1.

2.

3.

4.
5.

INFECTIUOS DISEASES
EXANTHEMATOUS FEVERS
Exanthem, meaning to bloom or to break out, refers to an eruption or rash
that is associated with fever and implies that the eruption is infectious in
origin
Exanthems may be caused by viruses, bacteria, Rickettsia, Mycoplasma,
and fungi. Moreover, certain allergic and immune-complex diseases such
as childhood arthritis can mimic infectious exanthems
Common in children. Clinical ranged from nonspecific viral infections to
classic viral
exanthems, bacterial infection or drug allergy.
Severity varies from self-limited viral diseases to potentially life
threatening severe bacterial diseases.
Fever with rash
Infectious:
Bacterial
-Scarlet fever
-Staphylococcal Scalded Skin Syndrome
-Toxic shock syndrome
-Meningococcemia
-Leptospirosis
Classic viral exanthems
-Measles
-Rubella
-Roseola
-Infectious mononucleosis
-Fifth disease

DISEASE
Enterovirus infection
Exanthem subitum
(roseola)
Erythema infectiosum
(fifth disease)
Rubella
(German measles)
Mumps
Infectious
mononucleosis

Rubeola
(measles)

Scarlet fever

CHARACTER OF RASH
Maculopapular; generalized to most of body; discrete
Maculopapular and discrete; begins on trunk and spreads to face
and usually spares the limbs
Red and flushed cheeks with circumoral pallor; subsequent
proximal maculopapular rash on extremities (lacelike)
Slapped-cheek appearance in otherwise healthy child
Pink, maculopapular, discrete; begins on face and spreads to
trunk and extremities
Maculopapular, discrete, concentrated on trunk; may have
urticaria; may be 1st sign of illness
Macular or maculopapular and discrete; when associated with
ampicillin administration, is confluent (morbilliform) and more
intense
Red to brown macular rash that spreads from face and neck to
trunk and extremities; confluent (morbilliform), particularly on
face; begins after onset of fever and fades after 6-7 days with
temporary staining of skin
Koplik spots
Erythematous papular eruption sometimes associated with
generalized erythema; concentrated on trunk and proximal
extremities; feels similar to fine sandpaper

Kawasaki disease

Rash ranges from maculopapular to scarlatiniform to urticaria;

marked erythema of palms and soles

ENTERIC FEVER
Etiology:
1. Typhoid fever is caused by Salmonella enterica serovar Typhi (S. Typhi), a
gram-negative bacterium.
2. A very similar but often less severe disease is caused by S. Paratyphi A
and rarely by S. Paratyphi B (Schotmulleri) and S. Paratyphi C
(Hirschfeldii).
3. The ratio of disease caused by S. Typhi to that caused by S. Paratyphi is
about 10 to 1.
Epidemiology:
1. The age-specific incidence of typhoid may be highest in children <5 yr of
age, with comparatively higher rates of complications and hospitalization
2. many strains of S. Typhi have developed plasmid-mediated multidrug
resistance to all 3 of the primary antimicrobials: ampicillin,
chloramphenicol, and trimethoprim-sulfamethoxazole.
Transmission:
1. Direct or indirect contact with an infected person (sick or chronic carrier)
is a prerequisite for infection.
2. Ingestion of foods or water contaminated with S. Typhi from human feces
is the most common mode of transmission, although water-borne
outbreaks due to poor sanitation or contamination can occur in
developing countries.
3. Oysters and other shellfish cultivated in water contaminated by sewage
or the use of night soil as fertilizer may also cause infection.
Pathogenesis:
1. Incubation period ranges from 4 to 14 days
2. Organisms invade the body through the gut mucosa in the terminal
ileum; then enter the mesenteric lymphoid system, and then pass into
the bloodstream via the lymphatics.
3. Patients who are infected with HIV and with Helicobacter pylori infection
have an increased risk for acquiring typhoid fever.
Clinical features:
1. The clinical presentation varies from a mild illness to a severe clinical
picture
2. Children <5 yr of age have comparatively higher rates of complications
and hospitalization.
3. Diarrhea, toxicity, and complications such as disseminated intravascular
complications are also more common in infancy, with higher case
fatality rates.
4. Complications of typhoid fever seen in adults, such as relative
bradycardia, neurologic manifestations, and gastrointestinal bleeding,
are rare.
5. Typhoid fever usually presents with high-grade fever with a wide variety
of associated features such as generalized myalgia, abdominal pain,
hepatosplenomegaly, abdominal pain, and anorexia.

6. In children, diarrhea may be present in the earlier stages of the illness

and may be followed by constipation.
7. The fever may rise gradually, but the classic stepladder rise of fever is
relatively rare.
8. In about 25% of cases, a macular or maculopapular rash (rose spots)
may be visible around the 7th10th day of the illness
9. If no complications occur, the symptoms and physical findings gradually
resolve within 24 wk; however, the illness may be associated with
malnutrition in a number of affected children.
Complications:
1. Clinically significant hepatitis and cholecystitis are relatively rare and
may be associated with higher rates of adverse outcome.
2. Intestinal hemorrhage (<1%) and perforation (0.51%) is infrequent
among children.
3. Rare complications include toxic myocarditis, which may manifest by
arrhythmias, sinoatrial block, or cardiogenic shock.
4. Neurologic complications are also relatively uncommon among children
and may include delirium, psychosis, increased intracranial pressure,
acute cerebellar ataxia, chorea, deafness, and Guillain-Barr syndrome.
5. Other reported complications include fatal bone marrow necrosis,
disseminated intravascular coagulation (DIC), hemolytic uremic
syndrome, pyelonephritis, nephrotic syndrome, meningitis, endocarditis,
parotitis, orchitis, and suppurative lymphadenitis.
Diagnosis:
1. blood cultures are positive in 4060% of the patients seen early in the
course of the disease, and stool and urine cultures become positive after
the 1st wk.
2. While blood leukocyte counts are low and in younger children
leukocytosis is a common
3. Thrombocytopenia may be a marker of severe illness and accompany
DIC.
4. The classic Widal test measures antibodies against O and H antigens of S.
Typhi but lacks sensitivity and specificity in endemic areas. Because
many false-positive and false-negative results occur, diagnosis of typhoid
fever by Widal test alone is prone to error.
5. A nested PCR is a promising means of making a rapid diagnosis.
D.D:
1. The early stages of enteric fever may be confused with alternative
conditions such as acute gastroenteritis, bronchitis, or
bronchopneumonia.
2. The differential diagnosis also includes malaria; tuberculosis, brucellosis,
tularemia, leptospirosis, and rickettsial diseases; and viral infections such
as Dengue fever, acute hepatitis, and infectious mononucleosis.
Treatment:
1. Adequate rest and hydration
2. Antipyretic therapy: acetaminophen 15 mg/kg mg every 46 hr PO
3. A soft, easily digestible diet

4. Thearpy with chloramphenicol or amoxicillin is associated with relapses,

whereas the quinolones and 3rd generation cephalosporins are
associated with higher cure rates.
SUSCEPTIBILITY

Antibiotic

Daily Dose (mg/kg/day)

Days

Fully sensitive

Chloramphenicol

5075

1421

Amoxicillin

75100

14

Fluoroquinolone or

15

57

cefixime

1520

714

Azithromycin or

810

ceftriaxone

75

1014

Multidrug resistant

Quinolone resistant

5. Relapse with all antibiotics may occur in 15% of previously treated

patients.
6. Although additional treatment with dexamethasone (3 mg/kg for the
initial dose, followed by 1 mg/kg every 6 hr for 48 hr) has been
recommended among severely ill patients with shock.
Prognosis:
1. Infants and children with underlying malnutrition and those infected with
multidrug-resistant isolates are at higher risk for adverse outcomes.
2. Despite appropriate therapy, 24% of infected children may relapse after
initial clinical response to treatment.
Prevention:
1. During outbreaks, therefore, a combination of central chlorination as well
as domestic water purification is important.
2. In endemic situations, consumption of street foods, especially ice cream
and cut fruit has been recognized as an important risk factor.
3. The human-to-human spread by chronic carriers is preventable by proper
handwashing.
4. Vaccine:
1. An oral, live-attenuated preparation of the Ty21a strain of S. Typhi has
been shown to have good efficacy (6782%) for up to 5 years.
Significant adverse effects are rare.
2. The Vi capsular polysaccharide can be used in people 2 yr of age. It is
given as a single intramuscular dose, with a booster every 2 yr and has
a protective efficacy of 7080%.
FEVER OF UNCERTAIN ORIGIN (FUO)
1. Definition: Petersdorf and Beeson (1961):
1. Fever higher than 38.3oC on several occasions recorded by
health personnel
2. Duration of fever 3 weeks as outpatient
3. One week of study in hospital (as inpatient)
2. New Definition: Durack and Street in 1987
1. 3 outpatient visits, or 3 days in hospital.
3. Expanded definitions:

1. Classical PUO: When temperature > 38C (101F) recorded on

several occasions occurring for more than three weeks in spite of
investigations on three OPD visits or three days of stay in hospital or
one week of invasive ambulatory investigations is called classic FUO
2. Nosocomial PUO: Three days of investigations including at least
two days incubtion of cultures, is the minimum requirement for this
diagnosis.
3. Neutropenic PUO: This diagnosis should be considered when
investigation including at least two days of incubation of cultures.
4. HIV-Associated PUO: This diagnosis is considered if appropriate
investigations over three days including two day of incubation of
cultures reveals no source.
4. Fever without a focus:
Acute onset of fever, present for less than a week without localizing
symptoms and signs and with no apparent infectious or noninfectious
causes.
5. Hyperpyrexia: temperature more than 41C:
6. Clues for FUO evaluation:
i. Age:
1. <6years: respiratory, genitourinary tract infection, osteomyelitis,
JRA, rarely leukemia
2. Adolescents: tuberculosis, inflammatory bowel disease,
autoimmune disease, lymphomas
ii. Exposure:
1. Wild or domestic animals: Zoonosis, leptospirosis
2. Pica: Toxocara, Toxoplasma
3. Visit to endemic area: malaria
4. Eye drops: atropine fever
iii. Genetic disorder in family: Nephrogenic Diabetes Incipitus; Reiley Dey
etc
iv. Absence of sweating:
1. Nephrogenic diabetes insipitus
2. Unhydrotic ectodermal dysplasia
3. Familial dysautonomia(Reily Dey)
v. Red weeping eyes: polyarteritis nodosa
vi. Palpebral conjunctivitis:
1. Measles
2. Cocksackie
3. TB
4. Infectious mononucleosis
vii. Bulbar conjunctivitis:
1. Kawaski
2. Leptospirosis
viii. Conjunctival hemorrhage: infective endocarditis
ix. Uveitis:
1. Sarcoidosis
2. JRA
3. SLE
x. Chorioretinitis:
1. CMV
2. Toxoplasma
xi. Proptosis: orbital cellulitis

xii. Lack of tears:

1. Familial dysautonomia(Reily Dey)
2. Sjogren syndrome: ("Sicca syndrome") is an autoimmune disorder
in which immune cells attack and destroy the exocrine glands that
produce tears and saliva. The hallmark symptoms of the disorder
are dry mouth and dry eyes
xiii. Sinus tenderness: sinusitis
xiv. Fever blisters: rules out enteric fever; staph infection
xv. Conjested pharynx:
1. Infectious mononucleosis
2. Kawaski
xvi. Bone pain and tenderness:
Osteomyelitis
Leukemia
xvii. Referred pain over trapezium: subdiaphramatic abscess
xviii. Tenderness per rectum: pelvic abscess
7. Lab:
i. CBC:
1. Poly < 5000:
i. no bacterial etiology
ii. enteric fever
2. Poly>10000 and > bands : bacterial sepsis
ii. ESR:
1. > 30 mm: infallamatory conditions
2. >100 mm:
i. Autoimmune
ii. TB
iii. Kawasaki
iii. Blood culture: aerobic, anerobic, enteric and AFB
iv. Urine culture: mid stream of suprapubic
1. Mantoux: positive primary TB; Negative in sarcoidosis
2. Xray : Chest, sinus and mastoid
3. Bone marrow: Leukemia and MP
4. Lyumphnode: biopsy or FNAC: TB and lymphoma
8. Ultimate causes as reported in various studies:
Infections

30 - 40 %

Malignancies

20 25 %

Collagen Vascular
Disease

10 20 %

Miscellaneous

15 20 %

Undiagnosed

10 15 %

9. Treatment:
1. Avoid empirical trials; it obscures diagnosis of infective
endocarditis , meningitis etc
2. ATT if the child is critically ill and TB is suspected
10.Prognosis:
1. Children with FUO has better prognosis than adults
2. More often FUO is due to atypical presentation of a common illness

3. In 25% cases the diagnosis remains unclear

MALARIA
1.

2.

3.

4.

5.

6.

7.

Definition:
Malaria is an acute and chronic illness characterized by paroxysms of
fever, chills, sweats, fatigue, anemia and splenomegaly.
Etiology:
Caused by intracellular parasite plasmodium protozoa; 4 species:
1. Falciparum
2. Malariae
3. Ovale
4. Vivax
Transmitted by:
1. Female anopheles mosquitoes
2. Blood transfusion
3. Contaminated needles
4. Trans placental to fetus
5. Organ transplant
Epidemiology:
1. Occurs in > 100 countries
2. P. Falcifarum and p.malariae are found in most places
3. P. Vivax is the predominant type in india
Pathogenesis:
1. The exoerythrocytic phase begins with inoculation of sporozoites by
female anopheles mosquitoes
2. Schizonts develop in hepatocytes and released into blood stream as
merozoites (1-2 weeks).
3. P.falciparum and p.malaiae have only one phase in hepatocytes.
4. P.ovale and p.vivax release merozoites after 6-9 days; hepatic phase
persists up to 5 years to cause relapse.
5. Merozoites enter RBCs to develop into ring forms and then to
trophozoites
6. Trophozoites multiply and released as merozoites by rupturing RBCs.
7. Some trophozoites in RBC develop into gametocytes to enter sexual
cycle in mosquitos.
Pathologic process:
1. Fever during release of merozoites from RBC
2. Anemia due to:
1. Haemolysis
2. Sequestration of RBCs in spleen
3. Bone marrow suppression
Immunopathology:
1. Intracellular parasites killed by macrophages, RES (spleen);
extracellular parasites killed by antibody mediated immunity
2. Immunity is not complete; does not eradicate or prevent
reinfection; prevents only severity of disease.
3. Immune mediated disorders:
1. No sufficient immunity after infection and hence re
infections can occur

2.

8.

9.

Hb F resist p.falciparum; hence newborn shows

resistance to malaria
3. Severe disease in pregnancy and infancy
Resistance to malaria:
b. Hb s resists malarial infection in general
c. Lack of blood group duffy resists p.vivax
d. Hb.F and ovalocytes resist p.falciparum
e. Newborn is resistant due to HB.F and maternal antibodies.
f. 3 m to 5 yrs: lack of immunity and develop severe disease
g. Severe disease in pregnancy
Clinical features:
i.
Incubation:
1. P.falciparum
9-14 days
2. P.vivax
12-17 days may go up to 12 months or more.
3. Hypnozoites are responsible for long incubation and late relapses
in these two species of malaria.
i. P.ovale
16-18 days
ii. P.malariae
6-12 months
ii.
Prodrome:
i. 2-3 days
ii. Headache
iii. Fatigue
iv. Anorexia
v. Myalgia
vi. Mild fever
vii. Pain chest and abdomen and joints
iii.

iv.

v.

Illness:
i. Paroxysms of fever alternate with wellness
ii. Fever coincides with rupture of RBCs and release of
merozoites
iii. Chills, swaets, headache, myalgia, nausea, vomiting,
diarrhea, pallor, and jaundice.
iv. Periodicity:
1. P.vivax and ovale
every 48 hrs
2. P.malairae
every 72 hrs
3. P.falciparum
less periodicity
4. Mixed infections
less periodicity
Children:
i. High fever
ii. Drowsiness
iii. Lethargy
iv. Cyanosis
v. Hepatoslenomegaly
vi. Convulsions
vii. Hypoglycaemia
viii. Hyperkalemia
ix. Acidosis
x. Dehydration
Recrudescence: relapse of fever due to dormant parasites
a. From liver: p. Vivax and p.ovale
b. From RBC: p.malariae

vi.

P.falciparum features:
a. Intense parasitemia > 60% (others only 2%) due to invasion
of both mature and immature RBCs;
b. High fatality
vii.
P.vivale:
a. Can cause death due to splenic rupture
b. Relapse from hepatic phase from 6 m to 5 yrs
viii.
P.malariae:
a.Low parasitemia
b.Infects only mature RBCs
c. Mildest form of malaria
d.Chronic infection
e.Recrudescence even after 30 yrs
ix.
P.ovale:
a.
Least common
b.
Acute and chronic
c.
Can occur in conjunction with P.falciparum
10.
Congenital malaria:
1. Abortion
2. Still birth
3. Prematurity and IUGR
4. Neonatal death
5. Affected NB may show fever, pallor, jaundice, and
hepatosplenomegaly.
11. Diagnosis of Malarial Fever:
a. P.falciparum: ring forms with double chromatic dots; RBC with more
than one parasites
b. Microscopy:
Thick smear:
1. Make thick smear by joining the 3 drops of blood and spreading it
with corner of another slide. Correct thickness is attained when
newsprint is barely legible through the smear.
2. It should be 10 mm diameter; 10 mm away from the edge of the
slide; contains 10 layers of RBCs and 10 wbcs should be visible per
oil immersion field of microscope.
Thin smear
1. With the edge of the slide spread a new drop of blood to the surface
of the first slide. Air dry, allowing 10 minutes for the thin smear.
2. It is uniformly spread over the slide. It is tongue shaped. Thin
enough so that newsprint can be read through the smear. Consists
of a single layer of RBCs.

3. After drying, only thin smear is fixed by dipping thin smear into
methanol for 5 seconds.
Staining:
1. Giemza staining:
Dry; fix thin smear with methanol and not thick smear; add 3%
giemza stain; allow 30-45 mts; wash with water; dry.
2. JSB stain:
After dehemoglobinisation by treating with distilled water for 10
mts, dip the thick smear in jsb ii stain two to three times.
Wash it by dipping in buffer water two to three times. Then keep the
thick film dipped in jsb i stain for 40-60 seconds. Wash it with buffer
water. Drain, dry and examine.
13. Rapid diagnostic tests:
1.
Immunochromatographic tests:
Are based on the capture of the parasite antigens from the
peripheral blood using specific antibodies. If the target antigen is
present in the blood, a labelled antigen/antibody complex is formed
and permits visualization as coloured lines.
2. Quantitative buffy coat (qbc) test:
QBC test is a new method for identifying the malarial parasite in
the peripheral blood. It involves staining of the centrifuged and
compressed red cell layer (buffy coat) with acridine orange and its
examination under uv light source.
14.

Treatment:
1. Uncomplicated malaria:
Drugs
Dose
Day 0: (first day of treatment) 10 mg/ kg of bw
single dose
Tab. Chloroquine
Day 1: 10 mg/ kg of bw single dose
Day 2: 5 mg/ kg of bw single dose
Single dose of 0.25 mg/ kg body weight daily for 14
Primaquin
days
2. Chloroquin resistant malaria:
4 mg/ kg bw of artesunate daily for 3 days plus 25 mg/ kg bw
of sulphadoxine + 1.25 mg/ kg bw of pyrimethamin on the
ACT
(or)
(artesuna first day
Oral quinine 10 mg/ kg bw daily for 3 days with tab doxycline
te
(100 mg)
combinati
(or)
on
Tab. Mefloquin (25 mg/ kg bw, but total dose does not exceed
treatment
1000 mg)
)
(and)
Tab. Primaquin in single dose of 0.75 mg/ kg bw

15. Treatment of complications:

1.
Corticosteroids are contraindicated as they cause prolonged coma
and increased mortality.
2.
Anemia is treated with RBC packed cells 10 ml/kg with frusemide
3.
Shock is treated with normal saline
16. CEREBRAL MALARIA:
1. Pathophysiology:
a. Cerebral malaria is the most important complication of falciparum
malaria.
b. The basic underlying defect seems to be clogging of the cerebral
circulation by the parasitized red cells.
c. This results in sequestration of the parasites in deeper blood
vessels.
d. Obstruction to the cerebral microcirculation results in hypoxia and
increased lactate production due to anaerobic glycolysis.
e. White retina is characteristic of malarial retinopathy.
2. Clinical features:
i. High-grade fever and failure to eat and drink.
ii. Vomiting and cough are common.
iii. Coma persists more than 30 minutes after a convulsion
iv. Deep breathing due to acidosis
v. Cold, clammy skin due to shock
vi. Opisthotonus posture, mimicking either tetanus or meningitis.
vii. Neurological signs:
a. Symmetrical upper motor neuron and brain stem
disturbances
b. Diconjugate gaze, decerebrate and decorticate postures.
c. Unarosable coma
d. Corneal reflex and 'doll's eye' movements may be absent.

e. Retinal haemorrhages and exudates are rarer than in adults.

f.

CSF examination in cerebral malaria is usually normal;

Increase in pressure, protein level and cell-count (mostly
lymphocytes, 50cells/ml) may be seen.

3. Other features:

i.

Severe anaemia

ii. Acute renal failure

iii. Pulmonary oedema or adult respiratory distress syndrome (ards).
iv. Hypoglycaemia
v. Circulatory collapse, shock, hypotension
vi. Spontaneous bleeding/disseminated intravascular coagulation.
vii. Jaundice
4. Treatment of Severe and complicated malaria and cerebral
malaria:
Quinine salt 20 mg/ kg bw on admission (iv infusion or divided
im injection) followed by maintenance dose of 10 mg/ kg bw 8
hourly; infusion rate should not exceed 5 mg/ kg bw per hour.
The parenteral treatment should be given for minimum of 48
hours and once the patient tolerates oral therapy, quinine 10
Iv quinine
mg/ kg bw three times a day with doxyclycline 100 mg once a
day or clindamycin in pregnant women and children under 8
years of age, shouldbe given to complete 7 days of treatment
in patient treated with parenteral quinine.
Or
(b) artesunate: 2.4 mg/ kg body weight iv or im given on
admission, then at 12 hours and 24 hours, then once a day for
7 days;
Or
Artemisini (c) artemether: 3.2 mg/ kg body weight im given on admission
n
then 1.6 mg/ kg body weight per Day for 7 days;
Derivative Or
(d) arteether: 150 mg daily im for 3 days in adults only (not
s
recommended for children);
Followed by full course of act to patients completed
treatment with artemisinin derivatives (b, c and d).
17. BLACKWATER FEVER:
1. Black water fever (BWF) is a severe clinical syndrome and
complication of falciparum malaria characterized by intra vascular
haemolysis, haemoglobinuria and kidney failure.
2. Black water fever is caused by heavy parasitization of red blood
cells with plasmodium falciparum. When the red blood cells burst,
hemoglobin leaks into the blood plasma.
3. This free hemoglobin damages the glomerulus in the kidney, and
begins to leak into the urine where it causes further damage to the
tubules of the kidney.

4. Within a few days of onset there are chills, with rigor, high fever,
jaundice, vomiting, rapidly progressive anemia and the passage of
dark red or black urine.
5. The cause of hemolytic crises in this disease is unknown. There is
rapid and massive destruction of red blood cells with the production
of hemoglobinemia, hemoglobinuria, intense jaundice, anuria
(passage of less than 50 milliliter of urine in a day), and finally death
in the majority of cases.
6. The most probable explanation for blackwater fever is an
autoimmune reaction.
7. Blackwater fever is much less common today than it was before
1950. It may be that quinine plays a role in triggering the condition,
and this drug is no longer commonly used for malaria prophylaxis.
8. The treatment is antimalarial chemotherapy, intravenous fluid and
sometimes supportive care such as intensive care and dialysis.
MEASLES (Rubeola)
Aetiology:
Single stranded RNA with lipid envelope; Genus: morbilivirus; Family:
paramyxoviridae
Human are the only host
Epidemiology
Most infectious viruses known to man.
Rarely will an un-immunized child escape.

Responsible for approximately 6 million deaths

Responsible for more deaths than any other single agent.
Median case fatality ratio of 3.7%, range 0 to 23.9%.
Vaccine from 1963 changed the epidemiology.
Transmission & Pathology
By droplets through respiratory mucosa and rarely conjunctiva.
Infective period: 3 days before and 5 days after rashes appear.
Necrosis of respiratory epithelium
Lymphocytic infiltration
Small vessel vasculitis of skin and mucosa
giant cells (up to 26 nuclei)
Fused cells with more than 100 nuclei called Warthin-Finkaldey giant cells
Pathogenesis: 4 phases
1. Incubation:
Infection of mucosa lympadenopathy viremeia RES secondary
viremia reach body surface to form exanthema
2. Prodrome:
It is charecterized by mild fever, conjunctivitis, coryza, cough and
photophobia.

Transverse linear injection of the lower lid margins, called a Stimson

line, is present before the more generalized conjunctival inflammation
obscures it.
3. Enanthem: Koplick spots is the pathagnamonic sign
1. Koplick spots 1-4 days before exanthem;
2. Inner cheek between premolars
3. Also rarely on conjunctiva and vaginal mucosa
4. Exanthem:
1. Symptoms abate as rash appears
2. Rash:
1. Maculopapular
2. First seen around hairline and behind ears
3. Spreads downwards to trunk and limbs
4. Finally confluence and fade over 7 days
5. Leaves brawny desquamation of skin
3. Febrile seizures may occur in children predisposed to them.
Types of measles:
1. Subclinical measles:
a) Occurs in vaccinated or those who received passsive antibodies like
or recipients of blood products
b) The rash may be indistinct, brief, or, rarely, entirely absent.
c) Persons with inapparent or subclinical measles do not shed measles
virus and do not transmit infection to household contacts.
2. Atypical Measles:
a) Atypical measles occurs in individuals who had previously received
killed measles vaccines
b) They have high fever, abdominal pain, cough, vomiting, and
pleuritic chest pain
c) Conjunctivitis and koplik spots are rarely present
d) Rash begins in limbs with little involvement of the face and upper
part of the trunk.
e) Pneumonia, hilar adenopathy, and pleural effusions are common.
f) Recovery from atypical measles may take 2 weeks or longer.
3. Black measles:
a) Severe hemorrhagic measles, or black measles, is most common in
infants in developing countries with high mortality
b) Sudden onset of high fever accompanied by seizures or altered
mental status.
c) Pneumonia, a hemorrhagic exanthem and enanthem, bleeding from
the mouth, nose, and gastrointestinal tract, and probable
disseminated intravascular coagulation follow
4. Modified Measles:
a) Modified measles occur in individuals who have received immune
globulin after exposure to measles.
b) The clinical manifestations are milder
c) The incubation period is prolonged from 14 to 20 days.
d) Complications are rare

Lab tests for measles:

1. Reduction in the total white blood cell count, with lymphocytes
decreased more than neutrophils.
2. Absolute neutropenia may occur
3. In measles not complicated by bacterial infection, the erythrocyte
sedimentation rate and c-reactive protein levels are normal.
Diagnosis:
1. Koplick spot with typical rash gives a definitive clinical diagnosis
2. Ig M antibody appears 12 days after the onset of the rash and remains
detectable for about 1 mo
3. A 4-fold rise in Ig G antibodies in acute and convalescent specimens
taken 24 wk later.
4. Viral isolation from blood, urine, or respiratory secretions can be doen
in viral labs
5. Molecular detection by polymerase chain reaction is possible
Differential diagnosis:
1. Rubella,
2. Scarlet fever,
3. Drug rashes
4. Serum sickness,
5. Roseola infantum,
6. Infectious mononucleosis,
7. Erythema infectiosum and
8. Echovirus and
9. Coxsackievirus infections and
10.
Kawasaki syndrome
Complications:
1. Mortality more in
1. <5 and > 20 yrs.
2. Vit.A def. and malnutrition.
3. Immune def.
4. Malignancy
2. Measles precipitates Vit.A def with blinding malnutrition
3. Respiratory complications:
1. Otitis media,
2. Pneumonia:
i. Interstitial pneumonia may be caused by the measles
virus (giant cell pneumonia).Also known as Hecht's
pneumonia; this is a deadly but fortunately rare
complication of measles.
ii. Bacterial: pneumococcus, group A Streptococcus,
Staphylococcus aureus, and Haemophilus influenzae type
b are common
3. Laryngitis, tracheitis, and bronchitis and bronchiolitis are
common and may be due to the virus alone.
4. Sinusitis and mastoiditis.
5. Retropharyngeal abscess

6. Measles may exacerbate underlying Mycobacterium tuberculosis

infection. There may also be a temporary loss of hypersensitivity
reaction to tuberculin skin testing.
7. Bronchiolitis obliterans: rare and life-threatening form of nonreversible obstructive lung disease in which the bronchioles are
plugged with granulation tissue. Causes death.
4. Gastro enteritis and dehydration
5. Appendicitis due to lymphoid hyperplasia
6. Febrile seizures in 3%
7. Encephalitis 1 in 1000
8. Black measles: black measles, a rare, severe, often fatal, form of
measles in which hemorrhage into the skin lesions and mucous
membranes is associated with a sudden rise in temperature,
convulsions, delirium, stupor, coma, and marked respiratory distress.
Called also hemorrhagic measles.
9. Myocarditis
10.Prgnancy: leads to fetal death, and neonatal mortality
11.Subute sclerosing pan encephalitis (SSPE)
1. Subacute sclerosing panencephalitis (SSPE) is a rare
chronic, progressive encephalitis that affects primarily children
and young adults, caused by a persistent infection of immune
resistant measles virus (which can be a result of a mutation of
the virus itself). 1 in 100,000 people infected with measles
develop SSPE.
2. Clinically: Insiduos onset, suble changes in behaviour, school
failure
3. Three stages:
i. Irritability; Reduced attention span; Temper outbursts
ii. Massive myoclonus; no loss of consciousness
iii. Disappearance of myoclonus ; Choreo athetosis;
Immobility; Dystonia; Lead pipe rigidity; dementia; stupor;
coma; death.
4. Diagnosis:
1. Clinical; myoclonus and consciousness
2. Measles antibody in CSF
3. EEG : Characteristic periodic activity (Rademecker complex)
4. Brain biopsy: eosinophilicinclusion bodies in the cytoplasm
nuclei of neurons and glial cells
5. Treatment:
Combinations of treatment for SSPE include:
a) Oral inosine pranobex (oral isoprinosine) combined
with intrathecal (injection through a lumbar puncture
into the spinal fluid) or intraventricular interferon
alpha.
b) Oral inosine pranobex (oral isoprinosine) combined
with interferon beta.
c) Intrathecal interferon alpha combined with intravenous
ribavirin.
6. Prognosis: death in 3 years
Treatment of Measles:

1. No antiviral drugs are effective

2. Hydration, antipyretics, O2
3. Ventilator support for severe respiratory involvement
4. Vit A 1-2 L units to prevent blinding malnutrition
5. IV ribaverin tried in immune def.
Prognosis: death 1 in 1000; 15 % in immune def.
Prevention:
1. Measles 9 month
2. MMR in 15 months
Post exposure prophylaxis:
1. Measles vaccine within 72 hrs
2. IM/IV IgG within 6 days
CHICKENPOX
Varicella-Zoster Virus (VZV)
ETIOLOGY.
1. VZV is a neurotropic human herpesvirus with similarities to herpes simplex
virus, which is also -herpesvirus.
2. These viruses are enveloped with double-stranded DNA genomes that
encode more than 70 proteins, including proteins that are targets of
cellular and humoral immunity.
EPIDEMIOLOGY.
1. It is a more serious disease with higher rates of complications and deaths
among infants, adults, and immunocompromised persons.
2. Within households, transmission of VZV to susceptible individuals occurs
at a rate of 6586%;
3. More casual contact, such as occurs in a school class room, is associated
with lower attack rates among susceptible children.
PATHOGENESIS.
1. VZV is transmitted in respiratory secretions and in the fluid of skin lesions
either by airborne spread or through direct contact.
2. Primary infection (varicella) results from inoculation of the virus onto the
mucosa of the upper respiratory tract and tonsillar lymphoid tissue.
3. Widespread cutaneous lesions occur during a 2nd viremic phase that
lasts 37 days.
4. Peripheral blood mononuclear cells carry infectious virus, generating new
crops of vesicles during this period of viremia.
5. VZV is also transported back to upper respiratory mucosal sites during the
late incubation period, permitting spread to susceptible contacts before
the appearance of rash.
6. In the immunocompromised child, it results in disseminated infection with
resultant complications in the lungs, liver, brain, and other organs.
7. Subsequent reactivation of latent virus causes herpes zoster, a
vesicular rash that usually is dermatomal in distribution
8. The skin lesions of varicella and herpes zoster have identical
histopathology, and infectious VZV is present in both.
9. Varicella elicits humoral and cell-mediated immunity that is highly
protective against symptomatic reinfection. Suppression of cell-mediated
immunity to VZV correlates with an increased risk for VZV reactivation as
herpes zoster.

CLINICAL MANIFESTATIONS.
1. It has variable severity but is usually self-limited.
2. It may be associated with severe complications, including bacterial
superinfection, pneumonia, encephalitis, bleeding disorders, congenital
infection, and life-threatening perinatal infection.
3. The illness usually begins 1416 days after exposure, although the
incubation period can range from 10 to 21 days.
4. Subclinical varicella is rare; almost all exposed, susceptible persons
experience a rash.
5. Prodromal symptoms may be present, particularly in older children and
adults. Fever, malaise, anorexia, headache, and occasionally mild
abdominal pain may occur 2448 hr before the rash appears. Temperature
elevation is usually moderate, usually from 100 to 102F but may be as
high as 106F; fever and other systemic symptoms persist during the 1st
24 days after the onset of the rash.
6. Exanthem:
a. Varicella lesions often appear first on the scalp, face, or trunk.
b. The initial exanthem consists of intensely pruritic erythematous
macules that evolve through the papular stage to form clear, fluidfilled vesicles.
c. Clouding and umbilication of the lesions begin in 2448 hr.
d. While the initial lesions are crusting, new crops form on the trunk
and then the extremities; the simultaneous presence of lesions in
various stages of evolution is characteristic of varicella.
e. The distribution of the rash is predominantly central or centripetal,
in contrast to smallpox, where the rash is more prominent on the
face and distal extremities.
f. Ulcerative lesions involving the mucosa of oropharynx and vagina
are also common; many children have vesicular lesions on the
eyelids and conjunctivae, but corneal involvement and serious
ocular disease is rare.
g. The average number of varicella lesions is about 300, but healthy
children may have fewer than 10 to more than 1,500 lesions.
The differential diagnosis of varicella:
1. includes vesicular rashes caused by other infectious agents, such as
herpes simplex virus, enterovirus, monkey pox, rickettsial pox, or S.
aureus; drug reactions; contact dermatitis; and insect bites.
2. Severe varicella was the most common illness confused with smallpox
before the eradication of smallpox.
Varicella in Vaccinated Individuals (Breakthrough Varicella).
1. Vaccine is >95% effective in preventing severe varicella and during
epidemic vaccinated children may develop breakthrough varicella.
2. The rash in breakthrough disease is frequently atypical, predominantly
maculopapular, vesicles are seen less commonly, and the illness is most
commonly mild with <50 lesions and little or no fever.
3. Breakthrough cases are less contagious than wild-type infections within
household settings.
Progressive Varicella.

1. Progressive varicella, with visceral organ involvement, coagulopathy,

severe hemorrhage, and continued vesicular lesion development, is a
dreaded complication of primary VZV infection.
2. Can occur in:
a. immunocompromised children,
b. pregnant women, and
c. newborns,
d. those with malignancy, particularly if chemotherapy was
e. varicella-related deaths usually occur within 3 days after the
diagnosis of varicella pneumonia.
f. Continued new lesion formation for weeks or months, have been
described in children with HIV infection.
Neonatal Chickenpox.
1. Newborns have particularly high mortality in the circumstances of a
susceptible mother contracting varicella around the time of delivery.
2. Infants whose mothers develop varicella in the period from 5 days prior to
delivery to 2 days afterward are at high risk for severe varicella.
3. The infant acquires the infection transplacentally as a result of maternal
viremia, which may occur up to 48 hr prior to the maternal rash.
4. Management:
a. Newborns whose mothers develop varicella 5 days before to 2 days
after delivery should receive human varicella-zoster immune
globulin (VariZIG)
b. Although neonatal varicella may occur in about half of these infants
despite administration of VariZIG, it is usually mild.
c. Because perinatally acquired varicella may be life threatening, the
infant should be treated with acyclovir (10 mg/kg every 8 hr IV)
when lesions develop.
DIAGNOSIS of varicella.
1. Leukopenia is typical during the 1st 72 hr; it is followed by a relative and
absolute lymphocytosis.
2. VZV can be identified quickly by direct fluorescence assay of cells from
cutaneous lesions, and by PCR amplification testing.
3. Although multinucleated giant cells can be detected with nonspecific
stains (Tzanck smear), they have poor sensitivity and do not differentiate
VZV from herpes simplex virus infections.
4. VZV IgG antibodies can be detected by several methods and a 4-fold rise
in IgG antibodies is also confirmatory of acute infection.
5. Testing for VZV IgM antibodies is not useful for clinical diagnosis because
commercially available methods are unreliable and the kinetics of the IgM
response are not well defined.
TREATMENT.
1. Oral therapy with acyclovir (20 mg/kg/dose, maximum 800 mg/dose)
given as 4 doses/day for 5 days should be used to treat uncomplicated
varicella.
2. Any patient who has signs of disseminated VZV, including pneumonia,
severe hepatitis, thrombocytopenia, or encephalitis, should receive
intravenous acyclovir (500 mg/m2 every 8 hr IV) therapy initiated within
72 hr of development of initial symptoms.

3. Treatment is continued for 7 days or until no new lesions have appeared

for 48 hr.
COMPLICATIONS.
1. Varicella hepatitis is relatively common but rarely clinically symptomatic.
2. Mild thrombocytopenia occurs in 12% of children
3. Purpura, hemorrhagic vesicles, hematuria, and gastrointestinal bleeding
are rare
4. Cerebellar ataxia occurs in 1 in every 4,000 cases.
5. Other complications: Encephalitis, pneumonia, nephritis, nephrotic
syndrome, hemolytic-uremic syndrome, arthritis, myocarditis, pericarditis,
pancreatitis, and orchitis.
6. Bacterial Infections:
1. Secondary infections due to group A streptococci and S. aureus, may
occur in up to 5% of children with varicella. These range from
superficial impetigo to cellulitis, lymphadenitis, and subcutaneous
abscesses.
2. Serious invasive infections caused by group A streptococcus, can have
a fatal outcome.
3. Bacterial toxin-mediated diseases (toxic shock syndrome) also may
complicate varicella.
7. Encephalitis and Cerebellar Ataxia.
1. Encephalitis (1/50,000 cases of varicella) and acute cerebellar ataxia
(,000 cases of varicella) are well-described neurologic complications
of varicella; morbidity from CNS complications is highest among
patients younger than 5 yr or older than 20 yr. Nuchal rigidity, altered
consciousness, and seizures characterize meningoencephalitis.
2. Patients with cerebellar ataxia have a gradual onset of gait
disturbance, nystagmus, and slurred speech. Neurologic symptoms
usually begin 26 days after the onset of the rash but may occur during
the incubation period or after resolution of the rash. Clinical recovery is
typically rapid, occurring within 2472 hr, and is usually complete.
8. Pneumonia.
1. Varicella pneumonia is a severe complication that accounts for most of
the increased morbidity and mortality in adults and other high-risk
populations, but pneumonia may also complicate varicella in young
children.
2. Smoking has been described as a risk factor for severe pneumonia
complicating varicella.
PROGNOSIS.
1. Primary varicella has a mortality rate of 23 per 100,000 cases with the
lowest case fatality rates among children 19 yr of age (-1 death per
100,000 cases).
2. Compared with these age groups, infants have a 4 times greater risk of
dying and adults have a 25 times greater high risk of dying.
3. Neuritis with herpes zoster should be managed with appropriate
analgesics. Postherpetic neuralgia can be a severe problem in adults and
may persist for months, requiring care by a specialist in pain
management.
PREVENTION.

1.

Vaccine.
1. Varicella is a vaccine-preventable disease. Live virus varicella vaccine
is available as a monovalent vaccine and is also available in
combination with measles, mumps, and rubella (MMRV) vaccines.
Administration of varicella vaccine within 4 wk of MMR vaccine has
been associated with a higher risk for breakthrough disease; therefore,
it is recommended that the vaccines either be administered
simultaneously at different sites or be given at least 4 wk apart.
2. Varicella vaccine is recommended for routine administration to children
at 1218 mo and at 46 yr of age.
3. Catch-up vaccination with the second dose is recommended for
children and adolescents who received only 1 dose.
4. Varicella vaccine is contraindicated in children with cell-mediated
immune deficiencies, and the vaccine may be considered for HIVinfected children with a CD4 count greater than 15%.
Postexposure Prophylaxis.
1. Vaccine given to normal children within 35 days after exposure (as soon
as possible is preferred) is effective in preventing or modifying varicella,
especially in a household setting where exposure is very likely to result in
infection.
2. High-titer anti-VZV immune globulin as postexposure prophylaxis is
recommended for immunocompromised children, pregnant women, and
newborns exposed to maternal varicella. The recommended dose is 1 vial
(125 units) for each 10 kg increment (maximum 625 units) given
intramuscularly as soon as possible but within 96 hr after exposure.
HERPES ZOSTER
1. Herpes zoster:
a. Reactivation of the latent infection of VZV causes herpes zoster
(shingles).
b. Because it is due to the reactivation of latent VZV, is uncommon in
childhood and shows no seasonal variation in incidence.
c. The lifetime risk for herpes zoster for individuals with a history of
varicella is 1015%, with 75% of cases occurring after 45 yr of age.
d. Herpes zoster is very rare in healthy children <10 yr of age except for
infants who were infected in utero or in the 1st year of life; herpes
zoster in children tends to be milder than disease in adults and is less
frequently associated with postherpetic neuralgia. However, herpes
zoster occurs more frequently, occasionally multiple times, and may be
severe in children receiving immunosuppressive therapy for
malignancy or other diseases and in those who have HIV infection.
Clinical fatures:
1. Herpes zoster manifests as vesicular lesions clustered within 1 or less
commonly 2 adjacent dermatomes.
2. In the elderly, herpes zoster typically begins with burning pain, with
clusters of skin lesions in a dermatomal pattern.

3. Almost half of the elderly with herpes zoster develop complications; the
most frequent complication is postherpetic neuralgia, a painful condition
that affects the nerves despite resolution of the shingles skin lesions.
4. In children, the rash is mild, with new lesions appearing for a few days;
symptoms of acute neuritis are minimal; and complete resolution usually
occurs within 12 wk.
5. In contrast to adults, postherpetic neuralgia is very unusual in children.
6. Immunocompromised children may have more severe herpes zoster,
which is similar to that in adults, including postherpetic neuralgia.
Managemnt:
1. Antiviral drugs are effective for treatment of herpes zoster. In healthy
adults, acyclovir (800 mg 5 times a day PO for 5 days), famciclovir (500
mg tid PO for 7 days), and valacyclovir (1,000 mg tid PO for 7 days)
reduce the duration of the illness and the risk for developing postherpetic
neuralgia;
2. Concomitant corticosteroid usage improves the quality of life in the
elderly.
3. In otherwise healthy children, herpes zoster is a less severe disease, and
postherpetic neuralgia is rare. Therefore, treatment of uncomplicated
herpes zoster in the child with an antiviral agent may not always be
necessary, although some experts would treat with oral acyclovir (20
mg/kg/dose, maximum 800 mg/dose) to shorten the duration of the
illness. Use of corticosteroids for herpes zoster in otherwise healthy
children is not recommended.
4. Patients at high risk for disseminated disease should receive acyclovir
(500 mg/m2 or 10 mg/kg every 8 hr IV). Oral acyclovir, famciclovir, or
valacyclovir are options for immunocompromised patients with
uncomplicated herpes zoster and who are considered at low risk for
visceral dissemination.
Prevention:
A new VZV vaccine formulation was licensed in 2006 for use as a single
immunization of individuals >60 yr of age for prevention of herpes zoster
reactivation and to decrease the frequency of postherpetic neuralgia. It is
not indicated for the treatment of zoster or postherpetic neuralgia
MUMPS
Etiology:
Single stranded RNA; Family Para myxoviridae; Genus Rubula virus
Human beings are the only host
Epidemiology:
1. Age: 5-9 yrs; epidemic at 4 yrs ; significant reduction after vaccination
2. Infectivity: 7 days before and 7 after parotid swelling appears
3. Pathology
4. Can involve Salivary glands; CNS; Testes; Thyroid; Ovaries; Heart; Kidneys;
Liver; Joints.
5. Infection epithelium lymphnode viremia target tissues necrosis with
lymphocytic infiltration focal ischemia healing
Clinical features
1. Incubation 12-25 days

2. Asymptomatic in some
3. Non specific symptoms in others
4. Typical illness :
Prodrome: 1- 2 days of fever; headache and vomiting;
Unilateral or bilateral (70%) swelling of parotids; tenderness; ear
pain
Parotid swelling:
Angle of lower jaw obscured
Ear lobe lifted up and out
Stensen duct opening red and swollen
Sub mandibular glands can be involved
Lymphatic obstruction leads to edema over sternum
Fever resolves in 3 days swelling in 7 days
Diagnosis
Increase in serum amylase
Leucopenia
Relative lymphocytosis
Viral isolation
PCR
Paired serology: rise in titre of acute and convalescent sera of IgG by
Compliment fixation
Hemagglutination
Enzyme immuno assay and ELIZA
Ig M by EIA demonstrates recent infection
D.D
Parotid swelling occurs in influenza; CMV; E.B virus; HIV; staph
infection(poly increased)
Sialidinitis due to calculus
Sjogren syndrome: autoimmune disorder in which immune cells attack and
destroy the exocrine glands that produce tears and saliva. The hallmark
symptoms of the disorder are dry mouth and dry eyes (part of what are
known as sicca symptoms).
SLE: a chronic autoimmune connective tissue disease that can affect any
part of the body.SLE is one of several diseases known as "the great
imitators" because it often mimics or is mistaken for other illnesses.
Parotid tumour
Complications
1. Meningitis; Encephalitis
2. Gonadal atrophy; 30% gonadal involvement; sterility if bilateral; oopheritis
can mimic appendicitis
3. Nerve deafness
4. Thrombocytopenia
5. Transverse myelitis
6. Pregnancy: fetal loss
7. Pancreatitis diabetes
8. Myocarditis
9. Thyroiditis myxaedema

10.Rare:
Treatment:
Prognosis:
Prevention:

optic neuritis; nephritis

Non specific; pain killers and rest
good rarely death due to encephalitis
MMR at 15 m and 5 yrs; contra indicated in egg and neomycin
allergy, pregnancy and HIV
DIPHTHERIA

1. Definition:
i.

Acute toxic infection caused by corynebacterium diphtheriae

ii.

Diphtheria in Greek means a piece of leather

iii.

I st infection in history conquered by the principles of bacteriology,

immunology and public health.

2. Etiology:
i.

corynebacterium diphtheriae are aerobic, nonencapsulated, nonspore forming, non motile, pleomorphic, gram positive bacilli

ii. Mitis, intermedius and gravis, belfanti are serotypes.

iii. Produce exotoxin after encoded by a bacteriophage
iv. C.ulcreans less commonly produces similar disease.
3. Pathogenesis:
i. Transmission by droplets sometimes by contact with skin lesion
ii. Asymptomatic carriers also spread the disease
iii. Children under 15 are susceptible
iv. Remain in superficial layers of respiratory mucosa and multiply
v. Induce cell necrosis by toxin
4. Psuedomembrane:
i.

Cell necrosis, fibrin, leukocytes, epithelial cells , RBCs and bacilli

together form a dense membrane

ii. Adherent to underlying tissues

iii. Bleeds on peeling

iv. Usually seen on tonsil and posterior fornix.

v. Nasal , laryngeal , conjunctival and cutaneous lesions possible
vi. Cervical glands enlarge to form bull neck
vii. Exotoxin affects heart, kidneys and CNS
5.

Clinical features
i. Incubation 2-5 days
ii. Nasal:

Membrane in nares and upper lip

iii. Faucial:

Membrane on tonsils, fornix, palate, pharynx and uvula

Cervical nodes enlarge

iv. Laryngeal:

Membrane on larynx and can spread to trachea and bronchi

Hoarseness, stridor and croup

6. Other sites:
i. Cutaneous:

Non healing ulcers with grey brown membrane

Spreads to others

Provides immunity to host

Ulcerative conjunctivitis

ii. Eye:

iii. Vulvo vaginitis

iv. Otitis externa
7. Diagnosis:

i. Culture from lesions

ii. Smear to identify organisms
iii. Toxigenicity to be determined ( Elek test)
iv. PCR for toxin gene
8. Complications:
i.

ii.

Cardiomyopathy (10-24%)

2nd week

Tachycardia

Prolonged P-R interwal

ST-T changes

Heart blocks

CCF

Neuropathy

Occurs after 2-3 weeks

Palatal palsy

Occulomotor

9. DD

Strabismus

ciliary paralysis

Blurred vision

Loss of accommodation

Peripheral neuritis

muscle weakness

Diaphragmatic paralysis

i. Infectious mononucleosus
ii. Vincents angina
iii. Streptococcal pharyngitis
iv. herpes
10.Treatment :
i. Antidiphtheritic serum after sensitivity tests

Nasal: 10 to 20000 U IM

Faucial: 15 to 25000 U IM/IV

Laryngeal 20 to 40000 IM/IV

Severe forms: 40 to 100 000 U half IM ; half IV

ii. Drugs:

Crystalline penicillin 25 to 50 000 U /kg IV in 3 doses for 14

days

Erythromycin is an alternative

iii. Tracheostomy
iv. ECG monitoring
v. Nutrition and hydration
11.Prognosis :
i. Mortality 30-50% reduced to 5-10% by effective management
ii. ADS within 72 hrs reduce mortality
iii. Mortality high in facial and laryngeal diphtheria
12.Prevention:
i. Antibiotic prophylaxis to carries
ii. Diphtheria vaccine 5 doses before 5 yrs
iii. Adult vaccine by 11-12 yrs

PERTUSIS
1. Etiology:
Bordetella pertusis: epidemic and sporadic causes
Bordetella parapertusis: sporadic cases
B.bronchiseptica: animal pathogen
2. Epidemiology:
World over 60 million cases and 500,000 deaths
Vaccine caused >99% reduction in incidence
1-6 yr more susceptible
More cases in older children
3. Pathogenesis
Gram negative coccobacilli
Droplet infection
Colonize only ciliated epithelium
Local epithelial damage
Pertusis toxin mechanism unclear; inhibits immune functions of
host
4. Clinical manifestations
Incubation 3-12 days
Catarrhal:
1-2 weeks; fever; rhinorrhea; lacrimation and conjunctival
suffusion
Paroxysmal:
2-6 weeks
Initial dry intermittent cough
Machine gun burst of uninterrupted cough
Loud whoop
Vomiting
Clutches a comforting adult
convalescent stage :
2 weeks
Symptoms regress
5. Infants:
a. No stages
b. No typical cough or whoop
c. After a trigger may develop signs of choking, cyanosis and apnea.
d. Paroxysm may continue intermittently for a longer period
SIDS
6. Immunized children and adults:
a. No distinct stages
Whoop not apparent
Uninterrupted cough
Post tussive emesis
Lasts for 3 weeks
7. Physical findings

a. Uninformative in many
b. Secondary infection may show signs of pneumonia
c. Conjunctival hemorrhage and petechiae on the face
d. Swollen eye lids
8. Diagnosis
a. Cough with whoop
b. Absence of fever and lung signs
c. Lymphocytosis
d. Normal CXR
e. Pharyngeal swap culture:
i. Bordet Gengou medium
ii. Colonies like mercury droplets
f. PCR from throat swaps
g. Serum for agglutinins
9. Treatment :
a. Azithromycin 10 mg/kg od for 5 days
b. Erythromycin for > 1 m infants (causes pyloric stenosis In NB )
c. Air way maintenance
d. Quiet environment
e. Mist inhalation
f. Small frequent feeding
10.Isolation: up to 5 days of treatment
11.Complications:
a. Apnea
b. Secondary infections
c. Otitis media
d. CNS hemorrhage
e. Hernia
f. Laceration of lingual frenulum
g. SIDS
h. Pertusis encephalopathy
12.Prevention:
a. DPT (DTwP)
b. Acellular pertusis vaccine (DTaP)
c. Tdap for adolescents
POLIOMYELITIS
1. Virus:
1.
2.
3.
4.

Single stranded RNA; Family: Picarnoviridae; genus:Enterovirus

Type 1,2,3 are antigenically different
Humans are the only host
PV1 is highly localized to regions in India, Pakistan, Afghanistan, and
Egypt, West and Central Africa. Wild poliovirus type 2 has probably
been eradicated; it was last detected in October 1999 in Uttar
Pradesh, India. Wild PV3 is found in parts of only five countries
(Nigeria, Niger, Pakistan, India, and Sudan).
2. Transmission:

3.

4.

5.

6.

7.
8.

1.
2.
3.
4.

1. Excreted from GIT and transmitted by feco oral method and disease
occurs in CNS
Epidemiology:
1. 90-95% subclinical or abortive
2. 5 % non paralytic illness
3. 1in 1000 paralytic polio in infants; 1 in 100 in adolescents.
4. Poor sanitation and overcrowding predisposes transmission
5. Infectivity: 2 weeks before and several weeks after the onset of
illness.
Pathogenesis:
1. Enter cells with specific polio receptors in GIT epithelium regional
lymphadenopathy pimary viremia RES & CNS through nerve
endings spinal motor neurons multiply Release by cell death
2. Vaccine virus similar course but no replication in CNS
3. Vaccine virus after acquiring neurovirulance can produce similar
illness (VAPP)
Pathology:
1. Motor neurons of spinal cord invaded; poly and lymphocytic
infiltration and inflammation; edema; more neuronal loss due to
inflammatory edema.
2. Anterior horn cell, internuncial neurons and dorsal ganglion can be
invoveld;
3. Vermis of cerebellum, substantia nigra, red nucleus of pons,
thalamus, hypothalamus, pallidum and motor cortex can be
involved to variable extent.
Immunity:
1. Infants 0-4 months have transplacental Ig.G
2. Type specific immunity by natural and vaccine virus through IgG
3. GIT gets IgA for surface immunity.
Incubation:
1. 8-12 days or longer.
Clinical Types:
1. Abortive:
Mild influenza like illness; fever, malice, head ache and
anorexia.
Recovery in 2-3 days.
2. Non Paralytic:
1. Minor illness: as above
2. Major illness:
1. Neck stiffness
2. Stiffness of muscles of trunk and limbs- spinal rigidity
3. Fleeting bladder paralysis
4. Constipation
5. Loss of head control
6. Depressed tendon reflexes
7. Loss of abdominal and cremastric reflexes
8. No sensory disturbances
3. Paralytic Polio: 1 in 100 cases
Spinal
Bulbar
Spino bulbar
Polio encephalitis

4. Spinal:
1.
2.

5. Bulbar:
1.
2.
3.
4.
5.
6.
7.
8.
9.

Phase I: Similar to abortive polio

Phase II:
1. Apparent recovery from phase I followed by
2. Fever, head ache, muscle pain, paresthesias, muscle
spasm
3. Asymmetrical and spotty paralysis
4. Proximal more than distal muscle groups
5. Diaphragm and intercostals paralysis
6. Reduced DTR
7. Bladder and bowel dysfunction
8. Provocation paralysis following IM inj.
9. Sensation is intact
10.Recovery 6-12 months

May occur alone

Nasal voice due to palatal palsy
Pooling of saliva
Irregular respiration
Diminished cough reflex
Deviation of uvula
Increase in BP
Hyperpyrexia
Cardiac arrhythmias
10. Skin mottling due to vasomotor instability
11. Aphonia due to vocal cord paralysis
12. Weakness of hyoid muscle and rope sign by pulling
hyoid backwards
13. Cranial nerve palsies
6. Polio encephalitis:
1.
Irrritabilty
2.
drowsiness
3.
Coma
4.
Tremors
5.
Seizures
9. Ventilatory insufficiency: due to
1. Pharyngeal and laryngeal weakness
2. Intercostal and diaphragmatic paralysis
3. Dysfunction of respiratory centres
4. Early diagnosis:
1. Anxious expression
2. Working of ala nasii
3. Week cough reflexes
4. Paradoxical abdominal movements
5.
Deltoid weakness as the area is adjacent to phrenic
nerve in spinal cord
10.Diagnosis:
1. Fever, asymmetry and spotty paralysis without sensory
involvement.
2. 2 Stool specimens in 24-48 hrs apart for viral solation
3. DNA sequence for wild, vaccine and non polio viruses
4. CSF: early polymorphic leukocytosis; later lymphocytosis
5. Paired serology for increasing titre.

11.DD:
1. VAPP Vaccine associated paralytic polio)
2. AFP:
1.
Guillain Barre Syndrome: symmetric; ascending with
sensory involvement
2. Transverse myelitis
3. Traumatic paralysis
12. Treatment:
1. Symptomatic
2. Pain killers
3. Bed rest
4. No Im inj and surgery; tonsillectomy can lead to bulbar polio
5. Hot tub baths
6. Splinting in neutral positions
7. Phsiotherapy after pain subsides
8. Air way maintenance
9. Tracheostomy
10.Ventilatory support
13.Prevention:
1. The first inactivated virus vaccine was developed in 1952 by Jonas
Salk, and announced to the world on April 12, 1955. The Salk
vaccine, or inactivated poliovirus vaccine (IPV), is based on
poliovirus grown in a type of monkey kidney tissue culture (Vero
cellline), which is chemically inactivated with formalin. After two
doses of IPV (given by injection), 90% or more of individuals develop
protective antibody to all three serotypes of poliovirus, and at least
99% are immune to poliovirus following three doses.
2. Subsequently, Albert Sabin developed another live, oral polio
vaccine (OPV). It was produced by the repeated passage of the virus
through non-human cells at sub-physiological temperatures.Three
doses of live-attenuated OPV produce protective antibody to all
three poliovirus types in more than 95% of recipients.
14.Eradication:
1. High infant immunization coverage with four doses of oral polio vaccine
(OPV) in the first year of life in developing and endemic countries, and
routine immunization with OPV and/or IPV elsewhere.
2. Organization of National immunization days to provide
supplementary doses of oral polio vaccine to all children less than five
years of age.
3. Active surveillance for wild poliovirus through reporting and laboratory
testing of all cases of acute flaccid paralysis among children less than
fifteen years of age.
4. Targeted "mop-up" campaigns once wild poliovirus transmission is
limited to a specific focal area.

5. Pulse Polio is an immunization campaign established by the

government of India in 1994 to eradicate poliomyelitis (polio) in India
by vaccinating annually all children under age five against poliovirus.
Every child receives a dose of Oral Polio Vaccine (OPV), a live,
attenuated virus which colonises the gastrointestinal tract. This virus
competitively inhibits the wild, disease-causing poliovirus. Not only
does this prevent pernicious infection in the host, it precludes
transmission of the wild poliovirus to other hosts. Since poliovirus
cannot survive outside a host for more than two weeks, theoretically it
would be eradicated, resulting in the eradication of poliomyelitis.

ACUTE FLACCID PARALYSIS

Definition of Acute Flaccid Paralysis
1. Flaccid paralys is one occurring over hours or few days with hypotonia,
hyporeflexia, loss of power and wasting if persists for longer period. It
involves lower motor neuron complex
WHO definition of AFP:
1. Flaccid paralysis of less than 4 weeks duration in children less than 15
years of age will be considered as a case of AFP
Acute: rapid progression of paralysis from onset to maximum paralysis
(hours to days)
Flaccid: loss of muscle tone, floppy as opposed to spastic or rigid
Paralysis: weakness, loss of voluntary movement
Differentail diagnoses of AFP
1. Anterrior horn cell:
1. Viral: poliomyelitis (1)
2. Immune mediated: acute transverse myelitis (4)
2. Nerve trunk:
1. Immune mediated: Guillain-Barre (2)
2. Toxin: Diphtheria; porphyria
3. Traumatic: IM injections (3)
3. Neuromuscular junction:
1. Tick toxin
2. Botulinum
4. Muscles:
1. Myositis
5. Metabolic:
1. Familial periodic paralysis: autosomal recessive; abnormal K
levels; episodic paralysis

AFP SURVEILLANCE:
WHO definition for polio surveillance:

Flaccid paralysis of less than 4 weeks duration in children less than 15

years of age will be considered as a case of AFP and should be
investigated for isolation of polio virus and confirmation of diagnosis.
This is the joint responsibility of PHC/Deputy Director of HS/SMO
(Surveillance MO)
Background rate
1. At least one case of AFP (excluding polio) occurs annually for every
100,000 children less than 15 years of age. This is referred to as the
background rate of AFP among children.
2. The non-polio causes of AFP including (but not limited to):
1. Guillian-Barr Syndrome (GBS),
2. Transverse Myelitis and
3. Traumatic Neuritis account
3. Sensitive surveillance for AFP must be able to detect a minimum of 1 case
per 100,000 children less than 15 years of age.
The Purpose of AFP Surveillance
1. AFP surveillance helps to detect reliably areas where poliovirus
transmission is occurring.
2. AFP surveillance helps us to identify areas of priority for focusing
immunisation activities.
3. It is the most reliable tool to measure the quality and impact of polio
immunisation activities.
4. It is necessary for polio free certification from WHO
AFP CASE INVESTIGATION
1. Case Notification: all health facilities, clinicians and other practitioners are
required to notify AFP cases immediately to the District Immunization
Officer (DIO), by the fastest available means
2. Case Investigation:
1. All cases should be verified and investigated within 48 hours
of notification
2. Collect two stool samples from the child at a minimum
interval of 24 hours within 14 days; from late-reported cases
for up to 60 days
3. Outbreak Response Immunization: is organized in the community and
performed as soon as possible.
4. Search: The investigation team searches for additional AFP cases in the
community called hot cases
5. Stool sample: the specimens to arrive at the laboratory within 72 hours of
dispatch in cold chain
6. Lab report: isolation result is reported to the surveillance program no more
than 28 days from the time the specimen by lab
7. Sixty day follow-up: is done between the 60 th and 90th day in certain
categories of AFP cases to determine the presence/ absence of residual
paralysis

8. Within 90 days of paralysis onset, all cases should undergo final

classification as confirmed polio, non- polio AFP or compatible with
poliomyelitis.
1. An AFP case is confirmed as polio only by the isolation of wild
poliovirus from any stool specimen.
2. An AFP case is classified as non-polio AFP if wild poliovirus is not
isolated from adequate stool specimens.
3. 60 day followup examination reveals persistent weakness or
paralysis, or the child has died or is lost to follow-up, the final
classification of the case is one as compatible
4. All other cases are discarded as non polio AFP
TETANUS
Definition:Tetanus is an acute, spastic paralytic illness caused by the neurotoxin
of Clostridium tetani
Bacteriology:
Clostridium tetani is a motile, gram positive, spore-forming, obligate
anaerobe; drum stick appearance in microscopy.
Ubiquitous and found in soil, dust, alimentary tract of animals.
Produce a single toxin tetanospasmin
Does not invade tissues and no inflammation
Epidemiology:
1. Ubiquitous; found in 90 developing countries; causes neonatal and
maternal mortality.
Causes of infection:
1. Penetrating injury by dirty nail, splinter, glass piece etc.
2. IM injection by drug abusers
3. Contaminated surgical instruments
4. Animal bites-dog, bats etc
5. Abscess including dental abscess
6. Chronic middle ear infection
7. Burns
8. Chronic ulcers
9. Compound fractures
10.Frost bite
11.Gangrene
12.Intestinal surgery
13.Ritual scarification-circumcision, female genital mutilation
14.Insect bites
15.Septic abortion
16.Unclean delivery
17.No obvious cause
Pathogenesis:
Tetanus occurs after introduction of spores which germinate and multiply
without tissue invasion; release toxin after cell lysis; toxin binds at the
neuromuscular junction; enters motor nerves; retrograde axonal transport;
enters the a-motor neuron; passes on to adjacent inhibitory interneuron;
prevents the release of g-amino butyric acid (GABA)leading to sustained
muscle contraction without relaxation.
Mechanism:

Tetanospamin is a Zinc containing enzyme protein; it inactivates

synaptobrevin that helps fusion of synaptic vesicles with terminal cell
membrane
Clinical features:
Incubation: 2-14 days or even more. Generalized and localized tetanus:
Features of Generalized tetanus:
1. Trismus or lock jaw due to masseter spasm.
2. Headache, restlessness, irritability.
3. Stiffness, difficulty in chewing and swallowing
4. Neck muscle spam
5. Facial muscle spasm leading to risus sardonicus (Origin: L. Risus=
laughter + Sardinia = herb fr, ref. to effects of Strychnos nux-vomica)
6. Opisthotonus (body arches in such a way only heel and occiput touch
the surface due to total contraction of opposing muscles acquiring an
equilibrium position.
7. Laryngeal and respiratory muscle spasm leading to asphyxia
8. Consciousness is intact; pain is preserved; anxious look.
9. Tetanic seizures characterized by sudden severe tonic contractions of
the muscles with fists clinching, flexion, and adduction of the arms and
hyperextension of legs. The spasm progresses in severity and duration.
The spasms are triggered by light, sound and touch.
10.Urinary retention due to bladder sphincter spasm.
11.Autonomic disturbances like tachycardia, dysarrythmias, labile
hypertension, sweating and cutaneous vasoconstriction.
12.Severe progression of symptoms in the first week, stabilization in 2nd
week, amelioration in 3rd week.
Neonatal Tetanus (Tetanus Neonatorum):
1. Spores contaminate umbilical stump due to unclean instrument or
applicants like cow dung.
2. Manifests in 3-12 days
3. Progressive difficulty in feeding
4. Diminished movements, stiffness and rigitity.
5. Progressive spasms
6. opisthotonus
Localized tetanus:
1. Results in painful spasms of muscles adjacent to the wound
2. May precede generalized tetanus
3. Cephalic tetanus, a rare form involves bulbar musculature due to
contaminated wound on head, nose or otitis media. It is characterized
by retracted eyelids, deviated gaze, trismus, risus sardonicus, spastic
tongue, and pharyngeal spasm.
Diagnosis:
1. One disease in Medicine that allows confirmation by clinical features.
Typical spasm with normal sensorium.
2. Leukocytosis
3. Normal CSF
4. Normal EEG and EMG.
5. Smear for C.tetani is usually negative.
6. In 1/3 cases isolation of organism is possible.
D.D:

1. Unmistaken diagnosis is possible

2. Trismus is seen in pharyngeal abscess and brain stem encephalitis.
3. Rabies has typical hydrophobia.
4. Strychnine poisoning has spasm but no Trismus.
5. Hypocalcaemia has laryngeal and carpopedal spasm but no Trismus
6. Epilepsy may mimic tetanus but normal sensorium in later condition.
Treatment:
1. Wound debridement and cleaning to clear tetanus bacilli and anaerobic
conditions.
2. Human tetanus immunoglobin 3000-6000 units as IM; infiltration
around wound not considered necessary now. Intra thecal not effective.
3. Intravenous immunoglobin as an alternative if TIG is not available.
4. Another alternative is tetanus antitoxin; 50,000 to 100 000 U half IM
and half IV. After sensitivity tests.
5. Penicillin G100000 U/kg in 4 divided IV doses for 10-14 days.
6. IV metronidazole 500 mg 8 hrly for adults.
7. Erythromycin and tetracycline for allergic patients.
8. Diazepam 0.1 to 0.2 mg/kg IV every 3-4 hrs later titrated to need.
9. Intra thecal baclofen in intensive care settings.
10.Vecuronium and pancuronium followed by ventilation improves
ultimate survival.
11.Autonomic instability is treated by b-blockers and morphine.
Supportive care:
1. Dark and secluded settings protected from sound, light and touch.
2. Suction of secretions
3. Maintenance of nutrition and hydration with electrolytes.
4. Avoid infection, ulceration and constipation.
Complications:
1. Aspiration pneumonia
2. Intramuscular haematomas.
3. Bone fractures
4. Renal failure due to myoglobinuria.
5. Hyperpyrexia
6. Cardiac arrhythmias
7. Venous thrombosis
Prognosis:
1. Synapses regenerate in spinal cord and recovers slowly.
2. No antibodies are formed and hence TT immunization is necessary.
3. High mortality in younger age groups.
4. Better prognosis in long incubation and localized tetanus.
5. Cephalic tetanus has poor prognosis
6. Long term sequelae include cerebral palsy, mental retardation.
7. Mortality: Generalized tetanus=5to 35%; neonatal tetanus=10-75%
Prevention:
1. DTP vaccination in early childhood
2. Boosters every 10yrs
3. Antenatal TT
4. TT and TIG 250 IU in tetanus prone wounds
5. Wound cleaning after injury.

CHILDHOOD (PRIMARY) TUBERCULOSIS

1. EPIDEMIOLOGY
2. world
1. 95% in developing countries
2. 1/3 of world population affected
3. 8 % MDR TB
4. HIV co epidemic
1.

India
1. 3.8 million cases
2. 4,400 die every day
3. 0.8 % among U5
4.

MDR 3%

2. Transmission:
a. airborne droplet from an adult with TB cavity and forceful cough
b. no transmission by children because:

3.

1.

paucibacillary

2.

less cough

3.

less tussive force

Clinical types:
1. Primary TB:

Latent tuberculosis

Primary complex

Progressive primary complex

Disseminated tuberculosis

Reactivation tuberculosis

2. Secondary TB: adult type

4.

5.

Difference between primary and secondary TB:

No

Primary TB

Adult TB

No prior immune sensitization

Very strong existing immunity

Disease spreads to regional

gland and further disseminates
to different organs

Localization of the disease to the

affected organ

Delayed hypersensitivity
develops during the course of
disease hence less tissue
destruction

More tissue destruction due to

delayed hypersensitivity

Sub pleural focus develops

anywhere in the lung- Ghon
focus

Apical region commonly affected due

to more Oxygen availability- simon
focus

Casseation and cavitation less

common

Casseation and cavitatation more

pronounced

Lesions leal by calcification

Healing by fibrosis

Pathogenesis:
1. An adult with tuberculous cavity coughs with enough tussive force
2. Child gets the infection; portal of entry is lung;
3. incubation 4-8 weeks;
4. Bacteria settle in a well ventilated sub pleural lung for eg. Rt middle
or lower lobe and this is called Ghon Focus
5. bacteria multiply in alveoli

6. Neutrophils try to eliminate bacilli but are not able to eliminate the
bacteria due to resistant bacterial wall
7. Monocytes enter the scene and engulf the bacteria but not able to
do intra cellular killing due to tough bacterial wall
8. Monocytes form special giant cells called Langhan type of giant
cells and epithelioid cells (macrophages)
9. Lymphocytes invade the area and get sensitized; CD4 cells secrete
specific lymphokines which activate CD8 cells which lyse bacilli
loaded monocytes and macrophages kill the bacteria. Delayed
hypersensitivity is developed by CD4 cells and Mantoux becomes
positive by the end of 4-6 weeks.
10.Delayed hypersensitivity is responsible for tissue destruction such
as casseation and cavitation and also allergic reactions like
phlectanular keratoconjunctivitis and erythema nodosum.
6. Clinical Types:
1. Latent Tuberculosis
i. Asymptomatic
ii. Mx + ve
iii. CXR normal
iv. No clinical signs
v. 40 % develop symptomatic TB
vi. Maximum progression in first 2 yrs
vii. Reactivation during adolescence
2. Primary complex:
i. The basic pathology is primary focus in some part lung and
lymphangitis and regional adenitis; all three constitute primar or
ghon complex
ii. More than 50% of infants and children with radiographically
moderate to severe PC have no physical findings and are
discovered only by contact tracing.
iii. Nonproductive cough and mild dyspnea are the most common
symptoms.
3. Progressive PC:

i. The primary focus enlarges steadily and develops a large caseous

center. Liquefaction may cause formation of a primary cavity
associated with large numbers of tubercle bacilli.
ii. The enlarging focus may slough necrotic debris into the adjacent
bronchus, leading to further intrapulmonary dissemination.
iii. Significant signs or symptoms are frequent in locally progressive
disease in children. High fever, severe cough with sputum
production, weight loss, and night sweats are common.
4. Disseminated TB:
i. Tubercle bacilli are disseminated to distant sites, including liver,
spleen, skin, and lung apices, in all cases of tuberculosis infection.
ii. Multiple organ involvement is common, leading to hepatomegaly,
splenomegaly, lymphadenitis in superficial or deep nodes, and
papulonecrotic tuberculids appearing on the skin.
iii. Bones and joints or kidneys also may become involved.
iv. Meningitis occurs only late in the course of the disease.
iv. Miliary TB:
i. The most clinically significant form of disseminated
tuberculosis is ^aemolyt disease, which occurs when massive
numbers of tubercle bacilli are released into the bloodstream,
causing disease in two or more organs.
ii. Miliary tuberculosis usually complicates the primary infection,
occurring within 2-6 mo of the initial infection. Although this
form of disease is most common in infants and young children,
it is also found in adolescents and older adults, resulting from
the breakdown of a previously healed primary pulmonary
lesion.
v. Because this form of tuberculosis is most common in infants
and malnourished or immunosuppressed patients, the hosts
immune incompetency probably also plays a role in
pathogenesis.
5. Reactivation Tuberculosis:
i. Older children and adolescents with reactivation tuberculosis are
more likely to experience fever, anorexia, malaise, weight loss,
night sweats, productive cough, hemoptysis, and chest pain than
children with primary pulmonary tuberculosis
ii. Tuberculous pleural effusions, which can be local or general,
originate in the discharge of bacilli into the pleural space from a
subpleural pulmonary focus or caseated lymph node.
iii. Asymptomatic local pleural effusion is so frequent in primary
tuberculosis that it is basically a component of the primary
complex. Larger and clinically significant effusions occur months
to years after the primary infection.
iv. Tuberculous pleural effusion is infrequent in children <6 yr of age
and rare in children <2 yr of age
6. CVS TB:
i. The most common form of cardiac tuberculosis is pericarditis.
Pericarditis usually arises from direct invasion or lymphatic
drainage from subcarinal lymph nodes.

7. Time line

9. Immunity
1. Mainly Cell mediated immunity; Humeral immunity less role
2. Bacilli land on well ventilated subpleural area of lung
3. Neutrophils migarate first but could not fight due to resistant bacterial
cell wall
4. Monocytes come for second line defense engulf the bacteria but could
not kill ; form epithelioid cells- multinucelate giant cells
5. Third comes T lymphocytes; CD4 get sensitized and release cytokines
6. CD4 release cytokines which activate CD8 cytotoxic cells
7. CD8 lyse monocyte and release bacteria
8. Activated macrophages ultimately kill the bacteria
9. After sensizitization of T lymphocytes, granuloma formation occurs to
prevent spread of infection
10.TB granuloma: Cntral area of casseation surrounded my epitheloid
cells, Langhan type of giant cells and lymphocytes with bacilli in
caseous material.
10. External markers
1. Wasting

2. Lanugo hair
3. Long eye lashes
4. Phlectenular conjunctivitis
5. Scrofuloderma
6. Sinus ulcers
7. Lupus vulgares
8. Tuberculids
9. Skin TB
10.Scrfuloderma
11.Veruka and lupus vulgares
11. TB in Prgnancy
1. Prematurity
2. IUGR
3. Increased peri natal mortality
4.

Congenital TB in NB is rare

12. Investications
1. Mantoux:
2. Bacterial isolation and culture:
1. Gastric aspirate- 3 consecutive morning samples
2. Bronchoscopy and aspirate
3. Negative culture and smear do not rule out TB
4. AFB staining:
Ziehl-Neelsen stain
1. Heat fix
2. Smear with carbol fuchsin

3. Steam 5 mts
4. Rinse
5. Add 3% acid alcohol - 5 minutes
6. Rinse
7. Methylene blue-1 mt
8. Rinse
9. Dry
10.

Bright red purple bacilli

5. Auramine-rhodamine florescent stain.

1. Requires a fluorescent microscope.
2. The fluorochrome dyes used
3. The fluorescing mycobacteria are seen as bright yelloworange bacilli against a dark background.
6. Culture:
Lowenstein-Jensen medium:
1. Egg medium
2. glycerol enhances the growth of M.tuberculosis
3.

also used in drug susceptibility testing

4. > 3 weeks for growth

5. > 4 weeks for sensitivity
6. rough, tough and buff colonies
3.

CXR

Primary focus

Miliary TB

Calcified hilar adenitis etc

4.

Other tests

Interferon release by T cells towards MT antigens

Quantiferon TB c-gold

T Spot- TB

Elispot (elliza identifies T cells specific for TB)

13. TB & HIV :

a. 30% more in HIV
b. Mx ve
c. Rapid progression
d. Lymphocytosis favours viral replication-vicious cycle
e. Rifampicin toxicity increased by ART
14: Treatment of Primary TB:
1. Pulmonary: 2HRZ/4HR
a. INH, Rifampicin and pyrazinamide for 2 months
b. INH, Rifampicin for next 4 months
2. MDR TB:
a. Add ehtambutol and SM
3. DOTS: Directly Observed Therapy, Short-course
a. 2 months drugs under direct observation by health worker
b. Intermittent course
i. Basis for Intermittent Chemotherapy
In vitro experiments have shown that after a culture
of M. tuberculosis has
been exposed to certain
drugs for sometimes, it takes several days (the lag
period), before multiplication starts again

ii. Higher dosing in intermittent treatment increase peek

plasma levels
4. Indications for Corticosteroids:
a. TBM
b. Tuberculoma
c. Endobronchial TB
d. Pericarditis
e. Miliary TB
15.Prevention :
BCG:
i. Live attenuated vaccine prepared from mycobacterium bovis Bacillus Calmette Gurin
ii. Heat and light sensitive vaccine
iii. Add 1 cc NaCl to vial; 0.05 ml intradermal; left arm; no spirit for
cleaning
iv. Time: Within 14 days after birth
v. Reaction:
a. 2 to 3 weeks - papule
b. 5 weeks - 4-8 mm in diameter
c. 6-12 weeks - shallow ulcer covered with a crust.
d. Healing with round scar 2-10 mm in diameter.
e. Scar not a must
vi.

Complications:
1. BCG Abcess
2. Keloid
3. Adenitis

4. Spread of tubercular disease

vii. Contraindications:
1. symptomatic HIV
2. Immunocompromised child
3. Mx + ve child
viii. Prevents serious forms of TB in infancy
ix. 50% effective in Primary TB
x. 80% protective in CNS TB
xi. No protection for adults as effect wanes after 5 years
12. Also used for diagnosis as accelerated BCG reaction
16. NB & TB Mother
Neonate:

INH for 3 months

Isolation for MDR TB

Pregnancy:

Pyrazinamide teratogenic

Isoniacid, Rifampicin and ethambutol

INTERPRETATION OF TUBERCULIN TEST (MANTOUX)

1. Mantoux skin test:
1. Basis: Delayed cellular hypersensitivity
2. 0.1 ml intradermal of 5 TU of PPD Tween 80
3. Read after 48-72 hrs
4. Early reaction is not positive

5. Delayed reaction also is positive

2. False positive:
1. Nontuberculous mycobacteria
2. Earlier BCG vaccination ( positive for Mx up to 5 yrs; usually
<10 mm in size)
3.

False Negative:
1. Anergy
2. Infant
3. Malnutrition
4. Suppressed immunity
5. Vaccine: Measles; MMR
6. Measles infection
7. Miliary TB
8. Technical error
4.

Mantoux reading :
positive reaction:
1. Contact history ; Symptoms of PC
2. HIV

}
}

3. Immuno supression

> 5 mm

4. High prevalence area

>10 mm

5. Low prevalence area

> 15 mm

6. Recent Mx conversion

>10 mm

7. Serial Mantoux in a patient:

becomes positive

PEDIATRIC HIV
1. Etiology
1. Family: Retroviridae
2. Genus: Lentivirus

2.

3.

4.

4.

6.

7.

3. HIV I: contains 2 copies of single stranded RNA

4. HIV II: common among monkeys; rare in Ped.HIV difficult to identify
with HIV I tests; specific antibody test or III generation ELIZA should
be used for testing
Epdemiology:
1. Affects sexually promiscuous people
2. Others:
a. Mother to child transmission to neonate
b. Sex victims
c. Hospital and lab personnel
d. IV drug users
e. Blood receipients
Infection
1. HIV 1: Gp 120 carries a binding site to CD4 molecule with co
recptors like CC5 of T Cell and gain entry into cell ;
2. Viral RNA enters into cell cytoplasm
3. Viral RNA transcribes viral DNA copies using reverse transcriptase
4. DNA copies enters chromosomal DNA to form provirus
5. Proviral DNA encodes production of viral RNA viral proteins
assembly buds out of cell as new HIV 1 virus
6. Virus attacks young CD4 cells
7. Viral release by CD4 cell lysis
8. Gradual decrease in CD4 population
HIV transmission
1. Penetrating sex with infected partner
2. Virtually vertical (MTCT) in pediatric population
3. Rarely through:
1. blood products, clotting factors- 3-6%
2. Homosexual contacts in adolescent boys
3. Heterosexual contact in adolescent girls
4. IV drug use
4. Transmission by household contacts is nonexistent
Risk factors for MTCT
1. Preterm < 34 weeks
2. Low CD4 count in mother
3. Birt weight < 2500 gms
4. Rupture of membranes for > 4 hours
5. Mothers viral load > 1000 copies/mL
6. Vaginal delivery
7. Instrumental delivery
8. Caserian + ART to infant decrease transmission by 87 %
Mother To Child Transmission
1. Transmission rate is 12-30 %
2. Intra uterine: 30-40 %
3. Intrapartum: 60-70 %
4. Breastfeeding:
Transplacental
1. PCR is positive in fetal tissue by 10 weeks of gestation

8.

9.

10.

11.

15.

2. In situ hybridization and immuno cytochemistry identify virus in

fetal tissue in 1st trimester
3. Viral detection soon after birth
Intrapartum
1. Infected blood, cervico vaginal secretions in birth canal
conjunctiva, skin abrasions, gastric mucosa
2. Infected infant negative for viral detection in first week of life
3. First born twin 3 times more infected
Breast feeding
1. Both virus and viral laden cells are present breast milk
2. Mother infected before pregnancy: 14 %
3. Mother infected postnatally: 29 %
4. Benefit of breastfeeding outweighs the risk of HIV in developing
countries
5. WHO: breastfeed first 6 months and rapid weaning thereafter
Pathogenesis
1. Virus enters via mucosal breaks
2. Virus infects T helper (CD4) cells, monocytes and macrophages
3. CD 4 receptors are also present in: Microglia, Astrocytes,
oligodentroglia, Placent. villus cells
4. Co receptor CXCR 4 and CCR 5 are also necessary for viral
attachmnt
5. Persons who lack CCR5 are highly protected from HIV
7. Lymphocyte proliferation against viral antigen produce generalized
lymphadenopathy
8. Younger the CD4 cells the more they are invaded
9. HIV is peculiar that it uses CD4 cells meant for eliminating them as
host cells
10.CD4 cell count decreases and viraemia increases in 3-6 weeks
producing flulike illness
11.Then by 2-4 months body mounts up cellular and humoral immune
defense to reduce viraemia
12.Now there is a symptom free period only for a short period to be
followed by gradual reduction CD4 cells and appearance of
symptom complex
Course of illness
1. Rapid course and death in 6-9 months- 15-25 %; in transplacental
transmission and is due to underdeveloped immune system in fetus
2. Slow progression with survival up to 6 years; 60-80% ; occurs in
intra partum infection
3. Long term survivors: < 5%; occurs in good immune system and
attenuated virus
4. CD4 < 1500 / mm is equivalent < 200 / mm in adults as infants
normally have lymphocytosis
Clinical manifestations:
Clinical categories
Category N: asymptomatic
Category A:

Any 2 of the following:

1. Lymphadenoapthy
2. Parotitis
3. Hepatomegaly
4. Splenomegaly
5. Dermatitis
6. Recurrent sinusitis
7. Otitis
Category B
1. Lymphocytic interstitial pneumonia
2. Oropharngeal thrush > 2 mo
3. Chronic diarrhea
4. Fever > 1 mo
5. Hepatitis
6. Herpes simplex
7. Pneumonitis
8. Varicella
9. Cardiomegaly
10.neuropathy
Category C
1. With 2 serious bacterial infections: sepsis, meningitis,
pneumonia in 2 years
2. Esophageal candidasis
3. Cryptococcoal infection
4. Encephalopathy
5. Malignancies
6. Disseminated TB
7. Pneumocystis pneumonia
8. Cerebral toxoplasmosis
9. Severe wasting
16.Immunologic category -CD 4 counts / L:
Immunity
< 12 yr
1-5 yr
6-12 yr
1.No suppression
>1500
>1000
>500
2.Moderate 750500200-500
suppression
1500
1000
3. Severe suppression
< 750
< 500
< 200
17. Combined categorization:
A1; A2; A3 etc
18. Oppurtunitic infections:
1. Pneumocysti carinii pneumonia- PCP
1. Most common OI in Ped. HIV ; Common in 3-6 mo of age
2. It accounts for 57% of AIDS-defining conditions
3. High Mortality at 1 yr
4. Fever, tacypnaea, hypoxemia
5. CXR: interstitial infiltrates
6. Diagnosis: staining of bronchial aspirtae for PC
7. Treatment:
1. IV TMP-SMZ; IV corticosteroids; Oral maintenance for 21 days

2. Pentamidine: 4 mg/kg/day, single dose IV for 21 deays

8. Prophylaxis: TMP-SMZ
1. Age (Year)
CD4 Count (Absolute
Count/Micro-Litre)
2. 1-5
<500
3. 6-12
<200
2. Non-tuberculosis mycobacterial infections:
1. Mycobacterium avium complex, M. kansasii, M. chelonei & M.
fortuitum
2. Slowly progressive. High-grade fever, weight loss, abdominal
pain and anemia are common.
3. Night sweats, diarrhea, malaise, hepatomegaly,
osteomyelitis, meningo encephalitis and intra abdominal and
soft tissue abscesses also occur with this infection.
4. Treatment: Clarithromycin or Azithromycin with Ethambutol
and/or Rifabutin
3. Tuberculosis:
1. Most common HIV-related OI;
2. High incidence of drug-resistant tuberculosis
3. Depletion and dysfunction of CD4 cells with defects in the
function of macrophages and monocytes
4. Miliary TB, hepatosplenomegaly, lymphadenopathy, TBM, and
genito-urinary tuberculosis may occur.
5. Mx is usually negative; positive if the induration is 5 mm
6. PCR test has high sensitivity and specificity. 4-drug regimen
of Isoniazid, Rifampin, Pyrazinamide and Ethambutol.
7. Duration of treatment is for 6-12 months for pulmonary, 12
months for extra-pulmonary disease.
8. ART & ATT :
1. In a patient with CD4 count less than 200, ART to be
started two weeks to two months after starting of
tuberculosis therapy.
2. If CD4 count is higher, ART after induction phase of
tuberculosis is complete
4. VIRAL INFECTIONS
HERPES SIMPLEX 1 & 2:
1. Recurrent self-limited cluster of orolabial ulcers with severe
stomatitis and cutaneous dissemination
2. Oral Acyclovir 80 mg/kg/day in 3-4 divided doses for 10 days
VARICELLA ZOSTER VIRUS (VZV):
1. Persistent lesions for more than one month after onset
2. pneumonia, hepatitis and encephalitis
3. IV Acyclovir 1500 mg/m2/day in 3 divided doses for 7-10
days;
4. Oral therapy 80 mg/kg/day in 4 divided
CYTOMEGALOVIRUS (CMV):
1. CMV infection is an AIDS defining condition.

2. More than 90% of HIV-infected pregnant women are CMVinfected; mother infects child pre or post natally
3. Chorioretinitis visual loss and retinal detachment
4. diarrhoea, abdominal pain
5. Pneumonitis
6. Encephalitis: It manifests as sub-acute dementia complex.
7. Ganciclovir 10 mg/kg/day in 2 divided doses, intra-venously,
over 1-2 hours for 14-21 days
8. Life-long prophylaxis with Ganciclovir (5 mg/kg/d IV 5 days
per week)
4. TOXOPLASMA GONDII INFECTION
1. Women transmits toxoplasma to the foetus
2. Low-birth weight, microcephaly hydrocephalus,
hepatosplenomegaly and chorioretinitis.
3. CNS: headache, fever, changes in the mental status, seizures;
hemiparesis, ataxia and cranial nerve palsies.
4. Multiple ring-enhancing lesions-granulomas is seen on the mri or
the ct scan of the brain.
5. The drugs used are sulfadiazine & pyrimethamine.
6. Folinic acid for prevention of drug-induced suppression of the bone
marrow.
5. CANDIDA INFECTIONS
1. Oral thrush and diaper dermatitis are common
2. Esophageal candidiasis present with substernal or abdominal pain,
dysphagia and weight loss.
3. Disseminated infection may manifest as sepsis and shock.
4. Nystatin, Amphotericin B and Azoles.
5. For esophageal candidiasis, Fluconazole is the drug of choice.
Amphotericin for treating for resistant cases
6. DIARRHEA
1. Diarrhoea may persist for several days leading to wasting and
cachexia.
2. Cryptosporidium: Paramomycin
3. Isospora: Oral TMP-SMX
4. Cyclospora: Oral TMP-SMX
5. Microsporidium : Albendazole 400 mg twice a day
6. Entamoeba Histolytica: Metronidazole
7. Giardia Lamblia: Metronidazole Furazolidone Tinidazole
19. Differences in pediatric and adult hivinfection:
1. Progression of disease is more rapid
2. Immune system is more immature with higher CD 4 counts
3. Recurrent invasive bacterial infections are more common
4. Disseminated CMV, Candida, Herpes Simplex and Varicella Zoster are
more common
5. LIP occur almost exclusively in children
6. CNS infections are common
7. Peripheral neuropathy, myopathy are rare in children

20.Skin manifestations in hiv-infected children:

Infectious Disorders and
Non-Infectious Disorders and
Lesions
Lesions
Viral Infections:
Atopic dermatitis; Seborrheic
Herpes simplex, Herpes zoster,
dermatitis, Generalized
Molluscum contagiosum, Warts
dermatitis, NutritionalDeficiency
Fungal Infections:
Candida, Tinea, Onchomycosis
Bacterial:Impetigo

Eczema, Psoriasis, Drug eruptions

Other: Scabies

Alopecia

Vasculitis

21.Hematological abnormalities:
Abnormality

Mechanism

Anemia

Auto-immune; Suppression of the bone marrow

by drugs Nutritional deficiency (folic acid,
Vitamin B12, micronutrients)

Thrombocytopenia

Immune-mediated, Nutritional deficiency

(Vitamin B12 deficiency)

Neutropenia

Immune-mediated destruction

Lymphopenia

Bone marrow suppression due to altered

cytokine production, CD4+ apoptosis induced
by HIV replication

Eosinophilia

Shifting of immune response from Th1 to Th2

cytokine profile

22.Other
1.
2.
3.

manifestations:
Cardiac: Myopathy
CNS: HIV Encephalopathy; peripheral neuropathy
Nephropathy: due to virus, immune complex mediated vasculitis, or
opportunistic infections
4. Respiratory: Lymphoid Interstitial Pneumonitis (LIP)
1. Cough and Tachypnea
2. Diffuse bilateral reticulondular or interstitial infiltrates on
chest radiograph
5. Malignancy:
1. Non-Hodgkins lymphoma, leiomyomas and
leiomyosarcomas and leukemia
2. Kaposis sarcoma is rare
23.Diagnosis
1. Viral Culture: 100% specific; costly and needs sophisticated laboratory
set up
2. Polymerase Chain Reaction (PCR) RNA/DNA:
1. Two PCRs have to be positive, done beyond one
month and at least one of them after age of 3
months.

2. Detect nearly 100% of infected newborns

3. Enzyme Linked Immunosorbent Assay (ELISA)
1. I Generation ELISA: antigen from crude viral lysate
2. II generation: part of virus
3. III Generation ELISA: synthetic peptides as the antigen
4. Rapid tests
ELIZA
1. Current kids are 100% sensitive and specific.
2. Detection of anti-HIV antibodies in patients sera.
3. The ELISA is performed by the use of purified antigen, bound to a plate
containing small wells.
4. The latest ELISA is the Rapid Test with results in 10 mts
5. Eliza test should be confirmed by Western Blot or repeated Eliza with
different antigens
ELIZA : method
1. HIV antigens pre-coated onto an ELISA plate
2. HIV antibodies of patient will bind to the HIV antigens on the plate.
3. Anti-human immunoglobulin is coupled to an enzyme is now added
which binds to human HIV antibodies
4. Chromogen or substrate is then added which changes color when
cleaved by the enzyme attached to the second antibody
Western Blot Analysis (WBA)
1. Plasma electrophoresis on a strip pre-impregnated with various HIV
antigens (i.e. p24, p28, gp41, gp120, gp160,).
2. show bands of all these antibodies depending on their presence in the
samples
3. In India, it is not mandatory to do WBA
24.Management Care immediately after birth
1. Cord clamped soon; no milking;
2. Early baby bathing
3. Single dose NVP to mother during labour and to the baby within 72
hours after birth.
4. Exclusive replacement feeding is afass acceptable, feasible,
affordable, sustainable and safe
5. Quick weaning at 6 mo
6. CTX prophylaxis from age of 46 weeks; 5 mg/kg/day
7. Growth monitoring
8. Screen for infections
25.When to start ART in children, guided by CD4
1. < 11 month infants : if CD4 < 1500 cells/mm3
2. 1235 months : if CD4 < 750 cells/mm3
3. 3659 months : if CD4 <350 cells/mm3
4. > 5 years old : < 350 cells/mm3 especially if symptomatic; or
5. Before CD4 drops below 200 cells/mm3.
26.ARV regimens
1. Zidovudine (AZT) + Lamivudine (3TC) + Nevirapine NVP
2. Stavudine (D4T) + Lamivudine (3TC) + Nevirapine (NVP)

3. Vaccine:
1. if the HIV-infected child is asymptomatic or mildly symptomatic
vaccinations should be given.
2. Withold vaccine (live vaccines) for HIV-infected children who are
symptomatic and severely immuno-compromised.
27.Prevention
1. Transmission from the mother to child is likely to be about 15-45%.
2. There is 16.2% greater risk of mother-to-infant transmission of HIV
when children are breast-fed as opposed to formula-fed.
3. Single dose NVP 200mg given at the onset of labour and
4. single dose of syrup NVP 2mg/kg weight to the baby within 72 hours
decreases risk of transmission by 13.1% (breast feeding)..
5. Transmission of the HIV virus occurs most commonly during the first
few months after birth
6. Avoid manipulations like amniocentesis and external cephalic version
increase the risk of transmission of HIV.
7. Long duration of rupture of membranes increase the transmission risk.
It has been estimated that with every hour, the risk of transmission
increases by 2%.
8. Placental disruption and infections also adversely affect transmission.
9. Invasive fetal monitoring should be avoided, as should all invasive
obstetric procedures.
10.Where facilities are available, elective LSCS should be offered.
11. If instrumental delivery is necessary, then forceps are a better option
than vacuum suction cup delivery.
12.Emergency LSCS is associated with high transmission
13.In India normal delivery is recommended unless the woman has
obstetric reasons
14.When replacement feeding (infant formula) is acceptable, feasible,
affordable, sustainable and clean water is available, HIV-infected
mothers should avoid breastfeeding completely.
15.Otherwise, exclusive breastfeeding is recommended during the first
months of life, with early abrupt weaning at 3-4 months or 6 months
of age

HIV AIDS DEFINING PULMONARY INFECTIONS:

1. The Centers for Disease Control and Prevention (CDC) defines an HIV+ person
with a CD4 cell count of 200 or less as having AIDS. The CDC has also
developed a list of more than 20 opportunistic infections (OIs) that are
considered AIDS-defining conditions (see below). If a child with HIV has one or
more of these OIs, it gives the diagnosis of AIDS.
2. Aids defining pulmonary infections are:

1. Candidiasis of bronchi, trachea, or lungs

2. Mycobacterium avium complex or M. Kansasii, disseminated or
extrapulmonary
3. Mycobacterium tuberculosis, any site (pulmonary or extrapulmonary)
Mycobacterium, other species or unidentified species, disseminated or
extrapulmonary
4. Pneumocystis carinii pneumonia
5. Pneumonia, recurrent
6. Histoplasmosis, disseminated or extrapulmonary
GUILLAIN-BARRE SYNDROME
1. It is a postinfectious polyneuropathy involving mainly motor and
sometimes sensory and autonomic nerves.
2. Progressive symmetric ascending muscle paralysis
Pathophysiology
1. Resemblance of the pathogens to antigens on peripheral nerves
(molecular mimicry) leads to an overzealous autoimmune response
mounted by T-lymphocytes and macrophages
2. Autoimmune process leads to:
1. Demyelination
2. Axonal degenerataion
Etiological agents
1. Symptoms start about 10 days after a nonspecific viral infection.
2. Usual infections are:
1. GIT: camphylobacter jejuni, Helicobacter,
2. R.S: Mycoplasma pneumonia
3. Vaccines: Rabies, influenza, oral polio and meningococcal and H1N1
vaccines.
Clinical
1. Paralysis starts from lower limbs and progress upward to involve
respiratory and bulbar muscles (Landry ascending paralysis)
2. Weakness is symmetrical and progress over days to weeks
3. Muscle pain is common in early phase
4. Paresthesia
5. Flaccid quadriplegia occurs in severe cases
6. Dysphagia and facial weakness indicate impending respiratory failure
7. Bulbar involvement occurs in 50% of cases
8. Aspiration is a risk leading to pneumonias
9. Papilledema can occur in some children
10. Urinary incontinence or retention of urine is a complication in about 20%
of cases but is usually transient.
11. Extraoccular muscles involvement is rare but more common in a variant
of this syndrome called Miller-Fischer syndrome:
External optholmoplegia
Ataxia
Areflexia

Signs:
1. Absent tendon reflexes
2. ANS: labile BP, bradycardia, hypotension
Congenital Guillain-Barre Syndrome has been reported
Laboratory Findings and Diagnosis
CSF:
1. The CSF protein is elevated to more than twice the upper limit of
normal,
2. glucose level is normal, and
3. There is no pleocytosis. Fewer than 10 white blood cells/mm 3 are found.
4. The results of bacterial cultures are negative, and viral cultures rarely
isolate specific viruses.
5. The dissociation between high CSF protein and a lack of cellular
response is diagnostic of Guillain-Barr syndrome.
ENMG
1. Motor nerve conduction velocities are greatly reduced, and sensory
nerve conduction time is often slow.
2. An electromyogram shows evidence of acute denervation of muscle.
Serology
1. Serum creatine phosphokinase (CK) level may be mildly elevated or
normal.
2. Antiganglioside antibodies, mainly against GM1 and GD1, are
sometimes
Muscle biopsy
1. Muscle biopsy is not usually required for diagnosis; specimens appear
normal in early stages and show evidence of denervation atrophy in
chronic stages.
Nerve biopsy
Sural nerve biopsy tissue shows segmental demyelination, focal
inflammation, and wallerian degeneration; usually not required for
diagnosis
Evidence for infection
1. Serologic testing for Campylobacter infection helps establish the cause
if results are positive but does not alter the course of treatment.
2. Antibodies for Helicobacter, Mycoplasma etc can be demonstrated
Treatment of GBS
1. Hospitalization
2. IV gamma globulin 400 mg/kg/day for 5 days
3. Interferon is also effective in combination with IVIG
4. Plasma exchange transfusion helps in removing antigen autoantibody
complexes
5. Steroids tried but less effective- high dose methyl prednisolone IV
6. Gabapentin or carbamzepine for neuropathic pain
7. No need for antibiotics
Prognosis
1. The clinical course is usually benign, and spontaneous recovery begins
within 2-3 wk.

2. Improvement usually follows a gradient inverse to the direction of

involvement, with recovery of bulbar function first and lowers extremity
weakness resolving last.
3. Bulbar and respiratory muscle involvement may lead to death if the
syndrome is not recognized and treated.
4. three clinical features are predictive of poor outcome with sequelae:
1. Cranial nerve involvement, intubation, and maximum disability at
the time of presentation.
DENGUE FEVER AND DENGUE HEMORRHAGIC FEVER
ETIOLOGY:
1. There are at least 4 distinct antigenic types of dengue virus, members of
the family Flaviviridae.
EPIDEMIOLOGY:
1. Dengue viruses are transmitted by mosquitoes of the Stegomyia family.
Aedes aegypti, a daytime biting mosquito is the principal vector and is
highly urbanized, breeding in water stored for drinking or bathing and in
rainwater collected in any container.
PATHOGENESIS:
1. It is usually associated with 2nd infections with dengue types 14.
2. Circulation of infection-enhancing antibodies at the time of infection is the
strongest risk factor for development of severe disease.
3. Mild degree of disseminated intravascular coagulation, liver damage, and
thrombocytopenia may operate synergistically.
4. Capillary damage allows fluid, electrolytes, small proteins, and, in some
instances, red cells to leak into extravascular spaces.
5. This results in hemoconcentration, hypovolemia, increased cardiac work,
tissue hypoxia, metabolic acidosis, and hyponatremia.
6. Minimal to moderate hemorrhages are seen in the upper gastrointestinal
tract, and petechial hemorrhages are common in the interventricular
septum of the heart, on the pericardium, and on the subserosal surfaces
of major viscera. Focal hemorrhages are occasionally seen in the lungs,
liver, adrenals, and subarachnoid space.
7. The liver is usually enlarged, often with fatty changes. Yellow, watery, and
at times blood-tinged effusions are present in serous cavities in about 3/4
of patients.
CLINICAL MANIFESTATIONS:
1. The incubation period is 17 days. The clinical manifestations are variable
and are influenced by the age of the patient.
2. In infants and young children, the disease may be undifferentiated or
characterized by fever for 15 days, pharyngeal inflammation, rhinitis, and
mild cough. A majority of infected older children and adults experience
sudden onset of fever, with temperature rapidly increasing to 39.4
41.1C , usually accompanied by frontal or retro-orbital pain,
particularly when pressure is applied to the eyes.
3. Occasionally, severe back pain precedes the fever (back-break fever).
4. A transient, macular, generalized rash that blanches under pressure may
be seen during the 1st 2448 hr of fever.

5. The pulse rate may be slow relative to the degree of fever.

6. Myalgia and arthralgia occur soon after the onset and increase in severity.
7. From the 2nd to 6th days of fever, nausea and vomiting and pronounced
anorexia may develop.
8. About 12 days after defervescence, a generalized, morbilliform,
maculopapular rash appears that spares the palms and soles. It
disappears in 15 days; desquamation may occur. Rarely there is edema of
the palms and soles.
9. About the time this 2nd rash appears, the body temperature, which has
previously decreased to normal, may become slightly elevated and
demonstrate the characteristic biphasic temperature pattern.
Dengue Hemorrhagic Fever:
1. Differentiation between dengue fever and dengue hemorrhagic fever is
difficult early in the course of illness. A relatively mild 1st phase is followed
after 25 days by rapid clinical deterioration and collapse. In this 2nd
phase, the patient usually has cold, clammy extremities, a warm trunk,
flushed face, diaphoresis, restlessness, irritability, and mid-epigastric pain.
2. Frequently, there are scattered petechiae on the forehead and extremities;
spontaneous ecchymoses are common.
3. Approximately 2030% of cases of dengue hemorrhagic fever are
complicated by dengue shock syndrome.
4. After a 2436 hr period of crisis, convalescence is fairly rapid in the
children who recover. The temperature may return to normal before or
during the stage of shock. Bradycardia and ventricular extrasystoles are
common during convalescence.
DIAGNOSIS:
1. The World Health Organization criteria for dengue hemorrhagic fever are:
a. Fever,
b. Minor or major hemorrhagic manifestations,
c. Thrombocytopenia (100,000/mm3), and
d. Objective evidence of increased capillary permeability (hematocrit
increased by 20%), serosal effusion (by chest radiography or
ultrasonography), or hypoalbuminemia.
e. Dengue shock syndrome criteria include those for dengue
hemorrhagic fever as well as hypotension or narrow pulse pressure
(20 mm hg).
2. The tourniquet test result may be positive. The test is performed by
inflating a blood pressure cuff halfway between the systolic and diastolic
blood pressures for approximately 5 minutes. After release, the number of
petechiae in a 2.5 x 2.5 cm patch is counted. Greater than 20 petechiae
indicate a positive test.
3. Virologic diagnosis can be established by serologic tests or by isolation of
the virus from blood leukocytes or serum.
4. In both primary and secondary dengue infections, there is a relatively
transient appearance of antidengue immunoglobulin M (IgM) antibodies.
These disappear after 612 wk, which can be used to time a dengue
infection.
5. In 2nd primary dengue infections, most antibodies are of the IgG class.

6. Serologic diagnosis depends on a 4-fold or greater increase in IgG

antibody titer in paired sera by hemagglutination inhibition, complement
fixation, enzyme immunoassay, or neutralization test.
7. Viral RNA can be detected in blood or tissues by specific complementary
RNA probes or amplified first by the polymerase chain reaction (PCR) or by
real-time PCR.
Other tests:
1. Other abnormalities include moderate elevations of the serum
transaminase levels, consumption of complement, mild metabolic acidosis
with hyponatremia, occasionally hypochloremia, slight elevation of serum
urea nitrogen, and hypoalbuminemia.
2. Roentgenograms of the chest reveal pleural effusions (left > right) in
nearly all patients with dengue shock syndrome.
DIFFERENTIAL DIAGNOSIS:
1. The differential diagnosis of dengue fever includes viral respiratory and
influenza-like diseases, the early stages of malaria, mild yellow fever,
scrub typhus, viral hepatitis, meningococcemia and leptospirosis.
TREATMENT:
1. Uncomplicated dengue fever:
a. It is mainly supportive. Bed rest is advised during the febrile period.
Antipyretics should be used to keep body temperature <40C
(104F). Analgesics or mild sedation may be required to control
pain.
b. Aspirin is contraindicated and should not be used because of its
effects on hemostasis.
c. Fluid and electrolyte replacement is required for deficits caused by
sweating, fasting, thirsting, vomiting, and diarrhea.
2. Dengue Hemorrhagic Fever:
a. Patients who are cyanotic or have labored breathing should be
given oxygen.
b. Rapid intravenous replacement of fluids and electrolytes can
frequently sustain patients until spontaneous recovery occurs.
Normal saline is more effective in treating shock than the more
expensive Ringer lactated saline. When pulse pressure is 10 mm
Hg, or when elevation of the hematocrit persists after replacement
of fluids, plasma or colloid preparations are indicated.
c. Care must be taken to avoid overhydration, which may contribute to
cardiac failure.
d. Transfusions of fresh blood or platelets suspended in plasma may be
required to control bleeding;
e. Disseminated intravascular coagulation may require treatment.
f. Corticosteroids do not shorten the duration of disease or improve
prognosis in children receiving careful supportive therapy.
g. Hypervolemia during the fluid reabsorptive phase may be life
threatening and is heralded by a decrease in hematocrit with wide
pulse pressure. Diuretics and digitalization may be necessary.
COMPLICATIONS:
1. Fluid and electrolyte losses, hyperpyrexia, and febrile convulsions are the
most frequent complications in infants and young children.

2. Epistaxis, petechiae, and purpuric lesions are uncommon but may occur at
any stage.
3. Infrequently, after the febrile stage, prolonged asthenia, mental
depression, bradycardia, and ventricular extrasystoles may occur in
children.
PROGNOSIS:
1. Death has occurred in 4050% of patients with shock, but with adequate
intensive care deaths should occur in <1% of cases.
PREVENTION:
1. Prophylaxis consists of avoiding mosquito bites by use of insecticides,
repellents, body covering with clothing, screening of houses, and
destruction of A. aegypti breeding sites.
2. The possibility exists that dengue vaccination may sensitize a recipient
so that ensuing dengue infection could result in hemorrhagic fever.

TOXIC SHOCK SYNDROME

TSS is an acute multisystem disease characterized by high fever, hypotension,
vomiting, diarrhea, myalgias, nonfocal neurologic abnormalities, conjunctival
hyperemia, strawberry tongue, and an erythematous rash with subsequent
desquamation on the hands and feet.
ETIOLOGY:
TSS is caused by TSST-1-producing strains of S. aureus, which may
colonize the vagina or cause focal sites of staphylococcal infection.
EPIDEMIOLOGY:
1. Menstrual TSS:
a. Many cases occur in menstruating women who is 1525 yr of age
and who use tampons or other vaginal devices (diaphragm,
contraceptive sponge).
2. Nonmenstrual TSS:
a. S. aureus infection of nasal packing
b. Wound infections, sinusitis, tracheitis, pneumonia, empyema,
abscesses, burns, osteomyelitis, and primary bacteremia.
3. During mass vaccination with multi dose measles vaccine; Staph.aureus
contamination is possible due to lack of specific preservative and TSS has
been reported in India as a complication of measles vaccine
PATHOGENESIS:
S. aureus strains produce a number of extracellular toxins, which causes
massive loss of fluid from the intravascular space directly or after production of
interleukin 1 and tumor necrosis factor
CLINICAL MANIFESTATIONS:
1. The diagnosis of TSS is based on clinical manifestations. The onset is
abrupt, with high fever, vomiting, and diarrhea, and is accompanied by
sore throat, headache, and myalgias.
2. A diffuse erythematous macular rash (sunburn-like or scarlatiniform)
appears within 24 hr and may be associated with hyperemia of
pharyngeal, conjunctival, and vaginal mucous membranes.

3. A strawberry tongue is common.

4. Symptoms often include alterations in the level of consciousness, oliguria,
and hypotension, which in severe cases may progress to shock and
disseminated intravascular coagulation.
5. Complications, including acute respiratory distress syndrome, myocardial
dysfunction, and renal failure, are commensurate with the degree of
shock.
6. Recovery occurs within 710 days and is associated with desquamation,
particularly of palms and soles; hair and nail loss have also been observed
after 12 mo.
DIAGNOSIS:
1. There is no specific laboratory test; appropriate selective tests for hepatic,
renal, muscular, gastrointestinal, cardiopulmonary, and central nervous
systems involvement.
2. Bacterial cultures of the associated focus (vagina, abscess) before
administration of antibiotics
Differential Diagnosis:
1. Group A streptococcus can cause a similar TSS-like illness from focal
streptococcal infection such as cellulitis or pneumonia.
2. Kawasaki disease closely resembles TSS clinically but is usually not as
severe or rapidly progressive. Kawasaki disease typically occurs in
children younger than 5 yr.
3. Scarlet fever, Rocky Mountain spotted fever, leptospirosis, toxic epidermal
necrolysis, sepsis, and measles must also be considered in the differential
diagnosis.
TREATMENT:
1. Parenteral administration of a -lactamase-resistant antistaphylococcal
antibiotic (nafcillin or a 1st generation cephalosporin) or
2. Vancomycin or
3. Clindamycin
4. Removal of any retained tampons
5. Drainage of focally infected sites
6. Fluid replacement
7. Inotropic agents
8. Corticosteroids and intravenous immunoglobulin may be helpful in severe
cases.
PREVENTION:
1. Using tampons intermittently during each menstrual period.
2. Discard measles vaccine on the same day of vaccine session
H1N1 INFLUENZA (SWINE FLU)
INTRODUCTION
1. Influenza A viruses have a complex epidemiology involving avian and
mammalian hosts that serve as reservoirs with the potential for infecting
the human population.
2. The segmented nature of the influenza genome allows reassortment to
occur between an animal virus and a human virus when co-infection
occurs.

3. Minor changes within a serotype are termed antigenic drift; major changes
in serotype are termed antigenic shift.
TRANSMISSION
1. Human-to-human transmission of swine flu can also occur.
2. Disease spreads very quickly among the population especially in crowded
places.
3. Cold and dry weather enables the virus to survive and epidemics appear in
winter.
4. People may become infected by touching/handling something
contaminated with flu viruses on it and then touching their mouth or nose.
SYMPTOMS
1. fever, lethargy, lack of appetite and cough.
2. runny nose, sore throat, nausea, vomiting and diarrhoea.
DIAGNOSIS OF SWINE FLU
1. Preferred respiratory samples : nasopharyngeal swab and throat
swab
2. Available Laboratory tests:
a. Rapid Antigen Tests: not as sensitive as other available tests.
b. RT-PCR
c. Virus isolation
d. Virus Genome Sequencing
e. Four-fold rise in swine influenza A (H1N1) virus specific neutralizing
antibodies.
3. Infectious period: The infectious period for a confirmed case of swine
influenza A (H1N1) virus infection is defined as 1 day prior to the onset of
illness to 7 days after onset
4. ANTIVIRAL TREATMENT
a. Oseltamivir is the recommended drug both for prophylaxis and
treatment.
b. Supportive therapy includes:
1. IV Fluids.
2. Parentral nutrition.
3. Oxygen therapy
4. Antibiotics for secondary infection.
5. Vasopressors for shock.
6. Paracetamol or ibuprofen is prescribed for fever, myalgia and
headache.
7. Patient is advised to drink plenty of fluids.
8. Smokers should avoid smoking.
9. Salicylate / aspirin is strictly contra-indicated
5. ANTIVIRAL CHEMOPROPHYLAXIS
a. Prophylaxis: Oseltamivir is given to all close contacts of
suspected and health care personnel coming in contact with
suspected, probable or confirmed cases
b. Prophylaxis should be provided till 10 days after last exposure
(maximum period of 6 weeks) infants 20 mg OD older children 3040 mg OD
6. Close Contacts of suspected, probable and confirmed cases should be
advised to remain at home (voluntary home quarantine) for at least 7 days
after the last contact with the case.

7.

Adult patients should be discharged 7 days after symptoms have

subsided.
8. Children should be discharged 14 days after symptoms have subsided.
AVIAN INFLUENZA (BIRD FLU)
Introduction:
Highly pathogenic avian influenza A(H5N1) virus has increased the risk of
human exposure to the virus since 2003; The largest number of cases has
occurred in Vietnam, particularly during the third, ongoing wave, and the
first human death was recently reported in Indonesia.
Transmission:
For human influenza A (H5N1) infections, evidence is consistent with birdto-human and limited, nonsustained human-to-human transmission to
date.
Incubation:
most cases occurred within two to four days after exposure; recent
reports indicate similar intervals but with ranges of up to eight days.
Initial Symptoms
a. Most patients have initial symptoms of high fever and an influenza-like
illness with lower respiratory tract symptoms.
b.

Diarrhea, vomiting, abdominal pain, pleuritic pain, and bleeding from

the nose and gums have also been reported early in the course of
illness in some patients.

Clinical Course
a.

Respiratory distress, tachypnea, and inspiratory crackles are common.

b. Sputum production is variable and sometimes bloody.

c. Almost all patients have clinically apparent pneumonia;
Radiology:
a. Radiographic changes include diffuse, multifocal, or patchy infiltrates;
interstitial infiltrates; and segmental or lobular consolidation with air
bronchograms.
b. Pleural effusions are uncommon.
Micrbiology:
a. Limited microbiologic data indicate that this process is a primary viral
pneumonia, usually without bacterial suprainfection at the time of
hospitalization.

Progression:
b. Progression to respiratory failure has been associated acute respiratory
distress syndrome (ARDS).
c. Multiorgan failure with signs of renal dysfunction and sometimes
cardiac compromise, including cardiac dilatation and supraventricular
tachyarrhythmias, has been common.
d. Other complications have included pulmonary hemorrhage,
pneumothorax, pancytopenia, Reye's syndrome, and sepsis syndrome
without documented bacteremia
Case Fatality:
The case fatality rate was 89 percent among those younger than 15 years
of age in Thailand.
Laboratory Findings
a. Common laboratory findings have been leukopenia, particularly
lymphopenia; mild-to-moderate thrombocytopenia; and slightly or
moderately elevated aminotransferase levels.
Virologic Diagnosis
a. Viral isolation
b. The detection of H5-specific RNA
c. Commercial rapid antigen tests are less sensitive
Management
a. Ventilatory support
b. Intensive care for multiorgan failure and sometimes hypotension.
c. Empirical treatment with broad-spectrum antibiotics, antiviral agents,
alone or with corticosteroids,
d. Isolation for clinical monitoring, appropriate diagnostic testing, and
antiviral therapy.
Antiviral Agents
a. Patients with suspected influenza A (H5N1) should promptly receive a
neuraminidase inhibitor pending the results of diagnostic laboratory
testing.
b. These viruses are susceptible in vitro to oseltamivir and zanamivir. Oral
oseltamivir and topical zanamivir are active in animal models of
influenza A (H5N1).

Prevention
Immunization
No influenza A (H5) vaccines are currently commercially available for
humans. Earlier H5 vaccines were poorly immunogenic and required two
doses of high hemagglutinin antigen content or the addition of MF59
adjuvant to generate neutralizing antibody responses
Hospital-Infection Control
a. Influenza is a well-recognized nosocomial pathogen. Current
recommendations are based on efforts to reduce transmission to health
care workers and other patients in a nonpandemic situation and on the
interventions used to contain SARS.
b. The efficiency of surgical masks, even multiple ones, is much less than
that of N-95 masks, but they could be used if the latter are not
available.
c. Chemoprophylaxis with 75 mg of oseltamivir once daily for 7 to 10
days is warranted for persons who have had a possible unprotected
exposure

CHILDHOOD IMMUNIZATION
VPD - vaccine-preventable disease
Definition of VPD:
1. An infectious disease for which an effective preventive vaccine exists.
2. If a person dies from it, the death is considered a vaccinepreventable death.
3. 1.4 million U5 deaths were from vaccine-preventable diseases.
4. With 100% immunization, one out of seven deaths could be prevented
5. The 8 targeted VPDs in India are:
1. Diphtheria,
2. Hepatitis B,
3. Measles,

4. Pertusis,
5. Poliomyelitis,
6. Tetanus,
7. Tuberculosis,
8. JE
6. Six killer diseases:
1. Polio,
2. Diphtheria,
3. Tuberculosis,
4. Pertusis (whooping cough),
5. Measles and
6. Tetanus.
7. Fully immunized child: A child who received
1. One dose of BCG,
2. Three doses of DPT and OPV
3. One dose of measles before one year of age
4. This gives a child the best chance for survival
BCG:
1. Live attenuated vaccine prepared from mycobacterium bovis - Bacillus
Calmette Gurin Danish 1331strain subcultured every 3 weeks for 13
years
2. Heat and light sensitive vaccine
3. Add 1 cc NaCl to vial; 0.05 ml intradermal; left arm; no spirit for cleaning
4. Within 14 days after birth
5. 2 to 3 weeks - papule
1. 5 weeks - 4-8 mm in diameter
2. 6-12 weeks - shallow ulcer covered with a crust.
3. Healing with round scar 2-10 mm in diameter.
4. Scar not a must
5. Prevents serious forms of TB in infancy
6. complications
1. Abcess
2. Keloid
3. Adenitis
4. Spread of tubercular disease
7. Contraindication:
1. HIV
2. Immunocompromised child
3. Mx + ve child
OPV:
1. Live attenuated whole virus vaccine
2. Trivalent- types I, II & III
3. Light and heat sensitive
4. From NB Up to 5 years of age
5. 4 doses at 6,10,14 weeks and 16-24 months
6. Pulse polio for U5 children as and when planned
7. Neurovirulance vaccine associated poliomyelitis

8. Contraindications: > 5 years; severe immune deficiency; severe

diarrhea
DPT:
1. Diphteria and tetanus: toxoid
2. Pertusis: whole cellular inactivated bacteria
3. 6,10,14 and 16-24 months
4. Should not freeze
5. Intramuscular vaccine- preferably antero lateral thigh
6. Site of injection
7. DPT-Vaccine reactions
8. Local redness and swelling, induration,
9. Fever
10.Prolonged crying
11.Febrile convulsions
12.Hypotonichyporesponsive episodes
13.Pertusis contrindicated in:
1.
Incessant crying for more than 3 hours
2.
Fever more than 40.5c
3.
Hypotonichyporesponsive episodes
4.
Progressive neurological disease
5.
> 6 years of age
Double antigen-DT :
1. Diphtheria and tetanus toxoid
2. 4 to 5 years age
3. No specific contraindications
4. Pain swelling and fever can occur
TT:
1. 6,10,14, 1 years, 4-5 years, 10, 16 years and later every ten
years
2. Antenatal 2 doses at 1 month interval
3. Pain, eryythema, tenderness and induration
4. No specific contraindications
5. No need for TT in trivial injuries
Measles:
1. Live attenuated virus
2. 0.5 ml subcutaneous
3. After completion of 9 months
4. Mild fever and cold few days later
5. Toxic shock syndrome is an important adverse reaction due to
contamination of staph.aureus.
6. contraindications:
1.
Neomycin and egg allergy
2.
Immune compromised children
Optional vaccines:
Mumps, measles and rubella vaccine (MMR):
1. Mumps can cause sterility, myocarditis and encephalitis

2. Rubella can cause fetal malformation- Congenital rubella

syndrome with CHD and mental retardation
3. MMR is given at 15 completed months
4. Adverse effects and contraindications similar to measles
5. ? autism
Hepatitis B vaccination:
1. Sexual and perinatal, needle stick transmission
2. Severe acute & chronic active hepatitis, hepatic carcinoma
3. HbB positive mother, NB to receive:
3.
HbB vaccine at birth
4.
HbB immune globulin 100 IU within 2-3
days
4. Normal schedule: 0,1,6 months or 6,10,14 weeks along with DPT
5. Child dose .5 ml; adult dose 1 ml IM, no boosters
6. May have Pain and fever
Haemophilus influenza Type B:
1. Produce otitis media, pneumonia and meningitis in children
2. Capsular polysaccharide vaccine
3. < 6 months:6,10,14 weeks combined with DPT
4. > 6 months: 2 doses at 1 month interwal
5. >15 months: 1 dose
6. Booster at 18 months
7. > 5 years: No need for vaccine
8. IM ; safe vaccine ; mild fever and pain
COLD CHAIN SYSTEM:
1. Cold chain definition:
1. Vaccines are sensitive to heat and freezing and must be kept at the
correct temperature from the time they are manufactured until they
are used.
i. The system used for keeping and distributing vaccines in good
condition is called the cold chain.
ii. The cold chain consists of a series of storage and transport links,
all designed to keep vaccines within an acceptable range until it
reaches the user.
2. Maintenance of the cold chain requires vaccines and diluents to be:
i. Collected from the manufacturer or an airport as soon as they
are available;
ii. Transported between 2c and 8c from the airport and from one
store to another;
iii. Stored at the correct temperature in primary/central and
intermediate
3. Vaccine stores and in health facilities;
i. Transported between 2c and 8c to outreach sites and during
mobile sessions;
ii. Kept between 2c and 8c range during immunization sessions;
and

iii. Kept between 2c and 8c during return to health facilities from

outreach sites.
4. After vaccines reach the health facility:
i. Keep them between 2C and 8C in health facility refrigerator
(ILR).
ii. Carry them to the immunization session in a vaccine carrier with
frozen ice packs or ice.
iii. Keep the vaccines cool using a foam pad in the vaccine carrier
while Health worker immunizes the children.
5. Cold chain equipments:
i. Primary vaccine stores need cold or freezer rooms, freezers,
refrigerators, cold boxes, and sometimes refrigerator trucks for
transportation.
ii. Intermediate vaccine stores, depending on their size/capacity,
need cold and freezer rooms, and/or freezers, refrigerators, and
cold boxes.
iii. Health facilities need refrigerators with freezing
compartments, cold boxes and vaccine carriers.
6. Vaccine vial monitors:
i. A vaccine vial monitor (VVM) is a label that changes colour when
the vaccine vial has been exposed to heat over a period of time.
ii. Before opening a vial, the status of the VVM must be checked to
see whether the vaccine has been damaged by heat.
iii. Use only vials with inner squares that are lighter in colour than
the outside circle

TT-1
Arm
TT-2
Upper Arm
TT- Booster

BCG
Hepatitis B
OPV-0
2 drops Oral
OPV 1,2 & 3
DPT1,2 & 3

National imuunization Schedule

For Pregnant Women:
Early in pregnancy 0.5 ml
Intra-muscular
4 weeks after TT-1*

0.5 ml

Upper

Intra-muscular

If received 2 TT doses in a pregnancy within the last 3 yrs 0.5

ml
Intra-muscular Upper Arm
For Infants:
At birth or as early as possible till one year of age (0.05ml
until 1 month age) Intra-dermal Left Upper Arm
At birth or as early as possible within 24 hours 0.5 ml Intramuscular Antero-lateral side of mid-thigh
At birth or as early as possible within the first 15 days
At 6 weeks, 10 weeks & 14 weeks 2 drops Oral

At 6 weeks, 10 weeks & 14 weeks 0.5 ml Intra-muscular

Antero-lateral side of mid thigh
Hepatitis B 1,2 & 3
At 6 weeks, 10 weeks & 14 weeks 0.5 ml Intramuscular
Antero-lateral side of mid-thigh

Measles

9 completed months-12 months.(give up to 5 years if not

received at 9-12 months age) 0.5 ml Sub-cutaneous Right
upper Arm
Vitamin A(1stdose)
At 9 months with measles 1 ml ( 1 lakh IU) Oral
For Children:
DPT booster
16-24 months 0.5 ml Intra-muscular Antero-lateral
side of mid-thigh
OPV Booster
16-24 months 2 drops Oral
Japanese
Encephalitis
16-24 months with DPT/OPV booster 0.5 ml Subcutaneous Left Upper Arm
Vitamin A
(2nd to 9th dose) 16 months with DPT/OPV booster Then, one dose every 6
months up to the age of 5 years. 2 ml (2 lakh IU) Oral
DT Booster
5-6 years 0.5 ml. Intra-muscular Upper Arm
TT
10 years & 16 years 0.5 ml Intra-muscular Upper Arm
Proposed Changes in the National Immunization Schedule: 2009-10
1. DT Booster to be replaced by DPT Booster at 5-6 years of age.
2. In select well-performing states, MR to be given with DPT Booster at 1624months (Dose: 0.5 ml; Route: Sub-cutaneous; Site: Right Upper Arm)
3. DPT and HepB vaccines at 6, 10 and 14 weeks to be replaced by DPT-HepBHib
(Pentavalent) vaccine.
NEWER VACCINES:
1. Conventional vaccines contained the whole of organism or the toxin whereas
the immunogenic protein component is not separated
2. Second-Generation or new vaccines
1. Conjugate Vaccines :
a. Pneumococci and H.Influenza produce serious diseases in
children
b. They are capsulated organisms with polysaccaride in the
capsule preventing immune reaction
c. The patient can not produce antibody
d. This antigen is combined with a protein from another
organism and this is called conjugate vaccine
2. Subunit Vaccines (polypeptide vaccines)
1. Vaccines are developed from antigenic fragments
2. They are able to evoke an immune response,
3. They have fewer side effects than a vaccine made from the
whole organism.
4. Subunit vaccines can be made from a part the actual
microbe, or in the laboratory using genetic engineering
techniques.
5. Eg:
Viral subunit : HBsAg
Bacterial subunit : Acellular pertussis
Against pneumonia caused by streptococcus
pneumoniae

3.

3. Recombinant subunit vaccine

a. The recombinant vaccine is made by inserting a tiny portion
of the virus genetic material into common bakers yeast.
b. This process induces the yeast to produce an antigen, which
is then purified.
c. The purified antigen, when combined with an adjuvant, a
substance that stimulates the immune system, results in a
safe and very effective vaccine.
d. Eg. Hepatitis B vaccine
4. Recombinant Vector Vaccines
a. A weakened virus or bacterium is made as a vector or carrier
b. Genetic material from the disease-causing organism is made
antigenic but not pathogenic is inserted into the vector
c. Eg.
d. Vaccinia virus acts as vector in which several genes from HIV
are inserted to produce a vaccine
e. Weakened bacteriumsalmonellacarry portions of the
hepatitis B virus to produce HB vaccine
5. DNA vaccines
1. DNA sequence used as a vaccine.
2. This DNA sequence code for antigenic protein of a pathogen.
3. As this DNA Inserted into cells (plasmids) it is translated to
form antigenic protein.
4. Immune response raised against this protein.
5. In this way , DNA vaccine provide immunity against that
pathogen.
6. Eg: Human papilloma virus vaccine; herpes vaccine and this
technology is also used to prepare vaccine against certain
cancers
6. VIROSOMES
1. virosomes represent reconstituted empty influenza virus
envelopes
2. Antigens can be incorporated into virosomes
3. Virosomes are small vesicles containing viral membrane
proteins
4. Virosomes fuse with cells of the immune system and thus
deliver their contents - the specific antigens directly to their
target cells, eliciting a specific first-class immune response
5. Eg. Hep A and Influenza vaccines
Some new vaccines:
i.
Inactivated polio vaccine: IPV
a. Dose .5 ml IM
b. Schedule: 6,10,14 weeks and at 18 mo ( in addition to
OPV)
c. Use: 1. immune compromised children; 2. for eradication
of polio where polio virus is circulating even after many
pulse polio sessions
ii.
Rota virus vaccine:

a.
b.
c.
d.

iii.

Oral vaccine 1 ml/dose

1st dose: 6 weeks; 2nd dose 10 weeks of life
Protects against rota virus gastroenteritis
RV5 (RotaTeq) is a live oral vaccine contains five re
assortant rotaviruses developed from human and bovine
parent rotavirus strains
e. RV1 (Rotarix) contains one strain of live attenuated human
rotavirus
f. Any rotavirus gatroenteritis - 74%-87% effective
g. Routine vaccination of all infants without a
contraindication
h. Intussusception was a suspected complication in older
vaccines
Human papilloma virus vaccine:
a. To protect women against cervical cancer
b. Two vaccines available:
i. Quadrivalent: mixture of L1 protein and sero types
16,18,6 & 11
ii. Bivalent vaccine: mixture of L1 protein and sero
types 16&18
c. Age: 9-26 years
d. Dose: .5 ml IM
e. Schedule: 0,2,6 months
VACCINES FOR ADOLESCENTS- IAP

Tdap/Td

10 years

TT

Booster at 10 and 16 years

Rubella

As part of MMR vaccine or (Monovalent) 1 dose to girls at 12-13

years of age, if not given earlier

MMR

1 dose at 12-13 years of age. (if not given earlier)

Hepatitis B

3 Doses (0, 1 and 6 m) if not given earlier

Typhoid

TA, Vi or Oral typhoid vaccine every 3 years

Varicella*

1 dose upto 12-13 years and 2 doses after 13 years of age. (if not
given earlier)

Hepatitis
A*

2 doses (0 and 6 months) if not given earlier

Human
Pappiloma
Virus
vaccine
For Girls
only

Studies show a rapid rise in ano-genital HPV infections by 15 yrs

age hence ensure immunization completed prior to it.
11-12 yrs endorsed by the Society for Adolescent Medicine (SAM),
9-10 yrs left to the discretion of the care provider.
3 doses of HPV given at 0, 2 and 6 months in the Deltoid.