Gastrointestinal Tract Infections PDF

# Gastrointestinal Tract Infections ## 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 ## General Principles in Pathogenesis - Encounter - Frequently from food o...

# Gastrointestinal Tract Infections ## 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 ## 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 ## Gastrointestinal Infections - Are viral, bacterial, or parasitic infections that cause gastroenteritis, an inflammation of the gastrointestinal tract involving both the stomach and the small intestine. - Symptoms include diarrhea, vomiting, and abdominal pain. Dehydration is the main danger of gastrointestinal infections. - (Newborns/infants, immunocompromised patients or elderly populations), they are potentially serious. ## Pathogenesis - General Mechanism - Diagram showing the steps of food poisoning: - Food, water, and fingers can be contaminated with pathogenic microbes or their toxins from humans or animals. - Ingestion of organisms and/or toxins. - Organisms multiply. - Organisms invade or toxins are absorbed in the gut. - Organisms spread and cause systemic symptoms such as fever. - Diarrhea. - Pathogens are excreted in feces. ## Types of GIT Infections and Their Symptoms - Gastroenteritis/Food Poisoning - Syndrome characterized by GIT symptoms like nausea, vomiting, diarrhea, and 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 (Typhoid) - Fever, headache, lethargy, shock, splenomegaly. - Stomach ulcers - Stomach pain. - Worm infestations - Blockage of GI tract, malnutrition. ## 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. ## Pathogenic Mechanisms Toxin Production - Enterotoxin - Vibrio cholerae, NCV, Enterotoxigenic E coli (ETEC) - Clostridium difficile (toxin A) - Campylobacter jejuni - Cytotoxin - Shigella spp - Enterohemorrhagic E coli, Clostridium difficile (toxin B) - Neurotoxin - Clostridium botulinum, Staphylococcus aureus - Bacillus cereus ## Pathogenic Mechanisms Invasion - Shigella spp - Enteroinvasive E coli - Yersinia entero colitica - Entamoeba histolytica - Balantidium coli - Norwalk virus ## 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 ## 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 ## Causes of Diarrhea ### Viruses - Rotavirus - Corona viruses - Norwalk virus - Adenovirus - Calicivirus ### Bacteria - Vibrio cholerae - Enterotoxigenic E. coli (ETEC) - Enteropathogenic E. coli (EPEC) - Enterohemorrhagic E. coli (EHEC) - Campylobacter jejuni - C. difficile ### Parasites - Giardia lamblia - Cyclospora and Cryptosporidium ## Causes of Dysentery - Shigella - Enteroinvasive E. coli - Campylobacter jejuni - Salmonella enterica - Vibrio parahemolyticus - Entamoeba histolytica ## More Causes - Enteric Fever - Salmonella typhi - Salmonella enterica - Stomach Ulcers - Helicobacter pylori - Others - Broad spectrum antibiotics - Antacids - Laxatives ## History - Ingestion of potentially contaminated food or untreated water. - Recent travel. - Sick contacts. - Recent antibiotic use. - Outbreaks. - Bloody diarrhea. ## Foodborne Illness (FBI) - 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). ## Incubation Periods - **Short (Minute to hours)** - Chemical toxins E.g., copper poisoning. - Neurotoxins, histamine, allergens E.g., Shellfish toxins. - **Short to medium (1-12 hours)** - Bacterial enterotoxins E.g., Staphylococcal or Bacillus cereus. - **Long (6 hours - 10 days)** - Bacterial infections E.g., Salmonella, E. Coli O157:H7 (Shiga toxin-producing), Campylobacter, Yersinia. ## Staphylococcal Food Poisoning - 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. ## Clostridium Perfringens Food Poisoning - 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 diarrhea. - Transmission - None. ## Bacillus cereus Food Poisoning - 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. ## Clostridium botulinum Food Poisoning - 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. ## Diagnosis - Gross & microscopic stool examination. - Stool culture. - Identification tests. - Endoscopy if noninfectious etiology suspected (inflammatory bowel disease). ## 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. ## Microscopic Examination by: - Direct wet mount - Ova & parasites, Fecal leukocytes. - Gram stain - Campylobacter, Vibrio. - Modified Acid fast - Cryptosporidium, Isospora. - Trichrome stain - Parasites. ## Screening Stool Cultures for Pathogens - Problem of the mixed microbial biota of fecal specimens. - All fecal specimens should be routinely screened for Salmonella, Shigella, EHEC, and Campylobacter. - Screening for the additional organisms on the basis of patient history and gross description of the specimen (bloody or watery). - Most clinical microbiologists inoculate stool samples on highly selective media, such as HE or XLD agars, in addition to regular MAC. ## Hektoen Enteric Agar - The carbohydrates and bile salts to inhibit growth of gram-positive bacteria and many nonpathogenic enteric bacteria. - A selective and differential medium for the primary plating of stool specimens to aid in the recovery of intestinal pathogens, e.g., Salmonella. - Should not be autoclaved or overheated. - Inoculated medium incubated aerobically (not in CO2) at 35° C for 18 to 24 hours. - Most nonpathogens appear bright orange to salmon pink. - Nonfermenters, such as Salmonella and Shigella spp., typically produce green to bluegreen colonies. ## CIN Agar for Screening for Y. enterocolitica and Most Aeromonas spp., ential Media. ## CHROMagar: Salmonella Produce Mauve-Colored Colonies. ## Thiosulfate Citrate Bile Salt Sucrose (TCBS) Agar - Is recommended to differentiates sucrose-fermenting (yellow colonies) of V. cholerae. - Although TCBS generally inhibits all other organisms, it should be monitored with stringent quality control measures. ## Microscopic Morphology of Vibrio sp. on Gram-Stained Smear (×1000). ## Aeromonas: β-hemolysis on Sheep Blood Agar. ## Aeromonas: Lactose Fermentation on MacConkey (MAC) Agar. ## Campylobacter Diagnosis - **Campylobacter Blood Agar**: - An enriched selective agar for Campylobacter spp. Contains Brucella agar base, 10% sheep red blood cells, and a combination of antimicrobials. - Incubating stool cultures at 42° C to recover C. jejuni. And, growth of colon microbiota is inhibited at this higher temperature. - Isolates from stool specimens and rectal swabs identified by a positive-oxidase, gram stain, can grow at 42° C in a microaerophilic environment. ## Helicobacter pylori - Linked to gastric infections. - Colonizes the stomach for a long time and can cause a low-grade inflammatory process. - The strong association between long-term H. pylori infection and gastric cancer. ## Urea Breath Test - Sensitive and specific for H. pylori and is recommended for monitoring therapy. - In this test, the patient is given 13C- or 14C-labeled urea orally. - Urea degraded by the urease activity of H. pylori in the stomach releases 13CO2 or 14CO2, which is absorbed into the bloodstream and detected in the exhaled breath by a counter. - H. pylori infection can also be diagnosed by fecal antigen detection using enzyme immunoassay. ## Serologic Grouping - When an isolate is biochemically identified as Salmonella or Shigella, serologic grouping of the isolate for the O serogroups (somatic antigen) must be performed for confirmation. - Serologic grouping is also important in the identification of enterovirulent E. coli strains. - **Salmonella**: Based on the common O antigens, Salmonella may be placed into major groups designated by capital letters. Salmonella Typhi, Salmonella Paratyphi, or Salmonella Choleraesuis. Identification is very important in providing proper therapy for the patient. - **Shigella**: Serologic grouping of Shigella is also based on the somatic O antigen. A (S. dysenteriae), B (S. flexneri), C (S. boydii), and D (S. sonnei). ## Latex Agglutination Tests for the Rapid Identification of Colonies of Enteric Campylobacters on Primary Isolation Media. ## H. pylori Antigen Test in Stool or Antibody in Serum. ## Acid Fast Stain - Useful in identifying patients, such as those with AIDS, who may be at risk for developing disseminated mycobacterial disease. - Stool specimens should be collected in clean containers without any preservative and sent directly to the laboratory for processing. - If processing within a few hours is not possible, the specimen should be frozen at -20° C until it is processed.