Parasite

Leishimania donovani

Disease
Visceral leishmaniasis (Kala-azar) Affects reticuloendothelial systems like liver, spleen, and bone marrow. Anemia, leukopenia, thrombocytopenia, low white blood cells, enlarge spleen, and increase IgG. intermittent fever, weakness, weight lost. Hyperpigmentation of skin. Post Kala azar dermal leishmaniasis (arises several years of treatment after primary infection. Lesion contain a lot of amastigote ) Cutaneous Leishmaniasis Immune response by body can lead to chronic inflation which results in granulomatous response. Red papule (raised edge and central crater), can enlarge to form satellite nodules that coalesce and ulcerate. Have depressed scar. Leishmania diffusa (cell mediated immunity doesnot develop the lesion continue to spread to large area of the skin. It resembles leprematous leprosy) Tropical (dry), major (wet), mexicana (disseminating form), aethipica (disseminating form).

Transmission
Sand fly (phlebotomus) for old world and Lutzomyia in the new world. Only female flies feed on blood. Promastigote (flagellated, infectious) Amastigote (non-flagellated and diagnostic) Life Cycle 1)fly takes a blood meal and injects promastigote stage (infective)into skin. 2)promastigote are phagocytized by macrophage. 3) Promastigotes transform into amastigotes (diagnostic) inside macrophage. 4) Amastigotes multiply in cell 5) fly takes a blood meal and ingest macrophage infected with amastigotes 6)ingestion of parasitied cell 7) amastigotes transform into promastigote in midgut 8) divide in midgut and migrate to probiscis

Treatment
diagnose through bone marrow, spleen, liver, or lymphnode biopsy. Giemsa stain to look for amastigotes. Culture the parasite. Serology (elevated serum globulin), PCR, skin test (leishimanin test/Montenegro): to see if there is hypersensitivity to antigen. Treatment Pentamidine isethionate Control No vaccine, use net, protective clothing, insect repellent

Leishinmania tropica, major, Mexicana, aethiopica

Same as above

Diagnose and control are the same Treatment: clean and remove tissue debris and treat with antibiotics for secondary infection by bacteria. Let it heal on its own. For non healing lesions use pentavalent antimony sodium glucoate or ketoconazole

parasite
L. Brasiliensis

Disease
Mucocutaneous Leishimaniasis Affects skin, mucus membrane, cartilages. Start as a papule at the site of the bite. Gradually forms metastatic lesion. This can lead to disfiguring granulomatous, ulcerating lesion. Lesion migrates to nasopharyngeal. After 20 years of tissue damage it can destroy nasal septum. Patient may die of asphyxiation from blockage of trachea.
African Sleeping Sickness (African trypanosomiasis) Antigenic variation in their surface glycoproteins to help evade the host immune response Primary lesion Parasite multiplies extracellularly and cause inflammation. Lesion may become tryanomosomal chancre. Lesions are painless, self-limited, and contain dividing parasite Stage 1 Intermittent fever every 2 weeks and skin rash Winterbotoms sign Lymphadenopathy in posterior triangle of neck Other symptoms Splenomegaly, myocarditis, leukocytosis, thrombocytopenia, anemia. High level of heterophile antibodies, anti DNA (rheumatoid factos), excess immune complex Terminal Stage Demyelinating encephalitis, increase pressure and protein in CSF, headache, insomnia, mood change, muscle tremors, slur speech. Sleeping sickness syndrome: lassitude, coma, death

Transmission same

Treatment
Same diagnose and control. Treatment: Use hot water compress at 39-42 degree Celsius and apply daily for 2030 min/day for 12-30 days. Exposure to UV or IR for 20 min/day. Patient develops permanent immunity after recovery.

Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense

Trypomastigote (diagnostice stage) Long for with kinetoplast posterior to the nucleus Epimastigote Stunt form, kinetoplast not posterior to nucleus Insect vector Tsetse fly (Glossina) 2nd host Gambience : human Rhodesiense: human and cattles form disease, but antelopes are disease carrier

Life cycle
Tsetes fly take blood mealinjected metacyclic trypomastigotes transform into bloodstream trypomastigotes which are carriersTrypomastigotes multiply by binary fission in body fluidTsetse fly take a blood mealbloodstream trypomastigotes transform into procyclic trypomastigotes and multiply by binary fission in the flys midgut. procyclic trypomastigotes leave the midgut and transform into epimastigotesepimastigotes multiply in salivary gland. Then transform into metacyclic trypomastigotes

Diagnose Blood, aspirate lesion or lymph node, CSF, Microscope (wet mount: motile trypomastigote, and giemsa stain), no culture, animal inoculation but not for gambiense Drugs Parasite in blood Suramin sodium (germanin) or Pentamidine isethionate. Parasite in tissue Melarsoprol Blood and CNS Eflornithine Prevention No vaccine, protect against fly bites, insecticide

Parasite Trypanosomia cruzi

Disease
American Trypanosomiasis (Chagas disease) Antigenic cross reactivity Acute Phase Chagoma, facial edema, unilateral swelling of the eyelids (Romanas sign), parasitemia, fever, acute regional lymphadenitis, hepatospenomegaly, myocarditis Asymptomatic phase 8-10 weeks after infection, may last for many years Chronic phase megaesophagus, megastomach, megacolon, dilated cardiomyopathy, Achalasia,

Transmission
Reduviid bugs Kissing bug because they bite around mouth and eyes of a sleeping person. Feed at night, both male and female transmit disease Animal host Human, cat, dog, rats, raccoon, armadillo, opossums Congenital chagas Fetus through placenta Trypomastigote: long flagellated found in animal blood and insect body, kenotoplast positioned anterior to nucleus Epimastigote: short flagellated, kenotoplast positioned posterior to nucleus and has undulating membrane Amastigote: non-flagellated form found intracellularly Life cycle Triatomine bug takes a blood meal (passes metacyclic trypomastigote in feces) metacyclick trypomastigotes penetrate human woundAmastigote multiply by binary fission in cells of infected tissuetransform into trypomastigoteburst out of cell and enter the bloodstreamtriatomine bug takes a blood meal and ingest trypomastigoteepigotes in midgut and multiplies metacyclic trypomastigoes in hindguy

Treatment
Diagnose Blood, fluid for centrifuge, microscope: wet mount for motile trypomastigote, and giemsa for trypomastigote or pseudocyst with amastigote form. Culture in trypomastigote form. Animal inoculation , ELISA, xenodiagnosis (only use for last resort) Treatment No treatment Nifurtimox with gamma interferon to shorten acute phase. Prevention No vaccine Modify habitat, insecticide

Parasite Toxoplasma Gondii

Disease
Acute Toxo Flu-like symptom (swollen lymph nodes, neckaxillaegroin) muscle pain, damage brain (encephalitis), damage eyes (necrotizing retinochoroids) Latent Toxo Only Bradyzoites present (cyst in nervous and muscle tissue). Infants may be asymptomatic at birth but have problems later on Congenital mom to fetus, infect in first trimester leads to abortion. Second and third trimester less severe. Infected before pregnancy will not give to fetus. Postnatal toxo (asymptomatic at birth, but handicapped in the future. Leading cause of blindness for children) Cutaneous Toxo Nodule, maculopapular lesions, blueberry muffin lesion Psychological issues Produce enzyme with tyrosine hydroxylasechange dopaminealter mood, social, attention, motivation

Transmission
Definitive host: cat Intermediate host: human Tachyzoites: Rapidly multiplying in macrophages, lunate shape, transplacental Bradyzoites Tissue cyst, slow growing, gamete formation, uncook meat Oocyst 8 sporozoites, cat feces Intestinal Phase Cat ingest tissue cyst in raw meat of intermediate hostbradyzoite in the tissue cyst are released in small intestineinfects epith cells and develop into male and female gametesgametes fuse and form oocyst which is excreted with feces oocyst develops into infective stage in the soil Extraintestinal phase Ingest oocyst from catin guy the cyst rupture and release trophozoitesmacrophage engulf them and multiply asexually to make tachyzoites spread to other places (brain, muscle, eye, lungs liver) bradyzoites(important diagnosis stage)

treatment
Diagnose Cutaneous toxo (tachyzoites form of t. gondii found in epidermis) Blood, sputum, bone marrow, CSF, exudates, biopsy from lymph nodes, tonsils, striated muscle. Giemsa stain, microscopic view for tissue cyst with bradyzoites, brain tissue stained. Animal inoculation. Tissue culture, PCR, skin test with antigen extract from toxo, immunoflourescent assay (IGM in new borns and IgG in adults) Drug Treatment Pyrimethamine, sulfadiazine, sulfonamide, clindamycin Prevention Eat properly cooked meat Avoid cat poo Change cat litter daily

Parasite Taenia Solium (pork tapeworm)

Morphology
Slightly smaller than T. saginata. Globular scolex with four suckers and a circular hooks (rostellum). Round yellowbrown egg. 5-10 uterine branches

Disease
Cysticerciosis, . Infestation is by multiple worms. Cysticercus in tissue forms space occupying lesion. Cysticerci in eye lead to blindness, in spinal cord lead to paralysis, in brain (neurocysticercosis) often misdiagnose as epilepsy. Secrets substance to suppress inflammation, but dies and calcify to cause inflammation

Transmission
Definitive host is human and intermediate host is pig and human. Life Cycle Eggs or gravid proglottids in feces and passed into environment (diagnostic)pigs become infected by ingesting contaminated eggs or gravid proglottidsoncospheres hatch, penetrate intestinal wall, and circulate to musculatureoncosphere convert to cysticerci in muscle (infective)human eat raw or uncook infected meatscolex attaches to intestineadults in small intestine

treatment
Diagnose CT scan, MRI, ELISA, but cant detect neurocysticercosis. Treatment Praziquantel, albendazole, surgery, steroids (suppress immune response from dying worm) Prevention Cook pork properly and freeze meat. Cysterci can not survive below -10 and above 50 degree Celsius. Good hygiene prevents autoinfection, and properly dispose human waste so pigs dont eat it.

Parasite Taenia Saginata (beef tapeworm)

Morphology
Pear-shaped head (scolex) with four suckers. Branch uterus (15-30). Same egg color and structure as solium.

Disease
One worm per person. Diarrhea, abdominal cramping, nervousness, nausea, and loss of appetite

Transmission
Definitive host is human and intermediate host is cattle. Life cycle Same as solium, but it be the cattle not pig

Treatment
Diagnose CT scan, MRI Treatment Same as solium Prevention Same as solium, but replace the word pork with beef
Diagnose Eggs in poo, increase eosinophils in blood, ELISA Treatment Praziquantel (side effects: interferes with Ca channels so it affects nervous system) Prevention No vaccines, proper sewage, avoid contaminated water, destroy snail and its habitat, avoid swimming in endemic areas

Schistosoma mansoni

Male and female attach together, 1020mm, males are thicker. Have a prominent lateral spine.

Form granuloma and proteolytic enzymes by eggs. In liver (hepatomegaly, splenomegaly, ascites), bladder (granulomatous lesions, hematuria, urethral occlusion, bladder cancer), intestine(polyp formation, dysentery), heart (arteriorlitis and fibrosis, failure of right ventricle) Acture phase Swimmers itch (Itching and dermatitis, type 1 and 4 hypersensitivity), 23 weeks later (fever, chills, diarrhea) Chronic phase GI hemorrhage, hepatomegaly, splenomegaly

Definitive host is human, baboons, mice. Intermediate host are snail (Biomphalaria) Life cycle Find mansoni egg in feces (diagnostic) eggs hatch releasing miracidiamiracidia penetrate snail tissuesporocyst in snailcercariae release by snail in water and free swimming (infectious)penetrate skincercariae lose tails schistosomulaecirculationg o to liver and become adultmigrate to mesenteric venules of bowel/rectumlay eggs that circulate to liver and shed in stools

Schistosoma japonicum

Male and female attach together, 1020mm, males are thicker. Have small lateral spine.

Same as above. Also this organism can go to CNS and cause headache, disorientation, amnesia, and coma

Definitive host (human, domestic animals, rodent) and Intermediate host (snails: oncomelania). Life cycle Find mansoni egg in feces and urine (diagnostic) eggs hatch releasing miracidiamiracidia penetrate snail tissuesporocyst in snailcercariae release by snail in water and free swimming (infectious)penetrate skincercariae lose tails schistosomulaecirculationg o to liver and become adultmigrate to mesenteric venules of bowel/rectumlay eggs that circulate to liver and shed in stools

same

Parasite Schistosoma haematobium

Morphology
Male and female attach together, 1020mm, males are thicker. Terminal spine.

Disease
Same as mansoni but the chronic phase leads to hematuria, UTI, secondary bacterial infection, bladder cancer

Transmission
Definitive host (human), Intermediate host (snail: bulinus) Life cycle Find mansoni egg in urine (diagnostic) eggs hatch releasing miracidiamiracidia penetrate snail tissuesporocyst in snailcercariae release by snail in water and free swimming (infectious)penetrate skincercariae lose tails schistosomulaecirculationg o to liver and become adultvenous plexus of bladder Life cycle Unembryonated eggs passed in feces (diagnostic)2-cell stageadvanced cleavageembryonated eggs are ingested (infectious)larvae hatch in small intestineadults in cecum Soil contamination

Treatment same

Trichuris trichiura (whip worm)

Onchocerca volvulus

Females 50 mm with slender anterior and thick posterior males smaller and has a coiled posterior end egg lemon shaped with two plugs that dont get stained. External layer is yellowbrown Males are smaller than females. Absence of sheath and absence of nuclei on terminal

Asymptomatic Less than 10 worms Massive infantile trichuriasis Chronic profuse mucus and bloody diarrhea with abdominal pains and edematious prolapsed rectum. Malnutrition, weight loss, anemia growth retardation, sometimes death.

Diagnose Symptoms and presence of eggs in feces. Eggs have to be lemon shape with two polar plug Treatment Mebendazole Prevention Proper disposal of waste and improve hygiene
Diagnosis Microfilaria in skin biopsy, adult worms in nodules, dont do blood examination. Treatment Ivermectin against microfilaria, suramin kills adult worms for people with eye disease, surgical removal of nodules. Prevention Insect vector control (insecticide), wear protective garments.

Skin Chronic inflamtion can lead to wrinkling of skin and lack of elsastic fibers and epidermal atrophy. Result in hyper or hypo pigmentation. Onchocercomata (nodules with adult worm, firm. In Africa they appear in lower parts of the body. In Latin America, they appear on upper parts of body) Eyes Microfilariae in eyes lead to blindness Hangin groin Due to lymphadenopathy

Human is the only host. Transmitted by black fly (Simulium damnosum) Obtain from streams and river Life cycle Blackfly takes a blood meal (infectious because L3 larvae enter bite wound)in human, it goes to subcutaneous tissueadults in subcutaneous noduleadults produce unsheathed microfilariae that are found in skin and in lymphatics of CT, but occasionally in peripheral of blood, urine, and sputum (diagnostic)black fly take blood meal (ingests microfilarae)microfilariae penetrate flys midgut and migrate to thoracic muscleL1 larvaeL3 larvaemigrate to head and flys proboscis

in inguinal and femoral area.

Parasite Wuchereria bancrofti And Wuchereria Malayi

Morphology Disease Brancrofti is Elephantiasisin Adult worms bigger than lymph nodes cause malayi. inflammation that Bancrofti obstruct lymphatic vessels, has no causing edema of nuclei at the legs, testis, lymph nodes. Recurrent tip of tail. high fever, Malayi has progressive lymphadenitis. As nuclei worm dies, it present at produce fibroproliferative the tail and granuloma that arranged in cause obstruction. Stretching of skin noncause injury, continuous microfilaria cause eosinophilia and fashion splenomegaly

Transmission
Host is human (bancrofti) and distributed in tropical areas. Host is wild and domesticated animals in south-east asia (malayi). Vectors are mosquito (culex, Aedes, Mansoni, Anopheles) Life cycle Mosquito takes a blood meal (L3 larvae enter skin, infectious)get inside humanadults in lymphaticsadults produced sheathed microfilariae that migrate into lymph and blood channels (diagnostic)mosquito takes blood meal (ingests microfilariae)microfilariae shed sheaths which penetrate mosquitos midgut and migrate to thoracic muscles. L1 larvaeL3 larvae migrate to head and mosquitos proboscis 10PM-2AM appear in blood

treatment
Diagnosis History of mosquito bites in endemic area, microfilaria in blood samples collected at night, presence of sheath and nuclei arrangements Treatment Diethycarbamazine can Kill adult worm and microfilariae. Steroids help alleviate inflammation. Antibiotics prevent secondary infections. Pressure bandages reduce swelling. Surgical removal of infected tissue to improve lymph flow Prevention avoid mosquito bite, insecticide, mass treatment

Parasite Ancyclostoma duodenale and Necator americanus (Hook worms)

Morphology
Americanus has two ventral semilunar cutting plates whereas duodenale has four ventral teeth. The eggs are ovoid, thin shelled, and transparent. Eggs in stools have 4-8 cell stage. Durodenal are larger and C shaped where as the americanus is S shaped.

Disease
Dermalreaction Ground itch occur at feet or hands, and secondary bacterial infection Pulmonary bronchitis, pneumonia and easinophilia GI Attach to intestine with buccal capsule causing pain, anorexia, or huge appetite with pica (desire to eat weird things like dirt, clay, paint), fever diarrhea, abdominal discomfort, weight loss, nausea, vomit, spleen, and liver enlargement Blood loss Anti-coagulant and mucosal feeding increase blood loss. Duodenal is more patho cuz it drains more blood from us. Children Mental retardations,

Transmission
Life cycle Eggs in feces (diagnostic)Rhabditiform larva hatchfilariform larvafilariform larva penetrate skin (infectious)adults in small intestine Obtain worm from soil

treatment
Diagnosis Identify hookworm eggs in feces Treatment Mebendazole Prevention Proper disposal of human waste and wear shoes

sex retard, high eos

Parasite Dracunculus medinensis (guinea worm or fiery serpent)

Morphology Females are larger. Longest nematode

Disease Abscesses, chronic arthritis, physical disability from chronic infection.

Transmission
Transmitted by water fleas (Cyclops). Host: humans, dogs, horses, cows, monkey. Life Cycle Juvenile worms ingested by copepods and mature into infective stagehuman drink water containing infected copepodsJuvenile worms exit the intestinal tract and migrate to subcutaneous tissuesmale and female worms mate and male worm diesfemale worms migrate to skin of legs, ankles, or feetfemales produce juveniles, blister forms on skin. The blister breaks open and juveniles liberated into water Man is the only host, no intermediate host. Infection occurs by ingesting embryonic egg from environment with food or by hand to mouth contact. Life cycle Eggs on perianal folds. Larvae is inside the eggs mature within 4-6 hours (diagnostic)Embryoncate d eggs ingested by human(infectious)larvae hatch in small intestineadults in lumen of cecum Gravid female migrates to perianal region at night to lay egg.

treatment
Diagnose Local blister with adult or larvae. Outline of worm under skin. Radiology Treatment Extraction of worm by rolling it or surgery. Metronidazole Prevention Dont drink contaminated water. Filter or boil water.

Enterobius vermicularis (Pinworm)

Males are smaller with coiled posterior end. Adult life of these worms are two months. Eggs are thin shelled, ovoid, and flattened on one side

Perianal and vaginal irritation. Scratching leads to secondary bacterial infection. Insomia and restlessness. GI symptoms (pain, nausea, vomit). Vaginitis. Can cause granulomas in uterus, fallopian tubes, liver, and peritoneum

2 doses of pyrantel pamoate or Mebendazole two weeks apart (effective against adults). Sanitize bedding and clothing. Be clean, bath, and change underwear

Parasite Ascaris Lumbricoides

Morphology
males are smaller with white creamy color. Both worms have three lips. Fertilized eggs have thick external layer whereas unfertilized egg are longer, more elongated, thin shell, and irregular smooth.

Disease
Intestinal Phase Asymptomatic, abdominal discomfort, nausea, malnutrition, ascaris can go to rectum, weight loss, fatal if worm blocks intestine Lung phase Loefflers syndrome (Hemorrhagic/ Eosinophilic, pneumonia, cough) Breathing problem and fever. Parasite proteins are highly allergenic and can cause asthma attacks, pulmonary infiltration, urticaria (hives)

Transmission
Human or pig is the only host. Man to man transmission Life cycle Ingestion of food contaminated with infective eggseggs hatch in the upper small intestinelarvae penetrate the small intestinal wallenters bloodstreamlarvae pass through liver, heart, and lung to reach alveoligo to bronchiascent to trachea to glottispass down the esophagus to the small intestine where they mature eggs are excreted in fecesinfective largae are formed within eggs (resistant to chem. Disinfectant)

Treatment
Diagnose Stool microscopy, eosinophilia, imaging, ultrasound Treatment Mebendazole, Albendazole, pyraneel, pamoate, ivermectin, piperazine, citrate, levanisole Prevention Good sanitation, no human feces fertilization, mass treatment

Echinococcus granulosus and multicularis (hyadatid cyst)

granulosus Body has three proglottids. The cyst consist of thick outer layer with several thinner internal layer and many protoscolices (hydatid sand) multicularis 4-5 proglotids The cyst grows by external budding forming diffuse growth. Does not have cyst wall, contains numerous cavity with gelatinous matrix within protoscolices and capsules.

Granulosus: Definitive host is dog and intermediate host is sheep, goat, and swine Multicularis Definitive host (foxes) intermediate ( rodents ) and human is dead end host Life cycle Eggs passed in feces eaten by sheep or humans (infectious)oncospher e penetrates gut wall and migrate to other organsHyatid cysts form in organs of intermediate host (diagnostic) after ingestion hydatid cyst is digested and solex evaginatesimmature scolex attaches to intestinal wall and develops into mature strobilla

Hepatic issue Abdominal pain, formation of mass, biliary duct obstruction. Pulmonary Chestin pain, cough, hemopeosis Rupture of cyst Fever, uticaria, eosinophilia, anaphylactic shock, cyst dissemination Hydatid cyst Mainly in liver and lungs, but can be found in brain, eye, kidney, muscle , bones

Diagnose Microscopy, Indirect hemagglutination, indirect fluorescent antibody test, enzyme immunoassay, Treatment Surgery and albendazole

Parasite Diphyllobotrium latum (fish tapeworm)

Disease
Pernicious anemia because the parasite takes up large amount of vitamin B12. Abdominal discomfort, nausea, diarhea

Transmission
First intermediate host is the copepod and the second intermediate host is the small fish. Definitive host is any fish eating carnivores Life cycle Unembryonated eggs passed in the feces (diagnostic)eggs embryonate in watercoracidia hatch from eggs and ingested by crustaceansprocercoid larvae in body cavity of crustaceans Infected crustaceans ingested by small freshwater fish procercoid larva released from crustacean, develops into plercocercoid larva (infectious)predator fish eats infected small fishhuman ingests raw or undercooked infected fishadults in small intestineproglottids release immature eggs Penetration of intact skin by filiariform larvae in the soil, or ingestion through contaminated food or waterlarvae enters lungsalveolimature into adult femalefemale go to intestinal mucosa and produce several eggs through parthenogenesishatch during transit through gut

Treatment
Diagnose Eggs in feces Treatment Praziquantel Prevention Dont eat raw fish or poo

Strongyloides stercoralis and strongyloides fuelleborni (threat worm)

Acute Infection Lower extremity itching (mild erythematous maculopapular rash at the site of skin penetration), cough, dyspnea, wheezing, lowgrade fevers Chronic infection Can be completely asymptomatic. Abdominal pain, intermittent diarrhea with constipation, weight loss, racing larva (recurrent maculopapular serpigo rash), chronic urticaria Severe infection Abdominal pain, distention, cough, hemoptysis, dyspnea, wheezing crackles, stiff neck, headache, brain abnormlities, fever/chills, hematemesis, hematochezia, rash (petechiae, purpura) Hyperinfection syndrome High fever, abdominal pain, bloating, intestinal ulceration, gram neg sepsis and shock, dyspnea, cough, hemoptysis, dissemination of worm, meningitis, heart, urinary tract, bacteremia

Diagnostics Elevated WBC for acute and chronic cases, and elevated Eosinophilia for acute infections. Check stools for S. stercoralis larvae, stool wet mount for direct exam, ELIZA, CXR (patchy alveolar infiltrates, diffuse interstitial infiltrates, pleural effusions). String test, and CT scan Treatment Antihelminitic therapy, Ivermectin, Albendazole, Thiabendazole, antihistamines for itching

disease

Transmission

Treatment

Parasite Toxocara canis (dog parasite) and Toxocara Cati (cat parasite)

Visceral Larva migrans Granulomas form around dead larvae due to delayed hypersensitivity response to larval protein. Blindness, fever, hepatmegaly, eosinophilia

Ancylostoma canine (dog hookworm) and Ancylostoma braziliense (cat hookworm)

Cause cutaneous larva migrans, creeping eruption. Lesion are erythematous, serpignious (spread by creeping), pruritic (extremely itchy), cutaneous eruption,

Life cycle Adult parasite live in the intestine of dogs and cats eggs are passed in the feces which contaminates the soileggs are then swallowed by manhatch in the intestinelarvae penetrate the mucosaenter circulation and are carried to liver, lungs, eyes, brain, and other tissed where they cause inflammatory necrosishuman is a dead end host Life cycle Dog and cats pass eggs with feceseggs hatch in the soillarvae penetrate human skin and migrate through subcutaneous tissue causing inflammatory responsehuman is a dead end host In US disease occurs among children and construction workers who are expose to soil with cat and dog poo

Diagnose Serologic diagnosis, demonstration of the larvae in the affected tissue Treatment Mebendazole or albendazole Prevention Treat dogs and cats, avoid contact of children with cats and dogs

Diagnosis Lab is little help, depends on clinical pictures Treatment Oral or topical thiabendazole

Parasite Disease Loa Loa (eye Calabar swelling(erythema and worm)

edema) due to hypersensitivity to the presence of the worm. The worm can also cause pain to the eye by migrating to the conjunctiva of the eye

Transmission
Humans get infected by bite of chrysops (deer fly) Life cycle Fly takes a blood meal (L3 larvae enter bite wound, infectious)Adults in subcutaneous tissueadults produce sheathed microfilariae that are found in spinal fluid, urine, sputum, peripheral blood and in lungs (diagnostic)fly takes a blood meal (ingests microfilariae)microfilariae shed sheath, penetrate fly midgut and migrate to thoracic musclesL1 larvae L3 larvaemigrate to head and fly sproboscis Female relase microfilaria that enter the blood during the day between 12:00 noon to 2:00 PM

treatment
Diagnose Microfilaria in blood smear. Bllod should be obtained during 12 noon to 2PM. PCR Treatment Diethylcarbamazine Is effective against larvae and may kill adult. Removal of the adult from eye may require surgical extraction Prevention insecticide

Parasite Paragonimus westermani (lung fluke)

Morphology
Body covered with spines, reddish brown, resembles a coffee bean. Adult worms are found in pairs or in threes in fibrotic capsules or cysts in the lungs. Yellowish brown may be seen in the sputum or in feces if sputum is swallowed

Disease
Invading and migrating stage After excystation the adolescents penetrate the intestinal wall and migrate to the lungs Suppurative stage Form a capsule, abscess Cystic stage cyst wall is formed due to progressive fibrosis of the surrounding tissue. If cyst communicates with the bronchilole, patients will cough up rusty sputum. Fibrous scar stage Worms are dead or escape from cyst. The exudate and pus are expelled or absorbed and replace by fibrous-scar tissue Pulmonary Resembles TB with low fever, loss of appetite, night sweat, chest pain, weight lost, rusty sputum. Brain Resembles epilepsy cerebral cystercosis

Transmission
Infective stage (metacercaria), infective mode (eating raw fresh water crabs and crayfish with metacercariae), Infective route (by mouth), site of inhabitation (lungs), intermediate hosts (1st host is melania snail, second hosts is crab and crayfish), reservoir hosts (carnivores like tiger, lion, wolf, fox, dog, lepard, cat). Life style Unembryonated eggs (diagnostic)embryonated eggmiracidia hatch and penetrate snailssporocystrediae cercariaecercariae invade the crustacean and encyst into metacercariae (infectious)humans ingest uncook or pickled crustacean with metacercariaeencyst in duodenumadults in cystic cavities in lungs lay eggs which are excreted in sputum.-->eggs are swallow and pass with stool

Treatment
Diagnose Sputum examination: (alkali digestive method, direct sputum smear.) Stool examination: (Alkali digestion, water sedeimentation method, direct fecal smear) Biopsy for subcutaneous type, CT for brain, immunological test Treatment Praziquantel, hexachloroparaxylol, Bithionol (bitin) Prevention Health education, avoid eating raw fresh water crabs and crayfish, avoid sputum and stool getting into water.

Abdomen Pain, diarrhea, dysentery with blood, mucus, ova in feces. Misdiagnosed as E. histolytica Subcutaneous Painless nodules

Parasite Clonorchiasis Sinensis (liver fluke)

Disease
Chill, high fever, slight jaundice, hepatomegaly, eosinophilia, splenomegaly, continuos reinfection (cirrhosis and portal ypertension), in children (malnutrition), acute or chronic cholecystitis, cholangeitis and cholelithiasis, portal liver cirrhosis (portal hypertension result in upper GI bleeding), pancreatitis, carcinoma of liver

Transmission
Host: cats, dogs, mice, pigs. Route of transmission: eating raw freshwater fish or shrimp. Humans are susceptible Life cycle Eggs into waterfirst intermediate host (special snail) swallow eggsmiracidiacercari a enter water and invade fresh water fish and shrimp (secondary internmediate host) eaten metacercariaeadult worm in human and mammals

Treatment
Diagnose Blood routine testeosinophilia, anemia in severe infection.) Eggs examination (dueodenal aspiration where we find eggs) ELISA, viral hepatitis, liver cirrhosis, fasciolopsiasis, fluke infection Treatment Praziquantel, albendazole Prevention Treat patient and pets, avoid eating raw freshwater fish and shrimp, sanitary disposal of excretament, avoid drinking raw water

Parasite Pneumocystis carinii and Pneumocystis jirovecii

Morphology
Lacks ergosterol and is not susceptible to antifungal drugs. Cyst contain eight intracystic bodies and intermediate precyst stage.

Disease
Opportunistic pulmonary pathogen. Penumonia in immunocompromised Host. Reduced CD4 positive helper T cells lower than 200 leads to pnuemocystic pnumonia. Cyst in alveoli induces inflammation on plasma cell so prevent oxygen exchange (plasma cell pneumonia). In immunosuppressed patients, the orgniasms increase alveolar capillary permeability and damage type 1 cells, thus block gas exchange and lead to dyspnea and hypoxia. Severe disease may cause interstitial edema, fibrosis, hylain membrane formation. Fever, cough, chest discomfort, weight loss, chills hemptysis, tachypnea, tachycardia, in children there could be cyanosis and nasal

Transmission
Airborne and person to person Sexual phase Haploid trophic forms conjugateproduc e a zygote or sporocyst (early cyst)zygote undergoes meiosis and subsequent mitosis to produce eight haploid nucleispore case usually collapses, but retains some residual cytoplasm

Treatment
Diagnose Methenamine-silver, giemsa, tissue stains, Fluorescent-antibody staining, PCR, Lactic dehydrogenase elevatin, CSR (butterfly shaped), respiratory alkalosis, sever dyspnea Treatment High dose of trimethoprimsulfamethoxazole (bactrim, sptra) and prednisone. Alternative drugs are Pentamidine and atovaquone Prevention Trimethoprimsulfamethoxazole or aerosolized pentamidine should be used as chemoprophylaxis in patient with CD4 below 200

flare

Parasite Entamoeba histolytica

Morphology
Trophozoite Metabolically active, move with pseudopodia, finger like projection unidirectionally. Found in colon, tissue, diarea. Divides by binary fission, ingested by red blood cell. Stain with ironhematoxylin Cyst Inactive, resistant to bad environment. Found in lumen of colon and pass with non-diarhea poo. Infective form resistant to stomach acid. Mature cyst has 4 nuclei. Less than 10um are non-patho. Has aggregation of ribosome, evenly distributed chromatin on nuclear membrane

Disease
Amoebic dysentery, liver, brain, lung abscesses. Bloody, mucousy diarrhea, fever, abdominal pain, no pus, but tissue necrosis metastatic Intestinal ameobiasis Trophozoites invade the colonic epitheliumsecret proteolytic enzymes that cause localized necrosisulcer Extraintestinal amoebiasis From submucosa trophozoites may join the portal circulation as microemboli and reach the liver, lung, brain, and form abscess Acute amebiasis Dysentery that is bloody and mucous containing diarrhea with lower abdominal discomfort and dehydration and incapacitation Chronic amebiasis Diarrhea, abdominal cramps, nausea, vomiting, need to poo, loss of appetite and weight loss Amebic abscess Pain in the upper right quandrant, weight loss, fever, tender enlarge liver. May penetrate diaphragm and trophozoit may invade lungs Amoebic liver abscess (fever, RUQ or epigastric pain / shoulder pain, diarhea

Transmission
Infects man, primates, dogs, cats, rats Life cycle Cysts ingested with food or water that is contaminated with human fecal materialcyst excyst in the small intestine and resulting trophozoites colonizing the large intestinetrophozoites Reproduce by division and invade the lining of the large intestine (diarrhea, colitis, dysentery)extraintestinal amoebiasistrophozoite s may invade the blood vessels of the large intestine and be transported to other organs in the body or become cyst and pass in feces.

Treatment
Diagnose
Amoebic (hematophagous trophozoites) in stool. Mixed WBC in stool, patchy inflammation on coloscopy, stool PCR, or antigen capture. Liver abcess : (Ultrasound, raised WBC, serology, aspirate microscope, response to metronidazole 750 t.i.d), fluid stool for trophozoit, formed feces for cyst, scraping and biopsies from colon walls by colonoscopy, liver abscess aspirates, blood for serological test (IgG for past and current infection, and IgM for recent infection, culture, iron hematozylin stain Treatment For carriers (iodoquinol or paromomycin) for symptomatic intestinal and extraintestinal abscess is metronidazole or tinidazole Prevention Personal hygiene and proper sweage, proper treatment of drinking water, carriers should not handle food. Cautious with high carb and low protein food

Parasite Acanthamoeba castellanii and Naegleria flowleri

Disease Naegleri flowleri

Meningitis and encephalitis, can infect immunocompetent individual, and highly fatal Acanthamoeba castellanii Issue associated with contact lens from puncturing of cornea. Can cause meningitis and encephalitis, keratitis

Transmission
Found in swimming pools and contaminated soil. Cyst is resistant to chlorination Naegleri flowleri life cycle Trophozoite stage enters the body through mucus membrane during swimmingpenetrate the nasal mucosa and enter the brain. Acanthamoeba castellanii life cycle Trophozoite state enters the body through broken skin, trauma, and eye

Treatment
Diagnose CSF, microscopic examination for trophozoites. Culture can be grown with Ecoli Treatment Amphotericin B

Parasite Giardia lamblia

Morphology
Trophozoite Actively metabolizing and dividing stage. Pear shaped, bilateral symmetry, 2 nuclei with central karyosome, two axostyles, basal bodies, 4 flagella, suction disk, axoneme (intracellular flagella) Cyst Metabolically dormant and resistant to bad environment like clorine. Oval shaped, thick wall, 4 nuclei, several internal fibers, can stay in water for 3 months

Disease
Does not invade tissue, but trophozoite attach to duodenal/jejunal wall (small intestinge). Mild inflammation, crypt of hypertrophy, villous flattening of the epith cell, malabsorption of food, lower IgA, children more affected. Nonbloody, foul smelling gas, diarrhea, stool would be watery, semisolid, greasy, bulky. Nausea, anorexic, weight loss, malaise, weakness, abdominal cramp, distention, farting, no fever

Transmission
Cyst ingested with contaminated water or foodcyst excyst and trophozoites colonize the small intestinecyst passed in fevergo to reservoir host (beever) or go to water streams

Treatment
Diagnose Stool, duodenal aspiration, detect antigen in stool with elisa, detect cyst or trophozoites in diarrhea. Formed stools will have cysts Treatment Metronidazole (flagy), quinacrine hydrochloride, Trinidazole (Fasign) Prevention Proper disposal of sewage, drink iodine treated or filtered or boil water, no vaccine, no chemoprophylactic

Parasite Balantidium coli

Morphology
Largest intestinal human parasite Trophozoite stage Posses cilia, have two nuclei (large kidney shape is macronucleus and small spherical is micronucleus). Cytoplasm contains vacules and food particles Cyst Spherical, when organisms encysts it secrets a double layered wall. The macro and micro nucleus, contractile vacuole, and cilia could be visible. It is the infective state Trophozoite only, pear shaped, central nucleus, four anterior flagella, undulating membrane that extends about 2/3 of body

Disease
Dysentery, infects the colon. Can invade mucosa and form abscesses and irregular ulceration. Chronic diarrhea, alternating with constipation. Bloody mucoid stool with tenesmus (difficulty defecating) and colic (severe abdominal pain caused by spasm, obstruction, or distention)

Transmission
Parasite of pig, rat, guinea pig, human, and others Humans are infected when they ingest cysts through food or water contaiminated with feces material. Excyst in the intestine, and trophozoite in the colon

Treatment
Diagnose Stool, aspiration from colon, microscopic examination to find trophozoite in liquid stools and cyst in formed stools Treatment oxytetracycline

Trichomonas vaginalis

Trichomoniasis Mild inflammation. However organism does not survive vaginal acidity of 3.8-4.4. in female infection is in vulva, vagina, cervix, and does not extend to uterus. In male infection is in prostate, seminal vesicles, and urethra. Infected mucosa surfaces become tender, inflamed and eroded. In female (watery, foul smelling, greenish vaginal discharge with itching and burning), in males its almost asymptomatic, but have urethritis with white discharge

Sextrophozoite in vaginal and prostatic secretion and urine (diagnostic)mutliply By longitudinal binary fissiontrophozoit in vaginal or orifice of urethra (infectious)

Diagnose Specimen such as vaginal or urethal discharge, microscopic examination like wet mount in saline (look for jerky motion of organism), use hematoxylin or gimesa staining. Culture Treatment Metronidazole (flagyl): both for topical and systemic Tinidazole (Fasign). Estrogen treatment for postmenopausal women Prevention no vaccine, safe sex, dont share shower stuff, treat both sex partner, maintain vaginal pH of 3.8-4.4

Parasite Dientamoeba fragilis

Morphology Disease
Only trophozoid, contain one or two nuclei, no cyst Invade the large intestine, abdominal discomfort and diarrhea.organisms Infect mucosal crypts of the large intestine that are located close to the mucosal epithelium, from cecum to rectum. The cecum and proximal colon are usually affected. Invoke eosinophilic inflammatory response in colonic mucosa (symptom is colonic mucosal irritation). Abdominal pain, flatulence, diarrhea, vomit, weakness, weight loss Babesiosis Infect RBC and lyse them. Onset of influenza. Hepatosplenomeg a And anemia. Asplenic patient affected more severely

Transmission
Trophozoit in feces (diagnostic)transmitted Through fecal oral route or helmith eggtrophozoite ingested (infectious)binary fissiontrophozoit in lumen of colon Trophozoit is extremely sensitive to environment

Treatment
Diagnosis Microscopic examination of stool (presence of two nuclei) Treatment Metronidazole (flagyl) Tetracycline (sumycin) Iodoquinol (vytone, yodoxin)

Babesia microti

Intermediate host (white-footed mouse) and the definitive host (tick: Ixodes dammini), dead end host is human Life cycle tick takes a blood meal (sporozyte introduced into host)go in mousetrophozoite--> merozoitegametetick takes a blood meal (ingests gametes)inside tickfertilize in gutookinete enter salivary glandsporogonysporozoite s (infectious)tick takes a blood meal (sporozoit gets in human)trophozoittransmit from human to human through blood transfusion

Diagnose Giemsa stain, Maltese cross (tetrad), and no pigment formation. Serology, PCR Treatment Quinine and clindamycin

Parasite Cryptosporidiu m parvum

Morpholog y
Oocyst (infective state, contains four sporozoites), trophozoites (release from oocyst), Schizonts (containing eight arc shaped merozoites), microgamates and macrogames fuse to give oocyst

Disease
Causes diarrhea mainly in immunocompromise d host. It inhibits the brush border of mucosal epithelial cells in GI tract such as villi of lower small intestine of jejunum. Watery, non-bloody diarrhea, dehydration, weight loss, abdominal pain, fever, nausea, vomiting. In immunocompromise d patient the CD4 count is less than 200 Causes diarrhea Invade small intestine. Low grade fever, lassitude, malaise, vague abdominal pain with watery diarrhea, weight loss, malabsorption of food. May be self limited for immunocompetent people, but it could also be chronic

Transmission
Host like rodent, fowl, monkey, cattle, and many herbivores. Sexual and asexual Life cycle Host is infected when it ingest oocysts in water or food contaminated with fecal materialoocyst excysts in small intestineparasite undergoes asexual reproduction in the small intestine and oocysts are producedoocysts are passed in host fecesoocyst become infective (sporulate) in the external environment Oocyst are resistant to chlorination

Treatment
Diagnose Stool specimen, wet mount, modified acid-fast staining, immunoflourscent staining, ELISA Treatment Stop using immunosuppressant drugs, supportive therapy, paromomycine or spiramycine No vaccines

Isospora belli

Oocyst excreted at large and have a ellipsoidal shape

Transmitted by fecal oral route. Has both sexual and asexual stage in the intestine Life cycle Oocyst in feces (diagnostic) Immature oocyst with sporoblast Immature oocyst with sporocystsmature oocyst with sporozoites get ingested by human (infectious)Mature oocyst with sporozoites (infectious) go through asexual process and create merozoitesgo through sexual processmicrogamet e and macrogamete fuse to form oocyst in feces (diagnostic)

Diagnose Microscopic examination of stool and detection of oocyst Treatment Trimethoprimsulfamethoxazol e

Parasite Fasiolopsis buski (Giant intestinal fluke)

Disease Inflammation, ulceration, haemorrage, abscess, diarrhea, hunger pains, edema of face and abdominal wall. Abdominal pain, nausea, vomiting. Skin becomes very dry and harsh

Transmission
Definitive host (human and pigs), first intermediate host (snail) second intermediate host (water plants) Life cycle Metacercaria (infectious) is ingested by definitive host (pig and human)and excysts in the small intestinethe adult, sexually mature parasite resides in the hosts small intestine eggs are passed in the hosts feces (diagnostics)eggs hatch and produce freeswimming miracidiuminfect snailparasite reproduce asexually in the snail, producing cercariaecercariae leave the snail and encyst on vegetation producing metacercariae

Treatment Diagnose Eggs in feces Treatment Praziquantel for all flukes

Parasite Trichinella spiralis

Morphology

Disease
Muscle fibers become enlarged edematous and deformed. Paralyzed muscles are infiltrated with neutrophil, eosinophils, and lymphocytes. Splenomegaly and worm induces IgE Intestinal (24-72 hours) Nausea, vomiting, diarrhea, abdominal pain, headache Circulation and muscle (10-21 days) Edema, peri-orbital conjunctivitis, photo phobia, fever, chill, sweating, muscle pain, spasm, eosinophilia Myocardium (10-21 days) Chest pain, tachycardia, EKG changes, edema of extremities, vascular

Transmission
Mammals, carnivores, omnivorous, pigs, human, bears, seals. Humans are infected by eating raw or undercook pork containing larvae encysted in muscle. Life cycle Juveniles are digested from muscles, penetrate into tissue of small intestine and grow to sexual maturitymale and female worms mate and females produce juvenilesjuveniles migrate into muscles of host and mature in infective stagehuman, carni, and omnis are infected by eating infected meat

Treatment
Diagnosis Labs (eosinophilia, serology, muscle biopsy to show presence of larvae inside muscle) Treatment Mebendazol to eliminate worms and steroids to treat inflammation Prevention Cook your meat and eliminate parasite infection in pigs

thrombosis Brain and meninges (14-28 days) Headache (supraoribital), vertigo, tinnitus, deafness, mental apathy, delirium, coma, loss of reflexes Acute trichinosis Fever, orbital oedema, myalgia, eosinophilia

Parasite Hymenolepsis nana (Dwarf tapeworm)

Morphology
Scolex has four suckers with a retractile rostellum equipped with 20 to 30 hooks. Shortest cestode. Egg is oval to spherical with six hooklets and almost colorless. Eggs are infective after they are released and are sensitive to environment.

Disease
Anorexis, abdominal pain, diarrhea.

Transmission
Defintive host (human, rats, mice, with both larvae and adult. Only cestode of human that doesnot require intermediate host), intermediate host (arthropods like beetles and fleas). Definitive host can be infected by ingesting the egg, ingesting an infected arthropod, or autoinfection in which egg hatch before leaving GIT. This is where they are burry in the tissues of the small intestine and develops into cystercoid and it move from tissue to lumen of gut and grows to sexual maturity. Definitive host(dogs, cats, fox, humans), intermediate host (dog and cat fleas and lice) Life cycle Adult worm lives in small intestinegravid proglottids detach and migrate to anus or pass in stooleach proglottid contains eggs packets and each packet has 20 embryonated eggscat and dog flea or lice ingest eggshexacanth embryo is release and cysticercoid develops in the body cavity of fleasdog or human ingest infected fleacystercoid develops into adult in gut

Treatment Diagnosis Eggs in stool Treatment Praziquantel

. Dipylidium caninum (dog tapeworm or cucumber tapeworm)

Gravid proglottids are elongated and resembles rice grains when dry. They have two genital pores laterally (doubled pored)

Eosinophilia, GIT symptoms

Diagnosis Observing gravid proglottids in feces or packets of eggs held by the embryonic membrain, in feces, egg-ball