Peter G. Sohnle

Predisposing factors that lead to blastomycosis remain unknown, although like other fungal infections, blastomycosis is an opportunistic infection. Here, we report on an unusual presentation in a Hmong woman with preexisting liver disease. This case highlights genetic and medical factors that may increase susceptibility to blastomycosis.

Background: Some non-antibiotic drugs, such as the phenothiazine antipsychotic agents, may have antimicrobial activity. Materials and Methods: We sought to determine the in vivo antimicrobial effects of the phenothiazine thioridazine in two mouse models of Staphylococcus aureus skin infection. Results: Thioridazine significantly suppressed dissemination from skin to spleen and kidney after inoculation of the skin surface. However, the drug did not affect infection parameters in the skin itself. Thioridazine did suppress the size of abscesses produced when the bacteria were injected intradermally. On the other hand, using the cutaneous abscess model we were not able to demonstrate synergistic activity between thioridazine and the beta-lactam drug cefazolin against methicillin-resistant S. aureus, as previously demonstrated in vitro. Conclusion: The phenothiazine drug thioridazine has in vivo antimicrobial activity against certain S. aureus skin infections, although the previously-demonstrated reversal of methicillin resistance by this agent may not be readily evident in vivo.

Staphylococcal skin infections are quite common in human patients. These infections often clear spontaneously, but may also progress locally and/or disseminate to cause serious and sometimes fatal deep infections. The present studies were undertaken to examine the clearance phase of experimental cutaneous Staphylococcus aureus infections in a mouse model system. Previous work in this system has shown that staphylococci applied to the skin rapidly disseminate to the spleen and kidney. In the present experiments the bacteria were found to persist at the skin infection site at a time (8 days after inoculation) when they had disappeared from the spleen and kidney. Examination of the infected skin at earlier times revealed rapid (within 6 h) invasion into the stratum corneum, stratum Malpighii, and dermis, but subsequent redistribution of bacteria (at 1–2 days) to more superficial sites, particularly crusts located just above the skin surface. The crusts seen in these infections were of two distinct types, which were termed type 1 and type 2. Type 1 crusts appeared first, consisted of bacteria, inflammatory cells, and debris, and developed over an intact epidermis. Type 2 crusts arose from the process of dermal necrosis previously reported to take place at 2 days in this model system. In the latter situation the bacteria were not really cleared from the epidermis and dermis; rather those layers were transformed into a superficial crust that contained the bacteria. Deep hair follicle infections in the dermis were found in these infections, but they did not persist and did not seem to be a reservoir for organisms in the dermis. Resolution of these experimental infections appeared to involve redistribution of invading bacteria to more superficial locations in crusts above the skin surface, marked proliferation of the epidermis, loss of the bacteria-laden crusts from the skin, and eventual healing of the cutaneous damage.

Background Previous studies in a murine cutaneous anthrax model have demonstrated that hairless and haired HRS/J mice are extremely resistant to Baci

Skin window procedures in humans have shown rapid accumulation of neutrophils into the exuded fluids above abraded skin. The present study was undertaken to determine if similar epicutaneous neutrophil accumulation might explain the extreme resistance of HRS/J mice, both hairless (hr/hr) and haired (hr/+), to experimental cutaneous Bacillus anthracis Sterne infections on abraded skin. In this study, very early (6 h) biopsies demonstrated a lack of bacilli in skin from the HRS/J hr/hr mice, indicating that the organisms never did invade in these animals as opposed to early skin entry and then efficient clearance by host responses in the tissues. Touch preparations of either the inoculation filter or the skin surface revealed more inflammatory cells, fewer bacilli, and a higher percentage of cell-associated bacilli in the HRS/J hr/hr mice than in comparator strains. In the HRS/J mice, cyclophosphamide treatment or separation of inoculated spores from the inflammatory infiltrates by a second filter below both produced marked increases in the number of bacilli observed. Examination of inoculation filter specimens demonstrated ingestion of spores and bacilli by neutrophils inside the filter at 6 h after inoculation. These findings suggest that an early and vigorous inflammatory cell infiltrate in HRS/J mice attacks the inoculated organisms above the skin surface and does not allow them to invade the tissues below.

Background. Cutaneous infection is the most common form of human anthrax, but little is known about Bacillus anthracis spore germination in these inf