Toxic shock syndrome with a cytokine storm caused by Staphylococcus simulans: a case report.
BACKGROUND
Exotoxins secreted from Staphylococcus aureus or Streptococcus pyogenes act as superantigens that induce systemic release of inflammatory cytokines and are a common cause of toxic shock syndrome (TSS). However, little is known about TSS caused by coagulase-negative staphylococci (CoNS) and the underlying mechanisms. Here, we present a rare case of TSS caused by Staphylococcus simulans (S. simulans).


CASE PRESENTATION
We report the case of a 75-year-old woman who developed pneumococcal pneumonia and bacteremia from S. simulans following an influenza infection. The patient met the clinical criteria for probable TSS, and her symptoms included fever of 39.5 °C, diffuse macular erythroderma, conjunctival congestion, vomiting, diarrhea, liver dysfunction, and disorientation. Therefore, the following treatment was initiated for bacterial pneumonia complicating influenza A with suspected TSS: meropenem (1 g every 8 h), vancomycin (1 g every 12 h), and clindamycin (600 mg every 8 h). Blood cultures taken on the day after admission were positive for CoNS, whereas sputum and pharyngeal cultures grew Streptococcus pneumoniae (Geckler group 4) and methicillin-sensitive S. aureus, respectively. However, exotoxins thought to cause TSS, such as TSS toxin-1 and various enterotoxins, were not detected. The patient's therapy was switched to cefazolin (2 g every 8 h) and clindamycin (600 mg every 8 h) for 14 days based on microbiologic test results. She developed desquamation of the fingers on hospital day 8 and was diagnosed with TSS. Conventional exotoxins, such as TSST-1, and S. aureus enterotoxins were not detected in culture samples. The serum levels of inflammatory cytokines, such as neopterin and IL-6, were high. CD8+ T cells were activated in peripheral blood. Vβ2+ population activation, which is characteristic for TSST-1, was not observed in the Vβ usage of CD8+ T cells in T cell receptor Vβ repertoire distribution analysis.


CONCLUSIONS
We present a case of S. simulans-induced TSS. Taken together, we speculate that no specific exotoxins are involved in the induction of TSS in this patient. A likely mechanism is uncontrolled cytokine release (i.e., cytokine storm) induced by non-specific immune reactions against CoNS proliferation.
['Goda|Ken|K|', 'Kenzaka|Tsuneaki|T|http://orcid.org/0000-0002-3120-6605', 'Hoshijima|Masahiko|M|', 'Yachie|Akihiro|A|', 'Akita|Hozuka|H|']
D000368:Aged D000900:Anti-Bacterial Agents D000071997:Blood Culture D002437:Cefazolin D002981:Clindamycin D000080424:Cytokine Release Syndrome D016207:Cytokines D005260:Female D006801:Humans D008826:Microbial Sensitivity Tests D012772:Shock, Septic D013183:Sputum D013203:Staphylococcal Infections D013210:Staphylococcus D013211:Staphylococcus aureus D013296:Streptococcus pneumoniae D016896:Treatment Outcome
Toxic shock syndrome Cytokine storm Staphylococcus simulans Coagulase-negative staphylococcus