Initial inoculum

Birth: vagina and external genitalia. Initial colonization takes 2 weeks. 1^st 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)

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