Heartworm (HW) infection is caused by a filarial organism, Dirofilaria immitis. At least 70 species of mosquitoes can serve as intermediate hosts; Aedes, Anopheles, and Culex are the most common genera acting as vectors. Patent infections are possible in numerous wild and companion animal species. Wild animal reservoirs include wolves, coyotes, foxes, California gray seals, sea lions, and raccoons. In companion animals, HW infection is diagnosed primarily in dogs and less commonly in cats and ferrets, due to diagnostic technique differences and the lifespan of the parasites in these animals. HW disease has been reported in most countries with temperate, semitropical, or tropical climates, including the USA, Canada, Australia, Latin America, and southern Europe. In companion animals, infection risk is greatest in dogs and cats housed outdoors. Although any dog or cat, indoor or outdoor, is capable of being infected, most infections are diagnosed in medium- to large-sized, 3- to 8-yr-old dogs.
Infected mosquitoes are capable of transmitting HW infections to humans, but there are no reports of such infections becoming patent. Maturation of the infective larvae may progress to the point where they reach the lungs, become encapsulated, and die. The dead larvae precipitate granulomatous reactions called “coin lesions,” which are medically significant because radiographically they appear similar to metastatic lung cancer.
HW infection rates in other companion animals such as ferrets and cats tend to parallel those in dogs in the same geographic region. No age predilection has been reported in ferrets or cats, but male cats have been reported to be more susceptible than females. Indoor and outdoor ferrets and cats can be infected. Other infections in cats, such as those caused by the feline leukemia virus or feline immunodeficiency virus, are not predisposing factors.
Mosquito vector species acquire microfilaria (a neonatal larval stage) while feeding on an infected host. Once ingested by the mosquito, development of microfilariae into the first larval stage (L1) occurs. They then actively molt into the second larval stage (L2) and again to the infective third stage (L3) within the mosquito in ~1–4 wk, depending on environmental temperatures. This development phase requires the shortest time (10–14 days) when the ambient temperature is >81°F (27°C) and the relative humidity is 80%. When mature, the infective larvae migrate to the labium of the mosquito. As the mosquito feeds, the infective larvae erupt through the tip of the labium with a small amount of hemolymph onto the host's skin. The larvae migrate into the bite wound, beginning the mammalian portion of their life cycle. A typical Aedes mosquito is only capable of surviving the complete developmental phase of small numbers of HW larvae, usually <10 larvae per mosquito.
In canids and other susceptible hosts, infective larvae (L3) molt into a fourth stage (L4) in 3–12 days. After remaining in the subcutaneous tissue, abdomen, and thorax for ~2 mo, the L4 larvae undergo their final molt at day 50–70 into young adults, arriving in the heart and pulmonary arteries ~70–120 days following initial infection. Only 2.5–4 cm in length upon arrival, worms rapidly grow in the pulmonary vasculature to adult worms (males ~15 cm in length, females ~25 cm). When juvenile heartworms first reach the lungs, blood pressure forces them into the more distal small pulmonary arteries of the caudal lung lobes; as they grow they occupy larger and larger pulmonary arteries, moving into the right ventricle and atrium when the worm burden is high. Microfilariae are produced by gravid females as early as 6 mo, but more typically at 7–9 mo postinfection.
Microfilariae are detectable in most infected canids (~80%) not receiving macrolide prophylaxis, and occasionally in those dogs placed on macrolide preventives when a heartworm infection was already present. The number of circulating microfilariae does not necessarily correlate strongly to adult female HW burden. Adults typically live 3–5 yr, while microfilariae may survive for up to 2 yr in the dog while awaiting a mosquito intermediate host.
Most dogs are highly susceptible to HW infection, and the majority (an average of 56%) of infective larvae (L3) develop into adults. Ferrets and cats are susceptible hosts, but the rate of infective larval development into adults is low (an average of 6% in cats and 40% in ferrets). In cats the adult burden is often only 1–3 worms. It appears that early death of juvenile worms on arrival at the respiratory system is largely responsible for the heartworm-associated respiratory disease syndrome in cats. Adult worm survival in cats is typically not longer than 2–3 yr. In all animals capable of being infected, aberrant larval migration may occur, resulting in lesions in the brain, systemic vascular system, and at visceral and subcutaneous sites.
The severity of cardio-pulmonary pathology in dogs is determined by worm numbers, host immune response, duration of infection, and host activity level. Live adult HW cause direct mechanical irritation of the intima and pulmonary arterial walls, leading to proliferative endarteritis, perivascular cuffing with inflammatory cells, including infiltration of high numbers of eosinophils. Live worms seem to have an immunosuppressive effect; however the presence of dead worms leads to immune reactions and subsequent lung pathology in areas of the lung not directly associated with the dead HW. Longterm infections, due to all of the factors noted (ie, direct irritation, worm death, and immune response) result in chronic lesions and subsequent scarring. Active dogs tend to develop more pathology than inactive dogs for any given worm burden. Frequent exertion increases pulmonary arterial pathology and may precipitate overt clinical signs, including congestive heart failure (CHF). High worm burdens are most often the result of infections acquired from numerous mosquito exposures. High exposures in young, naive dogs in temperate climates can result in severe infections, causing a vena caval syndrome the following year. In general, due to the worm size and smaller dimensions of the pulmonary vasculature, small dogs do not tolerate infections and treatment as well as large dogs.
The role of the endosymbiotic bacteria Wolbachia pipiens, which lives inside the worms, is still being determined. However, these bacteria have been implicated in the pathogenesis of filarial diseases, possibly through endotoxins. Recent studies have demonstrated that a primary surface protein of Wolbachia (WSP), induces a specific IgG response in hosts infected by D immitis.
HW-associated inflammatory mediators that induce immune responses in the lungs and kidneys (immune complex glomerulonephritis) cause vasoconstriction and possibly bronchoconstriction. Leakage of plasma and inflammatory mediators from small vessels and capillaries causes parenchymal lung inflammation and edema. Pulmonary arterial constriction causes increased flow velocity, especially with exertion, and resultant shear stresses further damage the endothelium. The process of endothelial damage, vasoconstriction, increased flow velocity, and local ischemia is a vicious cycle. Inflammation with ischemia can result in irreversible interstitial fibrosis.
Pulmonary arterial pathology in cats and ferrets is similar to that in dogs, although the small arteries develop more severe muscular hypertrophy. Some cats may never show clinical signs. Arterial thrombosis is caused by both blood clots and worms lodged within narrow lumen arterioles. In cats, parenchymal changes associated with dead HW differ from those observed in dogs and ferrets. Rather than type I cellular edema and damage as found in dogs, cats have type II cellular hyperplasia, which causes a significant barrier to oxygenation. Most significantly, due to restricted pulmonary vascular capacity and subsequent pathology, both ferrets and cats are more likely to die as a result of HW infection.
In dogs, infection should be identified by serologic testing prior to the onset of clinical signs; however, it should be kept in mind that at the earliest, HW antigenemia and microfilaremia do not appear until ~5 and 6.5 mo post-infection, respectively. When dogs are not administered a preventive and are not appropriately tested, infection can occur. Clinical signs of heartworm infection, such as coughing, exercise intolerance, unthriftiness, dyspnea, cyanosis, hemoptysis, syncope, epistaxis, and ascites (right-sided CHF) may develop. The frequency and severity of clinical signs correlate to lung pathology and level of patient activity. Signs are often not observed in sedentary dogs, even though the worm burden may be relatively high. Infected dogs experiencing a dramatic increase in activity, such as during hunting seasons, may develop overt clinical signs.
Dogs can be clinically classified as low- or high-risk patients based on clinical assessments of potential worm burden, the health of the dog, and its lifestyle. This replaces a more complex system in which dogs were classified from I to IV. Dogs 5–7 yr old are at higher risk of having a heavy worm burden. Other concurrent health factors (eg, existing pulmonary or organ system disease) affect risk assessment. The degree to which exercise can be restricted during the recovery period is another important factor to consider.
Infected cats may be asymptomatic or exhibit intermittent coughing, dyspnea, vomiting, lethargy, anorexia, or weight loss. When evident, signs usually develop during 2 stages of the infection: 1) the arrival of juvenile worms in the pulmonary vasculature ~3–4 mo postinfection, and 2) death of adult heartworms. The early signs are associated with an acute vascular and parenchymal inflammatory response to the newly arriving young worms and the subsequent death of many of these juveniles. This initial phase is often misdiagnosed as asthma or allergic bronchitis. However, this is now considered to be part of a newly recognized syndrome called heartworm-associated respiratory disease. Antigen tests in cats are negative during the early eosinophilic pneumonitis syndrome, although antibody tests may be positive. Subsequently, clinical signs often resolve and may not reappear for months. Cats harboring mature worms may exhibit intermittent vomiting, lethargy, coughing, or episodic dyspnea. Death of even 1 adult HW can lead to acute respiratory distress and shock, which may be fatal and appear to be the consequence of pulmonary thrombosis and/or anaphylactic shock.
The antigen detection test is the preferred diagnostic method for asymptomatic dogs or when seeking verification of a suspected HW infection. Antigen testing is the most sensitive and specific diagnostic method available to veterinary practitioners. Even in areas where the prevalence of HW infection is high, ~20% of infected dogs may not be microfilaremic. This figure is higher for adult heartworm-infected dogs consistently administered monthly macrolide prophylaxis, as this induces embryo stasis in mature female dirofilariae.
Timing of antigen testing is critical. A pre-detection period must be added (these tests only detect adult worms) to the approximate date on which infection may have been possible. A reasonable interval is 7 mo following possible exposure. There is generally no value in testing a dog for antigen or microfilariae prior to ~7 mo of age. To ensure that a previously acquired infection does not exist, young dogs or dogs not previously on heartworm prophylaxis should be tested 6–7 mo after beginning heartworm prophylaxis. Subsequently, annual antigen detection tests are recommended.
The level of antigenemia is directly related to the number of mature female worms present. At least 90% of dogs harboring ≥2 adult females will test positive with most available tests. For low-burden suspects, commercial laboratory-based microwell titer tests are the most sensitive.
In dogs, echocardiography is relatively unimportant as a diagnostic tool. Worms observed in the right heart and vena cava are associated with high-burden infection with or without caval syndrome. Severe, chronic pulmonary hypertension causes right ventricular hypertrophy, septal flattening, underloading of the left heart, and high-velocity tricuspid and pulmonic regurgitation. The ECG of infected dogs is usually normal. Right ventricular hypertrophy patterns are seen when there is severe, chronic pulmonary hypertension and are associated with overt or impending right-sided CHF (ascites). Heart rhythm disturbances are usually absent or mild, but atrial fibrillation is an occasional complication in dogs.
The diagnosis of HW disease in cats is based on historical and physical findings, index of suspicion, thoracic radiographs, echocardiography, and serology. Cats may develop a positive antigen test 8 mo post L3 inoculation. However, antigen tests alone are considered too unreliable as the initial screening test for cats because unisex infections are common in cats, light infections may occur with insufficient numbers of mature females to be detectable, and some cats may become ill with heartworm-associated respiratory disease and be tested before a detectable antigenemia develops.
Antiheartworm antibodies, produced by 90% of infected cats, may first appear 2–3 mo post L3 infection and are usually present by 5 mo. However, antibodies can persist for several months following worm death. Also, antibodies induced by larvae can persist after macrolide prophylaxis has been instituted and has killed the early larval stages. Thus, a positive antibody test is an indication of infection by the parasite and suggestive of heartworm-associated respiratory disease but not necessarily of persistent or continuing infection. In conjunction with other provocative findings, antibody seropositivity may be useful in making a clinical diagnosis of feline heartworm disease. False-positive results from cross-reactivity have not been observed. A negative antibody test indicates ≥90% probability of the absence of infection. Microfilariae are rarely detected by Knott's tests (<10%). An annual screening using both antigen and antibody detection tests for cats is recommended in HW-endemic areas.
In cats, worms can often be imaged on echocardiography. Parallel hyperechoic lines, which are an image from the heartworm cuticle, may be seen in the right heart and pulmonary arteries. High worm burdens may be associated with worms in the right heart. Echocardiography is more important in cats than dogs because of the increased difficulty of diagnosis and the high sensitivity of the test in experienced hands.
In addition to special diagnostic tests in both cats and dogs, a CBC, chemistry profile, urinalysis, and particularly thoracic radiographs are indicated. Laboratory data are often normal. Eosinophilia and basophilia are common and together suggest occult dirofilariasis or allergic lung disease. Eosinophilia surges as the L5 arrive in the pulmonary arteries. Subsequently, eosinophil counts vary but are usually high in dogs with immune-mediated occult infections, especially if eosinophilic pneumonitis develops (<10% of total infections).
Hyperglobulinemia may be present in dogs and cats due to antigenic stimulation. Hypoalbuminemia in dogs is associated with severe immune-complex glomerulonephritis or right-sided CHF. Serum ALT and alkaline phosphatase are occasionally increased, but do not correlate well with abnormal liver function, efficacy of adulticide treatment, or risk of drug toxicity. Urinalysis may reveal proteinuria that can be semiquantitated by a urine protein:creatinine ratio. Occasionally, severe glomerulonephritis or amyloidosis can lead to hypoalbuminemia and nephrotic syndrome. Dogs with hypoalbuminemia secondary to glomerular disease also lose antithrombin III and are at risk for thromboembolic disease. Hemoglobinuria is associated with high-risk clinical cases and occurs when RBC are lysed in the pulmonary circulation by fibrin deposition. Heparin therapy (75–100 U/kg, SC, tid) is indicated. Hemoglobinuria is also a classic sign of the vena caval syndrome.
In dogs, thoracic radiography provides the most information on disease severity and is a necessary screening tool for assessing the clinical status of dogs with dirofilariasis. High-risk infections are characterized by a large main pulmonary artery segment and dilated, tortuous caudal lobar pulmonary arteries. If the latter are ≥1.5 times the diameter of the 9th rib at their point of superimposition, then severe pathology is present. Right ventricular enlargement may also be seen. Fluffy, ill-defined parenchymal infiltrates of variable extent often surround the caudal lobar arteries, usually worst in the right caudal lobe, in advanced disease. The infiltrate may improve with cage confinement with or without anti-inflammatory dosages of a corticosteroid.
In cats, cardiac changes are less common. The caudal lobar arteries normally appear relatively large, but are larger still with heartworm infection. Patchy parenchymal infiltrates may also be present in cats with respiratory signs. The main pulmonary artery segment usually is not visible due to its relatively midline location.
Treatment in Dogs
The extent of the preadulticide evaluation will vary depending on the clinical status of the patient and the likelihood of coexisting diseases that may affect the outcome of treatment. Clinical laboratory data should be collected selectively to complement information obtained from a thorough history, physical examination, antigen test, and thoracic radiography.
Two important variables known to directly influence the probability of post-adulticide thromboembolic complications and the outcome of treatment are the extent of concurrent pulmonary vascular disease and the severity of infection. Assessment of cardiopulmonary status is indispensable for evaluating a patient's prognosis. Post-adulticide pulmonary thromboembolic complications are most likely to occur in heavily infected dogs already exhibiting clinical and radiographic signs of severe pulmonary arterial vascular obstruction, especially if CHF is present.
Prior to starting adulticide therapy, HW-infected dogs must be assessed and rated for risk of post-adulticide thromboembolism. Patients can be categorized as follows: 1) low risk of thromboembolic complications, light worm burden, and no evidence of parenchymal and/or pulmonary vascular lesions; or 2) high risk of thromboembolic complications. Dogs in the first category must fulfill all the following conditions: no clinical signs, normal thoracic radiographs, a low level of circulating antigen or a negative antigen test with circulating microfilariae, no worms visualized by echocardiography, no concurrent disease, and the owners are capable of completely restricting exercise. Dogs at high risk of thromboembolic complications include those with signs related to HW infection (eg, coughing, lipothymia, swelling of the abdomen), abnormal thoracic radiographs, high level of circulating antigens, worms visualized by echocardiography, concurrent disease, and low or no possibility that the owners will restrict exercise.
The only available heartworm adulticide is melarsomine dihydrochloride, which is effective against mature (adult) and immature heartworms of both genders. Melarsomine is given at 2.5 mg/kg, deep IM in the belly of the epaxial (lumbar) musculature in the L3–L5 region using a 22 g needle (1 in. long for dogs <10 kg or 1.5 in. for dogs >10 kg). Pressure is applied during delivery and maintained for 1 min after the needle is withdrawn to prevent SC leakage. In standard use, the procedure is repeated on the opposite side 24 hr later. Approximately one-third of dogs will exhibit local pain, swelling, soreness with movement, or sterile abscessation at the injection site. Local fibrosis is not uncommon (and is the reason for targeting the belly of the epaxial musculature). To reduce the danger of thromboembolism, a 2-phase treatment (alternate dosing regimen) is highly recommended. In this protocol, a single injection of melarsomine is given, followed by 2 injections 24 hr apart after an interval of at least 30 days. This alternate dosing regime is recommended by the American Heartworm Society regardless of the stage of the disease or the risk category.
Dogs with high worm burdens are at risk of severe pulmonary thromboembolism from several days to 6 wk post-adulticide. Administration of a single initial dose results in a graded (~50%) worm kill and reduced pulmonary complications. By initially killing few worms and completing the treatment in 2 stages, the cumulative impact of worm emboli on severely diseased pulmonary arteries and lungs can be reduced.
Other treatment protocols recommend the administration of prophylactic doses of macrolides for 3 mo prior to administration of melarsomine. The rationale for this approach is to eliminate susceptible migrating D immitis larvae, and allow nonsusceptible larvae 2–4 mo old to develop to an age at which they are more susceptible to melarsomine.
Following melarsomine injection, exercise must be severely restricted for 4–6 wk to minimize thromboembolic lung complications. A low cardiac output should be maintained in order to reduce thrombosis and endothelial damage and facilitate lung repair. Adverse effects of melarsomine are otherwise limited to local inflammation, brief low-grade fever, and salivation. Hepatic and renal toxicity are seldom seen.
High-risk patients should be stabilized prior to melarsomine administration. Stabilizing treatment variably includes cage confinement, oxygen, corticosteroids, and heparin (75–100 U/kg, SC, tid) for 1 wk prior to the alternate melarsomine treatment protocol.
Patients with right-sided CHF should be treated with furosemide (1–2 mg/kg, bid), a low-dose angiotensin-converting enzyme (ACE) inhibitor such as enalapril (0.25 mg/kg, bid, possibly increased to 0.5 mg/kg, bid after 1 wk pending renal function test results), and a restricted sodium diet. Digoxin, digitoxin, and arteriolar dilators, such as hydralazine and amlodipine, should not be administered. Digoxin is not effective for cor pulmonale; arteriolar dilators, and occasionally even ACE inhibitors, are likely to cause systemic hypotension.
Thromboembolic complications can occur 2–30 days after adulticide treatment, with signs most likely 14–21 days after treatment. Clinical signs are coughing, hemoptysis, dyspnea, tachypnea, lethargy, anorexia, and fever. Laboratory findings may include an inflammatory leukogram, thrombocytopenia, and prolonged activated clotting time or prothrombin time. A postinjection increase in serum CK may be noted. Local or disseminated intravascular coagulopathy may occur when platelet counts are <100,000/μL. Treatment for severe thromboembolism should include oxygen, cage confinement, a corticosteroid at an anti-inflammatory dosage (eg, prednisone at 1.0 mg/kg, PO, sid), and low-dose heparin (75–100 U/kg, SC, tid) for several days to 1 wk. Most dogs respond within 24 hr. Severe lung injury is likely if, after 24 hr of oxygen therapy, no improvement is noted and partial pressures of oxygen remain <70 mm Hg.
The standard melarsomine protocol and the 2-phase treatment regimen kill most adult worms in 50–85% of dogs. Controlled-study efficacy against younger, worms (4 mo), was lower, resulting in only 20% of dogs being effectively cleared of infection. Antigen testing should be performed 6 mo after the first 2 doses of the standard protocol and 6 mo after the third dose of the alternate protocol. A positive test result should be followed by retreatment (2 injections, 24 hr apart).
Longterm use of macrolides is seldom a substitute for melarsomine treatment because the slow kill may allow pulmonary pathology to progress in the interim.
In caval syndrome cases, surgical removal of worms from the right atrium and orifice of the tricuspid valve is typically necessary to save the life of the dog. This may be accomplished by using light sedation, local anesthesia and either a rigid or flexible alligator forceps, or an intravascular retrieval snare, introduced preferentially via the right external jugular vein. With fluoroscopic guidance, if available, the instrument should continue to be passed until worms can no longer be retrieved. Immediately following a successful operation, the clinical signs should lessen or disappear. Fluid therapy may be necessary in critically ill, hypovolemic dogs to restore hemodynamic and renal function. Within a few weeks following recovery from surgery, adulticide chemotherapy is recommended to eliminate any remaining worms. Particular care should be taken if many worms are still visible echocardiographically.
At specific preventive dosages, the macrolide preventive drugs are effective microfilaricides, although not approved by the FDA for this purpose. Adverse reactions may occur in dogs with high microfilarial counts (>40,000/μL), depending on the type of macrolide given. However, the microfilarial count is usually lower, and mild adverse reactions occur in ~10% of dogs. Most adverse reactions are limited to brief salivation and defecation, occurring within hours and lasting up to several hours. Dogs, especially small dogs (<10 kg), with high microfilarial counts (>40,000/μL) may develop tachycardia, tachypnea, pale mucous membranes, lethargy, retching, diarrhea, and even shock. Treatment includes IV balanced electrolyte solution and a soluble corticosteroid. Recovery is usually rapid when treatment is administered quickly. Microfilarial counts are not routinely performed, and thus severe reactions are seldom expected. Treatment specifically targeting circulating microfilariae may be started as early as 3–4 wk following adulticide administration. More commonly, microfilariae are eventually eliminated, even from non-adulticide-treated dogs, after several months of treatment with prophylactic doses of the macrocyclic lactones. As mentioned, no microfilaricides are approved by the FDA; however, licensed veterinarians are permitted extra-label use of certain drugs if a valid veterinarian-client-patient relationship exists. The use of monthly administered HW chemoprophylactics as microfilaricides is governed by this regulation. The macrocyclic lactones are the safest and most effective microfilaricidal drugs available. Livestock preparations of these drugs should not be used to achieve higher doses for the purpose of obtaining more rapid results. Performance of a microfilariae test is recommended at the time the antigen test is performed (6 mo after the adulticide treatment).
Treatment in Cats
There is currently no satisfactory treatment approach to heartworm infections in cats. Infection often is lethal, and a safe and effective melarsomine protocol has not yet been developed. Thus, all cats in canine HW-endemic regions should receive drug prophylaxis. The adult heartworm lifespan in cats is probably ≤2 yr, so spontaneous recovery is possible. Cats may remain asymptomatic, experience episodic vomiting and/or episodic dyspnea (resembling asthma), may die suddenly from pulmonary thromboembolism, or rarely, develop CHF. With each worm death, pulmonary complications occur. There does not appear to be an association between the presence, absence, or severity of clinical signs and the likelihood of acute complications.
Many cats are managed conservatively with restricted activity and corticosteroid therapy, such as prednisolone (1.0–2.0 mg/kg, PO, every 24–48 hr). Steroids reduce the severity of vomiting and respiratory signs. The hope is that episodes of pulmonary complications will not prove fatal as the worms die. Barring superinfection, 25–50% of cats may survive with this approach. Serial antigen and antibody testing (at 6-mo intervals) can be used to monitor status.
Surgical retrieval of worms from the right atrium, right ventricle, and vena cavae via jugular venotomy can be attempted in patients with high worm burdens detected by echocardiography. An endoscopic basket or horsehair brush can be advanced via the right jugular vein under fluoroscopy.
Heartworm infection is completely preventable with macrolide prophylaxis. Year-round prevention is advised. Preventive therapy in dogs is recommended beginning at 6–8 wk of age. No testing is necessary at this age. When started after 7 mo of age, an antigen test and a test for presence of microfilariae is recommended, followed by another antigen test 6–7 mo later. This series of tests will help to avoid unnecessary delay in detecting subclinical infections, as well as potential confusion concerning effectiveness of the preventive program, since it cannot be determined until the second test whether infection existed prior to beginning chemoprophylaxis.
Formulations of the macrolide preventives ivermectin, milbemycin oxime, moxidectin, and selamectin are safe and effective as prescribed for all breeds of dogs. Ivermectin/pyrantel pamoate (hookworms and roundworms) and milbemycin (hookworms, roundworms, and whipworms) also provide control of intestinal nematodes. At the approved dose, milbemycin kills microfilariae quickly, and in the face of high microfilarial concentrations a shock reaction may occur. Thus, milbemycin should not be administered without close monitoring as a preventive in dogs with high numbers of microfilariae. The injectable form of moxidectin is effective for at least 6 mo following 1 injection, but use in microfilaremic dogs is not advised.
Heartworm prevention is recommended for all cats in endemic regions, regardless of housing status, because of the potential for severe consequences. Ivermectin for cats is safe and effective at 24 μg/kg, PO, once monthly. At this dosage, the formulation is also effective against Ancylostoma tubaeforme and A braziliense. Preventive treatment should be initiated in kittens at 6 wk of age and continued lifelong.
Formulations of selamectin and a combination of imidacloprid/moxidectin are labeled for both dogs and cats. Selamectin is administered topically at a monthly dosage of ~6 mg/kg and also kills adult fleas and prevents flea eggs from hatching for 1 mo. It also is indicated for the treatment and control of Otodectes cynotis in dogs and cats, sarcoptic mange, Dermacentor variabilis infestations in dogs, Ancylostoma tubaeforme, and Toxocara cati in cats. A topical combined formulation of imidacloprid and moxidectin administered at dosages of 10 mg/kg imidacloprid and 1 mg/kg moxidectin is also effective against a series of ecto- and endoparasites.
Annual antigen testing is recommended in all cases.
Last full review/revision May 2012 by Jorge Guerrero, DVM, PhD, DEVPC (Ret)