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Microbiology > GI Infections > Flashcards

GI Infections Flashcards

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1
Q

What is unique about Food Poisoning?

A
  • preformed toxins
  • very short incubation (because they don’t need to multiply - its the exotoxin that is doing the damage)
  • examples: S. aureus, bacillus cereus
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2
Q

What do GRAM (+) cocci look like?

rods/spiral/sphere

A

GRAM (+) cocci:

grape-like clusters

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3
Q

meaning of

catalase +/-

A

catalase + (which means it breaks down peroxide into water and O2 (contributes to bubbling rxn)

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4
Q

Explain Mannitol Salt agar?

A

grows on manitol salt agar (MSA) and turns plate yellow
-only gram (+) can grow
-S. aureus metabolizes mannitol (yellow plate)
(S. Epi plate doesn’t turn yellow, stays pink)

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5
Q

S. aureus characteristics

A 
gram (+)
catalase (+)
grape like clusters
SALT tolerant
normally found in approx. 30% of humans (nose)
mannitol SALT agar (yellow)
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6
Q

S. aureus virulence

endotoxin / exotoxin

A
  • enterotoxin!
  • heat stable
  • don’t let food sit at room temp and it will not have a chance to grow
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7
Q

S. aureus signs and symptoms

A 
Symptoms: 3-6 hours after ingestion
Severe vomiting
Cramps
With/w.out diarrhea
Recovery 24-48 hours
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8
Q

S. aureus transmission

A

ingestion of contaminated food

-potato salad left out at room temp

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9
Q

Bacillus cereus characteristics

A 
gram (+) rod
produces endospores (you remember the other species anthrax)
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10
Q

Bacillus cereus virulence

A

2 forms of enterotoxins cause gastroenteritis:

  1. Emetic: *think RICE (buzz word)
    - incubation is less than 6 hours
    - duration is 8-10 hours
    - heat stable
  2. Diarrhea: think MEAT and VEGETABLES
    - incubation is great than 6 hours
    - duration is 20-36 hours
    - heat liable
    - profuse watery diarrhea (via increased cAMP)
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11
Q

Bacillus cereus transmission

A

ingestion

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12
Q

food poisoning

A

S. aureus, bacillus cereus

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13
Q

examples of enterobacteria?

A

E. Coli
Salmonella
Shigella

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14
Q

enterobaceria common characteristics

A 
Gram negative rods
Facultative anaerobes
Ferment glucose
MacConkey agar
Catalase positive
Oxidase negative
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15
Q

where are enterobacteria found?

A

-for E. Coli and Shigella fecal contamination of:
soil
water
vegetation

-for Salmonella:
intestinal tract of humans and animals

note: enterobacteria cause GI infections (IT’S the organism causing us problems - they survive the stomach and make it to the intestine)
(not the same as food poisoning - where its the preformed toxin causing us problems)

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16
Q

MacConkey agar

A

Light pink color
Selective: only Gram negatives
Differential: detects lactose fermentation
Lactose positive: pink/purple colonies
Lactose negative: colorless/beige colonies

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17
Q

EMB agar

A

Lactose fermenter: dark colonies

E. coli: metallic green sheen

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18
Q

What is the #1 cause of UTI infections in normal healthy people?

(hint:
we use this bacteria to test the fecal contamination of the water supply
-most strains of this bacteria are non-pathogenic)

A

E. Coli

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19
Q

Enterotoxigenic (ETEC)

A
  • travelers diarrhea (fairly common)

- strain of ecoli

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20
Q

ETEC virulence

A

2 toxins:

  • LT1 is heat liable and increases cAMP
  • STa is heat stable and increases cGMP
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21
Q

ETEC transmission

A

*consuming fecal contaminated water or food

returning from a few days in Mexico and suddenly it hits you: (even brushing teeth, salad wash – their water sanitation system just is not what ours is here – most people from the area probably are adapted to it

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22
Q

ETEC signs and symptoms

A

Watery diarrhea
Abdominal cramps
Fever
Nausea/vomiting (possible, but not always)

Onset: 24 to 72 hours
Duration: 3 to 5 days

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23
Q

Enteroinvasive (EIEC)

A

rare in US

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24
Q

EIEC virulence

A
  • no enterotoxin produced

* has to invade the GI epithelium to cause illness

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25
Q

EIEC symptoms

A 
Onset: 10 to 18 hours
Watery diarrhea
Fever
Abdominal cramps
Bloody diarrhea w/leukocytes
Duration: 3 to 5 days

*once bacteria has invaded the immune system is activated and the watery diarrhea turns into Bloody diarrhea w/leukocytes

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26
Q

Enterohemorrhagic (EHEC) characteristics

A
  • very infective, only requires 10 - 100 organisms

- Buzz word: undercooked hamburgers

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27
Q

EHEC transmission

A 
Normally found in GI tract of
Cattle
Goats
Sheep
-spread fecal to oral
examples:
Alfalfa sprouts
Unpasteurized milk, juice
Petting zoos
Lettuce, spinach
28
Q

EHEC virulence

A

Produces powerful shiga-like toxins
(The toxin this e. coli produces is actually picked up from shigella; moved via phage – transduction)

Stx1 and Stx2 (verotoxin)
disrupts protein synthesis
receptor found on intestinal cells and kidney cells

29
Q

EHEC symptoms

A 
Incubation: 3 to 4 days
Start with watery diarrhea
Progresses to gross bloody diarrhea
Severe stomach cramps 
Low grade fever
Vomiting (not common)
Duration: 3 to 7 days
30
Q

EHEC complications

A

This shit can cause LIFE LONG complications!

Two syndromes:

  1. Hemorrhagic Colitis (Bloody diarrhea) - attacking intestinal cells
  2. Hemolytic Uremic Syndrome (HUS) - infection gets into blood and travels to kidney and start killing kidney cells
31
Q

Discuss Hemolytic Uremic Syndrome (HUS)

Around 5–10% of O157:H7 cases - children/elderly
(EHEC complication)

A

Thrombocytopenia
-decrease in platelets – so cant clot and you bleed more

Hemolytic anemia

Renal failure

Death: 3-5% patients

32
Q

How much antibiotic should you give to a patient with HUS?

EHEC complication

A

*Antibiotics will actually stress the e. coli cells in this case and the e coli responds by pumping out more toxin (so don’t give an antibiotic!!)

Won’t need to know treatment specifically but))
instead:
Dialysis for kidneys
fluids to combat dehydration

*A kid could be on dialysis for the rest of his life (because he ate a hamburger)

33
Q

EHEC diagnosis (lab characteristics)

A

-collect fecal specimens
Plate on Sorbitol-MacConkey agar
select colorless colonies
95% E. coli are lactose +, sorbitol +, BUT O157:H7 is lactose +, sorbitol –

OR
Direct detection of the shiga-like toxin (verotoxin)
Direct PCR to detect presence of SLT genes

WHat won't work: 
urine specimen (infection is not in kidneys)
34
Q

Sorbitol-MacConkey agar?

A

95% E. coli are lactose +, sorbitol +
O157:H7 lactose +, sorbitol –

In sorbitol MacConkey agar, lactose is replaced by sorbitol.
O157:H7 is unable to ferment sorbitol (colorless colonies)

35
Q

Other infections caused by E. Coli

A

UTI (urinary tract infection):

Endogenous infection (coming from your bladder)
Colon to urethra, then ascends into bladder
*pili is most important virulence factor in UTI infection (if it didn’t have this the flow of urine would wash it away)

(E coli is one of the major causes of)
Neonatal meningitis:

Mother to child (vertical transmission)
Septicemia: starts in GI tract or urinary tract then spreads

36
Q

Salmonella characteritics

A

gram (–) rod
LPS
colorless on MacConkey agar (does not ferment lactose)
*H2S positive

Only two species of Salmonella
BUT over 2300 different strains
reptiles carry both species (S. enterica and S. bongori)
S. enterica enteritidis - causes enteric infections with diarrhea (this is the one she cares about for this lecture)

37
Q

salmonella transmission

A

*ingesting contaminated food or water

38
Q

salmonella virulence

A

Bacteria multiply and **invade the intestinal mucosa

Ability to attach (colonization)
Ability to enter (invasion) columnar epithelial cells and M cells
Divides in the phagocytic vesicles and does not escape to the cytoplasm of the host cell

39
Q

salmonella symptoms

A

Short incubation time: 12-72 hours

  • Diarrhea with mucus +/- blood (mucus, puss, leukocytes, it’s all the same, it’s from the immune response)
  • Fever
  • Abdominal cramping
    duration: 2 to 7 days
40
Q

shrigella transmission

A

super infective (infective dose: 10 cells)
again fecal - oral route
Day care , nursing home – coming in contact with fecal matter

41
Q

shrigella characteristics

A

Lactose non-fermenter
**H2S negative (differentiate from salmonella!)
No animal reservoir, only humans

4 species that are human pathogens
Shigella sonnei 
most common in U.S.
Shigella dysenteriae  
most severe disease

Shigella flexneri
Shigella boydii

42
Q

shrigella virulence

A

similar to salomella - *invades intestinal epithelium (mcell) then replicates in macrophage, and spreads from cell cytoplasm to cell cytoplasm

Shiga toxin

  • inhibits protein synthesis
  • another one that - Damages intestinal epithelial cells and kidney cells (Hemolytic Uremic Syndrome)
43
Q

shrigella symptoms

A 
Incubation 1-4 days
Watery diarrhea
Abdominal cramps
Fever
Bloody diarrhea with mucus
*Dysentery: frequent passage of stools containing blood and mucous (small amounts of diarrhea occurring many times throughout the day)
duration: 2 to 3 days
44
Q

lab diagnostics / characteristics of:

Vibrio cholera and Vibrio parahaemolyticus

A 
Gram negative, curved rod
Facultative anaerobes
Marine organisms
Halophiles** (organisms that live in high salt con.)
Oxidase positive
45
Q

Vibrio cholera transmission

A

ingestion of contaminated food or water.

46
Q

Vibrio cholera symptoms

A

incubation: 2 to 3 days
Presence of toxin causes cAMP concentration to rise, which results in massive loss of water and electrolytes

Buzz word: “rice-water stools” (rice is mucus and puss along with tons of clear liquid, no solids coming out anymore)

47
Q

vibrio cholera virulence

A

Organisms adhere to intestinal mucosa of small intestine:

  • secrete cholera toxin
  • Cholera toxin: phage mediated, ctxA and ctxB
48
Q

vibrio cholera complications

A

Huge volume loss, can die from dehydration in 12 hours

49
Q

Vibrio parahaemolyticus characteristics

A

Shellfish are natural reservoirs (Oysters)

More common in southeast US (Gulf Coast)*

50
Q

Vibrio parahaemolyticus virulence

A

*produces an enterotoxin
thermostable direct hemolysin (Kanagawa hemolysin)

Induces chloride secretion by increasing intracellular calcium

51
Q

Vibrio parahaemolyticus symptoms

A

Incubation: 5-72 hours

Explosive, watery diarrhea

52
Q

Vibrio parahaemolyticus lab diagnostics

A

TCBS - thiosulfate citrate bile salts sucrose agar

-green agar that turns orange when Vibrios grow

53
Q

campylobacter jejuni characteristics

A

Gram (-) curved/spiral rod

  • Microaerophile
  • Capnophilic – likes CO2
  • contaminated chicken food products!
  • *leading cause of bacterial gastroenteritis in US (she repeated this 3 times – this is more common than salmonella – so when you consume raw eggs you’re more likely to get campylobacter than salmonella)

1.4 to 2 million infections/annually in U.S.

54
Q

campylobacter jejuni transmission

A
  • ingestion of contaminated food, poultry, milk or water

- requires a large dose due to susceptibility to stomach acid

55
Q

campylobacter jejuni lab diagnostics

A

Prefers 42C – higher than body temp – isolate in lab by putting on two plates 42 vs. 37 (only survives on one)

56
Q

campylobacter jejuni virulence

A

C. jejuni invades epithelium of small intestine, causes inflammation

57
Q

campylobacter jejuni symptoms

A
  • bloody diarrhea
  • fever
  • abdominal pain
58
Q

campylobacter jejuni complications

A

Associated with Guillain-Barré syndrome:

  • Autoimmune disorder of the peripheral nervous system
  • Antigenic cross reactivity of LPS and gangliosides
  • antibodies cross react with peripheral nervous system (thinks its getting rid of campylobacter, but its attacking itself instead)

Reactive arthritis

  • painful inflammation of the joints
  • antibodies cross react with joints (BUT NO INFECTION IN the joint!)
59
Q

Helicobacter pylori characteristics

A 
Spiral shaped curved rod
As culture ages, changes shape
*Gram negative (has LPS)
Can live in the stomach! (Acidophile!)
Microaerophile
Fastidious

70-90% of the population in developing countries has H. Pylori

60
Q

Helicobacter pylori virulence

A

*Urease - produces cloud of ammonia that neutralizes the stomach acid

flagella - allow for invasion of stomach mucosa

  • Block acid production
  • Neutralize acid with ammonia
  • Burrow into mucus
  • Attach to epithelial cells
61
Q

Helicobacter pylori symptoms

A

Fullness
Vomiting
Nausea

Hypochlorhydria (increases your risk of infection):
– people with a decrease in stomach acid (those using tums/antacid/Nexium (purple pill) – ahh **bacterial infection that is directly linked to cancer!

62
Q

Giardia lamblia transmission

A
  • Streams, lakes
  • wild and domestic animals
  • Contaminated water, fruits and vegetables

need to ingest: (10-25 cysts)

63
Q

Giardia lamblia symptoms

A

Incubation: 1-4 weeks (average is 10 days)
*Acute, onset of foul smelling, watery *diarrhea
cramps
flatulence
*steatorrhea.
duration:: 10 to 14 days

64
Q

Giardia lamblia characteristics

A

-Protozoa (2 stages!)

-Cysts (resistant stage)
Typically shed in stools
Infective stage
Spread by fecal-oral route

-Trophozoites (active stage)
Live in the intestine

65
Q

Giardia lamblia virulence

A

Gastric acid causes change from cyst to trophozoite
Trophozoite attaches to intestinal villi
Localized tissue damage

66
Q

Giardia lamblia diagnosis

A

Diagnosis:

-microscopy of stool sample, 1/day for 3 days

67
Q

Shrigella and Enterohemorrhagic (EHEC) e coli. are both quite infective

A

10 cells : shrigella

10 - 100 cells: EHEC

Microbiology (9 decks)

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