B. anthracis - C. difficile

Question 1

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

Answer 1

Gram + ; catalase +

Question 2

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

Answer 2

spores; medusa

Question 3

What kind of hemolysis does B. anthracis show?

Answer 3

non-hemolytic

Question 4

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

Answer 4

string of pearls: +

capsule: +
motility: -

Question 5

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

Answer 5

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

note: protective antigen - EIA -do PCR for confirmation

Question 6

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

Answer 6

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

Question 7

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.

Answer 7

cutaneous anthrax

Question 8

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.

Answer 8

Inhalational Anthrax (Woolsorter’s disease)

Question 9

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.

Answer 9

intestinal anthrax

Question 10

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

Answer 10

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)

Question 11

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

Answer 11

G(+) rod; spore former

Question 12

What kind of hemolysis does B. cereus show?

Answer 12

beta-hemolytic

Question 13

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

Answer 13

String of pearls: -

capsule: -
motility: +

Question 14

How does one contract B. cereus?

Answer 14

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

Question 15

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

Answer 15

GI infections: diarrhea -> slow onset or fast onset

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

Question 16

What are the virulence factors associated with B. cereus?

Answer 16

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

PLC: eye destruction

Question 17

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

Answer 17

Gram +
spore forming
anaerobic rods

Question 18

C. perfringes grows very slowly. True or false?

Answer 18

false - rapidly (7 min)

Question 19

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

Answer 19

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

Question 20

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

Answer 20

box-car shaped; beta-hemolytic

Question 21

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

Answer 21

endogenously; exodogenously

Question 22

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

Answer 22

Clostridal cellulitis

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

Question 23

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

Answer 23

Clostridial myonecrosis (gas gangrene)

Question 24

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?

Answer 24

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

Question 25

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.

Answer 25

Necrotizing Enteritis

Question 26

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

Answer 26

Septicemia

Question 27

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

Answer 27

alpha toxin (phospholipase)

Question 28

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

Answer 28

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

Question 29

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

Answer 29

C. tetani

Question 30

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

Answer 30

mostly 3rd world countries and in newborns

Question 31

What disease does c. tetani cause?

Answer 31

tetanus

Question 32

What is the difference between cephalic and generalized tetanus?

Answer 32

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

Question 33

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

Answer 33

migrates into CNS (retrograde) and leads to muscle spasticity

Question 34

Death from c. tetani is the result of what?

Answer 34

muscle spasticity -> cardiac/respiratory complications

Question 35

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

Answer 35

C. botulinum

Question 36

Describe the foodbourne disease caused by c. botulinum

Answer 36

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

Question 37

Describe intestinal botulism caused by c. botulinum

Answer 37

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

Question 38

Which type of botulism is rare?

Answer 38

wound botulism - after traumatic injury with soil contamination

Question 39

Which type of botulism is considered considered bioterrorism?

Answer 39

inhalation botulism

Question 40

What is the mechanism of the botulism toxin?

Answer 40

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

Question 41

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

Answer 41

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

Question 42

Describe the structure of botulism toxins.

Answer 42

heterodimeric

Question 43

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.

Answer 43

c. diff | note: nosocomial; infants usually not susceptible

Question 44

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

Answer 44

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

Question 45

What are the symptoms of c. diff?

Answer 45

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

Question 46

What is special about c. diff spores?

Answer 46

they survive stomach pH and colonize the GIT

Question 47

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

Answer 47

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