1. Toxic shock syndrome (TSS) is a toxin-mediated multisystem disease characterized by the acute onset of high fever, hypotension, diffuse macular erythroderma, mucous membrane inflammation, severe myalgia, vomiting or diarrhea, and altered consciousness without focal neurologic signs.

a. It arises as a result of infection or colonization with toxin-producing strains of Staphylococcus aureus (S. aureus) or Streptococcus pyogenes (S. pyogenes, group A streptococcus). In the initial epidemic, 50% of cases of staphylococcal TSS occurred in menstruating women using tampons.

1. Staphylococcal TSS is mediated by S. aureus exotoxins (e.g., TSS toxin-1) that act as superantigens capable of activating large number of T cells. Activated T cells then release massive amounts of cytokines that mediate the signs and symptoms of TSS. The pathogenesis of streptococcal TSS appears comparable although the precise toxins involved have not been as clearly defined.

1. Five clinical features are needed for the diagnosis of TSS:

a. Fever.

b. Mucositis (often with rash).

c. Hypotension.

d. Desquamation over the palms and soles, typically 1 to 2 weeks after the onset of illness.

e. Evidence of multiorgan failure.

2. Additionally there should be evidence of S. aureus or S. pyogenes by Gram stain or culture from a wound, mucosal surface, or normally sterile body site. Blood cultures are usually negative in S. aureus TSS but are positive in streptococcal TSS.

1. Correct hypovolemic shock rapidly.

2. Surgical treatment of infected areas, drainage of abscesses, and removal of foreign bodies.

3. Empiric antibiotic therapy for presumed staphylococcal TSS must provide coverage for methicillin-resistant Staphylococcus aureus (MRSA); vancomycin is currently preferred. Alternatives include linezolid, daptomycin, or trimethoprim-sulfamethoxazole (this last agent is not reliably active for S. pyogenes). Patients with suspected TSS should receive clindamycin to suppress bacterial toxin production.

4. Intravenous immunoglobulin (IVIG) can be considered for severe cases.

1. Botulism is a rare but potentially life-threatening neuroparalytic syndrome resulting from the action of botulinum neurotoxins produced by Clostridium botulinum or other closely related anaerobic, spore-forming, gram-positive bacillus species.

2. The syndrome of botulism is characterized by acute onset of bilateral cranial neuropathies associated with symmetric descending weakness.

3. It occurs in five forms based on the route of toxin exposure.

a. Foodborne botulism.

b.

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