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Marek’s Disease Virus |   357

          induce the transformation of T lymphocytes, which provide a   severe and acute TP. However, some infected chickens can fully
          novel insight for better understanding of MDV pathogenesis.  recover or may transit to persistent neurological disease (PND),
                                                                which is characterized by persistent non-paralytic but neuro-
                                                                logical  related signs, including ataxia, torticollis, and nervous
          Pathogenesis                                          tics (Gimeno et al., 2001). PND is observed in chickens 12–15
          In MDV infected chickens, lymphoproliferative lesions appear,   days post infection, and chickens showing signs of PND usually
          as early as two weeks post infection, in various organs including   die within a week (Fig. 12.6A). Not all chickens infected with
          spleen, kidney, liver, skin, eye, nerve, and heart (Payne, 2004).   MDV develop neurological CNS lesions (like TP and PND),
          Sometimes, lymphoma lesions may regress (Sharma et al., 1973),   however most chickens develop lymphoproliferative lesions in
          but often progress to massive size compromising the function of   various tissues.
          the organ. Clinical manifestation of the disease depends on the
          organ being affected. MDV infection can result in paralysis when
          peripheral nerves are involved, blindness if the ciliary body of   Diagnosis
          the eye is infiltrated, or death due to visceral organ involvement   Outbreaks of MD usually occurs due to vaccine failure, which
          (Fig. 12.6). Lymphoma development is generally coupled with a   is  primarily  due  to  improper  vaccination  or  infection  with
          permanent immunosuppression which affects both humoral and   highly virulent field viruses. Manifestation of MD is typically
          cell-mediated immunity and may result in chickens succumbing   seen by  the presence  of gross lymphomas  in various visceral
          to lethal infection with other pathogens. It has also been reported   organs and skin (Zelnik, 2004). Lymphoproliferative lesions in
          that early exposure of chickens to very virulent plus MDV strains   peripheral nerves results in paralysis and sometimes blindness
          results in inadequate immune response to other vaccines resulting   is observed due to accumulation of tumour cells in the cili-
          in vaccine failures (Faiz et al., 2016).              ary body of the eye. In addition to clinical signs, other factors,
            Infection of chickens with very virulent plus MDV strains   such as vaccination program, history of disease, and the age of
          can result in the development of additional lesions in the cen-  affected chickens, should also be considered for accurate diag-
          tral nervous system (CNS) at 9–10 days post infection, called   nosis (Zelnik, 2004). Virulence of MDV and co-infection with
          transient paralysis (TP), which is characterized by sudden onset   other immunosuppressive viral pathogens aids in diagnosis as
          of flaccid paralysis in neck and wings (Gimeno et al., 2001).   well. Infection with avian leukosis virus (ALV) or reticuloen-
          Infected chickens usually die within 1 to 3 days after onset of a   dotheliosis virus (REV) will also cause lymphomas in poultry,



                   A                                           B
                                                               (B)
                   (A)















                                                               D
                   C                                           (D)
                   (C)

















          Figure 12.6  Marek’s disease pathogenesis. Chickens infected with vv+ strain of MDV showing neurological signs (A), paralysis (B), gross
          MD lymphomas in liver (C) and lymphoproliferative lesions in peripheral nerves (D).
                 Figure 6
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