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ENTERIC(TYPHOID)
FEVER
OBJECTIVE
• by the end of this session we should be able to understand about
1, definition
2, epidemiology
3, etiology & pathogenesis
4,clinical features
5, diagnosis and
6, prevention & control.
of Enteric(Typhoid) Fever and Relapsing Fever
INTRODUCTION
• Enteric (typhoid) fever is a systemic disease
characterized by fever and abdominal pain and
caused by dissemination of S. typhi or S. paratyphi.
EPIDEMIOLOGY
• In contrast to other Salmonella serotypes, the etiologic agents of enteric fever—S.
typhi and S. paratyphi serotypes A, B, and C—have no known hosts other than
humans.
• Most commonly,feco oral transmission results from contamination by ill or
asymptomatic chronic carriers. Sexual transmission between male partners has
been described. Health care workers occasionally acquire enteric fever after
exposure to infected patients or during processing of clinical specimens and
cultures
• Worldwide, however, there are an estimated 22 million cases of enteric fever, with
200,000 deaths annually.
• In endemic regions, enteric fever is more common in urban than rural areas and
among young children and adolescents
ETIOLOGY AND PATHOGENESIS
Ingestion of contaminated food and
water (inoculum dose 103-106cfu) by
susceptible host (Stomach acidity,
Achlorhydric diseases, Antiacid ingestion,
Age <1yr,  Intestinal integrity, IBD, GI
Surgery, Broad spectrum antibiotic use) 
they penetrate the mucus layer of the gut and
traverse the intestinal layer through
phagocytic microfold (M) cells that reside
within Peyer's patches  After crossing
the epithelial layer of the small intestine they
are phagocytosed by macrophages 
Dissemination throughout the body via
lymphatics and colonize RES  Re infection
of intestine as well as other body parts via
hematogenous dissemination.
• 1st week/Invasive
• •on set~:headache, bodyache,malise,sorethroat,anorexia
• •Gi symptoms-: constipation, tongue coated with raw tips &edges
• •Fever-:STEEP LADER low in morning high at night
• • bradycardia pulse
• •Bronchitis symptoms –cough
CLINICAL COURSE
• 2nd week /advanced
• •T°~high, rose spot rashes
• Spleen becomes palpable and constipation replaced by diarrhea
• 3rd week/decline
• •T° decrease
• Intestinal perforation & hemorrhage
• Patient may pass in to coma and die
• 4th convalescence
• Fever subsidies tongue clear pulse becomes rapid
DIAGNOSIS
;The definitive diagnosis of enteric fever is CULTURE.
In 15–25% of cases, leukopenia and neutropenia are detectable.
• Several serologic tests, including the classic Widal test for "febrile agglutinins," are
available
E X A M S A N D T E S T S
• CBC
• Blood culture
other tests
 ELISA
 Florecent antibody study
 Platelet count
 Stool culture
PREVENTION AND CONTROL.
• Consumptions of properly cooked meal, sanitation
• Vaccine for . Travelers to endemic areas
• People with close contact with chronic carrier
THANKS!!

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4 enteric(typhoid) fever and relapsing

  • 2. OBJECTIVE • by the end of this session we should be able to understand about 1, definition 2, epidemiology 3, etiology & pathogenesis 4,clinical features 5, diagnosis and 6, prevention & control. of Enteric(Typhoid) Fever and Relapsing Fever
  • 3. INTRODUCTION • Enteric (typhoid) fever is a systemic disease characterized by fever and abdominal pain and caused by dissemination of S. typhi or S. paratyphi.
  • 4. EPIDEMIOLOGY • In contrast to other Salmonella serotypes, the etiologic agents of enteric fever—S. typhi and S. paratyphi serotypes A, B, and C—have no known hosts other than humans. • Most commonly,feco oral transmission results from contamination by ill or asymptomatic chronic carriers. Sexual transmission between male partners has been described. Health care workers occasionally acquire enteric fever after exposure to infected patients or during processing of clinical specimens and cultures • Worldwide, however, there are an estimated 22 million cases of enteric fever, with 200,000 deaths annually. • In endemic regions, enteric fever is more common in urban than rural areas and among young children and adolescents
  • 5. ETIOLOGY AND PATHOGENESIS Ingestion of contaminated food and water (inoculum dose 103-106cfu) by susceptible host (Stomach acidity, Achlorhydric diseases, Antiacid ingestion, Age <1yr,  Intestinal integrity, IBD, GI Surgery, Broad spectrum antibiotic use)  they penetrate the mucus layer of the gut and traverse the intestinal layer through phagocytic microfold (M) cells that reside within Peyer's patches  After crossing the epithelial layer of the small intestine they are phagocytosed by macrophages  Dissemination throughout the body via lymphatics and colonize RES  Re infection of intestine as well as other body parts via hematogenous dissemination.
  • 6. • 1st week/Invasive • •on set~:headache, bodyache,malise,sorethroat,anorexia • •Gi symptoms-: constipation, tongue coated with raw tips &edges • •Fever-:STEEP LADER low in morning high at night • • bradycardia pulse • •Bronchitis symptoms –cough CLINICAL COURSE
  • 7. • 2nd week /advanced • •T°~high, rose spot rashes • Spleen becomes palpable and constipation replaced by diarrhea • 3rd week/decline • •T° decrease • Intestinal perforation & hemorrhage • Patient may pass in to coma and die • 4th convalescence • Fever subsidies tongue clear pulse becomes rapid
  • 8. DIAGNOSIS ;The definitive diagnosis of enteric fever is CULTURE. In 15–25% of cases, leukopenia and neutropenia are detectable. • Several serologic tests, including the classic Widal test for "febrile agglutinins," are available E X A M S A N D T E S T S • CBC • Blood culture other tests  ELISA  Florecent antibody study  Platelet count  Stool culture
  • 9. PREVENTION AND CONTROL. • Consumptions of properly cooked meal, sanitation • Vaccine for . Travelers to endemic areas • People with close contact with chronic carrier