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GI (Elaina) > Lower GI Micro > Flashcards

Lower GI Micro Flashcards

1
Q

Food poisoning vs. Food-associated infection

A

Poison - food contains pre-formed toxins. sxs begin w/ 30 min to 6 hrs
Food-associated - organisms produce toxin in GI tract or invade mucosal epithelium

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2
Q

staph aureus characteristics

A 
bacteria
gram + 
cocci
catalase +
coagulase +
s. aureus
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3
Q

bacillus cereus characteristics

A 
bacteria 
gram + 
large bacilli 
endospore-forming 
facultative anaerobe
mostly motile 
B-hemolytic 
b. cereus
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4
Q

clostridium botulinum

A 
bacteria
gram +
bacilli 
spore-forming 
obligate anaerobe
motile 
c. botulinum
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5
Q

s. aureus sxs

A

N/V, stomach cramps, diarrhea 1-3 days

appears 1-7 hours after ingestion of food

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6
Q

S. aureus food reservoirs

A

Reservoirs are food that sits around a long time, allowing bacteria to start producing toxin. High salt concentrations are not enough to keep S. aureus from growing.
potato salad, ham, eclairs

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7
Q

which bug is frequently found on skin and is a threat in hospitals because it produces biofilms

A

bacillus cereus

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8
Q

box-car shaped gram + rods

A

bacillus cereus

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9
Q

where are bacillus cereus spores commonly found

A

in the soil and sometimes in plant foods that are grown close to the ground – such legumes, cereals, spices etc..

reservoir = rice

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10
Q

two forms of bacillus cereus food poisoning

A

emetic: 1-6 hrs, N/V, looks like s. aureus illness
diarrheal: 6-15 hrs, watery diarrhea and cramping, looks like c. perfringens infection

lasts 24 hours

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11
Q

mechanism of emetic b. cereus illness

A

Caused by preformed enterotoxin that forms holes in membranes:
cereulide, an ionophoric low molecular-weight peptide that is pH-stable and heat- and protease- resistant
Self limiting

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12
Q

mechanism of diarrheal b. cereus illness

A

Caused by large molecular weight enterotoxin that causes intestinal fluid secretion, probably by several mechanisms
This toxin is not likely pre-formed!
Ingestion of large amounts of bacteria cause it to generate the toxin in the small intestine

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13
Q

types of botulism

A

Foodborne botulism - ingest toxin in food
Wound botulism - generating toxin in wound
Infant botulism - ingest spores

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14
Q

botulinum toxin

A

a neurotoxin
irreversibly blocks the release of acetylcholine from the motoric end plate which results in muscle weakness and paralysis

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15
Q

sxs botulism

A

botulism

double vision, blurred vision, drooping eyelids, slurred speech, difficulty swallowing, dry mouth, and muscle weakness

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16
Q

sxs infant botulism

A

Incubation period, spores have to produce toxin-forming bacteria
lethargic, feed poorly, are constipated, and have a weak cry and poor muscle tone
Can lead to paralysis of respiratory system and other muscles

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17
Q

bacteria generating pre-formed toxins in food

A

s. aureus
b. cereus
c. botulinum

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18
Q

bacteria that are primarily transmitted through food

A 
c. perfringens*
salmonella enterica ssp.*
campylobacter jejuni*
listeria monocytogenes
vibrio parahaemolyticus
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19
Q

characteristics c. perfringens

A 
bacteria
gram +
bacilli
spore-forming
obligate anaerobe 
non-motile
c. perfringens
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20
Q

salmonella enterica characteristics

A 
bacteria
gram - 
bacillii
non-spore forming 
H2S positive and Lactose negative
motile, flagellated 
salmonella enterica
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21
Q

campylobacter jejuni characteristics

A 
bacteria
gram - 
bacilli (spirilli)
motile
cold sensitive 
c. jejuni
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22
Q

listeria monocytogenes characteristics

A 
bacteria 
gram + 
bacillus
non-fastidious
flagellated, motile
non-spore forming 
oxidase (-)
listeria monocytogenes
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23
Q

vibrio spp. characteristics

A 
bacteria 
gram - 
vibrio (curved rod)
facultative anaerobes
flagellated, motile
oxidase +
vibrio spp.
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24
Q

c. perfringens also responsible for

A

gas gangrene

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25
Q

special thing about c. perfringens

A

non-motile

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26
Q

sxs c. perfringens food-assoicated illness

A

Diarrhea and abdominal cramps
Incubation 6 to 24 hours (typically 8-12)
Symptoms last for less than 24 hours
Usually NO fever or vomiting
The illness is not passed from one person to another

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27
Q

reservoir c. perfringens

A

“C. perfringens infection often occurs when foods are prepared in large quantities and kept warm for a long time before serving”

Gives spores in food a chance to start bacterial growth

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28
Q

campylobacter jejuni reservoir

A

Campylobacteriosis is a zoonosis, a disease transmitted to humans from animals or animal products. Harbored often in poultry

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29
Q

what agar for c. jejuni

A

Karmali agar is a selective medium:
Charcoal-based.
Because it is difficult to grow, must eliminate competing microorganisms
Contains vancomycin active against the gram-positive organisms, cefoperazone active against many normal flora, cycloheximide active against yeasts

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30
Q

sxs campylobacteriosis

A

diarrhea, cramping, abdominal pain, and fever
2-5 day incubation
Symptoms can last a week
Can have vomiting, diarrhea can be bloody

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31
Q

mechanism c. jejuni illness

A

Symptoms are an inflammatory response to cell invasion

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32
Q

important complication of c. jejuni

A

Guillain-Barré syndrome (also reactive arthritis)

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33
Q

guillain-barre presentation

A

Initial symptoms: weakness or tingling sensations in the legs.
Symmetrical weakness and abnormal sensations spread to the arms and upper body.
Possible increase in intensity until certain muscles cannot be used at all and, when severe, the person is almost totally paralyzed.

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34
Q

guillain-barre risk factors

A

Infection with Campylobacter jejuni or having the flu or other infections (such as cytomegalovirus and Epstein Barr virus, respiratory infection)
vaccination.

35
Q

salmonella serotypes for typhoid fever (not food-related)

A

s. paratyphi A

s. typhi

36
Q

salmonella serotypes for gastroenteritis (salmonellosis)

A

s. enteritidis
s. typhimurium
others

37
Q

agar for salmonella

A

Salmonella Shigella (SS) agar has bile salts that inhibit gram-positive and coliform organisms. Contains indicator, lactose fermenting organisms would appear red from the acid produced (not present here), Ferric citrate added for indication of H2S production (black color is the produced iron sulfide precipitate)

38
Q

sxs salmonellosis

A

diarrhea, fever, and abdominal cramps
12 hr to 3 day incubation
Symptoms typically last 4 to 7 days
Most persons recover without treatment

39
Q

possible complication of salmonellosis

A

reactive arthritis

40
Q

tx salmonellosis

A

Hydration. Antibiotics only necessary if infection spreads beyond gut.

41
Q

mechanism salmonellosis

A

Salmonella replicates in host cells as well as invades
Some genes expressed by Salmonella mediate closure of ion channels to that water and electrolytes are secreted to the lumen

42
Q

reservoir salmonella

A

eggs, raw milk, veggies

turtles/reptiles

43
Q

vibrio spp. causes

A

V. cholerae causes cholera, other species cause diarrhea and other GI distress

44
Q

how to identify vibrio in culture

A

Mixed culture of oxidase-negative Escherichia coli (colorless) and oxidase-positive Vibrio cholerae (purple) showing how the direct oxidase test differentiates between the two organisms.
Kovács oxidase reagent was added directly to the plate.

45
Q

what distinguishes vibrio from enterics

A

flagellated, motile

oxidase +

46
Q

sxs vibrio parahaemolyticus

A

Fairly mild bloody diarrhea, stomach cramps, fever, nausea, and/or vomiting,
Symptoms last less than a week.
In the immunocompromised, it can spread to the blood and cause serious or deadly infections in other parts of the body

47
Q

mechanism of disease v. parahaemolyticus

A

Likely through enterotoxins: hemolysins TDH (thermostable direct hemolysin) and/or TRH
V. parahaemolyticus lacking these toxins is not pathogenic
Form pores in red blood cells but also in epithelial cells, disrupting gut homeostasis

48
Q

vibrio parahaemolyticus reservoirs

A

shellfish

49
Q

listeria monocytogenes hemolysis

A

β-hemolytic but zone of discoloration is really only directly under the colonies

50
Q

Listeriosis presentation

A

Mild GI infection for most
More vulnerable are older adults, pregnant women, newborns, and adults with weakened immune systems OPPORTUNISTIC
Fever and muscle aches or stiff neck, or if you develop while pregnant: fever and chills
Meningitis and sepsis in vulnerable populations

51
Q

mechanism listeria monocytogenes

A

Invasive mechanism
If you have the classic clinical symptoms, the disease has already reached the invasive stage
Immune cells spread Listeria to other organs = Trojan horse
Once escaped from the vacuole, cells in cytosol utilize actin polymerization to move and spread to new cell
Liver is a major target

52
Q

listeria monocytogenes

A

Foods you don’t cook
Hardy bacterium can hang a long time at food processing facilities

sprouts, deli meats/hot dogs, smoked seafood, soft cheese, raw milk

53
Q

shigella subtypes

A

Shigella sonnei: most Shigella-caused GI illnesses
Shigella flexnori: causes bacillary dysentery
Shigella dysenteriae: rarest but most severe dysentery
Invasive and produces a toxin

54
Q

shigella transmission

A

Mostly bacterium passing from stools or soiled fingers of one person to the mouth of another person.

55
Q

shigella sxs

A 
diarrhea (often bloody)
fever
stomach cramps
Symptoms start 1-2 days following exposure
Usually resolves in 5 to 7 days.
56
Q

What is dysentery?

A

Frequent, small bowel movements with blood and mucus, accompanied by rectal pain and spasms (tenesmus)

57
Q

shigella characteristics

A 
bacteria 
gram (-)
Bacillus 
facultative anaerobe 
nonmotile 
non spore-forming
mainly lactose negative, H2S (-)
Shigella ssp.
58
Q

Shigella spp. mechanism of diesease

A

gain access through M cells - mediated by type III secretory system and other effector proteins and cytoskeletal rearrangements –> apoptosis of macrophage, survival of bacteria –> inflammation

59
Q

shigella use _____ to move around

A

actin rockets

60
Q

Do you treat shigella?

A

Since Shigella is invasive, if not treated it can spread beyond the GI tract and cause complications
Antibiotics for more severe cases, most usually resolve without antibiotics

61
Q

possible complcation of shigella

A

hemolytic uremic syndrome

s. flexnori can also cause reactive arthritis

62
Q

why is shigella systenteriae so bad?

A

Invasive, plus has a phage-borne toxin
Shiga toxin, also called the verotoxin (act on Gb3 receptor on epithelial cells)
Toxin acts on vascular endothelial cells
–> most severe dysentery

63
Q

Diseases caused by E. coli

A

Diarrhea
Urinary tract infection
Neonatal sepsis
Gram-negative sepsis

64
Q

e. coli characteristics

A 
bacteria 
gram (-)
bacillus 
facultative anaerobe
motile 
non spore forming 
mainly lactose positive 
e. coli
65
Q

STEC

A

Shiga toxin-producing E. coli (STEC)—Also known as VTEC or enterohemorrhagic E. coli (EHEC)
Outbreaks in U.S. O157:H7

66
Q

ETEC

A

Enterotoxigenic E. coli (ETEC)

Traveler’s Diarrhea, diarrhea in children

67
Q

how does ETEC deliver toxin

A

on top of microvilli - deliver of LT or ST enterotoxins

68
Q

mechanism of ETEC toxin

A

activates adenylate cyclase, end result water into lumen, NO bacterial penetration.

69
Q

How does STEC deliver toxin

A

intimate attachment of bacteria –> actin condensation and microvillus effacement –> delivery (much more, closer)

70
Q

sxs ETEC/STEC

A

profuse watery diarrhea and abdominal cramping
Can progress to bloody diarrhea for STEC
Fever, chills
Nausea with or without vomiting, loss of appetite
Less common: headache, muscle aches and bloating
Incubation:1-3 days ETEC, 3-8 for STEC
Illness typically lasts 3-4 days, less than 10.

71
Q

possible complications STEC

A

hemorrhagic colitis (HC) and/or HUS can result as a complication; children more vulnerable

72
Q

do you treat e. coli

A

abx NOT recommended (HUS)

73
Q

typical E. coli food reservoirs

A

fecal-oral

ground beef, leafy vegetables

74
Q

primary reservoir for V. cholerae

A

water

75
Q

vibrio cholerae: only ____ produce ____ and cause ____

A

Typically only serogroups O1 and O139 produce cholera toxin and thus cause cholera

76
Q

mechanism cholera toxin

A

Activates adenylate cyclase
inc. cAMP → dec. Na+ absorption, inc. Cl- excretion
Water moves into lumen

77
Q

cholera presentation

A 
profuse watery diarrhea, sometimes described as “rice-water stools,”
vomiting
rapid heart rate
loss of skin elasticity
dry mucous membranes
low blood pressure
thirst
muscle cramps
restlessness or irritability
78
Q

tx cholera

A

antibiotic therapy may help for severe cases, rehydration therapy is really the biggest factor in treatment.

79
Q

S. Typhi reservoir

A

Untreated water is the source, humans are the only carriers

80
Q

Typhoid fever

A

Life-threatening illness
In GI tract and then to bloodstream
High fevers (103-104 °F)
Weakness and headache
Stomach pains, loss of appetite, diarrhea or constipation
Sometimes, a rash of flat, rose-colored spots
After symptoms clear, person could become a carrier

81
Q

abx for typhoid fever?

A

YES. because of the danger of having a S. Typhi symptomless carrier…feces still contain the bacteria, and illness could reoccur.

82
Q

Low inoculum organisms

A

Tens to hundreds of virions/cysts/bacteria will cause disease
Shigella, Giardia, Entamoeba, Norovirus
STEC E. coli, only 100 organisms

83
Q

High inoculum organisms

A

Tens of thousands or more needed

Vibrio cholerae, C. perfringens

84
Q

clostridium difficile characteristics

A 
bacteria 
gram +  (variable?)
bacilli 
spore-forming 
obligate anaerobe
motile 
clostridium

GI (Elaina) (7 decks)

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