Gram Positive Rods Flashcards
What are the virulence factors for B. Cereus?
- emetic enterotoxin (cerulide): vomiting, nausea, cramps in less than 6hrs (lasts for 8-10hrs)
- diarrheal enterotoxins: profuse watery diarrhea, nausea, cramps in aboout 8hrs and lasts about 24 hours
- hemolysin (cereolysin): punches holes in RBCs membranes -> zone of clearing; similiar to streptolysin in structure/function
- proteases and phospholipases (collagenase and serine protease): eye and skin infections allowing dissemination through tissue (associated with nonsterile gauze and alcohol pads)
What’s the pathogenesis of emetic enterotoxins of B cereus?
binds 5-hydroxytryptamine (5-HT) receptor and stimulates afferent vagus n. causing stomach to contract quickly and eject toxins
What’s an important characteristic of cerulide?
heat-STABLE and proteolytic resistant peptide
(this is why cooking/microwaving/heating does not kill toxin)
How does diarrheal enterotoxin work?
just like cholera toxin!
stimulates adenylate-cyclase-cAMP in intestinal epithelial cells causing it to secrete fluids (dysregulation of Cl- secretion causing increase Cl- followed by water)
What’s significant characteristic of diarrheal enterotoxins?
large, heat labile protein complex -> will get destroyed if reheat food
Define panophthalmitis.
really bad inflammation and infection with proteases chewing up retina as a result of B. cereus getting into vitreal cavity
What are the disseminated infections seen in B. cereus?
septicemia, endocarditis, meningitis, etc. seen in immunosuppressed, IV drug users, and patients with indwelling shunts
What’s unique about emetic gastroenteritis?
an intoxication (not infection): toxins cause disease so more like poisoning
(extreme overdose of toxin can cause liver failure)
Why do diarrheal gastroenteritis appear AFTER emetic?
toxins are NOT premade!
bacteria has to enter intestine before secrete toxin
What culture is NOT done for B. Cereus?
fecal! bc it’s part of normal flora
How can spore stains be used to ID B.cereus?
spores DON’T STAIN bc spore coat doesn’t pick up reagents (will see gram + rod w/ white, unstained portion inside)
What’s the treatment for B. Cereus?
- for gastroenteritis: treat symptoms (so rehydrate and replenish electrolytes); no antibiotics bc self-limiting
- others: vancomycin, clindamycin, gentamicin (aminoglycoside), or ciprofloxacin
What is B. cereus resistant to?
have chromosomally encoded beta lactamase so resistant to beta-lactams, penicillin, and cephalosporin
What is listeria monocytogenes resistant to?
aminoglycosides bc they’re intracellular pathogens
What are the virulence factors for listeria monocytogenes?
- internalin A: adhesion and invasion of eukaryocytic cells by binding E-cadhedrin to be taken into endocytic vacuoles
- listeriolysin O (LLO): punches holes into phospholipid layers (hemolysin similar to streptolysin and pneumolysin) allowing bacteria to escape to cytoplasm from vacuoles before lysosomal fusion
- other hemolysin (phospholipase C’s): acts synergistically with LLO; affecting signal transduction pathways (short-circuiting intercellular communication networks)
- actA: directs host cell actin to polymerize behind it and propel bacterium in cytoplasm (flagella for environment; actA rockets intracellularly)
Where can we find Listeria normally?
soil, water, intestinal tracts of animals and man
What is essential for effective immune response to Listeria?
cell-mediated! (bc its intracellular)
What’s seen first after Listeria infection?
symptoms appear several weeks after, first flu-like (fever, chills, muscle aches, malaise, etc) then GI issues
What’s seen in pregnant women infected by Listeria?
may have mild symptoms or none at all
BUT: bacteria cross placenta (pale placenta) to infect fetus resulting in neonatal disease (granulomatosis infantiseptica- fetus with granulomas all over) or fetal death/miscarriage
What is seen in neonates and elderly infected with Listeria?
RAPID shift to septicemia or meningitis (stiff neck, headache, confusion, convulsions)
usu too late to treat and patient goes into septic shock -> HIGH MORTALITY RATE
What virulence factors cause the beta-hemolysis seen in Listeria?
LLO and phospolipase C
What should we culture to ID listeria?
blood and CSF
How do we treat patients infected with Listeria?
ampicillin+gentamicin (synergism), amoxicillin (penicillin)
bactrim (sulgamethoxazole w/ trimethroprim)
What’s Intralytix?
cocktail of phage approved to treat variety of processed meat to prevent listeria
What’s the most important virulence factor for Corynebacterium diphtheria?
Diptheria Toxin (DTx): A subunit (catalytic) and B subunit (binding)
How does the B subunit of Diptheria Toxin work?
helps the toxin translocate into cell bc it has translocation and receptor binding regions (for heparin binding epidermal growth factor [HB-EGF] on host)
What’s the mecahnism of action of DTx?
- toxin binds receptor and endocytosed
- drop in pH in vesicle causing toxin conformational change allowing A subunit to pop off and enter cytoplasm
- in cytoplasm, A subunit catalyzes ADP-ribosylation of elongation factor-2
- leads to inactivation of protein shutting down protein synthesis -> CELL DEATH
What’s significant about the DTx?
VERY POTENT: 1 molecule of A subunit is lethal for cell
How is DTx regulated?
- encoded by lysogenic phage (omega or beta) so has to infect to be pathogenic
- toxin production is regulated by iron reponsive protein (DTxR) that’s encoded on bacteria’s chromosome-> low iron turns on toxin production
What is the only sole reservoir for Corynebacterium diphtheria?
humans! (carried in oropharynx or skin of asymptomatic carriers of unvaccinated hosts)
What is seen first after infection with Corynebacterium diphtheria?
after 2-6 days, tired, achy, sore throat with exudate -> pseudomembrane (bacteria, lymphocytes, plasma cells, fibrin, dead epithelial cells)
1 in 10 infected -> death
What is the cutaneous presentation of Corynebacterium diphtheria?
chronic non-healin ulcer (RARE)
What makes up the metachromatic granules?
phosphates: form of storage vesicle or inclusion body for bacteria
What agar can be used to grow Corynebacterium diphtheria?
cysteine-potassium telluride agar (appears grey-black)
What is this?
Listeria (short gram + rods)
What is this?
C. Diptheria (note the club shaped pleiomorphic rods)
What is this?
Nocardia on blood agar (note the orange waxy appearance)
What is this?
Nocardia (note the filamentous rods)
Describe the Elek Test.
- used to determine whether or not strain isolated from throat is making toxin
- based on Ag-Ab precipitation reaction (precipitation occurs when antitoxin sees toxin)
What is the treatment of choice for C. Diptheria?
penicillin (1st) or erythromycin
antitoxin made in horses (used before antibiotics; beware of serum sickness)
Is there a vaccine for C. diptheria?
toxoid vaccine (“D” of DPT vaccine): toxin that’s heat activated or treated with formalin so not active but still immunogenic
*boosters every 10 years
What’s the Schick Test?
test immune status against DTx - similar to TB skin test
What’s the virulence factor for Nocardia?
unknown but knows it grows in non-activated macrophages
What’s unique about the pneumonia from nocardia?
opacity throughout entire lung field (others only consolidated in single lobe)
Describe the brain abscesses from Norcadia spread.
well-circumscribed lesions
What is collected for Nocardia culture?
sputum or abscess
What’s the mode of treatment for nocardia?
sulfonamides or amikacin + beta lactam
severe cases: ceftriaxone or imipenem
