SketchyMicro: Bacteria Flashcards
Bacteria -G+ Cocci (strep, staph, enterococcus) -G+ bacilli (bacillus, clostridium, listeria) -G+ filamentous rods (actinomyces, nocardia) -G- Diplococci (Neisseria
Which gram positive bacteria weakly stains acid fast
(a) Name another organism that stains acid fast that is not Tb
Nocardia species weakly stain acid fast
-b/c some mycolic acid in the cell wall
(pulmonary and brain abscesses, cutaneous lesions)
(a) Another acid fast positive = mycobacterium leprae (aka causes leprosy)
Main virulence factor of
(a) Staph aureus
(b) GAS responsible for rheumatic fever
(a) Staph aureus: protein A is the main virulence factor, binds Fc to prevent complement from binding (prevents opsonization)
(b) M-protein: prevents opsonization and molecular mimcry to cause mitral valve damage seen in rheumatic fever
2 features of clostridum species
- obligate anaerobes
- only flourish in environmnets w/o oxygen - spore forming
- often found in soil (C. tetani, C. perfingens)
- improper canning of food (C. Botulinum)
Tb virulence factors
(a) Cord factor
(b) Sulfatides
Tb virulence factors
(a) Cord factor (shows serpentine growth in vitro) causes granuloma formation to wall off infection
(b) Sulfatides inhibit phagolysosome formation
- prevents phagosomes and lysosomes from fusing = how Tb survives in macrophages
What type of hypersensitivity is seen in a positive PPD skin test?
Type IV hypersensitivity: delayed cellular response
Bacteria responsible for
(a) Scarlet fever
(b) MC cause septic arthritis in adults
(c) Impetigo
(d) MC cause osteo in adults
(e) TSS
(a) Scarlet fever (strawberry tongue, pharyngitis, face-sparing rash) = strep pyogenes = group A strep
- encapsulated w/ hyaluronic acid, beta-hemolytic
(b,d) MC cause of both septic arthritis and osteomyelitis in adults = staph aureus
-beta-hemolytic, protein A virulence factor, coagulase positive
(c) Impetigo = from group A strep
(e) TSSS = toxic shock syndrome from staph aureus
What are the two virulence factors of Neisseria species
Neisseria species (neisseria meningites and neisseria gonorrhea) virulence factors
- pili that demonstrates antigenic variation (why we can’t form super long lasting immunity to it)
- IgA protease: cleaves IgA and its hinge region
Abx of choice for
(a) MSSA
(b) MRSA
(c) Staph epidermidis
(d) VRE
Abx of choice for
(a) MSSA = Nafcillin “naf for staph”
(b) MRSA = Vanc
(c) Staph epidermidis (endocarditis) = Vanc
- or replace infected implanted joint
(d) VRE = Vanc-resistant enterococci- need to tx w/ Linezolid or Tigecycline
Tuberculoid vs. lepromatous leprosy
(a) T cell reaction
(b) Skin manifestation
Tuberculoid leprosy: bacteria very well contained inside marcophages
(a) Th1 reaction
(b) well demarcated hairless skin lesion: biopsy of this lesion shows small amount of bacteria
Lepromatous reaction
(a) Th2 reaction (if Th1 not strong enough so bacteria are not contained in macrophages)
(b) Poorly demarcated skin lesions on extensor surfaces
MC infections caused by
(a) Staph epidermidis
(b) Staph saprophyticus
Both gram positive cocci: catalase positive and coagulase negative
(a) Staph epidermidis infects artificial heart valves and artificial joints, also indwelling catheters
(b) Staph saprophyticus = UTIs in sexually active females
Which organism uniquely causes a double zone of hemolysis on agar
Clostridium perfinges (gas gangrene and food poisoning) causes a double zone of hemolysis
-differentiate it from other hemolytic strains (GAS/GBS) b/c it’s an obligate anerobe
How to diagnose CDif
(a) MC abx culprit
Detect toxin (not the organism) in stool
(a) Clindamycin
Name 2 gram positive filamentous rods
Gram positive filamentous rods = actinomyces israelii and nocardia
2 gram + bacilli that cause formation of pseudomembranes
- clostridium difficile: yellow pseudomembranes in colon
- corynebacterium diphtheriae: gray pseudomembranes in oropharynx
How to differentiate the 2 gram positive filamentous rods
(a) O2 use
(b) Clinically
(c) Tx
Actinomyces israelii vs. nocardia
Actinomyces israelii
(a) Obligate anerobe
(b) Gradual skin infection after jaw trauma
(c) PenG
Nocardia
(a) Obligate aerobe (like bacillus anthracis too)
(b) Pulmonary cavitations/abcesses, brain abscesses, cutaneous lesions
(c) Tx = sulfonamides
Differentiating neisseria meningities vs. neisseria gonorrhea
(a) Capsule
(b) Clinically
(c) Tx
Neisseria meningitides
(a) Has polysaccharide capsule (this is what the vaccine is made of)
(b) Clinically: meningitis w/ petechia, associated w/ Waterson-Freidhouse syndrome 2/2 shock
(c) Ceftriaxone- 3rd gen ceph w/ good CNS penetration
Neisseria gonorrhea
(a) No capsule!!!!
(b) White purulent discharge, PID, association w/ FItz-Hugh-Curtis syndrome
(c) Ceftriaxone AND azithromycin (for assumed chlamydial co-infection)
Gram positive cocci: beta-hemolytic vs. alpha hemolytic
Both staph aureus and strep A/B are beta-hemolytic (glow in red background)
While strep pneumo and strep viridans are alpha hemolytic (green color on agar plate)
Neisseria species
(a) 2 key organisms
(b) 2 agars on whcih they grow
(c) Which immunodeficiency increases risk specifically for neisseria infections?
Neisseria species
(a) Neisseria meningitis (encapsulated) and neisseria gonorrhea (non-encapsulated)
(b) Both grow on chocolate agar and VPN agar
- don’t grow on blood agar => need to heat up the blood agar which makes chocolate agar
(c) C5-C9 deficiency b/c pts can’t form MAC complex
Clinical features of lepromatous leprosy
- symmetric distal neuropathy (stocking glove distribution): mycobacterium leprosae prefers cold environments => extremities
- poorly demarcated skin lesion: biopsy shows tons and tons of bacteria
- profound facial deformity: “Leonine facies”
3 stages of Lyme’s disease (think the targets)
- Erythema migrans (‘bull’s eye rash’) w/ flu-like symptoms (fevers and chills)
- Heart block and b/l facial palsy (b/l Bell’s)
- Migrating polyarthritis of large joints (knees) and encephalopathy
Tx of Lyme’s disease
Doxyclcyine
If really severe infection = Ceftriaxone
Mechanism of Tb reactivation
(a) Clinical correlate
Immunosuppression (HIV etc) decreases release of TNF-alpha that was containing the infection in the granulomas in macrophages
=> reduced TNF-alpha increases risk of reactivation
(a) Clinical correlate: need to check PPD test before starting pt on TNF-alpha inhibitor
Treponema pallidum
(a) Direct visualization
(b) Treponemal vs. non-treponemal diagnostic tests
Treponema pallidum => syphilis
(a) Direct visualization under dark microscopy
(b) Non-treponemal tests = screening tests (VDRL and RPR): but these aren’t testing directly for the treponema
- can have false positives from cross-reactivitiy: seen in +RF, SLE, mono, leprosy
If one of those is positive, then do FTA-Abs test (direct treponemal test) to confirm dx
Differentiate CDif endotoxin A and B
Endotoxin A works at the intestinal brush border to cause watery diarrhea
Endotoxin B polymerizes actin filaments causing formation of yellow pseudomembranes in the colon (seen on colonoscopy)
Mycobacterium Tb
(a) Stain
(b) Primary infects what cells
(a) Lowenstein-Jensen stain
(b) Primarily infects macrophages
- so macrophages are the cells that are involved in reactivation (aka where Tb remains latent)
Differentiate the treatment for tuberculoid vs. lepromatous leprosy
Tuberculoid (well contained infection): Dapsone and Rifampin x6mo
Lepromatous (much more severe infection): Dapsone, Rifampin, and Clofazimine for 2-5 years
Name the main features of primary, secondary, and tertiary syphilis
Syphilis
Primary = painless chancre at site on infection Secondary = rash involving palms of hands and soles of feet, condyloma lata
Tertiary = gummas (soft growths w/ firm necrotic center)
- aneurysm of the ascending aorta
- tabes dorsalis = demyelination of the posterior column
- Argyll-Robertson’s pupils
Describe the make up of TDaP vaccine
Tetanus toxoid and corynebacterium diptheriae toxoid vaccines- meaning they have the inactivated toxin (NOT the bacteria’s antigens) bound to protein to spark immunogenic repsonse
Then have acellular pertussis
What feature causes positive AFB stain
Mycolic acid is a part of cell walls in mycobacterium (both tuberculosis and leprae)
-also partially acid fast = nocardia (gram positive branching filamentous rod)
Name 2 spirochetes that infect humans (and the disease they cause)
Spirchoetes = spiral shaped bacteria
Borrelia burgdorferi => Lyme’s disease
Treponema Pallidum => Syphilis
Clinical relevance of novobiocin test
Novobiocin test- used to differentiate coagulase negative gram positive cocci
-Staph epidermidis is novobiocin sensitive in culture while staph saprophyticus is novobiocin resistant
Catalase test is most helpful to differentiate which gram positive cocci
Catalase (enzyme that catalyzes H2O2 –> H2O) is used to differentiate staph and strep
Staph = catalase + (cocci in clusters) Streph = catalase - (cocci in long chains/pairs)
2 other body systems involved in Tb reactivation (besides pulmonary)
Spinal- Pott’s disease- infection of vertebral bodies
CNS- tuberculoma (cavitary lesions) or meningitis
Which staph species are coagulase positive vs. negative
Coagulase + = staph aureus
Coagulase - = staph epidermidis and staph saprophyticus
1st,2nd,3rd MC causes of neonatal meningitis
Neonatal meningitis
- GBS (strep agalactiae) = gram + cocci
- E. Coli
- Listeria monocytonegens = gram+ bacilli
Gram positive cocci in clusters vs. pairs
G+ cocci in
(a) Staph aureus grows in clusters, while strep genus grows in long chains or pairs
Differentiate the toxin excreted by clostridium tetani and clostridium botulinum
Both form toxins that are proteases against SNARE proteins
- tetanus toxin: cleaves SNARE protein preventing release of inhibitory nt (GABA and glycine), so no inhibitory signal => uncontrolled muscle spasms
- botulinum toxin: cleaves SNAREs in motor neurons preventing ACh release => causes descending flaccid paralysis (muscles can’t contract)
Test to differentiate group B strep from all other strep
CAMP test- increased zone of hemolysis when plated w/ staph aureus
GBS produces a CAMP factor that enlarges the area caused by staph aureus
-used to differentiate GBS from other strep species
What are Argyll-Robertson’s pupils?
“Prostitute’s pupils” highly specific for neurosyphilis
Pupils that react to accommodation, but not to light
-aka shrink when object nears, but don’t constrict to light
Clinical presentation of Clostridium botulinum
C. botulinum (G+ bacilli, obligate anaerobe, spore forming) presents w/ descending flaccid paralysis
Differentiate infection of C. botulinum in babies vs. adults
Adults do not get disease from the spores alone, instead the gut flora make a toxin (protease that cleaves SNARE in motor neurons) that cause disease
While babies don’t have this developed gut flora, so gut in an anaerobic environment in which C. botulinum can survive. So babies can get sick from the spores along (not the toxin formed by the gut)
-classically spores are found in honey
So babies get sick from the spores, while adults get sick from the preformed toxin
Why does the med student not get C. Dif but he/she transports it btwn pts who do get sick
C. Dif doesn’t compete well w/ normal gut flora, so it’s ppl who are on abx (therefore killing the normal gut flora) who are susceptible to infxn
Why do we test for C. Dif toxin instead of C. Dif bacteria in the stool
Tons fo ppl are colonized w/ C. Dif (it can be a normal part of gut flora), but most of those ppl aren’t colonized w/ toxin-producing strains
So want to test for the toxin and not the bacteria itself
Describe the clinical features of clostridium myonecrosis
Clostridium myonecrosis = gas gangrene, MC 2/2 Clostridium perfinges (G+ bacilli, obligate anaerobe, spore forming) = severe soft tissue infection
- palpable crepitus 2/2 gas production
- myocnecrosis due to alpha-toxin which is a lecithinase that leaves lecithin to damage the plasma membrane
Tx of clostridium myonecrosis
Tx = IV PenG
Clostridium myonecrosis = gas gangrene = soft tissue infxn MC 2/2 clostridium perfinges (G+ bacilli, obligate anaerobe, spore forming)
Hallmark clinical feature of Corynebacterium Diptheriae
C. diphtheriae classically presents w/ ‘Bull’s neck’ due to lymphadenopathy
-formation of grey pseudomembranes in the oropharynx
Describe the food poisoning caused by C. perfinges
Clostridium perfinges causes a late onset diarrhea
-slow onset watery diarrhea 2/2 spore ingestion
Late/slower onset b/c the toxin is not preformed, you consume the spores then toxin is produced