Pediatric lecture notes infectious diseases

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6. Lecture notes on Infectious (Communicable) Diseases1
Contents
6.1. Exanthematous fever.
6.1.1. Chicken pox.
6.1.2. Mumps.
6.1.3. Measles. (Rubeola)
6.1.4. German measles (Rubella) [3 Days measles].
6.1.4.1. Congenital Rubella Syndrome.
6.1.5. Erythema infectious (Fifth Disease)
6.1.6. Exanthem subitem (Sixth Disease)
6.2. Plague (Yersinia Pestis).
6.3. Poliomyelitis.
6.3.1. Acute flaccid paralysis (AFP).
6.4. Aids in children.
6.5. HIV testing strategies.
6.6. Whooping cough (Pertussis).
6.7. Diphtheria.
6.8. Tuberculosis.
6.8.1. Drug resistant tuberculosis.
6.8.2. Direct observed therapy short course (DOTS).
6.8.3. Tuberculin test.
6.8.4. Miliary tuberculosis.
6.9. Malaria.
6.9.1. Cerebral malaria.
6.9.2. Algid malaria.
6.9.3. Black water fever.
6.9.4. Congenital malaria.
6.9.5. Tropical splenomegaly syndrome.
6.10. Enteric fever.
6.11. Tetanus.
6.12. Infectious mononucleosis.
6.13. Pyrexia of unknown origin. (PUO)

6.1. Exanthematous fever.
A. Exanthems: It is as eruption of rash on skin, accompanied by eruption.
B. Enanthems: Eruptions on mucous membrane.
Skin rashes are following types:
C. Macule: It is a flat lesion on skin not raised above the surface. There is discoloration
only.
D. Papule: Small palpable rash elevated above the skin surface.
E. Vesicles: Small blisters with clear fluid.
F. Pustules: Pus filled vesicles are called pustules
G. Purpuric or petechiae: Rash associated with bleeding.
1. Causes of maculopapular rash:
1) Viral: Measles, Rubella, Coxsackie virus, Echo virus, CMV, Hepatis B
infection, Herpes virus, Epstein – Barr virus, adeno virus, chlamydia, HIV
virus.
2) Bacterial: Salmonella, Mycobacterium, Pseudomonas, Meningococcal,
Rheumatic fever, Scarlet fever, erysipelas.
3) Fungal: Histoplasma, Coccidiosis.
4) Rickettsial: Rocky mountain spotted fever, Typhus.
5) Others: Kawasaki disease, Rheumatoid arthritis.
2. Causes of Vesicobullous Lesion:
1) Viral: Varicella, Herpes virus, coxsackie virus, entero virus, meningococcal.
2) Bacterial: Streptococcal crops, pseudomonas infections, staphylococcal
erythema multiforme.
3. Causes of Petechial / Purpuric rashes.
1) Viral: Echo virus, CMV, Epstein – Barr virus, HIV virus, Atypical measles,
Congenital rubella, viral hemorrhagic fever.
2) Bacterial: Sepsis, Endocarditis.
3) Rickettsial disease.
4) Malaria.
5) Pneumococcal, meningococcal, listeria.
6) Vasculitis, Thrombocytopenia, Henoch – Schoenlein purpura.
6.1.1. Chicken pox.
It is highly contagious viral disease caused by varicella zoster disease (DNA
virus) It is a primary infection caused by VZV. Latent infection is in dorsal
root ganglia and can reactivate to causes herpes zoster.
1. Mode of transmission:
1) Airborne contacts through carriers.
2) Droplets.
• Reservoir of infection: Human are only reservoir.
• Infectivity: Patient is infective 1 day before and 5 days after the
appearance of Rash.
• Age: All ages but except infancy, peak age 5to9 years.
• Season: January to May.
2. Pathology: Vesicle of Rash are formed in prickle cells in vesicles

results in giant cell necrosis, may be seen in esophagus, pancreas, liver,
kidney and adrenals.
3. Clinical features:
1. Incubation period – 14 – 16 days (Range 11 to 21 days)
2. Prodromal symptoms are minimal and include mild fever for 1 to 3 days,
malaise, loss of appetite.
3. Rash
• Appears on first day in crops.
• Rash is centripetal i.e. more on central part of body and less on
extremities.
• Rash is pleomorphic – various stages are present at the same time.
Each stage progresses from macule, papule, vesicle on erythematous
base to pustule and crusts. Vesicles are not umbilicated. Rashes are
seen on scalp, conjunctiva, mucous membrane, GIT Respiratory
mucosa, but spares soles and palms.
• There is severe itching associated with Rash.
• Rash appear for 7 days.
4. Disease is more severe in immunocompromised patients and adults.
5. Fetal infection may cause limb atrophy, skin scarring, eye manifestations,
and neurological manifestations.
6. Breakthrough varicella – chicken pox can be occurred in immunized
children but is mild.
7. Complications:
1) Skin: Secondary bacterial infection, ITP, Purpura fulminans.
2) Neurological:
• Acute cerebral ataxia.
• GB Syndrome.
• Transverse Myelitis.
• Optic neuritis.
• Facial nerve palsy.
• Encephalitis Rarely.
3) Respiratory: Varicella pneumonia.
4) Hepatic: Reye’s syndrome, Hepatitis.
5) Miscellaneous: Arthritis, Appendicitis, Glomerulonephritis.
6) Late complications: Herpes zoster can occur after a year.
7) Progressive varicella: commen in immunodeficient children and in
malignancy. Rash with visceral organ involvement. Coagulopathy and
severe hemorrhage.
8. Treatment:
1) It is symptomatic and supportive.
2) For itching – antipruritic agents like Cetrizine can be given.
3) Antiviral drugs: Oral Acyclovir: if given within 24hrs of Rash, can reduce
severity of disease. Dose: 20mg/kg/dose 6hourly for 5 days max.
800mg/dose.

9. Prevention:
1) Chicken pox vaccine:
Age: After 1year of age two doses at an ideal interval of 12 weeks or
beyond.
Contraindication: Cell mediated immune deficiencies.
2) Post exposure prophylaxis:
VZ immune globulin.
Dose: 125 units/10kg/IM.
Maximum 625 unit within 4days after exposure.
6.1.2. Mumps.
It is viral infection of Salivary glands.
1. Etiology: It is caused by mumps virus. It is single stranded RNA virus of
paramyxoviridae family. Only one serotype is known.
2. Epidemiology:
• Mode of transmission:
I. Direct contact.
II. Airborne Droplets.
III. Fomites Contaminated saliva or urine.
• Age: Peak age 5to9yrs usually younger than 15 yrs. After vaccination seen in
adults also. Infectivity by saliva 1day prior and 3 days after appearance
of parotid gland swelling.
3. Pathogenesis: Virus multiplies in the cells of respiratory tract, then
through blood it reaches other organs including salivary glands.
• Incubation period: 14 to 24 days.
• Sub clinical infection in = 30 to 40%.
• Prodromal phase: Fever, muscular pain especially in neck, headache,
malaise.
• Salivary Gland:
a) Onset characterized by pain and swelling in one or both parotid glands.
First the enlarging parotid glands fills the space between posterior border of
mandible and mastoid and then extends downward and forward.
b) Edema of skin and soft tissue obscures the limit of parotid swelling so
that swelling is appreciated by sight than palpation.
c) Swelling peaks in 1 to 3 days and subsides within 3 to 7 days.
d) One parotid swelling usually precedes a day or two before the other. 25%
have swelling of one gland only.
e) Pain in parotid gland can be elicited by tasting sour liquids or lemon.
f) Redness and swelling at the opening of Stenson duct in mouth can be seen.
g) Edema over manubrium and upper chest can occur due to lymphatic
obstruction.
h) Parotid swelling is usually accompanied by low grade fever.
i) Parotid glands are commonly affected, submandibular glands can also be
involved.

• Submandibular swelling subsides slowly and is less painful.
• Sublingual gland is affected least.
5. Laboratory Diagnosis:
1) TLC – Leukopenia with lymphocytosis.
2) Serum amylase is raised.
3) IgM antibodies in serum are diagnostic by enzyme immunoassay.
4) Four-fold increase in IgG titer is diagnostic.
6. Differential Diagnosis:
1) Suppurative parotitis.
2) Other viral parotitis.
3) Salivary calculus.
4) Anterior cervical adenitis.
5) Recurrent benign parotitis.
7. Treatment: is Supportive only.
I. Antipyretics for fever and pain.
II. Orchitis treated with local support and bed rest.
III. Mumps arthritis treated by two weeks course of NSAIDS or corticosteroids.
8. Complications:
1. Meningoencephalomyelitis / Aseptic meningitis:
a) Most commen complication.
b) Males are Affected more.
c) More commen in adults>20yrs of age.
d) Clinically: Neck stiffness.
e) Pathogenesis: two types.
• Infective during disease.
• Post infectious encephalitis with demyelination. It follows
parotitis 10 days later.
CSF: Pleocytosis – lymphocytosis up to 2000 cells/mm3
2. Hydrocephalus due to Aqueductal stenosis (Mumps embryopathy)
3. Orchitis and Epididymitis (14-35%)
a) Bilateral orchiditis in 30% cases.
b) Rarely hydrocele.
c) Follows parotitis within 8days.
Clinically: Onset is abrupt with rise in temperature, chills, headache,
nausea, lower abdominal pain, testis are swollen and tender. Average
duration – 4days.
30 to 40% of affected testis atrophy.
Infertility is rare.
4. Oophoritis.
5. Pancreatitis: Mild is commen.
Clinically – Epigastric pain and tenderness accompanied by fever, chills,
vomiting and prostration, serum amylase is raised.
6. Myocarditis.
7. Arthritis – 2 weeks to 3months, big joints commonly affected.
8. Thyroiditis.
9. Deafness.

10. Ocular complications:
a) Dacryoadenitis.
b) Optic neuritis – recovery in 10 – 20 days.
11. Prevention:
Mumps immunization as MMR Vaccine.
Age: After 9months of age.
Second dose at 15months.
Women should avoid pregnancy for 3 months after immunization.
6.1.3. Measles. (Rubeola)
i. Definition: It is an acute viral infection characterized by maculopapular
rash accompanied by high fever.
ii. Etiology: It is caused by measles virus. It is an RNA virus of
paramyxoviridae family. Only one serotype is known.
iii. Epidemiology:
1) It is endemic throughout the world.
2) Age – Peak age preschool to 10years of age.
iv. Transmission:
1) It is highly contagious.
2) Mode – Droplet spread during catarrhal stage.
3) Infants acquire immunity transplacentally which persist up to 6to9
months.
4) Infectivity – 4days prior and 5days after the Rash.
v. Pathogenesis:
1) Essential lesions found on skin, conjunctiva and mucous membrane
of nasopharynx and bronchi and intestinal tract.
2) Serous exudates and proliferation of mononuclear cells and few
neutrophils occur around capillaries.
3) Hyperplasia of Lymphoid tissue especially in appendix. “
Warthin – Finkeldey reticuloendothelial giant cells” are seen.
4) “Hecht giant cell pneumonia”, an interstitial pneumonitis is seen in
measles.
vi. Clinical features: Three clinical phases.
• Incubation period 10-12 days,
• Features mild fever on 9 to 10th
day. Which subsides for 24 hours.
i. Phase I Prodromal phase 3 to 5 days.
Features:
1) Fever, dry hacking cough, coryza and
conjunctivitis (3C’s) lacrimation.
2) Koplik spots – Greyish white dots having reddish
areola may be hemorrhagic.
Size Grain of sand.
Day of appearance 2nd to 3rd day of fever.
Koplik spots: Pathognomonic sign of measles.

Site: Opposite lower molar teeth, may spread over
rest of buccal mucosa.
Disappear usually within 12-18 hours.
3) Photophobia and conjunctival inflammation may
suggest measles.
Transverse line of conjunctival inflammation
along eye lid margin may be of diagnostic
assistance during prodromal phase.
4) Occasionally this phase may be severe characterized
by high fever, convulsions and pneumonia.
5) Coryza, fever, cough is increasingly severe up till the
time of Rash has covered the body.
ii. Phase II Eruptive phase Rash on 4th or 5th day of fever and
persistent for 3 days. Starts as faint macules on upper lateral
part of neck behind ears, along hairline and on posterior part
of cheek. They become maculopapular and spread over
entire face, neck upper arms, and upper part of chest within
24hours.
During next 24 hours it spreads over back, abdomen, upper
arm and thighs. It reaches feet on 2nd
and 3rd
day. Rash fades
downward in same sequence as it appeared after 3rd
day. As
the rash appears fever increases. Rash may be severe and
hemorrhagic.
Black measles: it is hemorrhagic type of measles, there may
be petechiae and ecchymosis.
iii. Phase III Convalescence phase: As the rash fades after
7days brawny desquamation and brownish discoloration
occurs and disappears within 7 to 10days.
vii. Complications:
1) Respiratory Complications:
a) Pneumonia and Bronchopneumonia.
b) Otitis media.
c) Interstitial pneumonitis.
d) Exacerbation of underlying tubercular infection.
e) Laryngitis, Tracheitis, Bronchitis.
2) Neurological complications:
a) Encephalitis – Three types:
I. Measles encephalitis – During pre-eruptive period or
2 to 5 days after the appearance od rash.
II. Demyelinating encephalitis occur later.
III. Subacute sclerosing panencephalitis (SSPE)
It is immune mediated late complication.
b) Guillain – Barre Syndrome (GBS)
c) Hemiplegia.
d) Cerebral thrombophlebitis.
e) Retrobulbar neuritis.

3) Hematological –
4) Bacterial superinfections.
5) CVS – Myocarditis.
6) Malnutrition.
7) Immunosuppression.
8) Persistent diarrhea.
9) Late complication – SSPE (Subacute sclerosing panencephalitis)
viii. Treatment: Treatment is supportive:
a) Antipyretics for fever.
b) Adequate fluid intake.
c) Humidification for irritating cough and laryngitis.
d) Protection of eyes for photophobia.
e) Antibiotics for bacterial complications like otitis media,
bronchopneumonia.
f) Vitamin A: 2lakh units for children older than 1year and 1 lakh
units < 1years. Repeat on 2nd
day and 2 – 4 weeks later.
ix. Prevention:
1) Measles vaccine (Active immunization):
a) Age – 9 months.
During outbreak of measles, vaccine can be given from 6
months of age.
b) Repeat at 15 months as M.M.R.
2) Post exposure prophylaxis: Passive immunization with immune
globulin is effective.
Dose: 6months to 1year: 0.25 ml/kg/IM Max. 15ml given within 5
days of exposure, more than 1year or immune comprised child 0.5
ml/kg/IM, max. 15ml.
6.1.4. German measles (Rubella) [3 Days measles].
1. Etiology: It is an acute viral infection caused by rubella virus. It is RNA virus of
family Togaviride.
2. Epidemiology: Natural Host: Human only.
• Infectivity: 7days before Rash and 8days after Rash.
• Mode of Transmission
a) Oral Droplets.
b) Transplacentally causing congenital infection.
Sex: Both the sex equally.
Season: Mostly in spring.
Age: Peak age 5 to 14 yrs.
3. Pathogenesis:
1) Immune process is important.
2) If mother has disease during pregnancy during first 11weeks then chances of
congenital defects in fetus are 90%
Maternal infection after 16 weeks of pregnancy poses low risk of congenital
defect through infection of fetus may occur.

4. Clinical features: Incubation period: 14 to 21 days.
Three phases:
1) Prodromal phases are very mild. Mild catarrhal symptoms are present.
Tender lymphadenopathy is most is most characteristic sign.
Site: Retro auricular, Posterior cervical and post occipital
lymphadenopathy is evident 1 day before rash and remains for 1eek or more.
Enanthem (Forchheimer spots): It appears in 20% of cases just before the
onset of rash. It consists of discrete rose-colored spots on soft palate. These
spots may unite into red bluish and extend over faucets.
2) Eruptive phases: Discrete maculo-papular rash appears along with areas of
flush, which rapidly spread, from face to entire body within 24 hours.
During 2nd
day rash becomes pinpoint specially over trunk. There may be mild
itching. Eruption disappears on 3rd day. Spleen is slightly enlarged.
3) Convalescences: Desquamation is minimal.
In older girls and women: Polyarthritis may occur but commen in small
joints. Duration is usually several days to 2weeks.
5. Diagnosis:
1) Clinical Diagnostic features:
a) Mild constitutional features.
b) Fever mild only for 3days.
c) Tender lymphadenopathy.
d) No photophobia, headache, anorexia, malaise.
e) Rash appears on 1st
day and spreads fast within 24 hours.
2) Serological test: Antibody detection by enzyme immunoassay.
3) Virus culture: From nasopharynx and blood.
a) Measles.
b) Infectious mononucleosis.
• Generalized lymphadenopathy.
• Atypical lymphocytosis.
c) Enteroviral infections have accompanying respiratory and GIT features.
d) Drug rash: No lymphadenopathy.
e) Scarlet fever.
7. Complications: Rare.
1) Encephalitis very rare.
2) Congenital rubella syndrome in pregnant mother.
3) Progressive Rubella panencephalitis.
Immunity: Life long immunity though reinfection may occur in 3 – 10%
8. Treatment: Only supportive.
9. Prevention:
I. Active immunity:
Rubella Vaccine: Given as M.M.R. vaccine start by 9months of age with the
booster at 15th
month of age.
If not previously immunized then can be given at 11 to 12 years especially in
girls.
Precautions:

1) Avoid vaccine during pregnancy and women should avoid
pregnancy for 3months after active immunization.
2) Other contraindications to vaccine are allergy to vaccine component
neomycin.
3) Immunodeficiency.
4) Recent immunoglobulin administration.
5) Cancer and cancer therapy.
6) On long term high dose of corticosteroids.
II. Post exposure prophylaxis:
1) Vaccine to non – pregnant susceptible contacts.
2) I.V. immunoglobulin have not been studied.
6.1.4.2. Congenital Rubella Syndrome.
It occurs in fetus when mother has primary maternal infections with rubella
during first trimester of pregnancy.
There are 90% chances of congenital defects in fetus when mother is infected
during first 11 weeks of pregnancy.
• Features of syndrome
1) Intrauterine growth retardation (IUGR)
2) Eye: Cataract, Microphthalmia.
3) CVS:
• Myocarditis.
• CHD: PDA, Pulmonary artery stenosis.
4) Skin: “Blueberry muffin” skin lesion.
5) CNS:
• Meningoencephalitis.
• Sensory neural deafness.
• Mental retardation.
• Developmental retardation.
6) Respiratory: Pneumonia.
7) Liver: Hepatitis.
8) Hematological: Anemia, Thrombocytopenic purpura.
9) Bone: Bone Lucencies.
• Diagnosis:
1) Detection of IgM antibodies in serum of infant.
2) Virus culture from nasopharynx and urine. Virus is shed in urine for
1year.
6.1.5. Erythema infectious (Fifth Disease)
Causative agent – Human Paravirus B 19.
Mode of transmission – Respiratory secretion.
Incubation Period: 4 – 14 days.
Prodromal stage – Minimal or absent.
• Eruptive stage: Skin lesion occurs in three stages:
Stage I: Cheeks becomes erythematous Like slapped cheek.

Stage II: Erythematous or maculopapular rash appears on trunk or
extensor surface of extremities. Palms and soles – spread.
Stage III: Itching present rash fades from center giving reticula pattern.
Duration of Rash: Two weeks (1-6weeks)
Complication: Arthritis.
Treatment: Symptomatic.
6.1.6. Exanthem subitem (Sixth Disease)
Roseola infantum
• Causative agent Human herpes virus 6.
• Age: 6 months to 6years.
• Season: Spring and autumn.
• Non contagious.
Clinical features:
 Incubation period: 5-15 days.
 Onset: Fever, mild pharyngitis, coryza, fever subsides in 304 days.
 Rash: Macular or maculopapular rash appear on 3rd
or 4th
day of fever.
 Rash starts from trunk extend to face and extremities.
 Duration of rash 1day.
 Lymphadenopathy.
 Associated features: Edema lid, anterior fontanel bulging.
Treatment: Symptomatic.
6.2. Dengue: It is a syndrome caused by arthropod borne viruses. Dengue manifest as:
I. Dengue fever benign.
II. Dengue Hemorrhagic fever (DHF)
III. Dengue shock syndrome.
1. Etiology: Dengue is caused by four distinct antigenic types of dengue virus. Virus is
transmitted by bite of a mosquito Aedes aegypti.
Virus:
 It belongs to Flaviviridae family.
 Single stranded RNA.
 Four serotype Den 1,2,3,4.
 Lifelong immunity to one serotype but temporary and partial immunity
against other serotypes.
Vector:
oAedes Aegypti.
oMostly lives indoor.
oBites during day time.
oBreeds in stored water for drinking, bathing or rain water collected for
containers.
Host: DSS occurs in two immunological groups.
 Children with previous Dengue infection.
 Infants with warning levels of maternal dengue antibodies.

2. Pathogenesis:
1) Pathogenesis is not clear.
2) It is thought to have immunopathologic basis.
3) It is usually associated with second infections.
4) Dengue virus probably infects peripheral blood monocytes.
5) Cytotoxic lymphocytes release cytokines.
6) There is rapid activation of compliment system.
7) Cytokine interact with endothelial cells to produce increased vascular
permeability through nitric oxide.
8) Capillary damage allows fluid, electrolyte, small protein and RBC to leak
into extravascular space which results into hemoconcentration,
hypovolemia, tissue hypoxia, metabolic acidosis, hyponatremia and shock.
9) Mechanism of bleeding in dengue fever is not known but mild degree of DIV,
liver damage, thrombocytopenia, levels of factor XII are depressed,
activation of fibrinolytic system may operate synergistically.
3. Clinical features: Incubation period 1 – 7 days.
I. Dengue fever: It is characterized by:
1) Biphasic fever.
2) Myalgia, Arthralgia.
3) Frontal or Retroorbital pain.
4) Severe back pain. (Back break fever)
5) Rash: Transient macular generalized rash that blanches under pressure
and is seen during first two days.
6) Relative brady cardia.
7) Generalized lymphadenopathy.
8) Cutaneous hyperesthesia / /hyperanalgesia.
9) Nausea, vomiting, rhinitis, cough.
10) Taste aberration, Anorexia.
11) About 1 – 2 days after defervescence a generalized morbilliform,
maculopapular rash, appears that spares palms and soles. It disappears
in 1 – 5 days
Desquamation may occur.
2nd rash appears at this time with slight increase of temperature,
which is characteristic biphasic temperature pattern.
12) Leukopenia.
II. Dengue hemorrhagic fever:
1) Relatively mild first phase with rapid rise of fever, malaise, vomiting,
headache, anorexia and cough followed after 2 – 5 days by rapid clinical
detoriation and collapse.
2) Second phase – Patient has:
1) Cold clammy extremities, warm trunk.
2) Flushed face, epigastric pain.
3) Sweating irritability.
4) Hemorrhagic features like petechia, ecchymosis, easy bruising
hematemesis, Malena.
5) Rash – maculopapular.

6) Thrombocytopenia < 1 Lakh/mm3
7) Evidence of plasma leakage.
 Rise in hematocrit ≥20%
 Signs like pleural effusion, ascites, hypoproteinemia.
8) Positive tourniquet test.
III. Dengue shock syndrome: All the criteria of DHF plus features of shock.
a) Rapid and weak pulse.
b) Narrow pulse pressure.
c) Hypotension for age.
d) Cold clammy skin and restlessness.
4. Diagnosis of DHF/DSS:
Clinical
1) High fever of acute onset.
2) Hemorrhagic features.
3) Hepatomegaly.
4) Shock.
Laboratory diagnosis by:
1) Thrombocytopenia < 1 Lakh/mm3
2) Hemoconcentration (Rise of hematocrit ≥ 20mm%)
3) Plural effusion. (Chest x ray)
4) Specific lab diagnosis.
A. Detection of virus by
 Culture.
 PCR.
 Immunocytochemistry.
B. Detection of anti-dengue antibodies (IgM & Igg)
NS 1 antigen test: (NS1 stands for (Non structural protein 1) is a test
for dengue, introduced in 2006. It allows rapid detection in first day of
fever.
IgM: Appear first from 5days to 6weeks and disappear by 6-12 weeks.
IgG: Four-fold rise in significant.
1) Malaria.
2) Viral hepatitis.
3) Leptospirosis.
4) Typhus fever.
5) Viral influenza like disease.
6) Four arboviral disease without rash:
• Colorado tick fever.
• Sand fly fever.
• Rift valley fever.
• Rose river fever.
7) Meningococcemia.
8) Yellow fever.
9) Rickettsial disease.
6. Treatment:

1) No antiviral drug.
2) Treatment is supportive.
3) Bed rest during febrile period.
4) Antipyretics for fever, analgesics for pain, Aspirin is contraindicated.
5) Fluid and electrolyte for deficit, plenty of oral fluids.
6) DHF/DSS:
a) Evaluate and monitor vital signs. Degree of hemoconcentration,
Dehydration, Electrolyte imbalances.
b) O2
c) Rapid I.V. replacement of fluid & electrolyte:
oNormal saline is preferred Deficit+Maintainance.
o Colloid preparations or plasma for treating shock.
d) Management of bleeding:
oPacked cell transfusion if Hb low.
oPlatelet transfusion with plasma – Doubtful role of platelet
transfusion.
e) If DIC – Treatment of DIC.
6.3. Plague (Yersinia Pestis).
1) Etiology: Disease is caused by yersinia pestis. It is a gram-negative coccobacillus.
2) Epidemiology: Mode of transmission: It is from wild animal sources.
A. From bite of fleas that have acquired infection from feeding on infected urban
rats. Most common mode.
B. Less frequently is caused by contact with infectious body fluids or tissues.
C. Inhalation of infectious droplets.
3) Pathogenesis:
1. Infectious agent is transmitted to human skin from flea bite during feeding
attempts.
2. Bacteria migrate to lymph nodes via cutaneous lymphatics.
3. In lymph node pestis replicate resulting into Bubonic plague.
4. Bacteria occurs and bacteria are carried to various organs where they cause
purulent necrotic and hemorrhagic lesions.
5. Pneumonic plague: It occurs when infected material is inhaled.
4) Clinical feature: There are three principal clinical presentations of plague:
→ Bubonic plague (80 – 90%):
→ Septicemic plague:
→ Pneumonic plague
A. Bubonic plague:
1. Most commen form of plague.
2. Lymph nodes enlargement or bubo appears 2to8 days after fleabite.
Most commen lymphadenopathy is inguinal lymphadenopathy, which
are tender.
3. Fever, chills, weakness, prostration, headache and septicemia occur.
4. DIC may occur causing purpura and gangrene of extremities.
5. Black death can occur 2to4 days after onset of symptoms.

B. Septicemic plague: Occasionally systemic infection causes systemic
symptoms.
C. Pneumonic plague:
1. Least commen but most dangerous form.
2. It results from hematogenous dissemination.
3. There are features of pneumonia such as fever dyspnea, hemoptysis.
5) Complications:
a. Meningitis.
b. Tonsillitis.
c. Gastroenteritis.
6) Diagnosis:
1. Clinical:
I. Fever with exposure to small animals, fleas.
II. Painful swollen lymph nodes with fever prostration.
2. Laboratory Diagnosis:
I. Demonstration of Y. Pestis on smear of lymph node aspirate or blood
sputum or exudates stained by Gram’s stain or Giemsa stain.
II. Culture.
7) Differential diagnosis:
I. Lymphadenopathy – other causes.
II. Septicemia.
8) Treatment:
1. Isolation of patient till 2days after starting antibiotics.
2. Antibiotic
i. Streptomycin 30mg/kg/day, 12 hrly/ IM ×10 Days.
ii. Chloramphenicol for septicemia and meningitis. Dose:
60to100mg/kg/day/IV 6hrly.
iii. Oral tetracycline: For mild disease above the age of 8yrs.
3. Prophylaxis for:
oClose contacts of pneumonic plague. (Tetracycline / Doxycycline or
Trimethoprim+Sulphamethoxazole.
9) Prevention:
a) Avoid exposure to infected animals and fleas.
b) Isolate the patient pneumonic plague.
c) Vaccine.
6.4. Poliomyelitis.
A. Introduction:
1. Infectious agent:
• RNA polio virus.
• Genus enterovirus.
• Family – picornavirdae.
• Serotype – Three
• Frequent types are: type 1,3.
2. Transmission:

a) Person to person via faeco-oral oral route.
b) Poliovirus multiplies in intestine and spread through faeces.
c) Virus is intermittently excreted for up to 2months or more after infection.
d) Maximum excretion occurs just before paralysis and during first 14 days
after onset of paralysis.
3. Incubation period: 7to10 days (Range 4 – 35 days)
4. Reservoir: Only human beings.
5. Communicability:
a) It is highly communicable.
b) Most infectious 7 days before and after 14 days after onset of paralysis
6. Occurrence: Increase during rainy season.
7. Immunity:
a) Immunity is obtained through infection with wild virus or through
immunization.
b) Immunization with OPV results in both humoral and local intestinal cellular
response.
c) Vaccination with IPV confers humoral immunity mainly.
d) No cross immunity between poliovirus types.
e) Immunity is type specific.
B. Pathogenesis:
1. Poliovirus gains entry through GIT.
2. Primary site of replication may be M cells of mucosa of smell intestine.
3. Regional lymph nodes are infected.
4. Primary viremia occurs in 2to3 days.
5. Virus seeds multiple sites including RES, brown fat deposits, skeletal muscles.
6. Enters CNS along peripheral nerves probably.
7. It primarily infects motor neuron cells in spinal cord (anterior horn cells)
and medulla ablongata.
8. Variable involvement of vermis, cerebellum, substantia nigra, thalamus,
hypothalamus, motor cortex.
C. Clinical features: 90-95% cases are inapparent: Remaining 5-10% to present as one
of three syndromes as:
1) Abortive polio: 4-8%: Minor illness with low grade fever, sore throat, vomiting,
abdominal pain, loss of appetite, malaise, Recovery: Rapid & complete, No paralysis.
2) No paralytic: Aseptic meningitis (1-2%): Features: Headache, Stiffness – neck,
back, legs. Recovery: within 2to10 days.
3) Paralytic Poliomyelitis (1-5%) Symptoms in two phases:
I. Minor phase like abortive polio.
II. Major phase
 Muscle pain and spasm with paresthesias.
 Fever just prior to paralysis.
 Rapid onset of paralysis.
III. Paralysis – Three types.
a. Spinal paralytic poliomyelitis:
a) Most commen.

b) Cause: Lower motor neuron legion of anterior horn cells of spinal
cord.
c) Affects, legs, arms, trunk.
d) Muscle is floppy.
e) Reflex diminished.
f) Pain and touch sensation normal (No sensory loss)
g) Paralysis is asymmetrical.
h) Paralysis begins proximal and progressive to involve distal muscle
group.
i) Residual flaccid paralysis present after 60 days.
j) Bowel & Bladder: Paralysis of lower limb is often accompanied by
bowel and bladder dysfunction like transient incontinence to paralysis
with constipation and urinary retention.
b. Bulbar polio:
 Cause: Cranial nerve lesions and medullary center lesions.
 Features:
1) Respiratory insufficiency.
2) Difficulty in swallowing, eating and speaking.
3) Nasal twang.
4) Accumulation of pharyngeal secretions.
5) Absence of effective coughing.
6) Nasal regurgitation of saliva and fluids.
7) Deviation of palate, uvula or tongue.
8) Involvement of vital centers manifesting as:
 Irregular respiration.
 CVS alteration: BP changes especially increased BP.
 Paralysis of vocal cords – hoarseness, aphonic.
o Rope sign: Acute angulation between chin and larynx
caused by weakness of hyoid muscles.
c. Bulbospinal:
4) Polio Encephalitis:
a) Higher centers of brain are involved.
b) Features: Seizures, coma with spastic paralysis with increased reflexes:
 Irritability.
 Disorientation.
 Drowsiness.
 Coarse tremors.
 Peripheral and cranial N palsies coexist.
D. Residual paralysis:
1) Acute phase of illness lasts for about 0to4weeks.
2) As acute phase subsides recovery begins in paralyzed muscles.
3) At 60 days residual paresis can be there.
4) Maximum recovery occurs in first 6 months but slow recovery occurs up to
2years.
5) No recovery after 2years. Child is said to have post-polio residual paralysis.
E. Diagnostic tests:

1) Stool: Virus in shed in stool up to 2 months after paralysis with maximum
detection in first 14 days. Two stools specimen are collected within 48hrs for
culture within two weeks.
2) CSF Examination: Not likely to yield. How ever CSF examination helps in
differential diagnosis.
F. Treatment:
1. Treatment of acute phase:
a. Complete bed rest.
b. Correct positioning of affected limbs.
c. Warm moist fomentation to relieve pain and spasm.
d. Passive movements of joints 2-3 times a day for 10mins.
e. Analgesic to relieve fever and pain.
f. No massage or IM injection.
2. After acute phase is over:
a) Physiotherapy: Acute exercise is very beneficial.
b) Orthopedic surgery for fixed deformities and contractures
3. ORI (Outbreak Response Immunization)
a. After AFP case investigation and stool collection children aged 0to 59
months are given one dose of OPV regardless of previous
immunization.
b. Usually 500 children bellow 5yrs age are covered within that area.
c. Active case search in community.
d. Identification of hot cases.
Hot case: All cases which look like polio are labelled hot cases.
→ Age< 5yrs.
→ History of fever with asymmetrical or bulbar paralysis
involvement.
4. Cross notification.
5. Tracking of cases.
6. Action by reporting district immunization officer.
G. Strategies for polio eradication:
1. Sustain high level of routine OPV – three doses in first year of life
2. Pulse polio immunization to all children aged <5yrs during national
immunization Day, every year.
3. Surveillance of acute flaccid paralysis cases.
4. Conducting mop – up vaccination campaigns.
H. AFP Case investigation:
1) Case notification to district immunization officer (DIO).
2) Case investigation within 48hours.
a) Verification:
b) Investigation:
o History of 35 days travel.
o Collect 2 stool samples at an interval of 24 hours within two days.
o Specimen amount of stool 8gms.

6.3.1. Acute flaccid paralysis (AFP).
1. Definition: Sudden onset of weakness and floppiness in any part of body
in a child <15 years of age or paralysis in person of any age in whom
polio is suspected.
2. AFP surveillance purpose:
a) Helps to detect area where polio transmission is occurring.
b) Helps to identify areas of priority for focusing immunization.
c) Most reliable method to measure quality and impact of polio
immunization.
d) For polio free certification 3yrs after attaining zero polio case
status.
3. Pulse polio immunization:
a) Oral polio vaccine is given to all children between 0 to 5 yrs. Of
age in the country on single day regardless of previous
immunization.
b) Two round of pulse polio are given 4to6 weeks apart during low
transmission season of polio between November and February
(Three rounds in special circumstances)
c) These doses are extra doses, which supplement and do not replace
the doses receive during routine immunization services.
d) Pulse polio immunization helps in eradication of polio by replacing
wild virus by vaccine virus by vaccine virus in GIT.
Method: OPC is given at birth on 1st
day. On 2nd
& 3rd
day door to
door OPV is given to those cases who have not received OPV
vaccination on first day.
6.5. Aids in children.
1. Introduction: AIDS is retroviral disease characterized by profound
immunosuppression that leads to opportunistic infections, secondary
neoplasm and neurological features.
2. Epidemiological factors:
1) Agent:
a) HIV: it is lenti virus of retrovirus family.
b) They have unique Enzyme reverse transcriptase (RT) and
two more enzymes integrate and protease.
c) RT enzyme copies viral RNA into DNA.
d) This DNA integrates into host cell chromosome that is why it
cannot be eradicated.
e) It has several genes such as tat, rev, nef, vpr, vif which
regulate transcription.
2) Types of virus - two types:
a) HIV – 1.
b) HIV – 2.
3) Reservoir of infection: People harboring HIV in their body are
reservoir of infection.

4) Source of infection:
a) Prime sources:
• Infected blood.
• Semen.
• Vaginal fluids.
b) Infected Breast milk from mother to child. Saliva and tears
are not sources.
5) Mode of transmission in children:
a) Perinatal – 82%.
b) Blood born – 9%.
c) Sexual 8.5%. In adults it’s in >80%.
6) Host factors:
a) Age & Sex: Affect young people mostly aged 15 to 24 years.
Equal in both sexes.
b) High risk Groups:
I. I.V. Drug users.
II. Repeated blood transfusions.
III. Presence of sexually transmitted diseases.
IV. Increase frequency of unprotected sex.
V. Mixing pattern of population.
VI. Immunity – patient having less T helper cells are more
prone. They have profound lymphopenia.
7) Social and Economic factors:
a) Low literacy.
b) Urbanization.
c) Imprisonment.
d) High mobility.
e) Migration and separation from families.
f) Drug users.
g) Alcohol users.
3. Pathogenesis.
a) Major targets of HIV are immune system and CNS.
b) Virus damages CD4 + T cells.
c) Depletion of CD4 + T cells (Helper T cells) results in profound
immunosuppression.
4. Natural History of AIDS/HIV: Four stages:
1) Stage I Primary infection:
a) Rapid proliferation of virus in blood and lymph nodes.
b) CD4 cell count decline.
2) Stage II Early immune deficiency (CD4 cell count >500m3):
a) Viral replication is very high.
b) Signs and symptoms begin to appear.
3) Stage III Advanced immune deficiency (CD 4 cell count
<200/m3):
a) Viral is very high.
b) Sign and symptoms begin to appear.

4) Stage IV: Advanced immune deficiency (CD4 cell count <
200/m3)
a) Viral proliferation throughout body.
b) Patient has opportunistic infection and malignancies.
5. Specific Clinical features:
1) Asymptomatic at birth – mean age of presentation 17months
(4months to 7yrs)
2) Initial features:
a) Lymphadenopathy.
b) Chronic and recurrent diarrhea.
c) Failure to thrive, wasting.
d) Oral thrush.
3) WHO Clinical staging system:
• Stage I:
a) Asymptomatic.
b) General lymphadenopathy.
• Stage II:
a) Chronic diarrhea >30days in absence of etiology.
b) Severe persistent or recurrent diarrhea above
1month of age.
c) Weight loss (>10%) failure to thrive in absence of
known etiology.
d) Persistent fever >30 in absence of known etiology.
e) Recurrent bacterial infections other than septicemia
or meningitis.
• Stage III:
a) AIDS defining opportunistic infection.
b) Severe failure to thrive/ wasting in absence of known
etiology.
c) Progressive encephalopathy.
d) Malignancy.
e) Recurrent septicemia or meningitis.
6. General Clinical features:
a. Failure to thrive:
• Can be seen as early as 4-6 months in perinatally infected
children.
• Weight and height should be monitored.
b. Hepatomegaly:
• Hepatomegaly within 3 months of age has bad prognosis.
• Coinfection of Hepatitis C is known.
c. Lymphadenopathy:
d. Chronic Diarrhea:
e. Parotitis: Painless and recurrent.
f. Skin manifestation:

• Viral infections: Herpes simplex, Herpes zoster, molluscum
contagiosum, warts, CMV.
• Fungal infections: Candida tinea, onychomycosis
• Non infections: Seborrheic dermatitis, Atopic dermatitis,
Generalized dermatitis, Nutritional deficiency, eczema,
psoriasis, drug eruption, impetigo, vasculitis, scabies,
alopecia.
g. Oral candidiasis: It progresses to involve esophagus (20%)
presenting as fever, anorexia, dysphagia, vomiting.
h. Hematological abnormalities: Anemia, thrombocytopenia,
neutropenia, lymphopenia, and eosinophilia.
i. Cardiac manifestations: Cardiomegaly, CHF, Thrombotic
endocarditis, cardiomyopathy, pericardial effusion, cardiac
tamponade, conduction disturbances and sudden death.
j. Neurological manifestations: Present at least for 9 months.
HIV Encephalopathy: Progressive and static.
Features: Developmental delay, regression of milestones, cognitive
impairment, neuropsychiatric problem, weakness, spasticity,
hyperreflexia, cerebellar dysfunction, memory deficits,
microcephaly, Late features: Emotional liability, hyperactivity,
lethargy.
k. Nephropathy:
• More in adolescent.
• Proteinuria, Hematuria
• Hypertension.
• Renal tubular acidosis.
• Acute renal failure – May progress to end stage renal failure.
l. Respiratory:
• LIP: Lymphoid interstitial pneumonitis.
• Pulmonary lymphoid hyperplasia.
• PCP: Pneumocystis jiroveci pneumonia.
Features: Early features – cough, tachypnea (3-6 months)
Late features – dyspnea, clubbing.
X-Ray Chest: Diffuse bilateral reticulonodular or interstitial
infiltration (1-5 min) hilar lymphadenopathy.
m. Malignancy:
• Non-Hodgkin’s Lymphoma.
• Leiomyomas.
• Leiomyosarcoma.
• Leukemia.
• Rare Kaposi sarcoma.
n. Mycobacterial infections: MAC – Mycobacterium Avium
complex, M kansasi cheilonei fortuition occurs during first year of
life.
o. Recurrent bacterial infections.

7. Laboratory Diagnosis: Four types of tests.
1) Viral based tests:
a) Viral culture: Early diagnosis.
b) PCR – RNA.
c) PCR – DNA.
d) P24 antigen – during high viral load as early as 2 weeks.
2) HIV antibody tests:
a) HIV ELISA commonly used.
b) Western blot analysis – Detects antibody against antigen
like p24, p28, gp41, gp120, 160, pO1 gag.
c) HIV Immunofluorescence.
d) IgM, IgA, Anti-HIV antibody test.
3) Immunological markers:
a) CD4+Cell count.
b) CD8+Cell count.
c) CD4/CD8 Ratio.
d) Serum immunoglobulin.
e) Skin test for T cell function.
4) Surrogate markers:
a) Serum ꞵ2 macroglobulin.
b) Serum neopterin.
c) Serum IL – 2 level.
8. Window period: It is the time when an infected individual escapes
detection but is capable of transmitting immediately after infection.
Period lasts from few weeks to 6months.
Test to detect:
• PCR.
• p24 antigen.
6.6. HIV testing strategies. There are three strategies.
1) Strategy I:
• ELISA test once: If negative no HIV if positive HIV infected sample.
• Used to detect HIV infected blood at the time of blood donation, organ, tissue or
sperm donation.
• Donor not informed.
2) Strategy II:
• If ELISA is positive for HIV.
• Subject to second ELISA for different method (Western Blot).
• If positive it confirms earlier report.
• Indications – Surveillances, Diagnosis of AIDS disease.
3) Strategy III:
• Confirmation by 3rd reactive ELISA.
• Indications where specificity is required.
4) Management:
• Diagnosis.
• Initial evaluation.

• Timely chemoprophylaxis.
• Immunization.
• Management of opportunistic infection.
• ARV therapy.
• Infant feeding policy.
• Psychosocial care.
• Prevention.
1. Diagnosis:
a) ELISA detects antibodies against HIV not earlier than 18 months.
b) Before 18months it is diagnosed by PCR or by virus culture or by plasma
p24 antigen test after 1-month age. Repeat PCR after 2 months and 6
months.
2. Initial Evaluation: Every 3months up to 1 year then yearly.
a) Detailed history.
b) Baseline investigation.
c) Fundus examination.
d) CD4+Count.
e) Viral load evaluation.
f) Assess development.
g) CBC, LFT, CT, MRI, Echo cardiography.
3. Timely chemoprophylaxis: Prevention of vertical transmission
a) Counselling and voluntary testing of antenatal mothers.
b) Zidovudine prophylaxis of first 6weeks.
Infant HIV infection – dose 2mg / kg 6hrly into 6weeks. Single dose of
nevirapine can reduce 50% chances.
c) Start PCP prophylaxis in all HIV exposed infants at 4to 6 weeks (TMP –
SM)
d) Early diagnostic evaluation of HIV exposed infant. If positive start
multiple ART therapy.
4. Immunization: Immunize with all vaccine except live vaccines like OPV and
BCG vaccines.
5. Management of opportunistic infection.
a) PCP (Pneumocystis carinii infection.
Prophylaxis (TMP-SMX) Trimethoprim – Sulfa methazole. Dose
150mg/m2
/ 12hrly or 5 to 8mg /kg/day. 3day to 3weeks.
b) Serious bacterial infection TMP SMX 150mg/m2
I.V. Immunoglobulin
400mg/kg/month.
c) Mycobacterium tuberculosis infection:
Prophylaxis: Isoniazid 10mg / kg/ day×1year.
d) Disseminated mycobacterium avium intracellular infection:
Clarithromycin 15mg/kg/day. BID Daily
Azithromycin 20mg/kg/weekly.
e) Oral thrush (Oral candidiasis):
1% Gention violet ×7days, nystatin 1lakh unit 4-6 hours into 7days.

f) Eusopgeal candidiasis: Ketoconazole 3-6mg/kg ×7days OD or :
Fluconazole 3-6mg/kg ×7days OD.
g) Respiratory infection:
Trimethoprim + Sulfa methazole 4mg 6hours ×21days.
h) Resistant diarrhea: Trimethoprim + Sulfa methazole 5mg /kg BD. Or
Nalidixic acid 55mg/kg/BD.
i) Fever: Trimethoprim + Sulfa methazole 4mg ×10days or treatment of
Malaria.
6. Nutritional therapy:
• Calories 200 kcal/kg.
• Protein 4gm/kg.
• Vitamin supplementation as per RDA.
• Minerals supplementation as per RDA.
7. ARV therapy: Basic principles.
A. Never give monotherapy.
B. Give at least three drugs from two different group of drugs.
C. Classes of antiretroviral drugs – three classes.
a) NRTI: Nucleosides reverse transcriptase inhibitors:
i. Zidovudine (zdr, 360 mg/m2
/day)
ii. Stavudine (d4T, 2mg/kg/day)
iii. Lamivudine (3TC, 8mg/kg/day)
iv. Didanosine (ddl, 180-240mg/m2
/day)
v. Zalcitabine (ddl, 180-240mg/m2
/day).
vi. Abacavir (ABC 16mg/kg/day)
b) Non-Nucleosides reverse transcriptase inhibitors (NNRTI):
i. Nevirapine (NRP 300 to 400mg/kg/day).
ii. Delavirdine (DLV).
iii. Efavirenz EFV).
c) PI (Protease inhibitors)
i. Saquinavir (SQC 100mg/kg/day)
ii. Ritonavir (RTV 800mg/kg/day)
iii. Nelfinavir (NFV 90 – 110 mg/kg/day)
iv. Amprenavir (APV 20mg/kg/day)
v. Indinavir (IDV)
D. ART Therapy: Is based on:
i. Whether patient is asymptomatic or symptomatic
ii. CD4 cell count.
iii. Viral load.
iv. Age patient:
 If symptomatic always treat.
 If CD4 count is <200 always treat.
 If asymptomatic:
a. If CD4+count <200 treat.
b. If CD4+count >500 no ART.
c. Count between 200 and 350 consider other factors.
E. There are three types of regimens:

a) Protease inhibitor regime – 2NRTI + Ritonavir/ Lopinavir.
b) 2 NRTI based regime – age >3yrs – 2NRTI + Efavirenz, Age <3yrs – 2NRTI +
Nevirapine.
c) Nucleoside analog based usually not recommended Zidovudine + Lamivudine
+ Abacavir.
F. Best choice is:
a) Zidovudine + Didanosine/lamivudine.
b) Stavudine + lamivudine.
c) Dual NRTI + PI.
8. Infant feeding policy:
a) There are 16.2% greater risk of mother to infant transmission of HIV when
children are breast fed.
b) Replacement feeding at earliest may be considered. Exclusive breast
feeding for 4months followed by abrupt weaning.
c) Alternative modifications of mother milk to reduce infectivity.
1. Expressed milk that is allowed to stand reduce viral titers.
2. Pasteurized human milk.
3. Boiled human milk.
4. Frozen human milk.
5. Wet nursing by HIV negative lactating women.
6. Human milk bank.
7. Continuous ART while Breast feeding.
d) Reduce incidence of mastitis by advising correct positioning of infant while
feeding.
8. Psychosocial care.
9. Prevention of HIV:
a) Monogamy.
b) Using condoms.
c) Voluntary testing.
d) Screening of blood for HIV.
e) Counselling of adolescent and vulnerable groups.
f) Non formal teaching.
6.7. Whooping cough (Pertussis):
1. Definition: It is an acute respiratory tract infection causing intense cough.
2. Etiology: Agent – Bordetella pertussis; gram negative coccobacilli. Occasionally B
parapertussis.
3. Epidemiology: Age 1-5yrs usually <14yrs. Season July to October.
• Extremely contagious.
• Chronic carrier not known.
• Dose not provide lifelong immunity with natural disease or even after
vaccination.
• Mode of infection – droplet transmission.
4. Pathogenesis: Features of disease are caused by following biologically active
substances:

a) B pertussis has (Pertussis toxin – PT)
b) Surface protein called pertactin helps in attachment to ciliated respiratory
epithelial cells.
c) Tracheal cytotoxin, adenyl cyclase, and PT inhibit clearance of organism.
They cause local epithelial damage. (PT causes Lymphocytosis)
d) Filamentous hemagglutinins (FHA)
e) Fimbriae.
5. Clinical feature:
Infectivity: 1week prior and 3weeks after onset of symptom.
Incubation period 1-3weeks (7days)
Called “6 weeks disease”. In china called “100 days disease”.
Three stages:
oStage I: Catarrhal stage (3-12 days). Features of URI like fever, sneezing,
lacrimation and conjunctival suffusion.
oStage II: Paroxysmal stage.
Cough:
a) First it is dry intermittent, irritative, hacking which progress to severe cough
paroxysm. There are severe bouts of repetitive cough followed by whoop
(used for full inspiratory gasp) associated with apnea and choking.
b) During bout of cough face is reddened, tongue protrudes out face becomes
blue, eyes bulge with watering.
c) Precipitating factors for paroxysm – light sound, sucking, feeding.
d) Post tussive emesis is commen.
e) Post tussive exhaustion is universal.
f) Number and severity of paroxysm increase and remains for about 3weeks.
g) Infants less than 3months do not have classical stages.
Stage III: (Convalescent stage) Numbers, Severity and duration of episodes
diminish. In infants cough and whoops become louder and classic during
convalescence.
6. Diagnosis:
1) TLC: Leukocytosis.
2) DLC: Absolute lymphocytosis.
3) ESR: Decreased.
4) Culture.
5) Direct fluorescent antibody testing – DFA is a rapid test.
6) PCR.
7) Antibodies against pertussis toxin.
7. Complications:
1) Respiratory complications:
a) Flaring up of dormant tubercular focus.
b) Otitis media.
c) Pneumonia.
d) Collapse, emphysema, Bronchiectasis.
e) Pneumothorax.
f) Surgical Emphysema.
g) Pneumomediastinum.

h) Epistaxis.
2) CNS: Due to hypoxia and hemorrhage.
a) Hemiplegia due to necrosis.
b) Cerebral hypoxic encephalopathy.
3) Physical sequelae of severe cough:
a) Frenular ulcer.
b) Rupture of diaphragm.
c) Rectal prolapse.
d) Hernia.
e) Conjunctival and scleral hemorrhages.
f) Epistaxis.
g) Hemorrhage in CNS and Retina.
h) Pneumothorax, Emphysema.
4) Tetany following post tussive alkalosis.
5) Hyponatremia from excessive secretion of ADH.
8. Diagnostic triad:
a) Paroxysmal cough followed by whoop and vomiting.
b) Leukocytosis, lymphocytosis.
c) Decreased ESR.
9. Treatment:
1) Isolation for ≥5days after starting Erythromycin.
2) Antimicrobial Agents:
a) Erythromycin: 40-50 mg/kg/day/PO for 14days.
b) Clarithromycin: 15-20 mg/kg/day/BID for 5days.
c) Azithromycin: 10mg/kg/day for 5days.
Modest active drugs: Ampicillin, rifampicin and trimethoprim + sulfa
methazole.
Caution: Infantile hypertrophic pyloric stenosis has been reported with the
use of erythromycin in infants up to 6weeks of age but not with
clarithromycin or azithromycin.
3) Supportive therapies:
a) Salbutamol helps.
b) Corticosteroids not indicated.
c) I.V. use of human hyperimmune pertussis immunoglobulin is under
investigation.
4) Care of contacts:
a) Erythromycin 40-50 mg/kg/day/PO for 14days to all contacts.
b) Close contacts <7yrs of age who have received <4doses of pertussis
vaccine should be immunized again.
10. Prevention: Universal immunization before 7years.
6.8. Diphtheria:
1. Definition: Diphtheria is acute toxic infection caused by C. Diphtheriae.
2. Etiology: (Three biotypes – Mitis, Gravis & Intermedius)
3. Epidemiology & Immunity:
• Exclusive inhabitant of human mucous membrane and skin.

• Spreads airborne, respiratory droplets, direct contact with respiratory secretions
or exudate from skin lesion.
• Reservoirs asymptomatic respiratory tract carriers and skin infections.
• Incubation period respiratory 3-5 days, Cutaneous 7 days Average.
• Antitoxin immunity is indicated by Schick’s test.
• Infants become susceptible by 6-12 months of age as the transplacental
immunity decreases.
• Where diphtheria is endemic it primarily affects children < 15 days of age.
• In vaccinated era epidemiology has shifted to adults with low natural
exposure and low booster vaccinations.
Greater that 60% cases occur in more than 14years of age individual.
4. Pathology & Pathogenesis:
Causes skin and mucous infections rarely focal infections after bacteremia, remains in
the superficial layers of the skin lesion or respiratory tract mucosa including local
inflammatory reactions.
Mechanism of action of endotoxin is by inactivation of EF – 2 thus inhibiting
protein synthesis and causes local tissue necrosis.
Pseudo membrane is formed in the first few days of respiratory infection. Consists of
necrotic coagulum of organisms, epithelial cell, fibrin, leukocytes and erythrocytes.
Bleeding edematous submucosa is revealed on removal.
Diphtheria is actually a toxemia.
Toxin: Local & systemic effects:
• Local
 Pseudo membrane.
 Paralysis of the palate and hypopharynx.
• Systemic effects (Due to absorption of toxins)
 Cardiomegaly.
 Demyelination of Nerves.
 Necrosis of kidney tubules, liver cells, adrenal glands.
 Thrombocytopenia
As cardiac and neurological complications are 2-10 weeks after
infection, pathophysiological mechanism can be immunologically
mediated.
Depletion of carnitine may contribute to the pathogenesis of
diphtheritic myocarditis.
5. Clinical manifestation:
1) Respiratory tract Diphtheria: 94% - tonsil or pharynx followed by nose and
larynx.
A. Tonsillar diphtheria:
o Sore throat universal early symptom.
o 50% have low grade fever.
o Fewer have malaise, dysphagia, hoarseness and headache.
o Mild pharyngeal injection followed by membrane formation.
o Membrane extends to uvula, soft palate, posterior oropharynx,
Hypopharynx and Glottic area, membrane is dirty white.

o Bull neck is due to cervical adenopathy and soft tissue oedema.
Degree of local extension correlates directly with profound
prostration. Fatality due to airway comprise or toxin mediated
complications.
B. Nasal diphtheria:
o More commen in infants.
o Serosanguineous erosive rhinitis with membrane formation.
o Shallow ulcer of external nares and upper lip is characteristic.
C. Laryngeal diphtheria:
o Hoarseness, Stridor, Croupy cough, dyspnea.
o Edema of soft tissues and obstruction by membrane suffocation.
2) Cutaneous Diphtheria:
oIndolent infection.
oSuperficial, ecthymic, punched out non healing ulcer with gray
membrane.
oMinority of patients develops respiratory tract colonization or
symptomatic infection and toxic complications.
3) Other sites:
oEar – Otitis media.
oGenital tract – Purulent and ulcerative vulvovaginitis.
oEye – Purulent and ulcerative conjunctivitis.
o Septicemia – endocarditis, Pyogenic arthritis.
Three Diagnostic features are:
a) Mild Grade fever.
b) Dirty white membrane in throat.
c) Massive cervical adenopathy giving appearance of bull neck
6. Differential diagnosis:
A. Pharyngeal Exudates:
1) ꞵ hemolytic streptococcal infection.
2) Infectious mononucleosis.
3) Viral pharyngitis.
4) Fusopirochetal infection.
5) Candidiasis.
B. Pharyngitis: Due to group A streptococci and EBV:
1) High grade fever.
2) Dysphagia.
3) Membrane localized to tonsils.
4) Membrane is white in color.
C. Laryngeal obstruction:
1) Epiglottitis.
2) Viral croup.
3) Foreign body.
D. Neuropathy:
1) GBS.
2) Poliomyelitis.
E. Nasal diphtheria:

1) Foreign body.
2) Purulent sinusitis.
7. Complications:
1) Toxic cardiomyopathy:
o Subtle evidence of cardiac dysfunction in 50-60% patients.
o Clinical apparent myocarditis in 10-25% patients.
o Causes 50-60% deaths.
o2nd & 3rd week of illness (1-6 weeks)
oTachycardia out of proportion to fever diminished heart sounds, gallop,
rhythms, systolic murmurs, CHF, Cardiac arrhythmias.
oECG: Prolonged PR interval, Changes in ST – T waves.
Arrhythmias: Heart block, AV dissociation, AF, VF, VT.
oECHO: Dilated and hyperopic cardiomyopathy.
oBiochemical: Elevation of SGOT parallels severity of myonecrosis.
oRecovery: is usually complete although patient with more severe
dysrhythmias may have permanent conduction defect.
2) Toxic neuropathy:
 Present in 10% cases of average severity and 75% severe cases.
 Acutely or 2nd – 3rd week:
Paralysis of soft palate, weakness of posterior pharyngeal, laryngeal
fascial nerves, nasal voice, difficulty in swallowing, nasal
regurgitation, aspiration and death.
 5th week:
Cranial neuropathy and oculomotor and ciliary paralysis, strabismus,
loss of accommodation, dysfunction of the vasomotor center can cause
hypotension or cardiac failure.
 10 days – 3months:
i. Symmetric polyneuropathy causes principally motor deficits
with decrease DTR, mild weakness of pelvic muscle, with
unsteady gait to total paralysis. Generalized paresis usually occurs
after 4th
week.
ii. Paresthesias develop most often in glove and stocking
distribution.
iii. Intercostal and diaphragmatic palsy usually resolve completely.
iv. Time needed for improvement approximates time for exposure to
development of symptoms.
8. Other complications:
1) Pneumonia.
2) Renal failure.
3) Cerebral infarction, Encephalitis.
4) Pyogenic Arthritis.
5) Pulmonary embolism.
6) Bacteremia.
7) Endocarditis.
9. Laboratory diagnosis:
1) Throat smear examination.

2) Throat culture on selective media (Loeffler’s, Tellurite)
10. Treatment:
Case: Presence of C. Diphtheria in respiratory tract with pseudo membrane.
Carrier: Presence of C. Diphtheria in respiratory tract without pseudo membrane.
A. Specific measures:
1. Antitoxin – Mainstay of therapy (ADS).
Administered with in 48hours. It neutralizes free toxin.
Dose: 20,000 to 40,000 units – Disease of pharynx, larynx and present <
48hours.
40,000 to 60,000 units Nasopharynx.
80,000 to 1,20,000 units – Extensive disease, Brawny anterior cervical edema,
present >48hours.
Adverse Reactions:
 8% develop serum sickness.
 10% patients have pre-existing hypersensitivity to hoarse protein.
Sensitivity testing:
Intradermal test uses 0.02 ml of 1:100 saline diluted antitoxin (1:1000 if the
patient has prior exposure to animal serum or history of animal allergy)
Injection Adrenaline should be kept ready for use if required.
Immediate reaction is defined as wheal with surrounding erythema at least
3mms large than the control test read at 15-20min.
Desensitization is done in those showing immediate reactions with successive
doses every 15min.
Those with negative test results primary dose of 0.5 ml of antitoxin diluted
in 10ml of saline or 5% glucose solution is given slowly over 30min.,
remaining is then diluted 1:20 and given at the rate not exceeding 1ml/min.
2. Antibiotics.
Antibiotic therapy is not a substitute for antitoxin therapy.
Primary goal is:
1) Eradication of C. Diphtheria.
2) Prevention of transmission to susceptible contacts.
3) Halt toxin production
4) Treatment of carriers.
Drugs:
Erythromycin, rifampicin, clindamycin, penicillin G, tetracyclines only
erythromycin or penicillin is recommended.
Erythromycin is marginally better than penicillin for eradication of
nasopharyngeal carriage.
Dose of Erythromycin: 40 to 50 mg/kg/day.
Respiratory Diphtheria 14 days.
Cutaneous Diphtheria 7-10 days. Elimination should be documented by at
least successive cultures from nose and throat obtained 24 hours apart after
completion of therapy.
Treatment with erythromycin is repeated if culture is positive.
Isolation of the patient till cultures is negative.
3. Treatment of complications.

a) Obstruction by Pseudo membrane: Bronchoscopy, intubation and
mechanical ventilation.
Corticosteroid do not diminish myocarditis and neuritis hence not
recommended.
b) Oral therapy with DL carnitine (100mg/kg/day) in 2div. doses for
4days) may be beneficial in diphtheritic myocarditis.
4. Treatment of contact and carriers.
Asymptomatic case contacts:
 Observation for 7days.
 Cultures to be sent and if positive then repeat after 14days.
 Antimicrobial prophylaxis. Erythromycin (40mg/kg/day in 4div,
doses) for 10 days.
 Administer diphtheria toxoid.
 If, 3doses of toxoid or uncertain immunization status.
 Those who have not received their 4th
dose should be vaccinated.
 In immunized children who have not received booster within 5yrs.
Asymptomatic carriers:
 Antimicrobial prophylaxis for 7 days.
 Age appropriate diphtheria toxoid if no booster within 1yr.
 Place in isolation until 2subsequent cultures after cessation of therapy
are negative.
 Repeat cultures after 14 days for case and carriers and contacts if
positive repeat erythromycin for 10days.
People carrying diphtheria germs are contagious for up to 4weeks without
antibiotic therapy, even if they themselves do not symptoms.
Antitoxin is not recommended for asymptomatic close contacts or carriers
even if inadequately immunized.
B. General measures:
Bed rest in hospital for 10-14days.
Strict isolation for first 7days till secretions is non-contagious.
Isolation is discontinued when >2 cultures are negative.
C. At recovery administration of diphtheria toxoid is recommended as not all
patients develop antibodies after infection. Diphtheria toxoid at the time of
discharge.
5. Prevention:
→ Immunization.
→ Preventing secondary cases in exposed individuals.
→ Determining the source and carrier to halt spread.
6.9. Tuberculosis.
1) Definition: It is a chronic infectious disease caused by mycobacterium group of
bacilli.
2) Etiology: Caused by.
1. Mycobacterium tuberculi. (Most commen)
2. Mycobacterium Bovis.

3. Mycobacterium africanum.
3) Predisposing factors:
1. Poor nutrition, Poverty (PEM)
2. Overcrowding.
3. Inadequate health care.
4. Genetic may have role.
5. Age: more common in less than 3yrs or at puberty. Less in 5to14yrs.
6. Sex: Before puberty-equal in both sexes but during puberty more common in
girls.
7. Nursery school.
8. Child care centers.
9. HIV patients.
10. Immune comprised diseases and malignancies.
11. Immunosuppressant Drugs: Prolonged used of corticosteroids.
12. Infectious diseases – Like measles, whooping cough activate dormant
tuberculosis.
13. Drug users.
14. Health care persons.
15. Children exposed to TB positive contacts.
4) Transmission:
1. Airborne (Person to person by infected droplets).
2. By direct contact.
3. Milk born infection – if consuming raw cow’s milk (M Bovis)
4. Perinatal infection from infected mother to newborn through placenta.
5) Pathogenesis:
Portal of entry:
a) Lung in 98% cases.
b) Skin.
c) Mucous membrane.
d) Fetal liver in congenital tuberculosis.
e) Gastrointestinal tract in milk borne diseases.
Stages: Three stages:
1st stage Exposure to open adult case
2nd stage Tubercular infection:
• Tuberculi bacilli are inhaled into lungs through mucous droplets.
• They are deposited in distal airways i.e. alveoli.
• Ingested by alveolar macrophages and from phagosomes.
• Most of them are killed but few survive depending upon immunity of
person and virulence of organism.
• Bacilli multiply in macrophages until macrophage burst.
• Blood born monocytes and macrophages attach to it. They ingest bacilli but
do not kill. It takes 1to3weeks.
• Mantoux test is negative during this stage.
3rd stage of tubercular disease:
• Infected macrophages migrate to hilar lymph nodes.

• In lymph node bacterial antigen are presented to CD4 cells.
• CD4 cells are activated and cause delayed type of hypersensitivity.
• Cellular response leads to formation of tubercular Granuloma, which
contain macrophages, epithelioid cells, Langerhans Giant cells,
Lymphocytes and collagen fibers with central necrosis and liquefaction.
• Depending upon cell mediated immunity this primary focus heals by
fibrosis and calcification or lesion will enlarge and visible as tubercle
(Ghon focus) leading to formation of primary complex.
• During this stage Mantoux test will be positive.
Pulmonary primary complex (PPC): It comprises:
1. Primary focus of tubercular infection.
2. Draining lymphatics (Lymphangitis).
3. Draining Lymphadenitis collectively called (PPC).
Site – Common site mid zone of right lung 70% are sub plural.
Hallmark of primary tuberculosis is relatively large size of
adenitis compared with primary focus.
Mantoux test is positive during this stage.
Natural history Tubercular infection: (Fate of primary
complex).
Depending upon immune response there 3fates of primary
complex:
a) Heals by fibrosis and calcification.
b) Remains Dormant for years.
c) Progresses to progressive pulmonary complex.
Progression: If it progresses it causes following presentation:
a) Local progression causes:
1. Consolidation.
2. Cavity formation – Rare.
3. Bronchopneumonia.
4. Rupture into pleural space.
b) Lymphadenitis: It causes.
1. Bronchial obstruction either
a) Partial causing emphysema or
b) Complete causing Atelectasis.
2. Erode bronchial wall causing
a) T.B. Bronchitis.
b) Endobronchial tuberculosis.
3. Rupture in Bronchi causing: Bronchogenic spread
of tuberculosis to both lungs.
c) Hematogenous spread:
1. Acute spread (3to6months) Causes:
• Miliary tuberculosis.
• Tubercular meningitis.
2. Chronic spread – usually take more than 2years.
Causes: Tubercle lesions in

i. Bone.
ii. Joints.
iii. Genitourinary TB.
iv. Tuberculoma in Brain.
3. May localize in apex of lung (Simon focus)
6) Clinical features:
1. Primary infection usually passes unrecognized.
2. Asymptomatic infection is defined as infection associated with tuberculin
hypersensitivity and
a. Positive tuberculin test.
b. No clinical features.
c. No X-Ray finding.
3. Primary complex: Presents as.
a. Constitutional symptoms: Mild fever, Anorexia, Weight loss, Irritability,
Fatigue easily, Decreased activity Peevish, Off color, ill look.
b. Features of bronchial/tracheal compression due to enlarged lymph
node irritating dry cough.
c. Reduce growth
4. PPD (Progressive primary disease)
Primary focus
Healing by fibrosis and calcification Dormant Progression
Local Progression
• PPC.
• Consolidation.
• Cavity.
• Plural effusion.
• Bronchopneumonia.
Lymphadenitis Progression.
• Emphysema.
• Atelectasis.
• Endobronchial T.B.
• TB Bronchitis.
• Bronchogenic spread.
• Collapse consolidation.
Hematogenous Spread.
• Miliary T.B.
• Kidney T.B.
• Bone T.B.
• Simon focus in lung.
• Tuberculoma.

a. Present with high grade fever and cough.
b. In Advanced disease there may be expectoration of sputum and
hemoptysis.
• Finding of consolidation:
 Dull on percussion.
 Decreased air entry, crepitations and bronchial breathing on
auscultation.
5. Endobronchial tuberculosis: Present with fever, troublesome cough, dyspnea,
wheezing and cyanosis.
6. Atelectasis: Absent air entry, dullness, shifting of mediastinum to same side.
7. Miliary tuberculosis: Onset sudden 3to6 months after primary infection.
a. Age common in infants, Young child and adolescents.
b. High grade fever, dyspnea, cyanosis.
c. Pulmonary findings are less compared to dyspnea.
d. Crepitations, Ronchi on auscultations.
e. Hepatomegaly, generalized lymphadenopathy.
f. X-Ray chest Miliary mottling.
g. Fundus: Choroid tubercles in 50% of cases.
h. Meningitis in 20% cases.
i. Common in malnourished.
8. Pleural effusion: onset acute or insidious.
a. Fever with chest pain, cough, dyspnea.
b. More common above 5yrs of age.
c. More common in boys.
d. Mostly Unilateral.
e. Examination Early cases pleural rub:
o Decreased chest wall movement with fullness.
o Decreased or absent air entry, stony dull on percussion.
9. Tubercular lymph adenitis:
a. Usually present 6to9 months after primary infection.
b. Usually unilateral.
c. Tuberculosis of superficial lymph nodes is known as scrofula.
d. Onset can be: Acute, slow onset or infection.
i. Acute onset: Present as rapid enlargement of lymph nodes, high
fever, tenderness and fluctuance may rupture and form sinus.
ii. Slow onset: Present as painless enlargement of nodes which are
firm, not attached to skin soften slowly within 6months. Peri
adenitis can cause matting of nodes. There is early softening.
iii. Old infection: Soft painless, swelling calcification indicates
infection of many years.
Age – Usually in older children and adolescent.
10. Abdominal tuberculosis: Usually seen in malnourished children above the age of
5yrs: It manifest as:
a. Enteric fever: Present as tubercular enteritis in form of diarrhea or
ileocecal mass presenting as subacute intestinal obstruction (Vomiting,
diarrhea, constipation)

b. Peritoneal:
o Asities type 97%.
o Fibroadhsive type – 3% as mass, obstruction or enterocutaneous
fistula.
c. Mesenteric adenitis: presents as mass, obstruction or peritonitis due to
rupture, pain in abdomen.
d. Others: Hepatobiliary splenic, pancreatitis.
Clinical features:
a) Constitutional features like fever, night sweats, weight loss.
b) Abdominal distention and malnutrition are common presenting symptoms.
c) Other symptoms: Pain in abdomen, anorexia, fever, chronic diarrhea, loss of
weigh, vomiting diarrhea/constipation and cough.
d) Signs:
i. Abdominal distension.
ii. Ascites.
iii. Lump Abdomen.
iv. Peritonitis.
v. Doughy abdomen.
vi. Hepatosplenomegaly.
vii. Enterocutaneous fistula.
viii. Features of subacute intestinal obstruction.
11. Genitourinary Tuberculosis: Present as
a. Painless hematuria.
b. Sterile pyuria.
12. Pott’s Disease: Presents as:
a. Kyphosis.
b. Gibbus.
c. Paraplegia.
13. CNS: Tuberculosis as
a. Meningitis.
b. Tuberculoma.
7) Diagnosis: Diagnosis of tuberculosis in children is based on:
A. First line tests:
a) Clinical features: Prolonged fever, Persistent cough beyond 2week and
loss of weight.
b) History of contact with adult patient
c) Tuberculin testing:
M2TU = <5mm – negative.
= 5 to 100mm – Probable.
= > 10mm – Positive.
d) Chest X-Ray: Hilar lymphadenopathy with or without parenchymal
findings consolidation, collapse – consolidation, Miliary mottling,
effusion, bronchogenic spread and atelectasis.
Consolidation:
• Heterogenous.
• With ill-defined margins.

• Hilar lymphadenopathy.
e) Demonstration of mycobacterium in various clinical specimen like:
i. Gastric lavage.
ii. Sputum.
iii. Bronchial aspirate.
iv. CSF, Body fluid, Urine etc.
B. Second line tests:
1. FNAC: Fine needle aspiration cytology.
2. Biopsy of lymph nodes, liver and other tissues.
3. Culture:
4. GeneXpert TB: Cartridge based nucleic acid amplification test where
results are given in 2hours along with results of resistance to rifampicin is
present or not.
C. Third line tests:
1. Antibody detection by ELISA is banned by WHO.
2. Demonstration of cellular products like long chain fatty acids by gas
liquid chromatography (GLC) Fatty acids are species specific: this
method is reliable, economical but requires expertise.
8) WHO Diagnostic criteria:
1. Suspected tuberculosis: Any child with history of contact with confirmed
case of pulmonary TB who:
a) Is not gaining normal health after measles, whooping cough.
b) Has:
• Loss of weight.
• Cough.
• Wheeze
Not responding to Antibiotic therapy for Respiratory disease.
c) Has painless, lymph node enlargement (Superficial)
2. Probable tuberculosis: As suspected case and any of the following:
a. Positive Mantoux test (>10mm)
b. Suggestive X-Ray findings.
c. Biopsy suggestive.
d. Therapeutic response to treatment.
3. Confirmed tuberculosis: Detection of tubercle bacilli by microscopy or
culture. Identification of tuberculae bacilli as mycobacterium by culture
characteristic.
9) Treatment:
I. First principle of treatment of tuberculosis is drug treatment.
Basic principles of treatment are:
1. Early bacterial activity to reduce no. of bacilli by INH.
2. Sterilization – Ability of a drug to kill semi dormant bacteria. Rifampicin and
pyrazinamide are the most potent sterilizing agents.
3. Prevention of drug resistance Isoniazid and Rifampicin have highest activity
of preventing emergence of drug resistance.
4. Two phase chemotherapy:
a.Initial intensive phase – Multiple drugs are used for 2to3months.

b. Maintenance phase of sterilization for 4to10 months.
5. Single drug is never used.
6. An appropriate combination of drugs prescribed in correct dosage should be
ensured.
7. Compliance with therapy is major issue for treatment. All drugs should be
given in single dose empty stomach.
8. B6 is not necessary for children.
9. Nutrition of a child should be improved.
10. Intercurrent infections should be treated simultaneously and vigorously.
11. Always trace reservoir of infection that should also be treated.
12. Drug resistance is chromosomal and is not passed from one organism to other.
13. Short course intermittent therapy is an effective and least costly approacg to
treatment.
Drug Dose (mg/kg/day) Side effects
Isoniazid INH 5mg Hepatotoxicity, Hypersensitivity,
Rash, fever, peripheral neuritis,
seizures, psychosis, ataxia.
Rifampicin 10mg Hepatotoxicity, nausea, vomiting,
flu like syndrome, arthralgia,
wheezing, blood dyscrasia,
autoimmune reaction, Purpura.
Pyrazinamide 25-30mg Hepatotoxicity, GIT upset,
photosensitivity, Gout arthralgia,
fever, malaise, dysuria,
thrombocytopenia.
Ethambutol 15-25mg Rash, fever, Optic neuritis, GI
upset, confusion, Dizziness.
Streptomycin 10-30mg Ototoxicity, hearing loss, rash,
fever, arthralgia, peripheral neuritis,
anaphylaxis, Renal toxicity.
Second line drugs: Cycloserine, ethionamide, kanamycin.
Third line newer drugs: Ciprofloxacin, Ofloxacin, Clarithromycin, rifabutin,
rifapentine.
Category of
treatment
Type of patient Regimen
New New bacteriologically
confirmed.
New clinically diagnosed TB.
New Extrapulmonary.
2HRZE + 4HRE

Retreatment Bacteriological confirmed
recurrent.
Microbiologic positive failure.
Microbiologic positive
treatment after default.
Others – Sputum smear
negative or extrapulmonary
disease and have recurrence.
2SHRZE + 1HRE+
5HRE.
• H= Isoniazid.
• R= Rifampicin.
• Z= Pyrazinamide
• E= Ethambutol
• S= Streptomycin.
Use of steroids in Tuberculosis indications:
1. TBM.
2. Endobronchial tuberculosis.
3. Pleural effusions.
4. Tubercular pericardial effusions.
5. Genitourinary tuberculosis.
6. Tubercular ascites.
Drug used: Prednisolone
Dose: 2mg/kg/day.
Duration: 4weeks and tapered over 2-4 weeks.
Mechanism of action:
a. Decrease vasculitis.
b. Decrease inflammation.
c. Decrease intracranial pressure.
d. Decrease adhesions.
Treatment failure: AFB positive after 3-month therapy.
Positive contacts: Adult taking ATT or has taken ATT in past 2yrs.
DOTS: Directly observed therapy short course.
II. Monitoring of treatment:
1. Clinical: Improvement in fever, cough, appetite, feeling of wellbeing.
Drug resistant TB: AFB positive even after 3months of intensive
treatment.
2. Radiological improvement.
III. Monitoring of side effects. Like Hepatotoxicity, ocular toxicity, Peripheral
neuritis.
IV. Baby born to mother with tuberculosis.
a) Continue Breast feeding.
b) BCG vaccination at Birth.
c) If X-Ray chest is normal then 6H
d) If X-Ray chest is abnormal 2HRZE/4HR.

Defaulter: If Defaulter period is >1month restart full treatment.
BCG Adenitis: If lymph node <1.5 cm no treatment. If increasing size or
fluctuant then excision.
6.8.1. Drug resistant tuberculosis.
1. Primary Drug Resistance: When patient is infected with drug
resistance population without having received prior treatment. Infection
is transmitted from person with drug resistance tuberculosis.
2. Acquired or secondary resistance: When the patient harbors
organism, which was initially, drug responsive but resistance has
developed during the course of treatment. Cause is poor compliance or
faulty treatment plan.
3. Multi drug resistance tuberculosis (MDRTB): Resistance to
Isoniazid and rifampicin with or without resistance to other drugs.
Causes of Drug Resistance:
a) Inadequate or inefficient administration of effective treatment.
b) Use of substandard drug.
c) Inadequate or irregular drug supply.
d) Interruption of chemotherapy due to side effects.
e) Non adherence of patients to the prescribed regimens.
f) Availability of Anti TB drugs over the counter without
prescription.
g) Literacy.
h) Low socioeconomic status.
i) Ignorance of the patients.
j) Massive bacillary load.
k) Laboratory delay in identification and susceptibility testing.
4. Diagnosis:
a. Persistent sputum positivity even after anti-tubercular treatment
for 3 months.
b. Culture showing resistance to first line Anti-tuberculous drugs.
5. Laboratory diagnosis.
a. BACTEC.
b. Mycobacterium growth indicator tube (MGIT).
c. Luciferase reporter assay.
d. Polymerase chain reaction (PCR).
e. DNA fingerprinting.
f. SSCP (Single strand conformation. Polymorphism)
Category IV
6.8.2. Direct observed therapy short course (DOTS).
1. It is a short course therapy for treatment of tuberculosis.
2. In DOTS During:
a. Intensive phase treatment – Patient swallows the drugs in
presence of health worker or DOTS agent for the entire course of
intensive phase.

b. During continuation phase – Patient is issued medicine for one
week in multiblister combi pack of which first dose is
swallowed by patient in presence of health worker. Checking
of compliance is done by asking the patient to return empty
multiblister combi pack when patient comes to collect medicines
for next week.
3. Drugs are provided in blister packs to patient.
4. Advantages of DOTS.
a.Compliance of therapy.
b. Better cure.
6.8.3. Tuberculin test.
It is a skin test used for diagnosing mycobacterium tuberculosis disease.
I elicit characteristic delayed hypersensitivity reaction with induration.
Method: Intradermal Mantoux test (Mantoux test – MT)
Method: Test is performed by intradermal injection into ventral surface of forearm of
0.1ml of PPD. Ideal is 1TU strength. But till 5TU is accepted. It should raise wheal of
6to10 mm in diameter.
Reading:
a. Reading after 48 to 72 hours.
b. Look for induration either by palpation or pen method.
c. Diameter is measured transversely to the long axis of forearm and recorded
in mm.
Interpretation:
a. < 9 mm is negative.
b. > 10mm – positive.
In immunocompromised children and HIV infection cut off is 5mm induration.
Causes of false negative reaction to MT
1. Infectious diseases:
Viral: Mumps, Measles, Chicken pox, HIV.
Bacterial:
a) Recent overwhelming tubercular infection.
b) Leprosy.
c) Brucellosis.
d) Associated fungal infection
2. Severe tuberculosis like – Miliary tuberculosis, tubercular meningitis.
3. Attenuated viral vaccinations – mumps, polio.
4. Metabolic – renal failure.
5. PEM.
6. Lymphoreticular disorders.
7. Lack of circulating – T lymphocytes.
8. Drugs – corticosteroids, immunosuppressant drugs.
9. Age – Extremes of ages, new born or elderly.
10. Stress – Burn surgery, GVH disease.
11. Faulty technique.
12. Improper storage and dilution.
Causes of false positive:

• Repeating Mantoux at the same site.
• Reading error.
6.8.4. Miliary tuberculosis.
Definition: Hematogenous Dissemination of tuberculosis causes Miliary
tuberculosis. It occurs after primary infection usually within 6months to 1year.
Onset Acute: Presents as follows
a) Pulmonary type:
High grade fever with respiratory distress and cyanosis along with toxemia.
Distress is more than clinical signs in lungs.
Signs in lung – fine crepes Ronchi.
b) Septic type:
oFever with rigors.
oChild is delirious.
oResemble septicemia.
c) Meningitic type:
• Child appears peevish, irritable and has frequent vomiting and
photophobia.
• Shrill cry.
• Convulsions may occur.
• Neurological deficit may be there.
6.10. Malaria.
1. Definition: It is highly communicable protozoal infection characterized by
paroxysm of fever, chills, sweating, fatigue, anemia & splenomegaly.
Etiology: Malaria is caused by plasmodium.
2. Types: There are four types of species.
a) P. Vivax – Causing benign tertian malaria
b) P Ovale – Causing ovale malaria.
c) P. Malariae – Quartan malaria.
d) P. falciparum – causing malignant tertian malaria.
3. Transmission:
a) Humans are infected by Bite of an infected female anopheles’ mosquito.
b) Rarely by blood transfusion: Merozoite transmitted malaria.
c) Congenital malaria through placenta.
Vector: There are many species but commen are anopheles culicifacies in
rural area and A stephensi in urban area.
Life cycle:
4. Life cycle:
1) Asexual in human.
2) Sexual in mosquito
Asexual life cycle in humans
Infective stage is sporozoites
→ When female anopheles mosquito bites human beings sporozoites are injected
in capillaries.
→ Within minutes either they are cleared by phagocytes or they enter in liver.

Immunity:
I. Immunity after malarial infection is incomplete and doses not persists for whole
life.
II. In endemic areas – person develop Antitoxic immunity, which protects from
severe illness only.
III. Newborns can be protected by antibodies acquired transplacentally or through
Breast milk.
IV. Fetal HB also protects against malaria during first 4to 6 months.
V. P. Vivax does not grow in thalassemics.
VI. P. falciparum does not grow in sickle cell trait persons.
VII. Malnutrition also protects as it retards the growth of malarial parasite.
5. Pathophysiology:
1) All the clinical features of malaria are due to erythrocytic schizogony only.
2) Fever in malaria is due to cytokines released from macrophages and WBC
when they engulf merozoites which are released when RBC are destroyed.
3) All the complications of P. falciparum malaria are due to following
factors:
a) Very high density of parasitisation in P. falciparum.
b) P. falciparum infects both young and old RBC.
c) Cytoadherence property of P. falciparum: Trophozoites disappear
from peripheral blood within 24 hours and adhere to wall of venules
and capillaries in various internal organs especially brain, heart, kidney
lungs, intestines, bone marrow, placenta but not skin.
d) Sequestration: Cytoadherence causes sequestration of infected RBC in
organs.
e) Rosetting: Mature RBC adherence to uninfected RBC.
Ultimate effect of cytoadherence, sequestration and Rosetting is
impaired microcirculation of various organs causing anoxic
damage and is responsible for all the complications of P. falciparum.
1) Incubation period:
a. P. falciparum – 9to14 days.
b. P. Vivax – 12 to 17 days.
c. P. ovale – 16 to 18 days.
d. P. Malariae – 18 to 40 days.
2) Early symptoms: Nonspecific: Anorexia, malaise, irritability, headache,
myalgia, slight fever.
3) Classical features:
a. Periodic fever with rigors (Rigor is typically present with P. vivax
only)
b. Splenomegaly.
c. Anemia.
d. Classical febrile paroxysm of 8to12 hours consists of three stages:
A. Cold stage (15 to 60 mins): characterized by sudden rise of fever, feeling of cold and
uncontrollable shivering.

B. Hot stage (2 to 6 hours): Characterized by high fever along with hot feeling
associated with myalgia, headache, nausea, vomiting, tachypnea, palpitation,
prostration and delirium.
C. Sweating stage (2to3 hours): Characterized by fall of temperature with profuse
sweating.
D. Associate and atypical features: Commonly associated feature are intense periodic
headache, pain in neck, and pain in limb, pain in abdomen, urticaria, jaundice
and shock.
7. Complications (Severe Malaria): Most of the complications are associated with P.
falciparum:
1) Cerebral malaria.
2) Algid malaria.
3) Shock.
4) Severe anemia.
5) Black water fever.

6) Acute renal failure.
7) Pulmonary edema – ARDS.
8) Hypoglycemia.
9) DIC.
Relapse: New attack of malaria caused by hypnozoites after long period of 6months
to 5yrs after primary attack is called relapse seen in P. vivax and P. ovale only.
Recrudescence: New malarial attacks within 2months after culmination of primary
attack resulting from persistence of erythrocytic cycle of plasmodium.
8. Diagnosis:
I. Clinically periodic fever, rigors, splenomegaly and anemia if present in
endemic area malaria should be suspected.
II. Laboratory Diagnosis:
1) P.B. smear examination:
a. Make two smears of blood: Thick for presence of parasites. Thin
for identifying species.
b. Take smear late in febrile paroxysm.
c. Ring form parasites can be seen in RBC along with granules.
2) QBC (Quantity buffy coat):
a. Malarial parasite contains DNA.
b. DNA is stained with acridine orange.
c. Visualized by fluorescence microscopy.
d. Fast method, more sensitive, positivity, percentage is not more
than 30%.
3) Immunodiagnosis: It detects parasite specific antigens using
monoclonal antibodies. It includes following tests:
a. Parasite F test:
i. It is Dipstick antigen capture test.
ii. It detects histidine rich protein 2 (HRP 2)
iii. It is specific for P. falciparum.
iv. It is fast method takes 10 min.
b. Dipstick tests:
i. It detects specific lactic dehydrogenase.
ii. Test detects only live parasites.
iii. Test available for both P. Vivax & P. falciparum.
4) Molecular methods:
i. Dot blot assay.
ii. DNA probes.
iii. PCR amplification
Above tests are used in only specific situations.
5) Serological tests:
• It detects specific malarial antibodies.
• It includes following tests:
a. IFAT
→ Indirect Immunofluorescence tests.
→ Detect IgM, IgG and IgA.
b. IHA (Indirect hemagglutination.)

c. Immune precipitation.
d. ELISA.
e. RIA.
9. Treatment:
1) Antimalarial chemotherapy.
2) Symptomatic treatment.
3) Radical cure.
4) Chemoprophylaxis.
5) Malarial vaccine.
6) Combination and their treatment (Severe malaria)
I. Antimalarial chemotherapy:
Chloroquine:
a) It is the first Drug of choice.
b) Total dose 25mg in three days.
c) Uncomplicated P. Vivax malaria – Recommended treatment Chloroquine
10mg base/kg STAT orally followed by 5mg/kg at 6, 24, and 48hrs (Total
dose 25mg/kg) or Chloroquine 10mg Base /kg at 24h and 5mg /kg at 48h
(Total dose 25mg base/kg). Primaquine should be given in a dose of 0.25mg
/kg once daily for 14 days to prevent relapse.
d) Recommended treatment of uncomplicated P. falciparum malaria in all states
other than north eastern states of India. Artesunate 4mg/kg of body weight
orally once daily for 3days and a single administration of SP as 25mg/kg of
sulfadoxine and 1.25mg/kg of pyrimethamine on day 1 or Artesunate as above
and mefloquine 25mg /kg of body weight in two divided doses (15mg/kg and
10mg/kg) on day 2 and day 3 OR co-formulated tablets containing 20mg of
Artemether and 120mg of lumefantrine can be used as a six dose regimen
orally twice a day for three days. A single dose of primaquine (0.75mg/kg) is
given for gametocytocidal action.
e) Drug and dosage of antimalarials in complicated and severe malaria. Quinine
salt 20mg salt/kg (loading dose) diluted in 10ml of isotonic fluid /kg by
infusion over 4h. then give a maintenance dose of 10mg salt/kg every 8h,
calculated from beginning of previous infusion until the patient can swallow
then quinine tablet 10mg salt /kg 8hourly to complete a 7days course of
treatment (including both parental & oral) Tetracycline or doxycycline or
clindamycin is added to quinine as soon as the patient is able to swallow and
should be continue for 7days. Tetracycline above (8yrs) or doxycycline above
(8yrs) to be given for 7days 4mg/kg/dose 4times daily or 3.5mg/kg once a day
respectively. Clindamycin to be given 20mg/kg/day in 2divided doses for
7days. If controlled IV infusion cannot be administered then quinine salt can
be given in the same dosages by IM injection in the anterior thigh (not in
buttock). The dose of quinine should be divided between two sites, half the
dose in each anterior thigh. If possible, IM quinine should be diluted in
normal saline to a concentration of 60-100mg salt/ml (Quinine is usually
available as 300mg salt/ml) Tetracycline or doxycycline or clindamycin
should be added as above OR Artesunate 2.4mg/kg/IV stat and then at 12 to
24 hrs. then once a day. Once the patient is able to swallow oral medication,

complete the treatment by giving a course of – artemether + lumefantrine in
north eastern states – artesunate + sulfadoxine pyrimethamine in all states
other than north eastern states of India.
f) If no response within three days then treat it as chloroquine resistant.
II. Symptomatic treatment:
Fever – Cold sponging (Paracetamol 10-15mg/kg/dose SOS)
Anemia – Give hematinic (severe anemia – blood transfusion)
Headache:
• Dehydration give IV fluids.
• Vomiting. Give IV drugs like ondansetron or phenothiazines.
III. Radical cure: To prevent relapses.
Primaquine: For P. Vivax. (Dose – 0.3mg/kg/day×14days or 0.75mg/kg/for
5days. For P. Falciparum (Dose – 0.75mg/kg/for 1day only.
IV. Chemoprophylaxis:
1. Chloroquine – 5mg/kg/weekly.
2. Mefloquine – 20mg/kg/weekly. (one week prior to reaching endemic area
and up to 6weeks after leaving endemic area.
V. Malarial vaccine:
• No vaccine till date.
VI. Combination and their treatment (Severe malaria)
1. Hyperpyrexia:
a) Tapid sponging.
b) Wrap patient in wet sheet.
c) Paracetamol.
2. Dehydration:
a) I.V. saline or Glucose.
b) Maintain balance slightly on the negative side.
3. Acute renal failure (Oliguria or Anuria)
a) I.V. saline or Glucose.
b) Furosemide 2mg/kg/IV or IM in divided doses.
c) Hemodialysis or Peritoneal dialysis if no improvement.
d) Watch for Sr. Creatinine, Blood urea, Sr. potassium.
e) Alkaline urine.
f) Diet control.
4. Pulmonary edema.
a) Propped up position.
b) Oxygen.
c) Furosemide 20mg/kg/IV or IM
d) Monitor CVP.
e) Watch fluid balance.
f) Watch for Cyanosis, Hyperventilation, Pneumonia.
5. Hypoglycemia.
a) 10% Glucose IV.
6. Bleeding:
a) Parenteral Vit. K.
b) Blood transfusion.

7. Jaundice: I.V. Glucose.
8. Shock:
a) I.V. Dextran.
b) Plasma expander as required.
c) Dopamine.
9. Anemia: Blood transfusion.
Nursing Care:
a) Keep air passage clear.
b) Give oxygen if signs of air hunger.
c) Propped up position at 450
if hypostatic congestion.
d) Record oral/rectal temperature, pulse and Blood pressure 2hrly.
e) Tepid sponging when required.
f) Note fluid intake, output.
g) Note No. and size of stools.
6.9.1. Cerebral malaria.
1. Introduction:
• It is a serious complication of P. falciparum infection.
• It is characterized by fever, convulsions, and coma of at least ½ an hour
(Coma can be of either grade i.e. Drowsiness, Delirium, Coma)
2. Pathophysiology:
• RBC containing P. falciparum block the capillaries of brain.
Lead to coma due to nitric oxide produced by cytokines.
• Fever, convulsions, severe headache, decreased level of
consciousness, i.e. drowsiness, delirium and coma.
• Pallor, splenomegaly, hepatomegaly.
• Jaundice, vomiting.
• Variable muscle tone.
• Variable reflexes.
• Decerebrate and Decorticate posture.
• Pupils: Contracted and unequal.
• Retinal hemorrhages.
• Babinski sign positive.
4. Laboratory investigations:
• CSF may be normal or may show pleocytosis.
• PBS may be positive for malarial parasites.
• Blood sugar may be low.
5. Neurological sequelae:
• Hemiparesis.
• Ataxia.
• Cortical blindness.
• Aphasia.
• Mental retardation.
6. Treatment:

a) Quinine is the drug of choice.
Route: IV.
Dose: Loading dose 20mg/kg followed by 10mg/kg/8hrly till
patient is conscious and can take orally.
Dilution: 10% glucose.
Duration 7days.
b) Treat hypoglycemia. By giving 10% glucose.
c) Dexamethasone I.V. for 2to3 days.
d) Correction of fluid and Electrolyte imbalances.
e) Blood transfusion if severe anemia.
f) Treatment of shock by blood transfusion, I.V. fluids and
dopamine.
g) Treat seizure by Anticonvalscents.
6.9.2. Algid malaria.
• When patient having severe malaria develops shock with cold extremities it
called Algid Malaria.
• Causes: Secondary Gram-negative bacteremia and hypovolemia leads to
shock.
• Treatment: Treatment of malaria by:
a) Quinine.
b) Antibiotics to cover Gram negative bacteremia.
c) I.V. fluids to cover hypovolemia.
d) Oxygen administration.
6.9.3. Black water fever.
• It is a complication of P. falciparum malaria.
• Characterized by:
A. Sudden massive intravascular hemolysis.
B. Passage of chocolate color urine due to hemoglobinuria; and
C. Renal failure in severe cases.
• Predisposing factors:
A. When patient of malaria with G6PD deficiency are given oxidant drugs it causes
intravascular hemolysis.
B. When G6PD deficient patients get malaria and are treated by quinine they get
intravascular hemolysis.
• Pathogenesis: Anti RBC autoantibodies cause I.V. hemolysis.
6.9.4. Congenital malaria.
1) Definition: Malaria acquired by new born from mother prenatally is called
congenital malaria.
2) Effects:
Prenatal: It causes:
a) Abortion, miscarriages.
b) Still birth, IUGR.
c) Neonatal death.
Newborn:
a) Occurs within 10-30days of age usually.

b) Presents as fever, restlessness, drowsiness pallor jaundice poor feeding,
vomiting diarrhea, cyanosis.
c) Hepatomegaly
d) No exoerythrocytic stage.
6.9.5. Tropical splenomegaly syndrome.
• It is hyperreactive malarial splenomegaly resulting from abnormal
immunological response to chronic malaria or repeated malarial infection.
• Characterized by:
a) Massive splenomegaly
b) High titer of circulating anti-malarial antibodies.
c) Absence of malarial parasites in peripheral blood smear.
• It is chronic benign condition seen in endemic area of malaria.
• Associated features:
i. Hyperimmunoglobulinemia (IgM)
ii. Cryoglobulinemia.
iii. Decrease C3
iv. Presence of Rheumatoid factor without arthritis.
v. Anemia: Normochromic, Normocytic.
vi. Peripheral B-cell lymphocytosis
• Treatment: Prolonged antimalarial chemoprophylaxis for at least one year
(Chloroquine and/or proguanil)
6.11. Enteric fever (Typhoid fever).
1) Definition: It is severe systemic disease caused by salmonella typhi and para
typhi
2) Etiology: Typhoid fever is caused by following three organisms:
a. Salmonella typhi.
b. Salmonella para typhi A
c. Salmonella para typhi B.
3) Epidemiology:
a. Ingestion of contaminated food with human faces.
b. Feco-oral spread.
c. Contaminated water.
d. Oysters and shellfish cultivated in contaminated water.
e. Congenital transmission through placenta from mother to fetus.
f. Intrapartum transmission feco-oral route from carrier mother.
4) Pathogenesis:
Ingested Bacteria reach intestine.
Invade through peyer’s patches.
Reach intestinal lymph nodes; here they multiply in mononuclear cells
Carried to mesenteric lymph nodes.
Reach Blood stream through thoracic duct cause transient bacteria.

Localize in reticulo endothelial system – liver, spleen, bone marrow.
Bacteremia occurs and localizes in Gallbladder.
Bacilli multiply in gallbladder and are excreted in intestine through bile duct.
5) Pathological lesion.
1. Hyperplasia of peyer’s patches.
2. Sloughing of epithelium of intestine.
3. Intestinal ulcers:
• Heal without scaring.
• No stricture formation.
• No intestinal obstruction.
6) Clinicopathological correlation.
1. Fever is due to circulating endotoxins.
2. Systemic symptoms are due to cytokines produced by macrophages which
are simulated by endotoxins.
7) Clinical features: Age usually after 2yrs of age. Season Hot, (summer)
1. Incubation period 7-14 days (13-30 days)
2. Onset – insidious
3. Initial symptoms (First week)
a. Fever, increases step wise.
b. Anorexia, malaise.
c. Myalgia, Abdominal pain.
d. Headache.
e. Initially diarrhea – Pea soup consistency, later on constipation.
f. Cough, Epistaxis.
g. Lethargy.
2nd week to 4th week.
1. High fever is sustained.
2. Anorexia, cough, fatigue, abdominal pain increases.
3. Patient appears acutely ill, disoriented, lethargic, delirious – stupor may be
observed.
4. If untreated may have complications.
Physical findings
1. Relative bacteria.
2. Hepatosplenomegaly.
3. Distended abdomen with tenderness having doughy feel.
4. Rose spot Rash, which appear from 7th
to 10th
day. Lesions are discrete
erythematous, 1-5 mm in size, slightly raised, blanch on pressure, site lower
chest and abdomen, leave brownish discoloration on healing. Salmonella
organism can be grown from lesions in 60% cases.
5. Chest – Ronchi/rales.
Resolution in 2to4 weeks
Lethargy and malaise may persist for 1to2 months – Emaciation at the end of illness.
Infants and children <2yrs.
1. Rare in age group.

2. Mild disease can cause Gastroenteritis to septicemia.
3. Diarrhea more common
Carriers:
1. Convalescent carriers excrete bacilli in stool for 3months.
2. Chronic carrier excretes beyond one year.
Complications: common after first week
1. GIT:
a. Intestinal hemorrhage.
b. Intestinal perforation, site usually in ileum.
2. Sepsis.
3. Liver: Hepatitis.
4. Gall bladder: cholecystitis.
5. Pancreatitis.
6. Respiratory: More common in children, pneumonia, bronchitis.
7. CVS – Myocarditis, Endocarditis.
8. CNS:
a. Increased ICP, Toxic encephalopathy.
b. Thrombosis.
c. Acute cerebellar ataxia.
9. Bone marrow necrosis.
10. Kidney – Poly-nephritis, Nephrotic syndrome.
11. Others:
a. Parotitis, orchitis.
b. Suppurative lymphadenitis.
c. Suppurative Osteomyelitis.
d. Arthritis.
e. Alopecia.
8) Diagnosis (BASU):
a. First week – Blood culture (B).
b. Second week widal test (A for Antibody titer)
c. Third week – Stool culture (S).
d. Fourth week – Urine culture (U).
A. Cultures:
a. Blood culture – Positive in 40-60% cases during first week.
b. Urine culture – Positive after first week.
c. Stool culture – Positive after1st week.
d. Bone marrow culture – Single most reliable test positive in 85% to 90%
cases.
B. Antigen detection by PCR – More specific and sensitive.
C. Widal test – Measures antibodies against O and H antigen this method is prone
to error, Positive after 1st week, rising titer is diagnostic. Antibodies against O
Antigen are diagnostic if either rising titer or tier more than 1/80 are present
four-fold titer is diagnostic. Only rising H. titer indicates an amnestic reaction.
D. TLC: Leukopenia with reactive lymphocytosis and eosinopia.
9) Differential Diagnosis:
1. Sepsis.

2. Tuberculosis.
3. Brucellosis.
4. Tularemia.
5. Leptospirosis.
6. Rickettsial disease.
7. Infectious mononucleosis.
8. Leukemia, Lymphoma.
9. UTI.
10) Treatment:
I. Antimicrobial therapy:
a. Third generation of cephalosporin (Ceftriaxone 100mg/kg/day is the
drug of choice).
b. Quinolone – Not approved for children.
c. Chloramphenicol – 50-75 mg /kg/day.
d. Ampicillin – 200mg/kg/day.
e. Amoxicillin – 100mg/kg/day.
f. Azithromycin – 8mg/kg/day in one or two divided doses for 7days.
g. Oral cefixime 20mg/kg/BD for 7days is equally effective.
II. Supportive – Treatment.
a. Fluid and Electrolyte balance.
b. Blood transfusion if intestinal hemorrhage.
c. Platelet transfusion if thrombocytopenia.
d. Oral hygiene should be maintained.
III. Treatment of carriers:
a. High dose ampicillin or amoxicillin for 4to6 weeks.
b. Cholecystectomy for cholelithiasis or cholecystitis within 14 days of
antibiotic treatment.
IV. Surgical intervention of perforation
11) Prevention:
1. Improved sanitation.
2. Clean running water.
3. Personal hygiene.
4. Hand washing.
5. Eradication of carrier state.
6. Vaccines:
a) Typhoid conjugate vaccine: 2 doses 1year apart starting after
6months for life long protection.
b) Vi capsular polysaccharide vaccine (Vi antigen):
Age > 2yrs.
Dose – single IM injection.
Booster every 3 to 5 years.
c) Killed vaccine not used now days.
6.12. Tetanus.
1) Definition: It is an acute spastic paralytic illness caused by Tetanus toxoid
(Neurotoxin) produced by clostridium tetani.

2) Pathogenesis:
1. Clostridium tetani is not invasive organism. Spores introduced in wound
remain at site.
Spores germinate, multiply and produce neurotoxin, tetanospasmin
Toxin binds at neuromuscular junction.
Through retrograde axonal transport reaches to cytoplasm of alfa motor neuron
Toxin excites motor neuron at spinal cord and enters adjacent inhibitory inter neuron.
Prevents release of GABA.
Block normal inhibition of antagonist’s muscles.
Leads to coordinated muscle contractions.
2. Autonomous nervous (ANS) also becomes unstable.
3. Spores can be introduced by following ways:
a) Neonatal tetanus through infected umbilical cord in child of an
unimmunized mother.
b) Injury wounds.
c) Chronic otitis media.
d) Burn wounds.
e) Through animal bites.
f) Ear piercing.
g) Abscesses.
h) Chronic skin ulceration.
i) Compound fractures.
j) Insect bites.
k) Males circumcision.
l) Through contaminated suture material.
m) I.M. injection especially quinine.
3) Clinical features:
1. Incubation period 2to14 days to months.
2. Types:
a) Generalized.
b) Localized.
i. Cephalic Tetanus.
3. Important feature is – four.
a) Trismus (Lock jaw)
b) Muscular board like rigidity.
c) Tonic contractions of muscle triggered by sound, light and touch.
d) Clear sensorium.
4. Other features:
a) Fever.
b) Resus sardonicus.

Pediatric lecture notes infectious diseases

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