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Gastrointestinal Infections

Gastrointestinal Infections. III MBBS. Objectives. Impact General principles of pathogenesis in the GI tract Types of diseases Describe the usual cause of gastroenteritis Describe the signs and symptoms Interpret diagnostic tests to determine etiology of gastroenteritis

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Gastrointestinal Infections

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  1. Gastrointestinal Infections III MBBS Dr Ekta, Microbiology

  2. Objectives • Impact • General principles of pathogenesis in the GI tract • Types of diseases • Describe the usual cause of gastroenteritis • Describe the signs and symptoms • Interpret diagnostic tests to determine etiology of gastroenteritis • Treat selected patients with gastroenteritis Dr Ekta, Microbiology

  3. Impact • Diarrhoea • most common outcome of GIT infection • the greatest single cause of morbidity and mortality in the developing world • usually a self limiting condition Dr Ekta, Microbiology

  4. General Principles in Pathogenesis • Encounter - frequently from food or water contaminated by soil or feces; animals often the reservoir • Entry - feco-oral route (ingestion) • Spread - rare except for enteric • Multiplication - mostly extracellular; organisms that cause dysentery may invade intestinal epithelium • Evasion of Host Defenses - adherence, resistance to acid and bile • Damage - cell killing, toxins, inflammation • Transmission - lack of sanitation and clean water, improper food handling Dr Ekta, Microbiology

  5. Pathogenesis - General mechanism Dr Ekta, Microbiology

  6. Types of GIT Infections and Their Symptoms • Gastroenteritis / Food Poisoning – syndrome characterized by GIT symptoms like nausea, vomiting, diarrhoea & abdominal discomfort • Diarrhea – Excess fluid in the intestinal lumen results in frequent, loose, watery stools. • Inflammatory diarrhea or dysentery – inflammation of the intestine with passage of frequent stools containing blood and pus; abdominal cramps and fever • Enteric fever – fever, headache, lethargy, shock, splenomegaly • Stomach ulcers – stomach pain • Worm infestations – blockage of GI tract; malnutrition Dr Ekta, Microbiology

  7. Damage resulting from Infection of the GIT • Pharmacologic action of bacterial toxins, local or distant to site of infection e.g. cholera, staphylococcal food poisoning • Local inflammation in response to superficial microbial invasion e.g. shigellosis, amebiasis • Deep invasion to blood or lymphatics; dissemination to other body sites e.g. enteric fever, hepatitis A • Perforation of mucosal epithelium after infection, surgery or accidental trauma e.g. peritonitis, intra-abdominal abscesses. Dr Ekta, Microbiology

  8. Pathogenic Mechanisms Toxin production Enterotoxin Vibrio cholerae / NCV Enterotoxigenic E coli Clostridium difficile (toxin A) Campylobacter jejuni Cytotoxin Shigella spp Enterohemorrhagic E coli Clostridium difficile (toxin B) Neurotoxin Clostridium botulinum Staphylococcus aureus Bacillus cerues Dr Ekta, Microbiology

  9. Pathogenic Mechanisms Attachment to mucosal cells Enteropathogenic E coli Cryptosporidium parvum Isospora belli Rota virus Hepatitis A Norwalk virus Dr Ekta, Microbiology

  10. Pathogenic Mechanisms Invasion Shigella spp Enteroinvasive E coli Yersinia entero colitica Entamoeba histolytica Balantidium coli Norwalk virus Dr Ekta, Microbiology

  11. Gastroenteritis/ Food Poisoning • Inflammation of GI tract • Occurs due to consumption of food containing toxins, which may be due to • microbes secreting toxins (preformed toxins)or • chemicals (Heavy metal like arsenic, lead, Hg, cadmium) • Acute onset • Usually < 10 days • Self limiting Dr Ekta, Microbiology

  12. Causes of Food Poisoning • Staphylococcus aureus – most common cause • Clostridium perfringins – caused by cooked meat products that have not been properly stored • Bacillus cereus – “fried rice” food poisoning • Clostridium botulinum – neurological symptoms only, no GI symptoms Dr Ekta, Microbiology

  13. Bacteria Vibrio cholerae Enterotoxigenic E. coli (ETEC) Enteropathogenic E. coli (EPEC) Enterohemorrhagic E. coli (EHEC) Campylobacter jejeuni (most common in US) C.difficile Viruses Rotavirus Corona viruses Norwalk virus Adenovirus Calicivirus Parasites Giardia lamblia Cyclospora and Cryptosporidium Causes of Diarrhea Dr Ekta, Microbiology

  14. Causes ofDysentery • Shigella • Enteroinvasive E. coli • Campylobacter jejeuni • Salmonella enterica • Vibrio parahemolyticus • Entamoeba histolytica Dr Ekta, Microbiology

  15. More Causes • Enteric Fever • Salmonella typhi • Salmonella enterica • Stomach Ulcers • Helicobacter pylori • Others • Broad spectrum antibiotics • Antacids • Laxatives • Cardiac medicines Dr Ekta, Microbiology

  16. History • Ingestion of potentially contaminated food or untreated water • Recent travel • Sick contacts • Recent antibiotic use • Outbreaks • Bloody diarrhea Dr Ekta, Microbiology

  17. Shorter incubations go with intoxications and upper GI symptoms (e.g., nausea and vomiting) Longer incubations go with infections and lower GI symptoms (e.g., abdominal cramps and diarrhea) Foodborne Illness (FBI) - Rule of Thumb Dr Ekta, Microbiology

  18. Incubation Period: Short Minute to hours Chemical toxins E.g., copper poisoning VOMITING Neurotoxins, histamine, allergens E.g. Shellfish toxins Dr Ekta, Microbiology

  19. Incubation Period: Short to medium 1-12 hours Bacterial enterotoxins E.g., Staphylococcal or Bacillus cereus VOMITING +/- DIARRHOEA Dr Ekta, Microbiology

  20. Incubation Period: Long 6 hours – 10 days Bacterial infections E.g., Salmonella E. Coli O157:H7 Campylobacter Yersinia Dr Ekta, Microbiology

  21. Staphylococcal Food Poisoning • Scenario – church picnic • Encounter– from skin, nose, or wound of infected person • Entry – bacteria gets in food via contact; toxin gets in person via ingestion • Spread– toxin spreads • Multiplication – only in food, not person • Avoid Host Immune Response – resistant to stomach acid • Damage– enterotoxins (superantigens) • Transmission - none Dr Ekta, Microbiology

  22. Clostridium perfringens Food Poisoning • Scenario – cold meat pie • Encounter – spores contaminate meat, germinate on storage of cooked stews, etc. • Entry - ingestion • Spread – toxin may spread, bacteria do not • Multiplication – bacteria sporulate, don’t replicate; in a food borne infection the bacteria replicate • Avoid Host Immune Response – bacteria are acid resistant • Damage – toxin increases capillary permeability resulting in ileal fluid accumulation. It accounts for about 20% of bacterial diarrhoea. • Transmission - none Dr Ekta, Microbiology

  23. Clostridium perfringens Food- associated infections Dr Ekta, Microbiology

  24. Bacillus cereus Food Poisoning • Scenario – Chinese restaurant • Encounter – spores are in soil, on rice • Entry – toxin ingested • Spread – toxin may spread • Multiplication – only in food • Avoid Host Immune Response – toxin resistant to acid • Damage - toxin • Transmission - none Dr Ekta, Microbiology

  25. Bacillus cereus Food Poisoning Dr Ekta, Microbiology

  26. Clostridium botulinum Food Poisoning • Scenario • Encounter - Home canned vegetables, potatoes, fish & preserved sea food • food contaminated with spores • anaerobic conditions • Entry - Ingestion • Spread – toxin spreads from GI tract to nerve terminals hematogenously • Multiplication - NONE • Avoid Host Immune Response • Toxin: Resistant to proteolysis in stomach due to 2° accessory proteins • Absorption: Alkaline pH of intestine dissociates toxin from proteins, allows absorption into circulation • Damage – exotoxin produces flaccid paralysis Dr Ekta, Microbiology

  27. Pathogenesis of Viral diarrhoea Dr Ekta, Microbiology

  28. Diagnosis • Gross & microscopic stool examination • Stool culture • Identification tests • Endoscopy if noninfectious etiology suspected (inflammatory bowel disease) Dr Ekta, Microbiology

  29. Lab Diagnosis of GIT Infections Specimens Stool / feces Rectal swab Duodenal aspirate Specimens must be delivered to lab within 1 hr Delay of > 2 hr anticipated use transport medium (Cary-Blair TM) Rectal swab in Stuart’s transport or viral TM stored in refrigerated if delay > 2 hrs Dr Ekta, Microbiology

  30. Lab Diagnosis of GIT Infections Direct wet mount Ova & parasites Fecal leukocytes Gram stain Campylobacter Vibrio Modified Acid fast Cryptosporidium Isospora Parasites Trichrome stain Dr Ekta, Microbiology

  31. Lab Diagnosis of GIT Infections Antigen detection test Giardiasis Fluorescent antibody stain Cryptosporidiosis E coli 0157:H7 ELISA / LA Rota virus Cryptosporidium Giardia Dr Ekta, Microbiology

  32. Lab Diagnosis of GIT Infections Culture BA / MAC / XLD / SS / TCBS / Selenite F broth Identification tests Antibiotic susceptibility test – if needed Dr Ekta, Microbiology

  33. Lab Diagnosis of GIT Infections Report & Interpretations Simple diarrhea Antibiotic rarely beneficial Antibiotics indicated if evidence of invasion C difficile: stop antibiotics and start on metro / vanco Isolation of pathogens in stool samples must be notified to public health authority Dr Ekta, Microbiology

  34. Treatment • Rehydration – oral vs. IV • Antiemetics • Antidiarrheals • Decrease intestinal motility • Diphenoxylate, loperamide, codeine • +/- antibiotics • Shigella, Yersinia, campylobacter, cholera, C.difficile, giardia Dr Ekta, Microbiology

  35. Dr Ekta, Microbiology

  36. The End! Dr Ekta, Microbiology

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