1
Q
top 5 pathogens contributing to domestically acquired foodborne illnesses in US
A
- norovirus
- salmonella, non typhoidal
- c. perfringens
- campylobacter spp.
- s. aureus
2
Q
top 4 pathogens contributing to domestically acquired foodborne illnesses resulting in deaths in US
A
- Salmonella, nontyphoidal
- Toxoplasma gondii
- Listeria
- Norovirus
- Campylobacter
3
Q
most common causes of foodborne illnesses that cause the most hospitalizations
A
Salmonella non typhi
Campylobacter
4
Q
which two dudes are common contaminants but do not cause serious disease (toxin-mediated)
A
C. perfringens
S. aureus
5
Q
which two dudes are less common, but can cause fatal disease?
A
Listeria
E. coli O157:H7
6
Q
list the enteropathic bacteria
A
EHEC EIEC cholera shigella salmonella - typhi and non typhi campylobacter yersinia S. aureus (toxin) botulism (toxin) c. perfringens (toxin) B. cereus (toxin)
7
Q
enteropathic viruses
A
norwalk virus
enterovirus
polio virus
8
Q
enteropathic parasites
A
giardia
amoebae
ascaris
cryptosporiosis
9
Q
general pathogenesis of enteropathic bacteria
A
- ingestion of enterotoxins
- absorption of preformed toxin, short incubation time - hours - infection by colonizing toxigenic organisms
- hypersecretion reaction from bacterial adherence and toxin secretion
- incubation 1-3d - direct invasion of gut wall
- incubation time extended: days-weeks
10
Q
important virulence factors for adherence to mucosal cells
A
pili
flagella
11
Q
important virulence factors for production of enterotoxins
A
- prototype secretagogue toxin (vibrio cholerae)
- cytotoxins - Shiga toxin (shigella, E. coli O157:H7)
- T cell super Ag’s (staph enterotoxins)
12
Q
important virulence factors for capacity to invade
A
- intracellular proliferation, cell lysis, and cell-to-cell spread
- invasion and cytolysis result in bloody/pus diarrhea (dysentery)
13
Q
predisposing factors for enteropathic bacteria
A
- fecal contamination
- immunosuppression
- antispasmodic drugs (less movement through gut means more chance of overgrowth)
- antacids
- mucosal disease
14
Q
clinical presentation of enteropathic bacterias
A
- disease from absorbed toxin: local (staph) vs. systemic (botulism)
- secretory diarrhea (cholera)
- dysentery (shigella)
- systemic illness (typhoid fever)
15
Q
diarrhea vs. dysentery
A
diarrhea: excess fluid
- hypersecretion
- osmotic load (lactose intolerance)
dysentery: mucosal invasion
- inflamamtion + necrosis of wall
- loose stool + blood + leukocytes
16
Q
levels of tissue involvement/destruction in diarrhea
A
- toxin only (no bacteria)
- superficial colonization + toxin
- superficial colonization + inflammation
17
Q
levels of tissue involvement/destruction in dysentery
A
- mucosal invasion
- mucosal necrosis
- submucosal invasion
- systemic spread
18
Q
general characteristics of E. coli
A
G(-)
rods
green sheen on EMB agar
coliform - ferment lactose
19
Q
characteristics of E. coli disease
A
depends on strain:
- watery diarrhea, cramping pain, fever, malaise
- invasive or cytolytic disease (dysentery)
- verotoxin (shigatoxin) - hemolytic uremic syndrome
20
Q
hemolytic uremic syndrome
A
shiga toxin binds to glomerular endothelium -> clotting/inflammation
anemia
hemoglobinuria
renal failure
21
Q
pathogenic mechanisms of E. coli
A
- invasive disease (migrants, Indian reservations)
- toxigenic disease (traveler’s diarrhea)
22
Q
why do you not use imodium with Montezuma’s revenge?
A
it is an anti-motility drug: less motility of gut means more chance of overgrowth, easier overgrowth
23
Q
describe ETEC
A
watery “traveler’s diarrhea” from consumption of food contaminated with enterotoxin-producing strain
24
Q
describe EHEC
A
severe bloody colitis from consumption of hamburger, dairy products, or fruit juice, contaminated with invasive, verotoxin-producing (shiga toxin) strain (mainly O157:H7)
25
describe EAEC
primarily pediatric diarrhea in impoverished nations
26
describe where EHEC cannot grow
doesn't ferment sorbitol or grow at 45 degrees
27
sources of O157:H7
- cattle and beef products (hamburgers, unpasteurized milk)
- other ag products contaminated by products
- outbreaks: hamburgers, spinach, sprouts
-rarely transmitted person to person
28
O157:H7 mechanism of disease
- small infectious dose (less than 100 dudes)
- bacteria adhere to cell membrane, colonize large intestine
- produce shigatoxins -damage endothelial cells (inhibits mRNA translation, protein synthesis)
29
O157:H7 disease course
- onset 3-4d after ingestion
- severe abdominal cramping, watery diarrhea progressing to bloody after 3-4d
- occasionally vomiting
- fever low grade or absent
- duration average 8d
30
O157:H7 disease presentations
- asymptomatic
- mild/moderate illness (just watery diarrhea, abdominal pain, rare vomit, no fever)
- dysentery (grossly bloody diarrhea, severe abdom pain)
- hemolytic uremic syndrome (3-5% fatality rate, kids and elderly, acute renal failure - obstruction of glomeruli by microthrombi)
- TTP = thrombotic thrombocytopenic purpura (type of DIC)
31
how often do STEC non O157:H7 cause disease?
5-10% cause serious illness
32
what are STEC non O157:H7 associated with?
Stx2 and eae (intimin) genes (not as frequent or severe as O157:H7
33
general characteristics of shigella
G(-)
non-motile
non-coliform
34
how do you get shigella
fecal/oral transmission
daycare centers
MSM
35
pathogenesis of shigella
- invasive lesions of colonic mucosa which spreads to lymph nodes
- do NOT cause bacteremia
- exotoxin causes mucosal necrosis - fibrinosupporative exudate forms pseudomembrane as in diphtheria
- highly virulent: 12 dudes can cause disease
36
general characteristics of cholera
G(-)
comma
alkali tolerant
37
transmission of cholera
- direct fecal-oral transmission
| - asymptomatic carriers
38
pathogenesis of cholera
- no invasive lesions
- pathogenicity entirely due to enterotoxin
- induces secretion of isotonic fluid
- deaths due to dehydration and hypovolemic shock
39
where is cholera endemic?
endemic in India; recent pandemics in S. America
40
toxin of cholera - mechanism
- subunit A binds with ADP-ribosylates EF-2
- activates GTP-activated adenylate cyclase resulting in cAMP formation
- stimulates secretion of chloride and bicarb
41
hallmark symptom of cholera
rice water diarrhea
42
general characteristics of salmonella
G(-)
non coliform
H2S production
43
three forms of disease from salmonella
- typhoid (typhoid mary)
- enteric fever
- salmonella food poisoning
44
salmonella food poisoning: organisms
S. enteritidis
| S. typhimurium
45
salmonella food poisoning: transmission
- eggs
- undercooked chicken or meat
- contaminated waters
- turtles/reptiles
- cantaloupes
- mangos
46
salmonella food poisoning: symptoms
vomiting and diarrhea (gastroenteritis)
superficial lesions of colon
usually mild, self-limiting except in immunosuppressed
local epidemics traced to a single food source
47
salmonella food poisoning: pathogenic mechanisms
- invades mucosal cells - mucosal ulceration (superficial)
- NO enterotoxins
- multiply w/i neutrophils and macrophages
- can cause G(-) sepsis
48
normally osteomyelitis is caused by S. aureus. but in kids with sickle cell anemia, what is the main cause?
Salmonella!!
49
salmonella paratyphoid fever: organisms
- S. typhinurium
- S. paratyphi
- S. cholerae-suis
50
salmonella paratyphoid fever: symptoms
- fever
- bacteremia
- local lesions
associated with sickle cell disease, shistosomiasis
51
salmonella typhi - systemic disease. describe
typhoid fever
- fever
- rose spots on lower anterior chest and abdomen
- hepatosplenomegaly
- carrier state - 3-5% in gall bladder (not dissolved by bile)
- mild vomiting
- diarrhea uncommon
52
salmonella typhi pathogenesis
- systemic involvement: fever, rash
- invasion via involvement of mononuclear phagocytes
- results in splenomegaly; typhoid nodules throughout lymphoid tissues
- local ulceration of Peyer's patches
- colonization of gallbladder in carrier state
- neutropenia in peripheral blood
53
general characteristics of campylobacter enteritis (jejuni)
G(-)
comma
flagella
54
campylobacter jejuni presentation
one of the most common causes of gastritis, diarrhea, and dysentery in US - mostly self limited
55
campylobacter jejuni long term sequelae
associated with Guillain-Barre neuropathies
56
transmission of campylobacter jejuni
- ingestion of contaminated liquid or solid food, usually from animals (zoonotic)
- also think about when camping
57
campylobacter jejuni pathogenesis
- foul-smelling stools with blood or exudate***
- toxin/invasive lesions (colonic crypt abscesses)/adherence
-septicemia rare
58
yersinia entercolitica: who do you normally see it in + transmission
-mostly pediatric
- raw or undercooked pork
- unpasteurized milk
59
yersinia entercolitica pathogenesis
- upper and lower GI
- ulcerative intestinal lesions like typhoid fever, but NO systemic disease
- microabscess and granuloma formation
- deeply invasive and may be lethal (if extensive necrosis of GI tract)
60
rapid acting toxins: staph aureus
- common form of food poisoning from pre-formed toxin (enterotoxin)
- 2-4h
- more vomit than diarrhea
- resolves within 24h
61
rapid acting toxins: b. cereus
- fried rice syndrome
- associated with catering and buffets
- only 2-5% of food poisoning cases
- vomiting (1-5h) or diarrhea (8-15h), depends on strain
- production of enterotoxins (cereulide)
62
general characteristics of clostridiums
```
G(+)
spore forming
anaerobes
environmentally stable
produce fermentation products and degradative enzymes
```
63
what are clostridial diseases associated with?
elaboration of potent exotoxins and/or with invasive, destructive necrotic abscesses
64
transmission of clostridial diseases
"gut and soil" cycle - spores
- contamination of wounds (puncture wounds, necrosis)
- contamination of food (not killed during cooking)
65
pathologic mechanisms of clostridial diseases
- action of specific exotoxins cause specific disease even in absence of direct infection
- local growth leads to absorption and distribution of toxin
- spores difficult to kill
- growth favored in necrotic tissue/anaerobic environments
- growth accompanied by necrosis induced by several tissue damaging enzymes from bacteria
66
tell me EVERYTHING about C. tetani
- contamination of puncture wounds/necrotic tissue
- local growth + dissemination of toxin
- neurotoxin tetanospasmin
- affects presynaptic terminals of inhibitory spinal interneurons, resulting in severe convulsive contractions
- loss of sympathetic inhibition: high HR, HTN, CV instability, smooth muscle deficits (dysphagia, resp difficulty)
67
tell me all about C. perfringens
- gangrene/necrotizing cellulitis
- extracellular necrotizing enzymes (characteristic myonecrosis)
- invasion of traumatic/surgical wounds such as amputation stumps
- foul odor, thin and discolored exudate, wet gangrene
- gas gangrene: gas bubbles caused fermentative rxns; hemolytic destruction of RBCs
68
tell me about clostridial gastroenteritis
- one of the most common US forms of food poisoning
- improper preparation of meat, poultry w/ spores
- abdominal cramps + watery diarrhea
- incubation 6-24h
- usually resolves w/i 24h b/c no necrotic tissue for organism to grow in
69
tell me about C. diff
- pseudomembranous colitis
- diarrhea, clinical toxemia
- enterotoxin (toxin A) and cytotoxin (toxin B)
- nosocomial: associated w/ antibiotics, chemotherapy
- almost always hospital acquired, but if community acquired, shows suppression of gastric acid
70
tell me about botulism
- preformed neurotoxin cleaves synaptobrevin
- present in honey, improperly home canned foods
- usually does not involve direct infection of victim
- blocks release of ACh resulting in descending paralysis
- also get CN defects (diplopia, dysphagia)
- descending flaccid paralysis
- usually toxin w/o bacterial colonization
* *exception: neonates (honey) with necrotizing enterocolitis
Path
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