Fever, Rash, and Lung Crackles in a 25-Year-Old Woman

Jansen Tiongson, MD; John Sakles, MD; Harvey W. Meislin, MD


August 13, 2020

Patients with either type of TSS present with fever, rapid-onset hypotension, and generalized malaise after nonspecific prodromal symptoms. Subsequently, these patients quickly develop multisystem organ dysfunction, such as acute renal failure, ARDS, and disseminated intravascular coagulation. Serum creatinine levels may elevate to at least 2 mg/dL (or twice the baseline value in a patient with established renal disease). For 40%-50% of patients, it often precedes hypotension. Furthermore, in 55% of patients, ARDS also precedes hypotension, presenting as hypoxia and tachypnea.[5]

Differentiating between staphylococcal and streptococcal TSS is initially difficult. Both syndromes present with nonspecific constitutional symptoms and generalized signs. The infection is often in the nasopharynx, oropharynx, vagina, or skin; however, in about 50% of cases, no focus is identified.

Some symptoms and signs may assist in distinguishing between the two etiologies. Patients with staphylococcal TSS tend to present with diarrhea, vomiting, generalized erythroderma, conjunctival injection, and/or severe myalgia. Patients with streptococcal TSS often have soft-tissue necrosis (eg, cellulitis, abscess, myositis, or necrotizing fasciitis); influenza-like symptoms; and varicella (in those who have not been vaccinated against it).[1]

Laboratory tests for enterotoxins are often the only way to distinguish between the two etiologies. In staphylococcal TSS, TSST-1 is responsible for nearly 75% of cases (90% of menstrual cases and 50%-60% of nonmenstrual cases). Testing for this toxin involves detecting the presence of antibodies against it. If TSST-1 antibodies are present, the specificity of TSS being caused by S aureus is as much as 90%.

S pyogenes TSS is mediated by different enterotoxins, but all are linked to the M protein of the bacterial cell membrane. Streptococcal pyrogenic exotoxins A, B, and C are present in only about 13% of S pyogenes-mediated TSS-related cases; however, laboratory testing suggests that the M protein is present in about 75% of these cases. Unfortunately, at this time, no reliable tests detect M-protein.

Streptolysin O is another toxic immunogenic protein produced by S pyogenes and can be measured using the titer against antistreptolysin antibody (ASO titer). The sensitivity of this test ranges from 62% to 76%, with a specificity of 79% to 85%; therefore, elevated titers often identify S pyogenes as the cause.

Finally, blood culture findings are positive in about 75% of cases of streptococcal TSS; in staphylococcal nonmenstrual TSS, 50% of blood culture findings are positive, whereas less than 5% are positive in menstrual TSS cases.[3,6,7]


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