Updates-By Carol A. Kemper, MD, FACP
August 15, 2000 4 minutes read
Updates-By Carol A. Kemper, MD, FACP
Bacteriologic Warfare on the Home Front?
Source: Love DN, et al. Vet Microbiol 2000;74:179-193.
This intriguing review explores the clinical presentation and microbiological flora of infections due to cat bites in humans and in other cats. Evidence suggests that cat bites are a far more important "biological weapon" than cat scratches, despite the interest surrounding cat scratch disease. Cats (large or small) are natural predators, and their incisors are conveniently designed to inflict deep puncture wounds to the subcutaneous tissues of the neck, haunches, and tail of their prey. This is important because of the strictly anaerobic nature of cat bite infections. In contrast, Love and associates note that dog wounds are much more likely to tear flesh with wounds open to air.
Animals with infected cat bites often present with deep subcutaneous abscesses with or without fever, lethargy, and regional lymphadenopathy. In other cats, these abscesses can track extensively along the subcutaneous layer of skin, with the frequent formation of supporative draining fistulas. It is reasonable to assume that such deep bite wounds—though not immediately fatal—would later sufficiently weaken a host as to fall prey.
Unfortunately, cat bites in humans are often inflicted on hands and extremities, with introduction of bacteria into deeper tissue structures such as tendon sheaths, joints, and bone. The microbiological flora is the same whether inflicted in humans or cats. While Pasteurella multicida is the most commonly isolated organism in infected cat bites, other organisms that have not been well studied such as Porphyromonas (especially P. gingivalis), Bacteroides (especially B. tectum), and Fusarium are probably as important. These anaerobes have all been identified as part of the normal gingival flora of cats, which is distinct from the anaerobic oral flora of humans. How cats developed such unique and virulent anaerobic mouth flora is intriguing, but presumably evolutionary selection pressure played a role. P. gingivalis has also been shown to be more prevalent in cats with bad dentition and gingivitis. Is this the mechanism, Love et al wonder, by which older cats or cats with more significant periodontal disease (which may make it less likely for them to immediately fell their prey) maintain their social dominance and secure meat for food?
Sensitivity data for many of these anaerobic organisms is limited. Those that have been studied demonstrate frequent resistance to penicillin and clindamycin, and beta-lactamase production (see Kemper CA. Infect Dis Alert 1999;18:80). Ampicillin-clavulanate remains a useful agent in the treatment of these infections, coupled with aggressive debridement and drainage as appropriate.
Lactic Acidosis and D4T in HIV
Sources: Mokrzycki MH, et al. Clin Infect Dis 2000;30:198-200; Miller KD, et al. Ann Intern Med 2000;133:192-196.
The use of the nucleoside analog agents zidovudine, didanosine, and fialuridine has previously been linked to a rare, but life-threatening syndrome of lactic acidosis, myopathy, and hepatic steatosis. These two reports point to the additional association of stavudine (d4T) and severe lactic acidosis in nine patients, all of whom presented with abdominal pain, nausea and vomiting, complex acid-base disturbances, and elevated hepatic transaminases requiring intensive care. Several of the patients showed other signs of mitochondrial toxicity including myopathy and pancreatitis. One patient died of acute pancreatitis with extensive fat necrosis and steatosis. Recovery in the remaining patients was slow (weeks to months) despite the administration of parenteral fluids and bicarbonate, and the discontinuation of all antiretroviral therapy.
Only a minority of patients develop mitochondrial toxicity while receiving these agents for reasons that are not clear. Lactic acidosis should be looked for in any HIV-infected patient receiving antiretroviral therapy who develops a sepsis-like syndrome, abdominal pain, and acid-base disturbances.
Can Oral Sex Lead to Bacterial Vaginosis?
Source: Tchamouroff SE, Panja SK. Sex Transm Infect 2000;76:144-145.
This unusual report describes a strong association between the occurrence of bacterial vaginosis (BV) and receptive cunnilingus in two separate groups of women. BV was diagnosed in 55 of 256 (21%) heterosexual female patients presenting consecutively to the county hospital in Brighton, England. BV was significantly more common in women reporting receptive oral sex in the previous four weeks compared with those who reported no oral sex (37% vs 10%; P < 0.001). In addition, BV was diagnosed in six of nine homosexual female patients (67%) who practiced oral sex within the previous four weeks compared with none of the eight female homosexuals who had no oral sex in the previous month.
Tchamouroff and Panja raise the possibility that receptive oral sex in women may alter the vaginal microflora, either through biochemical means or through the introduction of differing oral flora. They also argue that, while the "dynamics of this practice vary considerably," women who practice receptive oral sex may be at higher risk for BV than those who do not. One wonders whether orodontal or gingival disease has any effect? Would brushing your teeth before bed sufficiently reduce the risk? Their intriguing observation deserves further investigation.
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