Virological and serological investigation of Equid herpesvirus 1 infection in New Zealand.

Infection with equid herpesvirus 1 (EHV-1) may be asymptomatic, or may result in respiratory disease, abortion, neonatal death, or neurological disease. The aim of this study was to estimate the prevalence of EHV-1 infection, including differentiation between genotypes with aspartic acid (D) and asparagine (N) at position 752 of the DNA polymerase sequence, within a selected population of New Zealand horses. The second aim was to determine the predictive value of serology for detection of latently infected horses. Retropharyngeal lymph nodes (RLN) and trigeminal ganglia (TG) were dissected from 52 horses at slaughter and tested for the presence of EHV-1 DNA using magnetic bead, sequence-capture enrichment followed by nested PCR. Sera were tested for EHV-1 antibody using type-specific glycoprotein G ELISA. Overall, 17/52 horses tested positive for EHV-1 DNA. All but one positive PCR results were obtained from RLN samples. Fifteen of the EHV-1 positive horses harboured EHV-1 with N752 genotype, one of which was additionally infected with the D752 genotypes of the virus. Our data comprise the first detection of EHV-1 with D752 genotype in New Zealand and suggest that the "neurovirulent" variant of EHV-1 had been present in New Zealand for at least two years before the first reported outbreak of EHM. All sampled horses tested positive for EHV-4 antibody, and 11/52 tested positive for EHV-1 antibody. The strength of agreement between results of EHV-1 PCR and EHV-1 serology was "fair" (Kappa 0.259, 95% CI: -0.022-0.539), which was likely a reflection of low levels of both EHV-1 antibody in sera and EHV-1 DNA in tissues tested.

Papillomaviral DNA sequences are not amplifiable from canine subungual squamous cell carcinomas.

AIM: To determine if papillomaviral DNA is more frequently present within canine subungual squamous cell carcinomas (SCCs) than in non-SCC digit lesions. METHODS: Total DNA was extracted from 23 canine subungual SCCs and 23 non-SCC digit lesions. The presence of amplifiable DNA within each sample was confirmed by amplifying a section of the glyceraldehyde-3-phosphate dehydrogenase (GADPH) gene. Two different consensus PCR primer sets were used to amplify papillomaviral DNA from the samples. RESULTS: The consensus primers only amplified papillomaviral DNA from the positive control samples. None of the 46 canine digit samples contained DNA that was amplifiable by the consensus PCR primers. CONCLUSION: Papillomaviruses are unlikely to be a significant cause of canine subungual SCCs. CLINICAL RELEVANCE: While circumstantial evidence suggests that canine subungual SCCs could develop due to papillomaviral infection, this study did not reveal any evidence to support papillomaviral aetiology of these neoplasms.

Dermatosparaxis in two white Dorper lambs.

CASE HISTORY AND CLINICAL FINDINGS: Two White Dorper lambs from the North Island of New Zealand, 2 and 4 weeks of age, were presented with large skin flaps hanging from the flanks, separation of skin from the subcutis over mobile joints, and de-gloving injuries of the limbs and tail. The lambs were subject to euthanasia on humane grounds. PATHOLOGICAL FINDINGS: Large skin tears with associated haemorrhage, periarticular S/C oedema and generalised skin fragility were observed in both lambs at post-mortem examination. Histology of the affected skin revealed diffuse hyalinisation of dermal collagen compared with control lambs, protein-filled peri-adnexal clefts and areas of deep dermal and S/C granulation tissue consistent with previous separation of skin from the subcutis. Analysis of hair follicles, collected from one of the lambs, using a commercially available genetic test in Australia was consistent with the lamb being homozygous for the mutation responsible for ovine dermatosparaxis. DIAGNOSIS: Likely dermatosparaxis. CLINICAL RELEVANCE: These findings strongly suggest that the mutation responsible for dermatosparaxis in White Dorper sheep is present in New Zealand. Dermatosparaxis should be considered when investigating skin fragility in lambs with White Dorper genetics. Confirmation of the disorder is possible through genetic analysis of hair follicles.

Immunoblot analysis to demonstrate antigenic variability of clinical isolated. Pseudomonas pseudomallei.

Pseudomonas pseudomallei (Ps.ps.) is the causative organism of melioidosis, and is widely distributed in Southeast Asia and Northern Australia. Clinical manifestations range from subclinical infection to fulminant septicemia. To demonstrate the antigenic variability of Ps.ps., 62 clinical isolates from 31 blood, 13 sputum, 9 pus, 3 urine and 6 body fluid culture specimens were studied by SDS-PAGE and immunoblotting. In SDS-PAGE, there were approximately 20 antigenic components with molecular weights ranging from 14 to 66 kilodaltons (KD) which suggested that there was antigenic variability among these 62 clinical isolates of Ps.ps. Attempts to correlate immunoblot profiles with clinical illness or sources of specimens were not successful but 6 common antigens were identified with molecular weight of 17.5, 21, 33, 34, 40 and 45 KD, respectively. Among these antigens, the 45 KD component was recognised by all patients' sera. Thus, the 45 KD protein antigen may be useful for the future approach in immunodiagnosis of melioidosis.