Staphylococcus Flashcards
What are 3 general characteristics of Staphylococci?
- Gram (+) cocci, arranged as grape-like clusters
- Facultative anaerobes
- Catalase (+)
What test can be used to differentiate Staph from Strep?
Catalase test
Staph are catalase (+)
Strep are catalase (-)
What are some general features of Staph in regards to infection? (Where are they commonly found? Do they survive well? Is antibiotic resistance a problem? What types of infections are they a common cause of?)
- Pyogenic (pus forming) bacteria
- Commonly found on the skin and mucus membranes of humans
- Survive for long periods of time on fomites under harsh conditions
- Common cause of community acquired (CA) and hospital acquired (HA) or nosocomial infections
- Antibiotic resistance is a problem
Staph can be separated into 2 classes based on what test/presence of…? What can those classes be further subdivided into?
- Staph aureus: coagulase (+) and contains protein A, beta-hemolytic
- Coagulase negative Staph (CoNS)
CoNS can be classified based on their novobiocin susceptibility
Novobiocin-susceptible: S. epidermidis, haemolyticus, hominis, lugdunesis, schleiferi
Novobiocin-resistant: S. saprophyticus, xylosus
Which CoNS is most similar to S. aureus with regards to its virulence?
S. lugdunesis
Which CoNS is a large cause of UTI’s in sexually active women?
S. saprophyticus
Which CoNS is a large cause of endocarditis?
S. epidermidis (think about IV drug users, common on the right side of the heart)
Which CoNS are prevalent in nosocomial infections?
S. epidermidis and haemolyticus
What is the most pathogenic species of Staph?
S. aureus
What types of conditions/diseases might a S. aureus infection produce? 6 things
- Skin/soft tissue => abscess
- Osteomyelitis
- Septic arthritis
- Respirator infections (ie aspiration pneumonia)
- Infective endocarditis (IVDU)
- Bacteremia
What type of Staph may lead to necrotizing pneumonia?
CA-methicillin resistant staph aureus (MRSA)
Approximately 90% of S. aureus are resistant to what…? What is the best way to treat them?
Pencillin/Methicillin resistant because they produce a beta-lacatamase.
Best treated using a cephalosporin (ie. nafcillin)
How might S. aureus cause problems without causing an infection?
Secretes enterotoxin A => severe vomiting and diarrhea with immediate onset (Food poisoning)
Toxic Shock Syndrome: foreign body (tampon or gauze pads) allow bacteria to grow to very high numbers which can then excrete a superantigen into the blood
What are the 7 virulence factors associated with S. aureus? Give examples and function when possible
- Fibronectin Binding Protein/Collagen Adhesin
- Protein A (binds Fc part of Ig)
- Cytolytic Exotoxins (hemolysins) (alpha, beta, delta, gamma, and Panton-Valentine leukocidin => nosocomial adolescent infections => necrotizing pneumonia)
- Slime production (biofilm)
- Superantigen Exotoxins
- Enzymes (Coagulase, catalase, hyaluronidase, fibrinolysin)
- Clumping factors A and B (fibrinogen binding)
* Certain types can go intracellular in endothelial cells and macrophages
What are the 2 primary methods by which S. aureus spreads?
- Direct contact
2. Aerosol/Large droplet (associated with respiratory infections)
There are 4 types of toxins that are produced by S. aureus. Name them with specific examples and describe how they behave and mediate disease.
- Cytolytic Exotoxins: alpha, beta, delta, gamma, and Panton-Valentine leukocidin => nosocomial adolescent infections => necrotizing pneumonia
- Exofoliative Toxins (ETA and ETB): act as superantigens, act as a serine protease that can split desmoglein-1, mediates staphylococcal scalded skin syndrome (SSSS)
- Enterotoxins (A-X): act as superantigens, heat stable and resistant to low pH and gastric enzymes. Enterotoxin A associated with food poisoning, enterotoxin B and C associated with 50% of non-menstruation associated TSS
- Toxic Shock Syndrome Toxin (TSST-1): act as a superantigen, responsible for 90% of menstruation associated TSS; also associated with the other 50% of non-menstruation associated TSS, is able to penetrate muscosal barriers
Name 3 types of skin infections that are caused by S. aureus
- Folliculitis/Styes: superficial infections of the hair follicles
- Furuncles: Deep tissue infection (abscess)
- Carbuncle: coalescent of furuncles that becomes even deeper in tissues with possible systemic effects such as fever and chills as the organism seeds into the blood
What 3 types of cytokines produced in TSS cause the symptoms?
- IL-1 => Fever
- TNFa/b => capillary leakage (hypotension)
- IFNy and IL-2 => rash
What is the main carrier or reservoir for Staphylococcal food poisoning? What causes it?
No reservoir for this disease, just has human carriers
Caused by ingestion of pre-formed staph enterotoxins
What is the antibiotic of choice for the treatment of MRSA? What is the next choice if the first one doesn’t work?
Vancomycin
If it is vancomycin resistant S. aureus (VRSA) then treat using linezolid, synercid, and daptomycin
S. aureus that has become methicillin resistant as well as resistant to other penicillins has done so by what mechanism(s)?
- Penicillin-binding protein 2a (PBP2a) is a transpeptidase that has been evolved to feature an alteration to the penicillin binding site that deceases affinity for both penicillin and cephalosporins.
PBP2a is encoded by different cassettes on the chromosome by the SCCmec gene. - Beta-Lactamase: present in 90% of strains, hydrolyzes classic penicillins, is encoded on a plasmid
There are 2 classes of PBP2a (SCCmec) genes? How do they differ and how are they classified?
- Hospital acquired strain: Larger SCCmec types I-III (34-67kb) which have greater antibiotic resistance than CA strains
- Community acquired strain: Shorter SCCmec type IV (~24kb) which has resistance to methicillin, beta-lactam antibiotics, but not other classes. So less resistant than HA strains
What are 3 major sites of infection for CoNS?
- Prosthetic heart valves (can also infect native heart valves but infection is more often associated with S. aureus)
- Artificial heart valves => endocarditis
- Catheters and shunts (ie foreign bodies) and account for ~50% of those types of infections
Where is S. epidermidis and saprophyticus found? What are their main virulence factors?
Both are part of the normal flora
- S. epidermidis: most abundant species on skin (can contaminate blood cultures or IV lines). Virulence via slime/biofilm formation
- S. saprophyticus: Genitourinary muscosa flora. Virulence via epithelial adhesions
What clinical diseases are most often implicated in S. lugdunesis and S. schleiferi infections?
Endocarditis of artificial valves (but can also be associated with native-valve endocarditis) and osteomyelitis
