Oncogenic Marek's Disease Herpesvirus in Avian Encephalitis (Temporary Paralysis)
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Kenzy, S. G.; Cho, B. R.; Kim, Y.

doi:10.1093/jnci/51.3.977

Cited by 26 publications

(21 citation statements)

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“…Thus, it seems clear that PN and MD are pathologically and aetiologically distinct, a conclusion consistent with the data of Julian (1992), J. L. Spencer (unpublished observations), and also of Biggs et al (1982), who found no association of the closely-linked IP syndrome with MD. PN also differs from transient paralysis (TP), a neurological syndrome induced by MDV (Kenzy et al, 1973) that is also influenced by the MHC, i.e. chickens with B * 6 are more susceptible than those with B * 13 (Schierman & Fletcher, 1980;Parker & Schierman, 1986).…”

Section: Discussionmentioning

confidence: 99%

Characterization and experimental reproduction of peripheral neuropathy in White Leghorn chickens

Bacon¹,

Witter²,

Silva³

2001

Avian Pathology

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A clinical neurological syndrome termed peripheral neuropathy (PN) that resembles Marek's disease (MD) occurred at low frequency in a commercial layer strain for several years. Study of chickens from six field cases showed that the PN syndrome could be distinguished pathologically from MD on the basis of several factors, including onset as early as 6 weeks, presence of B-type but not A-type lesions in peripheral nerves, and absence of visceral lymphomas. Serotype 1 MD virus could not be isolated from blood from any chicken or demonstrated in tissues by histochemistry or polymerase chain reaction assays. Moreover, the syndrome was not prevented by MD vaccination, either in the field or in laboratory trials. PN was induced in 3 to 54% of commercial line chickens inoculated at 1 or 6 days of age with whole blood or buffy coat cells from clinically affected donor chickens. Sonicated cells also induced PN, but plasma was ineffective. Chickens did not develop PN if reared in isolators without cellular transfer or when vaccinated solely against MD. However, PN was observed in 9% of 57 B*2/*19 commercial chickens reared in isolators following vaccination against MD, infectious bursal disease, Newcastle disease and infectious bronchitis, suggesting that common vaccines may predispose chickens to PN. The data confirmed a strong influence of the major histocompatibility complex (B-complex) on both naturally occurring and experimentally induced PN with the B*19 haplotype conferring susceptibility compared with other alleles. It is postulated that PN may represent an autoimmune reaction to nerve tissue that may result from response to a combination of common vaccines. These studies confirmed that PN is distinct from MD, provided criteria for its differential diagnosis, identified strategies for its control, and established a model for its experimental induction.

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Section: Discussionmentioning

confidence: 99%

Characterization and experimental reproduction of peripheral neuropathy in White Leghorn chickens

Bacon¹,

Witter²,

Silva³

2001

Avian Pathology

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“…Only a few of these chickens have lesions in, or symptoms attributable to, primary central nervous system (CNS) involvement (Wight, 1962b). In TP, 8 to 12 days post-inoculation of MDV, chickens develop a generalised flaccid paralysis which commonly disappears within 24 to 96 h (Kenzy et al, 1973;Schierman and Fletcher, 1980;Kornegay et al, 1983a, b). Resistance to the development of TP has been found to be a dominant trait controlled by genes within or closely linked to the major histocompatibility complex (MHC) (Schierman and Fletcher, 1980).…”

Section: Introductionmentioning

confidence: 99%

Marek's disease virus‐induced transient paralysis in chickens. 3. Differentiation of field cases from classical Marek's disease by central nervous system lesions

et al. 1989

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SUMMARYVasculitis with intramural pseudocyst formation primarily in the cerebellar white matter, but also in nuclei of the medulla, resulted in leakage of IgG and albumin and vacuolation of the neuropil (vasogenic oedema) in brains from chickens with clinical signs of Marek's disease virus (MDV)-induced transient paralysis (TP). Demyelination was absent. Chickens that had recovered from TP had a restored bloodbrain-barrier, indicated by the rarity of vasculitis and vascular intramural pseudocysts in the cerebellum. In addition, the vacuolation and protein leakage were greatly decreased. The minor vacuolation resulted primarily from intramyelinic (cytotoxic) oedema. The small quantity of extravascular protein was being removed by microglial cells and astrocytes. In one chicken which failed to fully recover from TP (TPprolonged) there was neither vasogenic oedema, cytotoxic oedema, nor vasculitis in the cerebellum. The medulla of the TP-prolonged chicken had a severe lymphocytosis, swollen axons, neuronal degeneration, secondary demyelination and some associated serum protein leakage. All TP-affected and TP-recovered chickens, and the TP-prolonged chicken, had perivascular mononuclear cell cuffs within all brain sections. Chickens with classical Marek's disease (MD) generally lacked CNS vacuolation, perivascular mononuclear cell cuffs, vasculitis and serum protein leakage. However, in a few cases of MD with severe perivascular mononuclear cell cuffs, focal demyelinating plaques were seen. These plaques had associated vacuolation, serum protein leakage, axonal spheroids and neuronal degeneration.

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“…Two neurological syndromes involving the brain have been reported to be induced by MDV: TP (Kenzy et al, 1973;Witter et al, 1999) and PND (Gimeno et al, , 2001. In this study, using strain 648A (vv+MDV) at different passage levels (from 10 to 100), we have shown that TP and PND are distinct syndromes, unrelated and differently regulated.…”

Section: Discussionmentioning

confidence: 64%

“…Changes in the brain consisting of oedema secondary to vasculitis, the presence of viral DNA, and viral antigen expression, as well as the presence of paralytic clinical signs, are common to both forms Witter et al, 1999). Although fatal cases were mentioned in early descriptions of TP (Cho et al, 1970;Kenzy et al, 1973), the unusually high frequency of fatal cases induced by highly virulent MDV strains created a need for a separate nomenclature. Therefore, the term 'acute' is used to designate birds that die from this syndrome.…”

Section: Introductionmentioning

confidence: 99%

“…The pathogenesis of MDV infection of the central nervous system (CNS) has received considerable study (Wight, 1968;Kenzy et al, 1973;Schierman & Fletcher, 1980;Lawn & Watson, 1982;Kornegay et al, 1983;Swayne, 1987;Cho et al, 1998Cho et al, , 1999Swayne et al, 1988Swayne et al, , 1989a). However, most of these studies focused attention on the CNS alone and provided little information on the relationship between alterations in CNS and other events of the pathogenesis of MDV infection.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Differential attenuation of the induction by Marek's disease virus of transient paralysis and persistent neurological disease: A model for pathogenesis studies

Gimeno¹,

Witter²,

Hunt³

et al. 2001

Avian Pathology

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Oncogenic Marek's Disease Herpesvirus in Avian Encephalitis (Temporary Paralysis) 2

Cited by 26 publications

References 0 publications

Characterization and experimental reproduction of peripheral neuropathy in White Leghorn chickens

Characterization and experimental reproduction of peripheral neuropathy in White Leghorn chickens

Marek's disease virus‐induced transient paralysis in chickens. 3. Differentiation of field cases from classical Marek's disease by central nervous system lesions

Differential attenuation of the induction by Marek's disease virus of transient paralysis and persistent neurological disease: A model for pathogenesis studies

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