Staphylococci Flashcards
General Staph Facts
Major cause of nosocomial bacteremia
Foreign bodies help colonization
Lots of resistance out there
General Staph Characteristics
Gram + cocci
GRAPE CLUSTERS
Facultative
Catalase positive
What is Coagulase?
Enzyme that clots plasma by activating fibrinogen
S. Aureus POSITIVE
Other staph NEGATIVE
Staph Aureus Epi
Found on skin, mucous membranes, nares
Colonizes diabetics, drug addicts, and hospitalized diabetics more
FOREIGN BODIES are often colonized
How do you take Staph outbreaks?
- DNA fingerprinting
- Ribotyping (ribosomal RNA)
- DNA sequencing of genes
- SPA
- MLST
How does Staph A. Toxin produce disease?
- Toxin Contamination
- enterotoxins -> food poisoning - Bacterial colonization
- toxin produced in host
a. TOXIC SHOCK SYNDROME TOXIN
b. Exfoliatins- scalded skin
How does Staph A cause invasive disease?
Damaged skin has lots of exposed matrix proteins
Easy for colonization through adhesive molecules
Can invade into tissue and blood
What Staph A toxins cause direct damage?
ALPHA TOXIN - lyse host cell membrane
Leukocidins - lyse leukocyte so
Proteases, COAGULASE, hyaluronidase, lipase
What toxins allow Staph A to evade our immune response?
PROTEIN A
- cell wall protein
- binds IgG
- less complement
- B-cell super antigen
ENTEROTOXINS
- many types
- T-cell super antigen
CAPSULAR POLYSACCHARIDE
-stops phagocytosis
EAP
-helps neutrophil evasion
What are the three toxin mediated SA diseases?
Food poisoning
Toxic Shock Syndrome (TSS)
Staphylococcal Scalded Skin Syndrome (SSSS)
What causes SA food poisoning and what does it look like?
Enterotoxins A-I except F
- HEAT STABLE
- A and C are Super antigens
Nausea
Vomiting
Non-bloody diarrhea
Does not require colonization
How does SA cause TSS and what does it look like?
Requires prior colonization
EXOTOXIN F / TSST-1
- super antigen
- IL-1/2 and TNF
Fever
Rash
Desquamation
HYPOTENSION AND SHOCK
What’s SSSS?
Caused by EXFOLIATINS A and B
encoded by eta genes
Superantigens
Usually infants
SUPERFICIAL LAYER OF EPIDERMIS DETACHES
What does superficial SA invasion look like?
Impetigo (red, vesicular lesions of the skin)
Folliculitis (follicle infection)
Furuncles and Carbuncles (skin boils)
Cellulitis
CATHETER SITE INFECTION
What are the deep seated SA infections?
Pneumonia (usually postoperative/hospitalized pts)
Endocarditis
Arthritis
Abscess
Sepsis
How do you treat SA?
Abscesses are surgically drained or removed
Semisynthetic penicillin
-dicloxacillin or oxtail in
VANCO last resort
-be judicious
How can we prevent SA infections?
WASHING HANDS
No ties?
Judicious use of antibiotics to curb resistance
Fight nasal infections with mupirocin
Staphylococcus Epidermidis distinguishing characteristics
Gram + cocci
WHITE colonies
COAGULASE NEGATIVE
CATALSE POSTIVE
Does not ferment mannitol
Sensitive to Novobiocin
S. Epiderm Epi
Skin colonizer, there normally
Very opportunistic
Loves FOREIGN BODIES (who doesn’t)
How does S. Epiderm infect?
Normally found on skin
indwelling device or immunosuppression makes it easy to colonize
Create biofilm
Can invade skin
How does S. Epiderm manifest?
Low fever
Pain
Discomfort
Diagnosing S. Epidermidis
TREAT PATIENT AND NOT THE CULTURE
Found normally on skin
-> common culture contaminant
How would you treat S. Epiderm?
Remove indwelling device
Treat with VANCO
If TSS use combination, rifampin or gentamicin
S. Saprophyticus distinguishing features
COAGULASE NEGATIVE
Catalase positive
Does NOT ferment mannitol
RESISTANT TO NOVOBIOCIN
S.S. Epi
Skin commensal
Common cause of UTI
Treating SS
Trimethoprim sulfamethoxazole (BACTRIM)
NORFLOXACIN (quinolone)
