No full-text available
To read the full-text of this research,
you can request a copy directly from the author.
Abstract
A three-year-old male neutered British Shorthair cat was treated for tick paralysis caused by L holocyclus. Ten days after discharge, the cat represented with left-sided congestive heart failure and was diagnosed with hypertrophic cardiomyopathy, characterised by diastolic dysfunction. It has been proposed that tick toxicity is associated with diastolic dysfunction and it is possible that residual toxin effects were a contributing factor to the development of left-sided congestive heart failure in this case.
ResearchGate has not been able to resolve any citations for this publication.
Serum growth hormone concentration was measured by radioimmunoassay in 31 cats with hypertrophic cardiomyopathy, 38 normal cats, and 35 cats with other cardiac disease. Cats with hypertrophic cardiomyopathy had a significantly increased serum growth hormone concentration when compared with normal cats and cats with other cardiac disease. The serum growth hormone concentration in cats with hypertrophic cardiomyopathy was less than that previously reported in cats with growth hormone secreting pituitary tumors. Pituitary tumors were not identified in eight of the cats with hypertrophic cardiomyopathy examined at necropsy. An increased serum growth hormone concentration may be measured in cats with hypertrophic cardiomyopathy but it is unclear if the increased serum growth hormone concentration is a cause or effect of hypertrophic cardiomyopathy.
Feline hypertrophic cardiomyopathy (HCM) is characterized by varying degrees and patterns of hypertrophy of the left ventricle. Compromise of the left ventricular chamber size along with some degree of impaired diastolic relaxation results in a reduction of ventricular filling, which can impair forward cardiac output. The myocardium may suffer ischemic injury often caused by abnormal coronary perfusion as well as excess oxygen consumption secondary to severe hypertrophy and tachyarrhythmias. In addition to diastolic dysfunction, feline HCM may be accompanied by systolic abnormalities, usually in the form of outflow obstruction. Physical examination, thoracic radiography, electrocardiography, and echocardiography are important tools in the diagnostic evaluation of HCM.
Tick paralysis caused by Ixodes holocyclus affects an estimated 20,000 domestic animals each year along the eastern coast of Australia (Stone 1988). Animals are presented with clinical signs ranging from mild paresis to ascending flaccid paralysis and varying degrees of respiratory and cardiac compromise. Mortality rates are significantly increased in animals presented with respiratory compromise compared to those animals without respiratory compromise, regardless of the degree of flaccid paralysis (Atwell et al 2001). Anecdotal evidence of ticks (collected from different sites in northern New South Wales) causing different clinical signs and mortality in hyper-immune dogs used for serum production, suggests that there may be a variation in toxin production and toxin content between individual ticks (Warne, N 2002 pers comm). This literature review suggests that two possible contributing factors to toxin variation may be the genetic variation within the I. holocyclus species and the variation in the host's response to tick feeding.
Under laboratory conditions 8 dogs were infested with Ixodes holocyclus and the clinical signs and histological findings were recorded. Seven of the dogs developed clinical signs of the disease, died and were subjected to a post-mortem examination, while the eighth dog remained normal. The clinical signs were consistent between animals and enabled the course of the disease to be subdivided into 5 stages to facilitate analysis of data in future experiments. The most prominent feature of the disease was dysfunction of the efferent motor system although some disturbance of the afferent pathways and involvement of the autonomic nervous system did occur. The period elapsing between attachment of the ticks and onset of signs varied from 5.5 to 7 days, while the mean duration of the disease was 23.3 h. The histopathology demonstrated moderate to severe congestion of the liver, kidney and lungs, and in some lung sections pulmonary oedema was present.
Hypertrophic cardiomyopathy (HCM) is the most common form of feline heart disease. Affected cats have concentrical or asymmetrical left ventricular hypertrophy without an identifiable cause. Although many diseases can cause concentrical left ventricular hypertrophy, the term hypertrophic cardiomyopathy is used here exclusively to refer to the idiopathic disease.
A litter of five, 18-month-old, mixed-breed cats were determined to have hypertrophic cardiomyopathy (HCM). Although no overt clinical signs were present in any cat, systolic heart murmurs were present in each. Electrocardiograms were normal, while subjective interpretations of heart enlargement on radiographs were made on four cats. Echocardiographic analyses indicated abnormalities consistent with HCM. Overt clinical signs are absent two years following diagnosis.
To determine current population characteristics of, clinical findings in, and survival times for cats with hypertrophic cardiomyopathy (HCM).
Retrospective study.
260 cats with HCM.
Information was obtained from the medical records. Cats were classified into 1 of 4 clinical groups (congestive heart failure [CHF] group, arterial thromboembolism [ATE] group, syncope group, or cats without clinical signs [subclinical group]) on the basis of the primary clinical signs at the initial examination.
120 cats were classified in the CHF group, 43 in the ATE group, 10 in the syncope group, and 87 in the subclinical group. Antecedent events that may have precipitated CHF included i.v. fluid administration, anesthesia, surgery, and recent corticosteroid administration. Median survival time was 709 days (range, 2 to 4,418 days) for cats that survived > 24 hours. Cats in the subclinical group lived the longest (median survival time, 1,129 days; range, 2 to 3,778 days), followed by cats in the syncope group (654 days; range, 28 to 1,505 days), cats in the CHF group (563 days; range, 2 to 4,418 days), and cats in the ATE group (184 days; range, 2 to 2,278 days). Causes of death included ATE (n = 56), CHF (49), sudden death (13), and noncardiac causes (27). In univariate analyses, survival time was negatively correlated with left atrial size, age, right ventricular enlargement, and thoracentesis. Cats with systolic anterior motion of the mitral valve lived longer than cats without this echocardiographic finding. In multivariate analyses, only age and left atrial size remained significant predictors of survival time.
Although overall survival time for cats with HCM was similar to earlier reports, survival times for cats with CHF or ATE were longer than previously reported.