Microbiology Flashcards
Which part of the bacterial structure contains Beta-lactamases?
Periplasm = space between cytoplasmic membrane and peptidoglycan wall in gram (-) bacteria
*note: Beta-lactamases = hydrolytic enzymes, resistant to antibiotics
Which bacteria contain sterols, but have no cell wall?
Mycoplasma
Which bacteria has a cell wall/membrane with mycolic acid and a high lipid content?
Mycobacteria
Bugs that don’t gram stain well?
“These Rascals May Microscopically Lack Color”
- Treponema (too thin)
- Rickettsia (intracellular)
- Mycobacteria (high lipid content in cell wall; need acid-fast stain)
- Mycoplasma (no cell wall)
- Legionella (mostly intracellular)
- Chlamydia (intracellular; and lacks muramic acid in cell wall)
Giemsa stain, stains:
- Borrelia
- Trypanosomes
- Chlamydia
- Plasmodium
PAS (periodic acid-Schiff): what structures does it stain? what’s it used to dx?
“PAS the sugar” –> it stains glycogen and mucopolysaccharides!
–dx Whipple’s disease (Tropheryma whippeli)
Ziehl-Neelson stain = carbol fushsin
stains acid-fast organisms (mycobacteria)
India ink–> what organism does it stain?
stains cryptococcus neoformas
silver stain:
- Fungi (ie pneumocystis)
- Legionella
chocolate agar with factors V (NAD+) and X (hematin)
H. influenza
Thayer-Martin/VPN media (Vancomycin, Polymyxin, Nystatin)
N. gonorrhea
- vancomycin –> inhibits gram +
- polymyxin –> inhibits gram -
- nystatin –> inhibits fungi
Bordet-Gengou agar (potato agar)
Bordetella pertussis
Lowenstein-Jensen agar
M. tuberculosis
–> takes 3-4 weeks to grow though! (can do acid-fast stain in mean time to help rule out…)
Eaton’s agar
Mycoplasma pneumonia
pink colonies on MacConkey’s agar
lactose-fermenters
- MacConkey’s agar:
- biosalts and crystal violet–> inhibit gram +
- lactose–> only carb in agar
- neutral red stain–> lactose fermenters take up lactose and neutral red; form pink colonies
**non-pink growth on MacConkey’s = gram (-), but not lactose fermenter
Tellurite plate, Loeffler’s media
C. diphtheriae
Sabouraud’s agar
Fungi
Obligate aerobes:
“Nagging Pests Must Breathe”
- Nocardia
- Pseudomonas
- Mycobacterium tuberculosis
- Bacillus
Obligate anaerobes:
“Can’t Breathe Air”
- Clostridium
- Bacteroides
- Actinomyces
- **Anaerobes lack catalase and/or superoxide dismutase, so susceptible to oxidative damage
- **Aminoglycosides = ineffective against anaerobes!
- **Treat anaerobes with:
- Metronidazole
- Clindamycin
Obligate intracellular bugs:
“stay inside (cells) when it’s Really Cold”
- Rickettsia
- Chlamydia
Facultative intracellular bugs
“Some Nasty Bugs May Live FacultativeLY”
- Salmonella
- Neisseria
- Brucella
- Mycobacterium
- Listeria
- Francisella
- Legionella
- Yersinia
bugs with a positive quellung rxn?
-who’s at increased risk of infection with these organisms?
encapsulated bacteria:
- SHiN SKiS:
- S. pneumonia
- H. influenza
- Neisseria meningitidis
- Salmonella
- Klebsiella pneumonia
- group B strep
*asplenic pts –> increased risk of infection with encapsulated organisms
Catalase-positive organisms:
-which pts have recurrent infections with these organisms?
- S. aureus
- Serratia
- Pseudomonas
- Candida
- E. coli
*pts with chronic granulomatous disease (NADPH oxidase deficiency) have recurrent infections with these organisms
Urease-positive bugs
“K-PUNCH”
- Klebsiella
- Proteus
- Ureaplasma
- Nocardia
- Cryptococcus
- H. pylori
*Urease splits urea into ammonium, which binds Mg and P –> forms stones –> stones deposited in renal calyces
Protein A
S. aureus virulence factor; binds Fc region of Ig; prevents opsonization and phagocytosis
IgA protease
virulence factor of SHiN: S. pneumonia, H. influenza, Neisseria
–> enzyme that cleaves IgA in order to colonize respiratory mucosa
M protein
virulence factor of Group A Strep: helps prevent phagocytosis
*Note: antibodies to M protein enhance host defenses against GAS, but can give rise to Rheumatic fever…
Which 2 bacteria produce a toxin that inhibits protein synthesis by inactivating elongation factor, EF-2?
C. diphtheriae –> Diphtehria toxin
Pseudomonas aeruginosa –> Exotoxin A
Which 2 bacteria produce a toxin that inhibits protein synthesis by inactivating the 60S ribosome by cleaving rRNA?
Shigella –> Shiga toxin
EHEC (including O157:H7) –> Shiga-like toxin
List 5 bacteria that produce an ADP-ribosylating A-B toxin:
1) Corynebacterium diphtheriae
2) Pseduomonas aeruginosa
3) ETEC
4) Vibrio cholerae
5) Bordetella pertussis
***Mechanism: B-binding component binds host cell surface receptor, enabling endocytosis; A-active component attaches ADP-ribosyl to disrupt host cell proteins
Which 2 bacteria produce a heat stable toxin? What’s the mechanism?
ETEC and Yersinia enterocolitica
*mechanism: increased cGMP –> decreased reabsorption of NaCl and H20 in gut –> increased fluid secretion
- note:
- ETEC –> watery diarrhea
- Yersinia –> bloody diarrhea
Which E. coli has a toxin that functions by the same mechanism as the cholera toxin? What’s the mechanism?
ETEC - heat labile toxin
*mechanism: increased cAMP by permanently activating Gs –> increased Cl secretion in gut and H20 follows it –> so increased fluid secretion
Which bacteria has a toxin that mimics adenylate cyclase (toxin acts like the enzyme!)?
Bacillus anthracis: toxin= edema factor –> mimics adenylate cyclase –> increased cAMP –> increased fluid secretion
2 toxins produced by ETEC (enterotoxigenic E. coli) and their mechanisms?
- heat labile toxin: increases adenylate cylcase–> increased cAMP–>iincreased Cl secretion in gut –> increased H20 secretion
- heat stabile toxin: increases guanylate cyclase –> increased cGMP –> decreased reabsorption of NaCl and H20 in gut
Which 2 bacteria produce a toxin that cleaves SNARE protein required for neurotransmitter release (and thereby inhibit release of neurotransmitter)?
Clostridium tetani and Clostridium botulinum
Which bacterial toxin acts through this mechanism?
–> overactivates adenylate cyclase by inhibiting Gi–> increased cAMP –> thereby, impairs phagocytosis, permitting survival of microbe
Pertussis toxin (Bordatella pertussis)
Tetanospasmin toxin: which neurotransmitters does it affect and how? what are the manifestations?
-tetanospasmin prevents release of inhibitory neurotransmitters (GABA and glycine) –> get muscle rigidity and “lock jaw”
Botulinum toxin: which neurotransmitters does it affect and how? what are the manifestations?
botulinum toxin prevents the release of stimulatory (Ach) signals at neuromuscular junctions –> get flaccid paralysis, “floppy baby”
Which bacteria produces Alpha toxin/Lecithinase (degrades phophospolipids)
Clostridium perfringens
-degradation of phospholipids–> myonecrosis (gas gangrene) and hemolysis (double zone of hemolysis on blood agar)
Streptolysin O toxin: mechanism?
- Streptococcus pyogenes (Group A strep)
- toxin lyses RBCs, contributes to Beta-hemolysis
- ASO antibodies can be used to dx rheumatic fever
Which 2 organisms have superantigens? what are the toxins? superantigen mechanism?
- Group A strep (Strep pyogenes) –> Exotoxin A
- Staph aureus –> TSST-1 (toxic shock syndrome toxin)
*superantigens bind MCH II and TCR simultaneously to stimulate a huge release of IL-2 and IFN-gamma –> results in shock; both can cause toxic shock syndrome (fever, rash, shock)
bacterial “competence”
-which bacteria are “competent?
competence = ability to take up DNA from environment = transformation (in bacterial genetics)
-many bacteria can undergo transformation, but especially common in SHiN (S. pneum, H. infl, Neisseria)
Conjugation: (F+ X F-) vs (Hfr X F-)?
(F+ X F-): only plasmid DNA can be transferred this way
(Hfr X F-): Transfer of plasmid AND chromosomal genes (because F+ plasmid can become incorporated into bacterial chromosomal DNA –> “Hfr cell”
Transduction:
bacterial genetic term –> spread of bacterial DNA via lytic (“generalized transduction”) or lysogenic (“specialized transduction”) bacteriophage (virus that infects bacteria)
What makes MRSA resistant to Beta-lactams?
Altered penicillin-binding protein
rusty sputum
pneumococcus! (strep pneumonia)
Strep pneumonia = most common cause of:
- Meningitis
- Otitis media (in kids)
- Pneumonia
- Sinusitis
Bacteria that causes acute bacterial endocarditis?
Staph aureus
Bacteria that causes subactue bacterial endocarditis at damaged valves?
-Strep sanguis (viridans group strep)
think of the sanguinistas in true blood :)
strawberry tongue
Scarlet fever –> toxigenic effect of group A strep
about 15% of colon cancer pts are colonized by which strep?
strep bovis (group D strep)
ABCDEFG of Corynebacterium diphtheriae
ADP ribosylation Beta-prophage (encodes exotoxin) Corynebacterium Diphtheria Elongation Factor 2 Granules (dx by gram + rods with metachromatic -blue and red- granules)
*exotoxin encoded by a beta-prophage–> exotoxin inhibits protein synthesis via ADP ribosylation of EF2
Spore-forming bacteria:
certain gram + rods:
- main ones:
- Bacillus anthracis
- Clostridium perfringens
- Clostridium tetani
- also:
- Bacillus cereus
- Clostrium botulinum
- Coxiella burnetti
Prevents glycine and GABA and glycine release from Renshaw cells in spinal cord?
Tetanospasmin (Clostridium tetani toxin) –> blocks inhibitory neurotransmitters, so causes spastic paralysis, trismus (lockjaw) and risus sardonicus
Treatment of C. difficile?
metronidazole or oral vancomycin (only case in which vancomycin is given orally!)
2 toxins produced by C. difficile, and how do they act?
Toxin A = enterotoxin: binds brush border of gut
Toxin B = cytotoxin: destroys cytoskeletal structure of enterocytes, causing necrosis of colon epithelium = pseudomembranous colitis
Only bacterium with a polypeptide capsule (that contains D-glutamate)?
Bacillus anthracis
move from cell to cell via “actin rockets”; bacteria is acquired by ingestion of unpasteurized milk/cheese and deli meats, or by vaginal transmission during birth
Listeria monocytogenes
treatment of actinomyces vs nocardia?
“ooooh SNAP!”
- Sulfa for Nocardia
- Actinomyces - use Penicillin
Langhans giant cells –> see multiple peripheral nuclei organized in the shape of a horseshoe
characteristic of TB caseating granulomas
Extrapulmonary tuberculosis:
- CNS–> tuberculoma or meningitis
- Pott’s disease in vertebral bodies
- lymphadenitis
- renal
- GI
Ghon complex =
-TB granulomas
= Ghon focus (calcified scar, usually in lower lobes) + lobar and perhilar lymph node involvement; reflects primary infection or exposure
Mycobacterium kansasii
pulmonary TB-like symptoms; more common in pts with COPD (chronic bronchitis or emphesyma)
Prophylactic treatment for Mycobacterium avium-intracellulare?
- Azithromycin
- ->MAI is often resistant to many drugs; causes disseminated disease in AIDS pts.
Reservoir in US is armadillos?
Mycobacterium leprae (Leprosy = Hansen’s disease)
Treatment for leprosy?
- long term oral Dapsone (but, toxicity = hemolysis and methemoglobinemia)
- alternatively: rifampin, or combination of clofazimine and dapsone
Lactose-fermenting bacteria (grow pink on MacConkey’s agar)…
macConKEES or CEEKS:
- Citrobacter
- Klebsiella
- E. coli
- Enterobacter
- Serratia
*note: E. coli produces Beta-galactosidase–> breaks lactose into glucose and galactose!
Which class of bacteria are resistant to Penicillin G (or rather, which class can Penicillin G be used to treat)?
Gram (-) bacilli are resistant to Penicillin G (but, may be susceptible to penicillin derivatives)
Penicllin G and V are mostly used to treat gram (+) organsims, and syphilis!
Fitz-Hugh-Curtis syndrome
caused by N gonorrhea
–>stars in lower genital tract, ascends through upper genital tract, ultimately infects liver capsule
Treatment for N. gonorrhea?
ceftriaxone
Waterhouse-Friderichsen syndrome
caused by N. meningitidis
–>adrenal hemorrhage –> adrenal insufficiency –> hypotension + DIC + electrolyte abnormalities
Prophylaxis and treatment for N. meningitidis?
- Vaccine available (not for type B)
- Rifampin prophylaxis in close contacts
- Treatment: ceftriaxone or penicillin G
Why can H. influenza be grown with Staph aureus?
H. infl requires Factors V (NAD+) and X (hematin) for growth; S. aureus provides factor V!
Prophylaxis for H. influenza?
Treatment for meningitis caused by H. infl?
- Vaccine: type B capsular polysaccharide conjugated to diphtheria toxoid or other protein
- Prophylaxis in close contacts: Rifampin
- Treatment for meningitis: Ceftriaxone
Legionnaires disease vs Pontiac fever?
Both caused by Legionella pneumophila
- Legionnaires’ disease = severe pneumonia and fever
- Pontiac fever - mild flu-like syndrome
***suspect Legionella in pts with recent exposure to contaminated water (ie cruise ship, hotel, etc…)
pt with Cystic Fibrosis + Pneumonia?
Pseudomonas
PSEUDOM of pseudomonas (presentations):
- Pneumonia (especially in cystic fibrosis pts)
- Sepsis (black lesions on skin–> ecthyma gangrenosum = cutaneous necrotic disease, common in imm-compromised pts)
- External otitis (swimmer’s ear)
- UTI
- Drug use endocarditis and Diabetic Osteomyelitis
- Malignant otitis externa in diabetics
- ->also: hot tub folliculits
- assoc with wound and burn infections
- water source
- produces pyocyanin = blue-green pigment
- grapelike odor
Treatment for Pseudomonas?
Aminoglycoside + extended-spectrum penicillin (ie piperacillin or ticarcillin)
E. coli virulence factors: What do they cause?
- Fimbriae?
- K capsule?
- LPS?
Fimbriae –>cystitis and pyelonephritis
K capsule –> pneumonia, neonatal meningitis
LPS –> septic shock
Anemia + Thrombocytopenia + Acute Renal Failure?
HUS = hemolytic uremic syndrome (EHEC O157:H7)
Which E. coli strain is the only one that does not ferment sorbitol?
EHEC
Which E. coli strains cause bloody diarrhea?
EIEC and EHEC
Which E. coli strain normally causes diarrhea in children?
EPEC (P for pediatrics :))–> doesn’t produce toxin; adheres to apical surface, flattens villi, prevents absorption
Which E. coli strains produce a toxin (and what toxin is it?) Which do not produce toxin?
EIEC –> no toxin
ETEC –> heat labile and heat staible toxins
EPEC –> no toxin
EHEC –> shiga-like toxin
Which antibiotic should be used to treat Salmonella?
TRICK QUESTION! Do not treat Salmonella with antibiotics; antibiotics may prolong symptoms!
Osteomyelitis in a sickle cell patient?
Think Salmonella!
spots on abdomen + fever + headache + diarrhea?
Salmonella typhi (rose spots on abdomen)
Which is more virulent: Shigella or Salmonella?
Shigella is more virulent –> only takes
10^1 organisms for infection, vs Salmonella –> takes 10^5 organisms!
Which bacterial infection is associated with Reiter’s syndrome/Reactive arthritis?
- Shigella flexneri
- Chlamydia
Causes mesenteric adenitis (which may mimc Crohn’s or appendicitis)?
Yersinia enterocolitica! (transmitted from pet fecies, contaminated milk, pork; outbreaks of diarrhea in daycare centers…)
Triple therapy for H. pylori treatment:
1) PPI
2) Clarithromycin (macrolide)
3) Amoxicillin or Metronidazole
- **Quadruple Therapy:
- Bismuth salicylate
- Metronidazole
- PPI
- Tetracylcine
flulike symptoms, jaundice, and photophobia with conjunctivitis, in person who was in contact with animal urine?
Leptospirosis (Leptospira interrogans)
–> severe form = Weil’s disease
Weil’s disease
=Icterohemorrhagic Leptospirosis
–> severe form of Leptospirosis (Leptospira interrogans): jaundice and azotemia (from liver and kidney dysfxn); fever, hemorrhage, anemia
water contaminated with animal urine? Think:
- Leptospira
- Hantavirus
Ixodes tick
vector for:
- Lyme disease (Borrelia burgdorferi)
- Babesia
3 stages of lyme disease:
“BAKE a key Lyme pie!” (Bell’s palsy, Arthritis, Kardiac block, Erythema migrans)
Stage 1: erythema chronicum migrans (bull’s eye rash), flu-like symptoms
Stage 2: Neurologic (bilateral or unilateral Bell’s palsy) and Cardiac (AV nodal block) manifestations
Stage 3: chronic monarthritis and migratory polyarthritis
Treatment for Lyme disease: at early stages (1 and 2)? Later disease?
Doxycycline –> for early stages
Ceftriaxone –> later disease
Treatment of choice for Syphilis?
Penicillin G!
primary syphilis:
painless chancre (localized)
secondary syphylis:
(secondary = systemic) disseminated disease with constitutional symptoms
- maculopapular rash (palms and soles)
- condyloma lata
- visualize treponemes from chancres and condyloma lata by darkfield microscopy
tertiary syphilis
- gummas (chronic granulomas)
- aortitis (VASO VASORUM DESTRUCTION!)
- neurosyphilis = tabes dorsalis
- Argyll Robertson pupil
- Signs: ataxia, + Romberg, Charcot joint, stroke but no HTN
FTA-ABS
test used to confirm syphilis (screening test = VDRL)
CN VIII deafness in a neonate?
Congenital syphilis (other signs = saber shins (ant bowing of tibia), saddle nose (flat nasal bridge), Hutchinson’s teetch (notching of upper incisors), mulberry molars)
What may cause a false positive VDRL (screening test for syphilis)?
Viruses (mono, hepatitis)
Drugs
Rheumatic fever
Lupus and Leprosy
- note: VDRL detects a nonspecific antibody that reacts with beef cardiolipin
- can confirm dx of syphilis with FTA-ABS
Transmitted by lice/louses?
Borrelia recurrentis and Rickettsia rickettsii
Transmitted by spores from tick feces and cattle placenta?
Coxiella burnetti –> causes Q fever
transmitted by animal/cat/dog bites? symptoms?
Pasteurella multocida –> cellulitis, osteomyelitis
Transmitted by fleas?
Rickettsia typhi, Yersinia pestis (Yersinia is also transmitted by rodents, prairie dogs…)
Treatment for all Rickettsial diseases?
Doxycycline
Headache + Fever + Rash that starts on palms and soles?
Rickettsia rickettsii = Rocky Mountain spotted fever (transmitted by tick)
Headache + Fever + Rash that starts centrally and spreads outward without involving palms or soles?
Rickettsia typhi = Rickettsia prowazekii (transmitted by louse) –> “Typhus on Trunk”
Q fever
- presents as pneumonia
- caused by Coxiella burnetti (part of Rickettsia)
- “Queer” b/c:
- no rash
- no vector (transmitted by inhaling aerosoles from ticks feces or cattle placenta)
- negative Weil-Felix
- no “Rickettsia” in genus name
Weil-Felix Reaction
DX Rickettsia (not Coxiella though)–> mix pt’s serum (with anti-Rickettsial antibodies) with Proteus antigens –> antirickettsial antibodies cross-react to Proteus O antigens and agglutinate
Cytoplasmic inclusions seen on Giemsa or Fluorescent antibody-stained smear
Lab dx for Chlamydia
Treatment for Chlamydia?
- 1st line = Azithromycin
- Or: Doxycyline
Chlamydia: What is associated with each types:
- A, B, C:
- D-K:
- L1, L2, L3
- A, B, C: blindness in Africa, chronic infection
- D-K: urethritis, PID, ectopic pregnancy, neonatal pneumonia, neonatal conjuctivitis
- L1, L2, L3: lymphogranuloma venereum (acute lymphadenitis)
3 main organisms that cause interstitial/atypical/walking pneumonia?
- Chlamydia pneumonia
- Mycoplasma pneumonia (most common)
- Legionella pneumophila
RBC agglutination or lysis in cold temperatures?
Mycoplasma pneumonia –> cold agglutinins (IgM)
–> this happens b/c Mycoplasma pneumonia shares antigens with human RBCs, so when body mounts a response against antigens, it also lyses RBCs, leading to anemia; antibodies that cause this RBC destruction = cold agglutinins
only bacterial membrane that contains cholesterol?
Mycoplasma pneumonia
Treatment for Mycoplasma pneumonia?
tetracycline or erythromycin
5 Infections associated with birds:
1) Histoplasmosis –> pneumonia
2) Cryptococcus –> meningitis in AIDS pts
3) Chlamydia psittaci –> atypical pneumonia
4) Avian influenza
5) West Nile Virus
Exotoxin A
2 organisms have an exotoxin A:
- Pseudomonas (similar to diphtheria toxin, inactivates EF2)
- Group A Strep (similar to TSST1of Staph aureus –> superantigen, causes shock)
*note: there’s also an alpha toxin (lecithinase) that Clostridium perfringens has…
Pneumonia, after pt was in:
1) Mississippi or Ohio river valleys
2) States east of Mississippi River and Central America
3) Southwestern US, California
4) Latin America
1) Histoplasmosis
2) Blastomycosis
3) Coccicidomycosis
4) Paracoccidioidomycosis
Dimorphic fungi: List them. What do they all cause? What makes them dimorphic?
- all cause pneumonia and can disseminate
- dimorphic: mold in cold (20 degrees); yeast in heat (37 degrees); exception = coccidiomycoides = spherule (not yeast) in tissue
- Includes:
1) Histoplasmosis
2) Blastomycosis
3) Coccidioidomycosis
4) Paracoccidioidomycosis
pneumonia-causing fungi that forms spherules filled with endospores in tissues (much larger than RBCs)
Coccidioidomycosis
meningitis, pneumonia, and dissemination to bone and skin following an earthquake?
Coccidioidomycosis
Budding yeast with “captain’s wheel” appearance?
Paracoccidioidomycosis
spaghetti and meatball appearance on KOH prep
Tinear versicolor (caused by Malassezia furfur); degrades lipids and produces acids that damage melanocytes –> so get hypopigmented and/or hyperpigmented patches
Dimorphic yeast: pseduohyphae and budding yeasts at 20 C; germ tubes at 37 C
Candida albicans