Enteric cholera amoebiasis- VIKramm.pptx

Bacteria adhere to mucosal cells and then invade the mucosa.
The M cells,
Specialized epithelial cells overlying Peyer’s patches
Site of the entry typhi and its transport to the underlying lymphoid tissue.
Microorganisms translocate to the intestinal lymphoid follicles and the draining mesenteric lymph nodes,
Some pass on to the Reticuloendothelial cells of the liver and spleen

1. ENTERIC FEVER DR VIKRANNTH V ASSOCIATE PROFESSOR

2. ENTERIC FEVER Gram-negative bacteria Belongs to Enterobactericiae Facultative anaerobe

3. Antigenic structure of salmonella Somatic or 0 antigens Contain heat stable long chain polysaccharides ( LPS ) Flagellar or H antigens Strongly immunogenic Induces rapid antibody formation High titers following infection or immunization. Encapsulation or Vi antigen

4. S. typhi causes typhoid fever S. paratyphi A, cause milder form of enteric fever Now Paratyphoid fevers are on rise Fecal-oral route of transmission Person-to-person spread by chronic carrier Fecally-contaminated food or water incubation period is 10-14 day

5. Pathogenesis-Small intestine Bacteria adhere to mucosal cells and then invade the mucosa. The M cells, Specialized epithelial cells overlying Peyer’s patches Site of the entry typhi and its transport to the underlying lymphoid tissue. Microorganisms translocate to the intestinal lymphoid follicles and the draining mesenteric lymph nodes, Some pass on to the Reticuloendothelial cells of the liver and spleen

6. Bactremic phase Salmonella survive and multiply within the mononuclear phagocytic cells Lymphoid follicles, liver, and spleen are involved Release of sequestered intracellular organisms into blood stream depends upon Number of bacteria Their virulence, and The host response, The incubation period is usually 7 to 14 days The organism is widely disseminated in this phase

7. Sites of secondary infection Liver, spleen, bone marrow, gallbladder, and Peyer’s patches Gallbladder invasion Either directly from the blood or Retrograde spread from the bile. Organisms excreted in the bile either reinvade the intestinal wall or excreted in the feces Necrosis of Peyer’s patches Results from intreaction between Immunologic mediators and bacterial factors

8. First week Step ladder pattern fever Morning high reduce in night Peak and trough rise progressively GI symptoms Diffuse abd pain and tenderness in the abdomen Occasionally colicky in RUQ Other symptoms Cough Dull Delerium stupor

9. Second week Fever plateaus 39-40*C Progression of the first week symptoms Rose red spots Abdominal distension Soft splenomegaly Relative bradycardia

10. Rose spots High fever Diarrhea Typhoid Meningitis Aches and pains Chest congestion

11. Rashes in Typhoid Rose spots 2 -4 mm in diameter Raised discrete irregular blanching pink maculae's Found in front of chest Appear in crops Up to a dozen at a time Fade after 3 – 4 days Sign of bacterial emboli

12. Third week – systemic manifestation Crackles over lung bases Severe abdominal distension Sometimes, pea-soup diarrhea foul, green-yellow, liquid diarrhea Typhoid state apathy, confusion, psychosis Bowel perforation and peritonitis Death may occur due to Severe toxemia myocarditis Intestinal hemorrhage

13. Other manifestations HepatoSplenomegaly Acute lobar pneumonia Arthralgias Urinary symptoms Severe jaundice Abscesses Neurological GBS/parkinsonism Pancreatitis Meningitis Orchitis Osteomyelitis

14. Complications

15. Typhoid face Cheeks are usually flushed and the eyes bright (1 st wk) A dull expressionless lethargic face (2 nd and 3 rd wk) Pupils dilated, and the skin and lips dry

16. Haemotological investigations Complete blood count Hemoglobin: Mild anemia Total leucocytic count (TLC):Low to normal Eosinopenia Platelets: Low to normal Liver function tests: Mildly abnormal Serum transaminase levels 2 to3 times the upper limit of normal

17. Diagnosis of enteric fever

18. Widal test Serum agglutinins raise during the 2nd or 3rd week Detects antibodies against O and H antigens Serum specimens tested at intervals of 7 – 10 days to read the raise of antibodies. False positives and false negative limits the utility Interpretation of single serum specimens tested vary Cross reactions limits the specificity

19. Significant Titers for Diagnosis When single sample is tested O > 1 in 160 H > 1 in 320

20. Criteria for the diagnosis Clinical features a. Prolonged pyrexia (more than one week duration) b. Toxemia c. Pulse and fever disproportion d. Splenomegaly and/or hepatomegaly e. Rose spots Laboratory Features a. Positive Widal Test b. Positive bacteriologic culture in the blood, stool or urine c. Histopathologic picture Favorable response to medications against enteric fever

21. Prevention And Treatment

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24. Antibiotic therapy Optimal therapy Alternative effective therapy Susceptibility antibiotic Daily dose mg/kg Days antibiotic Daily dose mg/kg Days Fully sensitive flouroquinolone 15 5-7 Choloramphinicol amoxycillin TMP/MTX 50-75 75-100 8-40 14-21 14 14 Multidrug resistance flouroquinolone Or Cefixime 15 15-20 5-7 7-14 Azithromycin Cefixime 8-20 15-20 7 7-14 Quinolone resistance Azithromycin Ceftrioxome 8-20 75 7 10- 14 Cefixime 20 7-14

25. Typhoid Mary Real name Mary Mallon, worked as a cook in Newyork city in the early 1900s. Was tracked as the common link for many people who had become ill from typhoid fever She was traced to typhoid outbreaks a second time She was put in prison again where she lived until she died.

26. Carriers may be Carriers may be temporary or chronic. Temporary carriers usually excrete bacilli up to 6-8 weeks . By the end of one year, 3-4 per cent of cases continue to excrete typhoid bacilli. Persons who excrete the bacilli for more than a year after a clinical attack are called chronic carriers.

27. Carrier Asymptomatic and have positive stool or rectal swab cultures for S. typhi a year following recovery from acute illness. Treatment: co-trimoxazole 2 tab twice/d for 6 wk, OR ciprofloxacin 750 mg twice/d for 4 wk

28. Prevention Two main typhoid fever prevention strategies:  1. Vaccination First type of vaccine: Contains killed Salmonella typhi bacteria. Administered by a shot. Second type of vaccine: Contains a live but weakened strain of the Salmonella bacteria that causes typhoid fever. Taken by mouth. 

29. Paratyphoid fever It is similar in its symptoms to typhoid fever, but tends to be milder, with a lower fatality rate. It is caused by Paratyphi A, B, and C Rash may be more abundant May present as gastroenteritis specially in children

30. Cholera is an acute diarrheal illness caused by infection of the intestine with the bacteria Vibrio cholerae. CHOLERA

31. CHOLERA Cholera is an acute diarrheal disease that can, in a matter of hours, result in profound, rapidly progressive dehydra- tion and death. Cholera is a toxin-mediated disease . Characteristic watery diarrhea is due to the action of cholera toxin, a potent protein enterotoxin elaborated by the organism after it colonizes the small intestine

32. Gram negative. Distinguishing factors: Oxidase- positive, motile via polar flagellum. Organism can multiply freely in water VIBRIO CHOLERAE

33. Most people remain asymptomatic. The symptoms of cholera include : SIGNS & SYMPTOMS profuse, watery diarrhea stoma c h pains leg cramps Mild fever V omiting Sunken eyes and cheeks Dry mucous membranes Decreased urinary output

34. After a 24- to 48-h incubation period- sudden onset of painless watery diarrhea Hypovolemic shock and death Fever - usually absent Muscle cramps Stool - characteristic : Nonbilious, gray, slightly cloudy fluid with flecks of mucus, no blood, inoffensive odour “ rice-water ” stool - resemblance to the water in which rice has been washed

35. severe dehydration Sho ck Renal failure D e ath COMP L IC A TIONS

36. Detected directly by dark-field microscopy on a wet mount of fresh stool Replacement of fluids, electrolytes, and base Doxycycline (300 mg) is effective in adults Not recommended for children <8 years of age because of possible deposition in bone and developing teeth Tetracycline resistance Ciprofloxacin Erythromycin Single 1-g dose of azithromycin

37. PREVENTION Strict personal hygiene is vital and drinking water should come from a clean piped supply or be boiled Parenteral vaccination and oral vaccines In epidemics, public education and control of water sources and population movement are vital

38. Entamoeba histolytica

39. LIFE CYCLE

40. Pathogenesis Both trophozoites and cysts are found in the intestinal lumen, but only trophozoites of E. histolytica invade tissue Trophozoites attach to colonic mucus and epithelial cells Amebas can lyse neutrophils, monocytes, lymphocytes, and cells of colonic and hepatic lines.

41. Intestinal Amebiasis The earliest intestinal lesions are microulcerations of the mucosa of the cecum, sigmoid colon, or rectum Proctoscopy reveals small ulcers with heaped-up margins and normal intervening mucosa

42. Contrast to bacterial dysentery, which typically begins abruptly , amebic colitis begins gradually over 1 to several weeks Although more than 90% of patients with amebic colitis present with diarrhea, abdominal pain can occur without diarrhea; Weight loss is common because of the chronicity of the illness. Microscopic blood is present in the stool of most patients with amebic dysentery

43. Intestinal Amebiasis Submucosal extension of ulcerations under viable-appearing surface mucosa causes the classic " flask-shaped” ulcer containing trophozoites at the margins of dead and viable tissues.  Rarely, intestinal infection results in the formation of a mass lesion, or ameboma, in the bowel lumen Most feared complication of amebic dysentery, acute necrotizing colitis with toxic megacolon , occurs in 0.5% of cases. This complication manifests as an acute dilatation of the colon