Biomedical subjects
Publications and source records attributed to K C Barnett.
Clinical and pathological observations of a naturally occurring disease in a British wild otter (Lutra lutra) are reported. Systemic lymphoreticular proliferative changes with plasmacytosis, glomerulonephritis, arteritis and biliary hyperplasia closely resembled the pathological changes in Aleutian disease of mink (Mustela vison). Feral mink provided a possible source of infection.
Progressive retinal atrophy was studied in 17 Tibetan Terriers. The diagnosis was made on the basis of clinical signs of the disease, retinal histopathologic findings, or both. Affected dogs were the progeny of matings of affected or ophthalmoscopically normal dogs. Results of the mating supported a simple autosomal recessive mode of inheritance. The disease initially could be diagnosed by findings of night blindness and ophthalmoscopic signs of tapetal hyperreflectivity in affected dogs that were approximately 1 year old. Electroretinograms recorded from affected dogs, compared with those of clinically normal dogs of the same age, did not reveal appreciable abnormalities until affected dogs were 10 months old, at which time a reduction in the amplitude of the b wave was seen in response to a Ganzfeld white-light stimulus. The peak times of the response were unaffected. With progression of the disease, the electroretinographic b-wave amplitude was gradually reduced, and the electroretinographic response was extinguished in affected dogs by the time they were 30 months old. Early in the disease, rod and cone functions were affected equally, with more rapid loss of rod function developing only later in the disease. Fluorescein angiography of affected dogs did not reveal abnormalities earlier than could be detected by ophthalmoscopy. Despite the electroretinographic findings, histopathologic findings included patchy disorientation and disorganization of the outer segments of rods and cones in affected dogs as young as 9 weeks. With progression of the disease, rods were lost at a faster rate than cones, and atrophy of the inner retinal layer was observed.
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Keratoconjunctivitis sicca (KCS) is a relatively common eye disease in the dog. The diagnosis is discussed, particularly of the early or mild case. The various types of medical treatment are described, including replacement therapy with artificial tears and ocular inserts, as well as other preparations; lacrimogenics; and other forms of medical treatment, including antibiotics, corticosteroids, mucolytics and hormones. Contraindicated drugs and agents are listed. Surgical treatments, including punctal occlusion, tarsorrhaphy, conjunctival flaps, contact lenses, superficial keratectomy, as well as parotid duct transposition, are discussed and the procedure indicated which is best suited to the case. The choice of treatment according to the severity of the KCS is also given.
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1 Keratoconjunctivitis sicca (KCS) is an inflammatory eye condition, affecting the cornea and conjunctiva, caused by a deficiency in the aqueous fraction of tears. The condition is relatively common in the dog with a varied aetiology. A number of drugs have been implicated in the production of KCS in the dog including salicylazosulphapyridine (sulphasalazine). 2 This paper details clinically evident KCS in a 12-month oral toxicity study with 5-aminosalicylic acid (5-ASA), the therapeutically active metabolite of sulphasalazine. 3 The condition was first diagnosed at study week 22 and subsequently progressed both in incidence and severity. There was a distinct sex-difference in the response, with treated females being more affected than males. 4 There was a close correlation between the production of KCS and reduced lacrimation as assessed by the Schirmer tear test. 5 Although sulphasalazine causes KCS in dogs there have been no reports of ocular lesions of this type in man with this drug. It is highly probable that the dog is not a predictive model for man with regard to KCS induction by sulphasalazine or its metabolite 5-ASA.
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The clinical and pathological features of an early-onset autosomal dominant photoreceptor degeneration in the Abyssinian cat are described. Ophthalmoscopic evidence of retinal disease at 8-12 weeks of age was always preceded by marked dilatation of the pupils, impairment of the pupillary light reflex, and nystagmus. The electroretinogram was unrecordable in all but one of the affected individuals examined. Abnormal photoreceptor development was observed by both light and electron microscopy in retinas of a 22-day-old kitten; in this individual, no outer segment material was detected, and inner segments showed impaired development which was more severe towards the posterior pole. In a 40-day-old kitten, the inner segments were relatively well-formed, whereas the outer segments, though present, showed marked disorganization and degenerative change. The retinas of older individuals showed more advanced photoreceptor degeneration, with thinning of the neural retina. This early-onset retinopathy, which may be classified as a rod-cone dysplasia, is distinct from the hereditary retinal dystrophy (progressive retinal atrophy) previously described in this breed. The gene symbol Rdy has been adopted.
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Thirteen cases of iatrogenic and bilateral keratoconjunctivitis sicca following the administration of the sulphonamide salicylazosulphapyridine (sulphasalazine) for the treatment of colitis were studied. No breed, age or sex incidence was noted in this series, unlike in keratoconjunctivitis sicca cases due to other causes. The lacrimotoxic effect of sulphasalazine was permanent except in one case and it is suggested that dogs on this drug should be monitored for tear secretion at regular intervals. Reports of a similar association between keratoconjunctivitis sicca and this drug and between the disease and other sulphonamides and compounds are discussed.
Prizidilol (SK&F 92657-A2 X H2O) is the dihydrochloride salt of D,L-3-[2-(3-t-butylamino-2-hydroxypropoxy)phenyl]-6-hydrazinopyridazi ne, a molecule combining the properties of precapillary vasodilatation and beta-adrenoceptor blockade. Prizidilol was administered to baboons daily for up to 1 year at sustained doses up to 800 mg/kg. During the 16th week of a 26-week study ophthalmoscopic examination revealed an orange tinge at the periphery of the normally pale pink optic disc in all high-dose (800-1225 mg/kg) baboons. The colour became more intense as the study progressed. By week 25 orange discolouration was seen in all baboons at 350 mg/kg and three out of six baboons at 100 mg/kg. The findings, except those at 100 mg/kg, were confirmed in a 12-month study. Optic disc discolouration was correlated with darkening of internal organs at necropsy. Discolouration of the optic disc did not appear to affect visual function. Slow regression of discolouration was demonstrated after withdrawal of treatment with 800 mg of prizidilol/kg at 6 months. No histological abnormalities were present in the optic discs of affected baboons. The study demonstrates the value of regular ophthalmoscopy in toxicity studies, combining the facility for the early detection of an unusual lesion with the ability to follow its time-course.
Keratoconjunctivitis sicca is a relatively common eye disease in the dog. The presenting signs are described and the aetiology due to canine distemper, trauma and hypothyroidism mentioned. A familial incidence in the West Highland White has been demonstrated, thirty-five per cent of two hundred cases occurring in this breed and of these cases over seventy per cent occurred in the female, the majority between 4 and 7 years of age. The indications are that keratoconjunctivitis sicca may be an autoimmune disease with similarities to Sjögren's syndrome. Keratoconjunctivitis sicca in the dog has also occurred following the use of sulphasalazine for the treatment of colitis. The operation of parotid duct transposition is described and its value in the dog discussed.
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