exam 4 Flashcards
HA-MRSA
Hospital-associated MRSA
- Resistant to all antibiotics but Vancomycin (only treatment) only treatment
- Methacilin resistant, so it has mec A gene
- Way more problematic and CA-MRSA
- No PVL
CA-MRSA
Community-associated MRSA
- Resistant Methcillin, but sensitive to most other antibiotics including Vancomycin
- Do not have to treat with vancomycin so you have other choices to treat with
- mec A gene
- Contains PVL (Panton-Valentine Leukocidin) gene
- All skin infections
–> CA has mec A gene AND PVL gene
Scalded Skin Syndrome
- bacteria colonize in the intesting of newborn and children <2
- adults can get it after toxic shock
- toxins enter bloodstream, goes to skin cells and the toxins affect the epidermis.
EXAMPLE OF TOXEMIA
Happens when a baby born (sterile), if they come across S. aureus before normal gut flora gets established, they can get S. aureus colonized in gut
If that s. aureus can make the toxin, they they will have scaled skin syndrome
The bacteria are multiplying in intestine but seeing affect on skin
THE TOXIN IS Exfoliative toxin A & B
Virulence factors of scalded skin
Exfoliative toxin A & B
- destruction of intracellular CT
- skin peels off in sheets
- must do histological testing to rule out other causes
Toxic shock syndrome
a. Colonization elsewhere
b. Toxin enters bloodstream
c, Body-wide effects
1) fever, vomiting
2) sunburn-like rash
3) Leads to peeling skin
(looks like scalded skin)
Staphylococcal Toxic shock syndrome
- S. aureus usually remains localized but may become systemic; all give rise to systemic superantigens (usually TSST-1, SEB, or SEC)
- Massive cytokine production: IL1-β (fever), TNF-αβ (hypotension), interferon-γ and IL-2 (rash and other symptoms)
- Menstrual TSS occurs primarily in association with tampons; incidence rises with increases in absorbency (oxygen) – the air lets S. aureus grow really well
Can grow in nasal sinuses with you get surgery and they pack sinuses - Must rule out other causes
- Culture on blood agar must Verify TSST-1 toxin
Acute glomerulonephritis (AGN)
Glomeruli – sterile water comes in, picks up trash from blood and you pass it as urine the antigen-antibody complexes get stuck in here; land on tissue, activate compliment against the tissue, and the complement then puts holes on kidney and causes kidney damage AKA ACUTE GLOMERULONEPHRITIS
Immune response to strep antigens where the antibodies are reacting with you own antigens after the antigen is gone
- Antigen is gone but you are still seeing effects; I THINK THIS IS CALLED late sequele
Necrotizing fasciitis
- Flesh-eating Streptococcus
- Have proven that S. aureus also causes it
- Rapid disease course
- Destroys tissue as quickly as it is removed
- has ability to travel through tissues
- this is a TOXEMIA OF S. PYROGENES
Epidemiology of necrotizing fasciitis
- can cause death
- loss of limbs
Virulence factors of necrotizing fasciitis
a) Pyrogenic exotoxin A (SPE A) - strepococcal
1) Superantigen (SPE A is superantigen –> cytokine storm)
b) Streptolysin O (SLO)
Diagnosis of necrotizing fasciitis
- culture on blood agar
- beta-hemolytic, Group A
- immunological assays for toxin
- catalase negative
- SPE A and SLO
Treatment of necrotizing fasciitis
- antibiotics-penicillins still drug of choice
- wound debridement necessary
Strep Toxic Shock Syndrome
- similar symptoms as staph toxic shock
- less frequent rash
- more frequent bacteremia
- shock and organ damage
- Toxin called strep TSS-1
pathogens attack in 3 ways
breach of intact skin
skin manifestation of a systemic infection
toxin-mediated skin damage
Subacute Schlerosing Panencephalitis (SSPE)
Rare event 1/million male children and young adults infected - 1-10 years after measles infection - fatal - subacute (no sign of it) LATE SEQUELAE OF MEASLES