Kaplan Microbiology A4

Front 1

What are the 4 most important genera of gram-positive bacilli? How do you distinguish these groups from each other?

Back 1

1) Listeria
2) Corynebacterium
3) Bacillus
4) Clostridium

Bacillis and Clostridium form spores, Listeria and Corynebacterium do not.

Front 2

1) What is the physical makeup of Listeria monocytogenes?
2) Microscopically, what does it resemble?
3) How is Listeria transmitted?
4) Who is at risk for getting this diease?

Back 2

1) Small, gram + coccobacillus that doesn't form spores
2) Nonpathogenic members of Corynebacterium (diptheroids), normal skin flora
3) Facultative intracellular pathogen, infects phagocytic cells. Contaminated meat or unpasteurized dairy products.
4) Neonates, pregnant women, immunosuppressed, alcoholics

Front 3

1) What are the physical characteristics of Corynebacterium diptheriae?
2) What is primarily responsible for the symptoms of infeciton?
3) Clinical manifestations of diptheria?
4) Is this organism invasive? How does it spread?
5) Diptheria toxin is especially toxic to?
6) DOC for tx?
7) Prevention for getting diptheria?

Back 3

1) Nonmotile, club-shape, nonspore-forming, Gram + rod
2) Diptheria toxin, encoded by a lysogenic phage
3) URI with **tonsillar grayish pseudomembrane**, can spread + compromise airway.
4) Not invasive, but toxin absorbed systemically/acts on other tissues.
5) The heart - can cause cardiac failure
6) Antitoxin, erythromycin ASAP
7) Vaccine containing diptheria toxin when 1 year old, booster every 10 years

Front 4

1) Physical characteristics of bacillus?
2) What is the major pathogenic species?
3) What are the major virulence factors?
4) How is bacillus anthracis transmitted?
5) 2 types of clinical manifestations?
6) How is the capsule of bacillus anthracis unique?

Back 4

1) Large gram + rods that produce spores
2) Bacillus anthracis
3) Capsule, and anthrax toxin made up of a) Protective antigen b) Lethal factor c) Edema factor
4) Skin cuts/abrasions, inhalation
5) Cutaneous or systemic
6) It's made of D-glutamate, not polysaccharide

Front 5

1) What kind of clinical manifestation of anthrax accounts for 95% of all infections? Characteristic presentation? What are other complications?
2) How fatal is cutaneous anthrax?

Back 5

1) Cutaneous - papules that develop into ulcers with necrotic centers. Regional lymphadenopathy and **edema**
2) 20% of untreated cases are fatal

Front 6

1) How do you get systemic anthrax? What is another name for inhalatory anthrax?
2) Symptoms?
3) How fatal is it?

Back 6

1) Inhalatory anthrax (Woolsorter disease) or GI.
2) Lymphadenopathy and septicemia
3) Almost always fatal

Front 7

1) DOC for B. anthracis?
2) How do you control anthrax?
3) What do you give to people who are often in contact w/ livestock?

Back 7

1) Penicillin
2) Prevention/cleanup of contaminated areas
3) Killed vaccine

Front 8

1) Bacillus cereus - where does it normally grow?
2) Virulence factor?
3) Principle clinical manifestation?
4) Tx/prevention?

Back 8

1) Foods - cereals/grains like rice
2) Two enterotoxins
3) Short incubation food poisoning (1-6 hrs, emetic type) - severe nausea and vomiting

Long incubation food poisoning (10-24 hrs, diarrhea) - abdominal cramps/diarrhea

4) Fluids, and vancomycin

Front 9

Clostridium:

1) Physical makeup?
2) Where is it usually found?
3) What are the 4 major pathogenic species? What do they produce that make them pathogenic?
4) What is notable about how the infections come about?

Back 9

1) Large obligate anerobe, spore forming
2) Soil or human GI tract
3) Clostridium perfringens, C. difficile, C. tetani, C. botulinum. Collagenase, protease, hyaluronidase, lecinthinase
4) They're mixed - aerobic organism grows first, reduces environment, allows anaerobic clostridia to grow.

Front 10

Clostridium perfringens:

1) How quickly does it grow? Motility? Where is it found?
2) All strains produce what kind of toxin? What effect does the toxin have?
3) How is this transmitted?
4) T or F: C. perfringens is part of the normal intestinal flora
5) Where are its spores frequently found?

Back 10

1) Fast growing, nonmotile, soil and intestine
2) Alpha toxin, aka lecithinase - lysis of erythrocytes/other cells
3) Disrupted skin, bowel, other epithelial tissues, traumatic surgery.
4) T
5) Soil

Front 11

1) 4 different clinical manifestations of C. perfringens?
2) Tx of gas gangrene?
3) Tx for food poisoning due to enterotoxin of type A?

Back 11

1) Gas gangrene, food poisoning, skin/soft tissue infections, suppurative infections
2) Surgical debridement + penicillin
3) Self-limiting, no antibiotic needed

Front 12

1) What is gas gangrene?
2) 3 most common causes of food poisoning, in order?
3) Where are skin and soft tissue infections found?
4) Suppurative infections are __ in origin. What does intra-abdominal infection cause? Pelvic infection?

Back 12

1) Myonecrosis - life threatening illness, muscle/connective tissue necrosis. Gas results from fermentation, forms in muscle tissue + causes crepitation. 80% caused by C. perfringens.
2) S. aureus, Salmonella, C. perfringens
3) Localized infections
4) Polymicrobial. Intra-abdominal - bowel perforation, emphysematous choleystitis. Pelvic -tubo-ovarian, pelvic abscesses, septic abortion.

Front 13

Clostridium dificile:

1) Where is it found in a small percentage of adults?
2) What kind of toxins can it produce?
3) Clinical manifestations?
4) Two antibiotics that are the most common causes of pseudomembranous colitis?

Back 13

1) Normal bowel flora
2) 2 heat labile ones - exotoxin A (enterotoxin) and exotoxin B (cytotoxin)
3) 25% of antibiotic associated diarrhea, 95% cases of pseudomembranous colitis
4) Clindamycin and ampicillin