Due to uncommon occurrence of staphylococcal toxic shock syndrome (TSS) in male patient, streptococcal origin is often suspected and treated as such. Pre-exposure to nonsteroidal anti-inflammatory drugs had been associated with masking of inflammatory symptoms. These two factors may lead to delay in receiving appropriate antibiotic treatment. We present a case of staphylococcal toxic shock in a diabetic male. He was initially presented to emergency department with abdominal pain, leg swelling and shortness of breath. The patient was having minor skin ulcerations twelve days before admission. He was prescribed with etoricoxib for his shoulder pain for 3 days prior to admission. Initial presentations upon admission showed upper gastrointestinal bleeding, metabolic acidosis and acute kidney injury. He developed TSS with multiorgan failure one day later. Initial diagnosis was streptococcal TSS and therefore intravenous immunoglobulin and clindamycin was initiated. Nevertheless, repeated culture from blood and wound showed staphylococcal infection. The diagnosis was changed to staphylococcal TSS and intravenous cloxacillin was initiated. However, the patient succumbed to the illness after 11 days of admission. In this case report, pre-exposure to etoricoxib may cause masking of inflammatory symptoms and rapid progression of a wound infection into TSS. Rarity of staphylococcal TSS in male and difficulties in differentiating between streptococcal and staphylococcal TSS led to delay in appropriate treatment.
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1. Lappin E, Ferguson AJ. Gram-positive TSSs. Lancet Infect Dis 2009; 9: 281-290.
2. Hajjeh RA, Reingold A, Weil A, et al. TSS in the United States: surveillance update, 1979-1996.
Emerg Infect Dis 1999; 5: 807-810.
3. Vincent JM. Staphylococcal and streptococcal TSSs; in: Yamamoto LG, Inaba AS, Okamoto JK, Patrinos ME, Yamashiroya VK (eds): Case based pediatrics for medical students and residents.
Honolulu, Department of Pediatrics, University of Hawaii John A, Burns School of Medicine, 2004, pp 218-222.
4. Gonzalez BE, Hulten KG, Hammerman WA, et al. Nonsteroidal anti-inflammatory drugs and invasive staphylococcal infections: the cart or the horse?: In reply. Pediatrics 2005; 115: 1791.
5. Stevens DL. Could nonsteroidal antiinflammatory drugs (NSAIDs) enhance the progression of bacterial infections to TSS? Clin Infect Dis 1995; 21: 977-980.
6. Hamilton SM, Bayer CR, Stevens DL, Lieber RL, Bryant AE. Muscle injury, vimentin expression, and nonsteroidal anti-inflammatory drugs predispose to cryptic group A streptococcal necrotizing infection. J Infect Dis 2008; 198: 1692-1698.
7. Mulla ZD. Nonsteroidal anti-inflammatory drugs and hypotension among patients hospitalized for invasive Group A streptococcal disease. Ann Epidemiol 2003; 13: 543-544.
8. Gonzalez BE, Martinez-Aguilar G, Hulten KG, et al. Severe staphylococcal sepsis in adolescents in the era of community-acquired methicillinresistant Staphylococcus aureus. Pediatrics 2005; 115: 642-648.
9. Bernard JJ, Gallo RL. Cyclooxygenase-2 enhances antimicrobial peptide expression and killing of Staphylococcus aureus. J Immunol 2010; 185: 6535-6544.
10. Legras A, Giraudeau B, Jonville-Bera AP, et al. A multicentre case-control study of nonsteroidal anti-inflammatory drugs as a risk factor for severe sepsis and septic shock. Crit Care 2009; 13:R43, DOI:10.1186/cc7766.
11. Chesney PJ. Clinical aspects and spectrum of illness of toxic shock syndrome: overview. Reviews of Infectious Diseases 1989; 11: 1-7.
12. Goldmann O, Hertzén E, Hecht A, et al. Inducible cyclooxygenase released prostaglandin E2 modulates the severity of infection caused by Streptococcus pyogenes. J Immunol 2010; 185: 2372- 2381.
13. Aronoff DM. Cyclooxygenase inhibition in sepsis: is there life after death? Mediators of Inflammation 2012; Doi:10.1155/2012/696897.