B. anthracis - C. difficile Flashcards
B. anthracis is large, Gram (__), and catalase (__)
Gram + ; catalase +
B. anthracis forms ___ and the colonies have ___ heads on agar plates
spores; medusa
What kind of hemolysis does B. anthracis show?
non-hemolytic
In regards to Identification of B. anthracis, give a + or - next to each category:
string of pearls
capsule
motility
string of pearls: +
capsule: +
motility: -
For the following specimens, how would you identify them:
cutaneous anthrax
GI anthrax
Inhalational anthrax
cutaneous anthrax: vesicular fluid
GI anthrax: blood, stool, rectal swab
Inhalational anthrax: blood, sputum
note: protective antigen - EIA -do PCR for confirmation
B. anthracis is commonly spread from human to human. True or false?
false - primarily a disease of grazing herbivores, human acquisition by contact with infected animals
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.
cutaneous anthrax
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.
Inhalational Anthrax (Woolsorter’s disease)
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.
intestinal anthrax
For the following virulence factors of B. anthracis, give their function: pXO2 pXO1 PA + LF PA + EF
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)
B. cereus is facultative G (_) __ and is a ___ former
G(+) rod; spore former
What kind of hemolysis does B. cereus show?
beta-hemolytic
In regards to identification of B. cereus, give a + or - next to the following:
String of pearls
capsule
motility
String of pearls: -
capsule: -
motility: +
How does one contract B. cereus?
Cells/spores can come from contaminated food (FRIED RICE!); also from penetrating injuries
B. Cereus causes two types of disease: GI infections and Non-GI infections (not too common). Describe each.
GI infections: diarrhea -> slow onset or fast onset
Non-GI infections: systemic - septicemia, endocarditis, respiratory, CNS; local - wound, ocular, and bone infections
What are the virulence factors associated with B. cereus?
Enterotoxin: heat-labile (diarrheal-slow onset), heat-stable(fast onset)
PLC: eye destruction
C. perfringes is Gram (_) , ___ forming, and has ___ rods
Gram +
spore forming
anaerobic rods
C. perfringes grows very slowly. True or false?
false - rapidly (7 min)
In regards to identification of C. perfringes, what is the Nagler reaction?
alpha toxin will degrade egg-yolk on lower half, upper half has an anti-alpha toxin Ab so you don’t see white
What shape are C. perfringes’ rods and what hemolysis does C. perfringes show?
box-car shaped; beta-hemolytic
C. perfringes is normal colonic flora and can infect both ____ and ____
endogenously; exodogenously
This disease caused by C. perfringes is described by damage to arteries, reducing O2 supply -> growth of clostridium
Clostridal cellulitis
note: doesn’t involve muscle - less aggressive than gangrene
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
Clostridial myonecrosis (gas gangrene)
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?
toxin binds brush border -> Ca2+ dependent increase in PM permeability leads to ion loss
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.
Necrotizing Enteritis
This disease caused by C. perfringes is due to myonecrosis and necrotizing eneritis patients being bacteremic.
Septicemia
C. perfringes has 12 different toxins. Which one produces gas gangrene?
alpha toxin (phospholipase)
What is the function of alpha and theta toxin in C. perfringes?
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
This bacterium is motile, forms spores, is a Gram + rod, a strict anaerobe, and its spores look like tennis racquets
C. tetani
Most cases involving c. tetani occur where and which individuals?
mostly 3rd world countries and in newborns
What disease does c. tetani cause?
tetanus
What is the difference between cephalic and generalized tetanus?
cephalic: head is site of infection, poor prognosis
generalized: most common form that includes lock jaw, sardonic smile, drooling, irritability, and back spasms
What is the role of the virulence factor, Tetanospasmin in c. tetani?
migrates into CNS (retrograde) and leads to muscle spasticity
Death from c. tetani is the result of what?
muscle spasticity -> cardiac/respiratory complications
This bacterium is anaerobic, spore forming, and a G+ rod. It’s ID is based on clinical presentation.
C. botulinum
Describe the foodbourne disease caused by c. botulinum
18-30 hr onset, homeade canned food - initial blurred vision, abd. pain, no fever -> descending paralysis, respiratory arrest
Describe intestinal botulism caused by c. botulinum
most common form in infants (can’t survive in adults) - initially causes constipation, weak cry -> flaccid paralysis with resp. arrest (spores)
Which type of botulism is rare?
wound botulism - after traumatic injury with soil contamination
Which type of botulism is considered considered bioterrorism?
inhalation botulism
What is the mechanism of the botulism toxin?
prevents ACh release at peripheral cholinergic receptors - cause of flaccid paralysis
Binding of botulism toxin to the cholinergic receptor is irreversible. Explain. How is recovery possible?
toxin degrades SNARE proteins involved in docking of NT vesicles; recovery: regeneration of receptors
Describe the structure of botulism toxins.
heterodimeric
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.
c. diff
note: nosocomial; infants usually not susceptible
There are three steps to getting C. diff infection. What are they?
- antibiotic treatment
- exposure to strain that makes toxins
- inadequate immune response
What are the symptoms of c. diff?
mild: diarrhea, abdominal cramps, fever, mild leukocytopenia
severe: up to 20 shits/day, abd. pain, peritonitis, marked leukcytopenia, high fatality rate
What is special about c. diff spores?
they survive stomach pH and colonize the GIT
C. diff toxin A is an enterotoxin and toxin B is a cytotoxin. What is their mechanism in infection?
toxins disrupt epithelial layer and cause cell death -> ulcers, necrosis, pseudomembranous colitis
