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Biomedical subjects

J S Guy

Publications and source records attributed to J S Guy.

At least 19 recordsLinked to original sources
PubMed2000

Limited transmission of turkey coronavirus in young turkeys by adult Alphitobius diaperinus (Coleoptera: Tenebrionidae).

We examined the role of lesser mealworm, Alphitobius diaperinus (Panzer), in the transmission of an enteric disease of turkeys caused by a coronavirus. Turkey coronavirus (TCV) from two sources was studied, one isolate (NC95) was embryo propagated, the second was TCV infected material from turkeys diagnosed with poult enteritis mortality syndrome (PEMS). Beetles were fed virus-infected feces mixed with chicken feed. Transmission of virus was effectively halted by surface sterilization of the beetles. Turkey poults administered beetle homogenates infected with TCV+ PEMS that had not been surface sterilized had reduced weight gains and 50% mortality. Mortality and weight gains were not effected in the NC95 group. Virus isolation procedures were performed to determine NC95 viability at varying time intervals. Beetles were dissected and the guts removed 1, 12, and 24 h after the initial viral feeding. Whole beetles were also examined for comparison. Whole beetles and beetle guts were homogenized and injected into turkey eggs for embryo propagation. Direct immunofluorescence was used to determine the presence of TCV. A. diaperinus were capable of mechanical transmission of TCV. However, only turkey embryos receiving whole beetle and beetle gut homogenates within 1 h of feeding on the virus were positive for TCV. Laboratory studies demonstrating PEMS transmission by A. diaperinus are continuing.

Animals↗
PubMed2000

Characterization of a coronavirus isolated from a diarrheic foal.

A coronavirus was isolated from feces of a diarrheic foal and serially propagated in human rectal adenocarcinoma (HRT-18) cells. Antigenic and genomic characterizations of the virus (isolate NC99) were based on serological comparison with other avian and mammalian coronaviruses and sequence analysis of the nucleocapsid (N) protein gene. Indirect fluorescent-antibody assay procedures and virus neutralization assays demonstrated a close antigenic relationship with bovine coronavirus (BCV) and porcine hemagglutinating encephalomyelitis virus (mammalian group 2 coronaviruses). Using previously described BCV primers, the N protein gene of isolate NC99 was amplified by a reverse transcriptase PCR (RT-PCR) procedure. The RT-PCR product was cloned into pUC19 and sequenced; the complete N protein of NC99 (446 amino acids) was then compared with published N protein sequences of other avian and mammalian coronaviruses. A high degree of identity (89.0 to 90.1%) was observed between the N protein sequence of NC99 and published sequences of BCV (Mebus and F15 strains) and human coronavirus (strain OC43); only limited identity (<25%) was observed with group 1 and group 3 coronaviruses. Based on these findings, the virus has been tentatively identified as equine coronavirus (ECV). ECV NC99 was determined to have close antigenic and/or genetic relationships with mammalian group 2 coronaviruses, thus identifying it as a member of this coronavirus antigenic group.

Amino Acid Sequence↗
PubMed2000

Parvovirus infection of keratinocytes as a cause of canine erythema multiforme.

Erythema multiforme major was diagnosed in a dog with necrotizing parvoviral enteritis. Skin lesions consisted of ulceration of the footpads, pressure points, mouth, and vaginal mucosa; vesicles in the oral cavity; and erythematous patches on the abdomen and perivulvar skin. Microscopic examination of mucosal and haired skin specimens revealed lymphocyte-associated keratinocyte apoptosis at various levels of the epidermis. Basophilic cytoplasmic inclusions were seen in basal and suprabasal keratinocytes. Immunohistochemical staining, performed with canine parvovirus-2-specific monoclonal antibodies, confirmed the parvovirus nature of the inclusions in the nucleus and cytoplasm of oral and skin epithelial cells. This is the first case of canine erythema multiforme reported to be caused by a viral infection of keratinocytes. This case study indicates that the search for epitheliotropic viruses should be attempted in cases of erythema multiforme in which a drug cause cannot be identified.

Animals↗
PubMed2000

Avian infectious laryngotracheitis.

Avian infectious laryngotracheitis (ILT) herpesvirus continues to cause sporadic cases of respiratory disease in chickens world-wide. Sources of transmission of ILT infection are three-fold, namely: chickens with acute upper respiratory tract disease, latently infected 'carrier' fowls which excrete infectious laryngotracheitis virus (ILTV) when stressed, and all fomites (inanimate articles as well as the personnel in contact with infected chickens). Infectious laryngotracheitis virus infectivity can persist for weeks to months in tracheal mucus or carcasses. Rigorous site biosecurity is therefore critical in ILT disease control. Furthermore, while current (modified live) ILT vaccines can offer good protection, the strains of ILTV used in vaccines can also produce latent infections, as well as ILT disease following bird-to-bird spread. The regional nature of reservoirs of ILTV-infected flocks will tend to interact unfavourably with widely varying ILT control practices in the poultry industry, so as to periodically result in sporadic and unexpected outbreaks of ILT in intensive poultry industry populations. Precautions for trade-related movements of chickens of all ages must therefore include an accurate knowledge of the ILT infection status, both of the donor and recipient flocks.

Animals↗
PubMed2000

Poult enteritis complex.

Poult enteritis complex (PEC) is a general term that encompasses the infectious intestinal diseases of young turkeys. Some diseases, such as coronaviral enteritis and stunting syndrome, are relatively well characterised, while others, such as transmissible viral enteritis, poult growth depression and poult enteritis mortality syndrome, remain ill-defined. All forms of PEC are multifactorial, transmissible and infectious. Salient clinical features include stunting and poor feed utilisation that result from enteritis. In the more severe forms, runting, immune dysfunction and mortality are reported. Gross and microscopic lesions of enteritis are present in all forms but tend to be non-specific. Other lesions may be present, depending on the agents involved. The basic pathogenesis involves the following: a) alteration of the intestinal mucosa, generally by one or more viruses infecting enterocytes; b) inflammation; c) proliferation of secondary agents, usually bacteria. Non-infectious factors interplay with infectious agents to modulate the course and severity of disease. Diarrhoea is believed to be primarily osmotic because of maldigestion and malabsorption, but may also have a secretory component. Transmission is primarily faecal-oral. No public health significance is recognised or suspected. Prevention is based on eliminating the infectious agents from contaminated premises and preventing introduction into flocks. This is accomplished by an effective cleaning, disinfection and biosecurity programme. All-in/all-out production or separate brooding and finishing units are helpful. Control may require regional co-ordination among all companies producing turkeys, especially if the production is highly concentrated, and a quarantine programme for more severe forms of PEC. No vaccines or specific measures for controlling the organisms involved in PEC are available. Treatment is supportive for the viral component, while antibiotics, especially those with efficacy against Gram positive bacteria, may help to reduce the impact to bacterial infections. Evidence suggests that PEC occurs wherever turkeys are raised commercially, but this is not well documented and distribution of the various organisms that have been associated with PEC is largely unknown. The disease causes enormous economic loss, mostly from failure of the turkey to reach its genetic potential.

Animals↗
PubMed1999

Sequence analysis of the turkey coronavirus nucleocapsid protein gene and 3' untranslated region identifies the virus as a close relative of infectious bronchitis virus.

The 3' end of the turkey coronavirus (TCV) genome (1740 bases) including the nucleocapsid (N) gene and 3' untranslated region (UTR) were sequenced and compared with published sequences of other avian and mammalian coronaviruses. The deduced sequence of the TCV N protein was determined to be 409 amino acids with a molecular mass of approximately 45 kDa. The TCV N protein was identical in size and had greater than 90% amino acid identity with published N protein sequences of infectious bronchitis virus (IBV); less than 21% identity was observed with N proteins of bovine coronavirus and transmissible gastroenteritis virus. The 3' UTR showed some variation among the three TCV strains examined, with two TCV strains, Minnesota and Indiana, containing 153 base segments which are not present in the NC95 strain. Nucleotide sequence identity between the 3' UTRs of TCV and IBV was greater than 78%. Similarities in both size and sequence of TCV and IBV N proteins and 3' UTRs provide additional evidence that these avian coronaviruses are closely related.

3' Untranslated Regions↗
PubMed1999

Hydranencephaly and cerebellar hypoplasia in two kittens attributed to intrauterine parvovirus infection.

Six weeks after vaccination with modified live feline parvovirus vaccine, a cat gave birth to five kittens, three of which died soon afterwards. The remaining two kittens (A and B) survived, but at 8 weeks of age were unable to walk and showed abnormal behaviour, with lack of menace and oculovestibular responses, and severe dysmetria. These signs suggested multifocal disease associated with the cerebrum and cerebellum. Magnetic resonance imaging demonstrated severe bilateral (kitten A) or unilateral (kitten B) hydrocephalus or hydranencephaly, combined with cerebellar agenesis (kitten A) or severe hypoplasia (kitten B). Hydranencephaly was confirmed histopathologically in both kittens. Parvovirus was isolated from the kidney of one kitten. Parvoviral DNA was amplified by the polymerase chain reaction (PCR) from paraffin wax-embedded brain of both kittens. The severe malformations observed in these kittens presumably resulted from an in-utero parvovirus infection, possibly due to vaccination, that occurred late in the first, or early in the second, trimester of pregnancy.

Animals↗
PubMed1999

Sequence analysis of the matrix/nucleocapsid gene region of turkey coronavirus.

A reverse transcriptase, polymerase chain reaction (RT-PCR) procedure was used to amplify a segment of the genome of turkey coronavirus (TCV) spanning portions of the matrix and nucleocapsid (MN) protein genes (approximately 1.1 kb). The MN gene region of three epidemiologically distinct TCV strains (Minnesota, NC95, Indiana) was amplified, cloned into pUC19, and sequenced. TCV MN gene sequences were compared with published sequences of other avian and mammalian coronaviruses. A high degree of similarity (>90%) was observed between the nucleotide, matrix protein, and nucleocapsid protein sequences of TCV strains and published sequences of infectious bronchitis virus (IBV). The matrix and nucleocapsid protein sequences of TCV had limited homology (<30%) with MN sequences of mammalian coronaviruses. These results demonstrate a close genetic relationship between the avian coronaviruses, IBV and TCV.

Amino Acid Sequence↗
PubMed1998

Virus infections of the gastrointestinal tract of poultry.

Several different viruses have been identified as causes of gastrointestinal tract infections in poultry. These include rotaviruses, coronaviruses, enteroviruses, adenoviruses, astroviruses, and reoviruses. In addition, a number of other viruses of unknown importance have been associated with gastrointestinal diseases in poultry based on electron microscopic examination of feces and intestinal contents. Viral infections of the gastrointestinal tract of poultry are known to negatively impact poultry production, and they likely contribute to the development of other, extragastrointestinal diseases. Our current understanding of the viruses that cause gastrointestinal tract infections in poultry is reviewed, with emphasis given to those of greatest importance.

Adenoviridae Infections↗
PubMed1997

Effect of a live attenuated intranasal vaccine on latency and shedding of feline herpesvirus 1 in domestic cats.

A prospective study was conducted that evaluated duration of virus shedding through acute and experimentally-induced recurrent disease episodes in 12 cats, and tissue distribution of latent infections, following intranasal vaccination with a temperature sensitive (ts) mutant strain of feline herpesvirus 1 (FHV1). Six of these cats were challenged with a virulent field strain of the agent to assess the extent to which vaccination affected subsequent shedding of virus and the establishment of latent infections. Virus isolation (VI) tests were done in parallel with a polymerase chain reaction (PCR) assay to compare the performance of each diagnostic method. The PCR confirmed that all 12 cats shed virus throughout the periods of vaccination, challenge or mock-challenge, and a cyclophosphamide-dexamethasone stress protocol to reactivate latent infections. Shedding to the tsFHV1 was documented by VI for up to 25 days following vaccination and for up to 15 days following challenge, but not after experimental stress. Overall, FHV1 was present in 144 of 300 (48%) cat-days of testing by PCR compared to 32 of 300 (11%) by VI. The frequency and distribution of latent FHV1 detected in neurologic, ophthalmic, and other tissues by PCR were identical for vaccine-only and vaccine-challenge groups, thereby disproving previous hypotheses that tsFHV1 mutants administered by this route protect against latency.

Administration, Intranasal↗
PubMed1995

Immunologic, histologic, and virologic features of herpesvirus-induced stromal keratitis in cats.

Sequential histologic, immunologic, and virologic features of herpesvirus-induced keratitis were studied in 18 experimentally infected cats. Histologic changes were assessed by use of light microscopy, and the presence of viral antigen, B lymphocytes, and T lymphocytes was verified immunohistochemically. Flow cytometry was used to monitor changes in blood T lymphocytes (CD4 and CD8 homologues) and B lymphocytes. Cellular immunity was assessed by use of the lymphocyte proliferation assay. Development of stromal keratitis was preceded by prolonged absence of corneal epithelium, decreased numbers of circulating lymphocyte subsets, decreased mitogen responses, and acquisition of viral antigen by the corneal stroma. Return to normal of circulating lymphocyte numbers and function was temporally associated with the arrival of neutrophils and B and T lymphocytes in the corneal stroma. Sequelae to stromal inflammation were fibrosis and scarring. Findings suggest that suppression of local immune responses allows virus access to the corneal stroma, and that subsequent keratitis is mediated by an immune response to viral antigen.

Adrenal Cortex↗
PubMed1993

Clinical and laboratory findings in chronic conjunctivitis in cats: 91 cases (1983-1991).

Clinical findings and laboratory test results from 91 cats with chronic conjunctivitis were studied to determine the causes of the disease and the sensitivity of diagnostic procedures used, and to identify correlations between results of various diagnostic procedures and clinical or signalment variations. Mean age of affected cats was 2.9 +/- 2.7 years (+/- SD), with a range from 1 month to 11 years. Conjunctivitis was more likely to be bilateral (56 cats) than unilateral (35 cats). In cats tested for FeLV or feline immunodeficiency virus infection, 15 and 8.5%, respectively, of the results were positive, compared with 4 and 2.6% for the general hospital population. Culturing or immunofluorescent assay (IFA) for feline herpesvirus 1 (FHV-1) and Chlamydia psittaci IFA resulted in identification of pathogens (positive test results) in 19% (FHV-1) and 18% (C psittaci) of tested cats. For FHV-1, culturing was more sensitive than was IFA, yielding positive results in 19 vs 8.8% of cases. In only 1 cat were FHV-1 and chlamydiae recovered. The probability of positive test results for FHV-1 or chlamydiae was unrelated to concurrent corneal disease, unilateral vs bilateral involvement, or age. Cause of conjunctivitis could not be definitively determined in the remaining 35 cases tested for both agents. Bacterial species considered to be potentially pathogenic were isolated from conjunctival sac specimens in only 1 of 38 attempts. Cytologic changes considered compatible with chlamydial or FHV-1 infection (intracytoplasmic inclusions or multinucleated epithelial cells, respectively) were found in 8 and 5 cases, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Reactivation of latent pseudorabies virus infection in vaccinated commercial sows.

Pseudorabies virus (PRV) was isolated from 9 of 44 PRV-vaccinated seropositive sows on 5 of 11 farms. Although serum-neutralization antibody titers were 1:16 to 1:256, 28 virus isolates were obtained from tonsil, nasal, or buccal swab samples from 9 sows given 2 ml of dexamethasone/kg of body weight IM for 5 days. Pseudorabies virus was isolated from 6 of 20 sows (3 of 5 farms) given a killed-virus vaccination. Virus was obtained from 3 of 24 sows (2 of 6 farms) given modified-live virus and killed-virus vaccination. Evaluation of the 9 PRV with 5 restriction endonucleases revealed 4 PRV existing genotypes. The 9 isolated types of PRV appeared to be indistinguishable by Kpn I and BamHI restriction endonuclease analysis; however, when analyzed with Sal I, HinfI, and Pst I, isolates 7 (farm D), 8 (farm C), and 9 (farm B) had numerous differences. Isolates 1, 2, 3, and 4 (farm F) and 5 and 6 (farm G) appeared to be the same genotype when further analyzed with Pst I, HinfI, and Sal I.

Animals↗
PubMed1989

Discovery of noninfectious viral genes complementary to Marek's disease herpes virus in quail susceptible to cholesterol-induced atherosclerosis.

Japanese quail genetically selected on the basis of atherosclerosis susceptibility were tested for infection by Marek's disease herpesvirus (MDV). Viral DNA was detected in the atherosclerotic aortas of susceptible (SUS) quail by the technique of DNA hybridization. Southern blot analysis demonstrated that restriction mapping of aortic DNA was specific and different from that of MDV. Screening of quail embryos by dot-blot hybridization detected that MDV DNA existed in 100% of SUS quail tested. Resistant (RES) quail were a mixed population, with 16% of embryos resembling the SUS group. Functional MDV was not found by a number of methods including virus isolation, serological test, and exposure of sentinel chicks to SUS quail. These results suggest that the SUS quail possess a portion of the MDV genome in the germline, and the viral genes have been coselected by their susceptibility to cholesterol-induced atherosclerosis.

Animals↗
PubMed1989

Experimental ocular herpesvirus infection in the cat. Sites of virus replication, clinical features and effects of corticosteroid administration.

Experimentally induced ocular feline herpesvirus 1 (FHV-1) infection was studied in 30 specific pathogen-free cats. In ten cats, the ability of five field isolates of FHV-1 to replicate in the epithelium and substantia propria of cornea and conjunctiva was demonstrated by histochemical techniques. Feline herpesvirus 1 was found to preferentially infect and induce necrosis of conjunctival epithelium. Although significant histologic lesions were not induced, all FHV-1 strains were observed to replicate in corneal epithelium; minimal viral antigen was detected in the corneal stroma. The course and clinical features of ocular FHV-1 infection were then studied over a period of 60 days in two groups of ten cats: in one group, infection was preceded by administration of subconjunctival betamethasone. In each of these groups, a distinct clinical syndrome developed. In cats not receiving corticosteroids, a course of epithelial keratitis, characterized by the formation of punctate and dendritic epithelial lesions, persisted for up to 24 days postinfection. In the corticosteroid treated group, a chronic (greater than 60 days) stromal keratitis developed, characterized by geographic epithelial ulceration, interstitial edema and deep vascularization. Other complications observed in corticosteroid-treated animals included decreased tear production, calcific-band keratopathy and a unique stromal disorder of cats termed corneal sequestration. The results of this study indicate that while epithelial keratitis may occur during primary infection, stromal keratitis does not, unless immune responsiveness to FHV-1 is concomitantly suppressed. This feature is similar to naturally occurring HSV-1 keratitis of humans, but contrasts to other animal model systems in which stromal keratitis predictably occurs during primary infection. Study of this animal model, therefore, may allow unique insights into the events preceding the establishment of stromal keratitis.

Animals↗
PubMed1989

In vitro susceptibility of feline herpesvirus-1 to vidarabine, idoxuridine, trifluridine, acyclovir, or bromovinyldeoxyuridine.

In vitro activities of 9-[( 2-hydroxyethoxy] methyl) guanine (acyclovir), (E)-5-(2-bromovinyl)-2'deoxyuridine, 9-beta-D-arabinofuranosyladenine (vidarabine), 5-iodo-2'-deoxyuridine (idoxuridine), and 5-trifluoromethyl-2'-deoxyuridine (trifluridine) were studied against 6 strains of feline herpesvirus-1. A significant difference was not detected among viral strains in their susceptibility to these compounds (P = 0.442). The relative potency of these compounds was trifluridine much greater than idoxuridine greater than vidarabine greater than bromovinyldeoxyuridine much greater than acyclovir. Concentrations of trifluridine and idoxuridine (0.67 and 6.8 microM, respectively) required to reduce plaque numbers by 50%, compared with that of controls, were significantly lower (P less than 0.001) than were those of other compounds.

Acyclovir↗
PubMed1986

Diagnosis of canine viral infections.

The diagnosis of canine viral infections frequently requires the correlation of clinical, hematologic, pathologic, and laboratory findings. When laboratory diagnostics are utilized, appropriate specimens must be collected. In addition, correct timing of specimen collection and the proper handling and transport of these specimens are essential. Whenever possible, the practitioner should not rely on any one laboratory procedure for making a diagnosis; rather, a combination of techniques should be used. Submission of tissue for histopathology, virus isolation, and antigen detection techniques (FAT), serum for serologic analysis, and feces whenever enteric infections are investigated will maximize the chances of making a successful diagnosis.

Animals↗