Membrana nictitans gland cyst in a dog

A cyst involving the gland of the 3rd eyelid was removed from an 8-year-old dog. Clinically the circumscribed mass resembled a pigmented neoplasm. Histologically the cyst was multiloculated, with homogeneous eosinophilic periodic acid-Schiff-positive content. Melanin pigment was present in epithelial cells and cystic lumens. Protective functions of the 3rd eyelid were retained following excisional biopsy.     

Fenbendazole treatment of pregnant bitches to reduce prenatal and lactogenic infections of Toxocara canis and Ancylostoma caninum in pups

A granulated formulation of fenbendazole was tested in a total of 23 treated and control, pregnant, parasite-free Beagle bitches experimentally infected with Toxocara canis and Ancylostoma caninum. The drug was administered to each treated bitch once daily in canned dog food at a dosage of 50 mg/kg body weight. Each of 2 treatment regimens tested was initiated on the 40th day of pregnancy. One regimen involved daily treatment continuing through the 14th postpartum day, and it resulted in 89% fewer ascarids and 99% fewer hookworms in pups born to medicated bitches, as compared with pups born to unmedicated controls. The other regimen of treatment, which was stopped on the day of parturition, was less effective in reducing ascarid and hookworm burdens (64% and 88% reductions, respectively). Three to 5 bitches from each of the treatment and control groups were allowed to whelp a 2nd litter without further treatment or further exposure to parasite infections. Hookworm burdens in 2nd-litter pups born of bitches that had initially received fenbendazole through the 14th postpartum day were significantly lower (P < 0.01; 85% reduction), when compared with the 2nd-litter control pups. All other parasite burdens were not significantly different. It was concluded that granulated fenbendazole is effective in reducing burdens of Ancylostoma caninum and Toxocara canis in newborn pups when the bitch is treated during the last third of pregnancy, especially when treatment (50 mg/kg/day) extends from the 40th day of pregnancy through the 14th postpartum day.     

Comparison of plasma aldosterone concentration among clinical status groups of dogs with chronic heart failure

The plasma aldosterone concentration (PAC) among clinical status groups of 23 dogs with chronic heart failure was compared at various times after diagnosis of the problem. Eighteen dogs admitted in New York Heart Association (NYHA) class IV clinical status had significant elevations in PAC (P<0.0001), when compared with clinically normal dogs. Five dogs admitted in NYHA class III status and 4 dogs that responded with a change to NYHA class III status had significant elevations in PAC (P<0.01), when compared with clinically normal dogs. In patients with NYHA class IV status, the PAC was significantly greater (P<0.01) than in patients in NYHA class III status. For patients with the poorest prognosis, ie, severe signs of NYHA class IV status, the PAC was not markedly different, when compared with that for patients with a favorable prognosis, ie, recent onset of signs of NYHA class IV status. Patients treated with captopril had significantly lower PAC after therapy (P<0.01), whereas patients treated with hydralazine had significantly higher PAC (P<0.05) after therapy. It was concluded that heart failure in the dog increases PAC, most likely because of renin-angiotensin-aldosterone-system activation, and that the increase is related directly to the clinical status of the patient. Further, it was concluded that treatment of dogs in heart failure with captopril causes a decrease in circulating PAC, whereas treatment with hydralazine causes an increase in circulating PAC.     

Cutaneous onchocerciasis in the horse: five cases in southwestern british columbia

Five horses were presented because of a dermatitis of the forehead. Unlike previous reports, ventral midline dermatitis was not the major problem, and was present in only two of five cases. All five horses responded to levamisole therapy at a daily dosage of 5.5 g for one week. Owners were cautioned that repeat therapy may be necessary.     

Equine herpesvirus abortion in Australia 1977 to 1982

Until 1977 no case of abortion caused by equine herpesvirus 1 (EHV1) had been recorded in Australia although the virus, called equine rhinopneumonitis virus, had been known to have been present at least since 1962. Outbreaks of EHV1 abortion occurred in New South Wales in 1977 and in 1981. Sporadic cases of EHV1 abortion had been confirmed in some parts of Australia each year since 1975. It was concluded that an abortigenic subtype of EHV1 had been introduced to Australia in 1977 and that the previously endemic respiratory subtype occasionally caused abortion. Virus isolation in a variety of cell cultures and histopathological examination of tissue were shown to be satisfactory methods of diagnosis of EHV1 abortion. Lung proved to be the specimen of choice. Slight serological differences between "abortigenic" and "respiratory" subtypes of EHV1 were found in cross neutralisation tests. A serological survey of 219 Sydney horses of various ages revealed that most yearlings had already acquired neutralising antibody to both subtypes.     

The genetic control of antibody formation

Studies of the molecular biology of lymphoid cells have markedly increased our understanding of how millions of different antibodies can be synthesized by a single animal. To date, the most detailed understanding has been achieved for the mouse, primarily because of the relatively greater experimental availability of this species. These studies, as well as those involving other species, have shown that the complete genes for antibody polypeptide chains are assembled from disparate genetic elements which are originally widely separated in the genome. The assembly process itself, together with the coding information present in the germ line genetic elements, contributes to the diversity of structure (and thus combining specificities) shown by mature antibody molecules. Specifically, the diversity of structure characteristic of antibody variable regions is due to three distinct mechanisms: innate variability of germ line genes; mismatching of individual gene segments during their somatic rearrangement leading to junctional diversity; and somatic mutation in variable region genetic material during or after the rearrangement. These processes lead to the wide array of combining specificities that permit the humoral immune system of a mature animal to interact with essentially any non-self antigen which it encounters. Complex genetic rearrangements are also responsible for the class switching phenomenon long known to be characteristic of the humoral immune response. A form of homologous recombination between constant region genes, possibly mediated by specific "switching" enzymes, is now believed to be involved in this phenomenon. It is also currently believed that the restriction of gene rearrangement processes to one of the two possible chromosomes of a diploid pair in each cell is responsible for the phenomenon of allelic exclusion that has long been associated with the normal functioning of mammalian B-cells.