Amoebiasis

Figure 1 Figure 2

Figure 1 - Trichrome stain of Entamoeba histolytica trophozoites in amebiasis. Two diagnostic characteristics are observed. Two trophozoites have ingested erythrocytes, and all 3 have nuclei with small, centrally located karyosomes. Figure 2 - Trichrome stain of an Entamoeba histolytica cyst in amebiasis. Each cyst has 4 nuclei with characteristically centrally located karyosomes. Cysts measure 12-15 mm.

Synonym: Amoebic dysentery History: Amoebic infection was first described by Fedor Losch in 1875 in St. Petersburg, Russia. In 1890, Sir William Osler reported the first North American case of amoebiasis, when he observed amoebae in stool and abscess fluid from a physician who previously resided in Panama. The species name E histolytica was first coined by Fritz Schaudin in 1903. In 1913, in the Philippines, Walker and Sellards documented the cyst as the infective form of E histolytica. The life cycle was then established by Dobell in 1925. Incubation Period: Severe infection is 3 days; Sub-acute and chronic form is several months; Average cases are 3-4 weeks. Causative Agent: Entamoeba histolytica

Pathophysiology: Ingestion of E. histolytica cyst Multiplication in the mucosa

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Endotoxin production, affecting the lining of the small intestines, colon, and capillaries

Necrosis of the mucosal layer

Ulceration Gangrene Toxemia Signs & Symptoms: Acute amoebic dysentery: Slight attack of diarrhea, altered with periods of constipation and often accompanied by tenesmus. Diarrhea, watery, and foul-smelling stools often containing blood-streaked mucus. Colic and gaseous distension of the lower abdomen. Nausea, flatulence, abdominal distension, and tenderness in the right iliac region over the colon.

Chronic amoebic dysentery: Attack of dysentery that lasts for several days, usually succeeded by constipation. Tenesmus accompanied by the desire to defecate. Anorexia, weight loss, and weakness. The liver may be enlarged. Stools at first are semifluid, but soon become watery, bloody, and mucoid. Vague abdominal distress, flatulence, constipation or irregularity of bowel movement. Mild toxemia, constant fatigue, and lassitude. The abdomen loses its elasticity when picked up between the fingers. On sigmoidoscopy, scattered ulceration, with yellowish and erythematous borders, is noted. The gangrenous type (fatal) is characterized by the appearance of large sloughs of intestinal tissues in the stools, accompanied by hemorrhage.
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Extraintestinal forms: Hepatic Pain in the RUQ with tenderness of the liver Jaundice Intermittent fever Loss of weight or anorexia Abscess may break through the lungs; patient coughs anchovy-sauce sauce.

Laboratory examinations: Stool examination - cyst; white and yellow pus with plenty of amoeba Blood examination - Leukocytosis Proctoscopy/Sigmoidoscopy

Medical Management: Medications: Metronidazole (Flagyl) Tetracycline Ampicillin, quinolone, sulfadiazine Streptomycin sulfate, chlorampenicol

Nursing Management: Observe isolation and enteric precaution. Proper collection of stool specimen: o Never give paraffin or any oil preparation for at least 48 hours prioi to the collection of specimen. o Instruct the patient to avoid mixing urine with stools. o If whole stools cannot be sent to the laboratory, select as large portions containing blood and mucus as possible. o Send the specimen immediately to the laboratory; stools that are not fresh are nearly useless for examination. o Label the specimen properly. Skin care: o Cleanliness and freedom from wrinkles on the sheet will be helpful with all the usual precautionary measures against pressure sores. Mouth care

Provide optimum comfort: o The patient should be kept warm. Dysenteric patient should never be allowed to feel cold, even for a moment. Diet: o During the acute stage, fluids should be forced. o In the beginning of an attack, cereals and strained meat broths without fat should be given. o Chicken and fish may be added when convalescence is established. o A bland diet without cellulose or bulk-producing foods should be maintained for a long time.

Health Teachings: Boil water for drinking or use purified water. Avoid washing food with water from open drums or pails. Cover leftover food. Wash hands after defecation and before eating. Avoid eating ground vegetables (lettuce, carrots and the like).

New Developments: Porcine colon explants in the study of innate immune response to Entamoeba histolytica.

Human amebiasis is caused by the protozoan Entamoeba histolytica. This protozoan is responsible for muco-hemorrhagic diarrhoea and liver abscess in affected populations. E. histolytica can be asymptomatic commensally confined to the intestinal lumen or can result in invasion of the colonic mucosa leading to ulceration and/or liver abscesses. Recently, human colonic explants have been identified as valuable in the study of host-parasite interactions. Here we investigated the potential of porcine colonic explants as an alternative to human tissues which are far less available. Porcine colonic explants were cultured with two strains of E. histolytica, one virulent (HM1:IMSS) and one avirulent (Rahman). Results from histopathological and real-time PCR analysis showed that porcine explants cultured with virulent ameba trophozoites react similarly to their human counterparts with an invasion of the tissue by the trophozoites and the triggering of typical innate immune response against the parasite. On the contrary, explants cultured with avirulent ameba trophozoites were preserved. The study open the way to the use of porcine colonic explants in the study of the complex interactions between the parasite and the host. Leptin signaling in intestinal epithelium mediates resistance to enteric infection by Entamoeba histolytica.

Leptin is an adipocytokine that links nutrition to immunity. Previous observation that a genetic polymorphism in the leptin receptor affected susceptibility
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to Entamoeba histolytica infection led to the hypothesis that leptin signaling has a protective role during intestinal amebic infection. In this study we show that mice lacking the functional leptin receptor developed devastating mucosal destruction after E. histolytica infection. Bone marrow chimera experiments demonstrated that leptin receptor expressed on hematopoietic cells was not sufficient to confer resistance. Similarly, peripheral knockout of the leptin receptor rendered animals susceptible, indicating that central expression of the leptin receptor was not sufficient to confer protection. The site of leptin action was localized to the gut via an intestinal epithelium-specific deletion of the leptin receptor, which rendered mice susceptible to infection and mucosal destruction by the parasite. Mutation of tyrosine 985 or 1138 in the intracellular domain of the leptin receptor, which mediates signaling through the SH2-containing tyrosine phosphatase/extracellular signal-regulated kinase (SHP2/ERK) and signal transducer and activator of transcription 3 (STAT3) pathways, respectively, demonstrated that both were important for mucosal protection. We conclude that leptin-mediated resistance to amebiasis is via its actions on intestinal epithelium rather than hematopoietic cells or the brain, and requires leptin receptor signaling through both the STAT3 and SHP2/ERK pathways.

Anthrax

Figure 1 Figure 3

Figure 2

Figure 1 -Polychrome methylene blue stain of Bacillus anthracis Figure 2 - Cutaneous anthrax Figure 3 - Inhalation anthrax. Chest radiograph with widened mediastinum 22 hours before death Figure 4 - Hemorrhagic meningitis resulting from inhalation anthrax Figure 5 - Note the central ulcer and eschar

History: Anthrax was described in the early literature of the Greeks, Romans, Egyptians, and Hindus. The term anthrakis means coal in Greek, and the disease is named after the black appearance of its cutaneous form. The fifth plague described in the Old Testament book of Genesis may be among the earliest descriptions of anthrax. At the end of the 19th century, Robert Koch's experiments with anthrax led to the original theory of bacteria and disease. John Bell's work in inhalational anthrax led to wool disinfection processes and the term woolsorter's disease.

A modern concern is use of anthrax as a biologic warfare agent. During the first Gulf War, Iraq reportedly produced 8500 L of anthrax. A total of 150,000 US troops were vaccinated with anthrax toxoid. In the weeks following the terrorist attacks of September 11, 2001, 22 confirmed or suspected cases of anthrax infection were disseminated via the US postal system; the spores mailed in these letters were ultimately traced to a US army medical research institute. Since there have been no cases of naturally occurring inhalational anthrax in the US since 1976, alarm should be raised for the occurrence of even a single infection. Incubation Period: few hours to 7 days Causative Agent:Bacillus anthracis

Pathophysiology: Precipitating factors: Inadequately-cooked food (meat) of infected animals Biological warfare Buthering Predisposing factor: Bacterium sporulates from soil

Skin contact w/ infected animal, animal product (raw meat), and insect bite Release of toxin in the skin

Ingestion of bacterium Infects intestines (terminal ileum and cecum) Abd. pain Nausea/ vomiting fever Occasional ascite Hemorrhagic lymphadenitis Sepsis

Inhalation of spores (Woolsorters disease) Deposits into alveoli or into alveolar Symptoms resembling severe viral resp. dse. Lymph nodes in mediastinum & thorax become inflamed & enlarged Septic shock Meningitis Hemorrhagic necrosis of affected lymph nodes

Small pimple or macule appears Ring of vesicle develop around papule Papules ulcerate Painless eschar develops and falls off Marked edema w/ pruritus, w/o pus and lesion not painful

Diarrhea (bloody)

Hypoxemia Signs & Symptoms: Cutaneous anthrax: Itching Papule Vesicle (vesicular fluid may exude) Lymph adenitis (inguinal area) Eschar

Hypotension

Hemorrhagic lymphadenitis

Inhalation anthrax: Resembles viral respiratory disease Hemorrhagic necrosis of nodes associated w/ hemorrhagic mediastinitis

GIT anthrax: Fever Nausea & vomiting Abdominal pain Bloody diarrhea Rapidly developing ascites

Acute phase o o o o o Fever Dyspnea Stridor Hypoxia Hypotension

Complications: Anthrax meningitis intense inflammation of the meninges of the brain and spinal cord. o Marked by elevated CSF pressure with bloody CSF, followed by rapid loss of consciousness and death. Anthrax sepsis develops after the lymphohematogenous spread of B. anthracis from the primary lesion. o Clinical features are high fever, toxemia and shock, with death following in a short time.

Laboratory examinations: Chest X-ray

Medical Management: Medications:

Parenteral penicillin G 2 million units every 6 hours, until edema subsides, with subsequent administration of oral penicillin for a seven-toten-day-course. Erythromycin, tetracycline, or chlorampenicol for patients who are sensitive to pencillin

Nursing Management: Careful history taking Thorough physical examination Skin care, psychological, emotional support Supportive measures are geared toward the type of anthrax exposure.

Health Teachings: Educate about modes of transmission Educate about care of skin abrasion Educate about personal cleanliness Educate about importance of disinfecting or sterilizing hair, wool, and bone meal or other feed of animal origin prior to pressing.

New Development: Sortase-conjugation generates a capsule vaccine that protects guinea pigs against Bacillus anthracis.

Capsules protect bacteria against phagocytic clearance. Capsular polysaccharides or polyglutamates have evolved also to resist antigen presentation by immune cells, thereby interfering with the production of opsonophagocytic antibodies. Linking capsular material to a carrier protein stimulates its presentation to the immune system. For many conjugate vaccines this is achieved by a process of random chemical cross-linking. Here we describe a new technology, designated sortase-conjugation, which generates a single amide bond between the C-terminal end of a carrier protein and the capsular material. Sortase-conjugation was used to link the poly-d--glutamic acid (PDGA) capsule of Bacillus anthracis to the receptor binding domain (D4) of protective antigen (PagA). When used as a vaccine, PDGAD4 conjugate elicited robust antibody responses against both capsule and D4. Immunization with PDGA-D4 afforded guinea pigs complete protection against anthrax challenge with wild-type or pagA mutant B. anthracis Ames.

Ascariasis

Figure 2

Figure 1

Figure 4

Figure 1 - Adult Ascaris lumbricoides. Figure 2 - The roundworm Ascaris lumbricoides causes ascariasis. Worms can reach 10-30 cm in length. Clinical disease results from effects of pulmonary larval migration, intestinal obstruction, or migration through the biliary tree. Figure 3 - Ascaris lumbricoides egg. Figure 4 - Adult Ascaris lumbricoides in biliary system.

Synonym: Roundworm infection History: Although A lumbricoides has been present in humans for many thousands of years, science only began to elucidate its biology in the 17th century, and effective chemotherapy was only developed in the late 20th century. The earliest recovered eggs
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are from the 30,000-year-old Upper-Paleolithic site of Arcy-sur-Cure in Yonne, France. Infertile eggs have been reported in coprolites dating to 2277 BCE from an archeological site at Los Gavilanes, Peru. Desiccated human feces from Big Bone Cave, Tennessee dating to approximately 2177 BCE contained A lumbricoides. In the Nubian aspect of the Nile River, eggs have been recovered inside a mummy dating to 2050-1750 BCE. In 1683, Tyson discussed " Lumbricus teres observations on the Round Worm bred in human bodies.that common Round Worm which children u[s]ually are troubled with." In 1758, Linnaeus proposed the name Ascaris lumbricoides. In 1856, Ransom reported that finding eggs in fecal samples was a reliable means of diagnosis. In 1862, Davaine concluded that ingested embryonated eggs produced ascariasis and that the infected host would produce eggs in feces that could pass the infection to another host. In the 1980s, several reviews noted the public health impact of STH infection and suggested control strategies using antihelminthic drugs, some of which were introduced in the 1960s (eg, pyrantel pantoate) and 1970s (eg, mebendazole). Causative Agent: Ascaris lumbricoides Pathognomonic Sign: Insatiable appetite, colicky periumbilical pain aggravated by cold stimulation (Nakamura sign) Pathophysiology: Embryonated ova is ingested to intestine Larvae penetrates the wall of the intestine (duodenum)

Larvae are picked up by lymphatics or bloodstream Carried to the liver Reach the stomach and esophagus Carried to the biliary tract Reach the heart RUQ pain

Nausea and vomiting

Poor appetite

Stays in the capillaries of the lungs Reaches the alveoli

URT Grows and molt for 10 days Migrates to the bronchioles, bronchi, trachea, and epiglottis Swallowed or ingested Cough Fever Rales Blood-tinged sputum

Nakamura sign

Adult ascaris stays in the small intestines

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Goes to the stomach, to the esophagus Intestinal obstruction Adult ascaris copulates in GIT Females lay eggs about 2-3 wks.

To the common bile duct and gall bladder Severe abdominal pain associated with vomiting Discharged into the feces and incubated in the soil for weeks

Signs & Symptoms: Larval stage: Nausea and vomiting, poor appetite Periumbilical pain RUQ pain Cough, fever, rales, blood-tinged sputum Nasal pruritus if larvae reach the nose

Adult stage: Colicky, periumbilical pain aggravated by cold stimulation (Nakamura sign) Intestinal obstruction may be caused by a bolus of entangled worms which may be palpable. Severe abdominal pain associated with vomiting.

Complications: Biliary tract obstruction; patient develops cholestatic jaundice Hepatic abscess and cholangitis Intestinal obstruction, perforation, peritonitis Malnutrition due to damage of the intestinal mucosa, which impairs the absorption of nutrients.

Laboratory examinations: Stool examination - Demonstration of fertilized or unfertilized eggs in the stools (Kato-Katz technique) Abdominal X-ray - Dense shadow of adult ascaris which looks like strands of spaghetti (dot sign)
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Routine blood counts - Significant eosinophilia

Medical Management: Medications: Albendazole or mebendazole Piperazine citrate Pyrantel pamoate

Nursing Management: Isolation is not needed. Preventive measures in each home and in the community should be enforced. All members of the family must be taught on sanitary practices such as washing of hands before handling food, washing of all fruits and vegetables that are eaten raw, and effective sewage disposal. Availability of toilet facilities must be ensured. Importance of personal hygiene should be explained. Proper disposal of diapers should be emphasized to mothers.

New Developments: Ascaris suum enolase is a potential vaccine candidate against ascariasis.

Ascariasis caused by Ascaris is the most common parasite problem in humans and pigs worldwide. No vaccines are available for the prevention of Ascaris infections. In the present study, the gene encoding Ascaris suum enolase (As-enol1) was amplified, cloned and sequenced. Amino acid sequence alignment indicated that As-enol-1 was highly conserved between different nematodes and shared the highest identity (87%) with enolase from Anisakis simplex s.l. The recombinant pVAX-Enol was successfully expressed in Marc-145 cells. The ability of the pVAXEnol for inducing immune protective responses against challenge infection with A. suum L3 was evaluated in Kunming mice. The immune response was evaluated by lymphoproliferative assay, cytokine and antibody measurements, and the reduction rate of recovery larvae. The results showed that the mice immunized with pVAXEnol developed a high level of specific antibody responses against A. suum, a strong lymphoproliferative response, and significant levels of IFN-, IL-2, IL-4 and IL10 production, compared with the other groups immunized with empty plasmid or blank controls, respectively. There was a 61.13% reduction (P<0.05) in larvae recovery compared with that in the blank control group. Our data indicated that A. suum enolase is a potential vaccine candidate against A. suum infection.

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Bacillary Dysentery

Figure 1

Figure 2

Figure 4

Figure 3

Figure 1 - Electron Micrograph of Shigella in a membrane-enclosed endosome of an epithelial cell Figure 2 - Endoscopic View of Colitis due to Shigellosis Figure 3 Shigella bacterium Figure 4 - This man developed necrosis of the intestines due to a Shigellosis infection resulting in his death.Shigella infection usually results in diarrhea, fever, and stomach cramps starting 1-2 days after exposure, which resolves in 5 to 7 days. However, the disease can be fatal, whereupon, necrosis of the bowel is also possible, as was the case here.

Synonym: Shigellosis History:

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They were recognized as the etiologic agents of bacillary dysentery or shigellosis in the 1890s. Shigella was adopted as a genus in the 1950s. Incubation Period: 7 hours 7 days; Average of 3 5 days Causative Agent: Shigella group: o o o o Shigella flexneri (Group B) Shigella boydii Shigella connei Shigella dysenteriae

Pathophysiology: Shigella bacterium ingested Invades intestinal mucosa Inflammation of the intestinal mucosa Dirty, green, fibrinous sloughing areas or ulcers are formed Rapid dehydration Colicky abdominal pain Diarrhea that is watery Loss of weight Diarrhea w/ bloody-mucoid stools Signs & Symptoms: Fever, especially in children Tenesmus, nausea, vomiting, and headache Colicky or cramping abdominal pain associated with anorexia and body weakness Diarrhea with bloody-mucoid stools that are watery at first Rapid dehydration and loss of weight

Complications:

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Rectal prolapsed, particularly in undernourished children Respiratory complications, such as cough and pneumonia Non-suppurative arthritis and peripheral neuropathy

Laboratory examinations: Fecalysis or microscopic examination of stools Isolation of the causative organism from rectal swab or culture Peripheral blood examination Blood culture Sheets of polymorphonuclear leukocytes seen in staining with methylene blue

Medical Management: Antibiotics are of question in the treatment of shigellosis; however, ampicillin, tetracycline, and cotrimoxazole may be useful in severe cases. IV might be infused with normal saline (with electrolytes) to prevent dehydration. Anti-diarrheal drugs are contraindicated because they delay fecal excretion that can lead to prolonged fever.

Nursing Management: Maintain fluid and electrolyte balance to prevent profound dehydration. Keep the patient warm and comfortable. Restrict food until nausea and vomiting subsides. Isolation can be carried out through medical aseptic technique. Personal hygiene must be maintained. Excreta must be properly disposed. Concurrent and terminal disinfection should be employed. Return to normal activities must be gradual because relapse may occur as a result of fatigue.

Health Teachings: Sanitary disposal of human feces. Sanitary supervision of processing, preparation, and serving of food, particularly those eaten raw.

New Development: Mucosal immunization with Shigella flexneri outer membrane vesicles induced protection in mice. Vaccination appears to be the only rational prophylactic approach to control shigellosis. Unfortunately, there is still no safe and efficacious vaccine available. We investigated the protection conferred by a new vaccine containing outer membrane
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vesicles (OMVs) from Shigella flexneri with an adjuvant based on nanoparticles in an experimental model of shigellosis in mice. OMVs were encapsulated in poly(anhydride) nanoparticles prepared by a solvent displacement method with the copolymer PMV/MA. OMVs loaded into NPs (NP-OMVs) were homogeneous and spherical in shape, with a size of 197nm (PdI=0.06). BALB/c mice (females, 9-weekold, 201g) were immunized by intradermal, nasal, ocular (20g) or oral route (100g) with free or encapsulated OMV. Thirty-five days after administration, mice were infected intranasally with a lethal dose of S. flexneri (110(7)CFU). The new vaccine was able to protect fully against infection when it was administered via mucosa. By intradermal route the NP-OMVs formulation increased the protection from 20%, obtained with free extract, to 100%. Interestingly, both OMVs and OMVNP induced full protection when administered by the nasal and conjuntival route. A strong association between the ratio of IL-12p40/IL-10 and protection was found. Moreover, low levels of IFN- correlate with protection. Under the experimental conditions used, the adjuvant did not induce any adverse effects. These results place OMVs among promising candidates to be used for vaccination against Shigellosis.

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AVIAN INFLUENZA

Definition Avian influenza (AI) is an infectious viral disease of birds (especially wild water fowl such as ducks and geese), often causing no apparent signs of illness. AI viruses can sometimes spread to domestic poultry and cause large-scale outbreaks of serious disease. Some of these AI viruses have also been reported to cross the species barrier and cause disease or subclinical infections in humans and other mammals. AI viruses are divided into two groups based on their ability to cause disease in poultry: high pathogenicity or low pathogenicity. Highly pathogenic viruses result in high death rates (up to 100% mortality within 48 hours) in some poultry species. Low pathogenicity viruses also cause outbreaks in poultry but are not generally associated with severe clinical disease.

History First identified in Italy in 1878, highly pathogenic avian influenza is characterized by sudden onset of severe disease, rapid contagion, and a mortality rate that can approach 100% within 48 hours. Human deaths from avian influenza were unknown until 1997, when six people in Hong Kong died from the particularly virulent H5N1 strain.

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In January 2004, a new major outbreak of H5N1 avian influenza surfaced again in Vietnam and Thailands poultry industry, and within weeks, spread to ten countries and religions in Asia including Indonesia, South Korea, Japan, and China. In February 2004, avian influenza virus was detected in pigs in Vietnam, increasing fears of the emergence of new variant strains. Fresh outbreaks in poultry were confirmed in Ayutthaya and Pathumthani provinces of Thailand, and Chaohu city in Anhui, China, in July 2004. In North America, the presence of avian influenza was confirmed at several poultry farms in British Columbia in February 2004. In August 2004 avian flu was confirmed in Kampung Paris, Kelantan, Malaysia. Two chickens were confirmed to be carrying H5N1.

Synonyms Avian Flu, bird flu, fowl plague, H5N1 Incubation Period The incubation period is three to five days. Causative Agent The causative agent is the avian influenza (A1) virus. A1 viruses all belong to the influenza virus, a genus of the Orthomyxoviridae family and are negative-stranded, and segmented.

Pathognomonic Sign

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Prolonged fever and body malaise

Pathophysiology

The pathophysiology of avian influenza differs from that of normal influenza. Avian influenza is still primarily a respiratory infection but involves more of the lower airways than human influenza typically does. This is likely due to differences in the hemagglutinin protein and the types of sialic acid residues to which the protein binds. Avian viruses tend to prefer sialic acid alpha (2-3) galactose, which, in humans, is found in the terminal bronchi and alveoli. Conversely, human viruses prefer sialic acid alpha (2-6) galactose, which is found on epithelial cells in the upper respiratory tract. One group has reported that ex vivo cultures of human tonsillar, adenoidal, and nasopharyngeal tissues can support replication of H5N1 avian influenza.

Colorized transmission electron micrograph shows avian influenza A H5N1 viruses (gold in color) Although this results in a more severe respiratory infection, it probably explains why few, if any, definite human-to-human transmissions of avian influenza have been reported: infection of the upper airways is probably required for efficient spread via coughing and sneezing. Many are concerned that subtle mutation of the hemagglutinin protein through antigenic drift will result in a virus capable of binding to upper and lower respiratory epithelium, creating the potential for pandemic spread. The functional role of these genetic markers has yet to be determined but likely involves replication enhancement and immune suppression. In contrast to human

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influenza, most deaths associated with avian influenza have been due to primary viral pneumonia, with no evidence of secondary bacterial infection.

Clinical Manifestations Fever Body weakness or muscle pain Cough Sore throat May have difficulty of breathing in severe cases Sore eyes Laboratory Examinations 1.) Polymerase chain reaction (PCR) tests Most laboratories and hospitals now offer nucleic acid (PCR)based studies. A nasal swab is submitted in special transport media to the laboratory, and results are reported within 24 hours. Some laboratories are able to differentiate between seasonal versus pandemic H1N1. Sensitivity for influenza is greater than 90%. These studies may be offered as respiratory panels, and they provide information on the presence of other viruses, such as respiratory syncytial virus (RSV) and adenovirus. 2.) Direct Immunofluorescent Tests Some laboratories offer direct immunofluorescent tests on fresh specimens, but these tests are labor-intensive and are less sensitive than culture methods. These tests require specially trained laboratory personnel for interpretation, and these personnel generally are not available during all shifts, even in large medical centers. 3.) Serologic Testing In order to overcome the expensive and time-consuming obstacle of culturing, several serologic tests have become available. In reality, many of these are not bedside tests; generally, 30-60 minutes are required to perform the test's multiple steps. Test sensitivities generally range from 60-70%. 4.) Testing for Avian Influenza a.) Hematology (CBC) may be more clinically useful in avian influenza than in seasonal influenza disease. Leukopenia (white blood cell count of 454-4900 cells/L), especially lymphopenia, is common and is observed in 50-80% of patients. In at least one study, lymphopenia at
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presentation (absolute lymphocyte count < 1500 cells/L) was a significant predictor of the progression to ARDS. More than half of patients will have mild-to-moderate thrombocytopenia.

b.) Liver function tests (LFTs) may be useful in differentiating illness from other febrile tropical diseases. Aminotransferase levels are elevated in more than half of all patients with avian influenza H5N1 infection. 5.) Radiography In elderly or high-risk patients with pulmonary symptoms, perform chest radiography to exclude pneumonia. Early radiographic findings include no or minimal bilateral symmetrical interstitial infiltrates. Later, bilateral symmetrical patch infiltrates become visible. Focal infiltrates indicate superimposed bacterial pneumonia. With avian influenza, pulmonary infiltrates are seen in almost all patients. The wide variety of radiographic characteristics range from diffuse or patchy infiltrates to lobar multilobar consolidation. Effusions and lymphadenopathy are also observed, as well as cystic changes (see the image below).

Chest radiograph of severe lung disease in a patient with avian influenza. In avian influenza, the severity of radiologically apparent disease is a good predictor of mortality, including findings consistent with acute respiratory distress syndrome (ARDS), such as a diffuse, bilateral ground-glass appearance. 6.) Alveolar-arterial gradient Severe hypoxemia is present in severe cases of influenza. The alveolararterial (A-a) gradient may be increased (>35 mm Hg). 7.) Lumbar puncture Patients with physical examination findings compatible with meningitis should undergo lumbar puncture.

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Medical Management The goals of pharmacotherapy are to reduce morbidity and to prevent complications. Agents include vaccines and antiviral drugs (i.e., amantadine, rimantadine, oseltamivir, zanamivir). The uricosuric agent probenecid may be used as an adjunct to antiviral treatment. Antiviral Agents Antiviral drugs indicated for treatment of influenza include neuraminidase inhibitors (i.e., oseltamivir and zanamivir) and amantadine and rimantadine. Neuraminidase inhibitors act directly on the viral proteins, decreasing the virulence of infection. a.) Amantadine (Symmetrel) Amantadine is active against influenza A virus. It has little or no activity against influenza B virus isolates. Its mechanism of antiviral action is unclear. It prevents release of infectious viral nucleic acid into the host cell by interfering with the function of the transmembrane domain of the viral M2 protein. In certain cases, amantadine is known to prevent virus assembly during virus replication. b.) Rimantadine (Flumadine) Rimantadine inhibits viral replication of influenza A virus H1N1, H2N2, and H3N2. It prevents penetration of the virus into the host by inhibiting uncoating of influenza A. Resistant virus strains may develop and be transmitted. c.) Oseltamivir (Tamiflu) Oseltamivir inhibits neuraminidase, which is a glycoprotein on the surface of influenza virus that destroys an infected cell's receptor for viral hemagglutinin. By inhibiting viral neuraminidase, oseltamivir decreases the release of viruses from infected cells and thus, viral spread. d.) Zanamivir (Relenza) Zanamivir is an inhibitor of neuraminidase, which is a glycoprotein on the surface of the influenza virus that destroys the infected cell's receptor for viral hemagglutinin. By inhibiting viral neuraminidase, release of viruses from infected cells and viral spread are decreased. This agent is
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effective against both influenza A and B; its efficacy against avian influenza is not well established. Vaccines Influenza A and B vaccine is administered each year prior to flu season. The CDC analyzes the vaccine subtypes each year and makes any necessary changes based on worldwide trends. In April 2007, the US Food and Drug Administration (FDA) approved the first vaccine for H5N1 influenza (i.e., avian influenza or bird flu). It is available only to government agencies and for stockpiles. a.) Influenza virus vaccine (Afluria, FluLaval, Fluarix, Fluvirin, Fluzone, Fluzone High-Dose, Fluzone Intradermal) Influenza vaccine is indicated for active immunization to prevent infection from influenza A and B viruses. The vaccine induces antibodies specific to virus strains contained in the vaccine. b.) Influenza virus vaccine, intranasal (FluMist, FluMist Quadrivalent) Intranasal influenza vaccine is indicated for active immunization to prevent influenza A and B viruses in healthy children, adolescents, and adults. Each year, the FDA-approved seasonal influenza vaccine includes three strains of influenza virus, two strains of influenza A and one of influenza B. The vaccine induces antibodies specific to virus strains contained in vaccine. c.) Influenza virus vaccine (H5N1) The H5N1 inactivated virus vaccine induces antibodies against viral hemagglutinin, thereby blocking viral attachment to human respiratory tract epithelial cells. The vaccine is estimated to reduce the risk of contracting avian influenza by 45%. This vaccine is indicated for active immunization of adults at increased risk of exposure to the H5N1 influenza virus subtype. Uricosuric Agents Agents that inhibit the tubular secretion of the active metabolite of the drug may be used as adjunctive therapy with the antiviral drug oseltamivir. a.) Probenecid This agent inhibits tubular secretion of the active metabolite of oseltamivir, reducing the clearance by approximately 50% and approximately doubling systemic exposure to oseltamivir.

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Nursing Management 1.) Patients will be isolated in designated hospital using hospital referral network. 2.) Early recognition of cases of highly pathogenic Avian Influenza (HPAI) during outbreak among poultry. 3.) Assign a specific area for triage of patients who may have avian influenza. 4.) Screen patients for travel history, symptoms and/ or close contact with cases. 5.) Barrier nursing technique for suspected and probable cases. 6.) Utilize personal protective equipment (PPE0 which include the wearing of N-95 respirator mask, goggles (protective eyewear), disposable gown and gloves, cap and shoe cover. 7.) Apply the principles of handwashing and when: before and after patient contact; after removing gloves; after contact with blood and other body fluids; after using the toilet; after blowing wiping of nose; before eating and before preparing the food.

Health Teachings Patient advisory is the most important in rendering the essential prevention for the disease. 1.) Wash hands thoroughly with soap and water before and after handling live and dressed chicken. 2.) Cook chicken thoroughly. 3.) Do not sell live chickens and other birds in the market while there is a threat of bird flu. 4.) Do not let chickens roam freely. Keep them in cages or pens. 5.) Do not place chicken, ducks and pigs together in one area, cage or pen. 6.) Do not catch, get near or keep in captivity wild birds. 7.) Report to the nearest agricultural/veterinary office any unusual death or illness of chickens and other birds. 8.) Report to the nearest local health centers any case of respiratory illness with history of exposure to sick or dead chickens and other birds. 9.) Individuals at risk are those directly exposed to sick chicken and other birds. The government thereby advises prospective travelers to countries affected with bird flu not to go to bird parks, poultry farms and markets where live chicken and other birds are sold. References Navales (2010)Handbook of Common Communicable and Infectious Diseases.3rd Edition. C & E Publishing, Inc.

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Cuevas et al (2007) Public Health Nursing in the Philippines. 10th Edition. Publications Committee. National League of Philippine Government Nurses, Incorporated.

BOTULISM

Definition Botulism is a serious illness that causes flaccid paralysis of muscles. It is caused by a neurotoxin, generically called botulinum toxin, produced by the bacterium Clostridium botulinum (and rarely by C. butyricum and C. baratii). The word came from the Latin botulus, (sausage), a rare butserious paralytic illness caused by the bacterium C. botulinum.

There are three human forms of botulism: 1. Foodborne (classical) botulism usually results from ingestion of inadequately cooked contaminated food, especially those with low acid content. 2. Wound botulism, also known as cutaneous botulism, is characterized by the formation of ulcers with sharply demarcated edges and a membranous base a result of deposition of toxin in the area. 3. Infant botulism usually afflicts infants aged 3-20 weeks. The disease can produce hypotonic (floppy) infant syndrome, manifested by constipation, feeble cry, depressed gag reflex, and inability to suck. History The recorded history of botulism begins in 1735, when the disease was first associated with German sausage (food-borne disease or food poisoningafter eating sausage). In 1870, a German physician by the name of Muller derived the name botulism from the Latin word for sausage. Clostridium botulinum bacteria were first isolated in 1895, and a neurotoxin that it
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produces was isolated in 1944 by Dr. Edward Schantz. From1949 to the 1950s, the toxin (named BoNT A) was shown to block neuromuscular transmissions by blocking the release of acetylcholine from motor nerve endings. Botulism toxin(s) are some of the most toxic substances known to man; while the toxin has been considered for use as a biological weapon, it has also been used to treat many medical conditions. In 1980, Dr. Scott used the toxin to treat strabismus (deviation of the eye), and in December 1989, BoNT-A (BOTOX) was approved by the U.S. Food and Drug Administration (FDA) for the treatment of strabismus, blepharospasm, and hemifacial spasm in young patients. The use of BOTOX to treat glabellar lines (wrinkles and frown lines) was approved in 2002 by the FDA for cosmetic improvements; the FDA has approved many additional uses (for example, underarm sweating, and muscle pain disorders) since 2002. Pathogenesis All the three forms produce disease via a final common pathway. The toxin is disseminated to peripheral cholinergic synapses and blocks acetylcholamine, causing impaired autonomic and voluntary neuromuscular transmission.

Clinical Characteristics Regardless of the source of botulinal toxin, i.e., whether ingested from food or produced in a wound or from infant gut, flaccid paralysis first affects and descends via the bulbar musculature. The somatic musculature is the next part to be affected and the patient may have generalized weakness. Because the toxin is blood-borne, paralysis almost invariably displays symmetry as it descends. Neurological symptoms are as follows: o Diplopia and blurred vision. o Ptosis, dry mouth, dysphagia and dysarthria. Classic symptoms of botulism include:

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o Double vision, blurred vision, drooping eyelids. o Slurred speech, difficulty swallowing, and dry mouth. o Muscle weakness. o Weak cry and poor muscle tone. o The symptoms may continue to paralytic ileus with severe constipation and lead to body paralysis. Complications Pneumonia Urinary tract infection Pulmonary embolism Decubitus ulcer Flexion contractures

Treatment/ Management Supportive care is needed, with particular attention to respiratory and nutritional needs. In foodborne botulism, emetics and gastric lavage are recommended. In wound botulism, exploration and debridement of the site need to be undertaken.

Common Nursing Diagnosis Impaired physical mobility Potential impairment of skin integrity Alteration in bowel elimination Pain and discomfort Altered nutrition: Less than body requirement Anxiety

Prevention and control Health education through instruction on proper preparation of food, specially on home canning is necessary. Infant botulism can be prevented by not giving infants food with honey, as it is known to contain C. Botulinum. Promptly report suspected cases or an outbreak of foodborne botulism.

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CANDIDIASIS

Synonym Moniliasis Candidasis

Definition A yeast infection results from an overgrowth of yeast (a type of fungus) anywhere in the body. Candidiasis is by far the most common type of yeast infection. An infection that ranges from a mild superficial fungal infection, to systemic and potentially life-threatening disease. Most often, candidiasis infects the: o Nails (onychomycosis) o Skin (diaper rush) o Mucous membrane particularly those of the oropharynx (thrush) o Vagina (monillasis) o Esophagus
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o GIT Infectious Agent Candida albicans o These organisms are part of the normal flora of the GIT, mouth, vagina, and skin. o There are more than 20 species ofCandida, the most common being Candida albicans. o These fungi live on all surfaces of our bodies. Under certain conditions, they can become so numerous they cause infections, particularly in warm and moist areas. Examples of such infections are vaginal yeast infections, thrush(infection of tissues of the oral cavity), skin and diaper rash, and nailbed infections. o Candidal infections commonly occur in warm moist body areas, such as underarms. Usually your skin effectively blocks yeast, but any breakdown or cuts in the skin may allow this organism to penetrate. Signs and Symptoms The skin is scaly, erythematous and popular rash is present, sometimes covered with exudates appearing below the breasts, between the fingers, and the axillae, groin and umbilicus. Nails are red and swollen; the nailbeds are darkened; there is occasional purulent discharge; and the separation of pruritic nails from nailbeds is evident. In women, signs and symptoms of avaginal yeast infection are a white discharge that is thick and often described as having a cottage cheese appearance. The infection typically causes itching and irritates the vagina and surrounding outer tissues. On occasion there may be pain with sexual intercourse or burning with urination. In infants and adults, a candidal infection can appear many different ways. Oral candidiasis is called thrush. Thick, white lacy patches on top of a red base can form on the tongue, palate, or elsewhere inside the mouth. These patches sometimes look like milk curds but cannot be wiped away as easily as milk can. If the white plaques are wiped away with a blade or cotton-tipped applicator, the underlying tissue may bleed. This infection also may make the tongue look red without the white coating. Thrush can be painful and make it difficult to eat. Care should be given to make sure a person with thrush does not become dehydrated. Thrush was formerly referred to as moniliasis, based upon an older name for Candid albicans (Monilia).

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In people with weakened immune systems, candidal infections can affect various internal organs and cause pain or dysfunction of the organ. People with suppressed immune systems due to AIDS, chemotherapy, or other conditions may contract a yeast infection called esophagitis in their upper gastrointestinal (GI) systems. This infection is similar to thrush but extends down the mouth and esophagus to the stomach. Candida esophagitis can cause painful ulcers throughout the GI system, making it too painful to swallow even liquids. If the infection spreads into the intestines, food may be poorly absorbed. People with this condition are in danger of becomingdehydrated. There may be associated pain in the area of the sternum (breast bone), pain in the upper abdomen, and/or nausea and vomiting.

Diagnosis Stool culture Gram staining of the skin, vaginal discharge, or scrapings

Nursing Management Avoid sharing utensils. Meticulous mouth care. Proper disposal of oral secretions.

Treatment Nystatin, for oral thrush. Clitrimazole, fluconazole, ketoconazole, for mucous membrane and vaginal infections. Fluconazole or amphotericin for infection.

Prevention Check high risk patient daily for patchy areas of irritation, sore throat, and gum bleeding. Check vaginal discharge and note the color, odor and amount.

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CHANCROID

Synonym Soft chancre Soft sore Sulcus mole

Definition Chancroid is a sexually transmitted disease characterized by painful genital ulcers and inguinal adenitis. It affects males more than females. Chancroid is a bacterial disease that is spread only through sexual contact.

Infectious Agent Chancroid is caused by a type of bacteria called Haemophilus discreyi. o The disease is found mainly in developing and third world countries.

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o Only a small number of cases (less than 50) are diagnosed in the United States each year. Most people in the U.S. who are diagnosed with chancroid have traveled outside the country to areas where the disease is known to occur more often. o Uncircumcised men are at much higher risk than circumcised men for getting chancroid from an infected partner. Chancroid is a risk factor for contracting the HIV virus. Incubation Period The incubation period is 1-14 days, with an average of 3-5 days.

Symptoms Small lesions appear at the groin or inner thigh. In males, it may appear on the penis andin females, on the vulva, vagina and the cervix. Within 1 day - 2 weeks after getting chancroid, a person will get a small bump in the genitals. The bump becomes an ulcer within a day of its appearance. The ulcer: o Ranges in size from 1/8 inch to 2 inches across o Is painful o Is soft o Has sharply defined borders o Has a base that is covered with a grey or yellowish-grey material o Has a base that bleeds easily if it is banged or scraped During the healing stage, phimosis may develop.

Diagnosis Gram stain of ulcer exudates Biopsy Darkfield examination and serologic test.
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Treatment The infection is treated with antibiotics, including azithromycin, ceftriaxone, ciprofloxacin, and erythromycin. Large lymph node swellings need to be drained, either with a needle or local surgery.

Nursing Management Standard precaution should be practiced. Check for drug allergy. Lotion, cream or oil should be applied on lesions. Instruct the patient to abstain from sexual contact until healing is complete. The patient should wash his/her genitalia daily with soap and water.

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CHLAMYDIAL INFECTIONS

Definition Chlamydia is a sexually transmitted disease caused by the bacteria Chlamydia trachomatis. Chlamydia infection (from the Greek, meaning "cloak") is a common sexually transmitted infection (STI) in humans caused by the bacterium Chlamydia trachomatis.

Infectious Agent The term Chlamydia typically refers to Chlamydia trachomatis, the STD. But two other types of this bacteria can also lead to illness: o Chlamydia pneumonia, which can be spread through coughing and sneezing, and o Chlamydia psittaci, which birds can pass to humans.

Mode of Transmission The disease is transmitted through vaginal or rectal intercourse. The disease is also transmitted through oral-genital contact with an infected person. Conjunctivitis, otitis media, and pneumonia may develop in children born to mothers with chlamydial infection passed through the birth canal.

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Signs and symptoms Diagnosis Swab from the site of infection. Culture of aspirated materials ELISA Direct fluorescent antibody test Women with cervicitis may develop cervical erosion, mucupurulent discharges, pelvic pain, and dyspareunia. Women with endometritis or saliphitis may experience signs of pelvic inflammatory disease, such as pain and tenderness of the abdomen. Women with urethral syndrome may experience dysuria, pyuria and urinary frequency. Menwith epididymitis may experience painful scrotal swelling and urethral discharge.

Treatment Doxycycline oral for seven days Azithromycin in single dose

Nursing Management Practice universal precaution. Suggest that both partners should submit for HIV testing. Check newborn for signs of chlamydial infection.

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Chickenpox

Synonym: Varicella Definition: Is an acute and highly contagious disease of viral etiology that is characterized by vesicular eruptions on the skin and mucous membrane with mild constitutional symptoms. Incubation Period: The incubation period is 10 to 21 days or may be prolonged after passive immunization against chickenpox. Causative Agent: Herpesvirus varicellae- a DNA- containing virus 1. Human beings are the only source of infection. 2. This is closely related or identical to herpes zoster virus. Pathognomonic Sign: Vesicular lesions

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Pathophysiology: After initial droplets inhalation of contaminate respiratory

Viral proliferation in regional lymph nodes of the upper respiratory tract

A second round of viral replication occurs in the bodys internal organs, the liver and the spleen

This secondary viremia is characterized by diffused viral invasion of capillary endothelial cells and the dermis

VZV infection of cells of the Malphigian layer produces both intercellular and intracellular edema

Resulting in the characteristic vesicle Signs and Symptoms: 1. Pre- eruptive manifestations are mi9ld fever and malaise. 2. Eruptive Stage: a. Rash starts on the trunk (unexposed area), then spreads to other parts of the body. b. Initial lesions are distinctively red papules whose contents become milky and pus- like within four days. c. In adults and bigger children, the lesions are more widespread and more severe. d. There is rapid progression so that transition is completed in six to eight hours. e. Vesicular lesions are very pruritic. f. All stages are present simultaneously before all are covered with scabs, leading to the appearance known as celestial map. g. The stages are characterized as follows: Macule is a lesion that is not elevated above the skin surface.

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 Papule is a lesion that is elevated above the skin surface with a diameter of about 3 mm. Vesicle is a pop- like eruption filled with fluid. The thin- walled vesicle easily bursts and dries up in three to five days. Pustule is a vesicle that is infected or filled with pus. If the lesion becomes infected that scar may be big and wide. Crust is a scab or eschar. This is a secondary lesion caused by the secretion of vesicle drying on the skin. The scars are superficial, depigmented and take time to fade out. Laboratory Exams: Determination of the V- Z virus through the complement fixation test. Determination of the V- Z virus through electron microscopic examination of vesicylar fluid. Complications: Chickenpox is rarely fatal, although it is generally more severe in adults than in children. Pregnant women and those with a suppressed immune system are at the highest risk of serious complications. The most common late complication of chickenpox is shingles, caused by reactivation of the varicella zoster virus decades after the initial episode of chickenpox. Secondary infection of the lesions- furuncles, cellulitis, skin abscess, erysipelas Meningoencephalitis Pneumonia Sepsis Medical Management: Oral acyclovir 800mg 3x a day for five days must also be given. Oral antihistamine can be taken to symptomatic pruritus. Calamine lotion eases itchiness. Salicylates must not be given. Antipyretic might be given for fever. Antihistamine must be given. Nursing Management: 1. Respiratory isolation is a must until all vesicles have crusted. 2. Prevent secondary infection of the skin lesions through hygienic care of the patient. 3. Attention should be given to nasopharyngeal secretions and discharges. Linens must be disinfected under the sunlight or through boiling. 4. Cut fingernails short and wash hands more often to minimize bacterial infections that may be introduced by scratching. 5. A child must wear mittens. 6. Provide activities to keep child occupied to lessen pruritus. 7. Observe oral and nasal care as rashes may appear in the buccal cavity.

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Cholera
Synonym: El Tor Definition: Is an acute bacterial enteric disease of the GIT characterized by profuse diarrhea, vomiting, massive loss of fluid and electrolytes, which could result in hypovolemic shock, acidosis and death. Incubation Period: The incubation period ranges from a few hours to five days, usually one to three days. Causative Agent: Vibrio cholera/ Vibrio coma

1. The organism is a slightly curved rod (comma- shaped), Gram negative and motile with a polar flagellum. 2. The organism survives well at ordinary temperaturs and multiplies well in temperatures ranging from 22- 40 degrees centigrade. 3. They survive longer in refrigerated foods. 4. An enterotoxin, choleragen, is elaborated by the organism as it grows in the intestinal tract. Pathognomonic Sign: Rice- water stools Pathophysiology:

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1. Fluid loss is attributed to the enterotoxin elaborated by the organism as it lies in opposition with the lining cells of the intestines. 2. The toxin stimulates adenylate cyclase, which results in the conversion of adenosine triphosphate (ATP) to cyclic adesine monophosphate (cAMP). 3. The mucosal cells are stimulated to increase the secretion of chloride. The increased secretion is associated with water and bicarbonate loss. 4. The toxin acts upon the intact epithelium on the vasculature of the bowel, thus resulting in the outpouring of intestinal fluids. 5. Fluid loss of 5 to 10% of the body weight results in dehydration and metabolic acidosis. 6. If treatment is delayed or inadequate, acute renal failure and hypokalemia become secondary problems. Signs and Symptoms: 1. There is an acute, profuse, waterydiarrhea with no tenesmus or intestinal cramping. 2. Initially, the stool is brown and contains fecal material, but soon becomes pale gray and rice water- like in appearance, with an inoffensive, slightly fishy odor. 3. Vomiting often occurs after diarrhea has been established. 4. Diarrhea causes fluid loss amounting to 1- 30 liters per day, owing to subsequent dehydration and electrolyte loss. 5. Tissue turgor is poor and eyes are sunken into the orbits. 6. The skin is cold; the fingers and toes are wrinkled, assuming the characteristic washerwomans hand. 7. Radial pulses become imperceptible and blood pressure unobtainable 8. Cyanosis is present. 9. The voice becomes hoarse and then is lost, such that the patient speaks in whispers (aphonia). 10. Breathing is rapid and deep. 11. Despite marked diminished peripheral circulation, consciousness is present. 12. The patient develops oliguria and sometimes even anuria. 13. Temperature could be normal at the onset of the disease but becomes subnormal in later stages, especially if the patient is in shock. 14. When the patient is in deep shock, the passage of diarrhea stops. 15. Death may come as rapidly as four hours after onset, but usually on the first or the second day if not properly treated. Laboratory Exams: Rectal swab Darkfield or phase microscopy Stool exam Medical Management: Treatment of cholera consists of correcting the basic abnormalitifes without delarestoring the circulating blood volume and blood electrolytes to normal levels.
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1. Intravenous treatment is achieved by rapid intravenous infusion of an alkaline saline solution containing sodium, potassium, chloride, and bicarbonate ions in proportions comparable to that in water- stools. 2. Oral therapy rehydration can be completed by the oral route ( ORESOL, HYDRITES) unless contraindicated or if the patient is not vomiting. 3. Maintenance of the volume of fluid and electrolytes lost after rehydration. This is done by careful intake and output measurement. 4. Antibiotics a. Tetracycline 500 mg every 6 hours might be administered to adults; 125 mg/ kg body weight for children every 6 hours for 72 hours. b. Furazolidone 100 mg for adults and 125 mg/ kg for children might be given every 6 hours for 72 hours. c. Chloramphenicol may also be given 500 mg for adults and 18 mg/ kg for children every 6 hours for 72 hours. d. Cotrimoxazole may also be administered 8 mg/ kg for 72 hours. Nursing Management: 1. Medical aseptic protective care must be provided. Handwashing is imperative before any food item is handled. 2. Enteric isolation must be observed. 3. Vital signs must be recorded accurately. 4. Intake and output must be accurately measured. 5. A thorough and careful personal hygiene must be provided. 6. Excreta must be properly disposed of. 7. Concurrent disinfection must be applied. 8. Food must be properly prepared. 9. Environmental sanitation must be observed. 10. Weighing the patient provides additional data that there is no deficit in fluid input. 11. Appropriate diet is given according to the stage of recovery. Health Teaching: Food and water supply must be protected from fecal contamination. Water should be boiled or chlorianated. Milk should be pasteurized. Sanitary disposal of human excreta is a must. Sanitary supervision is important.

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Diphtheria
Definition: Is an acute bacterial disease that can infect the body in two areas: the throat (respiratory diphtheria) and the skin (skin or cutaneous diphtheria). Incubation Period: After being exposed to the bacterium, it usually takes two to five days for symptoms to develop. Causative Agent: Corynebacterium diphtheria (Klebs- Leoffler bacillus) 1. It is a toxin- producing organism that manufactures an exotoxin which is responsible for major pathologic changes. 2. It is a Gram positive, non- sporulating, and generallyaerobic. 3. The bacilli invade the superficial tissues with very limited extension beyond the mucous membrane, but soluble toxin is capable of producing severe fatal sequelae. 4. It is unstable and easily destroyed by light, heat and aging. 5. It is capable of damaging muscles and especially the kidneys, liver, cardiac nerves, and other tissues. 6. It has 3 strains of organisms: a. Gravis (severe) is the strain that produces the most severe and greatest number of fatal cases in Europe. b. Mitis( mild) is the strain that produces lesions extending to the larynx and lungs but is rarely a cause of death. c. Intermedius (intermediate) is related to gravis but results in a tendency to bleed. Pathophysiology: 1. The toxin is absorbed into the mucous membranes and causes destruction of the epithelium and superficial inflammatory response takes place. 2. Necrotic epithelium becomes embedded in exuding fibrin so that a grayish pseudomembrane is formed by leukocytes, fibrin, and necrotic tissues. Microorganisms that adhere to the underlying tissues leave a raw bleeding when detached. The size of the pseudomembrane reflects the amount of toxin produced. ( The larger the pseudomembrane, the more toxins are present in the blood stream and in the tissues. 3. The microorganisms are commonly seen over the tonsils, pharynx or larynx, so that any attempt to remove the pseudomembrane, exposes the tears the capillaries and results in bleeding. 4. The bacilli within the pseudomembrane continue to actively produce toxins that result in distant damage, particularly parechymatous degeneration, fatty infiltration, and necrosis in the musclesof the heart and in the liver, kidney and adrenals, sometimes accompanied by gross hemorrhage. 5. The toxin also produces nerve damage, resulting in paralysis of the soft palate, eye muscles, or extremities.

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Types: 1. Nasal 2. Tonsilar 3. Facial Nasopharyngeal 4. Laryngeal 5. Wound or cutaneous diphtheria

Signs and Symptoms: a. The onset of the disease is insidious, marked by a feeling of fatigue, malaise, slight sore throat, and elevation of temperature usually not exceeding 38 degrees Celsius. b. Inflammatory reaction is initiated by the body. Exudates consisting of leukocytes, RBC, and necrotic tissues begin to form. c. The exudates forming the membrane are grayish in appearance as they begin to form. As they thicken, they become dull white. d. Cervical adenitis with tenderness of the glands occurs. e. There is the presence of body malaise, weakness, and apathy, with a rapid pulse rate that becomes disproportionate to the low- grade fever. f. In severe cases, the entire neck becomes swollen, with edema extending to the chest. g. The swelling of the neck was given the name bulls neck form. h. If the membrane forms in the larynx, it may extend to the trachea, resulting in respiratory problem, in which cases, tracheostomy may be necessary. i. After administration of the antitoxin, the membrane begins to curl at the edges, separate, and flake off in large pieces. Other common symptoms of respiratory diphtheria include: 1. Breathing difficulty 2. Husky voice 3. Increased heart rate 4. Stridor (a shrill breathing sound heard on inspiration) 5. Nasal drainage/ secretions (serosanguinous with a foul smell)

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6. Swelling of the palate 7. Low- grade fever Laboratory Exams: Swab from nose and throat or other suspected lesions Virulence test Schick test Molony test Loeffler slant Complications: Myocarditis caused by the action of diphtheria toxin on the heart muscles Polyneuritis that includes paralysis of the soft palate, the ciliary muscles of the eyes, pharynx, larynx, or extremities Airway obstruction may lead to death through asphyxiation. Cervical adenitis Otitis media Brochopneumonia Medical Management: a. Penicillin is usually effective in treating respiratory diphtheria before it releases toxins in the blood. b. Antitoxin can be given in combination with penicillin c. Erythromycin, 40 mg/ kg bw in 4 doses for x 7 to 10 days. d. Supportive therapy Nursing Management: 1. Bed rest for at least two weeks. The patient must not be permitted to bathe by himself. The patient must avoid exertion during defecation in order to conserve energy and decrease cardiac workload. 2. Soft diet is recommended. Small, frequent feeding are advised. 3. Patient must be encouraged to drink fruit juices rich in vitamin C to maintain the alkalinity of the blood and increase his/ her resistance. 4. Ice collar must be applied to the neck. 5. Nose and throat must be taken care of.

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Kawasaki Disease

Synonym: Kawasaki syndrome and mucocutaneous lymph node syndrome History of the disease: Kawasaki disease (KD), first described in Japan in 1967 by Dr. Tomisaku Kawasaki. Kawasaki disease was initially presumed to occur only in Japan; but now this disease is known in the whole world. The first cases in the United States were reported in Hawaii in 1976. In poland 5 cases were recognized, and first time described in 1981. Definition: Kawasaki disease is a rare childhood illness that affects the blood vessels. But then most children return to normal activities.Kawasaki disease can harm the coronary arteries, which carry blood to the heart muscle. Most children who are treated recover from the disease without long-term problems. The disease is most common in children ages 1 to 2 years and is less common in children older than age 8. It does not spread from child to child (is not contagious).

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Incubation Period: The incubation period for Kawasaki disease is not known. Causative Agent: 1. Unknown cause 2. Toxic, allergic and immunologic causes have been suspected, but most investigators favor an infectious cause or an immune response to an infectious agent. Among classes of microorganism suspected of causing Kawasaki disease were bacteria, fungi, rickettsiae and a number of viruses. Recently, there has been considerable interest in the possibility, that Kawasaki disease is caused by RETROVIRUSES. Pathophysiology: In the earliest stages of the disease, the endothelial cells and the vascular media become edematous, but the internal elastic lamina remains intact. Then, approximately 7-9 days after the onset of fever, an influx of neutrophils occurs, which is quickly followed by a proliferation of CD8+ (cytotoxic) lymphocytes and immunoglobulin A producing plasma cells. The inflammatory cells secrete various cytokines (ie, tumor necrosis factor, vascular endothelial growth factor, monocyte chemotactic and activating factor), interleukins (that target the endothelial cells and result in a cascade of events that eventuates in fragmentation of the internal elastic lamina and vascular damage. In severely affected vessels, the media develops inflammation with necrosis of smooth muscle cells. The internal and external elastic laminae can split, leading to aneurysms.

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Signs and Symptoms:

A fever lasting at least 5 days. Red eyes. A body rash. Swollen, red, cracked lips and tongue. Swollen, red feet and hands. Swollen lymph nodes in the neck.

Laboratory Exams:

Complete blood count. This test counts the number of red blood cells and white blood cells. Urinalysis. This test can help determine whether illness is present. Sedimentation rate or C-reactive protein (CRP). These blood tests can help find out if inflammation exists. Complications: pericarditi myocarditis myocardial failure mitral regurgitation pneumonia diarrhea arthritis aseptic meningitis otitis media obstructive jaundice Nursing Management: Monitor the vital signs every hour. Note the persistence of fever and refer to the physician. Instruct the mother to do tepid sponge bath. Encourage increase of fluid intake if patient is not vomiting. Provide comfortable clothes for the child. Alley the fears and hopes of the family. Observe proper hand washing before and after each nursing procedure in order to prevent further infection. Medical Management:

Immunoglobulin (IVIG) medicine. This is given through a vein (intravenous, or IV) to reduce inflammation of the blood vessels. Aspirin to help pain and fever and to lower the risk of blood clots.

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ENCEPHALITIS

Definition Encephalitis is an inflammatory disease involving part or all of the nervous system, resulting in abnormal functioning of the brain and spinal cord.

Synonym Brain Fever Incubation Period The incubation period is typically 5 to 15 days, but may range from 4 to 21 days. Causative Agent It may be caused by a variety of pathologic agents, including bacteria, viruses, fungi, rickettsia, toxins, chemical substances, or trauma. Arthropod-borne encephalitis viruses belong to the group of arboviruses. The natural habitat of these viruses appears to be many species of wild birds and some domestic birds that live in a symbiotic relationship with several known species of mosquitoes, many of which belong to the Culex group. Classification 1.) Primary encephalitis is an infection caused by direct invasion of the CNS by the virus, resulting in an inflammatory reaction. The arthropod-borne viruses are as follows:

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a.) Eastern equine encephalitis (EEE) This is considered as a serious epidemic disease of horses. It principally affects children under five years of age. The virus can multiply in the Aedes sullicitans mosquito.

Eastern equine mosquito b.) Western equine encephalitis (WEE) Is a milder and usually affects adults.

Western equine mosquito c.) St. Louis encephalitis The virus is transmitted by the bite of an infected mosquito. The organism is believed to gain entrance through the olfactory tract. d.) Japanese encephalitis This is a potentially severe vital disease that is spread by the bite of an infected mosquito, Culex tritaeniorynchus, which lives in rural rice-growing and pig-farming regions. The mosquito breeds in flooded rice fields and standing water around planted fields. Once the mosquito is infected, it carries the virus and is capable of transmitting the disease for life.
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It is a mosquito-borne viral disease that can affect the central nervous system and cause several complications and even death. Japanese encephalitis can be a risk to travellers to rural areas where the disease is prevalent. This affects children five to ten years old, more in males than in females with a ratio of 3:1. The case fatality rate is 30 to 35%. The peak season for Japanese encephalitis is March to April and September to October. There is no specific treatment for Japanese encephalitis. 2.) Secondary encephalitis a.) Post-infection encephalitis is usually a complication or sequel to some viral diseases like measles, chicken pox, and mumps. b.) Post-vaccinal results after the client receive a vaccine, most commonly with the anti-rabies vaccine. Pathognomonic Sign Decorticate and decerebrate rigidity

Pathophysiology Portals of entry are virus specific. Many viruses are transmitted by humans, though most cases of HSE are thought to be reactivation of HSV lying dormant in the trigeminal ganglia. Mosquitoes or ticks inoculate arbovirus, and rabies virus is transferred via an infected animal bite or exposure to animal secretions. With some viruses, such as varicella-zoster virus (VZV) and cytomegalovirus (CMV), an immune-compromised state is usually necessary to develop clinically apparent encephalitis. In general, the virus replicates outside the CNS and gains entry

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to the CNS either by hematogenous spread or by travel along neural pathways (e.g., rabies virus, HSV, VZV). Once across the blood-brain barrier, the virus enters neural cells, with resultant disruption in cell functioning, perivascular congestion, hemorrhage, and a diffuse inflammatory response that disproportionately affects gray matter over white matter. Regional tropism associated with certain viruses is due to neuron cell membrane receptors found only in specific portions of the brain, with more intense focal pathology in these areas. A classic example is the HSV predilection for the inferior and medial temporal lobes. In contrast to viruses that invade gray matter directly, acute disseminated encephalitis and post-infectious encephalomyelitis (PIE), most commonly due to measles infection and associated with Epstein-Barr virus (EBV) and CMV infections, are immune-mediated processes that result in multifocal demyelination of perivenous white matter.

Clinical Manifestations 1.) Japanese encephalitis a.) Flu-like symptoms (fever, chills, headache, nausea, and vomiting) b.) Stiff neck, confusion, and neurologic manifestations occur within 72 hours (drowsiness, seizures, bizarre, coma) c.) Decreased IQ d.) Serious brain damage 3.) General manifestations a.) During the prodromal period (one to four days), the patient experiences fever, headache, dizziness, vomiting, and apathy. b.) The patient may experience chills, sore throat, conjunctivitis, arthralgia, myalgia, and abdominal pain. c.) Later, the patient shows encephalitic signs such as nuchal rigidity, ataxia, tremors, mental confusion, speech difficulties, stupor or hyperexcitability, convulsions, coma, and death. d.) Ocular palsy, ptosis, and flaccid paralysis e.) The patient may feel disturbances in swallowing, mastication, phonation, respiration, and movements of the muscles of the eyes or face. f.) The muscles of the different parts of the body contract uncontrollably and twitch.

Laboratory Examinations

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1.) Cerebrospinal fluid (CSF) analysis - examine a sample of the fluid surrounding the brain and spinal cord. This fluid is an ultrafiltrate of plasma. It is clear and colorless. It contains glucose, electrolytes, amino acids, and other small molecules found in plasma, but has very little protein and few cells. 2.) Serologic test 90% confirmatory, done on the 7th day of illness

3.) Enzyme-Linked Immunosorbent Assay (ELISA) / IgM - are utilized to detect substances that have antigenic properties, primarily proteins (as opposed to small molecules and ions such as glucoseand potassium). Some of these include hormones, bacterial antigens and antibodies. 4.) Polymerase chain reaction - enables researchers to produce millions of copies of a specific DNA sequence in approximately two hours. This automated process bypasses the need to use bacteria for amplifying DNA. Sequelae 1.) Motor disturbances a.) Persistent convulsions b.) Parkinsonian syndrome or paralysis agitans c.) Epilepsy 2.) Mental disturbances a.) Mental dullness b.) Mental deterioration c.) Lethargy d.) Mental depression e.) Sleep disturbances 3.) Endocrine disturbances a.) Patient may grow either fat or thin. b.) Sexual interest or activity is lost.

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Medical Management 1.) Treatment must be symptomatic and supportive. 2.) Convulsions must be controlled. 3.) Nose and throat secretions should be sanitarily disposed of. 4.) Tepid sponge bath (TSB) or alcohol sponges may be given if the temperature is excessively high. 5.) Unless patient is comatose, oral fluid should be encouraged. 6.) Oral care should be done strictly. 7.) A mouth gag and protective devices, such as bedrails, should be available in case convulsions occur. 8.) Intake and output records should be closely monitored. 9.) Patients should be observed for neurologic signs involving speech, swallowing difficulty, twitching, eye movements, and indications of paralysis. 10.) The beginning, duration, and frequency of all convulsions should be carefully observed and recorded. Nursing Management 1.) Provide comfort. Keep the patient in a quiet, well-ventilated room. Stretch linens. Encourage or perform oral hygiene on the patient. Do bed baths if not contraindicated. 2.) Prevent complications. Turn the patient to sides at least every 3-4 hours. Encourage increased oral fluid intake. Encourage high caloric intake. Moisten lips with mineral oil. Render tepid sponge bath (TSB) if febrile. 3.) Monitor intake and output. Health Teachings 1.) Preventive measures are directed toward the identification of mosquito vectors. 2.) Prevention and control must be geared toward the elimination of breeding places, destruction of larvae, screening of homes, and use of repellents. 3.) A broad public education program about all phases of preventive programs is important. References Navales (2010)Handbook of Common Communicable and Infectious Diseases.3rd Edition. C & E Publishing, Inc.

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Cuevas et al (2007) Public Health Nursing in the Philippines. 10th Edition. Publications Committee. National League of Philippine Government Nurses, Incorporated.

FILARIASIS

Definition Filariasis is a parasitic disease caused by the microscopic, threadlike African eye worm. The adult worm can live only in the human lymphatic system. The disease is an extremely debilitating and stigmatizing and affects men, women, and children. It affects the poor in both rural and urban areas. The disease is rarely fatal; however, it causes extensive disability, gross disfigurement, and untold suffering of millions of men, women, and children.

Synonym Elephantiasis Incubation Period

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The incubation period which starts from the entry of the infective larvae to the development of clinical manifestation is variable. Nevertheless, it ranges from 8-16 months. Causative Agents Wuchereria bancrofti is the causative agent of filariasis. It is a thread worm four to five centimetres long and affects the lymph nodes and lymph vessels of the legs, arms, vulva, and breasts. Brugia malayi shows manifestations resembling that of the bancroftian, but swelling of the extremities is confined to the areas below the knees and below the elbows. Brugia timori rarely affects the genitals. Loa loa is another filarial parasite in humans transmitted by the deer fly.

Pathognomonic Sign Hardening and thickening of the skin

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Pathophysiology

57

Clinical Manifestations Asymptomatic Stage

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Characterized by the presence of microfilariae in the peripheral blood. No clinical signs and symptoms of the disease. Some remain asymptomatic for years and in some instances for life. Others progress to acute and chronic stages. Microfilariae rate increases with age and then levels off. In most endemic areas including the Philippines, men have higher microfilariae rate than women. Acute Stage Starts when there are already manifestations such as: Lymphadenitis (inflammation of lymph nodes) Lymphangitis (inflammation of lymph vessels) In some cases, the male genitalia is affected leading to funiculitis, epidydimitis, or orchitis (redness, painful and tender scrotum) Chronic Stage Develop 10-15 years from the onset of the first attack. Immigrants from areas where filariasis is not endemic tend to develop this stage more often and much sooner (1-2 years) than do the indigenous population of endemic areas.

Laboratory Examinations 1.) Nocturnal blood examination (NBE) blood is taken from the patient at the patients residence or in the hospital after 8:00pm. 2.) Immunochromatographic test (ICT) it is the rapid assessment method. It is an antigen test that can be done daytime.

Medical Management

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1.) Ivermectin, albendazole, or diethylcarbamazine (DEC) are used in treatment and act by: a.) Eliminating the larvae, b.) Impairing the adult worms ability to reproduce, and c.) Act killing the adult worms. The above medications are started at low doses to prevent immunologic reactions triggered by the large number of dying parasites. 2.) Surgery may be performed to remove surplus tissue and provide a way to drain the fluid around the damaged lymphatic vessels. Surgery may also be used to minimize massive enlargement of the scrotum. 3.) Elephantiasis of the legs can also be eased by elevating the legs and providing support with elastic bandages. 4.) Diethylcarbamazine-fortified salt is helpful. Nursing Management 1.) Health education and information dissemination as to the mode of transmission must be carried out. 2.) Environmental sanitation and the destruction of the breeding places of mosquitoes must be emphasized. 3.) Psychological and emotional support to client and the family are necessary. 4.) Personal hygiene must be encouraged. 5.) The course of the disease must be explained to the client and his/ her family. Health Teachings Mosquitoes that carry the microscopic worms usually bite between the hours of dusk and dawn. It is therefore advised that people living in an area with filariasis should: 1.) Sleep under a mosquito net, 2.) Use mosquito repellent in the hours between dusk and dawn, and 3.) Take a yearly dose of medicine that kills the worms circulating in the blood. References Navales (2010)Handbook of Common Communicable and Infectious Diseases.3rd Edition. C & E Publishing, Inc. Cuevas et al (2007) Public Health Nursing in the Philippines. 10th Edition. Publications Committee. National League of Philippine Government Nurses, Incorporated.

FUNGAL INFECTIONS

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Definition Fungi can be harmful or beneficial. Mushrooms are one type of fungus, but the term can also refer to microorganisms that live on us. These microorganisms are harmless most of the time, but they sometimes can cause a problem called fungal infection. Sometimes people get fungal infections, but they are usually easy to treat because they seldom spread below the skin. Tinea Flava is a common, benign, superficial, cutaneous fungal infection, characterized by hypo- or hyperpigmentation on the skin, usually on the back or chest.

Pathology 1.) Malassezia furfur is a member of the normal human flora and is found in 18% of infants and in 90% to 100% of adults. 2.) The organism can be found in both the spore stage and the filamentous (hyphal) form. 3.) Even though Malassezia furfur is a component of normal flora, it can also be an opportunistic pathogen. 4.) The organism is considered to be a factor in other cutaneous diseases, including Ptyrosporum folliculitis, confluent and reticulate papillomatosis, seborrheic dermatitis, and some forms of atopic dermatitis

Tinea Barbae is a colonization of the bearded areas of the face and neck and is restricted to adult males only.

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Trichophytosis is used to designate a group of diseases caused by vegetable fungi, affecting various portions of the body in different ways.

Tinea Pedis is an infection that is usually appears between the toes characterized by red, dry, cracked, and itchy skin between the toes and can also affect toenails.

Tinea Cruris is the infection of the groin and upper thighs. Both men and women can be infected with the disease.

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Synonyms Tinea Flava (Tinea alba/ Tinea versicolor) Tinea Barbae (Barbers itch) Trichophytosis (Ringworm) Tinea Pedis (Athletes foot) Tinea Cruris (Jock itch) Incubation Period 1 to 7 days and ranges of 2 weeks Causative Agent Malassezia furfur (Tinea Flava) Trichophyton mentagrophytes (Tinea Barbae) originating from cattle. Trichophyton verrucosum (Tinea Barbae) originating from horses. Vegetable fungi (Trichophytosis) Trichophyton rubrum (Tinea Pedis) Epidermophyton floccosum (Tinea Cruris) Pathognomonic Sign Intense pruritus

Pathophysiology

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Clinical Manifestations Tinea Flava (Tinea alba/ Tinea versicolor)

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Hypo- and hyperpigmentation of the skin usually on the back or chest. Tinea Barbae (Barbers itch) Lesions are of three types: 1.) Mild superficial form, which causes erythema and perifollicular papules and pustules. Hair of the area maybe affected with endothrix, which causes brittleness and lustreless hair. 2.) Inflammatory or deep, pustular, kerion crusting around the hair. a.) Unilateral involvement of the neck, chin, or maxillary area, sparing the upper lip. b.) Nodular lesions covered with crusts and seropurulent materials ending up in an abscess-like appearance. c.) Hair becomes loose and brittle. d.) Permanent alopecia and scarring may be the final consequence. 3.) Circinate variety has a spreading vesiculo-pustular border with central scaling. Trichophytosis (Ringworm) There are two types of ringworm, the dry and the moist. 1.) The dry type is characterized by the presence of rounded macular areas of reddish or yellowish-brown color of varying size (may be large as a coin). Sometimes these areas are slightly elevated above the surrounding skin. The center tends to be paler than the periphery of the lesion. 2.) The moist type is less frequently seen. This may arise from the dry lesion and rapidly becomes pustular in the presence of a secondary infection. Tinea Pedis (Athletes foot) Some people manifest red, scaly bumps filled with pus on the plantar area and the sides of the feet. Tinea Cruris (Jock itch) The rash in the groin and upper thighs is itchy and oftentimes feels like burning.

Laboratory Examinations

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1.) Specimen collection Specimens for fungal microscopy and culture may be: A scraping of scale, best taken from the leading edge of the rash after the skin has been cleaned with alcohol. Skin stripped off with adhesive tape, which is then stuck on a glass slide. Hair which has been pulled out from the roots. Brushings from an area of scaly scalp. Nail clippings. Skin biopsy. Moist swab from a mucosal surface (inside the mouth or vagina) in a special transport medium. A swab should be taken from pustules in case of secondary bacterial infection. They are transported in a sterile container or a black paper envelope. 2.) Direct microscopy The material is examined by microscopy by one or more of these methods: Potassium hydroxide (KOH) preparation, stained with blue or black ink Unstained wet-mount Stained dried smear Histopathology of biopsy with special stains. Microscopy can identify a dermatophyte by the presence of: Fungal hyphae (branched filaments) making up a mycelium Arthrospores (broken-off spores) Arthroconidia (specialized external spores) Spores inside a hair (endothrix) or outside a hair (ectothrix). Fungal elements are sometimes difficult to find, especially if the tissue is very inflamed, so a negative result does not rule out fungal infection.

3.) Culture Culture identifies which organism is responsible for the infection: To find out the source of infection e.g. a particular animal
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To select the most suitable treatment. Growing the fungus in culture may take several weeks, incubated at 2530C. The specimen is inoculated into a medium such as Sabouraud's dextrose agar containing cycloheximide and chloramphenicol. The cycloheximide is left out if a mould requires identification. 4.) Blood tests Blood tests are not useful for the diagnosis of superficial fungal infections. But in subcutaneous and systemic infection, several tests may be useful.

Medical Management 1.) Therapeutic options include topical agents and oral medications. Topical applications are cheaper and safer. Topical agents include: a.) Miconazole b.) Clotrimazole c.) Ciclopirox colamine d.) Propylene glycol lotion e.) Topical terbinafine f.) Benzoyl peroxide 2.) These drugs are given as regular doses for two to three weeks until clinical resolution is achieved. 3.) Systemic antibiotics may be beneficial. Nursing Management

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1.) Patients should be cautioned to wear protective footwear at communal pools and baths and should attempt to keep their feet dry by limiting occlusive footwear. When occlusive footwear is worn, wearing cotton socks and adding a drying powder with antifungal action in the shoes may be helpful. 2.) Keep the affected skin clean and dry. Wash daily. Take care to dry between the toes and in the skin folds; use a hair dryer if necessary. Use your own towel. 3.) Advise the patient to carefully clean the shower or bath using bleach. 4.) Advise the patient to provide hot wash socks, towels, bathmats at a temperature of at least 60C. 5.) Regularly wash floors where the patient walks bare foot. 6.) Administer antiseptics as ordered. Health Teachings (General) 1.) 2.) 3.) 4.) 5.) 6.) Avoid contact with infected animals. Avoid sharing of combs and razors with infected individuals. Observe oral hygiene. Wash feet every day. Dry feet completely, especially the areas between the toes. Wear sandals or shower shoes when walking around in locker rooms, public pools, and public showers. 7.) Wear clean socks. If they get wet or damp, be sure to change them as soon as possible. 8.) Use medicated powder to the feet to help reduce perspiration. 9.) Keep the groin always clean and dry. 10.) Wear clean, cotton underwear and loose-fitting pants.

References Navales (2010)Handbook of Common Communicable and Infectious Diseases.3rd Edition. C & E Publishing, Inc. Cuevas et al (2007) Public Health Nursing in the Philippines. 10th Edition. Publications Committee. National League of Philippine Government Nurses, Incorporated.

German Measles

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Synonyms Rubella, Three-day Measles Definition An acute contagious disease characterized by mild constitutional symptoms and a rose-colored macular eruption which sometimes resemble measles and at other times, scarlet fever. It causes mild, feverish illness associated with rashes and aches in joints. It has teratogenic effect on the fetus.

Background Rubella is now rare because of widespread compliance with childhood immunization programs. The disease is usually a benign and inconsequential viral illness unless exposure occurs in utero. Congenital rubella syndrome is associated with clinically significant congenital malformations. The live-attenuated virus vaccine has decreased the incidence of rubella significantly, thereby decreasing congenital disease.

Infectious Agent Rubella virus (family togaviridae; genus rubivirus) Incubation Period Usually 14 to 21 days Pathognomonic Sign none

Pathophysiology The causative organism is a single-stranded RNA togavirus that is transmitted by means of respiratory droplets. The virus replicates in the nasopharynx and

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regional lymph nodes, resulting in viremia. The virus then may spread to the skin, CNS, synovial fluid, and transplacentally to a developing fetus. Period of Communicability Approximately 1 week before and 4 days after the onset of the rash, but is at its worst when the rash is at its peak. Highly communicable infants with congenital rubella may shed virus from months after birth.

Mode of Transmission Direct contact with nasopharyngeal secretions Air droplets Transplacental transmission in congenital rubella Infected infants shed large quantities of the virus through their pharyngeal secretions and urine, which serve as sources of infection to other contacts

Clinical Manifestations 1. Prodromal Period Low-grade fever Headache Malaise Mild coryza Conjunctivitis Post-auricular, sub-occipital, and posterior cervical lympadenopathy which occurs on the 3rd to the 5th days after onset

2. Eruptive Period A pinkish rash on the soft palate (Forchheimers spot), an exathematous rash that appears first on the face, spreading to the neck, the arms, trunk and legs Eruption appears after the onset of adenopathy Children usually present less or no constitutional symptoms The rash may last for 1 to 5 days and leaves no pigmentation nor desquamation Testicular pain in young adults Transient polyarthralgia and polyarthritis may occur in adults and occasionally in children

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Complications Encephalitis Neuritis Arthritis Arthralgias Rubella syndrome, manifested by: o Microcephaly o Mental retardation o Cataract o Deaf-mutism o Heart disease Risk of Congenital Malformation 100 % when maternal infection occurs on the 1st trimester of pregnancy or 1st month of gestation 4 % in the 2nd and 3rd trimesters of pregnancy 90 % of congenital rubella cases excrete the virus at birth and are therefore infectious 10 % the virus remains contagious until the 1st year of age of the infected child

Clinical Manifestations (Congenital Rubella) 1. Classic congenital rubella syndrome Intrauterine growth retardation; infant has low birth weight All manifestations of congenital rubella syndrome Thrombocytopenic purpura known as blueberry muffin skin Lethargy and hypothermia

2. Intrauterine infection May result in spontaneous abortion Birth of a live child who may have one or multiple birth anomalies such as: o Cleft palate, hare lip, talipes, and eruption of teeth o Cardiac defects (patent ductus arteriosus, atrial septal defect ) o Eye defects (glaucoma, retinopathy, micropthalmia, unequal-sized eyeballs)
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o Ear defects (deafness usually bilateral, abnormally-shaped ears) o Neurologic (microcephaly, mental retardation,psychomotor retardation, behavioral disturbances, vasomotor instability) Diagnostic Procedure Certain diagnosis can be made only by virus isolation and identification or by changes in antibody titers Rubella hemaglutination inhibiting antibodies present by 2nd day of rash and increase in quantity over the next 10-21 days Hemaglutiantion inhibition (HI) antibody test - accepted as the most useful technique for diagnosis

Medical Management Very little treatment is necessary; treatment is essentially symptomatic. Nursing Management The patient should be isolated. The patient should be advised to rest in bed until fever subsides. The patients room must be darkened to avoid photophobia. The patient must take a mild liquid but nourishing diet. The patients eyes should be irrigated with warm normal saline to relieve irritation. The ears must be taken care, do not apply heat or cold compress unless ordered. Care of the skin at eruptive stage, soap is omitted (has irritating effect) instead bicarbonate of soda in water or lotion to relieve itchiness and has soothing effect. Good ventilation is necessary. The spread of infection must be prevented. The occurrence of complications must also be prevented.

Prevention Administration of live attenuated vaccine (MMR). Pregnant women should avoid exposure to patients infected with the rubella virus. Administration of immune serum globulin one week after exposure to rubella Prevent spread of infection by minimizing contact with visitors
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GONORRHEA

Synonyms Clap/Flores Blancas/Gleet Definition Gonorrhea is a sexually-transmitted bacterial disease involving the mucosal lining of the genitourinary tract, the rectum, and pharynx. History The exact time of onset of gonorrhea as prevalent disease or epidemic cannot be accurately determined from the historical record. One of the first reliable notations occur in the Acts of the (English) Parliament. In 1161 this body passed a law to reduce the spread of "...the perilous infirmity of burning." The symptoms described are consistent with, but not diagnostic of, gonorrhea. A similar decree was passed by Louis IX in France in 1256, replacing regulation with banishment. Similar symptoms were noted at the siege of Acre.

Coincidental to, or dependent on, the appearance of a gonorrhea epidemic, several changes occurred in European medieval society. Cities hired public health doctors to treat afflicted patients without right of refusal. Pope Boniface rescinded the requirement that physicians complete studies for the lower orders of the Catholic priesthood. Medieval public health physicians in the employ of their cities were required to treat prostitutes infected with the "burning", as well as lepers and other epidemic victims. After Pope Boniface completely secularized the practice of medicine, physicians were more willing to treat a sexually transmitted disease.
Infectious Agent Neisseria gonorrhea or gonococcus

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1. 2. 3. 4. 5.

This is a Gram-negative coccus found in pairs. This coccus is non-spore former and non-motile. It is fragile and does not survive long outside the body. It is readily killed by drying, sunlight, and ultraviolet light. It may be killed by ordinary disinfectants.

Incubation Period The incubation period is from three to twenty-one days and averages from three to five days. Period of communicability The period of communicability of the disease is varied. The infected person remains communicable as long as the organisms are present in secretions and discharges.

Mode of Transmission 1. Bacteria are transmitted by contact with exudates from the mucous membranes of infected persons, usually as a result of a sexually activity. 2. Transmission may occur in utero upon the rupture of membranes, as observed in infants delivered by cesarean section after the membrane ruptures. 3. Bacteria are transmitted through direct contact with contaminated vaginal secretions of the mother as the baby comes out of the birth canal. 4. It may be acquired through sexual contact (orogenital, angogenital) between opposite sexes, as well as of the same sex. 5. Bacteria may also be transmitted through fomites. Pathology 1. After infection, gonococci become adherent to the urethral epithelium. 2. Penetration of the mucosa usually elicits an acute inflammatory response consisting mainly of polymorphonuclear leukocytes in the submucosa. 3. Inflammatory edema of the gland ducts or plugs of debris obstruct drainage to form microabscesses that may coalesce to form large abscesses. 4. Infection tends to spread along mucosal surfaces and may involve the fallopian tubea and the endometrium and evenyually enter the peritoneal cavity of women. 5. Scarring from this abscess formation or tubal involvement may lead to strictures and sterility. 6. A similar mechanism, epididymitis, and therefore, possible sterility may occur in men. Clinical Manifestations 1. In Females a. b. c. d. Burning sensation and frequent urination Yellowish purulent vaginal discharge Redness and swelling of the genitals Burning sensation ad itching of the vaginal area. 74

e. Urinary frequency and pain on urination f. Urethritis or cervicitis occurs initially a few days after exposure g. Endometritis salpingitis or pelvic peritonitis are symptoms of uterine invasion which may lead to infertility. There is the presence of early signs of pelvic infection like fever, nausea and vomiting, and abdominal pain/ thderness. h. Pregnant women with gonorrhea may infect the eye of her baby during the passage through the birth canal.

2. In Males After a three-to-six day incubation period, the following may be noted: a. Dysuria with purulent discharge (gleet) from the urethra two to seven days after exposure. b. Rectal infection is common in homosexuals. c. Inflammation of the urethra can cause strictures which can prevent the passage of urine. d. Prostatitis e. Urethritis f. Pelvic pain and fever Other Clinical Features Vary According To Site Involved (Longworth, 2004) 1. Urethra a. Dysuria b. Urinary frequency and incontinence c. Purulent discharge d. Itching e. Red and edematous meatus 2. Vulva a. Ocassional itching b. Burning and pain due to exudates from the adjacent infected area c. Vulva symptoms are more severe before puberty and after menopause 3. Vagina a. Engorgement, redness, and swelling b. Profuse purulent discharge 4. Pelvis a. Severe pelvic and lower abdominal pain b. Muscle rigidity, tenderness and abdominal distention c. Tachycardia may develop in patients with PID and salpingitis 5. Liver a. RUQ pain 6. Other possible symptoms include pharyngitis, tonsilits, rectal burning

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Complications 1. 2. 3. 4. 5. 6. Sterility and pelvic inflammatory disease in women Epididymitis Arthritis Endocarditis Conjunctivitis Meningitis

Diagmostic exam 1. In females- culture of specimen taken from the cervix and anal canal (inoculation of specimen on Thayer-Martin medium. The medium conatins antibiotic that inhibits the growth of microorganisms. 2. In males- Gram stain Treatment Modalities 1. For uncomplicated gonorrhea in adults- ceftriaxone 125-250 mg IM single dose; doxycycline 100 mg orally BID x seven days. 2. For pregnant women- ceftriaxone, 125- 250 mg IM, single dose, plus erythromycin 500 mg orally for seven days. 3. Aqueous procaine penicillin- 4 million units injected intramuscularly after a negative skin test. 4. Recommended initial regimen for disseminated gonococcal infection in adults and adolescents is 1 gram ceftriaxone IM IV every 24 hours, or for patients allergic to betalactam antibiotics, 2 g spectinomycin IM every 12 hours. 5. All regimen should be continued for 24 to 48 hours after improvement begins, then therapy may be switched to the following regimens to complete one full week of antimicrobial therapy. a. 400 mg cefime p.o twice daily or 500 mg ciprofloxacin p.o 2x daily.Ciprofloxacin is contraindicated for children, adolescents, and pregnant lactating women. b. Treatment for gonoccoccal conjunctivits requires 1 g single dose ceftriaxone IM and irrigation of infected eye with normal saline solution. Nursing Management 1. Before treatment, ask the patient whether he/she has drug sensitivities and watch closely for adverse effects during therapy. 2. Explain to the patient that until cultures prove negative, he/she is still infectious and can transmit gonoccoccal infection. 3. Practice standard precautions. 4. All information concerning the patient is considered confidential. There should e no discussion concerning the patient and the laboratory reports. 5. The patient should be isolated until he/she recovers from the disease. 6. For a ptient with gonoccoccal arthririts, apply moist hea to relieve pain on the affected site. 7. Infants born to mothers positive for gonorrhea should e instilled with one percent silver nitrate or any recommended optahlmic prophylaxis onto both eyes at the time of birth. 8. Report all gonorrhoeal cases to health authorities, and for gonorrhea in children to Child Abuse Authorities. 76

9. Encourage patient to inform sexual contacts so that they can seek treatment. Advice them to refrain from sexual intercourse until treatment is completed. Signs of Gonoccocal Opthalmia Neonatorum Lid edema Bilateral conjunctival edema Abundant purulent discharge 2-3 days after birth Untreated gonoccocal conjunctivits can progress to corneal ulceration and blindness.

If not treated gonococcal ophthalmia neonatorum will develop in 28% of infants born to women with gonorrhea.

Common Nursing Diagnosis Altered sexuality pattern Social isolation Knowledge deficit Altered urinary isolation Risk for infection

Prevention and Control 1. Sex education, not only in schools, but also in the community, must emphasize the mode of transmission and the source of the inection. 2. Case finding, contact tracing. 3. Incidence of gonorrhea must be reported so that health authorities may be notified and contacts can be treated. 4.

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HEPATITIS

Definition Hepatitis is defined as inflammation of the liver, and is classified as either viral or nonviral. I. Hepatitis A ( Infectious hepatitis/ Catarrhal jaundice)

Hepatitis A is a liver disease caused by the hepatitis A virus. This inflammation of the liver is not really very severe and runs as acute course. This generally starts within two to six weeks after contact with the virus, and lasts no longer than two months. It is known as infectious hepatitis because it spreads relatively easy to individual who have close contact with the infected. Incubation Period The incubation period for hepatitis A ranges from 15 to 60 days, or three to five weeks, with a mean incubation period of 30 days.

Period of Communicability The infected patient is capable of transmitting the organism from a week before until a week after the appearance of symptoms. Mode of Transmission The virus is transmitted through the fecal-oral pathway: 1. ingestion of contaminated drinking water or ice, uncooked fruits and vegetables, and fruits and vegetables grown in or washed with contaminated water; and 2. contamination of food/drinks by infected food handlers. 3. 78

Groups at Risk for HAV 1. Children in day care centers can transmit the infection through diapers and toys. 2. Troops living in crowded conditions at military camps or in the field are at great risk. 3. Homosexual men are at an increased at risk of HAV infection from oral-anal sexual contact. 4. People who live in areas with a breakdown of sanitary conditions, such as after a flood or other natural disasters. Pathology/ Pathogenesis 1. Following ingestion, HAV enters the bloodstream through the epithelium of the oropharynx or intestines. 2. The blood carries the virus to its target, the liver, where it lives and multiplies within the hepocytes and Kupffer cells (i.e., liver macrophages). 3. Virions are secreted into the bile and released in stools. HAV is excreted in large quantities approximately 11 days prior to the appearance of symptoms or anti-HAV IgM antibodies in the blood. Clinical Manifestations 1. 2. 3. 4. 5. 6. 7. 8. Flu-like illness with chills and high fever. Diarrhea, fatigue and abdominal pain. Loss of apetite Nausea, diarrhea and fever Jaundice and dark-colored urine The infection in young children is often mild and asymptomatic. Hepatitis A does not have a chronic stage and does not case permanent liver damage. Following infection, the immune system makes antibodies against A virus that confer immunity against future infection. The disease can be prevented by A vaccine.

Complications 1. Progressive encephalopathy characterized by drowsiness and cerebral edema. 2. GIT bleeding progressing to stupor and later coma. Bleeding is not responsive to parenteral vitamin K administration. 3. Clonus and hyperflexia are later replaced by loss of deep tendon reflexes. 4. Edema and ascitis. 5. Aplastic anemia 6. In the late blood, respiratory failure, and cerebrovascular collapse may be present. Diagnostic Procedures 1. HAV and HBV- complement fixation rate 2. Liver function test- to determine the presence and extent of liver damage and check the progress of the liver. 3. Bile examination of stool and urine samples 4. SGOT- serum glumatic oxaloacetic transaminase SGT- Serum glutamic pyruvic transaminsae ALT- serum alanine transaminase 5. IgM level 79

Treatment Modalities 1. 2. 3. 4. 5. There is no specific treatment, although bde rest is essential. Diet must be high in carbohydrates, low in fat and low in protein. Patient must take vitamin supplements, especially the B complex group. Intravenous therapy is occasionally necessary. Isoprinosine (Methisoprenol) may enhance the cell- mediated immunity of the Tlymphocytes. 6. Alkalies, belladonna, and anti-emetics should be administered to control dyspepsia and malaise. Nursing Management 1. 2. 3. 4. 5. 6. 7. The patiet must be isolated (enteric solution). Patient should be encouraged to rest during the acute symptomatic phase. The patients nutritional status must be improved. Appropriates measures to minimize spread of the diseases must be taken. Observe the patient for melena and check for the presence of blood. Provide optimum skin and oral care. Increase the ability to carry out activities. a. Encourage the patient to limit the activity when fatigued. b. Assist the client in planning periods of rest and activity. c. Encourage gradual resumption of activities and mild exercise during recovery.

Prevention and Control 1. 2. 3. 4. 5. Hands should be washed thoroughly after using the toilet. Travelers should avoid water and ice if unsure of their purity. Food handlers should be carefully screened. Safe preparation and serving of food must be practiced. The public should be educated on the mode of transmission. II. HEPATITIS B (Serum hepatitis)

Hepatitis B is the inflammation of the liver caused by hepatitis B virus. This is considered to be more serious than hepatitis A due to the possibility of severe complications such as massive damage and hepatocarcinoma of the liver. It was once thought to be transmitted only through direct exchange of contaminated blood. Hepa B is now known to be transmitted also by contact with human secretions and stools. Recipient of plasma-derived products and hemodialysis clients are particularly at risk. Etiologic Agent The disease is caused by the Hepatitis B virus. 1. This virus has every limited tissue tropism. 2. HBV infects the liver and possibly the pancreas. 3. HBsAg appears in the blood 30 to 60 days after exposure and persist for variable periods of time.

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Incubation Period The incubation period is 50 to 189 days or 5 months with a mean equal to 90 days. Period of Communicability The patient is capable of transmitting the virus during the latter part of the incubation period and during the phase. The virus may persist in the blood for many years.

Mode of Transmission 1. Hepatitis B can be directly transmitted by person-to-person contact via infected body fluids. 2. It can be transmitted by through contaminated needles and syringes. 3. Transmission can occur through infected blood or body fluids introduced at birth. 4. It can also be transmitted through sexual contact. HBV transmission does not occur via: 1. the fecal-oral route 2. foodborne or waterborne transmission 3. arthropod (mosquito) transmission Pathogenesis 1. Hepatitis B virus primarily interferes with the functions of the liver by replicating in liver cells, known as hepatocytes. 2. During HBV infection, the host immune response causes both hepatocellular damage and viral clearance. 3. The virus replicates and large amounts of HBsAg are released into the blood, in addition to virons. 4. Initiation of virus replication may be soon as 3 days from acquisition,but symptoms may not be observed until after 45 days or much longer. 5. Replication of the virus is not cytopathic and proceeds for relatively long periods without causing liver damage. 6. During the acute phase of infection, the liver parenchyma shows degenerative changes consisting of cellular swelling and necrosis, especially in hepatocytes. Clinical Manifestations 1. Prodromal period a. fever, malaise, and anorexia b. Nausea, vomiting, abdominal discomfort, fever, chills c. Jaundice, dark urine and pale stools d. Recovery is indicated by a decline of fever and improved appetite. 2. Fulminant hepatitis may be fatal and manifested by severe symptoms like ascites and bleeding.

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Diagnostic Procedures 1. 2. 3. 4. 5. 6. 7. 8. Compliment fixation test Radio-immunoassay-hamaglutinin test Liver function test Bile examination in blood and urine Blood count Serum count Serum transaminase- SGOT, SGPT, ALT HBsAg

Prevention 1. Blood donors must be screened to exclude carriers. 2. Caution must be observed in giving care to patient infected with HBV. 3. Hands and other skin areas must be washed immediately and thotougly after contact with body fluids. 4. Avoid injury with sharp objects or instruments. 5. Use disposable needles and syringes only once and discard properly. 6. Avoid sharing toothbrushes, razors and other instruments that may be contaminated with blood. 7. Practice safe sex. 8. Get adequate rest, sleep, and exercise, and eat nutritious food. 9. Hepatitis B vaccine is recommended for pre-exposure. 10. Hepatitis immune globulin (HBIg) should be administered within 72 hours to those exposed directly to hepatitis B virus ingestion, prick or inoculation. III. HEPATITIS C

Is a blood-borne infectious diseased caused by the hepatitis C virus (HCV), originally known as non-A, non-B hepatitis The infection is often asymptomatic, but once established, can cause scarring of the liver (fibrosis) and eventually, cirrhosis (advance scarring). The hepa C virus is associated with a rate of chronic liver disease (chronic hepatitis, cirrhosis, and an increased risk for hepatocellular carcinoma). Clients with chronic hepatitis C are considered infectious. NO vaccine is available for hepatitis. IV. HEPATITIS D

Hepatitis D virus (also called delta virus) is a small, circular RNA virus. Hepatitis D virus is replication-defective and therefore cannot propagate in the absence of another virus. In humans, hepatitis D virus infection occurs only in the presence of hepatitis B infection. Hepatitis D virus infection is transmitted by blood and blood products. The risk factors for infection are similar to those in hepatitis B virus infection. A patient can acquire hepatitis D virus infection at the same time that he/she is infected with the hepatitis B virus. This is called co-infection. A patient can also be infected with hepatitis D virus at nay time during acute hepatitis B virus infection. This is called superinfection. 82

Found only in patients with an acute episode of or chronic hepatitis B and requires the presence of HbsAg. This virus depends on the double-shelled type B to replicate. For this season, type D infection does not outlast type B infection. Type D is rare in the United States, except among drug users. V. HEPATITIS E

Transmitted enterically (fecal-oral and waterborne routes), like hepatitis A. Hepatitis E virus is inconsistently shed in stools; therefore, direction is difficult. The hepatitis E virus (HEV) is a common cause of hepatitis that is transmitted via the intestinal tract. Spread is most often by drinking contaminated water. Hepatitis E never becomes a chronic (long-lasting) illness, but on rare occasions the acute illness damages and destroys so many liver cells that the liver can no longer function. This is called fulminant liver failure and may cause death. Pregnant women are at a much higher risk of dying from fulminant liver failure. The great majority of patients who recover from acute infection do not continue to carry HEV and cannot pass the infection to others.

Signs and Symptoms Assessment findings are similar for the different types of hepatitis. Signs and symptoms progress in three stages. Prodromal stage Patient complains of easy fatigue, anorexia, body malaise, headache, arthralgia, myalgia, photophobia and nausea with vomiting. There are changes in the patients senses of smell and taste. There is moderate grade fever ranging from 37.8-38.9 C As the prodromal stage draws to a close, urine may become dark-colored and stools are clay-colored. Clinical jaundice stage Patient manifest with pruritus, abdominal pain or tenderness and indigestion. There is yellowish discoloration of the sclerae, mucous membrane and the skin, which can last for one to two weeks. O inspection of the skin, rashes, erythematous patches and urticaria may be seen, especially if the client is suffering from hepatitis B or C. Pain, tenderness of the RUQ, an enlarged and tender liver, splenomegaly and cervical adenopathy are pesent.

Recovery stage During this stage, most of the patients symptoms decrease or subside. Recovery stage commonly last for 2-12 weeks.

Diagnosis Hepatitis A: Detection of antibodies to hepatitis A confirms the diagnosis. 83

Hepatitis B: The presence of HbsAg and hepatitis B antibodies confirms the diagnosis. Hepatitis C: The diagnosis depends on serologic testing for the specific antibody one or more months after the onset of acute hepatitis. Hepatitis D: Detection of intrahepatic delta or immunoglobulin M (IgM) establishes the diagnosis. Hepatitis E: Detection oh hepatitis E antigen supports the diagnosis.

Following are additional findings from liver function test that support the diagnosis: 1. Serum aspirate aminotransferase levels and serum alanine aminotransferase are increased in the prodromal stage of acute viral hepatitis. 2. Serum alkaline phosphotase levels are slightly increased. 3. Serum bilirubin levels are elevated and may continue to rise in severe liver damage. 4. WBC reveals transient neutropenia and lymphopenemia followed by lymphocytosis. 5. Liver biopsy is performed only if diagnosis is questionable. General Nursing Management 1. Suggest that a large meal be eaten in the morning because nausea tends to intensify as the day progresses. 2. Provide diversional patients to relieve boredom and anxiety. 3. Encouraged anorexic patients to take juices with occasional ice chips to maintain hydration without indusing vomiting. 4. Monitor the patients weight daily. Record intake and output. 5. Observe stools for color, consistency and amount. Record the frequency of bowel movement. 6. Before the patient is discharge, discuss restrictions and how to prevent recurrence of hepatitis. B. NON VIRAL HEPATITIS Non viral hepatitis is classified as either toxic or drug-induced (idiocyncratic) hepatitis. Most of the patients recover from this type of hepatitis, although a few develop fulminant hepatitis or cirrhosis. Causes 1. Alcohol overuse- follows heavy alcohol consumption 2. Diect hepatoxicity- hepatocellular damage and necrosis usually caused by toxins; it is a dose- dependent and occurs primarily in acetaminophen overdose. 3. Idiosyncratic hepatoxicity- follows a sensitization period of several weeks caused by the hosts hypersentivity to medication, such as, INH, methyldopa, lovastatin and halothane. 4. Cholestatic reactions- caused by a lack of bile excretion; direct hepatoxicity from hormaonal contraceptives or anabolic steroids; hypersensitivity to antibiotics, thyroid medications, anti-diabetics and cytotoxic drugs. 5. Metabolic and autoimmune disorders- acute exacerbations of sub-clinical liver disease. 6.

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Comparison of Types of Viral Hepatitis

VIRUS Mode of transmission Incubation (in weeks) Onset Carrier state Possible Complications

HEPATIS A (HAV) Fecal-oral

HEAPATIS B (HBV) Blood and body fluids;perinatal 6-24 Slow Yes Chronic hepatitis; Cirrhosis; Liver cancer Positive HBsAg (HBV surface antigen); anti-HBV antibodies present

HEAPTITIS C (HCV) Blood and bloody fluids 5-12 Slow Yes Chronic hepatitis; Cirrhosis

HEPATITIS D (HDV) Blood and bodu fluids; perinatal 3-13 Abrupt Yes Chronic hepatitis; Cirrhosis

HEPATITIS E (HEV) Fecal-oral

2-6 Abrupt No Rare

3-6 Abrupt Yes May be seen in pregnant women

Laboratory findings

Anti-HAV antibodies present

Liver cancer; Anti-HCV; Antibodies present

Fulminant hepatitis positive HDVAg (delta antigen) early, antiHDV antibodies later

Anti-HEV antibodies present

Reference: Principles of Medical-Surgical Nursing 4th Edition Volume 1 Page 705

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Herpes simplex

Definition Herpes simplex is a viral disease characterized the appearance of sores and blisters anywhere on the skin. These sores usually occur either around the mouth and nose or on the genitals and buttocks (thus the nickname virus of love). Herpes simplex is related to the viruses that cause infectious mononucleosis (Epstein Barr virus), chicken pox and shingles. Incubation Period 2-12days. Causative Agent Herpes simplex virus (HSV) Type 1 virus o Can cause cold sores that usually infect during infancy and childhood o The sore is characterized by tiny, clear, fluid-filled blisters. o Affects the lips, mouth, nose, chin, or cheeks and occurs shortly after exposure o Transmitted by kissing and sharing kitchen utensils and towels. Type 2 virus o Causes genital sores, affecting the buttocks, penis, vagina or cervix and lasts two-twenty days. o Transmitted through sexual contact with an infected individual. o It affects 20% of sexually active individuals. Pathognomonic Sign Cold sores or fever blisters

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Pathophysiology Etiologic agent (HSV) infect and invade the host multiply symptoms appear 2-20 days blister appears and spread primary infection usually last from 7-10 days. Sign and Symptoms Clinical manifestation of Herpes simplex infection ranges from mild to fatal disease, depending on the age and other characteristics of the host, the organs involved and the nature of the infection. Mild to moderate 1. Oral Herpes Gingivostomatitis o Inflammation of the gums, cervical adenopathy and fever o Vesicular and ulcerative lesions occur in the buccal mucosa and may involve the tongue o Excessive salivation results from pain on swallowing in infants and young children o Feeding is painful and fluid intake is poor. 2. Labial Herpes o Cold sores or fever blisters 3. Ocular Herpes o Herpetic keratitis accompanied by conjunctivitis and periauricular lymphadenopathy 4. Cutaneous Herpes o Deep burning pain, fever, skin edema. Ascending lymphagitis, and regional lymphadenopathy 5. Erythema multiforme o Sometimes appear as a zosteriform distribution that mimics herpes zoster 6. Genital Herpes Diagnostic test Tissue culture technique and smears Medical Management Oral antiviral drugs such as acyclovir, famicylcovir, valacyclovir Intravenous fluids Nursing Management Instruct personal hygiene Restoration of fluid and electrolyte balance Isolation of clients, especially those with eczema herpeticum and neonatal herpes. Practice of universal precaution and trough hand washing

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Herpes zoster

Definition Herpes zoster, commonly known as shingles, caused by the same virus responsible for chicken pox, the varicella zoster virus. Synonyms Shingles or Acute Posterior Ganglionitis Incubation Period Unknown, but is believed to be 13-17days Causative Agent Varicella zoster virus Mode of transmission Direct contact through droplet infection and airborne spread Indirect contact e.g, articles freshly soiled by secretions and discharges from an infected person Pathognomonic Sign Vesicles Pathophysiology VZV primary infection invade and multiply in the host produces localized vesicular skin lesions confined to a dermatome and severe neurologic pain in the peripheral nerves.

Sign and symptoms

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Cluster of vesicles appear to form patches with coalesce to form an irregular, band-like distribution along the couse of involved dermatomes. Pain Fever, malaise, anorexia, headache When the 5th cranial nerve is affected, corneal anesthesia occurs, the condition is called Gasserian ganglionitis Ramsay-Hunt Syndrome, when the facial nerve is affected.

Diagnostic Exam Characteristic of skin rash may be a diagnostic Tissue culture technique Smear of vesicle fluid Microscopy Complications Encephalitis Paralytic ileus, bladder paralysis Ophthalmic herpes Medical Management Symptomatic Antiviral drugs Analgesic to control pain Anti inflammatory drugs Nursing Management Personal hygiene Isolation to avoid the transmission Compliance to medications

Hookworm Diseases
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Definition Hookworm disease is an intestinal parasite of humans that usually causes diarrhea or cramps. Hookworm infection occurs mostly in tropical and subtropical countries. Synonym Ancylostomiasis/ Miners Disease/Egyptian Chlorosis Incubation Period 1. Hookworm ova appear in the stools about four to six weeks after the larval penetrate the skin. 2. 40-100 days or 2-8 weeks. Mode of transmission Transmitted trough the skin of the foot (ground itch) Through ingestion of contaminated drinking water Causative Agent 1. Ancylostoma duodenale- most prevalent in Europe and Asia 2. Necator americanus- distributed in central and South America and West Africa Pathophysiology Etilogic Agent larvae penetrate the unbroken skin of the feet and legs of the host Larvae penetrate the blood and lymph vessels and reach the heart larvae enter the lung capillaries enter the alveolar spaces migrate up to the trachea and swallowed and reach the small intestine maturation occurs and adult worms survives by attaching i8tself to the duodenal and jejuna mucosa worm continues to suck blood as much as 50 ml

Signs and symptoms

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Iron deficiency anemia Abdominal pain, diarrhea, allergic reactions like urticaria Infected children are lazy, no energy, lack ambition, tends to be malnourished, undersized. Pupils are more or less dilated Pedal edema

Diagnostic procedures Microscopic exam of the feces for the eggs Blood exam reveals eosinophilia

Medical management Pyrantel embonate(Quantrel) Tetrachloroethylene Carbon tetrachloride

Nursing Management Isolation is not necessary Diet should be high in calories, vitamins and minerals Personal hygiene should be maintained. Instruct not to walk barefooted.

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Influenza
Definition Influenza is an acute viral infectious disease affecting the respiratory system. Synonym La Grippe Incubation Period 24-48 hours Causative Agent -RNA- containing myxoviruses, types A, A-prime, B, and C - Influenza virus Mode of transmission Airborne spread among crowded places Through direct contact with the infected droplet Persist for hours in dried mucus

Pathognomonic Sign - Coryza Pathophysiology Influenza Virus invade the respiratory mucosa damages ciliated epithelium of tracheobronchial tree patient becomes vulnerable to secondary infection other organisms give rise to severe reactions, producing edema of the respiratory tree Serosanguinous discharge Complications

Signs and symptoms Onset is sudden and is marked by chilly sensation, hyperpyrexia, malaise sore throat, coryza, rhinorrhea, myalgia, and headache. Severe aches and pain usually at the back associated with severe sweating GI symptoms and vomiting Diagnostic tests Blood exam- usually normal but leukopenia may be noted Virus may be cultured from oropharyngeal washings / swabs during the first few days of illness
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Viral serology o Complement fixation test o Hemo-agglutination test o Neutralization test

Medical Management Untuil recently there has been no specific treatment for influenza. Advice the client to take the following to relieve pain and headache: a. Paracetamol b. Aspirin, unless contraindicated c. Ibuprofen or other anti- inflammatory drugs d. Nursing Management Drink plenty of fluids Bed rest Sponge down with tepid water Others Isolate the patient to decrease the risk of infecting others Limit strenuous activity especially in children Watch out for complications, especially among people at risk. Complication 1. Directly related to primary viral infections Hemorrhagic Pneumonia Encephalitis and other neurologic Syndrome Reyes Syndrome Myocarditis, which may lead to cardiac failure Sudden Death Infant Syndrome Myoglobinuria 2. Superimposed bacterial infections due to Streptococcus pneumoniae, Haemophilus influenza, Streptococcus pyogenes, and Staphylococcus aureus. Otitis media Sinusitis Pneumonia

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Impetigo Synonyms Impetigo Contagiosa, School sores

Definition Is a contagious, superficial infection of the skin. Background Impetigo is an acute, highly contagious gram-positive bacterial infection of the superficial layers of the epidermis. Impetigo occurs most commonly in children, especially those who live in hot, humid climates. The name is believed to be derived from the Latin impetere (to assail). Impetigo occurs in 2 forms: bullous and nonbullous, as shown in the photographs below. Nonbullous impetigo is the more common form, constituting approximately 70% of impetigo cases. It tends to affect skin on the face or extremities that has been disrupted by bites, cuts, abrasions, other trauma, or diseases such as varicella.

Infectious Agent Staphylococcus(Staph) and streptococcus (Strep) bacteria. Incubation Period 1 to 3 days Pathognomonic Sign ecthyma

Pathophysiology Caused by staphylococci producing exfoliative toxin that contains serine proteases acting on desmoglein 1, a structurally critical peptide bond in a molecule that holds epidermal cells together. This process allows Staphylococcus aureus to spread under the stratum corneum in the space
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formed by the toxin, causing the epidermis to split just below the stratum granulosum. Large blisters then form in the epidermis with neutrophil and, often, bacterial migration into the bullous cavity. This mechanism of lesion progression may explain how the body is usually able to resist entry beyond the superficial epidermis. In bullous impetigo, the bullae rupture quickly; causing superficial erosion and a yellow crust, while in nonbullous impetigo, Streptococcus typically produces a thick-walled pustule with an erythematous base. Histology of non-bullous established lesions shows a thick surface crust composed of serum and neutrophils in various stages of breakdown with parakeratotic material.

Period of Communicability Period of communicability varies. Mode of Transmission Direct contact Indirect contact Can also acquire in animals such as dogs and cats May spread to another part of the body trough scratching or picking at the blister and scabs

Clinical Manifestation Ecthyma Red sores that quickly rupture, ooze for a few days and then form a yellowishbrown crust Itching Painless, fluid-filled blisters In the more serious form, painful fluid- or pus-filled sores that turn into deep ulcers

Complications Acute glomerulonepritis Cellulitis in o Face and Ears o Arms and Hands o Legs and Foots o Abdomen and Breast
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Erysipelas Scarlet fever

Diagnostic Procedure Culture may be necessary to confirm the diagnosis or to rule out another cause. Medical Management Mupirocin (bactroban) Antibiotic ointment Clyndamycin for Drug resistant staphylococcus Methicillin- resistant staphylococcus aureus (MRSA) Penicillin and cephalosporin if developed resistance to antibiotic.

Prevention Importance of proper hand washing using soap and warm water. Isolate the person. Avoid sharing of clothes, towels or blanket.

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Influenza A (H1 N1) DEFINITION

INFLUENZA A VIRUS -causes influenza in birds and some mammals and is the only species of Influenza virus A. Itis a genus of the Orthomyxoviridae family of viruses. Influenza A viruses are negative sense, single-stranded, segmented RNA viruses. There are several subtypes, labeled according to an H number (for the type of hemagglutinin) and an N number (for the type of neuraminidase). There are 16 different H antigens (H1 to H16) and nine different N antigens (N1 to N9). HEMAGGLUTININ- is a type of hemagglutinin found on the surface of the influenza viruses. It is an antigenic glycoprotein. It is responsible for binding the virus to the cell that is being infected. NEURAMINIDASE- is a type of neuraminidase found on the surface of influenza viruses that enables the virus to be released from the host cell. Neuraminidases are enzymes that cleave sialic acid groups from glycoproteins and are required for influenza virus replication. RE-ASSORTMENT - is a process that happens if two different types of influenza virus infect a single cell and it can produce a new strain of influenza. This is because the virus genome is split between eight independent pieces of RNA, which allows pieces of RNA from different viruses to mix together and form a novel type of virus as new virus particles are being assembled.

SWINE FLU/INFLUENZA A(H1N1) Influenza A(H1N1) is caused by a new virus that resulted from the re-assortment of 4 viruses from pigs, birds, and human. It is a new virus causing illness to people. It was first detected in people in April 2009 at USA and Mexico, there were 7 cases reported and on May 7, it the disease spread rapidly, with the number of confirmed cases rising to 2,099 There was no vaccine yet to protect humans from this virus But there are existing and recommended medicine that are effective in treating A(H1N1) virus Influenza A(H1N1) can be fatal due to severe respiratory distress (pneumonia) On June 11, 2009, the World Health Organization declared the disease pandemic On May 30, 2010 worldwide update by WHO more than 214 countries and overseas territories or communities have reported laboratory confirmed cases of pandemic influenza H1N1 2009, including over 18138 deaths On August 10, 2010, the WHO declared an end to the 2009 A(H1N1) influenza pandemic. This declaration was based on strong indications that influenza, worldwide, is transitioning toward seasonal patterns of transmission.
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ETIOLOGY: There are two main types of influenza virustype A and type B. The 2009 outbreak is due to a new mixture of different kinds of influenza A. This strain passes from human to human, so it may spread rapidly.

MODE OF TRANSMISSION: Direct exposure to droplets when an infected person coughs and sneezes Touching mouth, nose, or eyes after touching infected things

Risk Factors: Contact with an infected person Age: children younger than two years old and people aged 65 or older People younger than 19 years old Being pregnant Having recently given birth (last two weeks) Diabetes Weakened immune systems, such as in: People infected with HIV People taking immunosuppressive drugs Disorders that may affect breathing Chronic lung, heart, kidney, liver, nerve, or blood conditions Being in a chronic care facility

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PATHOPHYSIOLOGY:

Transmission of the virus Virus attaches to and penetrates respiratory epithelial cells in the trachea and bronchi Viral replication Destruction of the host cell

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SIGNS AND SYMPTOMS: Fever and chills Sore throat Cough Severe muscle aches Severe fatigue Headache Runny nose, nasal congestion Sneezing Watery eyes Gastrointestinal symptoms (e.g. nausea, diarrhea, vomiting)

DIAGNOSTIC TESTS:

Chest x-ray films Pulse oximetry (a test in which a probe connected to a computer is placed on the finger or ear to measure oxygen saturation in the blood) Blood cultures Sputum (fluid from the respiratory tract) Gram stain and culture Reverse transcription polymerase chain reaction (RT-PCR) - this method allows a specific diagnosis of novel influenza (H1N1) as opposed to seasonal influenza. It is a variant of polymerase chain reaction (PCR), a laboratory technique commonly used in molecular biology to generate many copies of a DNA sequence, a process termed "amplification".

MEDICAL MANAGEMENT: If a person becomes sick with swine flu, antiviral drugs can make the illness milder and make the patient feel better faster. They may also prevent serious flu complications. For treatment, antiviral drugs work best if started soon after getting sick (within 2 days of symptoms). Beside antivirals, supportive care at home or in hospital, focuses on controlling fevers, relieving pain and maintaining fluid balance, as well as identifying and treating any secondary infections or other medical problems. The U.S. Centers for Disease Control and Prevention recommends the use of Tamiflu (oseltamivir) or Relenza (zanamivir) for the treatment and/or prevention of infection with swine influenza viruses; however, the majority of people infected with the virus make a full recovery without requiring medical attention or antiviral drugs. Oseltamivir is an antiviral drug that slows the spread of influenza virus between cells in the body by stopping the virus from chemically cutting ties with its host cellmedian time to symptom alleviation is reduced by 0.51 day. The drug is
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sold under the trade name Tamiflu and is taken orally in capsules or as a suspension. Zanamiviris a neuraminidase inhibitor used in the treatment and prophylaxis of Influenzavirus A and Influenzavirus B. Zanamivir works by binding to the active site of the neuraminidase protein, rendering the influenza virus unable to escape its host cell and infect others.

What can I do to protect myself from getting Influenza A(H1N1)? Always wash hands with soap and water You may use alcohol-based hand sanitizers Avoid close contact with sick people Increase your bodys resistance o Have at least 8 hours of sleep o Be physically active o Manage your stress o Drink plenty of fluids o Eat nutritious foods Make it a habit to cover your nose and mouth when coughing or sneezing Influenza A(H1N1) Vaccination

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Poliomyelitis (Infantile Paralysis / Heine-medin Disease)

Definition Is an acute infectious disease characterized by changes in the CNS which may result in pathologic reflexes, muscle spasms, and paresis or paralysis. It is a diseased of the lower motor neurons. There is anterior horn involvement, such that it is named anterior poliomyelitis. History The term derives from the Greek polis (), meaning "grey", myels (), referring to the "spinal cord", and the suffix -itis, which denotes inflammation. Poliomyelitis was first recognized as a distinct condition by Jakob Heine in 1840. Its causative agent, poliovirus, was identified in 1908 by Karl Landsteiner. Although major polio epidemics were unknown before the late 19th century, polio was one of the most dreaded childhood diseases of the 20th century. Polio epidemics have crippled thousands of people, mostly young children; the disease has caused paralysis and death for much of human history. Polio had existed for thousands of years quietly as an endemic pathogen until the 1880s, when major epidemics began to occur in Europe; soon after, widespread epidemics appeared in the United States.

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By 1910, much of the world experienced a dramatic increase in polio cases and epidemics became regular events, primarily in cities during the summer months. These epidemicswhich left thousands of children and adults paralyzedprovided the impetus for a "Great Race" towards the development of a vaccine. Developed in the 1950s, polio vaccines are credited with reducing the global number of polio cases per year from many hundreds of thousands to today under a thousand. Enhanced vaccination efforts led by the World Health Organization, UNICEF, and Rotary International could result in global eradication of the disease. Incubation Period 7 to 21 days for paralytic cases, with a repeated range of 3 to 35 days. Causative agent polio virus (Legio debilitans) Mode of transmission 1. Direct contact with infected oropharyngeal secretions and feces 2. Person-to-person transmission through healthy carriers 3. Indirectly, through flies and contaminated water food, utensils and other articles. Types of poliomyelitis 1. The abortive a. Does not invade the central nervous system b. Headache and sore throat c. Slight or moderate fever d. Occasional vomiting e. Low lumbar pain f. The patient usually recovers within 72 hours 2. Non-paralytic a. All signs of the abortive type is observed b. Types and spasm of the muscles of hamstring c. Changes in the deep superficial reflexes d. Pain in the neck, back, arms, legs and abdomen e. Inability to place the head in between the knees f. Positive pandys test g. Transient paresis may occur h. Usually lasts for about a week, with meningeal irritation persisting for about two weeks 3. Paralytic a. All signs of the abortive type and non-paralytic types are observed b. (+) Hoynes sign c. Paralysis occur
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d. e. f. g. h.

Less tendon reflex (+) Kerning and Brudzinski test Weakness of the muscle Hypersensitivity to touch There is usually urine retention, constipation and abdominal distention i. Spinal paralytic 1. Paralysis occurs in muscles innervated by the motor neurons of the spinal cord 2. It is characterized by asymmetry and scattered flaccid paralysis on one or both lower extremities 3. There is autonomic nervous system involvement manifested by excessive sweating 4. There is respiratory difficulty ii. Bulbar 1. Usually develops rapidly and is more serious 2. Motor neurons are attacked, affecting the medulla. This weakens the muscles supplied by the cranial nerves, especially the 9th (glossopharyngeal) and the 10th (vagus) 3. Facial, pharyngeal and ocular muscles are paralyzed 4. There are cardiac irregularities and cardiac failure 5. Impaired temperature regulation 6. Encephalitic manifestations, such as facial weakness, dysphagia, difficulty in chewing, inability to swallow or expel saliva, regurgitation of food through the nasa passages and dyspnea, are observed in about 30% of patients. iii. Bulbospinal 1. There is an involvement of neurons both in the brainstem and the spinal cord.

Pathophisiology Poliovirus enters the body through the mouth, infecting the first cells with which it comes in contactthe pharynx and intestinal mucosa. It gains entry by binding to an immunoglobulin-like receptor, known as the poliovirus receptor or CD155, on the cell membrane. The virus then hijacks the host cell's own machinery, and begins to replicate. Poliovirus divides within gastrointestinal cells for about a week, from where it spreads to the tonsils (specifically the follicular dendritic cells residing within the tonsilar germinal centers, the intestinal lymphoid tissue including the M cells of Peyer's patches, and the deep cervical and mesenteric lymph nodes, where it multiplies abundantly. The virus is subsequently absorbed into the bloodstream. Known as viremia, the presence of virus in the bloodstream enables it to be widely distributed throughout the body. Poliovirus can survive and multiply within the blood and lymphatics for long periods of time, sometimes as long as 17 weeks. In a small percentage of cases, it can spread and replicate in other sites, such as brown fat, the reticuloendothelial tissues, and muscle. This sustained replication causes a major

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viremia, and leads to the development of minor influenza-like symptoms. Rarely, this may progress and the virus may invade the central nervous system, provoking a local inflammatory response. In most cases, this causes a self-limiting inflammation of the meninges, the layers of tissue surrounding the brain, which is known as nonparalytic aseptic meningitis. Penetration of the CNS provides no known benefit to the virus, and is quite possibly an incidental deviation of a normal gastrointestinal infection. The mechanisms by which poliovirus spreads to the CNS are poorly understood, but it appears to be primarily a chance eventlargely independent of the age, gender, or socioeconomic position of the individual. Diagnostic Procedures 1. Stool cultures throughout the course of the disease 2. Culture from the CSF Modalities of treatment 1. Analgesics are helpful in easing headaches, back pain, and leg spasms. Morphine is contraindicated. 2. Moist heat application may reduce muscle spasm and pain 3. Bed rest is necessary 4. Physical therapy, braces corrective shoes and in some cases, orthopedic surgery. Nursing management 1. Carry out enteric isolation 2. Observed the patient closely for signs of paralysis and other neurologic changes 3. Perform neurologic assessment but dont demand any vigorous muscular activity 4. Check BP 5. Watch for signs of fecal impaction 6. Provide good skin care 7. Hand washing 8. Dispose excreta and vomitus properly 9. Provide emotional support 10. Maintain good personal hygiene particularly oral and skin care Complications 1. 2. 3. 4. 5. 6. Respiratory failure Circulatory collapse Electrolyte imbalance Bacterial infection Urinary problems r/t paralysis of the bladder Abdominal distention

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Prevention and Control 1. 2. 3. 4. 5. Immunization: OPV Proper disposal of GIT secretions Isolation Implementation of standard precaution Sanitation of the premises and proper food handling should be strictly observed to avoid contamination with flies

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Rabies (Hydrophobia /lyssa)

Definition Is a specific, acute viral infection communicated to man by saliva of an infected animal. History The term is derived from the Latin rabies, "madness". This, in turn, may be related to the Sanskrit rabhas, "to do violence". The Greeks derived the word "lyssa", from "lud" or "violent"; this root is used in the name of the genus of rabies lyssavirus. Because of its potentially violent nature, rabies has been known since c.2000 B.C. The first written record of rabies is in the Mesopotamian Codex of Eshnunna (ca. 1930 BC), which dictates that the owner of a dog showing symptoms of rabies should take preventive measure against bites. If another person was bitten by a rabid dog and later died, the owner was heavily fined. Rabies was considered a scourge for its prevalence in the 19th century. In France and Belgium, where Saint Hubert was venerated, the "St Hubert's Key" was heated and applied to cauterize the wound; by an application of magical thinking, dogs were branded with the key in hopes of protecting them from rabies. Fear of rabies related to methods of transmissions was almost irrational; however, this gave Louis Pasteur ample opportunity to test post-exposure treatments from 1885. In ancient medical times, the attachment of the tongue (the frenum linguae, a mucous membrane) was cut and removed as this is where rabies was thought to originate. This practice ceased with the discovery of the actual cause of rabies.
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Incubation period 1. One week to 7 months in dogs 2. 10 days to 15 years in human Causative agent Rhabdovirus Mode of transmission 1. Biting of infected animal to human 2. Saliva comes in contact with persons mucous membrane Pathognomonic sign Hydrophobia Profuse drooling Pathophisiology Infection occurs when the virus gains access to the body, usually though a bite wound, though contact of affected saliva on an open wound or mucosal surface may also occur (such as inhalation of virus laden particles in caves frequented by bats). The virus then incubates at the site of inoculation usually replicating within muscle cells. After an extended incubation time the virus gains entry to nerves and travels by retrograde axonal flow toward the central nervous system - first to the spinal cord then to the brain, except in cases of innoculation into or near a cranial nerve. Once in the brain the virus travels by axonal flow down the trigeminal nerve to the salivary glands. The virus is usually present in the saliva and the animal infective 3-5 days prior to the onset of clinical signs. As the virus first incubates in the site of inoculation, usually in muscle cells and then travels through the peripheral nerves by retrograde axonal flow to the central nervous system, the length of time until development of clinical signs is in part related to the distance the virus must travel. Hence, a bite to a distal periphery will have a longer incubation period than a bite to the face. This provides time for post-exposure vaccination to work, even if prior vaccination had not occurred. In dogs, the normal incubation period is 21-80 days, though it can be shorter or much longer depending on the location of the bite. One reported human case had an incubation of more than 6 years (Merck Veterinary Manual, Smith et al. 1991) Initially there is little immune response, though an antibody respose does develop as clinical signs progress, however at this point it is too late for antibodies to have an

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effect, as the virus is already within the central nervous system which is well protected by the blood-brain barrier, and hence has no exposure to antibodies. As the virus invades farther into the CNS there is an increase in nervous signs, causing either the raging of dumb forms (or some combination thereof) depending on the animal and what parts of the brain are affected as well as the source of the virus. Furious symptoms result from changes to the limbic system and the dumb form results from changes to the neocortex. Death results from respiratory paralysis from the virus affecting the breathing centres. Other signs such as excitement, salivation, and increased sexual activity result from the effects on the autonomic nervous system. In advanced disease there are viral inclusion bodies "Negri bodies" found in nearly all neurons within the brain (though the supporting cells are not affected). Signs and symptoms 1. Prodromal / Invasive phase a. Fever, anorexia, malaise, sore throat, copious salivation, lacrimation, perspiration, irritability, hyper excitability, apprehensive, restlessness, mental retardation, melancholia and marked insomnia b. Pain at the site of the bite, headache, nausea c. Light, sound and temperature sensitivity d. Pain and ache in different parts of the body e. Anesthesia, numbness and tingling, mild dysphagia 2. Excitement or neurologic phase a. Marked excitation and apprehension. b. Delirium associated with nuchal rigidity, involuntary twitching or generalized convulsions c. Maniacal behavior: eyes are fixed and glossy, glossy with cold clammy skin d. Painful muscle spasm of the mouth, pharynx and larynx e. Aerophobia f. Profuse drooling g. Tonic- clonic contractions of the muscle h. Death due to cardiac and respiratory failure 3. Terminal/ paralytic phase a. Quiet and unconscious b. Loss of bowel and urinary control c. Spasm cease and there is progressive paralysis d. Tachycardia and labored irregular respitaion e. Death due to respiratory paralysis, circulatory collapse and heart failure

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Diagnostic Procedures 1. Fluorescent rabies antibody (FRA)- confirmatory 2. Presence of Negri bodies in the digs brain Modalities of treatment 1. 2. 3. 4. Wash the wounds with soap and running water Check patients immunization status. Give Tetanus toxoid if needed Give tetanus antiserum infiltrated around the wound or IM ANST Give anti-rabies vaccine, both passive and active, depending on the site and size of the bite, as well as the health condition of the biting animal

Nursing Management 1. 2. 3. 4. 5. Isolate the patient Give emotional and spiritual support Provide optimum comfort Darken the room and provide quiet environment If IVF is to be given, it should be wrapped securing the needle acnchored to the vein 6. Concurrent and terminal disinfection should be carried out. Prevention and Control 1. 2. 3. 4. 5. Vaccination of all dogs Enforcement of regulations for the pick-up and destructions of stray dogs 10-14 day confinement of dog Availability of laboratory facilities for observation and diagnosis Providing public education

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Red Tide
(Blooms)

Definition It is caused by a population explosion of toxic, naturally occurring microscopic phytoplankton, specifically a subgroup known as dinoflegellates. History Red tide is a common name for a phenomenon also known as an algal bloom (large concentrations of aquatic microorganisms), an event in which estuarine, marine, or fresh water algae accumulate rapidly in the water column and results in discoloration of the surface water. It is usually found in coastal areas. These algae, known as phytoplankton, are single-celled protists, plant-like organisms that can form dense, visible patches near the water's surface. Certain species of phytoplankton, dinoflagellates, contain photosynthetic pigments that vary in color from green to brown to red. When the algae are present in high concentrations, the water appears to be discolored or murky, varying in color from purple to almost pink, normally being red or green. Not all algal blooms are dense enough to cause water discoloration, and not all discolored waters associated with algal blooms are red. Additionally, red tides are not typically associated with tidal movement of water, hence the preference among scientists to use the term algal bloom. Some red tides are associated with the production of natural toxins, depletion of dissolved oxygen or other harmful effects, and are generally described as harmful algal
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blooms. The most conspicuous effects of these kind of red tides are the associated wildlife mortalities of marine and coastal species of fish, birds, marine mammals, and other organisms. Causative agent 1. Allexandrium tamarense 2. Allexandrium catanella 3. Ptycodiscus brevis Seafoods that are unsafe to eat from infected waters 1. Quahogs 2. Soft shell clamps 3. Oysters 4. Mussels 5. Scallops 6. Moon snails Pathophysiology Eating of contaminated foods with A. catanella which produces saxitoxin that blocks sodium movement in muscle tissue. Severity depends on the amount of food ingested. Toxic shellfish taste and appear no different from non-toxic shellfish and cooking does not destroy the organism Clinical Manifestations 1. Tingling of the lips and tongue 2. Headache, dizziness, nausea 3. Symptoms maybe aggravated due to alcohol consumption 4. In severe cases, muscle paralysis and breathing difficulty may occur in 5 to 12 hours due to paralysis of the diaphragm 5. Death due to respiratory arrest Modalities of treatment 1. Charcoal hemoperfusion 2. Alkaline fluids such as sodium bicarbonates 3. Artificial respiration

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Dengue Fever
(Breakbone fever/ Hemorrhagic fever/ dandy fever/ infectious thrombocytopenic Purpura)

Definition It is an acute febrile disease caused by infection with one of the serotypes of dengue virus, which transmitted by mosquito genus Aedes. Dengue hemorrhagic fever is a severe, sometimes fatal manifestation of the dengue virus infection characterized by bleeding diathesis and hypovolemic shock. History The first record of a case of probable dengue fever is in a Chinese medical encyclopedia from the Jin Dynasty(265420 AD) which referred to a "water poison" associated with flying insects. There have been descriptions of epidemics in the 17th century, but the most plausible early reports of dengue epidemics are from 1779 and 1780, when an epidemic swept Asia, Africa and North America. From that time until 1940, epidemics were infrequent. In 1906, transmission by the Aedes mosquitoes was confirmed, and in 1907 dengue was the second disease (after yellow fever that was shown to be caused by a virus. Further investigations by John Burton Cleland and Joseph Franklin Siler completed the basic understanding of dengue transmission. The marked spread of dengue during and after the Second World War has been attributed to ecologic disruption. The same trends also led to the spread of different serotypes of the disease to new areas, and to the emergence of dengue hemorrhagic fever. This severe form of the disease was first reported in the Philippines in 1953; by the 1970s, it had become a major cause of child mortality and had emerged in the
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Pacific and the Americas. Dengue hemorrhagic fever and dengue shock syndrome were first noted in Central and South America in 1981, as DENV-2 was contracted by people who had previously been infected with DENV-1 several years earlier. The origins of the word "dengue" are not clear, but one theory is that it is derived from the Swahili phrase Ka-dinga pepo, which describes the disease as being caused by an evil spirit. The Swahili word dinga may possibly have its origin in the Spanish word dengue, meaning fastidious or careful, which would describe the gait of a person suffering the bone pain of dengue fever. However, it is possible that the use of the Spanish word derived from the similar-sounding Swahili. Slaves in the West Indies having contracted dengue were said to have the posture and gait of a dandy, and the disease was known as "dandy fever". The term "break-bone fever" was first applied by physician and Founding Father Benjamin Rush, in a 1789 report of the 1780 epidemic in Philadelphia. In the report he uses primarily the more formal term "bilious remitting fever".The term dengue fever came into general use only after 1828. Other historical terms include "breakheart fever" and "la dengue".Terms for severe disease include "infectious thrombocytopenic purpura" and "Philippine", "Thai", or "Singapore hemorrhagic fever". Incubation Period >3 to 14 days commonly 7 to 10 days Causative agent 1. Flavivirus 1, 2, 3, 4, a family of togaviridae 2. Arbovirus group B Mode of transmission 1. Bite of infected mosquito, principally the Aedes Aegypti Pathognomonic Sign >petechiae Pathophisiology Dengue fever is a mosquito-borne viral disease caused by 1 of 4 closely related but antigenically distinct serotypes of dengue virus, serotypes DENV-1 through DEN4.Infection with one dengue serotype confers lifelong homotypic immunity and a very brief period of partial heterotypic immunity, but each individual can eventually be infected by all 4 serotypes. Several serotypes can be in circulation during an epidemic.

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Clinical manifestation A. Dengue Fever 1. Prodromal symptoms a. Malaise anorexia b. Fever and chills accompanied by severe frontal headache 2. 3. 4. 5. Nausea and vomiting Fever 3 to 7 days Rash in the trunk and extremities Petechiae

B. Dengue Hemorrhagic Fever (DHF) a. Hemorrhagic diathesis b. Hepatomegaly c. Hypovolemic shock Classification according to severity Grade I a. Fever b. (+) tourniquet test Grade II a. All signs of grade I b. Spontaneous bleeding from nose gums and GIT Grade III a. Presence of circulatory failure (weak pulse, narrow pulse pressure, hypotension, cold clammy skin, restlessness) Grade IV a. Profound shock b. Undetectable BP and pulse Diagnostic test a. Tourniquet test b. Platelet count c. Hemoconcentration
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d. Occult blood e. Hemoglobin determination Treatment a. b. c. d. e. Analgesics IVF for rehydration Blood transfusion for severe bleeding Oxygen therapy Sedatives for anxiety

Nursing Management a. b. c. d. Keeping pt. in mosquito-free environment Periodic rest Monitor Vital signs In case of nose bleeding, elevate the trunk and apply icepacks on the bridge of the nose and forehead e. Observe for signs of shock f. Position the pt trendelenburg to restore blood volume

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Leptospirosis (Weils Disease/Canicola Fever/ Hemorrhagic Jaundice/Mud Fever/ Swine Herd Disease)

Definition: Is a zoonotic infectious bacterial disease carried by animals, both domestic and wild. Infected urine contaminates water or food, which causes disease when ingested or inoculated through the skin. The disease was first described by Adolf Weil in 1886 when he reported an "acute infectious disease with enlargement of spleen, jaundice, andnephritis." Leptospira was first observed in 1907 from a post mortem renal tissue slice. In 1908, Inada and Ito first identified it as the causative organism and in 1916 noted its presence in rats. Incubation Period: The incubation period varies from six to fifteen days. Causative Agent: A spirochete of genus Leptospira (Leptospira interrogans) 1. These are chiefly saprophytic aquatic organisms which are found in river and lake waters, sewage, and in the sea. 2. There are 150 serotypes divided among 28 serogroups; some species are pathogenic to man and animals. 3. Weils disease is specifically caused by the serovar icterohaemorrhagiae. Mode of Transmission: 1. Transmitted through ingestion or contact with the skin or mucous membranes of infected urine or carcasses of either wild or domestic animals. 2. The disease can be transmitted through the mucous membranes of the eyes, nose and mouth, and through breaks in the skin.

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Pathophysiology: Cattle, swine, and Other livestock Dogs Rodents wild animals

Contact with contaminated water and soil Entry through the eyes, mouth and Broken skin

Man Signs and Symptoms: 1. The symptoms range in severity from asymptomatic to fatal. 2. Clinical course is generally biphasic and the majorities of the cases are unicteric. 3. Three septic stages can be recognized: a. Septic stage This stage is marked by febrile lasting from four to seven days. There is an abrupt onset of remittent fever, chills headache, anorexia, abdominal pain and severe prostration. There is also respiratory distress. Fever subsides with lysis. b. Immune or toxic stage This stage can be with or without jaundice, and last for 4 to 30 days. Iritis, headache, meningeal manifestations like disorientation, and convulsions, with CSF findings of aseptic meningitis. Oliguria and anuria with progressive renal failure. Shock, coma, and congestive heart failure are also seen in severe cases. Death may occur between the 9th and 16th days. c. Convalescence At this stage, relapse may occur during the 4th and 5th weeks. Complications: 1. Meningitis 2. Respiratory distress 3. Renal interstitial tubular necrosis that results in renal failure.(Weils disease) 4. Cardiovascular problems Laboratory Diagnosis: 1. Blood urea-nitrogen and creatinine 2. Enzyme-linked immunosorbent assay (ELISA) 3. Liver function test usually are slightly to moderate elevated: aspartate aminotransferase (AST) alanine aminotransferase (ALT) gamme-glutamyltransferase (GGT) 4. Leptospira antigen-antibody test (LAAT)
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5. Leptospira antibody test (LAT) Management: 1. Medical. Treatment of leptospirosis is geared toward: A. Suppressing the causative agent B. Fighting possible complications Aetiotropic drug - penicillin, dexycycline, ampicillin, amoxicillin For prophylaxis, dexycycline 100 mg p.o. every 12 hours for 1 week Peritoneal dialysis Administration of fluid and electrolytes and blood, as indicated. 2. Nursing a. Isolate the patient; urine must be properly disposed of. b. Darken the patients room because light is irritating to the patients eyes. c. Observe meticulous skin care to ease pruritus. d. Keep client under close surveillance. e. Keep homes clean. Regularly replace water in pools, vases, aquaria, etc. to prevent stagnation. f. Eradicate rats and rodents. g. Provide health education on th modes of transmission of the disease. h. Encourage oral fluid intake.

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Malaria (Ague)

Definition: Is an acute and chronic parasitic disease transmitted by the bite of infected mosquitoes and is confined mainly to tropical and subtropical areas. This disease causes more disability and heavier economic burden than any other parasitic disease. Malaria is a mosquito-borne infectious disease of humans and other animals caused by eukaryotic protists of the genus Plasmodium. The disease results from the multiplication of Plasmodium parasites within red blood cells, causing symptoms that typically include fever and headache, in severe cases progressing to coma or death. It is widespread in tropical and subtropical regions, including much of Sub-Sahara Africa, Asia, and theAmericas Incubation Period: 1. 12 days for P. Falciparum 2. 14 days for P. vivax and ovale 3. 30days for P. malariae Causative Agent: Protozoa of genus plasmodia 1. The disease is caused by four species of protozoa: a. Plasmodium falciparum (malignant tertian)

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This is considered the most serious malarial infection because of the development of high parasitic densities in the blood (RBC). This type tends to cause agglunation, resulting in microembolus formation. b. Plasmodium vivax This is non-life-threatening, except for the very young and the very old. It is manifested by chills every 48hours on the 3rd day onward, especially if untreated. c. Plasmodium malariae (quartan) It is less frequently seen than the first two types. This species in non-life-threatening. Fever and chills usually occur 72hours, usually on the 4 th day after onset. d. Plasmadium ovale is the rare type of protozoan species. Pathophysiology: The infection of the red cells by malaria parasites, particularly P. falciparum, results in progressive and dramatic structural, biochemical, and mechanical modifications of the red cells that can worsen into life-threatening complications of malaria. While the vast majority of severe malaria and related mortality are caused by P. falciparum infection, complications can occur in non-falciparum infections as well. In recent years, several cases of severe infection and even deaths have been reported following infections with P. vivax and P. knowlesiinfections.[10-18] Several pathophysiological factors such as the parasite biomass; 'malaria toxin(s)' and inflammatory response; cytoadherence, resetting and sequestration; altered deformability and fragility of parasitized erythrocytes; endothelial activation, dysfunction and injury; and altered thrombostasis have been found to be involved in the development of severe malaria. All these phenomena are more profound and wide spread in P. falciparum infection compared to non-falciparum infections. As a result, except for severe anemia, complications such as cerebral malaria, hypoglycemia, metabolic acidosis, renal failure, and respiratory distress are more commonly seen in P. falciparum infections. Signs and symptoms: 1. 2. 3. 4. 5. 6. Paroxysms with shaking chills Rapidly rising fever with severe headache Profuse sweating Myalgia, with feelings of well-being in between Splenomegaly, hepatomegaly Orthostatic hypotension

Diagnostic Procedure: 1. Malarial smear In this procedure, a film of blood is placed on a side, stained and examined microscopically.
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2. Rapid Diagnostic Test (RDT) This is a blood test for malarial that can be conducted outside the laboratory and in the field. It gives results within 10 to 15 minutes. This is done to detect malarial parasite antigen in the blood. Management: 1. Medical a. Anti-malarial drugs Chloroquinine (all species, except for P. malariae) Quinine Sulfadoxine for the resistant P. falciparum Primaquine for relapses of P. vivax and ovale b. Erythrocyte exchange transfusion for rapid production of high levels of parasites in the blood. 2. Nursing Mnagement a. The patient must be closely monitored. b. Intake and output should be closely monitored to prevent pulmonary edema. Daily monitoring of patients serum bilirubin, BUN creatinine and parasitic count If the patient exhibits respiratory and renal symptoms, determine the arterial blood gas and plasma electrolytes. c. During the febrile stage, tepid sponges, alcohol and an ice cap on the head help bring the temperature down. d. Application of external heat and hot drinks during the chilling stage are helpful. e. Provide comfort and physiological support. f. Encourage the patient to take plenty of fluids. g. As the temperature falls and sweating begins, warm sponge baths may be given. h. The bed and clothing should be kept dry. i. Watch for neurologic toxicity (from quinine infusion) like muscular twitching, delirium, confusion, convulsion and coma. j. Evaluate the degree of anemia. k. Watch for any signs, especially abnormal bleeding. l. Consider severe malarial as medical emergency that requires close monitoring of vital signs.

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Measles (Rubeola/Morbilli)

Definition: Is an acute, contagious and exanthematous disease that usually affects children who are susceptible to upper respiratory tract infection (URTI). This may be one of the most serious of all childhood diseases. Incubation Period: 1. The incubation period is from ten to twelve days (the longest is 20 days and the shortest is eight days). 2. A single attack conveys lifelong immunity. Causative Agent: A filterable virus which belongs to the genus Morbilivirus of the family Paramyxoviridae is the agent measles. The measles virus is rapidly inactivated by heat, ultraviolet light and extreme degrees of acidity and alkalinity. Pathognomonic Sign: Kopliks Spots are pathognomonic of measles. These are inflammatory lesions of the buccal mucous glands with superficial necrosis. 1. They appear on the mucosa of the inner cheek opposite to the second molars, or near the junction of the gum and the inner cheek. 2. They usually appear one to two days before the measles rash.

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Pathophysiology: Measles virus is transmitted via droplets and infects epithelial cells of the nose and conjunctivae. Virus multiplies in these epithelial cells and then extends to the regional lymph nodes. Primary viraemia occurs 2 to 3 days after infection, and measles virus continues to replicate in epithelial and reticuloendothelial system tissue over the next few days. Secondary viraemia occurs on days 5 to 7, and infection becomes established in the skin and other tissues including the respiratory tract on days 7 to 11. The prodromal phase, which lasts 2 to 4 days, occurs at this time with fever, malaise, cough, coryza, and conjunctivitis. Koplik's spots may develop on the buccal mucosa about 1 to 2 days before the rash and may be apparent for 1 to 2 days after rash onset. The rash then develops at about 14 days after infection; at this time virus can be found in blood, skin, respiratory tract, and other organs. Over the next few days, viraemia gradually decreases as the rash coalesces and gradually resolves along with the other signs and symptoms. Viraemia and presence of virus in tissue and organs ceases by days 15 to 17 corresponding to the appearance of antibody. Signs and symptoms: Clinical manifestations come in three stages: 1. Pre-eruptive stage a. Fever b. Catarrhal symptoms (rhinitis, conjunctivitis, photophobia, coryza) c. Respiratory symptoms start from common colds to persistent coughing. d. Enanthem sign ( Kopliks spot, Stimsons line) 2. Eruptive stage a. A maculo-papular rash usually starts to appear late on the 4th day. b. The maculo-papular rash appears first on the cheeks, bridge of the nose, temples, earlobes or along the hairline. c. The rash is fully developed by the end of the second day and all symptoms are at their most severe this time. d. High-grade fever comes on and off. e. Anorexia and irritability. f. Abdominal tympnism, pruritus and lethargy. g. The throat is red and often extremely sore. h. S fever subsides, coughing may diminish, but more often it hangs on for a week or two and becomes looser and less metallic. 3. Stage of convalescence a. Rashes fade away in the same manner as they erupted. b. The fever subsides as rashes starts to fade. c. When the rashes have faded, desquamation begins. d. Symptoms subside and appetite is restored.

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Laboratory Examinations: 1. 2. 3. 4. Nose and throat swab. Urinalysis Blood exams (CBC, leucopenia,leukocytosis) Complement fixation or hemogglutinin test.

Medical Management; 1. Anti viral drugs (Isoprinosine) 2. Antibiotics of with complication 3. Supportive therapy ( oxygen inhalation, IV fluids) Nursing Management: 1. Isolation of the patient if necessary (the room must be quiet, well-ventilated and must have subdued light). 2. Control the patients high temperature with warm or tepid sponges. 3. Skin care is of utmost importance. The patient should have a daily cleansing bed bath. The water should be comfortably warm. 4. Oral and nasal hygiene is a very important aspect of the nursing care of a patient with measles. 5. Care of the eyes is necessary. The patient is sensitive to light. Therefore, position of the patient in such a way that direct glare of light is avoided. Keep eyes free of secretions. 6. Care of the ears is also important. It is the responsibility of the nurse to be on the alert for any signs of early mastoid infection. 7. Daily elimination is important. This can be accomplished with a mild laxative, as prescribed by the physician. 8. During the febrile stage, limit the diet to fruits, milk and water. If the patient is vomiting, give frequent, small servings of iced juices. 9. The patients position should be changed every three to four hours. 10. Penicillin or other prescribed medications, are usually given in cases where there is complication.

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Meningitis (cerebrospinal Fever)

Definition: is the inflammation of the meninges of the brain and spinal cord as a result of viral bacterial infection. Such inflammation may involve the three meningeal membranes-The dura matter, arachnoid membrane and the pia matter. Incubation Period: Incubation period varies, the extreme limits being set from one to ten days. Etiologic Agent: The disease can be caused by several kinds of organisms, including Pneumococcus, Staphylococcus and the tubercle bacillus. The species Neiseria meningitides (meningococcus) is the organism causing most epidemics meningitis. Pathophysiology: The infectious agents (ie, bacteria, virus, fungus, parasite) enter the central nervous system (CNS) from the nasopharynx and via the respiratory tract either through the bloodstream or via the nerves or by direct contiguous spread from the adjoining structures and replicate in uncontrolled fashion resulting in meningeal inflammation. Classificatios: 1. Acute meningococcemia a. Meningococci invade the bloodstream without involving the meninges. b. The onset is characterized nasopharyngitis, followed by a sudden attack f high-grade fever with chills, nausea, vomiting, malaise and headache.

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c. Petechial, purpuric or ecchymotic hemorrhages scatter over the entire body and mucous membranes. d. Adrenal lesions start to bleed into the medulla, extending to the cortex. e. The combination of meningococcemia and adrenal medullary hemorrhage is known as Waterhouse-Friderchsen syndrome. f. Waterhouse-Friderchsen syndrome is the rapid development of petechiae that become purpuric and echymotic spots in association with shock. g. The condition runs a short course and is usually fatal. This frequently occurs in the fulminant type. 2. Aseptic meningitis a. It is a benign syndrome characterized by headache, fever, vomiting, and meningeal symptoms. b. It begins suddenly with a fever of up to 40 degrees, alterations in consciousness (drowsiness, confusion and stupor), and the neck and spine stiffness, which is slight at first. c. Characteristic signs of meningeal irritation: Stff neck or nuchal rigidity Opsthotonos (+) Brudzinskis sign. (+) Kernigs sign Exaggerated and symmetrical deep tendon reflexes. d. Sinus arrhythmia, irritability, photophobia, diplopia and other visual problems e. Delirium, deep stupor and coma. f. Signs of intracranial pressure Bulging fontanels in infants nausea and vomiting (projectile) severe frontal headache blurring of vision alteration in sensorium Modalities of treatment: 1. If meningitis is left untreated it has a mortality rate of 70%-100%. 2. Treatment includes appropriate antibiotic therapy and vigorous supportive care. 3. IV antibiotics are usually given for two weeks and are followed by oral antibiotics such as: Ampicillin Cephalosporins (ceftriaxone) Aminoglycosides 4. Digitalis glycoside (digoxin) is administered to control arrhythmias. 5. Mannitol is given ti decrease cerebral edema. 6. An anticonvulsant or sedative is needed to reduce restlessness and convulsions. 7. Acetaminophen is helpful is relieving headache and fever.

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Nursing management: 1. Assess neurologic signs often. Observe the patients level of consciousness and check for increased intracranial pressure(ICP) (signs include plucking at bedcovers, vomiting, seizures and changes in motor functions and vital signs). 2. Watch out for the deterioration of the patients condition, which may signal an impending crisis. 3. Monitor fluid balance. Maintain adequate fluid intake to avoid dehydration, but avoid fluid overload because of the danger of cerebral edema. Measure central venous pressure and intake and output. 4. Watch out for any adverse reaction to the antibiotics and/or other drugs. Avoid infiltration and phlebitis. 5. Position the patient carefully to prevent joint stiffness and neck pain. Turn the patient often to avoid pressure sores and respiratory complications. Assist with ROM. 6. Maintain adequate nutrition and elimination. 7. Ensure the patients comfort. 8. Provide reassurance and support to the patient and the family. 9. Follow strict aseptic technique when treating patients with head wounds or skull fractures. 10. Isolation is necessary, especially if nasal culture is positive.

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Scabies

Synonyms None Definition Scabies is an itchy, highly contagious skin condition Background The burrows sometimes appear as short, wavy, reddish, or darkened lines on the skin's surface, especially around the wrists and between the fingers. A child who has contracted scabies can also develop a bumpy red rash. Mites are small eight-legged parasites (in contrast to insects, which have six legs). They are tiny, just 1/3 millimeter long, and burrow into the skin to produce intense itching, which tends to be worse at night. The mites that infest humans are female and are 0.3 mm-0.4 mm long; the males are about half this size. Scabies mites can be seen with a magnifying glass or microscope. The scabies mites crawl but are unable to fly or jump. They are immobile at temperatures below 20 C, although they may survive for prolonged periods at these temperatures.

Infectious Agent Sarcoptes scabiei

Incubation Period The itch mite may burrow the skin and lay ova within 24 hours of the original contact.

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Pathognomonic Sign Intense itching

Pathophysiology Sarcoptes scabiei undergoes four stages in its life cycle: egg, larva, nymph and adult. Females deposit 2-3 eggs per day as they burrow under the skin Eggs are oval and 0.10 to 0.15 mm in length and hatch in 3 to 4 days. After the eggs hatch, the larvae migrate to the skin surface and burrow into the intact stratum corneum to construct almost invisible, short burrows called molting pouches. The larval stage, which emerges from the eggs, has only 3 pairs of legs and lasts about 3 to 4 days. After the larvae molt, the resulting nymphs have 4 pairs of legs. This form molts into slightly larger nymphs before molting into adults. Larvae and nymphs may often be found in molting pouches or in hair follicles and look similar to adults, only smaller. Adults are round, sac-like eyeless mites. Females are 0.30 to 0.45 mm long and 0.25 to 0.35 mm wide, and males are slightly more than half that size. Mating occurs after the active male penetrates the molting pouch of the adult female. Mating takes place only once and leaves the female fertile for the rest of her life. Impregnated females leave their molting pouches and wander on the surface of the skin until they find a suitable site for a permanent burrow. While on the skins surface, mites hold onto the skin using sucker-like pulvilli attached to the two most anterior pairs of legs. When the impregnated female mite finds a suitable location, it begins to make its characteristic serpentine burrow, laying eggs in the process. After the impregnated female burrows into the skin, she remains there and continues to lengthen her burrow and lay eggs for the rest of her life (1-2 months). Under the most favorable of conditions, about 10% of her eggs eventually give rise to adult mites. Males are rarely seen; they make temporary shallow pits in the skin to feed until they locate a females burrow and mate.

Period of Communicability Entire period that the host is infected Mode of Transmission Direct- through an infected person Also acquired through sleeping on an infested bed or wearing infested clothing. Anyone may become infected and re-infected Scabies on dogs is called mange. When canine or feline mites land on human skin, they fail to thrive and produce only a mild itch that eventually disappear. Clinical Manifestation Itching usually starts first. It often becomes noticeable at night or after bathing and is sometimes mistaken for dry skin. Itching is caused by an allergic reaction
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to the scabies mite. Sometimes the itching is very intense, especially in small children and older adults. Irritated skin often appears as a rash and skin sores that look like tiny curving tracks. These symptoms are a result of the mite tunneling under the upper layers of the skin. Sometimes you can see a small blister or the mite itself, which looks like a tiny black dot, at the end of a burrow. The tracks may be hard to see after you scratch the area. Babies may only have red and inflamed skin, sometimes with small sores that are like blisters.

Symptoms are most likely to develop: Between the fingers and on the palm side of the wrists. On the outside surfaces of the elbows and in the armpits. Around the waistline and navel. On the buttocks. Around the nipples, bra line, and the sides of the breasts (in women). On the genitals (in men).

In babies and small children, itching and skin irritation may also occur: Around or on the scalp, neck, and face. On the palms of the hands and soles of the feet. Often the first symptom noticed in a baby is in these areas and is a series of tiny sores that are like blisters (vesicles).

Diagnostic Procedure Mineral drop oil placed onver the burrow, followed by superficial scraping and examination of expressed material under a low-powder microscope. Medical Management

Permethrin 5% cream (Elimite) is the treatment of choice for scabies. Permethrin 5% cream is applied from the head to the bottom of the feet, paying special attention to skin folds, the groin area, and the webs between fingers and toes. The cream should be applied to clean, dry skin. For best results, clip and clean all fingernails and toenails. Permethrin is usually left on the skin for 10-14 hours and then washed off in the shower. It is best to apply permethrin at bedtime and then wash it off in the morning.

Less common prescription agents

Lindane 1% cream or lotion is an older medication that is rarely used because it is not very safe in children and is potentially toxic to the nervous system (leading to symptoms such asdizziness, seizures). Some scabies have become resistant to Lindane.
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Ivermectin pill(s) (Stromectol) is an oral medication that is active against several parasites. It is not FDA-approved for use in scabies but has been used in cases with very heavy infestations. Ivermectin is not used in small children or in women who are pregnant or breastfeeding. Malathion 0.5% lotion (Ovide) is usually used for head lice but has been used successfully to treat scabies. It is irritating to the skin. It must taken only as directed and should be kept out of the reach of children because ingestion may cause organophosphate poisoning. Benzyl benzoate lotion is an older treatment for scabies. It can be irritating to the skin, especially in people who have eczema. Crotamiton lotion or cream (Eurax) is approved for use in adults with scabies. Treatment failures with this drug are more common than with permethrin. Sulfur-based lotions, creams, or soaps have been used, but are less effective than other options. They should not be used in people who are allergic to sulfa.

Nursing Management 1. Instruct patient to apply the cream at bedtime, from neck down to the toes, covering the entire body. 2. Contaminated clothing or bedclothes should be dry-cleaned or boiled. 3. Advise patient to report any skin irritation. 4. If patient is hospitalized, practice good hand washing techniques or use gloves while performing nursing procedures. 5. Terminal disinfection should be carried out after the discharge of the patient. Prevention 1. 2. 3. 4. Good personal hygiene Avoid contact with infested person All members of the household should be treated After the treatment, beddings and clothing worn next to the skin should be properly laundered.

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Schistosomiasis Synonyms Bilharziasis, Snail Fever

Definition Is a slowly, progressive disease caused by blood flukes of class Trematoda. It is a chronic wasting disease common among farmers and their families in certain parts of the Philippines. This is not only a public health concern but also a socio-economic problem because by causing illness, it reduces agricultural productivity.

Background Theodore Bilharz identified the parasite Schistosoma hematobium in Egypt in 1851. Schistosomiasis is the second most prevalent tropical disease in the world; malaria is the first. The disease is found mainly in developing countries in Africa, Asia, South America, the Middle East, and the Caribbean. About 207 million people in at least 74 countries are estimated to have the disease. In the U.S., it is diagnosed in tourists who have visited these developing countries and in visitors from these countries, or from lab accidents.

Infectious Agent Schistosoma japonicum. 3 major types of organism: Schistosoma japonicum.

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a. Infects the intestinal tract (Katayama disease) b. Found to be the only type that is endemic in the Philippines. c. Also known as Oriental Schistosomiasis Schistosoma mansoni a. Affects intestinal tract b. Common in some parts of Africa Schistosoma haematobium a. Affects urinary tract b. Found in some parts of the Middle East, like Iraq and Iran Incubation Period At least 2 months Pathognomonic Sign Swimmers itch

Pathophysiology In the body, the larvae develop into adult schistosomes, which live in the blood vessels. The females release eggs, some of which are passed out of the body in the urine or faeces. Others are trapped in body tissues, causing an immune reaction. In urinary schistosomiasis, there is progressive damage to the bladder, ureters and kidneys. In intestinal schistosomiasis, there is progressive enlargement of the liver and spleen, intestinal damage, and hypertension of the abdominal blood vessels.

Period of Communicability None Mode of Transmission Ingestion of contaminated water Through skin pores Through an intermediary host, a tiny snail called Oncomelania quadrasi

Clinical Manifestation Low-grade fever Pruritic rash swimmers itch

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Myalgia and cough Abdominal discomfort due to spleenomegaly, hepatomegaly and lymphadenopathy. Bloody- mucoid stools similar to dysentery Icteric and jaundice Abdominal enlargement In chronic disease, patient becomes weak and pale and there is a marked muscle wasting When reaches the brain, the victim experiences eevere headache, dizziness and convulsions.

Complications Liver cirrhosis and portal hypertension Cor pulmonale and pulmonary hypertension Heart failure Ascitis Hemaemesis as a result from rupture of esophageal varices Renal failure Cerebral schistosomiasis o Caused by the hosts reaction to schistosoma eggs. The mechanism of egg deposition is unknown, but the presence of the eggs suggests that they my cross the blood brain barrier or that some worm pairs may reach the venous side of the cerebral circulation. o Manifest increased intracranial pressure associated with focal neurologic signs. Diagnostic Procedure Fecalysis or direct stool exam Kato-katz technique Liver and rectal biopsy Enzyme-linked immunosorbent assay (ELISA) Circumoval precipitin test (COPT)- confirmatory test

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Medical Management Praziquantel tab for 6 months; 1 tab 2x a day for 3 months, then 1 tab a day for 3 months. Fuadin injection given either IM/IV. Patient consume 360 mg for the entire treatment.

Prevention Basic principle of its prevention and control is interrupting the life cycle of the worm and protecting people from infection through following measures: 1. Have a stool examination 2. Reduce snail density by: a. Clearing vegetation, thus exposing the snail to sunshine b. Constructing a drainage system (canals) to dry the areas where snails thrive c. Improve farming through proper irrigation and drainage, crop rotation and removal of weeds, thus disturbing the living conditions of the snail. 3. Diminish infection rate through: a. Proper waste disposal b. Control of stray animals c. Prohibition of people, especially children, from bathing in infested streams d. Construction of footbridges over snail-infested streams e. Provision of an adequate water supply for bathing and laundering and safe water for drinking. 4. Providing health education on the disease process, mode of transmission and prevention.

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Syphilis

Synonyms Lues venereal, Morbus Gallicus Definition Is a chronic, infectious transmitted disease that usually begins in the mucous membranes and quickly becomes systemic. Caused by a spirochete and is acquired through sexual contact. It may also be congenital in nature.

Background In 2008, 63% of the reported primary and secondary (P&S) syphilis cases were among men who have sex with men (MSM). During 20042008, rates of P&S syphilis increased the most among 1524 yearold men and women.

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Infectious Agent Treponema pallidum

Incubation Period 10 to 90 days. Average is 3 weeks Pathognomonic Sign Chancres, Gumma

Pathophysiology In the

Period of Communicability Is variable and indefinite

Mode of Transmission Direct contact Indirect contact Transplacental transmission Can be transmitted from a syphilitic baby to a wet nurse or to anyone carelessly handling diapers.

Clinical Manifestation 1. Primary syphilis a. Symptoms during this stage usually start about 3 weeks after a person becomes infected with the syphilis bacteria (Treponema pallidum), but the range is from 10 to 90 days. b. First symptom of primary syphilis is often a single, small, round, painless sore, called a chancre. c. The chancre disappears in about 3 to 6 weeks whether or not a person is treated. 2. Secondary syphilis a. Symptoms can begin 2 to 10 weeks after the chancre sore appears. b. The most common symptom is a rash on the palms of the hands and the bottoms of the feet. c. The symptoms of secondary syphilis will resolve with or without treatment. d. Rash can be macular, popular, pustular or nodular.
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e. Lesions are uniform size and well-defined and generalized. f. In warm, moist areas of the body such as the perineum, vulva and rolls of fats in the scrotum, the lesions enlarge and erode, producing highly contaminated pink or grayish white lesions (condylomata lata) g. Constitutional symptoms: headache, anorexia, malaise, weight loss, nausea and vomiting, sore throat and slight fever. h. Alopecia occur temporary i. Nails become brittle and pitted.

3. Latent syphilis a. This stage can start from 2 years to over 30 years after the initial infection. b. In early latent syphilis, you may not have syphilis symptoms, but the infection remains in your body. When you are in this stage, you can infect a sexual partner. 4. Late syphilis Considered as a destructive but non- infectious stage a. Late, benign syphilis Develops between 1to 10 years after the infection Gumma, a chronic, superficial nodule or a deep granulomatous lesion that is solitary, asymmetric, painless and endurated. May appear on the skin, bones, mucous membranes, upper respiratory tract, liver or stomach Gummas can be found in any bones, particularly the long bones of the legs.

b. The late syphilis Involves liver. It causes epigastric pain, tenderness, an enlarged spleen and anemia. Affects upper respiratory tract, it may cause perforation of the nasal septum or the palate. In severe cases, disease causes the destruction of bones and other organs which may lead to death.

c. Cardiovascular syphilis developed about 10 years after the initial infection

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Appear asymptomatic but may fuffer from aortic regurgitation and aneurysm.

d. Congenital syphilis Fetus may be overwhelmed by the infection and die. The fetus will then be expelled by the uterus, leading to either miscarriage or stillbirth, depending on the stage of pregnancy. If treponema infection does not prove to fatal, it may still show alterations in fetal development at various stages.

Early Congenital Syphilis a. Lesions of the skin and mucous membranes: Syphilitic pemphigus (bullous rash) Old man look Syphilitic nonychia

b. liver and Spleen Abdomen is proturbent Owing to the enlargement of the liver and the spleen Liver cells tend to be immature and imperfectly formed Hepatic insufficiency

Late Congenital Syphilis a. Interstitial keratitis is the commonest late lesion. Begin at any age from the 30 years or even later Appear as circumocorneal vascularization of the sclera followed by vascular infiltration extending from the sclera into the deep layers of the cornea. It usually affects a one eye at first and eventually ffects the other eye from a few weeks to many years. Severe lesions causing corneal scarring, giving rise to opacities which may cause slight impairment of vision or even complete blindness.

Complications Severe damage to several organs and the nervous system Heart disease, insanity and brain damage Severe illness or death in newborn

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Diagnostic Procedure Dark field illumination test is most effective if moist lesions are present Fluorescent treponemal antibody absorption test, in which the specimen consists of exudates from a lesion VDRL slide test and rapid plasma reagent test CSF analysis

Medical Management Penicillin G benzathine IM (2.4 million units) Oral tetracycline or doxycline for 15 days for early syphilis and for 30 days for late infections.

Nursing Management 1. Stress importance of completing the treatment even after the symptoms subside. 2. Instruct infected individuals to inform their partner that they should be test end if necessary, treated. 3. Practice universal precaution. 4. In secondary syphilis, keep the lesions dry as much as possible. If they are draining, dispose of contaminated materials properly. 5. In cardiovascular syphilis, check for signs of decreased cardiac output (decreased sensorium and urine output and hypoxia) and pulmonary congestion. 6. In neurosyphilis, regularly check the level of consciousness, mood and coherence. Watch for signs of ataxia. 7. Encourage patient to undergo VDRL testing 3, 6, 12 and 24 month to detect any possible relapse. 8. Be sure to report all cases of syphilis to local public health authorities. Prevention 3. Report cases to the Department of Health 4. Control prostitution 3. Require sex workers to have regular check up 4. Proper sex education should be given in early life t home, in schools and in the community. 5. Look for cases of syphilis infection 6. contact tracing

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Tetanus

Synonym Lockjaw

Definition Tetanus is an infectious disease caused by Clostridium tetani which produces a potent exotoxin with prominent systemic neuromuscular effects such as generalized spasmodic contractions of the skeletal musculature. Tetanus is fatal in up to 60% of unimmunized persons, with death occurring usually within ten days of onset. When symptoms develop within three days, the prognosis is poor.

Background The word tetanus comes from the Greek tetanos, which is derived from the term teinein, meaning to stretch. Tetanus was first described by the ancient Egyptians in the Edwin Smith Papyrus around 3000 BC. Tetanus has also appeared in military medical documents throughout the ages. Slapping dung on the umbilical cords of newborns (ie, as part of ritualistic ceremonies) caused rampant tetanus neonatorum or trismus nascentium in the West Indies and in Africa.

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In 1884, Arthur Nicolaier discovered the anaerobic bacillus Clostridium tetani.

Infectious Agent Clostridium tetani

Incubation Period Within 3 days to 3 weeks in adults and 3 to 30 days in the newborn (tetanus neonatorum)

Pathognomonic Sign Risus sardonicus

Pathophysiology Liberation of toxins Tetanospasmin Tetanolysin

Affects nerves specifically myoneural junction of muscles which causes localized spasm and pain

Deadly effect: lysis or destruction of RBC and WBC

Bloodstream CNS

Spinal cord -lockjaw -trismus -risus sardonicus -opisthotonos

Brain
-irritable -headache -laryngeal/pharyngeal spasms -general rigidity -convulsions

Sources of Infection Animal and human feces (the organisms are found in the intestinal wall of herbivorus animals,including man).

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Soil and dust Plaster of Paris; unsterile sutures, pins and scissors; and rusty materials

Mode of Transmission Normally through punctured wounds contaminated by dust ,soil, or animal excreta containing Cl. tetani. Rugged, traumatic wounds and burns The umbilical stump of the newborn, especially if delivered at home and thus have faulty cord dressings Babies delivered to mothers without tetanus toxoid immunization Unrecognized wounds (i.e., cleaning of the ears with sharp materials) Dental extraction, circumcision, and ear piercings

Clinical Manifestations 1. Neonate Feeding and sucking difficulties due to stiff jaw May cry excessively; most of the time, however, the cry is short, mild and voiceless An attempt to suck results in spasms and cyanosis Fever due to infection and dehydration Tonic or rigid muscular contractions, spasms or convulsion are provoked by stimuli Cyanosis and pallor develop Severe cases may end in flaccidity, exhaustion and death

2. Older children and adult If tetanus remains localized, signs of onset are spasm and increased muscle tone near the wound If it becomes systemic or generalized: o Hypertonicity, hyperactive deep tendon reflexes, tachycardia, profuse sweating, low-grade fever and painful involuntary muscle contractions o Neck and facial muscle rigidity (trismus) o Grinning expression (risus sardonicus) o Board-like abdomen or abdominal rigidity
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o Opisthotonos (arching of the back) o Intermittent tonic convulsions lasting for several minutes which may result in cyanosis and sudden death due to asphyxiation o In severe cases, laryngospasm is followed by the accumulation of secretions in the lower airways, resulting in respiratory distress due to the involvement of respiratory mucles o Fracture of the vertebrae may occur during severe spasms, yielding to coma and death In mild cases, after a period of weeks, spasms gradually diminish in frequency and severity, with trismus being the last symptom to disappear In fatal cases, death usually occurs during the 1st 10 days of the disease

Diagnostic Procedure CSF normal result Normal or slightly elevated WBC count

Complications 1. Results of laryngospasm and involvement of the respiratory muscles: Hypostatic pneumonia Hypoxia Atelectasis and pneumothorax Traumatic glossitis and microglossia

2. Changes related to sympathetic nervous system: Transitory hallucinosis Hypersalivation, diaphoresis and unusual tachycardia, especially with the use of aerosolized bronchodilators Cardiac standstill and bradycardia (high mortality)

3. Due to trauma: Laceration of the tongue and buccal mucosa Intramuscular hematoma Fracture of the spine and ribs

5. Septicemia

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Medical Management 1. Specific Within 72 hours after a punctured wound, the patient should receive anti-tetanus serum (ATS), tetanus antitoxin (TAT) or tetanus immunoglobulin (TIG), especially if the patient does not have any previous immunization Tetanus toxoid, 0.5 cc IM, given on standard schedule Penicillin G sodium, to control infection Muscle relaxant to decrease muscle rigidity and spasm

2. Non-specific Oxygen inhalation NGT feeding Tracheostomy Adequate fluid, electrolyte and caloric intake

Nursing Management 1. Prevention of respiratory and cardiovascular complications. Maintain an adequate airway titanic spasms of larynx, pharynx and respiratory muscles usually occurs during convulsions may lead to hypoxia, asphyxia and death. o Place patient in an intensive care unit requires expert respiratory management with early endotracheal intubation and mechanical ventilation Provide cardiac monitoring - overactivity of SNS may lead to sympathetic crisis and death. o Watch for isolated unexplained tachycardia, temporary hypertension premature ventricular contractions, sweating o Requires aggressive physiologic monitoring and pharmacologic treatment (propranolol to control tachycardia; phentolamine to control hypertensive episodes) Maintain an IV line for medication and emergency care if necessary

2. Carry out effective wound care. Debride all necrotic tissue that favors growth of tetanus bacillus. Irrigate wound copiously to wash out tissue fragments and foreign bodies, immune globulin may also be infiltrated into wound site 3. Ongoing assessment and support.
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Avoid sudden stimulation and light Prevent contractures and pressure sores Watch out for urinary retention Closely monitor vital signs and muscle tone Provide optimum comfort measures

Prevention Active immunization with tetanus toxoid for adults and pregnant women (in the latter to prevent tetanus neonatorum) DPT for babies and children

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Typhoid Fever

Synonyms Enteric fever, Typhus abdominalis Definition A bacterial infection transmitted by contaminated water, milk, shellfish and other foods. It affects the lymphoid tissues of the small intestines called Peyers patches.

Background The name Salmonella typhi is derived from the ancient Greek typhos, an ethereal smoke or cloud that was believed to cause disease and madness. In the advanced stages of typhoid fever, the patient's level of consciousness is truly clouded. Although antibiotics have markedly reduced the frequency of typhoid fever in the developed world, it remains endemic in developing countries.

Infectious Agent Salmonella typhosa/typhi

Incubation Period From 5 to 40 days, with a mean of 10 to 20 days

Period of Communicability Variable. As long as the patient is excereting the microorganism, he is capable of infecting others.
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Sources of Infection A person who has just recovered from the disease or has recently taken care of a patient with typhoid and was infected is considered as potential carrier Ingestion of shellfish (oysters) taken from waters contaminated with sewage disposal can be a source The stools and vomitus of an infected person are sources

Mode of Transmission Fecal-oral transmission The 5 Fs: food, fingers, flies, feces and fomites Ingestion of contaminated food, water and milk

Pathognomonic Sign Rose spots on the abdomen

Pathophysiology 5 Fs contaminated with S. typhi

GIT invading small intestines Peyers patches (lower ileum) Bloodstream

Infectious agent in the blood

Bacteremia 2ndary to the infection of liver, spleen, bone marrow, and lymph nodes

In the liver and kidneys, the focal necrosis of parenchymal cells at the site of colonization; lymphoid tissue hypertrophy and hyperplasia 149

Clinical Manifestations 1. Onset Headache, chilly sensation, and body aches Nausea, vomiting, and diarrhea During the 4th and 5th days, all symptoms are at their worst Fever is higher in the morning than in the afternoon Breathing is accelerated, the tongue furred, the skin dry and hot, and the abdomen distended and tender Rose spots appear on the abdominal wall on the 7th to the 9th days On the 2nd week, symptoms become more aggravated. Temperature becomes stable. Rose spots become more prominent.

2. Typhoid state Symptoms decline in severity The tongue protrudes, becomes dry and brown Teeth and lips accumulate a dirty-brown collection of dried mucus and bacteria known as sordes (preventable by good nursing care) Seems to be staring blankly (coma vigil) Twitching of the tendon sets in, especially those of the wrist (subsultus tendinum) Mutters deliriously and picks up aimlessly at bedclothes with his fingers in a continuous fashion (carphologia) Constant tendency to slip down to the foot part of the bed In severe cases, rambling delirium sets in, often ending in death

Complications Hemorrhage or peforation the 2 most dreaded complications Peritonitis Bronchitis and pneumonia Meteorism or excessive distention of the bowels (tympanites) Thrombosis and embolism Early heart failure
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Typhoid spine or neuritis Septicemia Reiters syndrome joint pain, eye irritation, and painful urination that can lead to chronic arthritis

Diagnostic Procedure Typhidot (confirmatory) ELISA Widal test Rectal swab

Medical Management Chorampenicol (drug of choice) Ampicillin Cotrimoxazole Ciprofloxacin or ceftriaxone 3rd and 4th generation of drugs if does not respond to chlorampenicol

Nursing Management Isolation by the medical aseptic technique Maintain or restore fluid and electrolyte balance by giving nourishing fluids in small quantities at frequent intervals Monitor vital signs Prevent further injury if with typhoid psychosis Maintain good personal hygiene and mouth care Cooling measures during the febrile state Watch out for signs of intestinal bleeding Terminal and concurrent disinfection

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Prevention Sanitary and proper disposal of excreta Proper supervision of food handlers Enteric isolation Provision of adequate amounts of safe drinking water supply Reporting of cases to health authorities Detection and monitoring of typhoid carriers Education of the general public on the mode of transmission

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