Bacteremic Nonmenstrual Staphylococcal Toxic Shock Syndrome Associated with Enterotoxins A and C

Czachor, John S.; Herchline, Thomas

doi:10.1086/318494

Cited by 11 publications

(8 citation statements)

References 29 publications

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“…We conclude from these results that cell-dependent costimulation of NK cells with monocytes is required to initiate the production of IFN-␥ by grampositive bacteria. portant gram-positive pathogens that cause a wide range of infections, including toxic shock syndrome (13,57). It seems controversial that lactobacilli, which have been carefully studied regarding safety (23,27), and pathogenic gram-positive bacteria induce similar immune responses in human leukocytes (21,22,25,26,40).…”

Section: Vol 9 2002mentioning

confidence: 99%

Activation of Human NK Cells by Staphylococci and Lactobacilli Requires Cell Contact-Dependent Costimulation by Autologous Monocytes

Haller

Serrant

Granato

et al. 2002

Clin Vaccine Immunol

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Section: Vol 9 2002mentioning

confidence: 99%

Activation of Human NK Cells by Staphylococci and Lactobacilli Requires Cell Contact-Dependent Costimulation by Autologous Monocytes

Haller

Serrant

Granato

et al. 2002

Clin Vaccine Immunol

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“…The prevalence of antibodies against one of the toxins, TSST‐1, is 90% in the general adult population. It has been hypothesized that an immune‐compromised host, with low humoral immunity, may be more susceptible to infection and the biological effects of superantigens (SAgs) [10–12].…”

Section: Introductionmentioning

confidence: 99%

Lack of muco-cutaneous signs of toxic shock syndrome when T cells are absent:S. aureusshock in immunodeficient adults with multiple myeloma

Kamel

Banks²,

Dosik³

et al. 2002

Clinical and Experimental Immunology

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Staphylococcal toxic shock syndrome (TSS) is an acute life threatening disease. The diagnosis can be made clinically based on diagnostic criteria. The clinical manifestations are caused in large part by there lease of high levels of T-cell-derived cytokines as a result of potent toxins, also called superantigens (SAg), produced by Staphylococcus aureus, but it is not clear which clinical symptoms/signs are strictly T-cell dependent. Here, we report on three adults with multiple myeloma (MM) presenting with S.aureus sepsis/shock, and two patients with typical TSS. The MM patients had compromised humoral immunity because of depression of normal immunoglobulin (Ig) levels at the expense of the M protein. In addition, their T cells were absent due to high dose chemotherapy initiated for bone marrow trans-plantation. The MM cases lacked mucosal hyperemia, erythroderma and desquamation, but were otherwise indistinguishable from the TSS cases. All patients grew S. aureus and in each case, SAg genes were detected by PCR. In several cases, the plasma contained biological SAg activity resulting in VP specific proliferation of indicator T cells in vitro. The same specific activity was observed with the supernatant fluids of S. aureus broth cultures from the respective bacterial isolates. This confirms the presence of bio-active toxins in the plasma but did not lead to full blown TSS when T cells were lacking.Thus, S. aureus sepsis/shock can be clinically distinguished from typical TSS, and we suggest that mucocutaneous manifestations of TSS are the most telling signs of massive T-cell-dependent cytokine release.

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“…The association of flucloxacillin (β-lactamase-resistant antistaphylococcal agent) with clindamycin (effective agent against aerobic gram positive, including methicillin-resistant SA and anaerobic gram negative) given to this patient provided an ideal empirical coverage for a complicated sacrococcygeal pilonidal abscess. There is some evidence that clindamycin has the ability to inhibit toxin production by SA 14. The adequate antibiotic therapy allied to the removal of the infectious nidus (abscess drainage) allowed a quick and significant improvement in our patient.…”

Section: Discussionmentioning

confidence: 66%

“…TSST-1 is accountable for 95% of the tampon use/menstrual cases and 40%–60% of the non-menstrual cases 13. The remaining cases of TSS are mediated through SA ETs A, B, C, D or E 14. Non-menstrual TSS is responsible for 30%–50% of all cases of TSS, one-third of which involve men 14.…”

Section: Discussionmentioning

confidence: 99%

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Teenage boy with high fever and rash: what could we be missing?

Oliveira

Costa²,

Costa³

et al. 2018

BMJ Case Reports

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A 15-year-old boy was admitted to a local hospital with high fever, generalised rash and a mild sore throat. He was started on intravenous flucloxacillin and 12 hours later develops a sustained low diastolic blood pressure (DBP), unresponsive to fluid volume expansion and cardiovascular support with dopamine. Intravenous clindamycin was added and transportation to paediatric intensive care unit arranged. Dopamine dosing was increased and norepinephrine infusion was added subsequently with immediate stabilisation of DBP. A sacrococcygeal pilonidal abscess was identified, requiring prompt surgical drainage. The microbiological culture of abscess material was positive for an enterotoxin-producing He was free of symptoms after 4 days. This case report summarises a potential severe complication of the pilonidal disease.

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Bacteremic Nonmenstrual Staphylococcal Toxic Shock Syndrome Associated with Enterotoxins A and C

Cited by 11 publications

References 29 publications

Activation of Human NK Cells by Staphylococci and Lactobacilli Requires Cell Contact-Dependent Costimulation by Autologous Monocytes

Activation of Human NK Cells by Staphylococci and Lactobacilli Requires Cell Contact-Dependent Costimulation by Autologous Monocytes

Lack of muco-cutaneous signs of toxic shock syndrome when T cells are absent:S. aureusshock in immunodeficient adults with multiple myeloma

Teenage boy with high fever and rash: what could we be missing?

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