• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/27

Click to flip

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)