Gastrointestinal Tract Infection & Food Poisoning PDF

Gastrointestinal tract infection and food poisoning DEPARTMENT OF MICROBIOLOGY COLLEGIUM MEDICUM 2018  Defensive mechanisms ▪ Lysosym in saliva ▪ Microflor ▪ more than 400 different bacterial specie...

Gastrointestinal tract infection and food poisoning DEPARTMENT OF MICROBIOLOGY COLLEGIUM MEDICUM 2018  Defensive mechanisms ▪ Lysosym in saliva ▪ Microflor ▪ more than 400 different bacterial species and subspecies ▪ pH in gastric juice ▪ Peristalsis Gastrointestinal tract infections and food poisoning ▪ Route of infection: ▪ Exogenous (contaminated food, water) ▪ Endogenous: ▪ microflora ▪ continuity of tissues ▪ autoinfection: fecal - oral Gastrointestinal tract infections and food poisoning ▪ Forms of infections / symptoms: ▪ gastritis ▪ gastroenteritis ▪ enterocolitis ▪ colitis ▪ diarrhea Gastrointestinal tract infections and food poisoning Intoxication bacteria -, toxin + Food poisoning (if the source of toxin or bacteria is in food) Toxins-related infection GTI/FP bacteria +, toxin + Infection Infection virus + / bacteria +, toxin - Intoxication  Intoxication ▪ definition ▪ disesae related with toxins produced before ingestion ▪ short incubation period ( 1 h) ▪ examples Staphylococcus aureus – related with enterotoxin Bacillus cereus – related with emetic toxin Clostridium botulinum – food-born Clostridium perfringens – food-born  Intoxication ▪ Staphylococcus aureus ▪ staphylococcal enterotoxins (SEs)– superantigenic activity ▪ source of toxins – human (during food preparation) processed meat and dairy products, ice creams, cakes) ▪ toxins are resistant to environment conditions (heat treatment, low pH) ▪ incubation period: 2 – 8 hours ▪ symptoms: nausea, violent vomiting, abdominal cramping, with or without diarrhea; self – limiting (up to 48 hours) ▪ laboratory confirmation – the presence of SEs in stool or vomit sample, food samples using ELISA- and PCR-based methods.  Intoxication ▪ Bacillus cereus (aerobic spore-forming bacteria) ▪ emetic toxins: ▪ vomiting toxin - cereulide – heat-resistant (121°C 90 minutes) ▪ it stimulates the vagus afferent through binding to the 5-HT3 receptor ▪ source - environment (rice, meat, milk, vegetables) ▪ incubation period: 2-3 h (up to 12 h) ▪ symptoms: nausea, vomiting and malaise ▪ self- limiting (up to 48 h) ▪ rrecognition based only on clinical manifestation of disease  Intoxication ▪ Clostridium botulinum (anaerobic, spore-forming bacteria) ▪ food-born botulism related with the presence of botulinum neurotoxin in food products, e.g. canned meat (homemade usually) ▪ the neurotoxin blocks the release of acetylcholine from motor nerve endings → paralyzes the nerves so that the muscles cannot contract → symptoms: ▪ early: constipation, double vision, feeling dry in the mounth/slurred speech, ▪ late: facial nerve paralysis, nausea and vomiting, abdominal distention, tachycardia, problem of urinating, muscle weakness leads to respiratory and musculoskeletal paralysis.  Intoxication ▪ Clostridium botulinum (anaerobic, spore-forming bacteria) ▪ laboratory examination – confirmation of neurotoxin presence in examined specimen ▪ specimen: stool sample, stomach contents, food samples, serum (only acute form of disease) ▪ mouse inoculation test ▪ enzyme-linked immunosorbent assays (ELISAs), electrochemiluminescent (ECL) tests, ▪ PCR-based methods  Intoxication ▪ Clostridium perfringens (anaerobic spore-forming bacteria) ▪ source of enterotoxins (A biotype): environment, contaminated food (meat stews) ▪ incubation period - 8 – 14 hours ▪ symptoms: intense abdominal cramps and watery diarrhea , self – limiting (12-24 hours) ▪ laboratory confirmation ▪ 105/g vegetative cells in food sample - using culture ▪ presence of enterotoxins using PCR-based methods, EIA, latex agglutination Toxin-mediated infection  Toxin-mediated infection ▪ definition ▪ toxins are produced in infected organism ▪ similar to endemic diarrheal infections ▪ examples Clostridium botulinum – infants botulism Clostridium perfringens – related with enterotoxins Clostridium difficile – antibiotic associated disease (AAD) Bacillus cereus – relateded with enterotoxin Bacteroides fragilis – enterotoxin Shigella sp., Vibrio sp. – related with enterotoxins  Toxin-mediated infection ▪ Clostridium botulinum – infants botulism ▪ severe infection in children younger than 1 year old ▪ ingest of Clostridium botulinum spores in gastrointestinal tract → intestinal colonization with Clostridium botulinum → neurotoxin synthesis in situ → symptoms similar like in food-borne botulism ▪ source of bacteria: honey, dust with spores of Clostridium botulinum ▪ in the classic case, the first sign of illness is constipation, lethargy, poor feeding, increasing weakness  Toxin-mediated infection ▪ Clostridium botulinum – infants botulism ▪ Laboratory confirmation: ▪ culture of Clostridium botulinum from stool sample, stomach contents, food samples ▪ AND confirmation of neurotoxin presence in examined specimen ▪ therapy: ▪ rinsing of toxins from gastrointestinal tract ▪ antitoxin ▪ prophylaxis: breast-feeding, not to feed honey to infants,  Toxin-mediated infection ▪ Bacillus cereus ▪ intestinal infection related with the presence of Bacillus cereus cell that syntheses enterotoxin → increasing of liquid secretion in intestine ▪ symptoms: watery diarrhea, abdominal cramps 12-24 hours – self-limiting ▪ laboratory confirmation: ▪ quantitative examination of food samples – the presence of Bacillus cereues spores or vegetative cells using culture ▪ the presence of enterotoxin in food samples and in stool samples using immunological techniques and PCR-based methods  Toxin-mediated infection ▪ Bacteroides fragilis (part of human colon microflora) ▪ subpopulation of strains produce enterotoxin (BFT) that increases the permeability of intestinal epithelial cell ▪ clinical manifestation ▪ onset 6-18 hours ▪ the clinical syndrome associated with ETBF diarrheal disease encompasses abdominal pain, tenesmus and inflammatory diarrhea ▪ treatment: metronidasole, penicillin+beta-lactamases inhibitors ▪ laboratory confirmation ▪ culture of Bacteroides fragilis ▪ detection of enterotoxin using cell line HT-29 or PCR-based methods  Toxin-mediated infection ▪ Clostridium difficile ▪ enterotoxin (toxin A) and cytotoxin (toxin B), binary toxin (CDT) ▪ quickly transmitted from person-to-person ▪ major pathogen in antibiotic associated disease/diarrhea (AAD) ▪ incubation period: 2-3 days ▪ symptoms in self-limiting form of infection: diarrhoea (watery or sometimes bloody), fever, loss of appetite, nausea, abdominal pain ▪ a serious form of the disease (pseudomembranous colitis) - severe inflammation of the lining of the gut  Toxin-mediated infection ▪ Clostridium difficile ▪ laboratory confirmation ▪ quick test (immunochromatographic kit): ▪ presence of GDH = presence of Clostridium difficile ▪ presence of toxin A or B ▪ PCR-based methods: GDH; A, B, CDT toxins ▪ treatment: metronidasole or vancomycine  Toxin-mediated infection ▪ Clostridium perfringens (spore-forming bacteria) ▪ enterotoxin is synthesized in intestinal by Clostridium perfringens strains (colonisation of human colon) ▪ usually as antibiotic associated diarrhea (AAD) ▪ symptoms: bloody diarrhea with mucus presence in stool sample – self limiting in 10 days ▪ laboratory confirmation: ▪ >106/g spores in stool sample - using culture ▪ presence of enterotoxins using PCR-based methods, EIA, latex agglutination  Gastrointestinal tract infection +/- toxin-mediated Patotypes of Escherichia coli related with gastrointestinal tract infections: EPEC enteropathogenic EIEC EHEC enteroinvasive enterohemorrhagic ETEC Escherichia EAEC enterotoxigenic coli enteroaggregative  Gastrointestinal tract infection +/- toxin-mediated  ETEC strains ◦ infection related with LT (heat labile), and/or ST (heat stabile), and Able to invade and destroy the colonic epithelium adhesion to enterocytes (adhesines) ◦ most common in developing countries: in travelers, young children – „traveler’s diarrhea” / „Delhi belly” / „Montezuma’s revenge” ◦ fecally contaminated food, water ◦ most common form: secretory diarrhea (infective dose 108-1010 cells)  Gastrointestinal tract infection +/- toxin-mediated  EPEC strains ◦ infection related with LA (localized adherence), A/E proteins, Able to invade and destroy the colonic epithelium enterotoxins ◦ most common form: infant watery diarrhea ◦ person to person spread (infective dose 108-1010 cells)  EAEC strains  infection related with adhesion to enterocyes ability, and enterotoxin EAST-1  most common form: infant in underdeveloped countries, travelers  might be related with chronic diarrhea  watery diarrhea (infective dose 1010 cells)  Gastrointestinal tract infection +/- toxin-mediated VTEC strains (previously EHEC) Able to invade and destroy the colonic epithelium – infection related with verotoxin VT1, VT2, and invasion to enterocytes ability – clinical manifestation: Children younger than 10 years - hemolytic uremic syndrome, HUS (acute renal failure, thrombocytopenia, microangiopathic hemolytic anemia) Adults – hemorrhagic colitis – reservoir of strains: gastrointestinal tract of sheep, pigs, chicken, wild birds, and pets – source: contamineted food, water, spread person-to-person – infective dose: 50 cells  Gastrointestinal tract infection +/- toxin-mediated EIEC strains Able to invade and destroy the colonic epithelium – infection related with invasion ability to enterocytes – most common form : bloody diarrhea – dysenteric form (fever, abdominal cramps, blood and leukocytes in stool specimens)  Gastrointestinal tract infection +/- toxin-mediated Laboratory confirmation of Escherichia coli gastrointestinal tract infection: – culture + serotyping – PCR-based methods using to identification bacteria and toxin/virulence factors presence  Gastrointestinal tract infection Shigella spp. – dysentery according to WHO – every disease caused by Shigella spp. rods infection related with invasionve ability and enterotoxins synthesis: ShET1, ShET2, and Shiga toxin (only in S. dysenteriae 1) infection dose: 10 – 103 CFU source: human (person-to-person spread), contaminated food (vegetables, salads, sour cream).  Gastrointestinal tract infection Pathomechanism of dysentery Infection Passage through the stomach 24 – 72 hours Bacteria in colon Phagocitosis (macrophages) Invasion to the submucosa Invasion to the enterocytes – replication 48 – 120 hours Swelling inflammatory, ulceration Diarrhea (blood, mucus)  Gastrointestinal tract infection Symptoms of dysentery Gastroenterocolitis nausea, vomiting watery diarrhea (increasing of body temperature) Shigellosis diarrhea (blood and mucus in stools) painful urges to defecate crampy abdominal pain increasing of body temperature symptoms of poisoning and dehydration  Gastrointestinal tract infection Laboratory confirmation in dysentery culture of stool sample / rectal swab in carrier state examination → serological typing PCR-based methods Treatment: bismuth subsalicylate antibiotic therapy only in severe cases: ciprofloxacin (in adults) azithromycin (in children) Gastrointestinal tract infections  Gastrointestinal tract infection Definition: diseases associated with bacterial presence, without enterotoxins Examples: listeriosis , campylobacteriosis stomach ulcers and duodenal ulcers (Helicobacter pylori) typhoid fever (Salmonella Typhi), and para-Typhoid fever (Salmonella Paratyphi A, B, C) salmonellosis (Salmonella Enteritidis, S. Typhimurium and other zoonotic species) 33  Gastrointestinal tract infection Listeria monocytogenes – intestinal listeriosis – infection usually in immunocompromised patients after ingestion contaminated food (cheese, fishes – L. monocytogenes can growth in 4°C) – invasion of bacteria to intestinal cells – symptoms: abdominal cramps, diarrhea, fever – self-limiting – laboratory confirmation: Culture of stool sample IgM, IgG in serum PCR-based methods 34  Gastrointestinal tract infection Campylobacter jejuni intestinal campylobacterosis – Reservoir: animals (birds, dogs) – Source: contaminated uncooked food, milk, water, direct contact with infected animals – Incubation period: 1-7 days – Symptoms: bloody diarrhae, fever, abdominal cramps, headache, muscle pain - self-limiting – Complication: Gullaina-Barré symdrome – Laboratory confirmation: - Immunochromatographic kit (quick test), - Culture +/- PCR-based methods  Gastrointestinal tract infection Helicobacter pylori stomach infection – according to WHO – 1st class carcinogen (stomach cancer) – reservoir: human (carriers increased by 10% with each decade of life developing countries - carriers 60-90%) – route of infection - direct contact with sick person – infection related with virulence factors: urease (↑pH in stomach), vacuolating cytotoxin vacA… → long-term infection of the gastric mucosa → chronic gastritis → peptic ulcer disease → mucosa-associated lymphoid tissue (MALT) lymphoma → gastric adenocarcinoma. Gastrointestinal tract infection  Gastrointestinal tract infection Helicobacter pylori stomach infection – Laboratory confirmation: Non-invasive methods: – urea-breath test – antigens in stool sample – antibodies in serum Ivasive methods – examination of tissue collected during gastroscopy: – Campylobacter Like Organisms Test (CLO test) – histopathologic examination – Culture (usually not used)  Gastrointestinal tract infection Helicobacter pylori stomach infection – Treatment: omeprazole, amoxicillin, and clarithromycin (OAC) for 10 days; bismuth subsalicylate, metronidazole, and tetracycline (BMT) for 14 days; lansoprazole, amoxicillin, and clarithromycin (LAC), which has been approved for either 10 days or 14 days of treatment.  Gastrointestinal tract infection Salmonella other species than S. Typhi, and S. Paratyphi - Salmonellosis – reservoir: intestine of wild and farm animals – source: contaminated food, water, rare person-to-person spread – symptoms: fever, abdominal cramps, diarrhea, vomiting in 12-72 hours after ingestion contaminated products – usually self-limiting – bacteria are able to invasion to enterocytes in immunocompromised patients → bacteremia → CNS infection – laboratory confirmation: culture – antibiotic treatment if necessary: ceftriaxone, ciprofloxacin  Gastrointestinal tract infection Salmonella Typhi - typhoid fever – reservoir of Salmonella Typhi – only human – source:  Insects Individual infections  Contaminated food, water Epidemic infections  Direct contact with carriers (after illness; chronic carrier-state (gallbladder, urinary tract, intestine) - laboratory confirmation: culture + serotyping - antibiotic treatment if necessary: ceftriaxone, ciprofloxacin, according to the susceptibility testing results  Gastrointestinal tract infection Typhoid fever - pathogenesis of infection Infection Passage through the stomach Attach to the mucosa of the small intestine and invade into the M cells (Peyer patches) 1st week Replication in entetocytes Relase into the blood and lymphatic system 2nd week Septicemia (LPS) Replication in gallbladder 3th week Ulceration in intestine  Gastrointestinal tract infection Typhoid fever - symptoms of disease: Incubaction period: „Flu-like” symptoms Increase of symptoms Increasing of temperature (to 40°C) Meningitidis symptoms, „stupor”, mental confusion A dry tongue with grey coating Hepatosplenomegaly Low presure of blood  Gastrointestinal tract infection Typhoid fever - symptoms of disease: Period of full-disease Strong „stupor” Low pressure of blood Flatulence of abdomen Typhoid rubella – single, round pocks (abdomen, chest) Bronchitis Recovery period Slowly decreasing of body temperature „wolfish appetite” Viral gastrointestinal tract infection  Viral gastrointestinal tract infection Frequency Who? Onset (among viral GTI) Children (