TOXIN MEDIATED FOODBORNE DISEASES

Epidemiology &
Organism Structure Pathogenesis Transmission/Source IP Lab Tests/Diagnosis Treatment/Prevention
Clinical Signs
- G(+) bacillus, Cat (-), - heat labile neurotoxin (A & B - animal/human feces into soil - symmetrical, upper extremity 12-36 hrs - clinical presentation & - evaluate respiration,
endospore, most common) and water à spores contaminate muscle weakness starting with history ventilatory support
anaerobic - degrades SNAP- food à spores germinate in food eyes then downwards - identify toxin via mouse - botulinum specific
Clostridium 25/Synaptobrevin/VAMP proteins (adult) or in GI tract (infant) à - respiratory failure bioassay antitoxin (hyperimmune
botulinum à ACh not released à no muscle toxin à ingested and/or - nausea & dry mouth globulin): neutralizes
contraction absorbed - 5 D’s: diplopia, dysarthria, dry circulating neurotoxin
- 2 forms = foodborne or infant - improperly prepared canned mouth, dysphagia, descending equine-derived heptavalent
- infant: spores germinate into foods paralysis botulinum antitoxin (HBAT)
vegetative cells in colon & - avoid dented/swollen/bulging - no fever, slow HR, -/+ for kids >1yr & adults
colonize à exotoxin cans or jars diarrhea/constipation -human derived bivalent
- prefer high moisture, low salt, - infant = honey & environmental - Infant: weak cry, irritability, lack (A&B) antitoxin for <1yo
low acid, no O2, no refrigeration dust of prior head control, lethargy,
drooling, refusal/inability to feed
à “floppy baby”
- colonize GI tract à feces in soil - roast beef, turkey, deli meats, - nausea, vomiting 8-16 hrs
Clostridium à spores contaminate food & gravy dishes
Perfringens resist cooking à germinate & Lasts
grow in food à vegetative <24-48
sporulate & produce enterotoxin hrs
- Enterotoxin is heat labile pore
forming cytotoxin
- damages ileal brush border à
loss of fluid & intracellular
proteins
- G(+) cocci in - enterotoxins - direct contact from food handler - diarrhea 1-6 hrs
clusters, Cat (+), Coat - SEA (most common) (has active infection or carrier)
Staphylococcal (+) - SEB - salty, high fat (mayo, ham, dairy) Lasts <24
aureus - B-hemolysis - SEC - hard boiled eggs hrs
- yellow colonies; - stable, withstands acid,
Mannitol Salt Agar proteolysis, heat at 100C for 30
min
- intestinal serotonin release à
stimulates receptors on vagal
afferent neurons à nausea,
vomiting
Bacillus - G(+) bacillus, - Emetic = performed toxin - Emetic = starchy foods - Emetic = vomiting, nausea, 1-6 hrs
Cereus endospore, Cat (+), ingested (cereulide), heat stable - Diarrheal: meats, veggies, dried abdominal cramps, diarrhea
aerobic polypeptide, binds serotonin beans, fried rice, dairy - Diarrheal = profuse diarrhea, 8-16 hrs
receptor of vagus n. abdominal cramps, nausea
- Diarrheal = replicates in SI, toxin Lasts <24
produce in vivo, heat labile, hrs
disrupts SI epithelial cell
membranes à inc fluid into SI
- G(-) comma, - O-antigen (O1 causes - human colon - mostly in developing countries 16-72 hrs - direct microscopy, rapid - fluid & electrolyte
facultative, oxid (+), pandemics; O139 produces - ingested via fecally- - watery diarrhea and vomiting antigen test replacement
alkalophile (likes capsule) contaminated water or food - liquid stool to hypovolemic - culture: thiosulfate citrate - antibiotic therapy
Vibrio salt), motile, - high dose required to infect shock in 4-12 hrs bile salts sucrose (TCBS) - Prevention: improve
Cholerae - TCP adheres to mucosal lining in agar sanitation, oral vaccines in
intestine (pilus) - alkaline pH, NaCl, yellow- some countries
- Lysogenic bacteriophage carries gold colonies (sucrose-
genes encoding cholera toxin fermenter)
subunits
- Cholera toxin: heat labile,
ganglioside receptors on
intestinal epithelial cells
- phosphyl. CFTR via Gas protein
 TOXIN MEDIATED FOODBORNE DISEASES
Epidemiology &
Organism Structure Pathogenesis Transmission/Source IP Lab Tests/Diagnosis Treatment/Prevention
Clinical Signs
Enterotoxigenic - G(-) baccili, - adhesion via CFA pili - fecally-contaminated food, - kids, infants in developing 24-48 hrs - antibiotics
E. coli facultative anaerobe, - stable toxin is heat stable: small water countries - antimotility agents to
(ETEC) ferment gluc & lact peptide, GTP to cGMP à - travelers to developing countries Lasts 3-4 reduce sxs
(hot pink on activates pKG à activates CFTR - watery diarrhea, frequent, may days - prevent via prophylaxis
MacConkey), reduce - labile toxin is heat labile: A:5B see mild fever, no RBC or WBC with bismuth subsalicylate
nitrate toxin is similar to cholera - vaccines available
- Cat (+), ox (-)
- motile

- bundle forming pilus BFP causes - direct contact - infants & children (2nd most
aggregation à intimate - hospitals usually implicated common cause of water diarrhea
attachment via lesions à Type 3 in infants in developing countries)
secretion injects Tir protein to act - can lead to hypovolemia,
Enteropathogenic as receptor for intimin à enzyme malnutrition, death
E. coli produces pedestal (rearranges - no RBC or WBC
(EPEC) actin)
- disruption of microvilli à
malabsorption
- tight junctions loosened à
watery diarrhea
- biofilm on surface of microvilli, - acute traveler’s diarrhea - antibiotics can help with
inflammation, toxin production - low grade fever, persistent persistent cases
Enteroaggregative - VF’s = fimbriae (aggregative - diarrhea in <6yo and adult HIV
E. coli adherence), cytotoxins, patients
(EAEC) enterotoxins
- shortening & rounding of villi à
malabsorption à watery diarrhea

ACUTE VIRAL GASTROENTERITIS

Epidemiology &
Organism Structure Pathogenesis Transmission/Source IP Lab Tests/Diagnosis Treatment/Prevention
Clinical Signs
- by contact - cooler months (Nov-March) 48 hrs
- usually in institutional settings - most common cause of acute
- resists chlorine infectious diarrhea Lasts 1-3
- children <2 yo, malnourished, days
Norovirus elderly, instutionalized
(Calciviridae) populations, personnel attending
sick
- sudden onset vomiting and/or
watery diarrhea
- no blood, no mucus, no fever
- serotype 40 & 41 are - usually single cases but can be in - <2yo, immunity by 3yo 8-10 days
Enteric responsible for gastroenteritis institutional settings - watery diarrhea, no blood
Adenovirurs - mucus in stool
- vomiting, abdominal pain, fever
- contaminated water or food - mostly children, some adults 3-4 days
- institutionalized populations
Astrovirus
- cooler months and during rainy
season
- childhood, malnourished, < 48 hrs - live attenuated vaccine,
elderly, institutional Rotarix, Rotateq
- temperate countries
Rotavirus
- sudden onset vomit (1-2 days)
(Reoviridae)
- watery diarrhea, abdominal
cramps, low grade fever,
dehydration
 INVASIVE FOODBORNE DISEASE
Epidemiology &
Organism Structure Pathogenesis Transmission/Source IP Lab Tests/Diagnosis Treatment/Prevention
Clinical Signs
Enterohemorrhagic - G(-) bacilli, - most common is O157:H7 - GI tract of cattle and herbivores - HUS = children <5yo and elderly 16-72 hrs - culture and direct toxin - supportive therapy
Shiga-Toxin facultative anaerobe, serotype - meat products contaminated - EHEC = most common cause of detection - antibiotics contraindicated
ferment gluc & lact - Shiga toxins 1 & 2 encoded by during butchering, undercooked renal insufficiency in children - Presumptive O157:H7 since doesn’t shorten
producing E. coli
(hot pink on lysogenic phage, A5B depurinates - veggies irrigated w/fecally- - severe abdominal cramping, screen: beige colonies on duration, inc release of
(EHEC, STEC)
MacConkey) adenine in 28S ribosome à contaminated water, not properly watery diarrhea, blood diarrhea SMAC, confirm E.coli Shiga toxin à inc risk of
- reduce nitrate inhibits protein synthesis à washed or cooked - can be complicated by - Confirm with anti-O157 HUS in kids
- cat (+), ox (-) attaches via sphingolipids hemolytic uremic syndrome serotyping - anti-motility agents
- motile - EHEC produces A/E lesions same (hemolytic anemia, schistocytes, - immunoassay for shiga contraindicated à inc HUS,
way as EPEC thrombocytopenia, azotemia, toxin in stool CNS dysfunction
leukocytosis, renal failure) - PCR for stx genes, serum
- blood cultures are neg IgM/IgG Abs
- Direct tissue invasion à fecal - Watery diarrhea, can progress to
Enteroinvasive leukocytes present, sometimes dysentery
E.coli (EIEC) mucus and blood
- no Shiga toxin
- G+ bacillus, - normal anaerobic intestinal - contact: spores survive for - risks = antibiotic exposure 5-10 - in vitro cytotoxin assay - Discontinue antibiotics
endospore, microbiota depletion permits months on surfaces days before, hospitalization, PPI - EIA for C. diff glutamate - Oral metronidazole or oral
anaerobic colonization & overgrowth of bug - endogenous: some people are usage DH vancomycin depending on
- opportunistic - Toxin A & Toxin B: endocytosed carriers - most common cause of - Toxin EIA for toxins A&B severity
Clostridium pathogen à glucosylate Rho proteins à antibiotic-associated diarrhea, or A - Oral probiotics with
difficile regulate cytoskeleton structure healthcare-acquired diarrhea, - PCR for toxin antibiotic therapy
à cell rounding, ulceration, antibiotic-associated colitis - Fecal transplant if
apoptosis, disrupt tight junctions - water diarrhea, low fever, antibiotics fail
- Toxin A: activates neutrophils leukocytosis - Prevention: hand hygiene
- Toxin B: more potent than A - severe form à higher fever, with soap and water NOT
- Hypervirulent strain: mutation in bloody diarrhea hand sanitizer (due to spore
toxin regulatory mechanism so - pseudomembranous colitis forming), contact isolation
produce more toxin; produces - fulminant colitis: perforation,
CDT (binary toxin) that ADP toxic megacolon
ribosylates A:B toxin; resistant to - post infectious IBS
fluoroquinolones
Vibrio - G – comma shaped, - thermostable direct hemoysin - raw or undercooked seafood - mild fever, vomiting, abdominal 16-72 hrs - leukocytes - antibiotics for severe
parahaemolyticus Ox + (Vp-TDH) an enterotoxin (mostly oysters) pain - halophilic vibrio, salt for cases
- cross contamination of food - explosive, watery diarrhea Lasts growth
- wound infection - cramping, headache, +/- RBC in <24hrs - isolation with TCBS agar
stools (blue green colonies)
- can become invasive, produce - B-hemolytic on blood agar
dysentery-like illness
- G – rod, ox – - Urease: protects against - vertebrates - mostly <5yo 4-7 days - Culture: MacConkey, small - Antibiotics for severe,
- ferments glu NOT stomach acid - meat (undercooked pork), - Risk: iron overload diseases, colorless colonies, complicated infections only
lact - Serum resistant via surface unpasteurized milk, tofu diabetes, malnutrition, Lasts 12- specialized selective
- non H2S producing proteins thalassemia 22 days medium
Yersinia - urease + - Yst enterotoxin similar to E.coli - winter peak - 25-28C for 48 hrs
enterocolitica - bipolar staining heat stable toxin - Watery diarrhea, low grade
- Inhibits phagocytosis (type 3 fever, abdominal pain
effectors) - Can lead to high fever and
- Invades intestinal epithelial cells leukocytosis
and localizes in local mesenteric - Sxs like acute appendicitis but
l.n. appendix normal
- terminal ileum inflamed
- fecal leukocytes found in stool
- nausea, vomiting, pharyngitis
- Complications = reactive arthritis
(Reiter Syndrome), erythema
nodosum, systemic infection
 INVASIVE FOODBORNE DISEASE
Epidemiology &
Organism Structure Pathogenesis Transmission/Source IP Lab Tests/Diagnosis Treatment/Prevention
Clinical Signs
- G – bacilli - Gallbladder colonization à - Human reservoir - Typhoid Fever (enteric fever): 10-14 - Culture of stool, urine, - Antibiotics based on
Salmonella typhi - ferment glu NOT asymptomatic carriers - “Typhoid Mary” diarrhea then constipation, high days rose spots, bone marrow susceptibility
lact (colorless on - Low/medium infectious dose - Ingestion of fecally fever - MDR stains
MacConkey) - Type 3 secretion contaminated food or water - Erythematous, maculopapular Lasts 1-3 - Prevention: live oral
- Produce H2S (black - Survive within phagocytes, rash on trunk wks vaccine, Vi polysaccharide
colonies) disseminate & infect bone - Complication: Guillain-Barre, Ag vaccine
- Motile marrow, liver, spleen, gallbladder, meningitis, GI bleeding,
ileal Peyer’s patches perforation

- Invade M cells in Peyer patches - All animals, reptilian pets - Salmonellosis (gastroenteritis) 6-48 hrs - Antibiotics do not reduce
& enterocytes via trigger - Eggs, poultry, dairy products, - watery diarrhea, cramping, duration & can increase
mechanism & membrane ruffling improperly stored food, cross fever, nausea/vomiting, myalgias, Lasts 2-7 carriage
Non-Typhoidal - Replicate in endocytic vacuoles contamination headache days - Prevention: inspection &
Salmonella spp. - Various proteins induce - Fecal-oral - no RBC, WBC+ monitoring of livestock,
neutrophil chemotaxis & - Can lead to bacteremia in proper preparation, avoid
inflammation à damage à fluid immunocompromised cross contamination
secretion
- G – bacilli - Attach to M cells on Peyer - Human reservoir - Shigella sonnei: developed Shigella - Methylene blue stools tain - Antibiotics for severe
- ferment glu NOT patches and enter via transcytosis - Fecal-oral transmission, low countries, day care centers, sonnei = WBC’s, RBCs cases, Shiga dysentery
lact (colorless on (T3SS injects proteins to induce infectious dose nurseries, custodial, 1-3 days - Stool culture, isolation of (reduces HUS), carriers
MacConkey) “membrane ruffling”) or - Resistant to acid and highly children/parents organism - Many strains are antibiotic
- doesn’t produce phagocytosis (via inflammatory communicable (hands, - Shigella fleneri: developing - MacConkey, EMB, XLD, resistant
Shigella H2S (green colonies) cytokine activation) food/water) countries Shigella-Salmonella agars - Antimotility agents
- Non-motile - Invades epithelial cells from - Shigella dysenteriae: type 1 is contraindicated and may
basolateral side most severe, developing prolong disease
- Lyses phagocytic vacuole, countries; complications = HUS,
replicates in cytoplasm seizures, reactive arthritis,
- Spreads to adjacent cells via hyponatremia, rectal prolapse,
actin “tails” toxic megacolon, obstruction,
- PMN infiltration loosens jxns perforation
- Enterotoxins induce further fluid - Watery diarrhea, progress to
secretion bloody and maybe dysentery,
- Infection moves from SI (watery) tenesmus (straining to pass stool)
to colon (bloody)
- S. dysenteriae: Shiga toxin
Campylobacter - G – curved rods - Invasive, inflammatory - Raw or undercooked - Guillain-Barre Syndrome: Abs to 2-4 days - Stool microscopy - Antibiotics for severe
jejuni/coli - gull wing shaped poultry/poultry products, O Ag recognize some human - Culture: cell morphology, disease
- ox + unpasteurized milk, untreated gangliosides biochemical tests, selective
- microaerophilic water - Reactive arthritis, rarely HUS medium, blood or charcoal
- Skirrow Agar = grey - Normal in animal GI tract but to remove ROS
contaminates food during
butchering, milking, egg shells
- Fecal-oral transmission, human
patients or carriers
Vibrio vulnificus - G(-) curved rod, - VF’s: capsule, RtxA toxin (pore- - Raw/undercooked seafood - Diarrhea, septicemia, cellulitis, - Stool, wound, blood - Antibiotics
motile forming and induces ROS à host (most common cause of death bullous, necrotic skin lesions culture on TCBS
cell death) from seafood) - nausea, vomiting, high fever, (blue/green)
- Wound infection chills, myalgias, hypotension

Listeria - G+, non- - Anaerobic & Intracellular - GI tract of animals - Headache, fever, muscle aches, 6hrs-10 - Blood cultures - Need to treat if invasive
monocytogenes sporeforming bacillus bacteria - Soil, water, vegetation, diarrhea days (GI), disease and fetal exposure
- Cat + contaminated foods (milk, soft - Nausea, vomiting, arthralgias 35 days
- tumbling motility cheeses, deli meats, hot dogs, - Complications: sepsis, mengitis, systemic
- B-hemolysis (grey unwashed veggies) fetal infection
colonies) - Can cross placenta