Abstract
Aleutian mink disease virus is one of the greatest threats to modern mink farming. The disease reduces fecundity and causes high mortality among kits. The aim of this study was to evaluate the effectiveness of methisoprinol in counteracting the effects of Aleutian disease, both by inhibiting replication of the virus and by mitigating the harmful effects of the disease on the fecundity and weight of infected animals. The study included 300 individuals with confirmed infection, divided according to antibody titres into three experimental groups, which received a 20% methisoprinol solution, and three control groups, which did not receive the immunostimulant. In the mink from the experimental groups, the number of copies of the genetic material of the virus in the spleens and lymph nodes was one order of magnitude lower than in the case of the control groups. Mink receiving the supplement also showed higher fecundity (on average 5.83 in the experimental groups and 4.83 in the control groups), and the weight of their offspring before slaughter was over 200 g higher. Given the lack of effective methods for immunoprophylaxis and treatment, methisoprinol supplementation can be an effective means of counteracting the effects of AMDV on persistently infected farms.
Highlights
Intensive mink farming and breeding are associated with increased exposure of the animals to infectious agents that have a negative impact on their health and well-being
The results indicate more-intensive replication of AMDV in the lymph nodes, where the pathogen reached 103copies in the experimental group, while the viral load in the spleen was one order of magnitude lower
Constant and long-term exposure to AMDV can lead to the development of mechanisms that reduce its harmful effects [11]
Summary
Intensive mink farming and breeding are associated with increased exposure of the animals to infectious agents that have a negative impact on their health and well-being. AD is a chronic and incurable disease in mink that results in breeding losses due to frequent abortion, low fecundity, and high juvenile mortality. The persistent and rapid replication of the virus in the body of infected mink leads to impairment of immune functions. The virus stimulates the host to synthesize excessive quantities of specific antibodies, leading to hypergammaglobulinaemia and the formation of immune complexes. When these complexes are deposited in tissues, they cause inflammation and pathological changes [2]. The disease can have a varied clinical course, from transient infections to persistent and progressive infections [3]
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