Public health education of veterinarians and veterinary students for the future.
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Animals↗
Biomedical subjects
M G Groves
Publications and source records attributed to M G Groves.
Isolation, genetic diversity, and geographic distribution of Bayou virus (Bunyaviridae: hantavirus).
Bayou hantavirus, previously implicated in human hantavirus pulmonary syndrome in Louisiana, was isolated from a rice rat (Oryzomys palustris) captured in Georgia. The presence of antibody among rice rats captured throughout the southeastern United States and the extent of diversity among the genetic variants of Bayou viruses suggest that the rice rat is the most likely natural reservoir of the virus and that both virus and host have probably co-evolved for some years.
Animals↗
Chronic obstructive pulmonary disease in horses in Louisiana.
OBJECTIVE: To evaluate chronic obstructive pulmonary disease of horses in Louisiana by assessing the signalment, history, environmental factors, clinical signs, and treatment of such horses. DESIGN: Epidemiologic mail survey. SAMPLE POPULATION: 83 of 240 veterinarians contacted by mail agreed to take part in the survey. Veterinarians contacted were listed as mixed-animal or equine practitioners in the 1991/1992 directory of the Louisiana Veterinary Medical Association or had submitted a specimen from a horse to the Louisiana Veterinary Medical Diagnostic Laboratory within the past 2 years. PROCEDURE: The survey contained 47 questions designed to elicit information from owners and veterinarians about horses reported to have chronic obstructive pulmonary disease (COPD). Questions were included to evaluate age, breed, sex, vaccination history, respiratory disease history, environment of primary activity, level of exercise, primary residence (pasture or stall), condition of pasture or barn, type and condition of feed, clinical signs, concurrent conditions, and treatment regimen prescribed. Information from the returned forms was analyzed by using a microcomputer program designed for epidemiologic data. RESULTS: Of the 83 veterinarians who agreed to participate, 31 returned 71 completed questionnaires for horses affected with COPD. Most affected horses were mature in age, kept on pasture, and had developed clinical signs during the summer months. The most consistent clinical signs were dry coughing, slight serous nasal discharge, labored expiratory effort, and flaring nostrils. CLINICAL IMPLICATIONS: Summer pasture-associated obstructive pulmonary disease appears to be precipitated by factors different than those associated with the traditionally diagnosed form of COPD and, thus, successful management measures may also vary.
Age Distribution↗
Rochalimaea henselae infections: newly recognized zoonoses transmitted by domestic cats.
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Angiomatosis, Bacillary↗
Characterization of factors determining Rickettsia tsutsugamushi pathogenicity for mice.
Pathogenicity of Rickettsia tsutsugamushi for laboratory mice is known to be influenced by at least three factors: (i) route of inoculation, (ii) antigenic strain, and (iii) natural resistance of the host. By using Karp, Gilliam, and Kato strains of R. tsutsugamushi, we examined the effect of these three pathogenicity factors on the kinetics of infection and the development of immunity in BALB/cDub and C3H/HeDub mice. The appearance of rickettsemia in the pathogenic infections generally preceded infections of reduced pathogenicity by 1 to 2 days in both magnitude and time of onset. Mice infected by the subcutaneous route with normally pathogenic rickettsiae, i.e., Gilliam-infected C3H/HeDub mice and Karp-infected BALB/cDub mice, consistently maintained a detectable rickettsemia over a 1-year period. Rickettsiae were recovered from the spleens of 95% (19 of 20) of these mice 52 weeks postinfection. In contrast, mice with infections of reduced pathogenicity, i.e., BALB/cDub mice infected by intraperitoneal and subcutaneous inoculation with Gilliam, did not have detectable rickettsemia from week 20 through week 52 postinfection except for a single mouse on week 44 postinfection. Rickettsiae were detected in the spleens of only 40% (8 of 20) of these mice after 1 year. In both Gilliam-infected mouse strains, protection against heterologous challenge with Karp or Kato rickettsial strains was incomplete up to 7 days postimmunization. Infections of reduced pathogenicity did not result from an enhanced systemic immune response by the host. The onset of the humoral response was not different for the pathogenic and reduced-pathogenicity infections. Pathogenicity differences seemed to result from the more rapid growth of the rickettsiae in the pathogenic infections.
Animals↗
Suppression of lymphocyte responsiveness during acute Rickettsia tsutsugamushi infection in mice.
Lymphocytes from Inbred Balb/cyJ mice infected subcutaneously with 10(3) MLD50 of Rickettsia tsutsugamushi Karp strain were unresponsive to rickettsial antigens and phytohemagglutinin in the lymphocyte transformation assay between 11 and 28 days post-infection. There was, however, no correlation between this suppressed responsiveness to rickettsial antigens and the immune capacity to resist a normally lethal ip challenge with the Karp strain. Fourteen days after infection, these mice survived a potentially lethal Karp challenge. Naive recipients of day 14 post-infection mouse splenic lymphocytes also were partially protected against ip challenge. Karp strain-specific anti-rickettsial antibody reached a peak geometric mean titer of 260 during the period of apparent cellular unresponsiveness. However, day 14 post infection mice showed a fourfold decrease of antibody response to a T-dependent antigen, which suggests the presence of T-dependent antibody suppression in these mice.
Animals↗
Detection of surface antigen in Rickettsia tsutsugamushi infected mouse reticuloendothelial cells.
Antibody produced by immunizing CBA/CaJ mice with RE cells from C57B1/6J mice infected 14 days earlier with R. tsutsugamushi Gilliam strain bound readily to Gilliam strain non-cell associated rickettsiae and less readily to the periphery of infected RE cells. Conversely, antibody produced by immunizing with RE cells infected 21 days earlier did not bind to Gilliam rickettsiae but bound to the surface of RE cells from mice infected 21 days earlier. This binding was not related to alloantibodies because these were absorbed prior to testing. The demonstration of rickettsial antibody staining of infected cell associated antigen(s) in this assay system provides a new method for the detection of R. tsutsugamushi infection.
Animals↗
A scanning and transmission electron microscopic examination of Rickettsia tsutsugamushi-infected human endothelial, MRC-5, and L-929 cells.
Monolayers of primary human endothelial cells were infected with the Karp strain of Rickettsia tsutsugamushi and examined by scanning and transmission electron microscopy. The results were compared with those obtained with similarly infected L-929 and MRC-5 cells and with uninfected cells of all three types. The rickettsiae grew to slightly higher titers in the human endothelial cells. Transmission electron microscopy revealed significant changes in the host cell organelles; a reduction in ribosome-coated endoplasmic reticulum and in Golgi activity, swelling of mitochondria, and an increase in vacuolation within the cytoplasm. Since human endothelial cells are known to retain their in vivo structural and functional qualities when cultured in vitro, it is likely that these effects are similar to those which occur during the infectious process in human scrub typhus.
Animals↗
Pathology of toxic death in mice following intravenous injection of Rickettsia tsutsugamushi strain gilliam: examination by light and scanning electron microscopy.
The pathologic manifestations of the toxic death elicited by the iv injection of mice with Rickettsia tsutsugamushi strain Gilliam were examined by light and scanning electron microscopic techniques to ascertain the cause of death. Light microscopic examinations of hematoxylin and eosin-stained sections of organs suggested the presence of fluid in the lungs; this was confirmed by an increase in the weight of the lungs of moribund mice. Scanning electron microscopy of blood cells demonstrated a marked crenation of erythrocytes from these mice. Death appears to be the result of shock brought on by vascular collapse secondary to plasma leakage.
Animals↗
Comparative studies on the karyotypes of Leptotrombidium deliense, L. fletcheri, and L. arenicola (Acari: Trombiculidae).
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Animals↗
Inbred mice as model hosts for cutaneous leishmaniasis. I. Resistance and susceptibility to infection with Leishmania braziliensis, L. mexicana, and L. aethiopica.
The susceptibility of 12 strains of inbred mice representing a broad genetic spectrum to infection of Leishmania braziliensis, L. mexicana and L. aethiopica was determined. Levels of susceptibility were evaluated by gross morphology of lesions, evidence of resolution, persistence of parasites at the site of inoculation, and visceralization to the spleen or liver following inoculation in noses. Very different patterns of responses were noted among the infections with the three species of Leishmania. Among the strains of inbred mice infected with L. braziliensis, patterns of cutaneous lesion development indicated a broad range of susceptibilities and responses. Two strains of inbred mice (AKR/J and CBA/J) showed only a slight and transient swelling of the nose. The SWR/J, C57L/J, A/J, A/HeJ and DBA/1J showed initial swellings or nodules which eventually resolved. In contrast, the BALB/cJ mice were ranked as most susceptible, based on progressive dermal lesions and visceralization. Four strains of inbred mice (C3H/HeJ, C57BL/6J, CBA/J and CBA/CaJ) showed no evidence of infection. Lesion development in most strains of inbred mice infected with L. mexicana occurred later than with L. braziliensis but was then more rapidly progressive with no indication of resolution. Two strains (C3H/HeJ and C57BL/6J) showed no evidence of infection. Only slight swellings of the nose were seen in the 12 strains of inbred mice infected with L. aethiopica; however, parasites were isolated by culture from apparently normal noses in five groups (A/HeJ, AKR/J, BALB/cJ, DBA/2J and SWR/J).
Animals↗
Lack of transplacental infection with scrub typhus organisms in laboratory mice.
Female mice were inoculated with either a virulent or avirulent strain of Rickettsia tsutsugamushi before (1 month and 1 week) or after (approximately 10 days) impregnation. From each group, two pregnant mothers were killed on day 20 post-impregnation, and fetuses and placentas were examined for rickettsiae. Organisms were isolated from 80% of placentas but not from the fetuses. Immediately following parturition, litters from 50% of the infected mothers were exchanged with litters from uninfected mothers. In all cases, no scrub typhus rickettsiae were found in the litters examined on days 1, 7, and 30 postpartum, and no antibody was found in sera collected 1 and 2 months postpartum.
Animals↗
Development of antibody to Rickettsia tsutsugamushi in soldiers in Malaysia.
Malaysian, British and New Zealand soldiers were tested for evidence of infection with Rickettsia tsutsugamushi after several weeks' exposure to the infection during field exercises in Malaysia. 39 (5.0%) of 787 British and New Zealand soldiers developed immunofluorescent antibody (IFA) to R. tsutsugamushi to a titre of 1:50 and two (0.3%) to a titre of 1:100. 11 (1.5%) of 751 Malaysian soldiers also developed low titres less than or equal to 1:100. These low antibody levels were not correlated with clinical disease, and their significance is unknown. Seven (0.9%) of the Malaysians showed an IFA rise to greater than or equal to 1:200, and three of these experienced febrile illnesses, one lasting two weeks. An additional eight Malaysian soldiers had an IFA titre of greater than or equal to 1:400 when first tested and six of these also had a Proteus OXK agglutinin titre of greater than or equal to 1:160, indicating infection shortly before the study.
Antibodies, Bacterial↗
Diagnostic criteria for scrub typhus: probability values for immunofluorescent antibody and Proteus OXK agglutinin titers.
The sensitivities and specificities of the indirect microimmunofluorescent antibody (IFA) and Weil-Felix (OXK) tests for scrub typhus were established for a range of titers using groups of diseased and control (other febrile illnesses) patients diagnosed by other methods. At a cut-off point of greater than or equal to 1:400, the IFA test was 0.96 specific, and at greater than or equal to 1:320, the OXK was 0.97 specific. Using either these highly specific levels of antibody or other rigorous diagnostic criteria (isolation or 4-fold rising titers), the prevalence of scrub typhus infection was determined to be 0.22 in an unselected population of febrile patients in a rural Malaysian hospital. Probability values (Pr) for the correct diagnosis of scrub typhus were then calculated from the specificity, sensitivity and prevalence determination for a range of titers. The Pr for an OXK titer of greater than or equal to 1:320 was 0.79, and the Pr for an IFA titer of greater than or equal to 1:400 was 0.78. When both these titers were present in a single specimen, the Pr increased to 0.96.
Agglutination Tests↗
Doxycycline propylaxis for human scrub typhus.
The use of doxycycline, as a prophylactic antibiotic against scrub typhus was investigated in a prospective, randomized, double-blind study. Twenty volunteers were divided into two similar groups. Beginning three days before exposure to Leptotrombidium fletcheri chiggers infected with Rickettsia tsutsugamushi, and continuing for six weeks after exposure, one group received weekly 200-mg oral doses of doxycycline and the other group received a placebo. Nine of 10 doxycycline-treated subjects remained well during prophylaxis but developed antibody to scrub typhus, whereas nine of 10 subjects given the placebo required treatment for scrub typhus. Therefore, the efficacy of the regimen in preventing scrub typhus was 89% (eight cases prevented of nine expected). Ten days after successfully completing prophylaxis, eight of nine subjects reported minor self-limiting symptoms. A single dose of doxycycline was given on day 3 of illness to volunteers who developed scrub typhus. Such therapy was initially effective but was frequently followed by relapse and cannot be recommended.
Adult↗
Transmission of scrub typhus to human volunteers by laboratory-reared chiggers.
Laboratory-reared, Rickettsia tsutsugamushi-infected Leptotrombidium arenicola and L. fletcheri chiggers were fed on 1 and 2 human volunteers respectively. All subjects developed typical clinical signs and symptoms of scrub typhus beginning days 8-10 post chigger attachment (PCA); these included fever, severe headache, myalgia, regional lymphadenopathy, and eschar. The two L. fletcheri subjects developed a transient generalized rash on days 3-4 after the onset of fever, and these two individuals also appeared to suffer a more severe clinical disease. Rickettsemias were detected in all three volunteers beginning on day 7 PCA, 1-3 days before the onset of clinical disease. Rises in indirect fluorescent antibody titers occurred starting on days 13-19 PCA (day 4-11 post fever) and in Weil-Felix OXK titers starting on days 26-22 PCA (days 7-14 post fever). These results strongly suggest that the use of laboratory-reared chiggers is a reliable means of transmitting scrub typhus infections to volunteers.
Adult↗
Leptospirosis in Nepal.
We present here a case report of a suspected leptospiral infection in a Nepali soldier, and the results of a serological survey of 188 residents of Eastern Nepal that indicate the infection may be common there. This is the first report of leptospirosis in Nepal although it is known to affect man and animals in most of the temperate and tropical regions of the world, and apparently occurs widely in India (Das Gupta, 1938; Khanna & Iyer, 1971).
Adult↗
Macrophages in resistance to rickettsial infections: early host defense mechanisms in experimental scrub typhus.
Several early nonspecific host defense mechanisms were examined in resistant (BALB/c) and susceptible (C3H/He) mice after intraperitoneal inoculation with Rickettsia tsutsugamushi strain Gilliam. Inflammatory exudates were formed in both mouse strains in response to rickettsial inoculation, but the inflammatory response of C3H animals was delayed several days, and influx of peroxidase-positive macrophages occurred late in infection. Peritoneal cells of C3H mice became progressively infected, with 40% of both macrophages and lymphocytes containing intracellular rickettsiae by day 10. The early flammatory response of BALB/c mice was unexpectedly associated with a low percentage of infected peritoneal cells (1 to 2%). In vitro, no difference was detected in ability of resident macrophages of either strain to support the growth of R. tsutsugamushi or to become activated by treatment with lymphokines for rickettsiacidal activity. In vivo, however, macrophages from C3H mice inoculated with Gilliam were not activated on days 6 and 7 after infection, whereas BALB/c macrophages were continuously activated beginning on day 4. The lack of in vivo C3H macrophage activation was not secondary to deficient lymphokine production by infected lymphocytes, as levels of lymphokines produced by peritoneal lymphocytes of both strains were similar and peaked on day 7 after infection. Susceptibility to infection appears to be related to defective regulation of macrophage responses rather than to defects in macrophage function.
Animals↗