Micrococcus, which, when limited in its extent and activity, causes acute suppurative inflammation (phlegmon), produces, when more extensive and intense in its action on the human system, the most virulent forms of septicaemia and pyaemia.1 In an elegant series of clinical observations and laboratory studies published in 1880 and 1882, Ogston described staphylococcal disease and its role in sepsis and abscess formation.1,2 More than 100 years later, Staphylococcus aureus remains a versatile and dangerous pathogen in humans. The frequencies of both community-acquired and hospital-acquired staphylococcal infections have increased steadily, with little change in overall mortality. Treatment of these infections . . .

https://www.nejm.org/doi/pdf/10.1056/NEJM199808203390806?articleTools=true

Staphylococcus aureus infections.

Toxic-shock syndrome (TSS) is an acute onset, multiorgan illness which resembles severe scarlet fever. The illness is caused by Staphylococcus aureus strains that express TSS toxin-1 (TSST-1), enterotoxin B, or enterotoxin C. TSST-1 is associated with menstrual TSS and approximately one-half of nonmenstrual cases; the other two toxins cause nonmenstrual cases, 47% and 3%, respectively. The three toxins are expressed in culture media under similar environmental conditions. These conditions may explain the association of certain tampons with menstrual TSS. Biochemically, the toxins are all relatively low molecular weight and fairly heat and protease stable. Enterotoxins B and C, share nearly 50% sequence homology with streptococcal scarlet fever toxin A; they share no homology with TSST-1 despite sharing numerous biological properties. Numerous animal models for development of TSS have suggested mechanisms of toxin action, though the exact molecular action is not known. The toxins are all potent pyrogens, induce T lymphocyte proliferation, requiring interleukin 1 release from macrophages, suppress immunoglobulin production, enhance endotoxin shock, and enhance hypersensitivity skin reactions. The genetic control of the toxins has been studied and suggests the exotoxins are variable traits. Some additional properties of TSS S. aureus which facilitate disease causation have been clarified.

Staphylococcal and streptococcal pyrogenic toxins involved in toxic shock syndrome and related illnesses.

In recent years, the importance of gram-negative organisms in the genesis of sepsis has been emphasized. However, this emphasis may no longer be correct; recent studies show an increasing incidence of gram-positive sources of sepsis, and it is possible that these cases may predominate in the coming years. This increase results from more than just a greater prevalence of infection—it appears that gram-positive organisms may also be more virulent in fomenting the disease, as can be evidenced by the emergence of streptococcal toxic shock syndrome and the resurgence of acute rheumatic fever. This may result from the ability of gram-positive organisms to produce more inflammation-causing cell wall constituents, as well as unbound exotoxins. Despite the recent emphasis on gram-negative causes, sepsis resulting from gram-positive sources is increasingly common. Research on these causes of sepsis should be encouraged. (Arch Intern Med. 1994;154:26-34)

Gram-positive Organisms and Sepsis

Toxic shock syndrome-associated staphylococcal and streptococcal exotoxins were tested for an ability to induce the production of tumor necrosis factor (TNF). Staphylococcal enterotoxins B and C1, along with streptococcal pyrogenic exotoxin A, all induced TNF production in a dose-dependent manner, with production peaking on the average at 3 days but continuing over the 6 days tested. This time course of exotoxin-induced TNF production contrasts with the 1-day peak-2-day duration observed with endotoxin as the stimulus and may be significant to development of toxic shock syndrome.

https://iai.asm.org/content/iai/57/1/291.full.pdf

Toxic shock syndrome-associated staphylococcal and streptococcal pyrogenic toxins are potent inducers of tumor necrosis factor production.

Microbiologic aspects of chronic ambulatory peritoneal dialysis.

Twenty-two women aged 13 to 44 years (mean, 22 years) with toxic shock syndrome (TSS) were hospitalized in Madison, Wis, between Aug 1, 1977, and Sept 1, 1980. Disease onset occurred during menses in 21 patients; all recovered. Notable sequelae included vocal cord paralysis and impaired finger sensation in two patients and recurrent disease in three. Coagulase-positive staphylococci were grown from the cervix or vagina in 11 of 12 women cultured. Previously undescribed features included vulvar cellulitis, hypocalcemia, hypophosphatemia, hypocholesterolemia, hyponatremia, lymphocytopenia, hypoferrinemia, and late convalescent hair and nail loss. Patients requiring dopamine hydrochloride had worse renal function, longer hospitalizations, and higher total serum bilirubin levels, and clinical onset earlier in menses. Originally reported in children, TSS now appears to be primarily a disease of menstruating women in whom recurrences are possible. (JAMA1981;246:741-748)

P J Wand

Papers

Clinical manifestations of toxic shock syndrome