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WVSOM - Staph
Staphylococci
| Question | Answer |
|---|---|
| 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
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