Seroprevalence of camel brucellosis (Camelus dromedarius) in Somaliland.

The present study was delineated to investigate the prevalence and risk factors of camel brucellosis in Northern Somalia (Somaliland). The study was carried out at three main districts of camel-rearing regions of Somaliland (Awdal, Waqoyi Galbed and Togdheer) in the period from July to November, 2008. A total of 1246 camel blood sera were randomly collected from 42 sporadic small scale camel herds. Two serological tests were used to screen all serum samples, Rose Bengal Plate Test (RBPT) and indirect ELISA (I-ELISA). Multivariate logistic regression was constructed to study the risk factors associated with Brucella seropositive cases. The overall prevalence of camel brucellosis in districts under investigation was 3.9% by RBPT and 3.1% by (I-ELISA). Multivariate logistic regression on animal level showed that locality (P < 0.05; OR: 6.254; CI, 1.186-32.976), herd size (P < 0.001; OR: 5.493; CI, 2.956-10-207), rearing with other ruminants (P < 0.001; OR: 12.433; CI, 3.957-39.060), and contact with other camels (P < 0.05; OR: 5.311; CI, 1.093-25.800) were the potential risk factors. However, herd size (P < 0.05; OR: 5.425; CI, 1.181-24.932), and rearing with other ruminants (P < 0.05; OR: 20.466; CI, 1.456-28.638) were recorded as risk factors on the herd level. The results of the present investigation indicate that the Brucella spp. exists within the camel herds in Somaliland. Further studies need to be done on Brucella infection in the other ruminants to determine which measure should be followed for control of brucellosis.

Molecular characterization of the equine herpesvirus 1 strains RacL11 and Kentucky D.

The pathogenicities of RacL11 and Kentucky D strains of equine herpesvirus 1 in the hamster infection model are different from those of Ab4p and the Japanese isolates. Virus genome restriction fragment length polymorphism analysis and sequence comparison of an intergenic region, glycoproteins and tegument genes showed higher conservation but with some strain-specific differences. These results indicate that point nucleotide differences in RacL11 and Kentucky D might be responsible for their pathogenicity in rodent models.