Flashcards in Microbiology: Bacterial Deck (241)
Two toxins produced by C. difficile:
What kind of toxin? What is its function?
Toxin A = enterotoxin = exotoxin, binds brush border.
Toxin B = cytotoxin = destroys enterocyte cytoskeleton -> pseudomembranous colitis.
Two antibiotics especially associated with C. diff:
Treatment for C. diff:
Dx of C. diff:
Toxin in stool
Most common E. coli strain causing bloody diarrhea:
Treatment for dysentery caused by E. coli:
Two toxins produced by enterotoxigenic E. coli:
Second messenger inside the cell for action of each?
Heat labile = cAMP increase = watery diarrhea like cholera
Heat stable = cGMP increase
Cause of traveler's diarrhea ("Montezuma's revenge"):
Enterotoxigenic E. coli
E. coli strain causing diarrhea in daycare:
Enterohemorrhagic E. coli
Triad of HUS:
Explain how this happens:
Acute renal failure
Shiga-like toxin from EHEC 0157:H7 damages endothelium, which swells, cuts off blood flow to the kidney. Narrow vessels shear RBC -> mechanical hemolysis. Damaged endothelium consumes the platelets -> thrombocytopenia.
Most E. coli ferment this sugar:
Which one does not?
EHEC does not ferment sorbitol
Tx for HUS:
Do not give abx.
Two E. coli strains causing dysentery:
E. coli strain causing watery diarrhea:
How would you distinguish EHEC from other forms of E. coli on culture?
It does not ferment sorbitol. The others do.
Organism responsible for causing staghorn calculi:
Urease-positive, ammonium-Mg-phosphate stones:
Common cause of osteomyelitis in sickle cell patients:
Four A's of Klebsiella:
Abscesses in lungs and liver
Mucoid colonies, lobar pneumonia in a diabetic:
Flagellated organism, hematogenous dissemination, produces H2S:
Very virulent organism, frequently causes bloody diarrhea, human and primate but not pet reservoirs:
Associated with Reiter syndrome:
Rose spots on abdomen:
Carried in the gallbladder, found only in humans:
Which organism ferments lactose: Salmonella or Shigella?
Which organism produces H2S: Salmonella or shigella?
Which organism produces a monocytic response: Salmonella or Shigella? A PMN response?
Monocytes = Salmonella
PMNs = Shigella
Leading cause of bloody diarrhea in the US:
Common antecedent to Guillain-Barre:
Fecal-oral transmission through poultry, meat, milk, grows at 42C:
Oxidase (+), grows in alkaline media:
Mesenteric adenitis that can look like Chron's, pet feces:
Egg salad -> delayed diarrhea:
Egg salad -> instant diarrhea / vomiting:
Permanently activates Gs, toxin is heat-stable:
Food poisoning from contaminated seafood:
Food poisoning from reheated rice:
Preformed toxin, food poisoning from custard:
Food poisoning from reheated meat:
Undercooked meat, bloody diarrhea:
E. coli 0157:H7
Infection with these three organisms can mimic appendicitis:
Most common cause of mesenteric adenitis:
Food poisoning as a result of mayonnaise sitting out:
Diarrhea caused by a gram (-) non-motile non-lactose fermenting organism:
Rice-water stools (2):
Diarrhea caused by an S-shaped organism:
Remember, campy=twisted, it's more of a corkscrew than a comma, but they might say "S-shaped"
Diarrhea caused by a non-lactose fermenting Gram (-) motile organism:
Diarrhea caused by a Gram (-) lactose fermenting bacterium:
A non-lactose-fermenting bacterium:
Salmonella or Shigella
Cause of Chagas disease?
Cause of African sleeping sickness?
Trypanosoma brucei, gambiense, or rhodesiense
This form of the malaria parasite looks like a diamond ring inside an RBC:
This form of the malaria parasite is the one that ruptures the RBC:
This form of the malaria parasite replicates inside RBCs:
This is the form of the malaria parasite injected by the Anopheles mosquito:
This form of the malaria parasite is banana-shaped:
Describe how Shigella gains access to the intestinal mucosa:
Via M cells in Peyer's patches, through endocytosis. It spreads laterally from M cells to other epithelial cells.
The _________ is where you will find b-lactamase.
This is in Gram (-)s
This bacterial structure protects against phagocytosis:
This bacterium is encapsulated, but its capsule is not polysaccharide like the others. What is it, and what is its capsule made of?
Capsule contains D-glutamate
What is the test for whether a bacterium is encapsulated or not?
This structure mediates adherence to surfaces:
This structure mediates adherence to cells:
Glycocalyx makes biofilms
Pilus is a glycoprotein projection that mediates cell-cell interactions
Feature of Gram (+) bacterial cell walls not shared with Gram (-)s:
What cytokines (2) does this cell wall component prompt release of?
This induces IL-1 and TNF-a production
Two structural features of Gram (-) bacteria not shared with Gram (+)s:
Endotoxin / LPS outer membrane
What is unusual about Mycoplasma's cell wall and membrane?
1. It has no cell wall
2. Membrane contains a lot of sterols
What is unusual about the cell walls of the Mycobacteria?
They contain mycolic acid and a ton of lipids.
These six organisms do not take Gram stain well:
Briefly think of why.
These Rascals May Microscopically Lack Color:
Treponema (too thin)
Mycobacteria (high lipid content, need carbolfuschin)
Mycoplasma (no cell wall)
Legionella (mostly intracellular)
How do you visualize Chlamydia?
When would you use the Ziehl-Neelsen carbol fuschin stain (2)?
For acid-fast organisms (2):
Six organisms you would stain with Giemsa:
Certain Bugs Really TRY His Patience
Four cases in which you would use silver stain:
What does PAS stain for?
Stain you would use to diagnose Whipple's disease:
Stain you would use to diagnose Cryptococcus:
Stain you would use to diagnose Nocardia:
Carbol fuschin (Ziehl-Neelsen)
Stain you would use to diagnose Borrelia:
Stain you would use to diagnose Legionella:
Stain you would use to diagnose Histoplasma:
Stain you would use to diagnose Pneumocystis:
Stain you would use to diagnose Chlamydia:
Gram (+) organisms stain ____.
Gram (-) organisms stain ____.
These four organisms are obligate aerobes:
Nagging Pests Must Breathe:
Pseudomonas AERuginosa (think aerate)
Obligate aerobe seen in burn wounds, causes pneumonia in patients with CF:
These three bugs are obligate anaerobes:
Can't Breathe Air:
They do not have catalase or SOD, cannot deal with oxygen.
Treatment for infection with obligate anaerobes:
This class of antibiotics requires oxygen to enter a cell:
These two bugs are obligate intracellular creatures, they cannot make ATP:
These bugs are facultative intracellular pests (7):
Some Nasty Bugs May Live FacultativeLY:
These bacteria are encapsulated (8):
Even Some Pretty Nasty Killers Have Shiny Bodies:
Asplenics are at risk for infection with these bacteria (8):
Even Some Pretty Nasty Killers Have Shiny Bodies:
group B Strep
These organisms make catalase (7):
You need PLACESS for CATs.
Organisms you may be susceptible to infection with if you have NADPH oxidase deficiency:
These organisms readily break down the limited amount of H2O2 people with this def. have. They are:
PLACESS for CATs:
Yellow-pigmented colonies (2):
Blue-green pigmented organism:
These organisms are urease-positive (8):
CHuck norris hates PUNKSS:
What is the function of bacterial protein A?
Which organism makes this?
This binds Fc of Ig and prevents host immune cells from phagocytosing the bacterium. S. aureus makes this.
Which bugs make IgA protease?
These are all respiratory pathogens:
What is M protein, and which bacteria make this?
M protein inhibits phagocytosis:
Don't Munch me, I will give you GAS:
Group A Strep
Where is the genetic material coding for exotoxin production located?
Exotoxin DNA is stored in plasmids or bacteriophages.
Endotoxin DNA resides in the bacterial chromosome.
Where is endotoxin found?
On Gram (-)s, their outer membrane.
Which kind of toxin is destroyed quickly by heat?
Which is more stable to high temps?
Exotoxin is easily destroyed by heat.
Endotoxin you can cook.
Six main toxins made by Staph aureus, two words about what they do:
1. a-toxin -> hemolysis
2. b-toxin -> sphingomyelinase
4. enterotoxins (A-E) -> food poisoning
5. TSST-1 -> toxic shock syndrome
6. Exfoliative / epidermolytic toxin -> scalded skin
Three main toxins made by Strep pyogenes, two words about what they do:
1. Streptolysin O (O2 Labile) &
2. Streptolysin S (O2 Stable) -> hemolysis
3. Erythrogenic pyrogenic toxins -> rash / fever, cause scarlet fever
These two toxins inhibit EF-2:
Which bacteria make them?
Exotoxin A (made by Pseudomonas)
These two toxins remove a residue from our rRNA coding for our 60S ribosomal subunit:
Which bacteria make them?
Shiga toxin (made by Shigella)
Shiga-like toxin (made by enterohemorrhagic E. coli)
This toxin mediates hemolytic uremic syndrome:
What was the triad again?
Shiga or shiga-like toxin
3. Acute renal failure
T/F: Enterohemorrhagic E. coli invades host cells:
F. Shigella does this, but E. coli does not.
This organism produces a toxin that behaves like cholera toxin. What is it, and how does the toxin work?
Enterotoxigenic E. coli makes a heat labile toxin, increases cAMP and Cl- secretion into the gut.
(The heat stable toxin increases cGMP and decreases NaCl resorption.)
A strain of E. coli makes a toxin that remains when the bacterium is heated and killed. What does this toxin do?
Another organism makes a similar toxin, which one?
This is heat stable toxin
Increases cGMP, slows NaCl and thus water resorption in the gut -> watery diarrhea
Yersinia enterocolitica does something similar
Four toxins that act to increase cAMP. Which organisms make them, what is their effect?
cGMP increase with:
E. coli heat-labile toxin, watery diarrhea
Cholera toxin, rice-water stools
(Both of these are high Cl- secretion mechs)
Bacillus anthracis makes edema factor
Pertussis toxin disables Gi, effect is impaired phagocytosis
Two toxins that cleave SNARE proteins:
What type of paralysis results from each?
Tetanospasmin (prevents inhibitory neurotransmitter release -> spastic paralysis)
Botulinum toxin (prevents ACh release -> flaccid paralysis)
Mechanism of action of pertussis toxin:
Mechanism of action of alpha toxin made by Clostridium:
Phospholipase, breaks down tissues and cell membranes, causes necrosis
This Strep. pyogenes toxin degrades cell membranes:
This is the toxin that LYSES cell membranes
This is also the SO of ASO, eg Ab titers for RF
These two superantigens cause shock:
Which organism makes them?
TSST-1 (made by Staph aureus)
Exotoxin A (made by Strep. pyogenes)
S. pneumo, H. influenzae, and Neisseria are able to undergo transformation. What does this mean?
Can take up naked DNA from their environment.
How is plasmid DNA transferred from bacterium to bacterium?
During conjugation, F+ x F- meet
What is a Hfr cell? What kind of genetic material is transferred when Hfr x F- during conjugation?
Hfr = an F+ plasmid (plasmid with the pilus instructions) incorporated into chromosomal DNA.
Conjugation -> transfer of plasmid and chromosomal information that just happened to be near the plasmid insertion point.
What is transduction?
Infection with a bacteriophage, can go two ways.
1. Phage carries some bacterial DNA with it when it lyses (vanilla)
2. Phage inserts itself into bacterial DNA, when it lyses it carries flanking genes with it.
These five toxins are carried by lysogenic phages:
Erythrogenic toxin (Strep pyo.)
Gram (+) cocci in clusters:
Gram (+) cocci in chains:
5 Gram (+) rods:
Two Gram (+) branching filaments:
Which is an aerobe?
Nocardia is the aerobe
What is alpha hemolysis?
Which Strep. sp are a-hemolytic?
Partial hemolysis = a-hemolysis
What is beta hemolysis?
Which Strep. sp are b-hemolytic?
b-hemolysis = complete hemolysis
Strep pyogenes (= GAS)
Strep agalactiae (= GBS)
What is the difference in antibiotic sensitivity between group A and B Strep?
GAS = pyogenes = bacitracin-sensitive
GBS = agalactiae = bacitracin-resistant
What is gamma hemolysis?
Which Strep. sp are g-hemolytic?
g-hemolysis = no hemolysis at all
Non-enterococci (Strep. bovis)
How do you tell between Strep pneumoniae and viridans group strep?
1. S. pneumo has a capsule, Quellung will be (+). It is Optochin sensitive.
2. Viridans strep. have no capsule (Quellung negative) and are Optochin resistant. Remember the viridans Strep. are mouth bacteria, they are OFF the CHIN resistant.
Which bacteria are beta-hemolytic, how will you tell them apart (4)?
Staph aureua (coag and cat +)
Strep pyogenes (GAS) (cat neg, optochin sensitive)
Strep agalactiae (GBS) (cat neg, optochin resistant)
Listeria monocytogenes (tumbling motility)
Mechanism by which MRSA are b-lactamase resistant:
Altered PCN binding proteins.
This Staph. sp is known for infecting prosthetic devices and IV catheters:
Most common cause of meningitis:
Gram (+) diplococcus associated with sepsis in sickle cell anemia:
This normal member of our oral flora causes dental caries:
Which of the a-hemolytic Strep. groups is optochin-sensitive?
Which is optochin-resistant?
Strep. pneumoniae = optochin sensitive
Strep. viridans = optochin resistant
These three organisms make an IgA protease:
Cause of rheumatic fever:
Strep pyogenes (GAS)
Which Strep pyogenes infection is most likely to precede glomerulonephritis?
Impetigo > pharyngitis.
Three organisms particularly deadly to babies:
Which is the more burly organism: Enterococcus or non-enterococcus group D?
Enterococci. You can grow them in bile AND salt.
This b-hemolytic Strep. is bacitracin-resistant as a rule:
Strep agalactiae (GBS) is bacitracin-resistant.
This titer detects recent infection with S. pyogenes:
Strep. sp associated with colon cancer:
Mechanism of action of diphtheria toxin:
(just like Pseudomonas)
Gram (+) club-shaped rods with metachormatic red-blue granules:
Black colonies on cystine-tellurite agar:
Treatment for diphtheria:
Penicillin or erythromycin.
May want to give diphtheria antitoxin.
Vaccinate (again) too.
Coxiella burnetii (rickettsial, causes Q-fever)
The two toxins produced by Clostridium dificile and their MOA:
1. Toxin A = enterotoxin, binds to enterocytes
2. Toxin B = cytotoxin, destroys cytoskeleton of enterocytes
This bacterium has a polypeptide capsule containing D-glutamate:
(Remember, it has a weird ENVELOPE. You would not want it at the post office.)
Some nice wool-comber develops pulmonary anthrax. What do you expect will happen to them?
Look like they have the flu.
Suddenly they have a fever, shock.
Pulmonary hemorrhage and mediastinitis.
Nausea and vomiting in 1-5 hours after eating reheated rice:
What is the toxin responsible?
Unpasteurized milk / dairy / vaginal transmission of an organism with tumbling motility:
What does this little guy look like on Gram stain?
Gram (+) rod
Treatment for Listeria:
Oral / facial abscess, yellow sulfur-granule appearance. How do you treat it?
This is Actinomyces.
Tx is penicillin.
Gram (+) filamentous branching aerobe. Treatment?
Nocardia, treatment is sulfonamides.
Why might someone be PPD (-) (3 reasons)?
Anergy (steroids, malnutrition, immunocompromised)
What is a Ghon complex?
A Ghon focus + hilar LAD, seen in primary TB.
What is the recommended prophylactic treatment for MAC?
Treatment for leprosy:
This form of leprosy is communicable. What T cell response will you characteristically see?
Lepromatous, TH2 dominant response. Diffuse presentation over the skin.
Second most common cause of Gram (-) sepsis:
Mesenteric adenitis that might look a lot like Chron's:
Three symptoms of leptospirosis:
Who gets this disease and from where?
Surfers in the tropics, it's found in water contaminated with animal urine.
What is Weil's disease?
Liver / kidney dysfx, azotemia
Hemorrhage / anemia
Question mark shaped organism, flu-like symptoms:
Treatment for Lyme disease:
Natural reservoir for Borrelia burgdorferi:
Carried by Ixodes tick
Characterizes primary syphilis:
Single painless chancre
Rash on palms and soles, 3 possibilities:
Coxsackie A virus
Alopecia areata, rash on palms and soles:
What is a Charcot joint?
Damage done to joints because they are insensate. Usually in DM, can be seen in tertiary syphilis.
This is an early sign of congenital syphilis:
(Cute. Or not.)
Blood-tinged nasal secretions.
Tertiary syphilis can do this to an aorta:
Destruction of the vaso vasorum that feed the aorta itself, causes "tree-barking"
What is an Argyll-Robertson pupil?
A pupil that constricts with accomodation but fails to react to light. AKA the prostitute's pupil. Seen in tertiary syphilis.
What are some common scenarios where you might see false positives with VDRL testing?
Viruses (mono and hepatitis)
Lupus / Leprosy
This organism causes the yaws:
Think of a couple features of the yaws.
Disease of skin / joints, healing with keloids, disfigurement, face commonly involved.
What happens to immunocompromised people who get cat scratch disease?
May develop angiomatosis that looks like Kaposi's sarcoma.
Appearance of Gardnerella vaginalis on LM:
Treatment for all the Rickettsial diseases:
How does the rash of RMSF differ from the rash seen in typhus?
RMSF: Rash starts at wRists and moves in.
Typhus: Rash starts on the Trunk and moves out.
(R. typhi is the endemic form)
Morula-like cytoplasmic inclusion, tick-borne:
What is Q fever?
Caused by Coxiella burnetii.
Causes interstitial pneumonia.
What is unusual about the cell wall of Chlamydia?
It has no muramuic acid
Treatment for chlamydial infections:
Azithromycin, single dose
Three most common causes of atypical pneumonia:
What are the three pathogenic Chlamydial sp?
What is lymphogranuloma venereum?
Infection with Chlamydia trachomatis type L1-L3, causes inguinal lymphadenitis with a primary ulcer, may mimic UC and cause rectal disease.
Why do we give babies azithromycin eye drops at birth?
Worry for congenital transmission of Chlamydia, which can cause conjunctivitis and neonatal pneumonia.
Chalmydia trachomatis serotypes associated with blindness in Africa:
A, B, C
T/F: C. trachomatis infection can cause ectopic pregnancy.
T. PID can make the uterus an unfriendly place, embryo might just go find another home.
Atypical pneumonia with a high titer of cold agglutinins:
How would you treat such an infection?
Tx is with fluoroquinolone or macrolide
This aminopenicillin is usually given orally.
This one is usually given IV.
What infections do they treat?
Ampicillin is usually used IV.
AmOxicillin is better Oral.
Used to HELPSS kill enterococci:
Usual mechanism of resistance to ampicillin / amox:
What is augmentin made of:
Amoxicillin + clavulanic acid = augmentin
What is unasyn composed of:
Ampicillin + sulbactam
What is zosyn made of:
Piperacillin + tazobactam
The three b-lactamase inhibitors:
Penicillin associated with development of pseudomembranous colitis:
Aminopenicillins, amp and amox
Good treatment of choice for neonatal infections with E. coli, Listeria:
Add gentamycin just to be safe
Treatment for uncomplicated URI with Gram (+) organisms:
Aminopenicillins +/- b-lactamase inhibitors
Three anti-pseudomonal penicillins:
Treats pseudomonas and Gram (-) rods:
Organisms not covered by cephalosporins:
These guys are LAME:
Atypicals (Chlamydia, Mycoplasma)
First generation cephalosporins are used to treat these infections:
The two first-generation cephalosporins:
Second-generation cephalosporins cover:
Drug of choice for OM due to non-typeable H. flu:
Second gen. cephalosporin
Consider Cefdinir (3rd gen) if resistant.
Four second-generation cephalosporins:
Third-generation cephalosporins add coverage for these two main infections:
Meningitis, gonorrhea, pseudomonas
What is it particularly good at?
Killing pseudomonas (and everything else)
Cephalosporins with a disulfiram-like reaction (3):
Mechanism of action of cephalosporins:
Inhibit cell wall synthesis.
Mechanism of action of aztreonam:
Binds PBP3 and prevents cross-linking of peptidoglycans.
Consider this drug for someone with a Gram (-) infection, renal insufficiency, and who is PCN-allergic:
These drugs can increase the nephrotoxicity of aminoglycosides:
These two drugs have a very broad spectrum but their use is limited to life-threatening infections of unknown origin and as last resort due to toxicity:
Drug you give with imipenam:
Inhibits renal dehydropepdisase I, which inactivates the drug.
T/F: Meropenam will cover MRSA.
F. You need to give vanc for that. Typical scenario is sepsis of unknown origin, must give carbapenam + vanc to cover for MRSA.
Mechanism of action of vancomycin:
Binds D-ala D-ala on cell wall of bacteria, inhibits peptidoglycan formation.
Spectrum of coverage for vancomycin:
Gram (+) only.
Especially useful for MRSA, enterococci, C. diff.
Three primary toxicities of vanc:
Also, Red Man syndrome
Mechanism of resistance to vancomycin:
D-ala D-ala becomes D-ala D-lac in resistant organisms.
Remember, D-lac = vancomycin activity LACking.
Prophylaxis for M. tb:
Prophylaxis for MAC:
Azithromycin / clarithromycin
When CD4 count < 50
Treatment for M. tb:
Pyrazinamide + pyridoxine (B6)
The B6 prevents isoniazid toxicity
Treatment for MAC infections:
Clarithromycin + ethambutol
Treatment for M. leprae infection:
Mechanism of action of isoniazid:
Decreases mycolic acid synthesis
Administering this vitamin can help prevent isoniazid neurotoxicity:
Three main toxicities associated with isoniazid:
Mechanism of action of rifampin:
Inhibits DNA-dependent RNA-pol.
This drug is used for prophylaxis of meningitis and HiB chemoprophylaxis:
Drug that causes orange body fluids:
Main pharmacokinetic consideration with rifampin:
Increases P-450 enzymes, speeds the metabolism of many drugs.
Mechanism of action of pyrazinamide:
It has a really great advantage for M. tb:
Blocks fatty acid synthesis in mycobacteria.
It works well at acid pH, ie in lysosomes where M. tb likes to hide.
This drug blocks arabinosyltransferase and therefor decreases carb. polymerization in Mycobacteria cell walls: