“…A significantly higher rate of virus isolations was found in blood plasma samples collected during spring than during the autumn. It is conjectured that a causal association exists with the initiation of the breeding season, which is known to reactivate latent viral infections including those caused by herpesviruses (Sharma, 1980;Kaleta & Docherty, 2007). However, definite proof for this assumption is currently lacking.…”
Herpesvirus isolations from peripheral white blood cells of 253 White Storks (Ciconia ciconia) were obtained during a long-term study (1983 to 2001). The storks lived for a few months to 20 years at four rehabilitation centres. Isolates were obtained from 83 of 253 storks. This herpesvirus is indigenous for storks and unrelated to any other avian herpesvirus. Significantly more herpesvirus isolates were obtained during spring than in autumn samplings. The intervals between the first and last virus isolation ranged from 1 to 15 years. Herpesvirus isolates were simultaneously obtained from white blood cells and from pharyngeal swabs of four of 34 storks but not from cloacal swabs. Neutralizing antibodies to stork herpesvirus were detected in 178 of 191 examined blood plasma samples. Neutralizing antibodies against stork herpesvirus did not correlate with herpesvirus viraemia. The results further substantiate the persistence of herpesvirus in White Storks and underline the previously unrecorded long periods of virus and antibody presence. Virulent avian paramyxovirus type 1 (APMV-1; Newcastle disease virus) was isolated from white blood cells during 1992 and 1993 from four healthy migrating storks, and possessed virulence markers on the cleavage site of the H and F genes. These properties resemble the NE type of APMV-1. Haemagglutination inhibition antibodies against APMV-1 were detected in 16 of 191 blood plasma samples. Avian influenza A virus was not isolated and antibodies against subtypes H5 and H7 were not detected.
“…A significantly higher rate of virus isolations was found in blood plasma samples collected during spring than during the autumn. It is conjectured that a causal association exists with the initiation of the breeding season, which is known to reactivate latent viral infections including those caused by herpesviruses (Sharma, 1980;Kaleta & Docherty, 2007). However, definite proof for this assumption is currently lacking.…”
Herpesvirus isolations from peripheral white blood cells of 253 White Storks (Ciconia ciconia) were obtained during a long-term study (1983 to 2001). The storks lived for a few months to 20 years at four rehabilitation centres. Isolates were obtained from 83 of 253 storks. This herpesvirus is indigenous for storks and unrelated to any other avian herpesvirus. Significantly more herpesvirus isolates were obtained during spring than in autumn samplings. The intervals between the first and last virus isolation ranged from 1 to 15 years. Herpesvirus isolates were simultaneously obtained from white blood cells and from pharyngeal swabs of four of 34 storks but not from cloacal swabs. Neutralizing antibodies to stork herpesvirus were detected in 178 of 191 examined blood plasma samples. Neutralizing antibodies against stork herpesvirus did not correlate with herpesvirus viraemia. The results further substantiate the persistence of herpesvirus in White Storks and underline the previously unrecorded long periods of virus and antibody presence. Virulent avian paramyxovirus type 1 (APMV-1; Newcastle disease virus) was isolated from white blood cells during 1992 and 1993 from four healthy migrating storks, and possessed virulence markers on the cleavage site of the H and F genes. These properties resemble the NE type of APMV-1. Haemagglutination inhibition antibodies against APMV-1 were detected in 16 of 191 blood plasma samples. Avian influenza A virus was not isolated and antibodies against subtypes H5 and H7 were not detected.
“…Concomitant infections, environmental factors and stress often contribute to morbidity and mortality of infections (Davison 2002, Kaleta & Docherty 2007. As a result, captive wild birds are more likely to have outbreaks than are free-living populations due to the high density and suboptimal environment that are intrinsic to captivity (Kaleta & Docherty 2007).…”
Section: Introductionmentioning
confidence: 99%
“…Herpesviruses cause a broad variety of diseases with distinct clinical presentations and lesions in birds (Kaleta 1990, Hansen 1999, Kaleta & Docherty 2007. Many avian herpesviruses have not yet been classified due to lack of gene sequencing information (Kaleta & Docherty 2007, Davison 2010, and this is further complicated by the fact that in many cases concurrent diseases obscure the primary effects of the herpesvirus on the host (Kaleta 1990). Horizontal transmission of herpesviruses can occur through inhalation of viral particles and is the predominant method of transmission (Kaleta & Docherty 2007).…”
Section: Introductionmentioning
confidence: 99%
“…Many avian herpesviruses have not yet been classified due to lack of gene sequencing information (Kaleta & Docherty 2007, Davison 2010, and this is further complicated by the fact that in many cases concurrent diseases obscure the primary effects of the herpesvirus on the host (Kaleta 1990). Horizontal transmission of herpesviruses can occur through inhalation of viral particles and is the predominant method of transmission (Kaleta & Docherty 2007). Concomitant infections, environmental factors and stress often contribute to morbidity and mortality of infections (Davison 2002, Kaleta & Docherty 2007.…”
Section: Introductionmentioning
confidence: 99%
“…Herpesviruses are large DNA viruses, and most species have a narrow host range (Hansen 1999, Davison 2002, Kaleta & Docherty 2007. Herpesviruses cause a broad variety of diseases with distinct clinical presentations and lesions in birds (Kaleta 1990, Hansen 1999, Kaleta & Docherty 2007.…”
Rehabilitation is an important strategy for the conservation of the Endangered African penguin Spheniscus demersus, and disease has been raised as a concern in the management of the species, both in the wild and in rehabilitation centres. We report 8 cases of herpesvirus-like respiratory infection in African penguin chicks undergoing rehabilitation between 2010 and 2013 at a facility in Cape Town, South Africa. Infection was confirmed through the identification of viral inclusions in the tracheal epithelium and demonstration of particles consistent with herpesvirus by electron microscopy, whereas virus isolation in eggs, serology and PCR testing failed to detect the virus. Only penguin chicks were affected; they were in poor body condition, and in 2 cases infection occurred prior to admission to the rehabilitation centre. The role played by the herpesvirus-like infection in the overall respiratory disease syndrome is uncertain, due to identification of lesions in only a small proportion of the chicks as well as to the occurrence of other concurrent pathological processes. Further studies are advised to characterise the specific virus involved through the development of sensitive diagnostic methods and to clarify the epidemiology and significance of these infections in wild African penguins.
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