Typhoid neo
- 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. 430–426 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”, “O”and “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, Münter 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. Hunter’s 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), PPI’s, 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
- 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 • It’s 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.
- 34. Bilateral Salmonella typhi breast abscess unmarried 35-year-old female without any predisposing conditions
- 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 Peyer’s patches of the small intestine
- 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 peyer’s 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
- 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
- 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 *Thickened gall bladder wall, sonographic Murphy's sign, pericholicystic collection in the absence of gall stones *Subha Rao SD, LewinS, Shetty B, et al. Acute acalculous cholecystitis in typhoid fever. Indian Pediatr 1992, 29: 1431-1435.
- 61. Chronic Cholecystitis (Carriers)TYPHOID Excretes bacteria in stools for more > 1 year1-4% of non- treated infected patients become chronic carriers Patients with cholelithiasis, biliary anomalies, females, Salmonella can be cultured from stools, duodenal aspirate, gall stones
- 62. Mary Mallon (September 23, 1869 – November 11, 1938) Forcibly quarantined twice, she infected 47 people, three of whom died. She died in quarantine.
- 63. Chronic CholecystitisTYPHOI D Biliary anomalies, stones--requires cholecystectomy + antibiotics 4-6 weeks antibiotic treatment
- 66. • Prophylaxis 1.control source of infection Isolation and treatment of patients stool culture one time per5 days. if negative continued two times ,without isolation. Control of carriers. observation of 25 days(15 days in paratyphoid) when close contact
- 67. 2. Cut of course of transmission key way avoid drinking untreated waterand food. 3.Vaccination side-effect more, less use
- 68. Ty21a—Oral live attenuated vaccine
- 70. Paratyphoid feverA,B,C • Caused by Salmonella paratyphoid A,B,C.respectively. • in no way different fromtyphoid feverin epidemiology, pathogenesis, pathology,clinical manifestations, diagnosis, treatment and Prophylaxis
- 71. Paratyphoid A,B: • incubation period 2~15days, in genaral,8~10 days. • milderin severity • fewerin complications. • Betterin prognosis, • relapse more common in Paratyphoid A. • Treatment same as in typhoid fever.
- 72. Paratyphoid C: • Always sudden onset. • Rapid rise of temperature. • Presented in different forms-- Septicemia, Gastroenteritis and Enteric fever • Complications--arthritis, abscess formation, cholecystitis, pulmonary complications are commonly seen. • Intestinal hemorrhage and perforation not as common as in typhoid fever.
- 74. 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.
- 75. Intestinal perforation: • a very severe condition in tropical countries • incidence ranges from 0.9 to 39% (8), • mortality rate ranging from 27% to 77% • the mortality and the morbidity rate depend – on the general status of the patient, – the virulence of the germs – the duration of disease evolution – Less on the surgical technique, • adequate pre-operative management • aggressive resuscitation with antibiotherapy
- 76. • Rent closure • Resection anastomosis – Last 60 centimeters of the ileum -high concentration of peyer’s patches whose infection is a source of intestinal perforation – Digestive fistula - most threatening – anastomotic leakage- suturing is performed in a septic environment – new perforation
- 77. postoperative complications • Resection with temporary ileostomy – avoiding any intestinal suture in septic tissues – management of stoma – Peristomal ulceration – awful skin pain –self limitation of food intake. denutrition, cachexia and death • postoperative septic shock
- 78. Intestinal perforation: • 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.
- 79. • 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
- 80. Othercomplications: • toxic encephalopathy. • Hemolytic uremic syndrome. • acute cholecystitis 、 • meningitis 、 • nephritis et al.
- 81. TREATMENT General treatment • isolation and rest • good nursing care and supportive treatment close observation T,P,R,BP,abdominal condition and stool . suitable diet include easy digested food orhalf- liquid food.drinkmore water intravenous injection to maintain waterand acid- base and electrolyte balance
- 82. • Symptomatic treatment: forhigh fever: • physical measures firstly • antipyretic drugs such as aspirin should be administrated with caution • delirium,coma orshock,2-4mg dexamethasone in addition to antibiotics reduces mortality.
- 83. Etiologic and special treatment 1.Quinolones: first choice it’s highly against S.typhi penetrate well into macrophages,and achieve high concentrations in the bowel and bile lumens • Norfloxacin (0.1～ 0.2 tid ～ qid/10～ 14 days). • Ofloxacin (0.2 tid 10～ 14days). • ciprofloxacin (0.25 tid) caution: not in children and pregnant
- 84. 2.Chloramphenicol: • Forcases without multiresistant S.typhi. • Children in dose of 50～ 60mg/kg/perday. • adult 1.5～ 2g/day. tid. • Unable to take oral medication, the same dosage given introvenously • afterdefervescence reduced to a half. complete a 10 ～ 14 day course. • But ,drug resistance, a high relapse rate,bone marrow toxicity.
- 85. 3.Cephalosporines: Only third generation effective Cefoperazone and Ceftazidime. 2～ 4g/day .10~14 days. 4.Treatment of complication. • Intestinal bleeding: bed rest, stop diet,close observation T,P,R,BP. intravenous saline and blood transfusion,and attention to acid-base balances. sometimes,operative.
- 86. • Perforation: early diagnosis. stop diet. decrease down the stomach pressure. intravenous injection to maintain electrolyte and acid-base balances. use of antibiotics. sometimes operative.
- 87. • Toxic myocarditis: bed rest, cardiac muscle protection drugs, dexamethasone, digoxin. 5.Chronic carrier: • Ofloxacin 0.2 bid orciprofloxacin 0.5 bid, 4～ 6 weeks. • Ampicillin 3～ 6g/day tid plus probenecid 1～ 1.5g/day. 4～ 6 weeks. • TMP+SMZ 2 tabs. Bid. 1～ 3 months. • Cholecystitis may require cholecystectomy.