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ENTERIC FEVER
By: Dr. SyedaWafa Zahra
House officer (peads- II)
CaseScenario:
 A 7- year old girl, who recently travelled to a village with her
family, presents with 4 day history of continuous fever, diarrhea,
and tenesmus and toxic look.There are palpable small
erythematous rash on the trunk only. Liver and spleen enlarged.
Stool examination revealed blood and leukocytes.
INTRODUCTION
 Typhoid fever is one of the commonest cause of PUO
(pyrexia of unknown origin)
 It’s a bacterial disease caused by typhoid bacillus.
 Characterized mainly by prolonged fever, abd pain,
diarrhea, rose spots, delirium, splenomegaly, intestinal
bleeding and perforation.
ETIOLOGY
 Typhoid fever is caused by SalmonellaTyphi
 Paratyphoid is caused by S. paratyphoid A, S. paratyphoid B ( S.
scottmuelleri) and S. paratyphoidC (S. hirschfeldii)
 Salmonella organisms are gram negative bacilli and they contain
three types ofAg:
1. Somatic or cell wall lipopolysaccharide (O)
2. Flagellar (H)
3. Capsular or polysaccharide virulence (Vi)
EPIDEMIOLOGY
 Adults and children of all ages and both sexes are equally
susceptible to infection. Most common in school age children and
young adults.
 Major reservoirs for salmonella are animals, contaminated water,
infected fruits and veges, and infected humans.
 Infection is transmitted by ingestion of contaminated food milk
water or contact with and infected animal.
 Person to person spread occur by faecal oral transmission. 10^5 -
10^6 viable organisms must be ingested for a clinical disease to
occur.
 Incubation period is usually 7-14 days. (Range 3-30 days)
PATHOGENE
SIS
PATHOGENE
SIS
 Bacteria enters by ingestion of contaminated food or water.
 After ingestion and surviving the acidity if stomach, it enters the
small intestine where it penetrates the mucous and enter
mononuclear phagocytes of ileal payers patches and mesenteric
LN.
 Then theres necrosis of payers leading to ulcers which causes
bleeding. It may also erode the intestinal wall and causes
intestinal perforations.
 Infection spreads to regional LN and multiply in mononuclear
cells.
 Via lymphatics it reaches the liver, spleen, mesenteric LN, bone
marrow and proliferate them.
 At the end of incubation period, they pass into bloodstream and
produce bacteremia and its associated symptoms.
 Large no. Of salmonella produce in the wall of GB and reach
intestine through bile.
CLINICAL
FEATURES
 First week: fever and chills gradually increasing and
persisting (95% cases), headache, abdominal
tenderness
 Second week: rash, abdominal pain, diarrhea or
constipation, delirium, prostration, rose spots,
hepatosplenomegaly
 Third week: complications of intestinal bleeding and
perforation, shock. Malena, ileus, rigid abdomen,
coma.
 Fourth week and later: restoration of symptoms,
relapse, wt loss, reappearance of acute disease,
cachexia.
DIAGNOSIS
 Isolation of causative organism ( culture )
1. Blood culture- positive early during the first 2 weeks
of illness in 40-60%
2. Bone marrow culture – positive during later sstage of
enteric fever, it’s the most sensitive procedure (
positive in 85-90%)
3. Urine and stool culture- it may be positive during the
incubation period
DIAGNOSIS
 Serological tests
1. Widal test- it measure the AB response to somatic O
and flagellar H Ag of salmonella. O titers of greater
than 1:160 is suggestive. H ab signifies prev
infections or immunization and is difficult to
interpret in endemic areas.
- It may give false positive or false negative results. So its
not a reliable test to diagnose.
 Polymerase chain reaction (PCR)
It gives results within few hours and its more specific abd
sensitive than blood culture.
DIAGNOSIS
 Supportive tests
1. CBC: -Leucopenia, in younger children leukocytosis is
common and may reach 20,000- 25,000 cell/uL.
- normochromic normocytic anemia
- thrombocytopenia
1. LFTs: it may be deranged.
DIFFERENTIA
LS
 Gastroenteritis
 Bronchopneumonia
 Sepsis
 Malaria
 Tuberculosis
 Acute hepatitis
 Amebic liver abscess
 Shigellosis
 Brucellosis
 Leptospirosis
 Bacterial endocarditis
 Infection mononucleosis
 Malignancies like leukemia or lymphomas
COMPLICATI
ONS
 Intestinal perforations- usually in distal ileum
 Intestinal hemorrhage
 Toxic encephalopathy
 Acute cholecystitis/ hepatitis
 Pneumonia
 Meningitis
 Osteomyelitis
 Septic arthritis
 Toxic myocarditis
Most of the complications occur after 2nd week of the disease.
MANAGEMENT
 Supportive:
 Corticosteroids are given in pt with toxemia or
prolonged ss. A short course of dexamethasone
improves the survival rates of pt with shock or coma.
Initial dose is 3 mg/kg, followed by 1 mg/kg every 6H
for 48hours.
 Blood transfusion in pt with anemia or severe intestinal
bleed.
 Adequate nutrition, hydration and electrolytes
balance.
 If intestinal perforations then surgical intervention
along with broad spectrum antibiotics.
 In case of thrombocytopenia, platelet transfusion is
needed.
MANAGEMENT
Specific
 Uncomplicated typhoid fever:
1. Fully sensitive:
 Chloramphenicol, 50-75 mg/kg/d PO or 75mg/kg/day IV in 4
divided doses for 14-21 days
 Amoxicillin 75-100 mg/kg/d Po in 3 divided doses for 14d
 Fluoroquinolones e.g Ciprofloxacin 15-20mg/kg/d PO for 10-14d
1. Multi drug resistant:
 Fluroquinolones
 Azithromycin 10-20mg/kg/d po for 7d
 Cefixime 20mg/kg/d Po for 7-14d
MANAGEMENT
Specific
 Uncomplicated typhoid fever
1. Quinolone resistant:
 Azithromycin
 Cefixime
 Ceftriaxone 60mg/kg/d in 2 doses IV for 14d
MANAGEME
NT
Specific
 Severe typhoid fever:
1. Fully sensitive:
 Fluoroquinolone
 Chloramphenicol
 Amoxicillin
1. Multidrug resistant:
 Fluoroquinolones
 Ceftriaxone
 Cefotaxime
1. Quinolone resistant
 Ceftriaxone
 Cefotaxime
 Azithromycin
PREVENTION
 Handwashing, improved personal hygiene and sanitary habits
 Protective health measures like provision of clean water, adequate
seepage disposal, control of flies
 Adequate temperature for cooking. Eggs should never be eaten
raw.Avoid preserving food at warm temp and avoid reheating it.
 Passive immunization with vaccination, parented ViCPS (typhim
Vi) for IM use. Oral live attenuated Ty21a vaccine is supplied as
enteric coated capsules.
PROGNOSIS
 Mortality rate is higher than 10% and its mainly due to delay in
diagnosis or treatment.
 Enteric fever with complications is associated with high mortality
and morbidity.
 Relapse may occur in 4-8% of the pt who haven’t got the
treatment, it may also occur in treated pt about 2 weeks after
stopping the antibiotics.
 Children have risk of becoming carriers at a rate of 1-5%.
 Chronic carriers are at increased risk to get biliary tract disease.
THANKYOU 

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ENTERIC FEVER

  • 1. ENTERIC FEVER By: Dr. SyedaWafa Zahra House officer (peads- II)
  • 2. CaseScenario:  A 7- year old girl, who recently travelled to a village with her family, presents with 4 day history of continuous fever, diarrhea, and tenesmus and toxic look.There are palpable small erythematous rash on the trunk only. Liver and spleen enlarged. Stool examination revealed blood and leukocytes.
  • 3. INTRODUCTION  Typhoid fever is one of the commonest cause of PUO (pyrexia of unknown origin)  It’s a bacterial disease caused by typhoid bacillus.  Characterized mainly by prolonged fever, abd pain, diarrhea, rose spots, delirium, splenomegaly, intestinal bleeding and perforation.
  • 4. ETIOLOGY  Typhoid fever is caused by SalmonellaTyphi  Paratyphoid is caused by S. paratyphoid A, S. paratyphoid B ( S. scottmuelleri) and S. paratyphoidC (S. hirschfeldii)  Salmonella organisms are gram negative bacilli and they contain three types ofAg: 1. Somatic or cell wall lipopolysaccharide (O) 2. Flagellar (H) 3. Capsular or polysaccharide virulence (Vi)
  • 5. EPIDEMIOLOGY  Adults and children of all ages and both sexes are equally susceptible to infection. Most common in school age children and young adults.  Major reservoirs for salmonella are animals, contaminated water, infected fruits and veges, and infected humans.  Infection is transmitted by ingestion of contaminated food milk water or contact with and infected animal.  Person to person spread occur by faecal oral transmission. 10^5 - 10^6 viable organisms must be ingested for a clinical disease to occur.  Incubation period is usually 7-14 days. (Range 3-30 days)
  • 7. PATHOGENE SIS  Bacteria enters by ingestion of contaminated food or water.  After ingestion and surviving the acidity if stomach, it enters the small intestine where it penetrates the mucous and enter mononuclear phagocytes of ileal payers patches and mesenteric LN.  Then theres necrosis of payers leading to ulcers which causes bleeding. It may also erode the intestinal wall and causes intestinal perforations.  Infection spreads to regional LN and multiply in mononuclear cells.  Via lymphatics it reaches the liver, spleen, mesenteric LN, bone marrow and proliferate them.  At the end of incubation period, they pass into bloodstream and produce bacteremia and its associated symptoms.  Large no. Of salmonella produce in the wall of GB and reach intestine through bile.
  • 8. CLINICAL FEATURES  First week: fever and chills gradually increasing and persisting (95% cases), headache, abdominal tenderness  Second week: rash, abdominal pain, diarrhea or constipation, delirium, prostration, rose spots, hepatosplenomegaly  Third week: complications of intestinal bleeding and perforation, shock. Malena, ileus, rigid abdomen, coma.  Fourth week and later: restoration of symptoms, relapse, wt loss, reappearance of acute disease, cachexia.
  • 9. DIAGNOSIS  Isolation of causative organism ( culture ) 1. Blood culture- positive early during the first 2 weeks of illness in 40-60% 2. Bone marrow culture – positive during later sstage of enteric fever, it’s the most sensitive procedure ( positive in 85-90%) 3. Urine and stool culture- it may be positive during the incubation period
  • 10. DIAGNOSIS  Serological tests 1. Widal test- it measure the AB response to somatic O and flagellar H Ag of salmonella. O titers of greater than 1:160 is suggestive. H ab signifies prev infections or immunization and is difficult to interpret in endemic areas. - It may give false positive or false negative results. So its not a reliable test to diagnose.  Polymerase chain reaction (PCR) It gives results within few hours and its more specific abd sensitive than blood culture.
  • 11. DIAGNOSIS  Supportive tests 1. CBC: -Leucopenia, in younger children leukocytosis is common and may reach 20,000- 25,000 cell/uL. - normochromic normocytic anemia - thrombocytopenia 1. LFTs: it may be deranged.
  • 12. DIFFERENTIA LS  Gastroenteritis  Bronchopneumonia  Sepsis  Malaria  Tuberculosis  Acute hepatitis  Amebic liver abscess  Shigellosis  Brucellosis  Leptospirosis  Bacterial endocarditis  Infection mononucleosis  Malignancies like leukemia or lymphomas
  • 13. COMPLICATI ONS  Intestinal perforations- usually in distal ileum  Intestinal hemorrhage  Toxic encephalopathy  Acute cholecystitis/ hepatitis  Pneumonia  Meningitis  Osteomyelitis  Septic arthritis  Toxic myocarditis Most of the complications occur after 2nd week of the disease.
  • 14. MANAGEMENT  Supportive:  Corticosteroids are given in pt with toxemia or prolonged ss. A short course of dexamethasone improves the survival rates of pt with shock or coma. Initial dose is 3 mg/kg, followed by 1 mg/kg every 6H for 48hours.  Blood transfusion in pt with anemia or severe intestinal bleed.  Adequate nutrition, hydration and electrolytes balance.  If intestinal perforations then surgical intervention along with broad spectrum antibiotics.  In case of thrombocytopenia, platelet transfusion is needed.
  • 15. MANAGEMENT Specific  Uncomplicated typhoid fever: 1. Fully sensitive:  Chloramphenicol, 50-75 mg/kg/d PO or 75mg/kg/day IV in 4 divided doses for 14-21 days  Amoxicillin 75-100 mg/kg/d Po in 3 divided doses for 14d  Fluoroquinolones e.g Ciprofloxacin 15-20mg/kg/d PO for 10-14d 1. Multi drug resistant:  Fluroquinolones  Azithromycin 10-20mg/kg/d po for 7d  Cefixime 20mg/kg/d Po for 7-14d
  • 16. MANAGEMENT Specific  Uncomplicated typhoid fever 1. Quinolone resistant:  Azithromycin  Cefixime  Ceftriaxone 60mg/kg/d in 2 doses IV for 14d
  • 17. MANAGEME NT Specific  Severe typhoid fever: 1. Fully sensitive:  Fluoroquinolone  Chloramphenicol  Amoxicillin 1. Multidrug resistant:  Fluoroquinolones  Ceftriaxone  Cefotaxime 1. Quinolone resistant  Ceftriaxone  Cefotaxime  Azithromycin
  • 18. PREVENTION  Handwashing, improved personal hygiene and sanitary habits  Protective health measures like provision of clean water, adequate seepage disposal, control of flies  Adequate temperature for cooking. Eggs should never be eaten raw.Avoid preserving food at warm temp and avoid reheating it.  Passive immunization with vaccination, parented ViCPS (typhim Vi) for IM use. Oral live attenuated Ty21a vaccine is supplied as enteric coated capsules.
  • 19. PROGNOSIS  Mortality rate is higher than 10% and its mainly due to delay in diagnosis or treatment.  Enteric fever with complications is associated with high mortality and morbidity.  Relapse may occur in 4-8% of the pt who haven’t got the treatment, it may also occur in treated pt about 2 weeks after stopping the antibiotics.  Children have risk of becoming carriers at a rate of 1-5%.  Chronic carriers are at increased risk to get biliary tract disease.