Heartworm disease in the dog. Report of a symposium.
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Copper and iron are involved in protection of the aerobic cell from highly toxic oxygen by-products, one of which is the superoxide anion-free radical. This protection is associated with a copper-zinc enzyme, superoxide dismutase. Increased hepatic superoxide dismutase activity correlated directly with hepatic nonheme iron, serum zinc, and serum copper concentrations and inversely with hepatic copper, hepatic zinc, and serum iron concentrations (P less than 0.001). Decrease in hepatic ceruloplasmin concentration was correlated with the decrease in hepatic copper concentration (P less than 0.001).
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Twenty-four dogs admitted for routine teeth cleaning were selected arbitrarily to undergo a periodontal examination and a dental radiographic examination before the dental procedure. Data pertaining to the physical and radiographic manifestations of periodontal disease of 783 teeth were collected. All dogs had lesions consistent with periodontal disease, ranging from mild gingivitis and minimal plaque accumulation to severely inflamed gingiva, exuberant calculus formation, and root exposure. Of the 783 teeth examined, 153 (20%) had a pocket depth greater than or equal to 4 mm and less than or equal to 9 mm. Data regarding these teeth were subjected to statistical analysis. The clinical signs of plaque, calculus, mobility, pocket depth, and furcation were positively associated with radiographic signs of periodonta disease. The association between grossly evident gingivitis and radiographic signs of periodontal disease was not significant. Conditional probability analysis was applied to determine confidence intervals for the probability of a radiographic sign of periodontal disease occurring given that a clinical sign of periodontal disease occurs.
A random epidemiological study was undertaken to estimate the prevalence of canine borreliosis (Lyme disease) in Castilla y León, the largest region in Spain. The presence of antibodies was determined by indirect immunofluorescence assay (IFA), using the Borrelia burgdorferi B31 strain as antigen. Sera from 308 dogs from 7 provinces in the region were tested. Of all the animals sampled, 37 (21%) were seropositive (titres of 1/64 or above). Almost all the provinces had seroprevalence of 20% or below, except for an important focus of borreliosis in the Zamora province (42.8%). Potential risk factors (age, sex, use, habitat, season, and presence of ticks on the animals) relating to the presence of antibodies were evaluated. Those dogs which had at some time had ticks were more often seropositive, at 24.2%, than those which had never had them, at only 6.2% (p < 10-n). No significant differences were discovered for the remaining factors studied. This work indicates that dogs in Castilla y León, even if in most cases they do not develop the disease, are exposed to the Lyme disease agent.
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Fourteen American Cocker Spaniels (ACS) with dilated cardiomyopathy (DCM) were studied to determine if individuals of this breed with DCM are systemically taurine- or carnitine-deficient and to determine if they are responsive to taurine and carnitine supplementation. American Cocker Spaniels with DCM were identified using echocardiography, and plasma was analyzed for taurine and carnitine concentrations. Each dog was randomly assigned to receive either taurine and carnitine supplementation or placebos. Echocardiograms and clinical examinations were repeated monthly for 4 months. During this period, the investigators and owners were blinded with respect to the treatment being administered. Each dog was weaned off its cardiovascular drugs (furosemide, digoxin, and an angiotensin converting enzyme inhibitor) if an echocardiographic response was identified. At the 4-month time period, each investigator was asked to decide whether he or she thought his or her patient was receiving placebo or taurine/carnitine, based on presence or absence of clinical and echocardiographic improvement. Unblinding then occurred, and dogs receiving placebos were switched to taurine and carnitine supplementation and followed monthly for 4 additional months. All dogs were reexamined 6 months after starting supplementation; survival time and cause of death were recorded for each dog. Data from 3 dogs were not included because of multiple protocol violations. Each dog had a plasma taurine concentration < 50 nmol/mL (mean +/- SD for the group 15 +/- 17 nmol/ mL) at baseline; normal range, 50-180 nmol/mL. The plasma taurine concentration did not exceed 50 nmol/mL at any time in the dogs receiving placebos (n = 5), but increased to 357 +/- 157 nmol/mL (range 140-621 nmol/mL) during taurine and carnitine supplementation (n = 11). Plasma carnitine concentration was within, only slightly below, or slightly above reported limits of normality at baseline (29 +/- 15 mumol/L); did not change during placebo administration; and increased significantly during supplementation (349 +/- 119 mumol/L; n = 11). Echocardiographic variables did not change during placebo administration. During supplementation, left ventricular end-diastolic and end-systolic diameters, and mitral valve E point-to-septal separation decreased significantly in both groups. Shortening fraction increased significantly but not into the normal range. Echocardiographic variables remained improved at 6 months. All dogs were successfully weaned off furosemide, an angiotensin converting enzyme inhibitor, and digoxin once an echocardiographic response was identified. Nine of the dogs have died since the onset of the study in 1992. One dog died of recurrence of DCM and heart failure 31 months after starting supplementation; six dogs died of noncardiac causes. Two dogs developed degenerative mitral valve disease and died of complications of this disease. Dogs less than 10 years of age lived for 46 +/- 11 months, whereas dogs older than 10 years of age lived for 14 +/- 7 months. Two of the 11 dogs were alive at the time of publication, having survived for 3.5 and 4.5 years, respectively. We conclude that ACS with DCM are taurine-deficient and are responsive to taurine and carnitine supplementation. Whereas myocardial function did not return to normal in most dogs, it did improve enough to allow discontinuation of cardiovascular drug therapy and to maintain a normal quality of life for months to years.
Eight Polled Dorset lambs were orally inoculated with Sarcocystis ovicanis sporocysts. Two lambs that received 100,000 or 200,000 sporocysts became clinically ill, recovered, and were killed 67 and 88 days after inoculation (DAI). Numerous intramuscular cysts were found in their skeletal and cardiac muscles. Three lambs received 100,000 sporocysts, three lambs received 1 million sporocysts, and three lambs received no sporocysts. After an acute clinical illness characterized by anemia, inappetence, weight loss, fever, and reduced serum protein, all lambs that received 100,000 sporocysts died 27 to 29 DAI and all that received 1 million sporocysts died 24 or 25 DAI. Hemorrhage involving the striated muscle and visceral organs was the most apparent gross lesion. The heart appeared most severely affected. Schizonts were found in vascular endothelial cells of all six inoculated lambs. Uninoculated lambs remained healthy, and neither lesions nor parasites were found in any tissues. Dogs fed tissues containing S. ovicanis cysts produced sporocytes 11 to 37 days after feeding; cats fed similar stages produced no sporocysts. Dogs fed tissues containing schizonts produced no sporocysts.