R. B. Atwell

Feline heartworm disease: a clinical review

Feline heartworm disease is caused by the filarial nematode Dirofilaria immitis, and is transmitted by mosquitoes in heartworm-endemic areas worldwide. While dogs are the definitive hosts for this parasite, cats can also be infected, and the overall prevalence in cats is between 5% and 10% of that in dogs in any given area. The spectrum of feline presentations varies from asymptomatic infections to chronic respiratory signs, sometimes accompanied by chronic vomiting to acute death with no premonitory signs. Ante-mortem diagnosis can be challenging and relies on a combination of tests, including antigen and antibody serology, thoracic radiography and echocardiography. As treatment with heartworm adulticidal drugs can be life-threatening and heartworm infection in cats is often self-limiting, infected cats are frequently managed with supportive treatment (corticosteroids, bronchodilators, and anti-emetics). Surgical removal of filariae using extraction devices may be considered in some acute cases where immediate curative treatment is necessary, but filarial breakage during the procedure may result in an acute fatal shock-like reaction. Necropsy findings are mainly pulmonary and include muscular hypertrophy of the pulmonary arteries and arterioles on histopathology. A number of safe and effective macrocytic lactone drugs are available for prophylaxis in cats. These drugs can kill a range of larval and adult life-cycle stage heartworms, which may be advantageous in cases of owner compliance failure or when heartworm infection status is undetermined at the time prophylaxis is commenced. An index of suspicion for feline heartworm disease is warranted in unprotected cats with respiratory signs, and perhaps chronic vomiting, in areas where canine heartworm disease is endemic. Many cats, once diagnosed and with appropriate supportive care and monitoring, will resolve their infection and be free of clinical signs.

Phylogenetic and phylogeographic relationships in Ixodes holocyclus and Ixodes cornuatus (Acari: Ixodidae) inferred from COX1 and ITS2 sequences

We inferred the phylogenetic and phylogeographic relationships in ticks, which were identified morphologically as Ixodes holocyclus and Ixodes cornuatus, from mitochondrial cytochrome oxidase subunit 1 (COX1) and nuclear internal transcribed spacer 2 (ITS2) sequences. We obtained COX1 (640bp) and ITS2 (527-568bp) sequences from 429 ticks from 49 localities in Tasmania, Victoria, New South Wales and Queensland, Australia. Our analyses show that there are two species of Ixodes in eastern Australia that cause paralysis in dogs and other mammals: I. holocyclus and I. cornuatus. Further, we conclude that the morphological criteria used to differentiate female I. holocyclus and I. cornuatus are equivocal but I. holocyclus can be distinguished from I. cornuatus using COX1 and/or ITS2 sequences. Intraspecific genetic variation in I. holocyclus and I. cornuatus was less than 0.86% and 0.19% for COX1 and ITS2, respectively. Ixodes holocyclus could be genetically distinguished between different geographic ranges. There were no significant genetic differences between I.cornuatus from Tasmania and mainland Australia, but there are some COX1 haplotypes of I. cornuatus from the mainland that were not detected in Tasmanian and vice versa.

Tick paralysis in Australia caused by Ixodes holocyclus Neumann

Abstract Ticks are obligate haematophagous ectoparasites of various animals, including humans, and are abundant in temperate and tropical zones around the world. They are the most important vectors for the pathogens causing disease in livestock and second only to mosquitoes as vectors of pathogens causing human disease. Ticks are formidable arachnids, capable of not only transmitting the pathogens involved in some infectious diseases but also of inducing allergies and causing toxicoses and paralysis, with possible fatal outcomes for the host. This review focuses on tick paralysis, the role of the Australian paralysis tick Ixodes holocyclus, and the role of toxin molecules from this species in causing paralysis in the host.

Tick toxicity in cats caused by Ixodes species in Australia: a review of published literature.

Tick toxicity in cats caused by Ixodes holocyclus and related species is a common medical condition on the east coast of Australia. Intoxication typically causes a flaccid ascending neuromuscular paralysis and clinical signs can include anxiety, dysphonia, hind limb weakness and/or ataxia, pupillary dilation, respiratory signs and possible bladder voiding dysfunction. Diagnosis is made with a combination of appropriate clinical signs and visualisation of tick(s) on a thorough body search. Cases are classified clinically using a scoring system, which grades neuromuscular weakness and respiratory compromise. The mainstays of treatment are tick removal, administration of tick antitoxin serum and intensive supportive care. Given a prompt and appropriate management regimen, prognosis is good, according to available literature. Most of the literature concerning tick toxicity in cats is anecdotal in nature and an evidence-based review of what is known of this condition has not previously been published.

Tumor necrosis factor-α at presentation in 60 cases of spontaneous canine acute pancreatitis

Tumor necrosis factor-α (TNF) is a pleiotropic cytokine with profound and broad ranging effects on many cell types. There have been few publications investigating the role of TNF in spontaneous disease processes of dogs, particularly the role of this cytokine during endotoxaemia, shock and multiple organ dysfunction syndromes. Plasma samples taken at presentation from 60 dogs with spontaneous acute pancreatitis of varying severity levels (scored 0–4 in ascending severity) were assessed for TNF activity by bioassay and total TNF protein levels through a dot-blot immunoassay. TNF activity by bioassay was detected in 31% (4/13) of dogs presenting with severe disease (>50% expected mortality) as defined using a scoring system for organ compromise, and was not detectable in the remaining animals or healthy controls. TNF activity was detected in 66% (4/6) animals in the highest severity group (Score 4), these animals were showing severe multiple organ dysfunction. Total TNF protein levels, measured by dot-blot immunoassay, exhibited a wide range in all severity groups and healthy dogs. Dogs with detectable TNF activity were not distinguished from the other severity or healthy groups by immunoassay. The absence of detectable differences in total TNF protein levels between the various severity groups suggests that other factors may be crucial in determining the role of TNF in spontaneous canine acute pancreatitis and subsequent endotoxaemia and shock.

Acute death in heartworm-infected cats : Unraveling the puzzle

Although the acute death syndrome in feline heartworm disease is widely recognized, its pathogenesis remains a mystery. The most widely held hypothesis is that an acute anaphylactic reaction, perhaps precipitated by the death of the parasite, is the underlying cause. This study investigated the role of the physical form of antigen (Ag) in the ensuing reaction when Dirofilaria immitis-sensitized cats are challenged by intravenous (IV) administration of heartworm Ag. Healthy D. immitis-naive cats (n = 23) were sensitized using subcutaneous injections of adjuvanted D. immitis Ag administered weekly for 6 weeks. After sensitization, cats (n = 20) were anaesthetized and challenged with IV D. immitis Ag in various forms or with IV sterile 0.9% saline (n = 3). Systolic blood pressure, respiratory rate, degree of dyspnea, blood oxygen saturation, and heart rate were measured immediately before and at 10-15 min intervals after challenge until terminal apnea occurred or until euthanasia at 140 min after challenge. Blood samples were collected for complete blood count and measurements of serum serotonin immediately before and at 10, 20, and 35 min after challenge. Clinical observations were recorded as they occurred, or at 10-15 minute intervals, whichever was the more frequent. The most severe post-challenge reactions occurred in cats challenged with Ag from dead worms, live worms, and 20 ng/mL Ag. Dyspnea increased significantly after challenge in all three groups (p < 0.001; p = 0.04, and p = 0.002, respectively), and blood oxygen saturation dropped post-challenge in the Dead Worm (p < 0.001) and the 20 ng/mL Ag (p = 0.002) groups. In the 20 ng/mL Ag group, systolic blood pressure decreased (p <0.05) and respiratory rate increased (p < 0.05) post-challenge. Clinical observations included dyspnea, gastrointestinal signs (retching, defecation, or flatulence), urination, and less commonly, hemorrhage from the nostrils or anus, or cutaneous swelling (general or specifically facial). The 20 ng/mL Ag group had the highest rate of clinical signs, followed by the Dead Worm group. The most common and reliable hematologic change associated with severe clinical effects of D. immitis Ag challenge was increased hematocrit, which was statistically higher after challenge than at baseline in the Dead Worm group (p = 0.012). The model demonstrated that the physical form of heartworm Ag used for IV challenge in D. immitis-sensitized cats is an important factor for determining the characteristics of the post-challenge reaction, and the amount of exposed internal filarial Ag presented to the feline immune system may influence the severity of the response to challenge.

Adverse drug reactions in the treatment of filarial parasites: Haematological, biochemical, immunological and pharmacological changes in Dirofilaria immitis infected dogs treated with diethylcarbamazine

Abstract In order to understand the mechanism of the shock reaction that can occur in Dirofilaria immitis -infected dogs, following treatment with diethylcarbamazine (DEC), a variety of blood parameters were measured. A decrease in red blood cell parameters occurred in reactive dogs, followed by an increase, suggesting a possible sequestration of erythrocytes followed by peripheral vasoconstriction. Changes in leucocytes were consistent with stress reactions. Thrombocytopenia occurred, but no evidence of coagulopathy was seen. Alanine aminotransferase and creatinine phosphokinase (especially CK1 and CK3) concentrations increased suggesting cell damage and possibly liver cell necrosis, possibly due to hypoxia. Complement was not activated during the reaction and there was no increase in circulating immune complexes. No changes in plasma concentrations or histamine, 5-hydroxytryptamine, kininogen or prostaglandin F metabolite were found. Bradycardia was not caused by changes in potassium or calcium ion concentrations. These results suggest that the shock reaction is not an anaphylactic Type 1 reaction and is not caused by mast cell degranulation or by immune complex activation of mediators. The most likely cause of the reaction is that DEC causes the liberation of substances from microfilariae or adult worms which are able to constrict the hepatic vein directly or via its sympathetic innervation.

Pulmonary changes associated with dead filariae (Dirofilaria immitis) and concurrent antigenic exposure in dogs

Initially, a group of 5 dogs had their left pulmonary artery ligated 7 months prior to the insertion of filariae (Dirofilaria immitis). A second group of 3 dogs was used as controls for the various components of the experiment. Antigen (D. immitis) was injected subcutaneously on 3 occasions and necropsy was performed 5 weeks after insertion of filariae. These results were then compared to those from the control dogs. With exposure to antigen, severe pulmonary arterial and parenchymal disease was produced in association with the insertion of dead D. immitis filariae into the pulmonary artery. In the dogs receiving antigen, the arterial and peri-arterial pathology was generally more intense and at a more advanced stage of organization than in the control animals. Interstitial pneumonitis was also more prominent in the antigen-stimulated dogs. The advanced nature of the reaction was also reflected in the skin histology of the injection sites. The pathology was similar to that reported for natural dirofilariasis and it appears that most of the pathology of dirofilariasis is associated with reactions to dead filariae or filarial by-products and concurrent antigenic experience.

Surgical extraction of transplanted adult Dirofilaria immitis in cats.

A jugular venotomy technique was developed to attempt extraction of Dirofilaria immitis in cats. Seven cats were first examined by cardiac ultrasound to establish the location of adult D. immitis that had been inserted by jugular venotomy. The efficiency of an extractor catheter in surgically removing filariae similarly inserted into 13 experimental cats was then assessed. A mean extraction success rate of 96% was achieved. This technique would seem to be worthy of clinical use provided the filariae are in the right atrial area.

CARDIAC β-ADRENOCEPTOR CHANGES IN EXPERIMENTAL HYPERTHYROIDISM IN DOGS

1. Triiodothyronine (T3; 1.0 mg/kg per day subcutaneously) was administered to 10 dogs for 14 days; 10 saline‐treated dogs served as controls. T3‐treated dogs showed the expected physiological responses of hyperthyroidism; further, chronotropic responses to isoprenaline in vivo were significantly increased in T3‐treated dogs.