Gastrointestinal Tract Infections PDF
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This document provides an overview of gastrointestinal tract infections, covering topics such as causes, general principles in pathogenesis, types of infections, and their symptoms. It details the various factors contributing to these infections, including bacterial, viral, and parasitic agents, and presents information on treatment and diagnosis.
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# 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.