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Biomedical subjects

K J Davis

Publications and source records attributed to K J Davis.

At least 37 records · Page 2Linked to original sources
PubMed1996

Lethal experimental infection of rhesus monkeys with Ebola-Zaire (Mayinga) virus by the oral and conjunctival route of exposure.

OBJECTIVE: The source of infection or mode of transmission of Ebola virus to human index cases of Ebola fever has not been established. Field observations in outbreaks of Ebola fever indicate that secondary transmission of Ebola virus is linked to improper needle hygiene, direct contact with infected tissue or fluid samples, and close contact with infected patients. While it is presumed that the virus infects through either breaks in the skin or contact with mucous membranes, the only two routes of exposure that have been experimentally validated are parenteral inoculation and aerosol inhalation. Epidemiologic evidence suggests that aerosol exposure is not an important means of virus transmission in natural outbreaks of human Ebola fever; this study was designed to verify that Ebola virus could be effectively transmitted by oral or conjunctival exposure in nonhuman primates. MATERIALS AND METHODS: Adult rhesus monkeys (Macaca mulatta) were exposed to Ebola-Zaire (Mayinga) virus orally (N=4), conjunctivally (N=4), or by intramuscular inoculation (N=1, virus-positive control). RESULTS: Four of four monkeys exposed by the conjunctival route, three of four monkeys exposed by the oral route, and the intramuscularly inoculated positive control monkey (one of one) were successfully infected with Ebola-Zaire (Mayinga). Seven monkeys died of Ebola fever between days 7 and 8 postexposure. One monkey was given aggressive supportive therapy and a platelet transfusion; it lived until day 12 postexposure. CONCLUSIONS: Findings in this study experimentally confirm that Ebola virus can be effectively transmitted via the oral or conjunctival route of exposure in nonhuman primates.

Animals↗
PubMed1996

Pathology of experimental pneumonic plague produced by fraction 1-positive and fraction 1-negative Yersinia pestis in African green monkeys (Cercopithecus aethiops).

OBJECTIVE: The protein capsule of Yersinia pestis, known as Fraction 1 or F1, is a protective immunogen and is an assumed, but not proven, virulence factor. Our objectives were to determine if inhaled F1-negative and/or F1-positive strains of Y pestis were virulent in the African green monkey and, if so, to differentiate F1-negative from F1-positive monkeys. Because F1-negative strains have been isolated from natural sources and have caused experimental fatal disease, we felt that this information was crucial to the development of future vaccines and diagnostic tests. MATERIALS AND METHODS: Adult African green monkeys were exposed by aerosol to F1-positive (CO92, n=15) or F1-negative (CO92-C12, n=6; Java-9, n=2) Y pestis strains. RESULTS: All monkeys died 4 to 10 days postexposure and had lesions consistent with primary pneumonic plague. Antibodies to F1 antigen and other Y pestis antigens allowed us to differentiate F1-positive from F1-negative Y pestis strains in fixed tissues. CONCLUSIONS: In this study, F1 antigen was not a required virulence factor. Therefore, there may be a need for vaccines and diagnostic assays that are not solely based on the F1 antigen.

Acute Disease↗
PubMed1996

Venezuelan equine encephalitis in BALB/c mice: kinetic analysis of central nervous system infection following aerosol or subcutaneous inoculation.

OBJECTIVE: To investigate the routes of entry of Venezuelan equine encephalitis (VEE) virus into the brain, we infected BALB/c mice with a virulent strain (V3000) by aerosol or subcutaneous inoculation. METHODS: Immunohistochemistry and in situ hybridization methods were used to detect VEE virus in tissues taken at daily intervals postinfection. RESULTS: In both groups, virus in the brain first appeared in olfactory regions. Aerosol exposure caused early massive infection of olfactory epithelium, which developed into bilaterally symmetrical infection of the olfactory nerves, olfactory bulbs, and lateral olfactory tracts by day 2 postinfection. After subcutaneous inoculation, VEE in the brain also appeared first in olfactory regions, but was not detected until day 3 postinfection. By day 4 postinfection, VEE viral infection had spread throughout the brain in both groups. Vascular endothelium and the choroid plexus remained uninfected during the entire study. CONCLUSIONS: Our findings suggest that VEE virus, whether given by aerosol or subcutaneously, first enters the brain through the olfactory tract.

Aerosols↗
PubMed1995

Pathology of experimental inhalation anthrax in the rhesus monkey.

BACKGROUND: The inhalation form of anthrax, although rare, is nearly always fatal because of the rapid progression of the disease with little host response until the terminal stages of the disease. The Gulf War heightened the concern that anthrax could be used as a biologic weapon. Past studies modeling pathologic changes in human inhalation anthrax have used the rhesus monkey. EXPERIMENTAL DESIGN: We studied pathologic changes in the rhesus monkey model of inhalation anthrax. Gross examination as well as light and electron microscopy were used to define pathologic alterations. Immunolabeling techniques were used to identify the anthrax bacillus by light and electron microscopy. RESULTS: Gross changes included hemorrhage in mesenteric (54%) and tracheobronchial (46%) lymph nodes, meninges (38%), lungs (31%), and small intestinal serosa (31%). Histopathologic changes included suppurative meningitis (77%); hemorrhages in the meninges (54%), neuropil (31%), and pulmonary alveoli (31%); and pneumonia (15%). Spleens and various lymph nodes from all monkeys had one or more of the following changes: hemorrhage, acute inflammation, extracellular bacilli, lymphocytic depletion, and histiocytosis. Spleens of two monkeys were devoid of extracellular bacilli, but degraded intrahistiocytic bacilli reacted with Ab to Bacillus anthracis cell wall polysaccharide. CONCLUSIONS: In our study, compared with previous reports, meningitis and mesenteric lymph node hemorrhages were more common, whereas mediastinal and tracheobronchial lymph node hemorrhages were less common. Immunostaining highlighted intracellular bacilli that would have been otherwise missed by light microscopic examination.

Animals↗
PubMed1993

Spontaneously generated non-Hodgkin's lymphoma in twenty-seven simian T-cell leukemia virus type 1 antibody-positive baboons (Papio species).

Simian T-cell leukemia virus type 1 (STLV-1), a type C retrovirus associated with leukemia/lymphoma in Old World monkeys, is closely related to human T-cell leukemia virus type 1, the etiologic agent of adult T-cell leukemia/lymphoma in humans. In a colony of 3200 baboons, the prevalence of antibodies to STLV-1 is more than 40%. Seropositivity is more frequent in female baboons than in males and increases with age. Of 27 STLV-1 antibody-positive baboons with non-Hodgkin's lymphoma, 20 were females and 7 were males, ranging in age from 3 to 21 years (mean, 13 years). Non-Hodgkin's lymphoma was not found in STLV-1 antibody-negative baboons. Clinical signs and laboratory findings were variable but generally included lethargy, low body weights, anemia, dyspnea, lymphadenopathy, hepatosplenomegaly, pneumonia, nodular skin lesions, and leukemia with or without multilobulated lymphocytes in peripheral blood. Radiography revealed pulmonary infiltrates consistent with pneumonia in 17 of the baboons. Serum chemical values were normal except for hypercalcemia in one baboon. Lymphocytosis was found in 18 of the baboons, with leukemia diagnosed in 11. At necropsy, variable enlargement of lymph nodes and other lymphopoietic tissue was usually found. Pale tan to white space-occupying foci typical of proliferative lymphoid tissue were often found in various organs, including lungs, spleens, livers, skin, and hearts. The lungs in 14 baboons had thickened pleuras, congestion,edema, and large tan to brown areas of consolidation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Cancer statistics by race and ethnicity.

Key findings on cancer incidence and mortality are presented for five racial and ethnic groups in the United States--African Americans, American Indians, Asians and Pacific Islanders, Hispanics, and whites. Information on the prevalence of cancer risk factors and screening examinations among these racial and ethnic groups is also included.

Black or African American↗