Lecture 18: Lower Alimentary Tract Infections

(Lower Alimentary Tract Infections) Lecture 18 Diseases of the GI Tract Infections: Intoxications: · pathogen multiplies in mucosa or passes through · usually sudden onset and no fever · ingesting pathogen to other systemic organs · characterized by fever, release of endotoxin (LPS) · ingesting preformed toxin or other systemic symptoms both cases lead to diarrhea, major cause of infant mortality (dehydration) Transmission of Infections/Intoxications · most GI infections are fecal-oral transmission · requires hygiene to prevent it ↳ proper disposal and treatment of sewage ↳ disinfection of drinking water Predominant Flora of Intestine · G-, both anaerobes and aerobes · Bacteriodes species are dominant ↳ anaerobic G- rod ↳ proper food preparation and handling Main Pathogenic Mechanisms of LAT · attachment (with ligand and receptor) · +/- cell invasion · loss of microvilli · exotoxin production (2 actions) ↳ increase secretion of water and electrolytes eg. Vibrio cholerae enterotoxin ↳ inhibit protein synthesis and cause cell death eg. Clostridium difficile cytotoxin (A and B) · remember: that many GI pathogens are G- and have both endotoxins and exotoxins Dysentery · Severe diarrhea with blood, often pus and/or mucous Gastroenteritis · inflammation of the stomach and the intestinal mucosa, no pus in diarrhea but lots of it eg. Entamoeba histolytica eg. Vibrio cholerae Shigella dysenteriae Cryptosporidium sp. common symptoms: diarrhea, vomiting, abdominal cramps, nausea Intoxications: Cause % of cases Time to Staphylococcus 5-25 blast off 2-4 hr Bacillus cereus 1-2 1-6 hr aureus Main clinical Characteristic foods Vomiting Meats, custards, salads symptoms Vomiting, diarrhea Rice, meat, vegetables Neuromuscular Improperly preserved (vomiting toxin*) Clostridium botulinum 5-15 12-72 hr paralysis vegetables, fish, meat Bacillus cereus can cause either an intoxication or an infection Staphylococcal Food Poisoning · leads to lots of recalls · S. aureus produces exotoxins called enterotoxins, which are heat stable (to 30 min boiling) and resistant to enzymatic destruction in the GI tract ↳ grow quickly and easily in food Staphylococcal Enterotoxin ↳ fairly high resistance to heat (60°C) 30 min · causes abdominal cramps · triggers vomiting reflex ↳ salt tolerant, osmotically stable due to cell wall · usually occurs in 2-4 hours after ↳ temperatures in food kept "warm" conducive to growth ingestion ↳ requires adequate refrigeration for prevention · complete recovery within 24 hours · no lasting side effects Bacillus Cereus · food associated disease can have two forms: ↳ 1. diarrhea: from production of enterotoxin in gut (8-16hr) (infection) ↳ 2. vomiting: due to ingestion of enterotoxin in food (1-6hr) · G+ bacilli, aerobic, spore forming · heating food may not kill spores · commonly acquired from rice · self limiting disease Salmonellosis (Salmonella Gastroenteritis) · G- non-spore forming bacilli, motile · Two types of Salmonella infection: Common Causes of GI Infections: · Salmonella · Shigella · Campylobacter · E. coli (ETEC, EIEC, EPEC, EHEC ) · Clostridium perfringens · Bacillus cereus (intoxication & infection) Gastroenteritis Typhoid Fever · Vibrio cholerae (S. enterica) (S. typhi) · Rotavirus, Norovirus, Sapovirus S. enterica enterica ↳ from eating meat S. enterica typhi · E. histolytica, Giardia, Cryptosporidium ↳ contaminated food/water · Hepatitus A Salmonella Gastroenteritis · over 2000 serotypes for human disease (zoonotic) · Salmonella enterica is the group name, then each serotype has its own name ↳ Salmonella (enterica) enteritidis and Salmonella (enterica) typhimurium · incubation period 12-36 hours · bacteria killed by gastric acid (therefore you need lots of bacteria for infection) · meat products, eggs, poultry, reptile skin · S. enteritidis can infect chickens - eggs then have bacteria inside of them (the egg shell) · usually not treated with antibiotics because it prolongs shedding and makes it last longer · no vaccine Typhoid Fever · caused by S. typhi · spread ONLY from human to human · characterized by high fever >40°C, headache · diarrhea starts in 2nd or 3rd week but is not the main characteristic · causes sepsis (enteric fever) · bacteria multiply in phagocytic cells, therefore disseminate quickly to blood · after recovery, carrier state in gall bladder eg. Typhoid Mary story · treatment: always antibiotics (ceftriaxone) Shigellosis · infection (not intoxication) · G- bacilli, non-motile · severity depends on the infecting strain ↳ Type A contains a plasmid essential for attachment and entry of bacteria into cells · transmitted from person to person, no animal reservoir · growing bacteria produce Shiga toxin (a cytotoxin) ↳ main virulence factor* · 4 Species: ↳ S. dysenteriae (A)*** ↳ S. boydii (B) ↳ S. flexneri (C) ↳ S. sonnei (D) Campylobacter Gastroenteritis · facultatively anaerobic G-, spiral formed bacilli · leading cause of foodborne bacterial illness in US/Canada · Commensals of poultry and cattle (live on their bodies without harming them) · self limiting disease · prevention: hygienic measures when handling poultry and monitoring water · complications: IBS and Guillan Barre Syndrome · no vaccine Escherichia coli Gastroenteritis · most strains of E. coli are harmless and normal flora of GI tract · pathogenic strains have specialized fimbriae for attachment into intestinal cells and produce toxins ↳ Enterotoxigenic E. coli (ETEC) ↳ Enteroinvasive E. coli (EIEC) ↳ Enteroadhesive E. coli (EAEC) ↳ Enteropathogenic E. coli (EPEC) ↳ Enterohemorrhagic E. coli (EHEC) (Hamburger disease) Enterohemorrhagic E. coli (EHEC) · poorly handled meat, poultry, raw alfalfa · best known serotype O157:H7 · self limiting in adults, children and · "Hamburger Disease" · produce shiga-like toxins sprouts, contaminated water immunocompromised at risk for ↳ hemorrhagic colitis: inflammation of intestine w/bleeding complications ↳ HUS: hemolytic uremic syndrome · HUS complication: ↳ Kidney failure ↳ 5-10% of small children with EHEC get HUS ↳ mortality rate 5% · treatment: rehydration, supportive care · no vaccine Clostridium Gastroenteritis (perfringens, welchii) · G+ bacilli, spore forming, anaerobic · grows in intestinal tract and produces an exotoxin that causes abdominal pain and diarrhea · most cases mild, occur 8-12 hours after ingestion · can be serious in folks who lack trypsin or eat a diet rich in trypsin inhibitors (like soybeans) ↳ result is Pigbell: gangrene of intestines · meat dishes (stews) · often not treated · no vaccine Vibrio Cholerae · facultatively anaerobic G- "vibrio" (comma shaped) · up to >20L fluid loss per day → can die of dehydration · survives in high PH and high salt · killed by gastric acid, many bacteria required for disease · Virulence factors: exotoxin, cholera enterotoxin, heat labile, TCP (toxin co-regulated pili ) · transmitted often by fecally contaminated water · global pandemic · vaccine exists, 40-60% effective (oral vaccine Dukoral) · treatment: rehydration glucose + electrolytes Viral Gastroenteritis · major cause of dealth in developing countries · not distinguishable clinically from other cases of gastroenteritis · viruses are specific to humans · fecal-oral transmission · 90% of cases caused by rotavirus or norovirus Rotavirus Gastroenteritis · RNA, wheel shaped virus, non-enveloped · most common cause of viral gastroenteritis in children · same incidence in developed and underdeveloped nations · disease of children, most severe cases <2 years · incubation 2-3 days · often nosocomial · symptoms: low grade fever, diarrhea, vomiting (1 week duration) · new vaccines available (Rotorix, Rotateq) Norovirus Gastroenteritis · RNA, small round, non-enveloped · causes major epidemics of viral gastroenteritis (2/3 of all cases cause food poisoning) · 2 day incubation period, pathogenesis similar to Rotavirus (damages microvilli) · Symptoms: nausea, abdominal cramps, diarrhea, vomiting for 1-3 days, sudden onset · self limiting · no prodrome · cruise ship virus Parasitic Diseases of the GI · Protozoan Diseases (often diarrhea) ↳ Giardia lamblia ↳ Cryptosporidiosis ↳ Entamoeba histolytica · Helminthic Diseases (no diarrhea) ↳ tapeworm (cestode) ↳ roundworm (nematode) Infections of Auxillary Organs · hepatitis ↳ inflammation of the liver ↳ hepatitis A, B, C, D, E (5 different viruses) ↳ CMV and EBV can also cause infectious hepatitis Hepatitis A (HAV) · RNA, non-enveloped · transmission: fecal-oral, contaminated water and mollusks · virus is resistant to chlorine!! · incubation period 2-4 weeks · Pathogenesis: ↳ after infection the virus multiplies in intestinal epithelial cells, enters the blood stream and infects the liver ↳ virus excreted in feces · Symptoms: nausea, fever, anorexia, vomiting, jaundice ↳ usually sudden onset · Clinical course: self-limiting, 50% of infections are subclinical (unaware) ↳ no chronic form · Diagnosis: HAV IgM antibodies in serum · Immunity: lifelong vaccine exists Hepatitis B (HBV) · enveloped DNA virus (Hepadnaviridae family) · transmission: STI, bloodborne disease · can cause both acute and chronic disease: ↳ acute: liver inflammation, vomiting, jaundice (10% of adults become chronically infected) ↳ chronic: cirrhosis, hepatocellular carcinoma (liver cancer) -infected for life if chronic b/c of DNA virus · vaccine available · U of A connection: one antiviral drug for HBV (lamivudine) · drugs for treatment expensive (Harvoni and Sovaldi) → lifetime treatment Hepatitis C (HCV) · enveloped RNA virus · transmission: bloodborne disease · can cause acute and chronic disease: ↳ acute: mild and vague symptoms (malaise) (80% become chronically infected) ↳ chronic: cirrhosis, liver cancer · no vaccine available · drugs can completely cure HCV (Harvoni and Ribovirin) Hepatitis E (HPE) · non-enveloped RNA virus (Caliciviridae family) · transmission: Fecal-oral, like Hep A · endemic in areas with poor sanitation (always present) eg. India and SE Asia · no chronic disease (only acute) · risk for pregnant women, up to 20% mortality Hepatitis D (HDV) · Enveloped RNA virus but is a satellite virus (needs HBV) · transmission: similar to HBV · can only grow in the presence of HBV (uses the HBAg coating) · coexists with HBV to cause disease*