EN TER IC FEV ER IN

P ED IATR IC S

Dr.Padmesh. V

 ETIOLOGY:
Caused by Salmonella enterica serovar Typhi
(S. Typhi). (Gram negative bacterium).
Similar but less-severe disease is caused by

Salmonella Paratyphi A and rarely by S.

Paratyphi B (Schotmulleri) and S. Paratyphi C
(Hirschfeldii).
Ratio of disease caused by S. Typhi to S.

Paratyphi is approximately 10 : 1
Polysaccharide capsule Vi (virulence) is present

in 90% of S. Typhi . (Protects the bacteria)

 PATHOGENESIS
Ingestion
Invade body through gut mucosa in terminal ileum.
Pass through intestinal mucosa
S. Typhi enter mesenteric lymphoid system
Lymphatics
Bloodstream (Asymptomatic bacteremia, Culture
negative)
Colonize Reticuloendothelial system (replicate in
macrophages)
Shed back into blood (Secondary bacteremia-Symptoms
appear)

 PATHOGENESIS
Surface Vi polysaccharide capsular antigen

interferes with phagocytosis by preventing binding

of C3 to bacterial surface.
Ability to survive within macrophages is an

important virulence trait encoded by PhoP regulon.

Occasional occurrence of diarrhea: Due to presence

of a toxin, related to cholera toxin and E.coli heatlabile enterotoxin.

Clinical syndrome of fever and systemic symptoms:

Due to release of proinflammatory cytokines (IL-6,

IL-1, and TNF-) from infected cells.
Patients with Helicobacter pylori infection have an

increased risk of acquiring typhoid fever.

 CLINICAL FEATURES:
Incubation period: 7 - 14 days (3-30 days)
Clinical presentation varies from mild illness with

low-grade fever, malaise, and slight, dry cough

to
Severe clinical picture with abdominal
discomfort & multiple complications.
Diarrhea, toxicity, & complications such as

disseminated intravascular coagulopathy are

more common in infancy. (increased fatality)
However, some features & complications seen in

adults, like relative bradycardia,neurologic

manifestations,and gastrointestinal bleeding are
rare in children.

 CLINICAL FEATURES:
FEATURE RATE (%)
High-grade fever 95
Coated tongue 76
Anorexia 70
Vomiting 39
Hepatomegaly 37
Diarrhea 36
Toxicity 29
Abdominal pain
21
Pallor
20
Splenomegaly
17
Constipation 7
Headache 4
Jaundice 2
Obtundation 2
Ileus 1
Intestinal perforation 0.5

 CLINICAL FEATURES:
In children diarrhea may occur in earlier
stages and may be followed by constipation.
Classic stepladder rise of fever is rare.
In 25% of cases, a macular or maculopapular

rash (rose spots) around the 7th-10th day;

May appear in crops of 10-15 on the lower
chest and abdomen and last 2-3 days.
If no complications occur, symptoms and

physical findings gradually resolve within 2-4

wk;

 COMPLICATIONS:

Altered liver function is found in many

patients.
However, clinically significant hepatitis,

jaundice, and cholecystitis are rare.

 COMPLICATIONS:
Extra intestinal complications:
Central nervous system (3-35%): Encephalopathy,
cerebral edema, subdural empyema, cerebral abscess,
meningitis, ventriculitis, transient parkinsonism, motor
neuron disorders, ataxia, seizures, Guillain-Barr
syndrome, psychosis.
Cardiovascular system (1-5%): Endocarditis,
myocarditis,pericarditis, arteritis, congestive heart failure.
Pulmonary system (1-6%): Pneumonia, empyema,
bronchopleural fistula.
Hepatobiliary system (1-26%): Cholecystitis, hepatitis,
hepatic abscesses, splenic abscess,peritonitis, paralytic
ileus

 DIAGNOSIS
Mainstay: Culture from blood or another

anatomic site.
Blood cultures are positive in 40-60% ,

early in the course.

Stool & urine culture become positive

after 1st wk.

 DIAGNOSIS
Results of other lab investigations are nonspecific.
Although WBC counts are frequently low in

relation to fever and toxicity, there is a wide

range in counts; in younger children leukocytosis
is common & may reach 20,000-25,000 cells/L.
Thrombocytopenia may be a marker of severe

illness & may accompany disseminated

intravascular coagulopathy.
Liver function test results may be deranged, but

significant hepatic dysfunction is rare.

 DIAGNOSIS
Widal test measures antibodies against O

and H antigens of S. Typhi but lacks

sensitivity and specificity in endemic areas.
O antibodies appear on days 6-8 and
H antibodies on days 10-12 after the onset
of the disease.
'O' titer is considered to be of greater

diagnostic significance.

 DIAGNOSIS: Other tests:

Nested PCR using H1-d primers
Typhidot: Test kit uses 50 kD antigen to

detect specific IgM and IgG antibodies to S.

typhi
Typhidot-M
IDL Tubex: detects IgM antibodies but not

IgG
Dip-S-Ticks test

 TREATMENT: (WHO, Nelson)

 TREATMENT: (WHO, Nelson)

 TREATMENT: (IAP)
3rd generation cephalosporins, both oral and

injectables are recommended for first line

treatment.
Oral: Cefixime , Cefpodoxime proxelil
Parenteral: Ceftriaxone, Cefotaxime, Cefoperazone.
Oral 3rd generation cephalosporin to be used in

higher dose in typhoid fever.

Azithromycin: Alternative in uncomplicated typhoid.
Aztreonam,Imepenem are potential 2nd line drugs.
For life threatening infection resistant to all other

recommended antibiotics fluoroquinolones may be

used.

 PROGNOSIS:
2-4% of infected children may experience
relapse after initial clinical response to
treatment.
Individuals who excrete S. Typhi for 3 months

or longer after infection are regarded as

chronic carriers. The risk for becoming a
carrier is low in children (<2% for all infected
children) and increases with age.
A chronic urinary carrier state can develop in

children with schistosomiasis.

 PREVENTION: Vaccines:
Oral, live-attenuated Ty21a strain of S.

Typhi has good efficacy (67-82%) for up to

5 yr.
Vi capsular polysaccharide for 2 yr of age

and older. Booster every 2 yr. Protective

efficacy of 70-80%.
Vi-conjugate vaccine has a protective

efficacy
children.

> 90% in younger

THANK
YOU!
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