Typhoid neo

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

2. Definition of Typhoid fever mesenteric fever by BAGLIVI in 1696, typhoid fever was given its universal name in 1834. Potentially fatal, multi-systemic illness caused primarily by Salmonella typhi and paratyphi Earlier 100% death rate for the perforations Nowadays, 1 to 39% 3. Typhoid---ancient Greek Typhos, smoke or cloud that was believed to cause disease or madness 4. 430426 B.C. Killed 1/3 of the population of Athens, including their leader Pericles. The power shifted from Athens to Sparta. 2006 study detected DNA sequences similar salmonella 5. Etiology Serotype: Dgroup of Salmonella Gram-negative rod non-spore flagella 6. 1. H(flagellarantigen). 2. O(Somatic orcell wall antigen). 3. Vi (polysaccharide virulence) widel test Antigens: located in the cell capsule 7. Georges Fernand Isidor Widal (1862-1929) Demonstrated specific agglutinins in the blood of Typhoid patient in 1896---- The Widal Reaction 8. Susceptibility and immunity all people equally susceptible to infection immunity is not associated with antibody level of H, Oand VI. No cross immunity between typhoid and paratyphoid. 9. 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 10. epidemiology sporadic occurusually, sometimes have epidemic outbreaks. 11. Susceptibility and immunity All seasons, usually in summerand autumn. Most cases in school-age children and young adults. both sexes equally susceptible. 12. Infects roughly 21.6 million people each year * International Estimate Ramsden AE, Mota LJ, Mnter S, Shorte SL, Holden DW.The SPI-2 type III secretion system restricts motility of Salmonella-containing vacuoles.Cell Kills 200,000 people each year 13. 62% of these occurring in Asia and 35% in Africa * International Estimate * Taylor TE, Strickland GT. Malaria. In: Strickland GT, ed. Hunters Tropical Medicine and Emerging Infectious Diseases. 8th ed. Philadelphia: WB Saunders, 2000:614-43. Highest in Pakistan & India in Asian countries (451.7 per 100,000) 14. fecal-oral route close contact with patients orcarriers contaminated water and food flies and cockroaches. 15. Best prevention Scrub of them off your handsBest prevention Scrub them off your hands 16. S. typhi are able to survive a stomach pH as low as 1.5. Antacids, (H2 blockers), PPIs, gastrectomy, facilitate S typhi infection TYPHOID FEVER RISK FACTORS 17. 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 mononuclear phagocytes spread to blood. initial bacteremia (Incubation period). Pathogenesis 18. Pathogenesis enterspleen, liverand bone marrow (reticulo-endothelial system) furtherproliferation occurs "typhoid nodules A lot of bacteria enter blood again.(second bacteremia). 19. 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 20. PRESENTATION Incubation period is 7-14 days 21. FIRST WEEK TEMPERATURE PATTERN 22. Diffuse abdominal pain, Inflamed Peyer patches narrow the lumen-- Constipation. Dry cough, dull frontal headache, delirium, increasingly Stupor & malaise FIRST WEEK OTHER SYMPTOMS 23. Rose spots, blanching, truncal, maculopapules usually 1-4 cm wide, < 5 in number; these generally resolve within 2-5 days (bacterial emboli to the dermis) FIRST WEEK OTHER SYMPTOMS 24. Distended abdomen, Soft splenomegaly, Relative bradycardia & dicrotic pulse (double beat, the second beat weaker than the first) SECONDWEEK 25. Patient may descend into the typhoid state---apathy, confusion, and even psychosis THIRD WEEK TYPHOID STATE 26. Necrotic Peyer patches, bowel perforation, Peritonitis, intestinal hemorrhage may cause death THIRD WEEK Week of complications 27. Fever, mental state, and abdominal distension slowly improve over a few days, complications may still occur in surviving untreated individuals FOURTH WEEK WEEK OF CONVALESCENCE 28. Clinical forms: Mild infection: symptomand signs mild good general condition temperature is 380 C short period of diseases Persistent infection: diseases continue than 5 weeks Ambulatory infection: mild symptoms,early intestinal bleeding orperforation. Fulminate infection: rapid onset, severe toxemia and septicemia. High fever,chill,circulation failure, shock, delirium, coma, myocarditis, bleeding and othercomplications, DIC 29. Recrudescence 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. Relapse serumpositive of S.typhi after 1 3 weeks of temperature down to normal. Symptomand signs reappear 30. Diagnosis Epidemiology data Typical symptoms and signs Laboratory findings. 31. Laboratory findings Routine examinations: white blood cell count is normal ordecreased. Leukocytopenia(specially eosinophilic leukocytopenia). Blood culture: 80~90% positive during the first 2 weeks of illness Serological tests (Widal test) 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. BASU 32. Serological tests(Vidal test): five types of antigens: somatic antigen(O),flagella(H) antigen, and paratyphoid fever flagella(A,B,C) antigen. "O"agglutinin antibody titer 1:80 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 nonspecifically elevated by immunization previous infections or anamnestic reaction. 33. MINORCOMPLICATIONS 34. Bilateral Salmonella typhi breast abscess unmarried 35-year-old female without any predisposing conditions 35. MEDICALCOMPLICATIONS 36. MAJORSURGICALCOMPLICATIONS 37. Morbidity 55.4%mortality 28.5 % INTESTINAL PERFORATIONS 5% of people withtyphoid fever experience this complication DS00538 April 10, 2008 1998-2009 Mayo Foundation for Medical Education and Research (MFMER). Typhoid enteric perforation, Dr Y. Akgun *, B. Bac, S. Boylu, N. Aban, I. Tacyildiz, British Journal of Surgery Volume 82 Issue 11, Pages 1512 - 1515 Published Online: 8 Dec 2005 38. Pathology in ileum 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 39. (PEYERS PATCHES) 40. (TYPHOID NODULE) 41. 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. 42. 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 43. MECHANISM OF INTESTINAL PERFORATION Intestinal peyers patches 44. Ileum especially distal ileum,jejunum usually doesnot perforate in typhoid, usually happens in the third week 45. 2 or 3 weeks hx of disease, with suddenly worsening of pain & general conditions, Tenderness starts in his right lower quadrant, spreads and eventually becomes generalized, Guarding , (seldom the board-like rigidity) Erect film, shows gas Under diaphragm (50% positive) lateral decubitus film, shows gas under his abdominal wall PRESENTATINPERFORATION The bradycardia and leucopenia of typhoid may occasionally mask the tachycardia and leucocytosis of peritonitis 46. PATIENTPERFORATION 47. If peritonitis seems to be localized, signs confined to only part abdomen, general condition is good, patient not deteriorating, consider non-operative treatment. CONSERVATIVE SURGICALVS If signs of generalized peritonitis, do a laparotomy 48. Suck and drip Resuscitation, antibiotics, pass a NG-tube, Monitor abdominal tenderness, pulse, temperature, white blood count. If any of these rise, suspect that peritonitis is extending, so take an erect X-ray film of his abdomen CONSERVATIVE MANAGEMENT 49. MDR-area MDR+NAR-area MEDICATION TREATMENT WHO RECOMMENDATIONS 50. Operate as early as possible, Do as much as necessory & as little as possible SURGICAL MANAGEMENT PREPARATION Adequately resuscitate, Maintain good urine output, pass nasogastric tube down, Start chemotherapy. 51. SurgerySteps 52. SurgerySteps 53. SurgerySteps 54. SurgerySteps 55. INTESTINAL HEMORRHAGE Occurs in 10-20 per cent of the cases 56. Intestinal bleeding is often marked by a sudden drop in blood pressure and shock, followed by the appearance of blood in stool Hemorrhagepresentation 57. replace the blood loses. Bleeding usually stops spontaneously Only operate if bleeding is persistent, or alarmingly INTESTINAL HEMORRHAGE 58. Surgery Intestinal Hemorrhage 59. Occurs in 1-2% of cases *According to Indian study 8% More common in children Antibiotic resistance & virulence of bacteria *M.L. Kulkarni, SJ. Rego, Department of Pediatrics, J.J.M. Medical College, Davangere 577 004. Acute Acalculous CholecystitisTYPHOID 60. Acute Acalculous CholecystitisTYPHOID *Thi