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WVSOM - Staph

Staphylococci

QuestionAnswer
Size and shape of staphylococcus Spherical and 1 um
Staphylococcus oxygen requirement Facultative anaerobes
Do staphylococci form spores? NO
Are staphylococci motile? NO
Staphylococcus gram staining Gram +
Metabolic requirements of staphylococcus Ferment wide variety of sugars -> acids (NO gas production)
Growing conditions for staphylococcus High salt concentrations (NaCl > 7.5%)
What media to staphylococci grow on? Most lab media (particularly mannitol salts agar) provided they are supplemented with amino acids and B vitamins
Three staphylococci associated with human diseases S. aureus, S. epidermidis, S. saprophyticus
S. aureus characteristics + for coagulase, golden yellow color of colony, + for mannitol fermentation, S (novobiocin)
S. epidermidis characteristics - for coagulase, white color of colony, - mannitol fermentation, S (novobiocin)
S. saprophyticus characteristics - for coagulase, white color of colony, - mannitol fermentation, R (novobiocin)
Purpose of peptidoglycan layer of S. aureus Provides shape & rigidity to cell; serves as chemotractant for PMNs; activates complement via alternate pathway (C3b); has endotoxin-like properties (anti-inflammatory response)
Purpose of teichoic acids of S. aureus Characteristized as polymers of ribotol / glycerol phosphates; used for adherence; in deep seated infections = antibodies are used as a diagnostic tool
What can gram + bacteria cause? SHOCK!
Effects of peptidogclycan fragments and lipoteichoic acids released during gram + infections Binds TLR-2,6 on macrophage -> releases cytokines (IL-1,6,8, TNF-a, PAF) -> activates complement, coagulation, prostaglandins / leukotrienes -> blood clotting, MAC lysis, inflammation -> ARDS, DIC, damage BV, MULTIPLE ORGAN FAILURE
Factors that allow for S. aureus infections Protein A (anti-opsonin effect, binds Fc portion of IgG -> Fab portion free to bind specific antigen); fibronectin-binding protein (promotes binding to mucosal cells); bound coagulase; micro-capsule (antiphagocytic)
Toxins and enzymes related to S. aureus infections Catalase, coagulase (free / bound), other enzymes (hyaluronidase, staphylokinase, B-lactamase), hemolysins (alpha, beta, delta, gamma), leukocidin (panton-valentine)
Bound coagulase causes _________ of S. aureus Agglutination
Free coagulase causes _____ ________ of S. aureus Clot formation
What is leukocidin? A pore forming toxin that destroys WBCs
How do you characterize staphylococcus strains for epidemiological studies? Phage typing (historical), DNA sequencing
Staphylococcal strain that is more resistant to antibiotics than S. aureus Staphylococcus epidermidis
What does Staphylococcus saprophyticus cause? UTI infections in F
Where are you likely to have an S. epidermidis infection? How does it infect these sites? Prosthetic joints, IV catheters, heart valves; capsule adheres to specific sites
# of deaths in USA related to MRSA 18,000 / year
How many people die annually from hosptial-acquired infections? 99,000
What are some risk factors for MRSA? Hospitalizaton w/i last 12 months, nursing home residency, surgery, catheterization; crowded living space (homeless shelter, camps, boarding schools, daycare centers); drugs by injection; incarceration; contact sports; frequent antibiotic use
How to reduce the risk of MRSA infections Wash hands often w/ alcohol or soap; use air blowers / paper towels; don't use personal items; wash linens & clothing in detergent; clean regularly touched areas; covers areas to protect against abrasions while exercising
What are two ways in which someone can get methicillin-resistant S. aureus? Hospital acquired and community acquired
Hospital acquired MRSA is _________ to most other antibiotics Resistant
What is used to treat hospital acquired MRSA? Vancomycin
What strain is responsible for community acquired MRSA? USA300 (has panton-valentine leucocidin)
Community acquired MRSA is resistant to ... Cephalosporins, tetracyclines, erthromycin, clindamycin (sometimes)
How is community acquired MRSA treated? Trimethoprim / sulfoxazole, fluoroquinoline, clindamycin (if susceptible), vancomycin
What mechanism is responsible for methicillin resistance? Altered penicillin binding proteins; transpeptidases fails to bind methicillin
What is the mechanism responsible for resistance to penicillin? B-lactamase enzyme; breaks b-lactam ring
What is used to treat S. aureus minor skin infections? Tetracycline
What is used to treat S. aureus abscesses? Incision and drainage; treat w/ penicillinase resistant penicillin (methicillin, nafcillin, oxacillin)
What is the problem with trying to treat S. aureus strains with methicillin? Many are resistant to methicillin
What causes scalded skin syndrome? Epidermolytic toxins A and B
What enterotoxins cause food poisoning? A, B, C, D, G
What causes toxic shock syndrome? Toxic shock syndrome toxin-1
Osteomyelitis is an example of what? Dissemination; abscess spreads via lymphatics -> enters bloodstream (bacteremia) -> abscesses in other parts of the body (metastatic disease)
What is cellulitis? A wound infection in which S. aureus is spread to subcutaneous tissues
An abscess formation in the skin is called? Furuncle / boil -> carbuncles
Examples of skin and soft tissue infections caused by S. aureus Impetigo, furuncles and carbuncles, wound infections, cellulitis
Bacteremia are often associated with? Metastatic abscesses
Diseases caused by S. aureus Endocarditis, pulmonary infections, genitourinary infections
Examples of CNS infections caused by S. aureus Brain abscess, epidural abscess
Examples of musculoskeletal infections caused by S. aureus Osteomyelitis, arthritis
Examples of toxin mediated diseases caused by S. aureus Toxic shock syndrome, scalded skin syndrome, food poisoning
List 3 specific toxins that contribute to S. aureus infections Exofoliatin (A - phage and B - plasmid); toxic shock syndrome toxin (acts as superantigen); enterotoxins (A, B, C, D, E, G - act as superantigens)
Characteristics of enterotoxins Resist gut enzymes and low pH; found in 30-50% of strains; most common kind of food poisoning in US; ingestion -> vomitting and diarrhea w/i 2-6 hours
Describe superantigens Attach to side of binding site btw T cell and APC; results in unregulated production of regulatory molecules from T cell (ex: IL-2, IFN-gamma, TNF) in toxic amounts
How do we encounter S. aureus? Part of normal flora (25-50% colonize external nares); survive on fomites (inanimate objects)
How does S. aureua gain access? Penetrate skin, enter through damaged skin / mucous membranes
How does S. aureus spread and survive? Number of organisms, virulence of strain, site of entry, inflammatory response of host, immunological history of patient
What kind of damage can S. aureus cause? Infections and toxinoses
Created by: JaneO