Background: Bacteria have been suggested as a possible cause of hidradenitis. Different species have been found in several small studies, and particularly the presence of Streptococcus milleri has been linked to disease activity. Objective: To investigate the possible role of bacteria in hidradenitis. Methods: Cultures of active lesions and serological analysis of circulating IgG antibodies were studied in 41 patients. Results: Bacteria were found in 49% (20/41) of all lesions: Staphylococcus aureus, 8; S. milleri, 1; Staphylococcus epidermidis, 11; Staphylococcus hominis, 1. Corynebacterium spp., Acinetobacter and Lactobacillus spp. were found once each and considered as contaminants. Patients in whom S. aureus was found had a shorter duration of disease (mean 1.7 vs. 9.7 years for sterile lesions). No other significant correlations were found between location of disease or antibody response and the bacterial species found. Conclusion: S. milleri appears to be an unusual pathogen, and bacteria are only found in approximately 50% of all active hidradenitis lesions. It is suggested that S. aureus may play a temporary role in the early phase of the disease, but additional longitudinal studies of cohorts of patients are needed to clarify this point.
Twenty-four patients, including 12 with meningitis, were admitted with meningeal symptoms and fever. Their serum and spinal fluid tumor necrosis factor-alpha (TNF alpha) levels were determined by ELISA. TNF alpha immunoreactivity was found in spinal fluid of 10 meningitis patients and one nonmeningitis patient, whereas 7 sera, 5 from meningitis patients, contained TNF alpha. Levels were significantly higher in spinal fluids than in serum samples, and the TNF alpha bioactivity of spinal fluids and sera was considerably below predictions based on ELISA measurements. Gel filtration chromatography demonstrated the presence of both polymeric (greater than 200 kDa) and oligomeric (10-40 kDa) TNF alpha in spinal fluid. Significant bioactivity was obtained only from samples containing oligomeric cytokine. In agreement with previous in vitro findings, these results strongly indicate that bioactive TNF alpha oligomers form inactive polymers and monomers, which could contribute to the observed in vivo discrepancies between immunoreactive and bioactive protein. Finally, the data support the concept of local central nervous system production of TNF alpha in meningitis.
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