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Biomedical subjects

E W Howerth

Publications and source records attributed to E W Howerth.

At least 37 records · Page 2Linked to original sources
PubMed1997

Experimental vesicular stomatitis in swine: effects of route of inoculation and steroid treatment.

An enzootic focus of vesicular stomatitis virus New Jersey serotype (VSV-NJ) exists on Ossabaw Island, Georgia. Many questions regarding the epizootiology of this virus at this focus still exist, but evidence suggests that the vector for this virus is a phlebotomine sand fly (Lutzomyia shannoni), with feral swine serving as a potential source of virus for the sand fly and for other swine via contact transmission. We conducted 2 experimental trials in domestic swine using VSV-NJ isolated from a sand fly from Ossabaw Island to determine if route of inoculation or immunosuppression via steroid administration affected the development of disease, viremia, viral shedding, or the neutralizing antibody response. In a third trial, we studied the potential for contact transmission among swine using this isolate. Virus isolations were made from nasal cavity or palatine tonsil of the soft palate, and VSV-NJ neutralizing antibodies developed when pigs were inoculated intradermally in the apex of the snout, ear, or coronary band, intravenously, intranasally, or via scarification of the apex of the snout or coronary band. Vesicles developed only in pigs inoculated in the apex of the snout or coronary band, and these vesicles were at the site of inoculation. Steroid treatment did not potentiate the development of secondary vesicles and did not prolong the period of virus shedding from VSV-NJ-infected swine. Contact transmission, as determined by shedding of virus from the tonsil of the soft palate and the development of VSV-NJ neutralizing antibodies, occurred in pigs in contact with animals inoculated in the apex of the snout but not in contact animals exposed to pigs inoculated intradermally in the coronary band or intranasally. These trials show that contact transmission can occur and VSV-NJ can be shed without the development of clinical disease (i.e., vesicle formation). Viremia was never detected in any of the experimental pigs, suggesting that swine may not be a good amplifying host for VSV-NJ.

Animals↗
PubMed1997

Evaluation of low-level aflatoxin in the diet of white-tailed deer.

We evaluated the response of white-tailed deer (WTD) (Odocoileus virginianus) to dietary aflatoxin. Fourteen 4-to-5-mo-old WTD were used in this 8-wk study, conducted between November 1993 and January 1994. Seven animals received a ration containing 800 parts per billion (ppb) total aflatoxin (AF). Seven control animals received the same ration without AF. At 0, 1, 3, 6 and 8 wk, feed consumption, feed conversion, liver enzymes, bile acid levels, and immune function via lymphocyte proliferation assays and delayed type hypersensitivity reactions were determined. At the conclusion of the 8-wk feeding trial, deer were euthanized and necropsied. Clinical illness was not evident in any of the animals, but by the end of the study, AF-fed deer had reduced feed consumption and body weight as compared to control deer; the differences were not statistically significant. The AF-exposed group had a significant increase (P = 0.03) in serum bile acid concentration as compared to control deer. Two AF-exposed deer had gross and histologic hepatic lesions indicative of a mild degenerative hepatopathy. Residues of an aflatoxin metabolite, aflatoxin M1, were found in the livers of all treated animals. No differences in immune function were detected between the two groups. We conclude that consumption of 800 ppb AF in the diet of young WTD over an 8-wk period can produce subclinical hepatic injury.

Administration, Oral↗
PubMed1997

Shell disease in river cooters (Pseudemys concinna) and yellow-bellied turtles (Trachemys scripta) in a Georgia (USA) lake.

A disfiguring shell disease was detected in river cooters (Pseudemys concinna) and yellow-bellied turtles (Trachemys scripta) from Lake Blackshear, Georgia (USA). The turtles used were part of a mark-recapture study conducted from September 1991 to June 1993. Histologic changes on four turtles included acute segmental necrosis of the epidermis, followed by ulceration, necrosis of the underlying dermis and dermal bone, and exaggerated remodeling of bone. Additional findings included visceral inflammatory lesions and bacterial infection, sepsis and marked trematode ova granulomatosis. The cause of the shell lesions was not determined.

Animals↗
PubMed1997

In vitro replication of epizootic hemorrhagic disease and bluetongue viruses in white-tailed deer peripheral blood mononuclear cells and virus-cell association during in vivo infections.

In vitro and in vivo infections were conducted to determine if the epizootic hemorrhagic disease (EHD) and bluetongue (BT) viruses would replicate in peripheral blood mononuclear (PBM) cells of white-tailed deer (Odocoileus virginianus). All of the North American EHD and BT viruses (EHD virus serotypes 1 and 2, and BT virus serotypes 2, 10, 11, 13, and 17) replicated in vitro in cultures of white-tailed deer PBM cells. However, this replication appeared to be monocyte-dependent and was not enhanced by lymphocyte blastogenesis induced by the addition of concanavalin A. In white-tailed deer infected with either EHD virus serotype 2 or BT virus serotype 10, virus could be isolated consistently from PBM cells only from post-infection day 4 through 8, although they remained viremic through post-infection day 21. In deer, highest viral titers were associated with the erythrocyte fraction, and in no cases did viral titers detected in the platelet, PBM cell or polymorphonuclear cell fractions approach titers observed in whole blood. In the in vitro infections of white-tailed deer erythrocytes, the EHD and BT viruses were associated with pits in the erythrocyte membrane. This association may be important in the long-term viremia observed in deer.

Animals↗
PubMed1997

Host defense responses associated with experimental hemorrhagic disease in white-tailed deer.

Our objectives were to examine the immunity conferred by epizootic hemorrhagic disease virus serotype 2 (EHDV-2) infection in white-tailed deer (Odocoileus virginianus) and determine if this immunity was protective during challenge with homologous (EHDV-2) or heterologous (bluetongue virus serotype 10; BTV-10) virus. Trials were conducted in the fall of 1992 and 1993. In the first experiment, naive white-tailed deer were infected intradermally and subcutaneously with EHDV-2 and monitored via physical examinations, complete blood counts, alpha and beta interferon (IFN) assays, viral isolation, and serology. Infected deer had a wide range of clinical signs in response to infection. Eleven of the 16 deer had body temperature elevations > or = 0.5 C between post-infection day (PID) 4 and 8. Infected deer had decreased lymphocyte counts between PID 6 and 10 that returned to normal levels by PID 17. Severely lymphopenic animals had the most severe clinical signs; five of 10 deer with lymphocyte counts less than 1000 cells/microliters succumbed to the infection. Viremia was detected in all 16 EHDV-2 infected animals by PID 4, and peak viremias occurred between PID 4 and PID 10. Three deer remained viremic until PID 56, the study endpoint. Interferon was first detected between PID 2 and 6. Peak alpha and beta IFN levels coincided with peak viremia in 11 deer. Precipitating and neutralizing antibodies were detected in infected deer by PID 10. In the second experiment, convalescent deer were challenged subcutaneously and intradermally with either EHDV-2 or BTV-10 and similarly monitored. Virus was detected in the blood of all four deer challenged with BTV-10, but viremia was not detected in three EHDV-2-challenged deer. Temperature fluctuations, blood cell parameter changes, and IFN and antibody responses seen in BTV-10-challenged deer were similar to those seen in the initial experiment. Deer challenged with EHDV-2 had mildly increased temperatures, but minimal IFN response and lymphocyte alterations.

Acute Disease↗
PubMed1995

Glycogen storage disease type Ia in two littermate Maltese puppies.

Glycogen storage disease type Ia (GSD-Ia) (von Gierke's disease) was identified in two 47-day-old littermate Maltese puppies. The puppies were presented for necropsy with a history of failure to thrive, mental depression, and poor body condition. Gross findings included small body size and emaciation (212 and 246 g versus 595 g for normal littermate), severely enlarged pale livers (48 and 61 g), and pale kidneys. Histologically, there was marked diffuse vacuolation of hepatocytes with large amounts of glycogen and small amounts of lipid. Renal tubular epithelium was mildly to moderately vacuolated. Soft tissue mineralization was present in renal tubules and pulmonary alveolar septa. Biochemical analysis showed that levels of glucose-6-phosphatase were markedly reduced in liver (0.3 and 0.4 microM/minute/g tissue versus 4.7 +/- 1.5 microM/minute/g tissue for controls) and kidney (0.45 and 0.4 microM/minute/g tissue versus 4.1 microM/minute/g tissue for controls) and that glycogen content was increased in liver (9.4% and 9.4% versus 1.3% +/- 1.4% for controls). This is the first confirmed report of animals with glycogen storage disease type Ia.

Animals↗
PubMed1995

Isolation and culture of large vessel endothelium from white-tailed deer (Odocoileus virginianus).

Endothelial cells were obtained from white-tailed deer carotid arteries and umbilical vessels by instilling a weak collagenase type II solution. Cell growth was best when cultures were grown in plates coated with either fibronectin or laminin. Several commercially available media supported the growth of these cells when supplemented with a commercially available endothelial growth supplement and 10% fetal calf serum. Cells obtained could be characterized as endothelium by ultrastructural characteristics and by the uptake of fluorescent acetylated low-density lipoprotein. Cells stained positive for factor VIII-related antigen up to passage 2, but staining was inconsistent by passage 3, and no immunoreactivity could be demonstrated after passage 4.

Animals↗
PubMed1995

Epizootic hemorrhagic disease virus and bluetongue virus serotype distribution in white-tailed deer in Georgia.

Serum samples collected from 1,396 white-tailed deer (Odocoileus virginianus) in five areas of Georgia (USA) from 1989 to 1991 were tested for precipitating and serum neutralizing (SN) antibodies to the enzootic North American epizootic hemorrhagic disease virus (EHDV) and bluetongue virus (BTV) serotypes. Precipitating antibodies to the EHDV or BTV serogroups, as detected by agar gel immunodiffusion (AGID) tests, were present in 35%, 29%, and 39% of deer sampled in 1989, 1990, and 1991, respectively. Significant differences (P < 0.05) in precipitating antibody prevalence were detected between physiographic regions during all years. Antibody prevalence consistently was highest in deer sampled from the Coastal Plain (77%), followed by the Piedmont (33%), Ridge and Valley (29%), Barrier Island (5%), and Blue Ridge (2%) regions. All AGID-positive samples were tested by SN tests for antibodies against all North American EHDV and BTV serotypes (EHDV serotypes 1 and 2, BTV serotypes 2, 10, 11, 13, and 17). Criteria for previous exposure to a specific serotype were either detection of monospecific results or clusters of positive results against that serotype. Serologic evidence of previous exposure to EHDV serotypes 1 and 2, and BTV serotypes 11 and 13 was detected during all years. Predominant serotypes varied among years. In general, evidence of exposure to EHDV serotype 2 appeared annually while exposure to BTV serotype 13 and EHDV serotype 1 decreased and increased, respectively. To determine serotype diversity prior to 1989, 134 AGID-positive white-tailed deer serum samples collected from 1967 to 1988 also were tested by SN. Evidence of exposure to EHDV serotypes 1 and 2 and BTV serotypes 11, 13, and 17 was detected.

Age Distribution↗
PubMed1994

Susceptibility of white-tailed deer (Odocoileus virginianus) to infection with Ehrlichia chaffeensis, the etiologic agent of human ehrlichiosis.

Although more than 320 cases of human ehrlichiosis have been diagnosed in 27 states since 1986, the reservoir host or hosts remain unknown. Since antibodies reactive to Ehrlichia chaffeensis, the etiologic agent of human ehrlichiosis, have been found in white-tailed deer (Odocoileus virginianus), we experimentally evaluated the susceptibilities of four white-tailed deer to infection with E. chaffeensis and Ehrlichia canis, a closely related species. A fifth deer served as a negative control. Isolation and nested PCR amplification results from peripheral blood indicated that E. chaffeensis circulated for at least 2 weeks. The deer developed antibodies to E. chaffeensis by day 10 after inoculation, but there was no indication of clinical disease. Immunohistochemical staining identified E. chaffeensis within macrophage-type cells in lymph nodes. The deer inoculated with E. canis did not become infected and did not seroconvert. These results indicate that white-tailed deer can support an E. chaffeensis infection with resulting rickettsemia of at least 2 weeks. The resistance to infection and the absence of seroconversion upon exposure to E. canis indicate that antibody responses previously detected among wild deer are not E. canis cross-reactions. The role of deer as competent reservoirs in the life cycle of E. chaffeensis remains to be explored with suspected tick vectors.

Animals↗
PubMed1994

Experimental infection of Borrelia burgdorferi in white-tailed deer.

Four white-tailed deer (Odocoileus virginianus) were experimentally inoculated with Borrelia burgdorferi to determine serologic response by enzyme-linked immunosorbent assay (ELISA) and immunoblotting. Deer had antibodies by ELISA by 2 to 3 wk post-inoculation (PI) and remained positive for 10 wk. Deer demonstrated immunoblotting reactivity between 10 and 14 days PI and consistently showed antibody response to nine B. burgdorferi antigens. Attempts were made to recover the spirochete from blood and tissues; B. burgdorferi was isolated from an ear punch biopsy from one of the inoculated deer.

Animals↗
PubMed1994

Survey for selected diseases in nutria (Myocastor coypus) from Louisiana.

Thirty-two trapper-caught nutria (Myocastor coypus) from East Baton Rouge, Iberville, Tangipahoa, and St. Helena Parishes in Louisiana (USA) were sampled for several disease agents. Antibodies against Toxoplasma gondii, Chlamydia psittaci, Francisella tularensis, Leptospira spp., and encephalomyocarditis virus were detected in 7%, 14%, 0%, 7%, and 0% of nutria, respectively. Both animals seropositive for leptospirae were positive for L. interrogans serovar canicola. No Salmonella spp. were isolated from feces, and no Giardia spp. were seen in trichrome-stained fecal preparations.

Animals↗
PubMed1993

Neuroaxonal dystrophy in a group of related cats.

A syndrome resembling previously described feline hereditary neuroaxonal dystrophy (FHND) was diagnosed in a litter of cats. The disorder was characterized by a sudden onset of hind limb ataxia that slowly progressed to hind limb paresis and paralysis. The cats were between 6 and 9 months old when clinical signs were first noted. Histologically, there was marked ballooning of axonal processes, with spheroid formation and vacuolation in specific regions of the brain and spinal cord. Some dystrophic axons contained a central periodic acid-Schiff (PAS)-positive core. Neuronal loss and gliosis were seen in certain brain stem nuclei, spinal cord nuclei, and the cerebellum. Ultrastructurally, there was hypomyelination and dysmyelination of affected axons. The PAS-positive core in dystrophic axons corresponded ultrastructurally with accumulations of electron-dense, flocculent, amorphous material. In addition, these axons contained membrane-bound osmiophilic bodies and large nonmembrane-bound vacuoles. The syndrome in this report differs from the previously described FHND in that no inner ear involvement was seen and onset of clinical signs occurred at a later age. In addition, although some of the affected cats did have diluted coat colors, abnormal coat color was not always associated with clinical disease. This disease is similar to juvenile neuroaxonal dystrophy in children and to neuroaxonal dystrophies described in horses, dogs, cattle, and sheep.

Animals↗
PubMed1992

Anaerobic bacterial infections causing osteomyelitis/arthritis in a dog.

A 3-year-old German Shepherd Dog was examined for lameness, signs of pain, swelling, a draining fistulous tract, and osteolysis after a dog bite on the left carpus. After failure of the lesion to respond to several antibiotics, Peptostreptococcus sp and Propionibacterium sp were isolated from swab specimens and then from surgically collected bone and soft tissue specimens. The bone fragments had mild purulent osteomyelitis associated with numerous gram-positive rods and cocci. The dog was successfully treated by surgical debridement of the lesion and clindamycin administration.

Animals↗
PubMed1992

Zidovudine serum, cerebrospinal fluid, and brain concentrations following chronic administration of a new zidovudine formulation via an implantable pump in dogs [corrected].

Zidovudine (AZT), prepared as an alkaline solution, was administered iv and intraarterially (ia) by continuous infusion via an implantable pump in dogs. The AZT serum and cerebrospinal fluid (CSF) concentrations were measured over a 28-day treatment period by HPLC. Terminal brain AZT concentrations were also measured. Control (vehicle only) animals were also studied. All animals were evaluated for pathological changes associated with the AZT and vehicle infusions in catheterized vessels and other organs. In the iv AZT treatment group, serum AZT concentrations were relatively constant, with individual coefficients of variations (%CV) of 20% or less. Mean CSF:serum and brain:serum AZT concentration ratios were 0.149 and 0.212, respectively. In the ia AZT treatment group, serum AZT concentrations were more variable than in the iv group, with %CV ranging from 22 to 79%. The fluctuations in serum concentrations were attributed to temporary blockages of the outflow catheter. Mean CSF:serum and brain:serum AZT concentration ratios were 0.126 and 0.249, respectively. Pathological changes, similar in both control and treatment groups, included endothelial denudation and myointimal proliferation at the infusion sites. The conclusions of the study are (1) steady-state greater than 1 microM AZT serum concentrations can be maintained chronically by use of an implantable pump containing a basic pH AZT solution; (2) ia delivery of AZT did not increase central nervous system uptake compared with iv administration; and (3) morbidity associated with the infused solutions does not seem to be a limitation for this mode of therapy.

Animals↗
PubMed1992

Copper and selenium deficiencies do not enhance the cardiotoxicity in rats due to chronic doxorubicin treatment.

This study tests the hypothesis that Cu and Se deficiencies enhance doxorubicin-induced cardiotoxicity and anemia. Male Sprague-Dawley rats (n = 48) were fed Cu and Se-adequate (+Cu+Se), Cu-deficient (-Cu), Se-deficient (-Se) or Cu and Se-deficient (-Cu-Se) diets for 5.5 wk. Doxorubicin (4 mg/kg body wt) or saline was administered once weekly for the last 4 wk of the study. Copper deficiency was confirmed by 79% lower liver Cu, 67% lower liver Cu,Zn superoxide dismutase (Cu,Zn SOD) activity and 76% lower erythrocyte Cu,Zn SOD activity. Selenium deficiency was confirmed by 90% lower liver glutathione peroxidase activity. Rats fed the -Cu diet had greater reductions in hematocrit than did those fed the +Cu diet after administration of doxorubicin. Doxorubicin, Cu deficiency and Se deficiency all produced electrocardiographic abnormalities and ultrastructural anatomical lesions. However, the dietary deficiencies did not enhance doxorubicin-induced cardiotoxicity. Doxorubicin, but not Cu or Se deficiency, raised lipid peroxidation 16% in liver (P < 0.01) and 18% in heart (not significant). These data suggest that the cardiomyopathies caused by doxorubicin and Cu and Se deficiencies have some similarities, but cardiac changes may be related to mechanisms other than lipid peroxidation.

Animals↗
PubMed1992

Diseases diagnosed in gray foxes (Urocyon cinereoargenteus) from the southeastern United States.

Diagnostic findings were reviewed on 157 sick or dead gray foxes (Urocyon cinereoargenteus) from the southeastern United States examined during the period 1972 through 1989. Most foxes (n = 118) originated from Georgia; fewer animals were from Florida, Kentucky, Maryland, Mississippi, North Carolina, South Carolina, Tennessee, Virginia and West Virginia. Etiologic diagnoses included canine distemper (n = 125), congenital absence of guard hairs (n = 7), traumatic injuries (n = 7), rabies (n = 3), suspected toxicoses (n = 3), verminous pneumonia due to Paragonimus kellicotti (n = 1), bacterial septicemia secondary to Dracunculus insignis (n = 1), and tick paralysis (n = 1). Concurrent toxoplasmosis or toxoplasmosis or cryptosporidiosis was noted in six and three foxes with canine distemper, respectively. Only lesion diagnoses were attainable for three foxes, and six cases were classified as undetermined. Canine distemper was diagnosed in 78% of the foxes, was geographically widespread, was detected in 16 of 18 yr, and exhibited a seasonal pattern of occurrence. These facts indicate that canine distemper is more significant as a mortality factor for gray foxes than all other infectious and noninfectious diseases combined.

Animal Diseases↗