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Flashcards in L 73 Toxic Syndromes Deck (25):

What is staphylococcal scalded skin syndrome?

A syndrome of toxin-mediated dermatitis
Superficial blistering and exfoliation
Follows an erythematous rash
The bacteria is often elsewhere in the body and the toxin is carried through the blood to affect the skin


Staph Scalded Skin Syndrome epidemiology

Generally in children


Previous name for Staph Scalded Skin Syndrome and the causative agent

Previously known as Ritter's disease
Caused by S. aureus


Exotoxins from S aureus

S aureus produces two toxins that affect the skin, botha re Epidermolytic toxins
ET-A: chromosome
ET-B: plasmid


Actions of the epidermolytic toxins from S aureus

Cleaves desmoglein-1 which is a protein of desmosomes that mediates keratinocyte adhesion
Leads to intaepidermal splitting of tissues and necrosis
Forms bullae and can look like a blistering sun burn


Difference between Impetigo and SSSS

The bullae from impetigo are infectious and focal whereas the one from SSSS are systemic and not infectious


SSSS clinical manifestations

Site of infection: Oral/nasal cavities, throat, umbilicus, conjunctiva

Early Stage: Fever, irritability, pururlent rhinorrhea, diffuse blanching erythema

Acute Stage: Rash progresses (scarlatiniform–blistering eruptions), mucous membranes hyperemic, but otherwise not affected, conjunctivitis
Skin looks like tissue paper wrinkling, large flaccid bullae at flexures of body
Nikolsky's sign= press on skin and epidermis separates
Sheet-like desquamation, moist erythematous base revealed


What frequently follows an SSSS infection for adults?

Bacteremia and pneumonia


SSSS diagnosis

Culture and biopsy needed for definitive diagnosis–try conjunctiva, nasopharynx, feces, pyogenic skin, blood neg for kids might be pos for adults


What other conditions present like SSSS and must be considered?

Toxic Epidermal Necrolysis
Stephen Johnson Syndrome
Both stem from drugs that cause a similar presentation except that they also involve the mucous membranes


SSSS treatment

Find the focus and treat
IV antibiotics initially
Check for MRSA strains–vancomycin
Supportive care with emollients, fluid and electrolyte balance
Isolate patient and find the carriers


What is a superantigen?

Instead of activating only the T-cells that are specific to it, the superantigen activates a much larger number of T-cells and causes a cytokine storm for the activated T-cells


Staphylococcal Toxic Shock Syndrome STSS epidemiology

S. aureus present in nares, vagina, rectum, and on skin

Became a significant disease when new highly absorbent tampons were marketed that women left in longer and promoted the growth of S aureus that was already present

Also seen in surgical wounds and wounds packed (kind of like a tampon)


Specific reasons why some people were more likely to develop STSS and others were not

Lack antibodies to TSST-1 and fail to develop antibodies in part because of cytokine storm that releases IFN-gamma that inhibits production of antibodies


Toxins involved in STSS

Staph Enterotoxin B & A (SEB, SEA)


Streptococcal Toxic Shock Syndrome (GAS TSS) epidemiology

Often assoc. with a break in the skin, an invasive disease
Many necrotizing fasciitis cases develop STSS
All ages, most are not immunosuppressed
Risk Factors: diabetes, alcoholism, minor trauma, muscle injury=>vimentin production attracting bac, surgery, child delivery, viral infections, varicella, NSAID use (affects renal clearance)


GAS TSS causative agents

GAS–Strep pyogenes most frequent
Group B (Strep agalactiae)


GAS TSS virulence factors

GAS: Strep Pyrogenic Exotoxins SpeA, SpeB
All cause massive cytokine release
Streptolysin O–synergist with SpeA for TNF & IL-1 production

M type proteins 1,3,12,28: creates more virulent strain of GAS, antiphagocytic

Mucoid colonies

SSA: streptococcal superantigen
MF: mitogenic factor


Clinical manifestations of Staph TSS

S aureus:
1) Fever>102
2) Rash, diffuse macular erythroderma
3) Desquamation 1-2 weeks after, particularly palms and soles
4) Hypotension: Systolic bp in adults


Staph TSS diagnosis

Labs negative for other pathogens, never actually have to isolate S aureus
5 of 5 clinical manifestations


When to consider GAS TSS

Patient presents from the community in shock
No clear etiology


Clinical manifestations of GAS TSS

1) Isolation of GAS from normally sterile sites (blood, CSF, pleaural/peritoneal fluid, tissues, surgical wounds)
2) Hypotension
3) Multiorgan involvement (2 or more)
Renal: creatinine high
Coagulopathy: thrombocytopenia, DIC
Hepatic dysfunction:
Erythematous macular rash
Soft tissue necrosis (necrotizing fasciitis, myositis, gangrene)


Differences between STSS and GAS TSS

STSS has no soft tissue necrosis, no mention of coagulopathy


GAS TSS diagnosis

Meets criteria, GAS isolated form sterile site


TSS treatment

1) Supportive of hypotension
2) Nidus therapy: remove tampons & anything else from vaginal canal, drain infectious focus
3) IVIG: immunoglobulins, more effective strep vs staph
4) Eradication of carrier state: S aureus, nares and other sites
5) Antibiotic therapy:
Staph: IV clindamycin, vancomycin
MSSA: Clindamycin and Oxacillin or Nafcillin
MRSA: Clindamycin and vancomycin or Linezolid

Strep: Clindamycin and pnicillin