Pathologic activity of Plasmodium berghei prevented but not reversed by dexamethasone.

Dexamethasone has recently been shown to block the production of cachectin (implicated in the pathogenesis of cerebral malaria) if administered prior to endotoxin induction of mouse macrophages. Using the hamster cheek pouch-cerebral malaria model, we tested the hypothesis that dexamethasone is effective as a therapeutic agent in severe malaria if given before some yet undefined trigger point in the disease. Infected hamsters were treated with dexamethasone (0.7 mg/kg) daily on days 7-12, 4-12, or 1-12 post-challenge. When treatment was started on day 1, whole body oxygen consumption (used as a measure of erythrocyte transport to sites of diffusion) on day 12 was greater than (P less than 0.05) that of infected control animals, though the degree of anemia was no different in treated and untreated groups. Furthermore, treatment produced a reduction in monocyte accumulation, capillary malfunction, and monocyte/red blood cell aggregate formation observable in the cheek pouch in vivo and a similar reduction in monocyte presence, capillary pathologic change, and multifocal hemorrhage in the brain on postmortem. These data suggest that mediator(s), whose production can be blocked by pretreatment with dexamethasone, are involved in the pathogenesis of disease leading to death of the Plasmodium berghei infected hamster.

An epizootic of measles in captive silvered leaf-monkeys (Presbytis cristatus) in Malaysia.

An epizootic of measles occurred in a group of 31 silvered leaf-monkeys (Presbytis cristatus) that had been in captivity for 4-12 months. Twenty-four of the monkeys exhibited a maculopapular rash that persisted for 6-9 days. A serous to mucopurulent nasal discharge and conjunctivitis were seen in some animals. Eight monkeys died during the epizootic; however, their deaths could not be directly attributed to measles. Serum samples from the surviving monkeys collected 1-2 months prior to, and 5 weeks after, the epizootic were examined by the complement-fixation and hemagglutination-inhibition tests for antibodies to measles virus. The preepizootic complement-fixation titers were all less than 1:4 and hemagglutination-inhibition titers, less than 1:10. The postepizootic complement-fixation titers in 21 of 23 surviving monkeys ranged from 1:8 to 1:128, and hemagglutination-inhibition titers in 22 of 23 monkeys ranged from 1:40 to 1:80 or greater.

Comparison of experimental Rickettsia tsutsugamushi infections in silvered leaf (Presbytis cristatus) and cynomolgus (Macaca fascicularis) monkeys.

Both silvered leaf and cynomolgus monkeys were infected with the Gilliam, Karp and Kato strains of Rickettsia tsutsugamushi. The two species developed similar clinical syndromes, but the antibody responses were greater in cynomolgus monkeys. In both species of monkeys, the Gilliam strain induced more severe clinical manifestations. At 10 months post-infection, silvered leaf monkeys were immune to homologous intradermal (id) challenge. Cynomolgus monkeys, at 15 months post-infection, were relatively resistant to homologous intravenous challenge, but not to a homologous or heterologous id challenge.

Clinical responses of silvered leaf monkeys to infection with selected strains of Rickettsia tsutsugamushi.

Minimal clinical and hematologic signs were observed in silvered leaf monkeys inoculated intradermally with four strains of Rickettsia tsutsugamushi, both virulent and avirulent for laboratory mice. The clinical response of the monkeys to the infection was related to neither the virulence of the strains in mice nor the antigenic characteristics of the strains.

Experimental Rickettsia tsutsugamushi infections in dogs.

Dogs were infected intravenously and intradermally with the Gilliam and Karp strains of R. tsutsugamushi. Although the development of clinical signs was related to the dose of the organism, Gilliam-infected dogs developed severer infections than those infected with Karp. Specific antibodies were demonstrated in sera of experimentally infected dogs.