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Med Micro > B. anthracis - C. difficile > Flashcards

B. anthracis - C. difficile Flashcards

1
Q

B. anthracis is large, Gram (__), and catalase (__)

A

Gram + ; catalase +

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2
Q

B. anthracis forms ___ and the colonies have ___ heads on agar plates

A

spores; medusa

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3
Q

What kind of hemolysis does B. anthracis show?

A

non-hemolytic

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4
Q

In regards to Identification of B. anthracis, give a + or - next to each category:
string of pearls
capsule
motility

A

string of pearls: +

capsule: +
motility: -

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5
Q

For the following specimens, how would you identify them:
cutaneous anthrax
GI anthrax
Inhalational anthrax

A

cutaneous anthrax: vesicular fluid
GI anthrax: blood, stool, rectal swab
Inhalational anthrax: blood, sputum

note: protective antigen - EIA -do PCR for confirmation

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6
Q

B. anthracis is commonly spread from human to human. True or false?

A

false - primarily a disease of grazing herbivores, human acquisition by contact with infected animals

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7
Q

This disease caused by B. anthracis is located on the head, neck, and extremities. There are painless lesions which turn black (eschars). There is no pus or fluid close to eschar but surrounding tissue has edema. 10% of cases are fatal.

A

cutaneous anthrax

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8
Q

This disease caused by B. anthracis can start as an mild URT infection (like viral) and after 1-3 days it can cause dyspnea, strident cough, chills, and is mostly fatal. This disease can also cause mediastinum widening and if untreated, the patient will die in 2-3 days.

A

Inhalational Anthrax (Woolsorter’s disease)

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9
Q

This disease caused by B. anthracis starts as a GI infection from eating infected meat (25-60% fatal). It then progresses to vomiting with blood, diarrhea, acute inflammation of bowel, and spreads via blood making more toxins along the way.

A

intestinal anthrax

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10
Q 
For the following virulence factors of B. anthracis, give their function:
pXO2
pXO1
PA + LF
PA + EF
A

pXO2: capsule (D-glutamic acid)
pXO1: edema factor, lethal factor, protective antigen
PA + LF: lethal toxin (degrades MAPK -> cell death)
PA + EF: edema toxin (massive edema, adenylate cyclase -> cAMP -> fluid accum)

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11
Q

B. cereus is facultative G (_) __ and is a ___ former

A

G(+) rod; spore former

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12
Q

What kind of hemolysis does B. cereus show?

A

beta-hemolytic

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13
Q

In regards to identification of B. cereus, give a + or - next to the following:
String of pearls
capsule
motility

A

String of pearls: -

capsule: -
motility: +

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14
Q

How does one contract B. cereus?

A

Cells/spores can come from contaminated food (FRIED RICE!); also from penetrating injuries

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15
Q

B. Cereus causes two types of disease: GI infections and Non-GI infections (not too common). Describe each.

A

GI infections: diarrhea -> slow onset or fast onset

Non-GI infections: systemic - septicemia, endocarditis, respiratory, CNS; local - wound, ocular, and bone infections

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16
Q

What are the virulence factors associated with B. cereus?

A

Enterotoxin: heat-labile (diarrheal-slow onset), heat-stable(fast onset)

PLC: eye destruction

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17
Q

C. perfringes is Gram (_) , ___ forming, and has ___ rods

A

Gram +
spore forming
anaerobic rods

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18
Q

C. perfringes grows very slowly. True or false?

A

false - rapidly (7 min)

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19
Q

In regards to identification of C. perfringes, what is the Nagler reaction?

A

alpha toxin will degrade egg-yolk on lower half, upper half has an anti-alpha toxin Ab so you don’t see white

20
Q

What shape are C. perfringes’ rods and what hemolysis does C. perfringes show?

A

box-car shaped; beta-hemolytic

21
Q

C. perfringes is normal colonic flora and can infect both ____ and ____

A

endogenously; exodogenously

22
Q

This disease caused by C. perfringes is described by damage to arteries, reducing O2 supply -> growth of clostridium

A

Clostridal cellulitis

note: doesn’t involve muscle - less aggressive than gangrene

23
Q

This disease caused by C. perfringes produces gas due to replicating organism, crepitus intense pain, rapid muscle necrosis, shock, renal failure, and the patient is dead in 2 days. Extensive surgical debridement is needed/amputation

A

Clostridial myonecrosis (gas gangrene)

24
Q

C. perfringes is the 2nd -3rd most common source of food poisoning. How does it cause ion loss through watery diarrhea in 8-22 hrs?

A

toxin binds brush border -> Ca2+ dependent increase in PM permeability leads to ion loss

25
Q

This disease caused by C. perfringes is 50% fatal! It is caused by strains that produce alpha and beta toxin which get high after a high-protein meal and sweet potato (trypsin inhibitor). There is necrotic destruction of jejunum and or ileum followed by abdominal pain, bloody diarrhea, and shock.

A

Necrotizing Enteritis

26
Q

This disease caused by C. perfringes is due to myonecrosis and necrotizing eneritis patients being bacteremic.

A

Septicemia

27
Q

C. perfringes has 12 different toxins. Which one produces gas gangrene?

A

alpha toxin (phospholipase)

28
Q

What is the function of alpha and theta toxin in C. perfringes?

A

leukocyte aggregation

note: requires a ton of AA’s and growth factors not available in normal tissues, but present in necrotic tissues, which is where the infections thrive

29
Q

This bacterium is motile, forms spores, is a Gram + rod, a strict anaerobe, and its spores look like tennis racquets

A

C. tetani

30
Q

Most cases involving c. tetani occur where and which individuals?

A

mostly 3rd world countries and in newborns

31
Q

What disease does c. tetani cause?

A

tetanus

32
Q

What is the difference between cephalic and generalized tetanus?

A

cephalic: head is site of infection, poor prognosis
generalized: most common form that includes lock jaw, sardonic smile, drooling, irritability, and back spasms

33
Q

What is the role of the virulence factor, Tetanospasmin in c. tetani?

A

migrates into CNS (retrograde) and leads to muscle spasticity

34
Q

Death from c. tetani is the result of what?

A

muscle spasticity -> cardiac/respiratory complications

35
Q

This bacterium is anaerobic, spore forming, and a G+ rod. It’s ID is based on clinical presentation.

A

C. botulinum

36
Q

Describe the foodbourne disease caused by c. botulinum

A

18-30 hr onset, homeade canned food - initial blurred vision, abd. pain, no fever -> descending paralysis, respiratory arrest

37
Q

Describe intestinal botulism caused by c. botulinum

A

most common form in infants (can’t survive in adults) - initially causes constipation, weak cry -> flaccid paralysis with resp. arrest (spores)

38
Q

Which type of botulism is rare?

A

wound botulism - after traumatic injury with soil contamination

39
Q

Which type of botulism is considered considered bioterrorism?

A

inhalation botulism

40
Q

What is the mechanism of the botulism toxin?

A

prevents ACh release at peripheral cholinergic receptors - cause of flaccid paralysis

41
Q

Binding of botulism toxin to the cholinergic receptor is irreversible. Explain. How is recovery possible?

A

toxin degrades SNARE proteins involved in docking of NT vesicles; recovery: regeneration of receptors

42
Q

Describe the structure of botulism toxins.

A

heterodimeric

43
Q

This bacterium is an anaerobic Gram + rod, spore forming, motile, and identified by 3 or more unformed stools per day for 2 or more days, as well as the presence of toxins A/B in stool. Its disease almost always follows antibiotic treatment.

A

c. diff

note: nosocomial; infants usually not susceptible

44
Q

There are three steps to getting C. diff infection. What are they?

A
  1. antibiotic treatment
  2. exposure to strain that makes toxins
  3. inadequate immune response
45
Q

What are the symptoms of c. diff?

A

mild: diarrhea, abdominal cramps, fever, mild leukocytopenia
severe: up to 20 shits/day, abd. pain, peritonitis, marked leukcytopenia, high fatality rate

46
Q

What is special about c. diff spores?

A

they survive stomach pH and colonize the GIT

47
Q

C. diff toxin A is an enterotoxin and toxin B is a cytotoxin. What is their mechanism in infection?

A

toxins disrupt epithelial layer and cause cell death -> ulcers, necrosis, pseudomembranous colitis

Med Micro (25 decks)

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