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Typhoid Fever

Typhoid Fever. Dr.kibruyisfawe OCT, 2012. Epidemiology. Typhoid/enteric fever is endemic in most developing countries in Africa, Asia and Latin America It is primarily a disease of children and young adults In developed countries it occurs in travelers to endemic regions

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Typhoid Fever

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  1. Typhoid Fever Dr.kibruyisfawe OCT, 2012

  2. Epidemiology • Typhoid/enteric fever is endemic in most developing countries in Africa, Asia and Latin America • It is primarily a disease of children and young adults • In developed countries it occurs in travelers to endemic regions • Man is the ONLY reservoir of Salmonella typhi • It is transmitted by ingestion of food/water contaminated by feces of patients/carriers

  3. Epidemiology contd. • Up to 10% of patients continue to excrete the organism in feces for three months • 2-3% become chronic carriers; excrete the organism for > six months • S. typhi had become increasingly resistant to a number of 1st line antibiotics

  4. Etiology • Typhoid fever is caused by S. typhi; S. enterica, subspecies enterica, serotype typhi • It is a Gram negative, aerobic, non spore forming organism • It contains: • LPS, lipolysaccharide • Oligosaccharide somatic antigen “O” antigen • Flagella “H” antigen • Virulence “Vi’ antigen

  5. Pathogenesis • The portal of entry is the gastrointestinal tract • Infecting dose, ID50, is 1000,000 organism • Organism destroyed by acid in stomach • Achlorhydria, treatment with H-2 receptor antagonists lowers the infecting dose • Incubation period is 7-10 days • Organism multiplies within mononuclear phagocytic cells of the intestinal lymphoid follicles

  6. Pathogenesis contd. • After initial intracellular replication the organism is released into the circulation: • Sustained bacteremia • Widely disseminated and seeds the liver, spleen, bone marrow, gall bladder, Peyer’s patches • It induces local and systemic humoral and cellular responses • Endotoxin may activate clotting/fibrinolytic cascade • Local inflammation at Peyer’s patches may cause tissue necrosis

  7. Clinical manifestations • The onset is usually sub acute • During the 1st week, temperature rises in stepladder fashion, and remains constant • Patients develop headache, dry cough, abdominal pain • By the end of the 1st week patients become ill/confused • Liver and spleen palpable in about 50% of cases

  8. Clinical manifestations contd. • Relative bradycardia, pulse temperature dissociation may be observed • Rose spots, pink macules, may be present • During the 2nd and 3rd week patients are more ill • They have apathetic affect, “typhoid facies” • Various neurological complications may occur in 10-40% of cases

  9. Complications • With appropriate therapy mortality <1% • In some endemic regions it may be as high as 30% • Perforation is the most serious complication • Occurs in about 1-3% of patients • GI bleeding, in about 10% of patients • Relapse occurs in 5-10% of patients • Chronic carriers in about 3%

  10. Laboratory diagnosis • In the 1st week blood culture positive in nearly all patients • Bone marrow cultures may be positive • Serological test, the Widal test becomes positive in 7-10 days • A four-fold rise in titer • A single titer of >1/160 WITH compatible clinical illness • False positive/negative results are common

  11. Blood culture Urine Culture Stool culture 100 Serum agglutinins 90 80 % Positive 70 60 50 40 Presence of S. typhi in blood urine and stool, and rise of antibodies after ingestion of the organism 30 20 10 0 1 2 3 5 6 7 8 Weeks 4

  12. Management • The aim of management is to kill the organism and correct effect of septicemia • Most patients are treated at home • For hospitalized patients, good nursing care, adequate nutrition, fluid/electrolytes • Recognition and management of complications • Multi drug resistant S. typhi increasing

  13. Antibiotic treatment • 1st line drugs • Amoxicillin,50-100mg/kg, 14 days • TMP/SMX,8/40mg/kg, 14 days • Chloraphenicol, 50-75mg/kg, 14 days • 2nd line drugs • Floroquinolones, ciprofloxacin 15mg/kg, 5-7 days • 3rd generation cephalosporin, ceftrixone 50mg/kg/day, IV/IM

  14. Adjunct therapy • Dexamethasone, 3mg/kg, IV for 48 hours • Perforation is usually managed by surgery • Sever GI bleeding may require blood transfusion

  15. Prevention and control • Provision of clean, piped water supply • Proper waste disposal • Vaccines • TAB, parentral inactivated whole organism • Ty21A, oral mutant strain, 60-70% protection for up to 3 years • Vi based, single injection, 65-70% protection after 1 year

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