1985 Volume 59 Issue 6 Pages 646-652
The patient was a 13 year, 6 month old girl who was admitted in our hospital by lupoid hepatitis and improved soon after administration of glucocorticoid, though SLE-related laboratory tests, for example, LE cell test, anti-DNA antibody titer, hypergammaglobulinemia, etc, further continued positive. She was treated by daily oral administration of small dosis of aspirin and/or anti-inflammatory drugs after the glucocorticoid therapy.
On June 25, 1983, her temperature elevated to 39.5°C and she complained general malaise and joint pains at bilateral elbows and knees.
The next morning, the fever still continued and she showed hypotention with systolic pressure at 66 mmHg. Confusion, menigeal signs and abnormal findings of spinal fluid with increased leukocyte counts (1662/ 3/cumm with 92% of neutrophils), increased, protein content (200 mg/dl) and decreased sugar content (36 mg/dl) were also observed. White bloodcell counts were 21900/cumm in peripheral blood with 95% neutrophils with left shift.
With intensive care, her blood pressure was stabilized in 48 hours after the onset of the illness. However she had hyperemia of her conjunctivae, lips, oral mucosa, pharynx and skin, especially at the cheeks and the palms. She also showed manifestations of multisystem involvement; diarrhea and vomiting, elevated values of GOT, GPT, LDH, CPK, BUN and creatinin in serum, prolonged P-Q interval in ECG, muscle pains, alteration of consciousness without any focal signs even after recovering from shock and hyperexia, etc.
She was treated by peritoneal dialysis for 5 days from June 27 owing to acute renal failure.
At 7th day of the illness, the spinal fluid was normalized and no pathogen was detected from central nervous system, suggesting that the abnormal findings of the spinal fluid had not been due to direct invasion of pathogen, but due to temporary reaction of central nervous system against exotoxin and/or some products of the pathogen.
The patient was finally recovered without any sequelae.
Staphylococcus aureus was isolated from throat and the lesions of angular stomatitis as well as pustle of chest wall at the onset of the illness; the isolate from throat was 52A/79/84/85 of phage type, those from angular stomatitis and pustule were 79/84. All the isolates produced enterotoxin A and coagulase type VII, though toxic shock toxin (TST) was not detected.
Serum ASO titer was not significantly changed. Agglutinins against Yersinia, Leptospira and Proteus OX strains (Weil-Felix reaction) were not detected.
Serum levels of complement C3, C4 and CH50 were decreased at the shock state.
We reported a unique case of TSS with temporary manifestations of aseptic meningitis at the onset of the illness.
