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Food Microbio > Foodborne bacterial infections > Flashcards

Foodborne bacterial infections Flashcards

1
Q

what are two microorganisms that cause foodborne intoxication

A

Staphylococcus aureus and Clostridium botulinum

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2
Q

how does food borne intoxication occur?

A

it occurs from ingestion of a food containing a preformed toxin

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3
Q

what are 5 general characteristics of a foodborne intoxication?

A
  1. toxin is produced by a pathogen while growing in the food
  2. the toxin can be heat liable or heat stable
  3. ingestion of a food containing active toxin, not viable cells, is necessary for poisoning
  4. symptoms generally occur quickly, as early as 30 minutes after ingestion
  5. febrile symptoms are not present (no fever because there’s no immune response/no infection)
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4
Q

How does Staphylococcus aureus causes illness?

A

through the ingestion of the toxin NOT the organism

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5
Q

what is an enterotoxin?

A

a toxin that acts on the gastrointestinal tract

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6
Q

action of enterotoxin

A

toxin stimulates the vagus and sympathetic nerves

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7
Q

when are enterotoxins produced?

A

throughout most of the exponential growth phase

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8
Q

what is the optimal temperature for organism growth

A

37-40C (only 3h required at this temperature for sufficient toxin production)

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9
Q

what is the onset time for intoxication?

A

very quick onset (30min/toxin concentration), mean incubation is 4.4h (too fast for infection), 10hrs is maximum time to onset

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10
Q

what is infant Botulism

A

ingestion and intestinal proliferation of Clostridium botulinum, internal production of the toxin (infection) [GI of baby isn’t as diverse -> C. botulinum can grow in there and produce the toxin]

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11
Q

what is a common food known for C. botulinum

A

HONEY

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12
Q

how do you treat C. botulinum intoxication

A

with antibiotics/anti-toxins

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13
Q

to avoid C. botulinum spores to germinate in food, what is the ideal pH?

A

pH < 4.2

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14
Q

mechanism of action of botulinum toxin onces ingested

A
  1. following ingestion/production the toxin molecules are absorbed by the gut and are spread via the blood to peripheral nerves
  2. normally the axon termine of the neutron connects with muscle tissue through SNARE proteins and releases acetylcholine into the muscle cells which causes the contraction
  3. BoNT acts as a protease cleaving the SNARE proteins
  4. this deprives the muscle of acetylcholine signal and results in a flaccid paralysis
  5. this becomes a major issue when it comes to lung or heart muscles
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15
Q

what are 6 symptoms of Salmonella enteric infection

A
  • weakness
  • nausea and vomiting
  • fever
  • abdominal pain, bloating
  • muscle and joint pain
  • diarrhea
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16
Q

the genus Salmonella has … species

A

two

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17
Q

Salmonella enterica is grouped in to … subspecies

A

six

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18
Q

which subspecies of the genus Salmonella causes illness in humans?

A

Salmonella enterica subsp. enterica

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19
Q

which serovars of salmonella enterica subspecies enterica are associated with foodborne illness?

A

Serovars Typhimurium and Enteritidis

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20
Q

how do we treat uncomplicated cases of salmonella enterica infection?

A

supportive therapy, such as fluid and electrolyte replacement
=> Antibiotics prolong carrier state and increase AMR so they generally are not used!

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21
Q

how does a non-typhoidal salmonella infection manifests itself in immunocompromised people?

A

as an invasive disease, characterized by bacteria and high mortality rate

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22
Q

what are the growth conditions for Listeria monocytogenes? (temp, pH, salt content]

A
  • can grow and divide from 4-45C
  • It grows in the refrigerator and outcompetes other bacteria in this environment
  • in media as low as pH 4.4
  • in salt contents as high as 10% (and heat resistance increases as salt content decreases)
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23
Q

lowering the temperature doesn’t stop the Listeria monocytogenes growth BUT ….

A

it does slow it down

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24
Q

what are some sources of Listeria monocytogenes?

A

raw milk, ready-to-eat meats, cold-meats, deli (sausage/ham/hot dogs)

25
Q

why do Listeria monocytogenes survive well during cheese manufacturing?

A

due to both the cold temperature and high salt content , while many of its competitors die

26
Q

who should avoid eating raw milk cheeses and cold-meat products?

A

pregnant women and immuno-compromised people

27
Q

when can contamination of animal muscle with L. monocytogenes happen?

A

during or after slaughter

28
Q

which meats are especially good for L. monocytogenes?

A

ready-to-eat meats that are heated and then cooled in brine (competing bacteria are reduced)

29
Q

mechanism of action of Listeria moncytogenes infection

A

listeria monocytogenes-contaminated food -> intestine -> lymph node (kills macrophages and divide in lymph nodes if immunocompromised) -> blood stream -> liver and spleen -> brain and placenta (fetus)

30
Q

how do you render chicken liver safe for consumption (kill Campylobacter)

A

washing + cooking to an internal temperature of 70C for 2 min

31
Q

what are the clinical manifestations of Campylobacter infection?

A
  • gastroenteritis
  • typically following an incubation period of 24-72h acute diarrhea occurs and may be accompanied by fever, chills, headache, and abdominal cramping
32
Q

what is the most extensively studied extraintestinal manifestation associated with Campylobacter infection

A

Guillain-Barre syndrome (GBS) and Miller Fisher Syndrome

33
Q

what are the symptoms of Guillain-Barre syndrome (GBS) and Miller Fisher Syndrome

A

Symptoms generally begin with motor and sensory deficits in the lower extremities and spread to the upper extremities the trunk – this can lead to the need for ventilator support.

34
Q

what is the main difference between Miller Fisher Syndrome and more common variants of GBS

A

the main difference is that the first nerve groups to be affected by paralysis in patients with MFS are those in the head, resulting in difficulty controlling eye muscles and balance. Paralysis in other forms of GBS typically begins in the legs.

35
Q

when do most cases of Guillain-Barre Syndrome occur?

A

after C. jejuni infection

36
Q

how do patients infected with C. jejuni develop immunity?

A

antibodies are thought to be produced against certain antigens in the bacteria LPS that could cross react with peripheral nerve cell surface gangliosides

37
Q

what are the 3 factors taken into account when categorizing Escherichia coli ?

A

categorized into different pathotypes based on their:

  • ability to produce toxins
  • ability to adhere to epithelial cells
  • ability to invade epithelial cells
38
Q

how have the pathogenic traits of Escherichia coli been acquired?

A

through horizontal gene transfer

39
Q

are all E. coli dangerous?

A

no they can either be probiotics/neutral/bad/very very bad

40
Q

what are the means of E. coli invasion?

A
  1. actin rearrangement
  2. invasion through mucus attachement
  3. attachment by pili (part of bacteria)
  4. vacuole formation
  5. lateral spread by using actin tail
41
Q

what are the sources of E. coli?

A
  • fecal contaminant -> irrigation water
  • cross contamination
  • sewage
42
Q

what is Cronobacter infection almost exclusively associated with?

A

powdered infant milk formula

43
Q

who is at the greatest risk for Cronobacter infection?

A
  • powder infant formula fed infants less than 1 year old
  • immunocompromised and neonates younger than 28 days old are at the greatest risk
  • low birth-weight neonates
    premature infants born <37 weeks
44
Q

why are premature neonates at a particular risk for Cronobacter infection?

A

Premature neonates secrete less gastric acid than older infants which is important in the long-term survival of Cronobacter

45
Q

which bacterial genus is predominant in estuarine waters?

A

Vibrio sp.

46
Q

why can a few strains Vibrio sp. found in potential pathogenic species cause illness in humans?

A

because they have picked up virulence factors. However, most vibrio isolates found in potentially pathogenic species are non-pathogenic.

47
Q

which vibrio sp. strains cause illness in humans?

A

V. cholerae
V. parahaemolyticus
V. vulnificus

48
Q

what is Vibrio infection generally associated with?

A

seafood consumption (or seafood contact)

49
Q

what is “Vibrio season”?

A

when water that oysters are harvested from goes above 17C and causes Vibrio infection through Vibrio parahaemolyticus ingestion found in raw oysters
(colder waters produce safer seafood if only considering Vibrio infections)

50
Q

what is a key feature of Vibrio parahaemolyticus and what does it imply?

A

V. parahaemolyticus has a generation time of 8 to 9 minutes at 37C
The ability to grow rapidly means that contaminated food becomes highly colonized if temperature abused

51
Q

what is the onset time of Vibrio infection and what are the symptoms?

A

Symptoms appear 4 to 30 hours after the ingestion of contaminated food
Symptoms include diarrhea, abdominal cramps, nausea, vomiting, and fever

52
Q

which microorganism grows faster: E. coli or Vibrio sp.?

A

Vibrio sp.

53
Q

what is a physical symptom of Vibrio vulnificus?

A

microvascular petechial rash that can progress to dark, fluid-filled bullies lesions

54
Q

mechanism of action of Vibrio cholerae

A

It releases Cholera Toxin (CT) that binds to gangliosides receptors on the surface of intestinal epithelium cells
CT is internalized by endocytosis and triggers the production of cAMP within the cell
cAMP activates specific ion channels within the cell membrane, causing an efflux of ions from the cell
-> the build-up of ions in the intestinal lumen draws water from cells and tissues lai osmosis - causing acute diarrhea
As water is being removed from body tissues, dehydration will result if left untreated (can be fatal if untreated)

55
Q

growth environment of V. parahaemolyticus vs. V. vulnificus vs. V cholerae

A

cool water but warmer than 15C vs. warm water vs. tropical water

56
Q

symptoms of infection of V. parahaemolyticus vs. V. vulnificus vs. V cholerae

A

diarrhea, fever, abdominal cramps, nausea, vomiting
VS. fever, chills, nausea, skin lesions
VS. rice water stools (pale gray color), abdominal pain, loss of appetite

57
Q

Mortality rate of V. parahaemolyticus vs. V. vulnificus vs. V cholerae

A

very low vs. 40-60% vs. ~1% in worse case scenarios

58
Q

Virulence factors of V. parahaemolyticus vs. V. vulnificus vs. V cholerae

A

tdh and trh VS. Capsule, LPS, vvhA VS. Cholera toxin (CTX)

Food Microbio (11 decks)

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