Typhoid neo

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Typhoid

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  • 1.TYPHOID FEVER AND PARATYPHOID FEVER Dr nawin kumarDr nawin kumar

2. Typhoid and Paratyphoid Definition Etiology Pathogenesis Epidemiology Clinical manifestations The laboratory and other examinations Complications Diagnosis and differential diagnosis Prognosis Treatment Preventions Paratyphoid Fever 3. Definition of Typhoid fever Acute enteric infectious disease caused by Salmonella typhi (S.Typhi). prolonged fever, Relative bradycardia, apathetic facial expressions, roseola, splenomegaly, hepatomegaly, leukopenia. 4. haemorrhage; perforation; cholecystitis; phlebitis; genitourinary inflammation; arthritis osteomyelitis. 5. Etiology Serotype: Dgroup of Salmonella Gram-negative rod non-spore flagella Culture characteristics 6. Antigens: located in the cell capsule H(flagellarantigen). O (Somatic orcell wall antigen). Vi (polysaccharide virulence) widel test 7. Endotoxin A variety of plasmids Resistance: Live 2-3 weeks in water. 1-2 months in stool. Die out quickly in summer Resistance to drying and cooling 8. Epidemiology continues to be a global health problem areas with a high incidence include Asia, Africa and Latin America affects about 6000000 people with more than 600000 deaths a year. 80% in Asia . sporadic occurusually, sometimes have epidemic outbreaks. 9. Source of infection Cases and chronic carriers Cases discharge fromincubation, more in 2~4 weeks afteronset, a few (about 2~5%) last longerthan 3 months chronic carrier TyphoidMary 10. Transmission fecal-oral route close contact with patients orcarriers contaminated waterand food flies and cockroaches. 11. Susceptibility and immunity all people equally susceptible to infection acquired immunity can keep longer, reinfection are rare immunity is not associated with antibody level of H, Oand VI. No cross immunity between typhoid and paratyphoid. 12. Susceptibility and immunity All seasons, usually in summerand autumn. Most cases in school-age children and young adults. both sexes equally susceptible. 13. Pathogenesis gastrointestinal tract host- pathogen interactions The amount of bacilli infection (>105 baeteria). 14. ingested orally Stomach barrier(some Eliminated) enters the small intestine Penetrate the mucus layer entermononuclearphagocytes of ileal peyer's patches and mesenteric lymph nodes proliferate in mononuclearphagocytes spread to blood. initial bacteremia (Incubation period). Pathogenesis 15. Pathogenesis enterspleen, liverand bone marrow (reticulo- endothelial system) furtherproliferation occurs A lot of bacteria enterblood again. (second bacteremia). Recovery 16. S.Typhi. stomach Lower ileum peyer's patches & mesenteric lymph nodes thoracic duct 1st bacteremia (Incubation stage) 10-14d (mononmonon uclearuclear phagocphagoc ytesytes ) 2nd bacteremia liver spleen gall BM ,ect early stage&acme stage (1-3W LN Proliferate,swell necrosis defervescence stage 3-4w Bac. In gall Bac. In feces S.Typhi eliminated convalvescence stage (4-5w) Enterorrhagia,i ntestinal perforation 17. Pathology essential lesion: proliferation of RES (reticuloendothelial system) specific changes in lymphoid tissues and mesenteric lymph nodes. "typhoid nodules Most characteristic lesion: ulceration of mucous in the region of the Peyers patches of the small intestine 18. (PEYERS PATCHES) 19. (TYPHOID NODULE) 20. Majorfindings in lowerileum Hyperplasia stage(1st week): swelling lymphoid tissue and proliferation of macrophages. Necrosis stage(2nd week): necrosis of swelling lymph nodes or solitary follicles. 21. Majorfindings in lowerileum Ulceration stage(3rd week): shedding of necrosis tissue and formation of ulcer----- intestinal hemorrhage, perforation . Stage of healing (from4th week): healing of ulcer, no cicatrices and no contraction 22. Clinical manifestations Incubation period: 3 60 days(7 14). The initial period (early stage) First week. Insidious onset. Feverup to 39~400 C in 5~7 days chills ailment tired sore throat cough ,abdominal discomfort and constipation 23. The fastigiumsatge second and third weeks. Sustained high fever partly remittent feverorirregularfever. Last 10 14 days. Gastro-intestinal symptoms: anorexia abdominal distension orpain diarrhea orconstipation Neuropsychiatric manifestations: confusion blunt respond even delirium and coma ormeningism 24. Circulation system: relative bradycardia ordicrotic pulse. splenomegaly hepatomegaly toxic hepatitis. roseola :30%, maculopapularrash a faint pale color, slightly raised round orlenticular, fade on pressure 2-4 mmin diameter, less than 10 in number on the trunk, disappearin 2-3 days. 25. fatal complications: intestinal hemorrhage intestinal perforation severe toxemia 26. defervescence stage feverand most symptoms resolve by the forth weekof infection. Fevercome down, gradual improvement in all symptoms and signs, but still danger. convalescence stage the fifth week. disappearance of all symptoms, but can relapse 27. Clinical forms: Mild infection: very common seen recently symptomand signs mild good general condition temperature is 380 C short period of diseases recovery expected in 1~3 weeks seen in early antibiotics users young children mild more easy to misdiagnose 28. Persistent infection: diseases continue than 5 weeks Ambulatory infection: mild symptoms,early intestinal bleeding or perforation. 29. Fulminate infection: rapid onset, severe toxemia and septicemia. High fever,chill,circulation failure, shock, delirium, coma, myocarditis, bleeding and othercomplications, DIC 30. Special manifestations In children Often atypical sudden onset with high fever. Respiratory symptoms and diarrhea, dominant. Convulsion common in below 3. relative bradycardia rare. Splenomegaly, roseola and leucopenia less common. 31. In the aged temperature not high, weakness common. More complications.high mortality. 32. clinical manifestations reappear less severe than initial episode Its temperature recrudesce when temperature start to step down but abnormal in the period of 2-3 weeks and persist 5~7 days then backto normal. seen in patients with short therapy of antibiotics. Recrudescence 33. relapse serumpositive of S.typhi after 1 3 weeks of temperature down to normal. Symptomand signs reappear the bacilli have not been completely removed Some cases relapse more than once 34. Laboratory findings Routine examinations: white blood cell count is normal or decreased. Leukocytopenia(specially eosinophilic leukocytopenia). recovery with improvement of diseases decreased in relapse 35. Bacteriological examinations: Blood culture: the most common use 80~90% positive during the first 2 weeks of illness 50% in 3rd week not easy in 4th week re-positive when relapse and recrudesce attention to the use of antibiotics 36. The bone marrow culture the most sensitive test specially in patients pretreated with antibiotics. Urine and stool cultures increase the diagnostic yield positive less frequently stool culture betterin 3~4 weeks The duodenal string test to culture bile useful forthe diagnosis of carriers. Rose spots: Not use routinely 37. Serological tests(Vidal test): five types of antigens: somatic antigen(O),flagella(H) antigen, and paratyphoid fever flagella(A,B,C) antigen. Antibody reaction appearduring first week 70% positive in 3~4 weeks and can prolong to several months in some cases, antibodies appearslowly, orremain at a low level, some(10~30%) not appearat all. 38. "O"agglutinin antibody titer1:80 and "H" 1:160 or"O"4 times highersupports a diagnosis of typhoid fever "O"rises alone, not "H", early of the disease.Only "H" positive, but "O"negative, often nonspecifically elevated by immunization orprevious infections or anamnestic reaction. Antibody level maybe lowerwhen have used antibiotics early. 39. Some cross reaction between group D and A. False positive in some infectious diseases. Some positive in blood culture ,but negative in vidal test. 'Vi" often useful forcarrier(1:40) molecularbiological tests: DNA probe orpolymerase chain reaction (PCR) 40. Complications Intestinal hemorrhage Commonly appearduring the second-third week of illness difference between mild and greaterbleeding often caused by unsuitable food, diarrhea etc serious bleeding in about 2~8% a sudden drop in temperature rise in pulse and signs of shockfollowed by darkorfresh blood in the stool. 41. Intestinal perforation: The more serious .Incidence,1-4% Commonly appear during 2-3 weeks. Take place at the lowerend of ileum. Before perforation,abdominal pain or diarrhea,intestinal bleeding . When perforation, abdominal pain, sweating, drop in temperature, and increase in pulse rate, then, rebound tenderness when press abdomen, abdomen muscle entasia, reduce ordisappearin the sonant extent of liver, leukocytosis . Temperature rise .peritonitis appear. celiac free airunderx-ray. 42. Toxic hepatitis: common,1-3 weeks hepatomegaly, ALT elevated get betterwith improvement of diseases in 2~3 weeks Toxic myocarditis. seen in 2-3 weeks, usually severe toxemia. Bronchitis, bronchopneumonia. seen in early stage 43. Othercomplications: toxic encephalopathy. Hemolytic uremic syndrome. acute cholecystitis meningitis nephritis et al. 44. Diagnosis Epidemiology data Typical symptoms and signs Laboratory findings. 45. Differential diagnosis Viral infections: such as upperrespiratory tract infection. abrupt onset with fever, headache, leucopenia, sore throat, cough, coryza. no rose spots, no enlargement of liver& spleen. The course of illness no more than 2 wks. differential diagnosis depends on typical manifestations and blood culture. 46. Malaria history of exposure to malaria. Paroxysms(often periodic) of sequential chill,high feverand sweating. Headache, anorexia, splenomegaly, anemia, leukopenia Characteristic parasites in erythrocytes,identified in