1. BACTERIAL INFECTIONS OF GIT Assistant Professor Microbiology Syed Yousaf Kazmi College of Medicine, Majmaah University

2. OBJECTIVES 1.Maj Bacteria causing GIT Infections, epidemiology, etiology and pathogenesis 2.Mechanism of transmission, Enlist clinical conditions 3.Discuss laboratory diagnosis

3. INTRODUCTION Digestive system-maj route of entry of pathogen Local defenses are strong to keep infection away o Mechanical & Physiological o Immunity (MALT etc) o Microbial Flora Digestive diseases are usually associated with: o Crowding o Poor hygiene o Contaminated food or water

4. INTRODUCTION GIT Infections are of two types o Exogenous infection -where org are introduced from outside o Endogenous infection -where infection is associated due to normal flora Endogenous infections are caused by organisms that are part of the normal flora. o Viridans Streptococcus, Actinomyces isreali In the right circumstances they can cause: o Dental diseases. o Infections of the bowel, appendix, and liver. o Diverticular abscesses.

5. CLINICAL CONDITIONS 1.GASTROENTERITIS a.Non inflammatory (No WBCs in stool) b.Inflammatory (WBCs in stool) c.Invasive (WBCs, RBCs, Mucus in stool) 3.FOOD POISONING 4.DYSENTERY 5.ENTEROCOLITIS, PSEUDOMEMBRANOUS COLITIS 6.PEPTIC ULCER DISEASE 7.DIVERTICULITIS 8.APPENDICITIS 9.DENTAL CARIES, PERIODONTITIS

6. GASTROENTERITIS Most infections of GIT are Gastroenteritis Mainly of two types o Intoxication (Ingestion of toxins) e.g. Staph aureus, Bacillus cereus, Clostridium perfringens o Infections ( Ingestion of bacteria) e.g. Vibrio cholerae, Shigellosis, Campylobacter jejuni Modes of contamination of food or water Many microbes are present in healthy animal’s intestine- contaminate during slaughter e.g. Campylobacter spp, Salmonella spp Washing of fruits/ veg with contaminated water Hands of food handler Sewage contamination of drinking water

7. NON INFLAMMATORY GASTROENTERITIS

8. INTOXICATION- STAPH AUREUS Gram positive cocci, Catalase & coagulase +ve Secretes enterotoxin Food contaminated from boil/ abscess of food handler or from nose during sneeze Type of food meat, fish, cream filled pastries, egg salad Incubation Period 1-6hrs Nausea, vomiting, abdominal cramps, diarrhea Mnemonic: (Staph starts with S, Shank for vomiting)

9. INTOXICATION- CLOSTRIDIUM PERFRINGENS  C. pergringens-Obligate anerobe, Gram +ve spore forming rod  Protein rich food-beef, poultry, fish,  Survive cooking-germinate & secrete enterotoxin  Moderate to severe abdominal cramps, diarrhea  Recovery usually in 1-2 days  Antimicrobials usually not req  Mnemonic C. perf starts with C, C for Commode

10. INTOXICATION- BACILLUS CEREUS Gram +ve spore forming rod Spores germinate after reheating of rice/ Chinese food Vomiting after 2-6 hours Recovery in 2-3 days Antimicrobials usually not req

11. INFLAMMATORY GASTROENTERITIS

12. INFECTION- VIBRIO CHOLERAE Gram –ve curved rod Contaminated water or raw seafood Extremely susceptible to acid 10 5 -10 8 org req Release toxin-enterocytes - ↑cAMP-loss of water & electrolytes Profuse vomiting and diarrhea (rice water stool) Extreme dehydration Renal failure, acidosis- death

13. INFECTION-ESCHERICHIA COLI Gram –ve facultative anaerobe Normal fecal flora but various serotypes can be pathogenic Enterotoxigenic E. coli (ETEC) T for Traveller o Commonest cause of Traveller’s diarrhea o Secrete enterotoxins like cholera o Eating of raw veg, fruits, drinking unhygienic water o Diarrhea, vomiting, abd cramps, fever o Diarrhea last for 3-7 days Enteropathogenic E. coli (EPEC) P for Pediatric o Diarrhea in infant o Associated with poor sanitation

14. INVASIVE GASTROENTERITIS

15. SHIGELLOSIS Shigella spp are Gram –ve facultative anaerobe, non motile bacillus Shigella dysenteriae most severe, Shigella sonnei most benign form Outbreaks in school, daycares, etc. Consumption of water or food e.g. eggs, veg, dairy products contaminated by food handler, flies, hands Even 10 1 to 10 2 org can initiate infection Acid resistant- reach colon- secrete toxin and invade epithelium Blood, mucus, WBCs passed in stool Severe diarrhea, tenesmus, vomiting, dehydration Stool exam shows WBCs, RBCs, non motile bacilli

16. ENTERO-HEMORRHAGIC E. COLI EHEC-H for Hemolytic Uremic Syndrome Dangerous Undercooked beef, unpasteurized milk, juices, lettuce, 10 3 org can initiate infection Release toxin in high conc in large intestine Serotype O157:H7 secretes toxin- inhibits protein synthesis-cytolysis Hemorrhagic colitis Older, young children, weak immunity- HUS Hemolysis, renal failure, seizure, coma, etc

17. SALMONELLOSIS Salmonella typhi causative agent of typhoid fever Salmonella enterica serotype Enteritidis and serotype Typhimurium Salmonella typhi source is humans, Salmonella enterica spp source is poultry chicken & turkeys Transmitted through food handlers IP 6-48 hours, nausea, diarrhea, abdominal pain, fever Colonic ulceration Infection lasts 3-7 days Septicemia rare

18. CAMPYLOBACTER JEJUNI Gram negative motile curved bacillus Normal gut flora of chicken, turkey, dairy cattle Contaminated raw food, water, eggs, poultry Fecal-oral route IP 2-7 days – small /large intestine invasion Ulceration of mucosa Symptoms variable- mild to severe dysentery Association with GB Syndrome weeks later ( Markus Babbel liverpool)

19. LAB DIAGNOSIS OF INFECTIVE GASTROENTERITIS Clinical history Appropriate Samples Vomitus Stool Left over food Blood Microbiological Testing Microscopy (Direct and after Gram staining) Culture & Sensitivity of Stool, vomitus, left over food or blood Blood complete picture Toxin detection in stool or vomitus, food Cl. Perfringens in stool

20. LAB DIAGNOSIS Vibrio cholerae colonies on TCBS Campylobacter jejuni in stool Toxin detection kit C. difficile

21. PEPTIC ULCER- HELICOBACTER PYLORI Peptic ulcer –smoking, alcohol, diet, stress etc. Association of peptic ulcer with infectious etiology in 1982 Australians Dr. Barry J Marshall & J Robbin Warren believed that infection is responsible Microaerophilic Gram –ve curved rod, urease producer Person to person via food or water In stomach, attaches to stomach surface- secrete urease- produces ammonia Locally pH ↑, neutralize acid, mucus cells destroyed Ulcer develop 2% of ulcer patients develop cancer Gastric ulcer

22. HELICOBACTER PYLORI LAB DIAGNOSIS Urea breath Test o Urea breath test- use radioactive C labeled urea o Patient drinks the sol- urea broken down by urease of H. pylori- CO 2 released radiolabeled detected by special equipment Serological tests like ELISA Culture of gastric biopsy Rapid urease test of gastric biopsy