1 Introduction

Cerebellar hypoplasia is the result of abnormal development during the foetal period to the section of the brain that coordinates motor movement, resulting in a calf that is born weak, trembling, or stumbling (Gul et al., 2013). Even though observed in many animal species (calf, lamb and foal), it is mostly reported in the Hereford, Holstein-Friesian, Guernsey, Shorthorn, Ayrshire and Angus breeds of cattle (Smith, 2009). Cerebellar hypoplasia as nervous system disorders in cattle represents a medium financial loss to cattle breeders’ worldwide (Galiza et al., 2010). The congenital form of cerebellar hypoplasia is reported to be non-progressive and sporadic (Radostits et al., 2008). The emergence of this malformation depends not only on genetic factors, but also on some intra-uterine viral infections like bovine viral diarrhoea (BVD), blue tongue and border disease, feline panleukopenia, hog cholera (Rosenberger, 1994; Ok, 2010). Sometimes the ingestion of toxic plants like Astragalus species, Veratrum californicum, Lupinusspecies, Conium species, Nicotiana species (Garland et al., 1998) and Mimosa tenuiflora (Pimentel et al., 2007) by the pregnant animals also results in the cerebellar hypoplasia in calves. The BVD virus infection of sensitive cattle during 90-170^th day of gestation terminates with abortion, stillbirth, hydranencephaly or cerebellar hypoplasia in foetuses (Ok, 2010). This is first communication of cerebellar hypoplasia from Kashmir.

1.1 History and clinical examination

A female Holstein- Friesian calf of 05 days old and weighing 21 kg was brought to the Veterinary Clinical Services Complex. The anamnesis of case was that the calf was weak, not able to stand without assistances and had head pulled backwards since birth. However the calf had normal sucking reflex. Clinical examination revealed hypertonous and exaggerated movements of the limbs with hyperaesthesia (Figure 1). Upon physiological examination the various physiological parameters like respiratory rate, heart rate and rectal temperature were observed to be within normal physiological range.

1.2 Treatment

The animal was treated with 0.5 mL Neuroxin-12-V injection (thiamine hydrochloride 30mg, pyridoxine hydrochloride 13.75 mg, cynocobalamine 500 mcg in 1 mL), 1 ml Advet injection (250 000 IU vitamin A, 25.00 IU vitamin D₃, 100 mg vitamin E in 1 mL) and 0.1ml of siquil injection (20 mg triflupromazine in 1 mL) for three days however, the animal showed no recovery, except that animal limb movements decreased and further physical examination showed that the animal was still unable to stand, lay in a lateral recumbency with exaggerated movements of the limbs, was weak despite having normal sucking reflex, had soft hoofs, unerupted teeth, exhibited hyperaemic mucosa and harsh vesicular sound on lungs auscultation, opisthotonos and lacked papillary and palpebral reflexes (Figure 2). Body temperature, heart and respiratory rate were 102.3^oF, 128 beats/min and 88 beats/min, respectively. Cerebellar hypoplasia was diagnosed on the basis of clinical signs and poor response to treatment. Euthanasia of calf was recommended to owner depending on the severity of the diseased condition.

2 Discussion

Clinical findings including inability to stand, lateral recumbency, weakness despite having sucking normal reflex, opisthotonos, incoordinated limb movements, the lack of papillary and palpebral reflexes are consistent with cerebellar hypoplasia as described in earlier reports in the literature (Radostits et al., 2008). Additional findings of soft hoofs and unerupted teeth support the claims (Smith, 2009). Cerebellar hypoplasia was diagnosed through specific clinical findings in the present report (Radostits et al., 2008). The present findings where differentiated from neural symptoms like opisthotonos and blindness observed in cerebrocortical necrosis (CCN), hypovitaminosis A and encephalitis in colibacillosis. The clinicopathological changes of cerebrocortical necrosis (CCN) quite closely resemble with those of the bovine viral diarrhea-mucosal disease virus infection (Narita et al., 1979) suggest that care should be taken to avoid confusing with Cerebellar hypoplasia. Since BVD virus infections are commonly observed in cattle and lead to significant economic losses, they must be considered as possible cause of cerebellar hypoplasia in calves and such calves show motor defects at birth like failure to stand, ataxia (stumbling), head tremors, weakness and/or extension of all four limbs, and a general failure to coordinate their motor movements (Gul et al., 2013). Cerebellar hypoplasia is characterized by lowered head carriage, a wide-based stance and inco- ordination, particularly of the hind legs but with preservation of normal muscle strength (Recai et al., 2006). Due to the fact that the cerebellum controls the strength of motor movements, calves may show hypermetria, or exaggerated movements of the limbs when walking (Allen, 1977).The presentation of symptoms can vary widely according to the severity of the lesion, ranging from mild improper development to complete lack of cerebellar growth. However, in the present clinical case, BVD virus infection in cattle was most unlikely as the arboviruses are not present in Jammu & Kashmir due to the absence of its vector. Therefore, the cause in present case may be ingestion of toxic plants such as Astragalus and Conium species by dam during later half of pregnancy. As there was no specific treatment and the symptomatic treatment was given as owner was not initially willing to euthanize the calf.

3 Conclusion

In the present case report cerebellar hypoplasia was diagnosed through specific clinical findings and owner was advised to euthanize the animal. Therefore as with any genetically inherited condition, known carrier sires and dams should be removed from the breeding stock so that the source of such diseases conditions are controlled. Also there should be paper identification of toxic plants in place.

Acknowledgement

The authors are highly thankful to Dr. M. R. Fazili, Associate Professor, Teaching Veterinary Clinical Service Complex, F.V.Sc & A.H, SKUAST-K, for his persistent & valuable guidance in the preparation of this communication.

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