Ebola (subtype Reston) virus among quarantined nonhuman primates recently imported from the Philippines to the United States.

In April 1996, laboratory testing of imported nonhuman primates (as mandated by quarantine regulations) identified 2 cynomolgus macaques (Macaca fascicularis) infected with Ebola (subtype Reston) virus in a US-registered quarantine facility. The animals were part of a shipment of 100 nonhuman primates recently imported from the Philippines. Two additional infected animals, who were thought to be in the incubation phase, were identified among the remaining 48 animals in the affected quarantine room. The other 50 macaques, who had been held in a separate isolation room, remained asymptomatic, and none of these animals seroconverted during an extended quarantine period. Due to the rigorous routine safety precautions, the facility personnel had no unprotected exposures and remained asymptomatic, and no one seroconverted. The mandatory quarantine and laboratory testing requirements, put in place after the original Reston outbreak in 1989-1990, were effective for detecting and containing Ebola virus infection in newly imported nonhuman primates and minimizing potential human transmission.

Combined simian hemorrhagic fever and Ebola virus infection in cynomolgus monkeys.

Simian hemorrhagic fever (SHF) virus and a new strain of Ebola virus were isolated concurrently in recently imported cynomolgus monkeys (Macaca fascicularis) being maintained in a quarantine facility. Ebola virus had never been isolated in the U.S. previously and was presumed to be highly pathogenic for humans. A chronology of events including measures taken to address the public health concerns is presented. The clinicopathologic features of the disease were abrupt anorexia, splenomegaly, marked elevations of lactate dehydrogenase, alanine aminotransferase, and aspartate aminotransferase, with less prominent elevations of blood urea nitrogen, creatinine, and other serum chemistry parameters. Histologically, fibrin deposition, hemorrhage, and necrosis of lymphoid cells and reticular mononuclear phagocytes were present in the spleens of SHF and of Ebola virus-infected animals. Intravascular fibrin thrombi and hemorrhage were also present in the renal medulla and multifocally in the gastrointestinal tract. Necrosis of lymphoid and epithelial cells was occasionally noted in the gastrointestinal tract. The histopathologic findings considered specific for Ebola virus infection include hepatocellular necrosis, necrosis of the zona glomerulosa of the adrenal cortex, and interstitial pneumonia, all of which were generally associated with the presence of 1 to 4 mu intracytoplasmic amphophilic inclusion bodies. The disease spread within rooms despite discontinuation of all direct contact with animals, and droplet or aerosol transmission was suspected. Antibody to Ebola virus developed in animal handlers but no clinical disease was noted, suggesting a less virulent strain of virus.(ABSTRACT TRUNCATED AT 250 WORDS)

Dietary fat and blood pressure.

Until recently most experimental research linking diet to hypertension was related to dietary salt levels. However, recent evidence suggests that elevations in blood pressure, initially attributed to high salt intake, may be due to other factors in the diet, such as the level and type of fat consumed. Studies in animal models and humans suggest that blood pressure can be lowered during high salt feeding by supplementing the diet with polyunsaturated fatty acids such as linoleic acids. This review outlines key points that delineate the effect and possible interactions of dietary lipids on blood pressure regulation.

Atherosclerosis in the Erythrocebus patas, an old world monkey.

Fifty monkeys of the species Erythrocebus patas were fed a control monkey chow, a semi-synthetic diet containing 25% lard, or a semisynthetic diet containing 25% lard and 0.5% cholesterol for 2 years. The patas monkeys had naturally occurring atherosclerosis that was greatly accelerated by feeding a diet containing cholesterol. The atherosclerosis involved the aorta, predominantly the abdominal portion, the coronary arteries, and various peripheral vessels. Histologically, the atherosclerosis was characterized by intimal proliferative lesions associated with intra- and extracellular lipid deposition. Complicated lesions that developed after 2 years on the cholesterol-containing diet were associated with lipid crystals, necrosis, mineralization, and encroachment upon the media. Adventitial reactions characterized by increased vascularity and the presence of inflammatory cells were seen. All of these observations have been described as components of the human atherosclerotic disease process. The similarity of the patas monkey atherosclerosis to human atherosclerosis, the relatively large size and easy handling of the animals, and the fact that previous studies have shown the lipoproteins of both control and cholesterol-fed monkeys to resemble human lipoproteins all contribute to making the patas monkey a useful model for the study of experimental atherosclerosis.

An outbreak of cecal mucosal hyperplasia in hamsters.

Cecal mucosal hyperplasia associated with diarrhea, runting, and high mortality in suckling and weanling hamsters occurred as a natural disease outbreak in a production colony. Young hamsters were runted, and their perineal hair was stained and matted with liquid feces. Their ceca were thickened, contracted, congested, and had scant luminal content. There were severe hyperplasia of cecal crypts, accompanied by increased mitotic activity, inflammation, and focal mucosal erosion. A variety of bacteria was isolated, but none was considered pathogenic. No relationship of cecal hyperplasia to transmissible ileal hyperplasia of hamsters was found. Hyperimmune serum from hamsters with transmissible ileal hyperplasia did not react by immunofluorescence against hyperplastic cecal mucosa. Electron microscopy did not reveal a caustive agent. Transmission attempts have been unsuccessful. Cecal mucosal hyperplasia is apparently a newly discovered disease entity in hamsters with the clinical sign of diarrhea.

Effects of prolonged high temperature on testicular development and fertility in the male rat.

High temperatures for more than 2 days in a large rat production colony resulted in the death of one-third of the animals. The temperature in the room was as high as 89 degrees F (31.6 degrees C) and it is estimated that temperatures in individual cages reached 100 degrees F (37.7 degrees C). In addition to the deaths, 25% of the surviving males, 4-66 days of age at the time of exposure to the high temperature, were found after 18 days, to have irreversible bilateral testicular atrophy. These animals were sterile whereas survivors with normal testes bred successfully.

Elimination of the Shigella carrier state in rhesus monkeys (Macaca mulatta) by trimethoprim-sulfamethoxazole.

The Shigella carrier state was eliminated from its nonhuman primate host, Macaca mulatta. Each of 31 animals was treated twice a day for ten consecutive days with 16 mg trimethoprim and 80 mg sulfamethoxazole delivered via stomach tube. Fresh rectal swab and stool enrichment cultures were taken for seven consecutive days as well as the 35th and 78th days after treatment, and all were negative for shigellae. In addition, no clinical signs of shigellosis were observed during or following an extensive period of stress.

Multiple testing for the detection of B virus antibody in specially handled rhesus monkeys after capture from virgin trapping grounds.

Eight groups of rhesus monkeys totaling over 1,000 animals were captured in the virgin trapping grounds of Jammu and Kashmir, India. Individual caging and special handling technics were utilized to prevent cross-contamination during capture, holding, and subsequent shipment to quarantine facilities in the United States. Immediately following the arrival of the monkeys, 5 consecutive blood samples were obtained at approximately 2-wk intervals, and the sera were rested for neutralizing antibody against Herpesvirus simiae. In order to assure the greatest sensitivity possible, sera were not heat-inactivated and were tested against only 10 TCID50 units of virus in addition to the more commonly used concentration of 100 TCID50 units. The first test detected 80-90% of the positive animals within each group, and only 1 seroconversion was noted after the second test. Seventy-three percent of the adults, 36.6% of the young adults, and 12.4% of the juvenile macaques were found to be antibody-positive. Considering the measures employed to prevent cross contamination, these percentages probably reflect the true prevalence of B virus infection in these rhesus monkeys at the time of their capture in the wild.