A New Inherited Muscular Disorder in Japanese Quails (Coturnix coturnix japonica)

Author:

Braga I. S.1,Oda K.2,Kikuchi T.2,Tanaka S.1,Shin Y.1,Sento M.1,Itakura C.1,Mizutani M.3

Affiliation:

1. Department of Comparative Pathology, Faculty of Veterinary Medicine, Hokkaido University, Sapporo, Japan

2. Division of Animal Models for Human Disease, National Institute of Neuroscience, NCNP, Kodaira, Tokyo, Japan

3. Laboratory of Animal Research Station, Nippon Institute for Biological Science, Kobuchizawa, Yamanishi, Japan

Abstract

Thirteen adult mutant (LWC strain) Japanese quails ( Coturnix coturnix japonica), between the ages of 8 and 60 weeks were examined for a progressive muscular disorder. The disorder, inherited as an autosomal dominant trait, was clinically apparent as early as 28 days of age; it was characterized by generalized myotonia, muscle stiffness, and muscle weakness. Affected birds were identified by their inability to lift their wings vertically upward and by their inability to right themselves when placed on their dorsum. Electromyographic studies in two mutant quails showed high-frequency repetitive discharges comparable to those of myotonic runs. These discharges persisted after nerve resection. The distinctive histopathologic changes in the various muscles examined were ring fibers, sarcoplasmic masses, and internal migration of sarcolemmal nuclei. A slight decrease in the size of type IIB muscle fibers and a slight increase in the size of type IIA fibers were observed in the M. pectoralis thoracicus of affected quails. In older affected birds, inter- and intrafascicular fatty infiltration with replacement of type IIB fibers by fat cells was seen in the pectoral muscles. Single fiber necrosis, nonspecific lymphorrages, and variations in the muscle fiber size and shape were also noted. The typical muscle lesions and multisystem involvement, which was manifested by testicular degeneration and atrophy in the male LWC specimens and bilateral lenticular cataracts in 6 of 13 affected mutant quails, suggest resemblance of this new inherited muscular disorder to myotonic dystrophy in man.

Publisher

SAGE Publications

Subject

General Veterinary

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