Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
27 Cards in this Set
- Front
- Back
How many categories of gram positive rods are there and what are they?
(MIP B1 Pg 1) |
3
Endospore formers: Bacillus Cereus, Bacillus Anthracis, and Clostridium sp. Regular rods: Listeria monocytogenes and Erysipelothrix rhusiopathiae Irregular Rods: Corynebacterium diptheriae, mycobacterium sp., proprionibacterium sp., Actinomyces, and Nocardia asteroids |
|
What is the special stain necessary to be used for Endospors because they don't take up typical gram reagents?
(MIPB1,1) |
Malachite Green
|
|
Discuss the virulence factors of Bacillus cereus (How many are they and what do they do)?
(MIPB1,1-2) |
There are 5 classes.
1.) Emetic enterotoxin (aka cerulide) (Intoxication - ingestion of preformed toxin): Causes emetic Gastroenteritis. Binds 5'HT (serotonin) receptor and stimulates vagal nerve afferents to produce symptoms - heat stable and proteolytic resistant. Diarrheal enterotoxins (2 types)(Infection - ingest organism then secrete toxins): causes diarrheal gastroenteritis. stimulates adenylate cyclase causing net secretion of fluids into intestines, heat labile Hemolysin (aka cereolysin [1 of 3]): Perforates cell membranes, heat labile, similar to Streptolysin-O, inhibited by cholesterol (beta hemolysis) Phospholipases (3 forms): Phosphotidylinosital hydrolase, phosphotidylcholine hydrolase, and hemolytic sphingomyelinase (they destroy membrane integrity by destorying integral membrane proteins) Proteinases - collagenase and serine proteinases: Lare role in extra-intestinal infections (cutaneous wound and eye infections), important for spreading |
|
What is the etiology of Bacillus cereus?
(MIPB1,2-3) |
Ubiquitous in the environment with both the spores and vegetative state being infectious causing: food borne illnesses, eye infections, and disseminating infections.
|
|
What is the pathogenesis of Bacillus cereus' Emetic gastroenteritis?
(MIP B1,3) |
Symptoms appear around 2 hours after ingestion and last 8-10 hours (Remember: intoxication)
Toxin is heat stabile and binds 5'HT receptors of vagal afferents |
|
What is the pathogenesis of Bacillus cereus' Diarrheal gastroenteritis?
(MIP B1,3) |
Heat labile
Watery diarrhea 8-24 hours after ingestion and last a day or two (Remember: infection - takes time to produce bacteria then toxin) |
|
What is the pathogenesis of eye infections (Panopthalmitis) for bacillus cereus?
(MIP B1,3) |
Usulaly involves trauma to the eye
Replication in the vitreous Pain, swelling, and increased intra-ocular pressure, destruction fot he retina within 2 days of the infection (loss of eye) |
|
What are some other pathogenic effects of bacillus cereus?
(MIP B1,3) |
Septicemia causing: Meningitis, pneumonia, or endocarditis
Skin lesions causing: necrotic lesions through collagenases and serine protienases |
|
What can be used to clinically identify bacillus cereus?
MIP B1, 4 |
Isolation of bacteria from sterile body fluids:
Gram stain - gram positive bacilli with intracellular clearings (endospores) Spore stain - cell appears red and spore appears green within the cell Differentiation of different bacillus species requires sugar and motility tests |
|
What can be done to treat or prevent bacillus cereus infection?
MIP B1, 4 |
For gastroenteritis - treat symptoms
For systemic infections - vancomycin, gentamycin, ciprofloxacin (drug of choice because lacks toxic side effects), clindamycin (also B. cereus has a chomosomal encoded beta-lactamase) |
|
How many and what are the virulence factors of Listeria Monocytogenes?
MIP B1, 4 |
There are 4 virulence factors
Internalins - Mediate the adhesion and penetration of eukaryotic cells (Internalin A and B) bind to E-caherin receptors on host cells to facilitate uptake Listeriolysin O (LLO) - hemolysin similar to streptolysin O, allows escape of organism before the endocytotic vesicle fuses with the lysosome Phospholipases (2 types) - Phosphoinositol specific phospholipase and phospholipase C. These are synergicstic with LLO (they disrupt eukaryotic cell membrane) Act A - protein that directs polymerization oft he host cell's actin at the pole of Listeria (as a side - it is catalase positive) |
|
What is the infectious cycle of Listeria monocytogenes?
MIP B1, 5 |
Internalins - bacteria taken into host phagocytic vesicles
Phospholipase and LLO - break down and escape vesicle Act A - actin propulsion system to another cell causing a double layer coat around the cell Phospholipase and LLO - break down new membrane coats |
|
What is the etiology of Listeria Monocytogenes?
MIP B1,5 |
Everywhere
Cell mediated immunity because intracellular 3 main targets for infection: Fetuses, neonates, immunocompromised adults - associated with eating contaminated dairy and processed meats (cold cuts and hot dogs) Grows well at 4 degrees |
|
What is the pathogenesis of Listeria monocytogenes?
MIP B1, 5-6 |
Symptoms - weeks after eating contaminated food
Non specific signs - flu-like symptoms, GI upset Pregnant women - effect on fetus dependent on time of infection and severity (spontaneous abortion with early infection) Granulomatosis infantseptica (infection closer to term) - baby covered with granulomatous lesions full of pus Immunocompromised individual develop septicemia (septic shock or meningitis) |
|
How is listeria monocytogenes identified clinically?
MIP B1, 6 |
Gram stain - short, gram pos. rods
Cultured - cold enrichment (fridge like environment to grow) Complete hemolysis on BAP Wet mount - 20 degree broth tumbiling motility |
|
What are the treatments and prevention of listeria monocytogenes?
MIP B1, 6 |
Ampicillin or erythromycin (drugs that can permeate host cells - aminoglycosides can't permeate host cells)
|
|
What is the virulence factor of Corynebacterium diptheriae?
MIP B2, 1 |
Diptheria toxin2 subunits linked by a disulfide bond:
A-subunit has a catalytic domain (endogenous host protease clips the disulfide bond to activate) B-subunit responsible for binding and translocaiton HB-EGF receptor for the B subunit. |
|
How does diptheriae toxin function?
MIP B2, 1 |
DTx binds to its receptor and is endocytosed. Once endocytosed the pH of the vesicle drops due to lysosomes allowing the A subunit to be released into the cytoplasm. A subunit catalyses the transfer of ADP-ribose from NAD to the elongation factor-2 which inactivates EF-2 a protein needed for protein synthesis. (1 A subunit is lethal for 1 cell) (side note: Pseudomonas aeruginosa exotoxin A has same function but is structurally different)
|
|
Where does DTx come from?
MIP B2, 2 |
a lysogenic phage that incorporates the genetic material for DTx into the bacteria's chromosome
|
|
What other factors are needed to activate DTx?
MIP B2, 2 |
A protein DTxR - iron responsive protein that activates the transcription and production of DTx in the presence of low iron conditions. DTxR is encoded already in the bacteria chromosome
|
|
What is the pathogenesis of Corynebacterium Diptheriae?
MIP B2, 2-3 |
Spread by respiratory route or direct contact
Humans are the only reservoir of infection. Bacteria infects tissue of the throat, replicate, and secrete toxin. Incubation 2-6 days feel tired, achy, sore throate with exudates (flu-like symptoms) Exudates evolves pseudomembrane - obstructs breathing DTx - absorbed systemically causing bull neck due to infection of the cervical lymph nodes. Toxin can cause cardiac arrhythmia and/or arrest 1/10 with Diptheria will die can appear as a cutaneous form of a chronic non-healing ulcer |
|
How do you clinically ID corynebacterium diptheriae?
MIP B2, 3 |
Club shaped pleomorphic rod (like chinese characters)
Metachromatic granules (deposits of phosphates not spores) 3 distinct colony morphologies on telluride agar: Gravis - colonies are large, irregular and gray Intermedius - colonies are small, flat, and gray Mitis - colonies are small, round, convex, and black Test for toxin production (not all have omega or beta phage) - Elek test PCR for toxin gene |
|
How is Corynebacterium diptheriae treated?
MIP B2, 3-4 |
Antibiotics - penicillin or erythromycin
Antitoxin - horse anti-DTx passive immun. Vaccination - DPT Verification - inject small amount of toxin intradermal like in PPD |
|
Nocardia asteroides can grow in non-actiavted macrophages yes or no? (duh)
MIP B2,4 |
Yes
|
|
What is the pathogenesis of Nocardia asteroides?
MIP B2, 4 |
Organism is inhaled with contaminated dirt or dust resulting in bronchopulmonary disease of hte immunocompromised
Lobar pneumonia Meningitis from lungs to brain (abscess can form) |
|
How is nocardia asteroides clinically ID?
MIP B2, 4 |
Collect sputum or abscess
Grow aerobically on blood agar to form orange, wrinkly, waxy colonies Poorly staining with gram stain so acid fast (b/c of waxy esters) |
|
What is the treatment of nocardia asteroides?
MIP B2, 4 |
Sulfonamides or Amikacin plus a beta0lactam (ceftriaxone or imipenem)
|