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Micro lecture 15.1
Micro lecture 15.1 Staphylococcus!
| Question | Answer |
|---|---|
| What does staphylococcus look like? | Gram-positive cocci in a grape-like cluster. |
| Name some staphylococcus traits | facultative anaerobes, facultative halophiles, catalase positive, have peptidoglycan relatively resistant to lysozyme |
| What is a facultative halophile? | Something that can live in environments with a high salt concentration but don't have to. |
| What is catalase positive? | When the bacteria produces catalase which deactivates peroxide radicals and allows the cell to live in the host. |
| What can staphylococci withstand? | Drying for weeks, heating up to 60°C for 30 min, pH fluctuations from 4.0-9.5, NaCl concentrations up to 10% |
| What are staphylococci inhibited by? | Bacteriostatic dyes i.e. crystal violet, bile salts, disinfectants, several antimicrobial drugs |
| Name some important staphylococci. | S. aureus, S. epidermidis, S. saccharolyticus, S. haemolyticus, S. lugdunensis, S. saprophyticus, S. schleiferi, S. intermedius |
| How can you tell if something is catalase positive once you test it with 3% hydrogen peroxide? | It produces O2 and produces bubbles |
| Where is S. epidermidis found? | Normal flora on human/some other species' skin. |
| What does S. epidermidis look like on a BAP? | Small, white, nonhemolytic colonies. Doesn't ferment mannitol, coagulase negative, suceptable to novobiocin. |
| How are S. epidermidis biofilms held together? | With a slime coat. (THERE IS A PICTURE HERE) |
| Where are most S. epidermidis infections acquired? | The hospital. |
| Is S. epidermidis susceptible to penicillin G? | No, but the majority of isolates are susceptible to other penicillins. |
| Where is S. saprophyticus found? | Normal flora on human genitourinary skin. |
| What does S. saprophyticus look look on a BAP? | White, nonhemolytic colonies. Does not ferment mannitol, coagulase negative, resistant to novobiocin. |
| Is S. saprophyticus susceptible to penicillin G? | yes |
| What does S. saprophyticus cause? | UTIs/cystitis in sexually active women. |
| What does S. aureus look like on a BAP? | pale yellow, β-hemolytic colonies. Ferments mannitol, coagulase positive, susceptible to novobiocin. |
| Where is S. aureus found? | Part of normal flora on anterior nares and skin on humans and other animal species. |
| Why is S. aureus the most virulent member of the staphylococci? | Its surface proteins facilitate attachment and immune system evasion; secretes a large assortment of toxins. |
| What does S. intermedius look like on a BAP? | Unpigmented, β-hemolytic colonies. Often ferments mannitol, coagulase positive, susceptibel to novobiocin. |
| Where is S. intermedius found? | Normal flora on skin of domestic dogs, mink, fox, and raccoons. |
| What are 2 differences between S. aureus and S. intermedius? | Composition of the cell wall peptidoglycan glycine interpeptide bridges and the teichoic acid sugar composition. |
| What does β-hemolysis look like on a RBC plate? (there is a picture) | white, with yellowy edges due to incomplete hemolysis |
| What happens in a coagulase-positive tube test? | The coagulase from the bacteria causes the plasma to coagulate inside the tube. |
| What does DNase positive bacteria look like in blood agar? | DNase from the bacteria are released into the blood and digests the DNA, clearing the agar. |
| What does Mannitol-Salt agar test for? How does it show halophilic bacterial presence? | It tests for halophilic (salt-loving) bacteria. The pink agar turns yellow in the presence of halophilic bacteria due to a release of acid fermentation products from mannitol. |
| There is a flow chart we should probably know | on slide 24 |
| Name the disease types caused by S. aureus | infection, intoxication, infection + intoxication |
| What is an S. aureus infection? | colonization and growth of S. aureus without release of exotoxins |
| What is an S. aureus intoxication? | Ingestion of S. aureus exotoxins; not an infection, often seen with food poisoning. |
| What is an S. aureus intoxication + infection? | Colonization and release of exotoxins. |
| Name the S. aureus virulence factors. | Protein A, Fibronectin-Binding Protein, Cytolytic Exotoxins, Enzymes, Slime Production, Superantigen Exotoxins |
| What do Fibronectin-Binding Proteins do? | promote binding to mucosal cells and tissue matrices |
| What does Protein A do? | binds to the Fc portion of IgG and thus "hides" the host cell behind host cell immunoglobulins. This is part of the immunological disguise. |
| What do cytotoxic proteins/enzymes do? | Promote bacterial spread in tissues. They kill RBCs, WBCs, and a lot of other stuff. |
| What do membrane-damaging toxins do? | disrupt eukaryotic cell membranes and contribute to pus formation. |
| Pus | mixture of host cell debris, living and dead PMNs, and living and dead bacteria |
| Impetigo | localized superficial skin infection with pus filled vesicle on reddened base (like acne, but often found in children) |
| Folliculitis | infection of hair follicles, sweat, or sebaceous glands |
| Furuncles (single boil)/Carbuncles (multiple openings) | abcesses that form around foreign bodies (i.e. splinters) |
| Bacteremia | visible bacteria in blood stream |
| Pneumonia | exudate within alveoli |
| empyema | collection of pus in body cavity |
| osteomyelitis | growth on ends of long bones and vertebral bodies |
| Staphylococcal Scalded Skin Syndrome (SSSS) | Ranges from local blistering to generalized exfoliation; toxin is a protease, causes stratum corneum to shed. |
| Toxic Shock Syndrome (TSS) | multisystem intoxication with fever, hypotension, rash, high mortality without proper prompt antibiotic treatment. |
| Menstrual TSS | Shows up within 2 days of menses and associated with use of high absorbency tampons. |
| Why is TSS rare despite ~20% of S. aureus isolates are TSST-1 producing strains? | TSST-1 requires special growth requirements. |
| Why is S. aureus often antibiotic-resistant? | It often has a penicillinase. MRSA also has an altered penicillin-binding protein. Also VISA and VRSA have thickened cell walls or carry vanA genes from Enterococci. |
| HA-MRSA | often ~50% of S. aureus isolates, Methicillin resistant. Hospital acquired. |
| CA-MRSA | mostly skin and soft tissue infections. Community acquired. |
| Vancomycin intermediately resistant S. aureus (VISA) strain | thick cell wall, allows them to sequester more vancomycin than non-VISA strains. |
| highly-vancomycin-resisting S. aureus (VRSA) strain | carries vanA from Enterococcus |
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