Gastrointestinal tract
Initial inoculum |
Birth: vagina and external genitalia. Initial colonization takes 2 weeks. 1st E. coli & Streptococci arrive in 4-7 days. Bifidobacterium, Clostridium & Bacteroides are initially high but disappear. Differences between breast and bottle fed. 2 years until bacterial population resembles that of adults. |
Breast-fed infants |
Bifidobacterial numbers stay high, E. coli, Streptococci, Bacteroides & Clostridia decline. Once weaning begins, starts to look like formula fed. Eventually leads to Bacteroides and anaerobic G+ predominating. |
Formula-fed infants |
Lactobacilli predominate. Eventually leads to Bacteroides and anaerobic G+ predominating. |
Gastric flora |
Usually non-existent. 0-103 bactera. May rise in abnormal states. H. pylori gastritis. 105-107 bacteria/mL indicates abnormality such as achlorhydria or malabsorption syndrome |
Small intestinal flora |
Small numbers increasing as distance from stomach increases. Aerobic Streptococci, Staphylococci, Lactobacilli, yeasts, anaerobic Streptococci and Lactobacilli. |
Duodenum flora |
Complete absence of coliforms and Bacteroides |
Jejunum-Ileum flora |
Presence of large numbers of Enterobacteria & some Streptococci, Staphylococci, Lactobacilli, Bacteroides, Bifidobacterium, Clostridium. |
Colonic flora |
95-99% anaerobic organisms. Bacteroides, Bifidobacterium, Eubacterium, Peptostreptococcus & Clostridium + Enterobacteria |
Allogenic |
Originate outside ecosystem. Diet, age, geographic location |
Diet |
Western: high Bacteroides, low enterococci (other anaerobes) |
Antibiotic therapy |
Disturbance or removal of flora increases susceptibility to colonization by pathogenic organisms |
Surgery |
Alters bacterial population. Ileostomy effluents – unique ecological niche. Does not correspond to bacterial #'s or types in ileum or colon. |
Autogenic |
Arising from within ecosystem. Temperature, [H+], peristalsis, epithelial shedding, mucus, conjugated bile salts, immunological response (IgA) |
Activities of microorganisms |
Nutritional competition, production of bacterial inhibitors, bacteriocins, antibiotics, toxic metabolic end products, H2S production, competition for attachment sites, maintenance of low-oxidation-reduction potentials. |
Worst GI infections |
Campylobacter jejuni, Salmonella, Shigella spp, E. coli O157:H7, Yersinia enterocolytica |
Food-poisoning |
Consumption of food containing toxins (chemical and bacterial) |
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Food-associated infections |
Consumption of food containing organism (vehicle for entry) |
Enteritis |
Inflammation of the intestinal mucosa |
Colitis |
Inflammation of the colon |
Enterocolitis |
Inflammation of small & large intestines |
Diarrhea |
Frequent || fluid stool |
Dysentery |
Inflammation of GIT w/ blood & pus in faeces |
Exotoxin |
Protein toxin secreted by living microorganisms into the surrounding environment |
Enterotoxin |
specific for cells of the intestine, causing inflammation, ~excessive secretion of fluid & electrolytes |
Cytotoxin |
(Inhibits ^^ prevent) functions of cells || causes destruction of cells |
Enteroadherent |
Organisms that adhere to microvilli |
Enteroinvasive |
Organisms invade intestinal mucosa |
Stool samples |
Easy to collect but include liquid part of stool. Also mucus if present. |
Vomitus |
Rarely obtained, but may contain viruses in acute viral gastroenteritis or bacteria in some toxic food poisoning. Worth collecting in patients who do not have coexisting diarrhea |
Blood cultures |
Mandatory for patients w/ fever. Serum may contain enterotoxins, botulinum toxin of antibodies to toxins |
Mucosal specimens |
For parasites and ova of Entamoeba histolytica or Schistosoma spp. |
Intestinal fluids |
Giardiasis or strongyoidiasis parasites in duodenal aspirate |
Diagnosis of infective diarrhea |
Depends upon identification of the pathogen from the faeces: EM, culture, demonstration of antigens |
Selective - enrichment |
designed to encourage growth of certain types of organisms in preference to any others that may be present |
Differential – combined selective |
Growth of certain types of organisms leads to visible changes in appearance of medium (dyes – inhibit Gram+ growth; bile salts – inhibit non-enterics; CH2O & pH indicator – acid production; iron & iron salts – H2S production |
*MacConkey agar |
Select and recover enterics. Bile salts, crystal violet, neutral read (selective agents); peptone protease peptone (source of aa); amino acid (none); fermentable sugars (lactose 1%); pH indicator (neutral red: acid = red; alkaline = white/lgiht; non-fermenters colourless. |
*Eosin methylene blue |
EMB. Differentiate E. coli. Selective isolation and differentiation of G- enterics. Aniline dyes (eosin, methylene blue) inhibit G+ and fastidious organisms. |
Deoxycholate citrate |
DCA. Select salmonella from other coliforms or G+ |
Xylose lysine deoxycholate |
XLD. Detects Shigella sp. & Salmonella sp in feces. |
Differentiation on MacConkey agar |
Lactose+ (red color: E. coli, Klebsiella sp, Enterobacter sp), Lactose – (not red) --> oxidase- (glucose+, Proteus sp, Salmonella sp), oxidase+ --> glucose- (Pseudomonas sp, Campylobacter jejuni), Glucose+ (Vibrio sp) |
O antigen |
External part of cell wall; resistant to heat and blood. Detection by agglutination; antibodies to O antigen: IgM 150 types identified |
K antigen |
Cell surface antigen (capsule). Some polysacc (E. coli) some proteins. 100 types identified (> 2000 serotypes Salmonella Vi antigens) |
H antigen |
Flagella. Denatured by heat or alcohol; agglutinate w/ anti-H antibodies (IgG). 50 identified |
Pilin proteins |
Colonisation factor antigens (CFA's) |
Agglutination reaction |
Bacterial suspension + antiserum --> reaction |
Oral rehydration |
Until normal rehydration restored. Sodium: 150-150mmol/L; glucose 200-220mmol/L; K 2-5 mmol/L |
Intravenous rehydration |
Shock, exhaustion, precluding oral feeding and oral rehydration failure |
Antiemetic drugs |
Reduce filling loss; therefore, oral rehydration becomes effective |
Anti-diarrheal drugs |
Rarely successful. Reduce gut motility – allow accumulation of fluid filled feces |
Escherichia coli |
Raw foods! 3 types: enterotoxogenic, enteroinvasive, enterohemorrhagic. Enterohemorrhagic from cattle & other ruminants, otherwise fecal contamination. Enteroinvasive: dysentery. Enterohemorrhagic: watery diarrhea progresses to blood, w/ kidney failure. Member of normal intestinal flora. UTI, sepsis/meningitis, enteric/diarrheal disease. Diagnosis: MacCokey's agar; Sorbitol MacCokey's agar (no fermentation EHEC); (ETEC) inoculate mouse adrenal cells: stimulation of adenylate cyclase by LT/ST; ELISA on toxin bound to antibody; DNA probe to detect toxin genes. |
Salmonella spp |
5hr-3days:1-4 days. Diarrhea, abdominal pain, chills, fever, vomiting, cramps. Raw/undercooked eggs, meat & paultry; raw milk. Infected food source animals; human feces. Prevent: cook eggs, meat, poultry; pasteurised milk. Vi antigens. S. typhirium***, S. paratyphi, S. schottmulleri, S. enteritidis most common. TYPHRIUM DOES NOT CAUSE TYPHOID FEVER. |
Shigella spp |
.5-4days:4-7 days. Diarrhea, fever, nausea, sometimes vomiting & cramps. Raw food contaminated w/ human fecal contact (direct or via water). Prevention: General sanitation; cook foods. Groups A-D. Endotoxin and exotoxin. 4F's. Rarely invade blood. antibiotics |
V. parahaemolyticus |
.5-1:4-7 days. Diarrhea, cramps, sometimes nausea, vomiting, fever & headache. Fish & seafood. Marine, coastal environment. Cook fish and seafood thoroughly |
V. vulnificus |
People w/ high serum iron 1 day. Chills fever, prostration, often death. Raw oysters & clams. Marine coastal environments. Cook shellfish thoroughly. |
Yersinia enterocolytica |
3-7 days:2-3weeks. Diarrhea, cramps, |
Enterobacteriacea |
Produce variety of toxins (VIRULENCE FACTORS). G- bacilli. |
ETEC |
E. coli Enterotoxinogenic. Non-invasive. LT: cAMP (heat labile) and ST: cGMP (heat stable). Traveller's diarrhea. Rapid onset watery diarrhea. Transmission by contaminated food/water. High infective dose. Management: rehydration therapy. CFA's allow colonization. Enterotoxin has effect and Cl-, Na+, H2O, K+ are secreted --> watery diarrhea. PLASMID ENCODED. |
EIEC |
Non-toxigenic enteroinvasive E. coli. Similar to shigellosis, but less severe. No shiga toxin. Infection w/ only 10 microorganisms. Invasion of enterocytes of LARGE INTESTINES. Inhibits protein synthesis killing host cell. Dead WBCs, RBCs and mucosal cells in stool. Rehydration therapy. Vaccule lysis allows for spread. |
EPEC |
Non-invasive Enteropathogenic E. coli. Infantile diarrhea. Bundle forming pilus (BFP) attaches epithelial cells. Destruction of microvilli. Rehydration therapy or antibiotics |
EAEC |
Enteroadhesive E. coli. NO PLASMID ADHERENCE FACTOR. Fimbriae attach to mucosa, enhanced mucus production making biofilm encrusted w/ EAEC, cytotoxin production --> damage to intestinal cells. |
EHEC |
Enterohemorrhagic E. coli. Cytotoxin (VT). HUS. Hemorrhagic colitis w/o invading cells of colon. Bloody diarrhea. Reservoir in dairy cattle. |
Infection strategy |
Colonization of mucosal site. Evasion of host defences. Multiplication. Host damage |
Heat labile toxin |
LT. E. coli toxin similar to cholera toxin. Increase cyclic AMP. ETEC |
Heat stable toxin |
ST. increase cGMP. ETEC |
Cholera toxin |
Binds (B subunit) --> reduction --> A subunit enters membrane, ADP-ribosylation of S protein. Inactivation of GTPase --> activating adenylate cyclase |
Bundle forming pilus |
BFP. Plasmid borne. Attaches to epithelial cells. Found in EPEC. |
Evolution of HUS??? |
Hemolytic uremic syndrome. |
Shigella dysenteriae |
Group A. Only Shigella species produce Shiga toxin. Inhibits protein synthesis. Enterotoxin produces diarrhea. Exotoxin inhibits sugar and AA absorption in SI. Neutotoxin affects CNS (all same toxin) |
NAD glycohydrolase |
Found in Shigella species. (destroys all NAD in human cells, stops metabolism and causes cell death) |
Shigella sonnei |
Children < 5 years (DAY CARE) |
Shigella flexneri |
Sexually active gay men. |
Shigella boydii |
rare |
4 F's |
Food, flies, fingers, feces |
Diagnosis of shigella |
Isolation from stool. MacConkey agar: pale/colorless colonies. S-S agar (Salmonella-Shigella agar). Non-motile, G- rod, no lactose fermentation, no utilization of citric acid, no H2S production (except S. flexneri), no gas from glucose. |
Salmonella septicemia |
Uncommon. S. cholerasuis. |
Salmonella Enteric fever |
S. typhi only!! high grade fever, headache, initial constipation, low WBC. Ingested species make it to SI. Intraluminal multiplication. Passes between epithelia in ileocecal area. Intracellular multiplication. enter lymphatics (multiplies in intestinal lymph nodes) and proceded to blood stream. Carried in blood to other organs. Multiply in intestinal lymphoid tissue. Chloramphenicol/ciprofloxacin. |
Salmonella gastroenteritis |
S. typhimurium, S. enteritidis, S. newport. Incubation in hours. Localized infection; NO SPREAD OF ORGANISM. Excessive fluid excretion of fluids from ileum and jejunum. |
S. enteritidis pt4 |
Causative agent in UK eggs |
Salmonella pathogenesis |
Invasion of intestinal mucosa. Lysosomal digestion ^^ deep tissue invasion --> Phaocytosis by macrophages and neutrophils --> systemic dissemination. |
Reptile associated salmonellosis |
Infants/children: direct or indirect contact. Lizards, snakes or turtles. Turtles < 4 inches banned in US (1975). 77% reduction in turtle-associated salmonellosis |
Typhoid mary carriers |
Asymptomatic carriers: establish in gall bladder (resists bile & bile salts); continuous feedback into intestine. Re-establish infections. 2-5% of typhoid patients become carriers |
Salmonella susceptibility |
Stomach: achlorhydria, gastric surgery. Intestines: antibiotics, GI surgery, idiopathic inflammatory bowel disease. Hemolytic anemias (sickle cell). Impaired immune system: cariconmatosis, leukemia, lymphomas, diabetes mellitus, immunosuppressice drugs, AIDS, ... |
Salmonella diagnosis |
Isolation from stools, water & food. MacConkey agar: pale/colorless colonies. S-S agar. Motile; G- rod, no lactose fermintation, H2S production, gas from glucose, serotyping. |
Yersinia pestis |
Rodent. Bubonic and pneumonic plague. |
Yersinia pseudotuberculosis |
Rodent. Severe enterocolitis. |
Yersinia enterocolytica |
Cattle, deer, pigs and birds. Diarrhea & local abscess. Children > 7 yrs. Gastroenteritis*. Psychroptroph*, self-limiting enterocolitis*. Abdominal pain & diarrhea; mild fever, vomiting rare. Oxytetracycline and doxycycline. Spreads to mesenteric lymph nodes (infrequent) and causes abscess, peritonitis, diarrhea. Invasion induces inflammatory response. Mimics appendicitis. Heat stable enterotoxin (increase cGMP). |
Positive reactive arthritis |
Pathogenesis poorly understood (maybe polyclonal T-cell stimulation). |
Yersinia diagnosis |
from stool. Rising antibody titers in paired serum. MacConkey (pinpoint colonies/48 hours). Specialized Yersinia media |
Vibrionaceae |
Curved G- rod. May be linked forming S shape. Motile by single polar flagellum. Non-spore forming. Oxidase+, O & H antigens. Cause toxigenic water-loss diarrhea (cholera), wound infections, rare systemic infections. |
Vibrio cholerae |
2-3 days: hours-days. Profuse watery diarrhea, ~vomiting, dehydration, often fatal if untreated. Food w/ Fecal contamination. Prevent by general sanitation. Differentiate: ferment sucrosse, mannose, !arabinose. Acid sensitive, halotolerant (NaCl stimulates growth). Single LT flagella H antigen. O1 serotype is classic. Not invasive. Tetracycline reduces duration of diarrhea |
Cholera toxin |
Potent enterotoxic exotoxin. Enterotoxin LT (AB toxin). Ganglioside GM1 serves as mucosal receptor. Activates adenylate cyclase via G protein activation. Results in diarrhea. 20-30L/day. Replace ION loss* |
Vibrio parahaemolyticus |
Ingestion of raw/poorly cooked seafood. Acute abdominal pain, vomiting & watery diarrhea. #1 cause of food-borne infection in Japan = raw fish, US = shellfish |
Vibrio vulnificus |
Diarrhea & infection of cuts. Salt water abrasions (fishermen) virulent/invasive strain. Intense skin lesions; gastroenteritis & rvrn severe bacteremia. Management: tetracycline |
Diagnosis of cholera |
Clinical presentation. Screening of stool samples. Oxidase activity. Thiosulphate-citrate-bile salts-sucrose (TCBS) agar. Sucrose (differentiating agent), sucrose+ = V. cholerae, sucrose- = V. parahaemolyticus, V. vulnificus |
Campylobacter jejuni/coli |
3-5:2-10 days. #1 cause of food-borne infections in developed countries. g- curved rod (vibrio). Non-sporing, motile. Do not ferment carbohydrates. No growth at 25C, grow well at 37C and better at 42-43C. Epidemiology: GI tract of wide range of animals (zoonotic). Fecal contaminated water. 60% of all infections from contaminated food (unpasteurized, raw, partially cooked: dairy, poultry, contaminated water). ETEC LT-like enterotoxin. Verotoxin: similar to shigella toxin. OMPs LPS has endotoxic activity. Slight vomiting, profuse diarrhea, abdominal pain, prostration, pyrexia, bloodstained feces |
C. jejuni v. H. pylori |
H. pylori is aseasonal, C. jejuni peaks in Summer. H. pylori is more common in elderly and C. jejuni in 20-40 year olds |
Campylobacter diagnosis |
Microscopy: G-, single flagella, darting motility. Culture: spreading mucoid, grayish colonies. Biochemical analysis: oxidase, catalase, hippurate hydrolysis |
H. pylori |
Most common cause of gastritis. Associated w/ duodenal ulcers and maybe cancer. < 20% of people < 30 years old. 40-60% of people 60 years old. G-, non spore-forming, curved to spiral, microaerophilic, catalase+, urease+, motile polar 5-6 flagella, coccoidal pordms under culture. Route of infection is unknown. Urease production allows survival at pH of 2.0. able to split ammonia from urea --> alkaline environment. Toxin & lipposac may damage mucosla cells. Treatment requires multiple antibiotics. Antacids heal ulcers, but have no effect on H. pylori. Amoxicillin and omerprazole 3X daily each has 91% cure rate. Resistance is spreading (metroidazole and clarithromycin) |
H. pylori diagnosis |
Noninvasive: breath test, serology. Invasive: urease test, stain of histologic section, culture. |
Helivax |
H. pylori whole cell vaccine |
Clostridium perferingens |
8-22:12-24 hours. Diarrhea, cramps/abdominal pain, rarely nausea & vomiting. Cooked meat/meat products. Soil; raw food. Prevent by heating and rapid cooling. Release 2 toxins. CPE and beta toxin. Diagnosis by case history and symptoms; Large # of C. perfringens spores in feces; Incubate anaerobically for 24 hours at 37C; TSC; selective plating (black colonies) |
Clostridium |
G+ rods. Anaerobes. Motile or non-motile. Carb fermentation --> gas. Some produce exotoxins and others non-pathogenic. Soil, lower GIT, humans & animals. Susceptible to penicillin. |
Clostridium difficile |
Motile. Weak toxin producing. Nosocomial pathogen. Uncomplicated antibiotic-associated diarrhea to fatal antibiotic-associated colitis. Diarrhea can evolve into enterocolitis. Pseudomembranous colitis. Ampicillin, cephalosporins, clindamycin, amoxicillin can predispose to illness. Antineoplastic agent: methotrexate. Fever >101F & severe weakness. Hypoalbuminemia & leukocytosis common. Diarrhea when on antibiotic. |
Clostridium Type A |
Food-borne infection. Necrotic enteritis. Found in soil and dust (vegetables, fruits, meats, fish, poultry). 50% of meats contain Clostridium. Must ingest 106 – 107 organisms. Sporulation in gut. CPE --> diarrhea and cramps |
Spore-formation |
Clostridium and bacillus. Resistance to environmental stress. Resistant to heat when cooking. Ingestion of vegetative cells. |
CPE |
Clostridium perferingens enterotoxin. Watery diarrhea. Directly affects the permeability of the plasma membrane of mammalian cells causing fluid and electrolyte loss from the GI. Target thought to be SI but ileum is sensitive. |
C. difficile Toxin A |
Fluid accumulation in bowel. Weakly cytotoxic most mammalian cells. Causes extensive mucosal damage resulting in formation of hemorrhagic fluid, rich in albumin. |
C. difficile Toxin B |
Decrease cellular protein synthesis & disrupts microfilament system of cells (similar to diphtheria toxin) |
Diagnosis of C. difficile |
Differentials: ulcerative colitis, Crohn's disease. Endoscopic |
Treatment of C. difficile |
Discontinue antibiotic! Or use vancomycin or metronidazole. |
Clostridium botulinum |
12-26 hours:months. Food poisoning***: Fatigue weekness, double vision, slurred speech, respiratory failure --> death. In infants: constipation, weakness, respiratory failure --> death. In infants associated w/ honey. In food poisoning type A&B: soil and dust (vegetables, fruits, meat, fish, poultry); type E: water and sediments (fish). Thorough heating and cooling of food. Non-motile, produce potent exotoxins & extracellular enzymes (7 groups A-G). can progress from mild to severe disease fatal within 24 hours. |
C. botulinum toxin A |
Most potent. 10-8g will kill a human. A, B (most common in Europe), E found in humans but rarely F |
Infant botulism |
Most common form in the USA. Organism grows and produces toxin in intestines of infants. No known reason why only children. Toxins A and B. initial symptoms of illness and constipation are often overlooked. Proceeds to lethargy, child sleeps more than normal. Suck and gag reflexes diminish. Dysphagia becomes evident as drooling. Head control lost and infant becomes flaccid. Severe cases proceed to respiratory arrest. |
Food poisoning |
Ingestion of toxin. Preformed toxin contaminating food. Toxin is ingested along w/ food. Incubation time of about 18-36 hours. Small % of toxin absorbed through intestinal mucosa. 1/3 of type A/B have GI disturbances, all type E have GI disturbances. Toxemia symptoms apparent. No fever in absence of complicating infections. |
Wound botulism |
Organism grows in necrotic tissue of wound w/ no GI disturbance |
Botulism diagnosis |
Toxin demonstration in feces. Differential diagnosis: neurologic + GI. Treat w/ horse C. botulinum antitoxin + supportive measures (maintain respiration). |
Bacillus cereus |
2 types: emetic (onset 1-5, duration 6-24 hours; rice and pasta) and diarrheal (8-16:12-24 hours; meats, soups, sauces, vegetables). Soil and dust. Preventable by heating and rapid cooling of food. G+ rod. Arranged in chains. Aerobic or facultative. Emetic toxins and enterotoxin. |
Bacillus cereus diarrheal infection |
Resembles C. perfringens. Characterized by diarrhea and abdominal pain for 12-24 hours. LT enterotoxin production during vegetative growth in SI. |
Bacillus cereus emetic infection |
Resembles S. aureus. ST enterotoxin production by cells in food (peptide), when vegetative cells in late exponential/stationary phase |
Bacillus cereus diagnosis |
>105 org/g. Non-selective medium used, i.e. Blood agar. Diarrhea toxin by latex agglutination kit |
Staph aureus |
1-6:6-24 hours. Nausea, vomiting, cramps, diarrhea. Ham, meat, poultry, cream-filled pastries, whipped butter, cheese. Food handlers transmit. Prevention by heating and rapid cooling. Coagulase positive, catalase+, ST enterotoxin (7 types). Poor personal hygiene. Externsive food handling during processing. INTAKE OF TOXIN not organism. Self-limiting. Some emesis w/in 6 hours of ingestion, but not all vomit. Infective dose: 105-108 organisms. Does not stimulate adenylate cyclase. |
S. aureus identification |
Baird-Parker (selective, diagnostic, recovery) Lithium cholride & tellurite (selective agents), egg yolk and pyruvate. Reduction of tellurite --> shiny, jet-black colonies surrounded by clearing zone. Confirm w/ coagulase test** |
Listeria monocytogenes |
3-70 days. Non-enteric nature. Meningo-encephalitis, still births, septicemia or meningitis in new borns. Dairy, meat, vegetables. Via soil, infected animals, manure, handling of food and preperation practices. Demographic changes (elderly and immunocompromised). Prevent: pasteurised milk, deli meats & patés. G+ rod (short: appears cocci). Motile, non-sporing, non-capsulated. Aerobic/faculatative anaerobic. Resistant to low pH, high NaCl. Mother asymptomatic* or flu-like* --> fetus spontaneous abortion, still birth, neonatal septicemia, meningitis. Non-pregnant adult --> meningitis, meningoencephalitis. High fatality rate. Nonperinatal: bacteremia. Infective dose unknown. Intracellular pathogen. Engulfed by phagocytes. Produces listeriolysin O. multiply in phagocyte – invade other tissues. |
L. monocytogenes diagnosis/treatment |
Culture from blood, cerebrospinal fluid or stool. Enrichment broth (naladixic acid) selective enrichment agar. Listeria selective. Selective agents: lithium chloride, moxalactam. Ampicillin, cholramphenicol |
Enteroviruses |
No diarrhea or GI symptoms. Picornaviridae. Poliovirus 1-3, coxsackieviruses, echoviruses. Infect, inhabit and shed in GIT. Asymptomatic infections. Direct or indirect orol-fecal transmission; sewage contaminated water; insect vectors. Multiplication in tonsils, lymph nodes of neck and intestinal mucosa. Dissemination via bloodstream. Shedding in feces. |
Poliomyelitis |
Poliovirus. 3 classes of disease: abortive poliomyelitis, nonparalytic (aseptic meningitis), paralytic. Inactivated (killed) polio vaccine: Salk (1955) and sabin live attenuated(1963) |
Aseptic meningitis |
Primary echoviruses (coxsackieviruses A and B also) |
Herpangia |
Fever & sore throat, ulcerated lesions on mucous membrane of oral cavity. Primary children 3-10 years, self-limiting. |
Respiratory illness |
Associated w/ pharyngitis. Military recruits. Several coxsackieviruses & echoviruses. |
Conjunctivitis |
Echoviruses, coxsackieviruses and enteroviruses. Acute hemorrhagic conjunctivitis (tropical coastal) |
Neonatal disease |
Primary coxsackievirus B and echoviruses. Transplacentally aquired. Asymptomatic response or cardiac/respiratory distress & death |
Myocarditis |
Primary coxsackieviruses A & B. newborn, children and adults. Neonatal: often fatal, rapidly developing cyanosis & circulotory collapse precede death. Older children & adults recover but heart damage may occur. |
Pleurodynia |
Coxsackie group B. children 5-15yrs & adults. Characterized by pain over lower rib cage (upper abdomin). Self-limiting w/ duration of 4-7 days. |
Hepatitis A virus |
enterovirus 72. 15-50 days:weeks-months. Fever, weakness, nasuea, discomfort, often jaundice. Raw or undercooked shellfish; sandwiches, salads contaminated w/ human feces. Cook shellfish thoroughly; general sanitation & overcrowding. Virus shed in feces. |
Viral diarrhea |
Importance: half of diarrheal disease. |
Viral criteria |
Visualization of virus particles. 108/gram stool. Establish virus detection in symptomatic more frequently than asymptomatic patients. Demonstrate humoral and/or secretory antibody response in patients shedding virus. Reproduce disease – experimental inoculation of animal host. Exclude all other known causes of diarrhea. |
Rotavirus |
1-3:4-6 days. Gastroenteritis 1-3 days. Sudden onset watery diarrhea w/o vomiting up to 6 days. Diarrhea esp in infacts and young children. Complication: dehydration may kill. Raw/mishandled food w/ human fecal contamination. General sanitation. Distinctive wheel shape. 11 segment double stranded DNA. Double-layered capsid. Infants and children world wide. Almost all kids under 4 will have been infected. Unsafe water, inadequate sanitation. < 6 months and > 5 years asymptomatic. Protection against diarrheal infections. Temperate developed countries: winter gastro. Tropical, developing countries: year long (Summer). |
Rotavirus pathogenesis |
Feco-oral, water-borne, air-borne. Incubation period < 48 hours. Multiplies in epithelial cells of SI. Feces contain 108 – 1010 virus particles/mL. Shedding may persist for 10 days or more. Peak within 8 days. |
Rotavirus detection |
Virus in stool. Latex agglutination, ELISA, EM, elecrophoresis of RNA segments. |
Rotashield |
Live oral tetravalent vaccine. Vaccine given w/ or w/o food. Not necessary to repeat if regurgitated. Reduce risk of feco-oral spread. Prevent 50% of rota cases. Some people developed virus w/ shorter period of vomiting and diarrhea. Associated w/ intussusception. |
Calcivirus |
Non-enveloped. SsRNA. Star of David appearance. Not cultured in vitro. Infants, young children and elderly. Rarely sporadic or epidemic gastroenteritis. |
Norwalkviruses |
Non-enveloped. ss+RNA. Leading cause of viral food-borne infections. 1-2:1-2 days. Nausea, vomiting, diarrhea, abdominal pains, headache, mild fever. Raw or undercooked shellfish, sandwiches, salads w/ human fecal contamination. Cook thoroughly, general sanitation. Winter seasonality |
Norwalk pathogenesis |
Feco-oral transmission. Water and food borne. Raw shellfish. Virus grows in SI. Transient lesions in intestinal mucosa. Spares LI (No fecal leukocytes). Shed in feces. |
Norwalk-like viruses |
Considerable genetic homology w/ Norwalk. Shared virological characteristics. (MMWR 50*). cycles of infection says fomites (toilets) can transmit as well as contaminated foods. |
Astroviruses |
Astroviridae. Non-enveloped. Smooth or slightly indented outer shell. Inner 5 or 6 pointed star shaped core. 6.8kb +sense ssRNA. Responsible for 2-8% of sporadic cases in infants. 7 serotypes |
SRSV's |
Small round structured viruses. Some are calciviruses and some astroviruses. More molecular data is needed. |
Adenoviruses |
2 genera: mastadenoviruses and aviadenoviruses. Icosohedral protein shell. 252 capsomeres. Protein core. dsDNA. 12 vertices pentons each w/ fiber. 2 serotypes associated: 40 & 41 (Group F). conjunctivitis, pharyngitis, gastroenteritis. Main target respiratory tract. Pharynx, conjunctiva, SI, and occasionally other organ systems. Spread beyond local lymph nodes not usual. Many replicate in intesine and are present in stool. Diarrhea w/ or w/o vomiting. Sencond only to Rotavirus. |
Hepatitis E virus |
Nonenveloped symmetrical +sense ssRNA. Incubation period longer then HAV (mean 6 wks). |
Toroviruses |
Emerging pathogen. First found in calves |
Short-acting Mushroom toxin |
Museinol, muscarine, psilocybin, coprius, artemetaris, ibotenic acid. Incubation < 2 hours. Vomiting, diarrhea. |
Long acting mushroom toxin |
Amantia. 4-8hrs. Diarrhea, abdominal cramps FATAL |
Ciguatera poisoning |
Carribean/tropical pacific. Dinoflagellates: ciguatoxin. Large predatory reef fish: barracuda, grouper & amberjacks. Acute GI symptoms 3-6 hours after ingestion. Watery diarrhea, nausea, abdominal pain (12 hours). Neurologic symptoms: circumoral & extremity paresthesia, severe pruritis, hot/cold temp reversal. |
Scrombroid poisoning |
Bacteria: histamine (scrombotoxin) Fish: tuna, mahi-mahi, marlin & bluefin. Burning sensation in mouth, metallic taste. Acute GI symptoms: mins-3hrs after ingestion: watery diarrhea, nausea, lasting 3-6 hours. Dizziness, urticaria (rash), facial flushing, generalised pruritus, paresthesias |
Gastroenteritis |
Vomiting as primary symptom; diarrhea may be present. Viral gastroenteritis, most commonly rotavirus. Preformed toxins (S. aureus, B. cereus), |
Noninflammatory diarrhea |
(normally) No fever, dysentery, watery diarrhea. Classic symptoms of ETEC, V. cholerae, and enteric viruses, but may be caused by virtually all enteric pathogens. |
Inflammatory diarrhea |
Invasive gastroenteritis, grossly bloody stool and fever maybe present. Shigella sp., Campylobacter sp., Salmonella sp., EIEC, V. parahemolyticus, Y. enterocolytica |
Neurologic manifestations |
Parastheisias, respiratory depression, bronchospasm. Botulism (Clostridium toxin), Guillan-Barre syndrome (associated w/ infectious diarrhea due to C. jejuni) |
Systemic illness |
L. monocytogenes, V. vulnificus, HAV |