L 73 Toxic Syndromes Flashcards

1
Q

What is staphylococcal scalded skin syndrome?

A

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

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2
Q

Staph Scalded Skin Syndrome epidemiology

A

Generally in children

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3
Q

Previous name for Staph Scalded Skin Syndrome and the causative agent

A

Previously known as Ritter’s disease

Caused by S. aureus

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4
Q

Exotoxins from S aureus

A

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

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5
Q

Actions of the epidermolytic toxins from S aureus

A

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

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6
Q

Difference between Impetigo and SSSS

A

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

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7
Q

SSSS clinical manifestations

A

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

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8
Q

What frequently follows an SSSS infection for adults?

A

Bacteremia and pneumonia

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9
Q

SSSS diagnosis

A

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

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10
Q

What other conditions present like SSSS and must be considered?

A

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

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11
Q

SSSS treatment

A
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
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12
Q

What is a superantigen?

A

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

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13
Q

Staphylococcal Toxic Shock Syndrome STSS epidemiology

A

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)

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14
Q

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

A

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

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15
Q

Toxins involved in STSS

A

TSST-1

Staph Enterotoxin B & A (SEB, SEA)

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16
Q

Streptococcal Toxic Shock Syndrome (GAS TSS) epidemiology

A

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)

17
Q

GAS TSS causative agents

A

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

18
Q

GAS TSS virulence factors

A

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

19
Q

Clinical manifestations of Staph TSS

A

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

20
Q

Staph TSS diagnosis

A

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

21
Q

When to consider GAS TSS

A

Patient presents from the community in shock

No clear etiology

22
Q

Clinical manifestations of GAS TSS

A

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:
ARDS
Erythematous macular rash
Soft tissue necrosis (necrotizing fasciitis, myositis, gangrene)

23
Q

Differences between STSS and GAS TSS

A

STSS has no soft tissue necrosis, no mention of coagulopathy

24
Q

GAS TSS diagnosis

A

Meets criteria, GAS isolated form sterile site

25
Q

TSS treatment

A

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