Congenital Chondrodysplastic Dwarfism in a Fischer’s Lovebird (Agapornis fischeri)

Ken S. Frazier and Kitty H. Remington

Veterinary Diagnostic and Investigational Laboratory, College of Veterinary Medicine, The University of Georgia, P.O. Box 1389, Tifton, GA 31793 (Frazier), and Animal House Veterinary Services, 800 Sharpe St. , Bainbridge, GA, 31717 (Remington)

Abstract. Although chondrodysplastic dwarfism is a common congenital disease of humans, cattle, dogs, and occasionally other species, it has rarely been reported in caged aviary birds. We describe a case of congenital malformation in a Fischer’s Lovebird that had gross and chondrodystrophic histologic lesions similar to those described in congenital dwarfs of other animal species. The gross and histologic changes in cartilage and bone of the necropsied lovebird were consistent with disturbed endochondral ossification, and included short limb length, disorganized columns in the growth plate with cartilage fibrillation, and widening of the metaphysis. A genetic basis for chondrodysplasia is suggested by the consanguinity of the parents and the presence of another bird with proportionate dwarf characteristics hatched in a subsequent clutch.

Keywords: Avian, Fischer’s Lovebird, Agapornis fischeri, Dwarfism, Chondrodysplasia, Congenital malformation

  Introduction

Although chondrodysplastic dwarfism is a common congenital disease of humans, cattle, dogs, and occasionally other species, it has rarely been reported in caged aviary birds. ¹¹ Avian cases of dwarfism have been described in fowl, quail, pheasant, black-headed gulls, and a great- crested flycatcher, and anecdotal accounts of dwarf birds have been mentioned sporadically. ^1-6,9,11 In humans and dogs, chondrodysplasia is divided into proportionate and disproportionate types depending on limb length compared to body size. Different genes are involved in each syndrome. In chickens, dwarfism is a sex-linked recessive trait,⁶ while in quail it is autosomal recessive. ⁴ Specific point mutations and polygenic inheritance patterns have been described in other species. ¹¹ Several hormonal alterations have been demonstrated in dwarf chicks including reduced insulin-like growth factor-1 and T₃, and increased growth hormone and T₄ levels. ^5,7 Growth hormone stimulated conversion of T₄ to T₃ reportedly does not occur in dwarf chickens, and growth hormone receptor deficiency has been suggested as a cause of other associated hormonal irregularities. ⁷ Chondrodysplasias have also been attributed to defects in chondroitin sulfate and glycosaminoglycans. ^2,3 We describe a case of congenital malformation in a Fischer’s Lovebird (Agapornis fischeri) that had gross and chondrodystrophic histologic lesions similar to those described in congenital dwarfs of other animal species. A genetic basis for the chondrodysplasia is suggested by the consanguinity of the parents and the presence of another bird with dwarf growth characteristics hatched in a subsequent clutch.

Case Report

A 16 day old male Fischer’s Lovebird was presented to a veterinary clinic with a history of retarded growth and development. The bird was from a clutch of four and was the only hatchling to survive. The lovebird’s parents were siblings and this was their first clutch. The lovebird’s feet were contracted and curled ventrally. It was getting adequate nutrition via hand feeding (Exact diet); however, it had the size and weight of only a 4 day old lovebird. Due to problems with perching and concerns of the potential for communicable disease, the owner’s elected euthanasia.

The lovebird was submitted for necropsy to the Veterinary Diagnostic and Investigational Laboratory. There was marked shortening, thickening and bowing of the tibiotarsus; decreased length of the humerus; and widening of the metaphyseal region of developing long bones. Neither brachycephaly nor micromelia, described in other cases of avian hereditary chondrodystrophies, were found. Microscopic examination of the skeleton of the bird revealed decreased mineralization, cartilage maturation, and ossification when compared to age-matched controls (Figs. 1 & 2).

Fig. 1. Fischer's Lovebird, proximal tibiotarsus, H&E stain.   Note disorganization, poor mineralization, cartilage fibrillation, and irregular spongiosa.	Fig. 2. Fischer's Lovebird, developing bone, H&E stain. Note widened bone proximally and disorganized columns in hypertrophic (maturation) zone of developing ossification center.

Trabeculae of primary and secondary spongiosa were focally coarse and mildly disorganized. At growth plates, the zone of proliferation was decreased in length while the hypertrophic zone (zone of maturation) often appeared lengthened. The avian physis is more cellular and less well organized than mammalian growth plates,⁸ but irregularities of the cartilage columns in ossification centers of long bones were pronounced when compared to those in normal birds. Columns lacked parallel growth and multiple islands of cartilage fibrillation were noted (Figs. 3 - 5).

Fig. 3. Fischer's Lovebird, developing bone. Note island of degenerative cartilage at interface between hypertrophic and ossification zones.	Fig. 4. Fischer's Lovebird humerus, H&E stain.    High power view of proliferative and hypertrophic zones in developing bone. Note lack of alignment and disorganization of columns. Chondrocyte nuclei are atypical.

Fig. 5. Fischer's Lovebird, femur, H&E stain. Area of more normal column organization in femur. Compare to Figures 3 and 4.

Scattered chondrocytes had degenerative basophilic nuclei and vacuolated cytoplasm. Interstitial growth was generally reduced whereas appositional growth was normal or increased with adequate mineralization, resulting in an overall decrease in long-bone length and increase in width relative to body size.

A chick hatched from a second clutch several months later is also very small for its age when compared to siblings. The bird (now an adult) weighs 42 grams, whereas siblings average 50 to 60 grams. In contrast to the earlier bird, it has no problems with distal limb contracture. No thickened joints are palpable, and limb length in the lovebird appears proportional. Mentation, appetite, clinical history and laboratory data are normal.

Discussion

The histologic changes in cartilage and bone of the first lovebird are consistent with disturbed endochondral ossification. These changes, particularly in a bird of 16 days of age, are highly suggestive of a congenital defect in chondrocyte/osteocyte maturation. The history of inbreeding and presence of offspring in a subsequent clutch with dwarf stature suggests a hereditary etiology. Fischer’s Lovebirds are not particularly common in aviaries and founding stock are likely genetically closely related with a high number of identical recessive mutations. The problem was probably amplified in this case by breeding siblings. The potential genetic defect could involve any of the phases of ossification including chondrocyte proliferation, extracellular matrix production, chondrocyte hypertrophy, matrix calcification, vascular invasion, or matrix degradation. Whether this case represents an analogous condition to chondrodysplastic dwarfism in mammals, sex-linked dwarfism such as that found in chickens, or a condition similar to pseudochondrodysplastic dwarfism remains undetermined.

Various histologic features found in the lovebird’s long bones have been described in many other animals with chondrodysplasia. ^1-4,11 Histologic lesions may vary with individuals afflicted by the same hereditary syndrome, but particular features (e.g. , endochondral ossification defects in the growth plates of chondrodysplastic dogs or premature synostosis of cranial synchondroses in Telemark dwarf cattle) are often consistent and reproducible. ¹¹ Limb contracture, as noted in this case, is common, and has been reported in chondrodysplastic chickens, cattle and dogs. ¹¹ The pathogenesis probably involves incongruous growth and development of ligamentous soft tissue and adjacent bone. Although disrupted endochondral ossification occurs commonly in fast-growing domestic broilers (avian tibial dyschondroplasia) as a consequence of ill-defined nutritional, metabolic and genetic factors,¹⁰ the signalment and presentation differ from those described here. Avian tibial dyschondroplasia develops as islands of immature cartilage in the metaphysis as the animal grows and more closely resembles osteochondrosis. Hypovitaminosis D, calcium deficiency, and other nutritional disorders may also affect the maturation of bone and cartilage, but a nutritional deficiency would be unlikely in a bird of this age hand-reared on a commercial diet.

Since the lovebird from the later clutch has proportionate limb features, it could be argued that it is not a true dwarf, but only a "runt. " However, the severity of the size differential (70-80% of normal) would be more consistent with classification as a dwarf in this species. Histologic examination of its skeleton would be necessary to confirm the presence of any underlying abnormalities in bone maturation, and backcross matings with the female parent would be the most direct method of determining a genetic basis for the condition. The proportionality of the limbs in this second bird could represent decreased phenotypic expression or penetrance of the same defect or conversely, could represent an entirely separate gene mutation. The inbreeding of consanguinous parents could support either possibility.

After the second instance of offspring with markedly retarded growth, the breeder separated the mating pair to prevent additional occurrences of potential genetic anomalies. Identification of chondrodysplastic diseases in animals is important for both alerting breeders of potential genetic defects and as serving as models of pathogenesis for human genetic diseases.

References

1. Ash JS: Another dwarf pheasant. Bull Brit Ornithol Club 86:95-96, 1966.

2. Bingel SA, Sande RD, Wight TD: Chondrodysplasia in the Alaskan malamute, characterization of proteoglycans dissociatively extracted from dwarf growth plates. Lab Invest 53:479-485, 1985.

3. Bingel SA, Sande RD, Wight TD: Undersulfated chondroitin sulfate in cartilage from a miniature poodle with spondylo-epiphyseal dysplasia. Conn Tiss Res 15: 283-302, 1986.

4. Hermes JC, Abbott UK, Johnston E, Owens M: A new chondrodystrophy mutation in Japanese quail (Corturnix japonica). J Hered 81:222-224, 1990.

5. Hoshino S, Wakita M, Suzuki M, Yamamoto K: Chjanges in a somatomedin-like factor and immunoassayable growth hormone during growth of normal and dwarf pullets and cockerels. Poult Sci 61:777-784, 1982.

6. Hutt FB: Sex-linked dwarfism in the fowl. J Hered 50:209-221, 1959.

7. Kuhn ER, Decuypere E, Huybrechts LM, Darras VM: Hormonal control of the hepatic 5'-monodeiodination activity and its relation to the somatomedin production in the chicken. In: Wada M, Ishii S, Scanes CG: Endocrinology of Birds. Molecular to Behavioral. Springer Verlag, Berlin, pp. 129-142, 1990.

8. Leach RM, Gay CV: Role of epiphyseal caritilage in endochondral bone formation. J Nutr 117:784-790, 1987.

9. Murray BG: A small great-crested flycatcher. Bird Banding 42:119, 1971.

10. Orth MW, Cook ME: Avian tibial dyschondroplasia: A morphological and biochemical review of the growth plate lesion and its causes. Vet Pathol 31:403-414, 1994.

11. Palmer N: Diseases of Bones. In: Pathology of Domestic Animals, Jubb KVF, Kennedy PC, Palmer N (eds), 4^th ed. , vol. 1. Academic Press, San Diego, CA, pp. 27-361993.

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