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Heartworm for Dog Last updated: 2016-10-01

Synopsis

CAPC Recommends

 

  • Annual testing of all dogs for both antigen and microfilariae of heartworm. 

  • Protect all dogs from heartworm infection by using preventives year round.  

  • Treat infected dogs with labeled adulticides and microfilaricides (if microfilaria are present) as soon after diagnosis as medically practical. 

Life Cycle and Stages


  • Microfilariae reside in the blood of most, but not all, infected canids. 
  • Microfilariae (300-322 µm x 6.8-7.0 µm) are ingested by feeding female mosquitoes. After two molts (approximately 2 weeks), infective third-stage larvae (L3s) are present in mosquito mouth parts. Development may be slower at cooler temperatures and ceases at temperatures below 57°F. Development progresses in the mosquito relative to ambient temperature; if ambient temperature increases, development will resume. 
  • L3s (1,000 µm x 40 µm) are deposited on the skin of the dog during subsequent feeding and migrate through the bite wound into the host. Most L3s molt to fourth-stage larvae (L4s) in canine subcutaneous tissues within 1-3 days after infection. 
  • L4s migrate through tissues for several weeks. 
  • A final molt to the sexually immature adult stage occurs approximately 2 months (50 to 70 days) after infection. 
  • The young adults (2-3 cm in length) enter the vascular system and are carried to the heart and pulmonary arteries, arriving as early as 70 days after infection. Final maturation and mating occurs in the pulmonary vessels. By 4 months after infection, the worms in the pulmonary arteries are around 10-15 cm in length.  Fully mature adults at 6.5 months after infection reach lengths of 15-18 cm (5-6 in) for males and 25-30 cm (10-12 in) for females. 
  • Canine hosts typically demonstrate microfilaremia 6 to 7 months after infection. 
  • Heartworms live approximately 5 to 7 years in the dog. 
800X600 Heartworm Canine Life Cycle

Heartworm Life Cycle

Disease

  • Heartworm infection in the dog induces pulmonary endothelial damage, villous proliferation, and activation and attraction of leukocytes and platelets due to live worms as well as thrombosis, granulomatous, and villous inflammation due to dead and/or dying worms. 
  • Pulmonary vessels may become thickened and tortuous. 
  • Cardiac output may be reduced. Pulmonary hypertension may lead to compensatory right heart enlargement and right heart failure. Clinical signs include cough, dyspnea, weight loss, ascites, jugular venous distension, exercise intolerance, and arrhythmias. 
  • Heartworm infection may induce glomerulonephritis and proteinuria secondary to antigen-antibody complex deposition. 
  • Rarely, ectopic infections of the eye, central nervous system, peritoneal cavity, systemic circulation, or skin have been reported. 
  • Caval syndrome occurs in a small number of cases, typically associated with large numbers of adults in the pulmonary arteries 
    • Worms may be found in the post cava and right atrium, causing interference with tricuspid valve function. This results in a peracute life-threatening hemolytic anemia and right heart failure. 
    • Associated findings include: 
      • pallor, weak pulses, tachycardia, and sudden collapse 
      • hemoglobinemia and hemoglobinuria 
      • disseminated intravascular coagulopathy  
      • murmur caused by tricuspid regurgitation auscultated best on right side of thorax

Prevalence

  • Surveys indicate that heartworm infections continue to increase in number and geographic distribution. 

  • The greatest numbers of cases are seen in the southeastern U.S. and the Mississippi River Valley.  There is an apparent high level of prevalence documented in northern California.

    Click here to view our Prevalence Maps and to sign up for updates on reported cases in your area

800X600 Heartworm Canine Raw Data Map 2011 12

Raw reported heartworm prevalence rates for 2011 and 2012

800X600 Heartworm Canine Map Smooth Data 2011 12

Head-banging smoothes heartworm prevalence rates for 2011 and 2012

Host Associations and Transmission Between Hosts

  • Mosquito species capable of transmitting heartworms can be found in most geographical areas. More than 70 species of mosquitoes are capable of transmitting heartworm. 
  • Transmission can occur anytime infected mosquitoes are active and feeding. 
  • Rare instances of transmission of microfilariae from infected bitches to fetuses via the placenta and from dog to dog via blood transfusion have occurred.  These microfilariae will not develop into adult worms without first developing to the L3 stage in a mosquito.  However, such microfilariae are problematic because they can confound diagnosis and because they are infectious to mosquito vectors. 
  • Although the domestic dog is the primary host for heartworm, other species have been infected, including wild canids, ferrets, cats, wild felids, marine mammals, and people;  disease caused by heartworm infection in these different hosts varies. 

Prepatent Period and Environmental Factors

  • Microfilariae appear in circulation 6 to 7 months after introduction of infective larvae (L3). Infection and successful development of heartworm larvae in mosquitoes is dependent on mosquito feeding habits, mosquito longevity, and ambient temperatures. 

Site of Infection and Pathogenesis


See Life Cycle and Stages and Disease. 

Diagnosis

  • All dogs, including those on heartworm prevention, should be tested annually using both antigen and microfilariae tests.  In some areas, testing dogs twice each year may be indicated, particularly in dogs that are highly exposed to mosquitoes. 
    • Antigen tests detect a glycoprotein found predominantly in the reproductive tract of the female worm. Only mature infections (older than 6 months) with at least one female worm are usually detected. Low worm burdens (fewer than two adult females) and infections with only male worms may not be detected. 
    • A number of commercial antigen-capture diagnostic tests are available. Formats include well enzyme-linked immunosorbent assay (ELISA) tests, solid substratum ELISA tests, immunochromatograhic (immunomigratory) tests, and colloidal gold agglutination tests 
  • Heartworm infection and/or disease is confirmed or ruled out in light of antigen detection, microfilarial detection methods, radiography, echocardiography, and/or electrocardiography. These tests may also be used to identify appropriate therapies, monitor the course of the infection or disease, and determine the success of any treatment. 
  • Laboratory tests 
    • Antigen tests 
      • Due to high specificity (98-100%) of the available tests in dogs with several female worms, it is better to accept than reject a positive test result. Because no test is 100% accurate, it is prudent to repeat positive tests for animals from hypoendemic areas or animals on preventives. Similarly, a negative test for an animal exhibiting clinical signs of heartworm disease should be repeated. Repeat tests can be submitted to a reference laboratory for testing with a test that is different from the original test. 
      • In the southern United States, samples from as many as 5-10% of dogs provided false-negative on results with antigen tests, possibly due to formation of antigen-antibody complexes.  Heat treatment of these samples prior to testing resulted in detection.  
      • Although helpful when a diagnosis of heartworm is suspected but the initial antigen test is negative, routine heat treatment of all samples prior to testing is not recommended.  Although it can improve antigen detection, heat treatment denatures antibodies and is likely to render subsequent antibody detection assays invalid. 
      • Mixing samples prior to testing is not recommended, because it can block antigen detection through formation of antigen-antibody complexes and it can dilute circulating heartworm antigen below detectable limits. 
    • Clinical pathological parameters 
      • Clinical pathology changes are not uniquely diagnostic for heartworms. 
      • Hematological changes associated with heartworm infection include
      • Biochemical changes may include elevated liver enzymes, azotemia, and hyperbilirubinemia. eosinophilia, basophilia, neutrophilia, nonregenerative anemia, and thrombocytopenia.
      • Urinalysis may indicate proteinuria and albuminuria. 
    • Detection of microfilariae 
      • Microfilariae are not present in all heartworm-infected dogs. Dogs may be microfilariae negative (“occult”) for several reasons: 
        • single sex adult infections 
        • elimination of microfilariae by administration of monthly preventives 
        • host immune responses 
        • occurrence of circulating antigen prior to microfilariae production (In rare cases, the appearance of microfilariae may precede antigenemia.) 
    • Microfilariae may be identified microscopically by several methods: 
      • direct examination of fresh blood or blood treated with an anticoagulant 
      • examination of liquid-cell interface (buffy coat) in a microhematocrit tube 
      • concentration using a stained or unstained Millipore filter 
      • concentration by centrifugation using the modified Knott procedure 

 Microfilariae of D. immitis must be differentiated from those of Acanthocheilonema (=Dipetalonema)reconditum and, rarely in the U.S., from other Dirofilaria spp. The following compares characteristics of D. immitis and A. reconditum; these guidelines are only useful with fresh blood samples.


Acanthoceilonema reconditum

Number in blood:  Usually few

Motion:  Progressive

Shape:  Curved body, blunt head, curved or "button-hook" tail

Length (modified Knott test):  250 to 288 µm


Dirofilaria immitis

Number in blood:  Usually many

Motion:  Stationary

Shape:  Straight body and tail, tapered head

Length (modified Knott test):  300 to 322 µm

800X600 Heartworm Canine Microfilariae

Microfilariae of D. immitis (bottom) and A. reconditum (top) as they appear in a Knott's test.  In these preparations, the microfilariae of D. immitis will be wider at middy than the red blood cells while those of A. reconditum are narrower than the red blood cells.

Radiography

  • Radiographic evidence of heartworm infection consists of changes to the pulmonary arteries (increased size, tortuosity, and pruning) and right-sided cardiomegaly (evidenced by a reverse “D” shape to the heart). 

  • Pulmonary parenchyma should be evaluated for infiltrates and nodules. 

  • Additional radiographic findings may include lymphadenopathy and pleural effusion. 

  • Radiographic lesions are more pronounced in the caudal lung lobes.

20170117 Capc Image Bkgd F V1

Control and Prevention

  • Heartworm infection is prevented by the routine administration of a number of macrocyclic lactone preventives.  Limiting contact with mosquitos further reduces risk of heartworm infection. 
  • These preventives vary in their claims against other internal and external parasites and are available in different formulations (tablets, topicals and injectable preparations). 
  • Macrocyclic lactone (a.k.a., macrolide) preventives currently available include oral ivermectin, oral milbemycin oxime, topical or injectable moxidectin, and topical selamectin (Visit CAPC’s “Parasite Product Applications” webpage). 
  • RESISTANCE - Recent work indicates that some heartworm isolates can develop to adults even in dogs receiving routine prophylaxis with any of the available macrocyclic lactones.  These infections in treated dogs results in different heartworm numbers, depending on the preventive used.
    • Infected dogs must be treated promptly with an approved adulticide (see below) and unaffected dogs should be maintained on macrolide preventives year round to protect them from heartworm disease.
    • Annual antigen testing of dogs receiving preventives is extremely important to verify that they are not becoming infected despite precautions.  Annual testing will ensure that infected dogs are identified and treated as soon as possible.  For dogs living in high endemic areas, twice-a-year testing is advised.
    • At this time, the geographic extent of these resistant heart worms is not known.
  • Available heartworm preventives for dogs include: 
    • Advantage Multi® Topical Solution for Dogs (imidacloprid/moxidectin) (Bayer Animal Health) 
    • HEARTGARD® Chewables for Dogs (ivermectin) (Merial) 
    • HEARTGARD® Tablets for Dogs (ivermectin) (Merial) 
    • HEARTGARD® Plus Chewables for Dogs (ivermectin/pyrantel) (Merial) 
    • HeartShield™ Plus Flavored Chewables (ivermectin/pyrantel) (TruRx) 
    • Interceptor® Flavor Tabs® for Dogs & Cats (milbemycin oxime) (Elanco) 
    • Iverhart Max® Chewable Tablets (ivermectin/pyrantel pamoate/praziquantel)  (Virbac) 
    • Iverhart Plus® Flavored Chewables (ivermectin/pyrantel) (Virbac) 
    • Paradyne® (selamectin) (Zoetis) 
    • PetTrust™ Plus Chewable Tablets (ivermectin/pyrantel) (Sergeant's) 
    • ProHeart® 6 (moxidectin) (Zoetis) 
    • Revolution® (selamectin) (Zoetis) 
    • Sentinel® Flavor Tabs® (milbemycin oxime/lufenuron) (Virbac) 
    • Sentinel® Spectrum® Chewables (milbemycin oxime/lufenuron/praziquantel) (Virbac) 
    • Trifexis® (milbemycin oxime/spinosad) (Elanco) 
    • Tri-Heart® Plus Chewable Tablets (ivermectin/pyrantel) (Intervet/Merck Animal Health) 

Treatment

The goals of treatment are to address the clinical condition of the animal, to eliminate adult heartworms that cause disease, and to eliminate microfilariae that are infectious to mosquitoes that can vector the infection to other hosts, including back to the treated dog. 

  • Stabilize dogs presenting with clinical heartworm disease. Any or all of the following may be medically indicated: 
    • corticosteroid therapy 
    • fluid therapy 
    • diuretics 
    • vasodilators 
    • positive inotropic agents 
  • Dogs receiving a macrocyclic lactone should be maintained on preventive if it is already being administered.  If a dog is not receiving a macrocyclic lactone preventive, administration of preventive should be instituted as soon as any severe medical condition has been stabilized.  The purpose of preventive use is to kill recent infections of new larvae that can be transmitted by additional infected mosquitoes, preventing the development of additional adult heartworms. Treatment with melarsomine for removal of adult worms will not kill newly introduced larvae. 
  • CAPC recommends treating infected dogs with adulticide promptly, as soon as medically practical.  Delaying treatment while maintaining dogs on preventives may contribute to selection for resistance, allows pathology to progress, and, when treatment is delayed for several months, could lead to more infected dogs remaining untreated if practical concerns interfere with completing an extended treatment protocol.  No experimental studies have been conducted to determine if delaying treatment while maintaining dogs on preventives improves clearance of worms with subsequent adulticide treatment. 
  • Infected dogs are staged by veterinarians into one of three classes based on clinical signs: asymptomatic or mild disease (stage 1), moderate disease (stage 2), or severe disease (stage 3). 
    • For Stage 1 and 2 dogs, melarsomine dihydrochloride (2.5 mg/kg) can be administered intramuscularly twice over a 24-hour period, followed by at least 1 month of strict exercise restriction.  This treatment regimen will kill greater than 90% of the worms present and clear a similar percentage of dogs of their infections.  The treatment can be repeated for dogs that remain antigen-positive 4 months after the previous treatment. 
    • The prescribed method for treating Stage 3 dogs is to administer melarsomine dihydrochloride (2.5 mg/kg) intramuscularly once, followed in 1 month (or longer if the dog’s condition dictates) by two intramuscular injections (2.5 mg/kg each) 24 hours apart. Any excitement or exercise beyond slow walking for should be restricted for at least 1 month following each set of injections. This treatment regimen will kill up to 98% of the worms present. 
    • The greater efficacy obtained using the 3-injection regimen developed for Stage 3 dogs also makes this approach the treatment of choice for Stage 1 and 2 dogs.  Other, off-label regimens for administration of melarsomine dihydrochloride are not recommended. 
    • Melarsomine is not effective against heartworms younger than 4 months of age.  Because infected mosquitoes can bite dogs over a period of months, heartworms of different ages can be present within a given season.  Thus, melarsomine treatment may not be completely efficacious in all situations, which may necessitate additional therapy or alternate therapeutic strategies. 
    • All melarsomine-treated dogs should be antigen tested 4-6 months after therapy to determine if infection has been cleared. 
  • Adulticidal therapy using long-term macrocyclic lactone administration - the "slow kill" method - is not recommended, especially in light of resistance.  Repeated macrocyclic lactone administration to infected dogs increases the proportion of circulating microfilariae that possess resistance markers (i.e., application of long-term drug pressure will select for survival of drug-resistant microfilariae).
    • Depending on the macrocyclic lactone used, as many as 20% of adult heartworm-infected dogs will continue to have circulating microfilariae for at least a year or longer when receiving monthly preventative.  
    • In a recent study, false-negative antigen test results were observed for approximately half of dogs managed with slow-kill protocols, presumably because of antigen-antibody complex formation.  Antigen test results from dogs on slow-kill may not be a reliable indicator of infection status. 
    • Although the “slow-kill” method should be avoided, if it is the only medically acceptable option, microfilariae should be eliminated prior to exposure to preventive doses of macrocyclic lactones and dogs should be maintained on a mosquito repellent. 
    • Topical moxidectin/imidacloprid is label approved in dogs for removal of microfliariae when used monthly. 
  • Post-adulticide microfilaricidal treatment 
    • Microfilariae present after treatment should be cleared from the circulation.  Microfilariae can persist for more than a year in the presence of very high levels of some macrocyclic lactones, and these microfilariae put other dogs at risk of infection (or re-infection) with potentially resistant phenotypes. 
    • Advantage Multi® Topical Solution for Dogs (imidacloprid + moxidectin) (Bayer Animal Health) is approved for the removal of circulating microfilariae in heartworm positive dogs. 
  • Additional considerations for adulticide and microfilaricidal therapy 
    • Wolbachia 
      • Most filarial nematodes, including D. immitis, harbor obligate, intracellular, gram-negative bacteria belonging to the genus Wolbachia (a rickettsial symbiont). 
      • Although more research is needed, initial data suggest treatment of dogs with doxycycline prior to adulticide therapy may i) reduce the gross pulmonary pathology that occurs as a result of thromboembolic shower of dead worm fragments, ii) decrease the number of microfilariae after adulticide therapy, and iii) interfere with the ability of the microfilariae to develop into infective larvae in mosquito vectors.  Importantly, further investigations are needed to test each of these hypotheses. 

Public Health Considerations

  • Dirofilaria immitis is of public health concern even though the number of reported cases is small. 
  • More than 100 human cases of pulmonary dirofilariasis have been reported in the United States in the last fifty years. 
  • Human heartworm Infections have also been recorded in the eye, skin, testicle, and elsewhere. 
  • Human dirofilariasis results in nodular inflammation of the lungs. 
    • Pulmonary nodules are usually solitary and form around dead immature heartworms. 
    • Nodules are often mistaken for lung tumors or tuberculosis, resulting in unnecessary surgery. 
  • Prevention is best accomplished through mosquito abatement programs (including screening outdoor kennels), and by using mosquito repellents, wearing protective clothing, and remaining indoors during mosquito feeding periods. 
    • Reducing the prevalence of heartworm infection in the definitive canine host will also reduce the risk of D. immitis transmission to people

Selected References

  • Blagburn BL, Carmichael J, Kaminsky R, Schenker R, Kaplan R, Moorhead A, Prichard R, Geary T, Bourguinat C, Malone J, Bowman DD.    2013.   Resistance and heartworm preventives: historical perspective and overview of research.  ABSTRACT 28, 58th Annual Meeting of the American Association of Veterinary Parasitologists, Chicago, IL, July 20-23.
 
  • Blagburn BL, Dillon AR, Arther RG, Butler JM, Newton JC.  2011. Comparative efficacy of four commercially available heartworm preventive products against the MP3 laboratory strain of Dirofilaria immitisVet Parasitol. 176(2-3):189-94.
Bowman DD. 2012. Heartworms, macrocyclic lactones, and the specter of resistance to prevention in the United States. Parasit Vectors. 5:138.
 
  • Bowman DD, Atkins CE. 2009. Heartworm biology, treatment, and control. Vet Clin North Am Small Anim Pract. 39(6):1127-58
 
  • Lee AC, Montgomery SP, Theis JH, Blagburn BL, Eberhard ML. 2010. Public health issues concerning the widespread distribution of canine heartworm disease. Trends Parasitol. 26(4):168-73.
 
  • Little SE, Munzing C, Heise SR, et al. 2014. Pre-treatment with heat facilitates detection of antigen of Dirofilaria immitis in canine samples.  Veterinary Parasitol. 203(1-2):250-2. 

Synopsis

CAPC Recommends

 

  • Annual testing of all dogs for both antigen and microfilariae of heartworm. 

  • Protect all dogs from heartworm infection by using preventives year round.  

  • Treat infected dogs with labeled adulticides and microfilaricides (if microfilaria are present) as soon after diagnosis as medically practical. 

Life Cycle and Stages


  • Microfilariae reside in the blood of most, but not all, infected canids. 
  • Microfilariae (300-322 µm x 6.8-7.0 µm) are ingested by feeding female mosquitoes. After two molts (approximately 2 weeks), infective third-stage larvae (L3s) are present in mosquito mouth parts. Development may be slower at cooler temperatures and ceases at temperatures below 57°F. Development progresses in the mosquito relative to ambient temperature; if ambient temperature increases, development will resume. 
  • L3s (1,000 µm x 40 µm) are deposited on the skin of the dog during subsequent feeding and migrate through the bite wound into the host. Most L3s molt to fourth-stage larvae (L4s) in canine subcutaneous tissues within 1-3 days after infection. 
  • L4s migrate through tissues for several weeks. 
  • A final molt to the sexually immature adult stage occurs approximately 2 months (50 to 70 days) after infection. 
  • The young adults (2-3 cm in length) enter the vascular system and are carried to the heart and pulmonary arteries, arriving as early as 70 days after infection. Final maturation and mating occurs in the pulmonary vessels. By 4 months after infection, the worms in the pulmonary arteries are around 10-15 cm in length.  Fully mature adults at 6.5 months after infection reach lengths of 15-18 cm (5-6 in) for males and 25-30 cm (10-12 in) for females. 
  • Canine hosts typically demonstrate microfilaremia 6 to 7 months after infection. 
  • Heartworms live approximately 5 to 7 years in the dog. 
800X600 Heartworm Canine Life Cycle

Heartworm Life Cycle

Disease

  • Heartworm infection in the dog induces pulmonary endothelial damage, villous proliferation, and activation and attraction of leukocytes and platelets due to live worms as well as thrombosis, granulomatous, and villous inflammation due to dead and/or dying worms. 
  • Pulmonary vessels may become thickened and tortuous. 
  • Cardiac output may be reduced. Pulmonary hypertension may lead to compensatory right heart enlargement and right heart failure. Clinical signs include cough, dyspnea, weight loss, ascites, jugular venous distension, exercise intolerance, and arrhythmias. 
  • Heartworm infection may induce glomerulonephritis and proteinuria secondary to antigen-antibody complex deposition. 
  • Rarely, ectopic infections of the eye, central nervous system, peritoneal cavity, systemic circulation, or skin have been reported. 
  • Caval syndrome occurs in a small number of cases, typically associated with large numbers of adults in the pulmonary arteries 
    • Worms may be found in the post cava and right atrium, causing interference with tricuspid valve function. This results in a peracute life-threatening hemolytic anemia and right heart failure. 
    • Associated findings include: 
      • pallor, weak pulses, tachycardia, and sudden collapse 
      • hemoglobinemia and hemoglobinuria 
      • disseminated intravascular coagulopathy  
      • murmur caused by tricuspid regurgitation auscultated best on right side of thorax

Prevalence

  • Surveys indicate that heartworm infections continue to increase in number and geographic distribution. 

  • The greatest numbers of cases are seen in the southeastern U.S. and the Mississippi River Valley.  There is an apparent high level of prevalence documented in northern California.

    Click here to view our Prevalence Maps and to sign up for updates on reported cases in your area

800X600 Heartworm Canine Raw Data Map 2011 12

Raw reported heartworm prevalence rates for 2011 and 2012

800X600 Heartworm Canine Map Smooth Data 2011 12

Head-banging smoothes heartworm prevalence rates for 2011 and 2012

Host Associations and Transmission Between Hosts

  • Mosquito species capable of transmitting heartworms can be found in most geographical areas. More than 70 species of mosquitoes are capable of transmitting heartworm. 
  • Transmission can occur anytime infected mosquitoes are active and feeding. 
  • Rare instances of transmission of microfilariae from infected bitches to fetuses via the placenta and from dog to dog via blood transfusion have occurred.  These microfilariae will not develop into adult worms without first developing to the L3 stage in a mosquito.  However, such microfilariae are problematic because they can confound diagnosis and because they are infectious to mosquito vectors. 
  • Although the domestic dog is the primary host for heartworm, other species have been infected, including wild canids, ferrets, cats, wild felids, marine mammals, and people;  disease caused by heartworm infection in these different hosts varies. 

Prepatent Period and Environmental Factors

  • Microfilariae appear in circulation 6 to 7 months after introduction of infective larvae (L3). Infection and successful development of heartworm larvae in mosquitoes is dependent on mosquito feeding habits, mosquito longevity, and ambient temperatures. 

Site of Infection and Pathogenesis


See Life Cycle and Stages and Disease. 

Diagnosis

  • All dogs, including those on heartworm prevention, should be tested annually using both antigen and microfilariae tests.  In some areas, testing dogs twice each year may be indicated, particularly in dogs that are highly exposed to mosquitoes. 
    • Antigen tests detect a glycoprotein found predominantly in the reproductive tract of the female worm. Only mature infections (older than 6 months) with at least one female worm are usually detected. Low worm burdens (fewer than two adult females) and infections with only male worms may not be detected. 
    • A number of commercial antigen-capture diagnostic tests are available. Formats include well enzyme-linked immunosorbent assay (ELISA) tests, solid substratum ELISA tests, immunochromatograhic (immunomigratory) tests, and colloidal gold agglutination tests 
  • Heartworm infection and/or disease is confirmed or ruled out in light of antigen detection, microfilarial detection methods, radiography, echocardiography, and/or electrocardiography. These tests may also be used to identify appropriate therapies, monitor the course of the infection or disease, and determine the success of any treatment. 
  • Laboratory tests 
    • Antigen tests 
      • Due to high specificity (98-100%) of the available tests in dogs with several female worms, it is better to accept than reject a positive test result. Because no test is 100% accurate, it is prudent to repeat positive tests for animals from hypoendemic areas or animals on preventives. Similarly, a negative test for an animal exhibiting clinical signs of heartworm disease should be repeated. Repeat tests can be submitted to a reference laboratory for testing with a test that is different from the original test. 
      • In the southern United States, samples from as many as 5-10% of dogs provided false-negative on results with antigen tests, possibly due to formation of antigen-antibody complexes.  Heat treatment of these samples prior to testing resulted in detection.  
      • Although helpful when a diagnosis of heartworm is suspected but the initial antigen test is negative, routine heat treatment of all samples prior to testing is not recommended.  Although it can improve antigen detection, heat treatment denatures antibodies and is likely to render subsequent antibody detection assays invalid. 
      • Mixing samples prior to testing is not recommended, because it can block antigen detection through formation of antigen-antibody complexes and it can dilute circulating heartworm antigen below detectable limits. 
    • Clinical pathological parameters 
      • Clinical pathology changes are not uniquely diagnostic for heartworms. 
      • Hematological changes associated with heartworm infection include
      • Biochemical changes may include elevated liver enzymes, azotemia, and hyperbilirubinemia. eosinophilia, basophilia, neutrophilia, nonregenerative anemia, and thrombocytopenia.
      • Urinalysis may indicate proteinuria and albuminuria. 
    • Detection of microfilariae 
      • Microfilariae are not present in all heartworm-infected dogs. Dogs may be microfilariae negative (“occult”) for several reasons: 
        • single sex adult infections 
        • elimination of microfilariae by administration of monthly preventives 
        • host immune responses 
        • occurrence of circulating antigen prior to microfilariae production (In rare cases, the appearance of microfilariae may precede antigenemia.) 
    • Microfilariae may be identified microscopically by several methods: 
      • direct examination of fresh blood or blood treated with an anticoagulant 
      • examination of liquid-cell interface (buffy coat) in a microhematocrit tube 
      • concentration using a stained or unstained Millipore filter 
      • concentration by centrifugation using the modified Knott procedure 

 Microfilariae of D. immitis must be differentiated from those of Acanthocheilonema (=Dipetalonema)reconditum and, rarely in the U.S., from other Dirofilaria spp. The following compares characteristics of D. immitis and A. reconditum; these guidelines are only useful with fresh blood samples.


Acanthoceilonema reconditum

Number in blood:  Usually few

Motion:  Progressive

Shape:  Curved body, blunt head, curved or "button-hook" tail

Length (modified Knott test):  250 to 288 µm


Dirofilaria immitis

Number in blood:  Usually many

Motion:  Stationary

Shape:  Straight body and tail, tapered head

Length (modified Knott test):  300 to 322 µm

800X600 Heartworm Canine Microfilariae

Microfilariae of D. immitis (bottom) and A. reconditum (top) as they appear in a Knott's test.  In these preparations, the microfilariae of D. immitis will be wider at middy than the red blood cells while those of A. reconditum are narrower than the red blood cells.

Radiography

  • Radiographic evidence of heartworm infection consists of changes to the pulmonary arteries (increased size, tortuosity, and pruning) and right-sided cardiomegaly (evidenced by a reverse “D” shape to the heart). 

  • Pulmonary parenchyma should be evaluated for infiltrates and nodules. 

  • Additional radiographic findings may include lymphadenopathy and pleural effusion. 

  • Radiographic lesions are more pronounced in the caudal lung lobes.

20170117 Capc Image Bkgd F V1

Control and Prevention

  • Heartworm infection is prevented by the routine administration of a number of macrocyclic lactone preventives.  Limiting contact with mosquitos further reduces risk of heartworm infection. 
  • These preventives vary in their claims against other internal and external parasites and are available in different formulations (tablets, topicals and injectable preparations). 
  • Macrocyclic lactone (a.k.a., macrolide) preventives currently available include oral ivermectin, oral milbemycin oxime, topical or injectable moxidectin, and topical selamectin (Visit CAPC’s “Parasite Product Applications” webpage). 
  • RESISTANCE - Recent work indicates that some heartworm isolates can develop to adults even in dogs receiving routine prophylaxis with any of the available macrocyclic lactones.  These infections in treated dogs results in different heartworm numbers, depending on the preventive used.
    • Infected dogs must be treated promptly with an approved adulticide (see below) and unaffected dogs should be maintained on macrolide preventives year round to protect them from heartworm disease.
    • Annual antigen testing of dogs receiving preventives is extremely important to verify that they are not becoming infected despite precautions.  Annual testing will ensure that infected dogs are identified and treated as soon as possible.  For dogs living in high endemic areas, twice-a-year testing is advised.
    • At this time, the geographic extent of these resistant heart worms is not known.
  • Available heartworm preventives for dogs include: 
    • Advantage Multi® Topical Solution for Dogs (imidacloprid/moxidectin) (Bayer Animal Health) 
    • HEARTGARD® Chewables for Dogs (ivermectin) (Merial) 
    • HEARTGARD® Tablets for Dogs (ivermectin) (Merial) 
    • HEARTGARD® Plus Chewables for Dogs (ivermectin/pyrantel) (Merial) 
    • HeartShield™ Plus Flavored Chewables (ivermectin/pyrantel) (TruRx) 
    • Interceptor® Flavor Tabs® for Dogs & Cats (milbemycin oxime) (Elanco) 
    • Iverhart Max® Chewable Tablets (ivermectin/pyrantel pamoate/praziquantel)  (Virbac) 
    • Iverhart Plus® Flavored Chewables (ivermectin/pyrantel) (Virbac) 
    • Paradyne® (selamectin) (Zoetis) 
    • PetTrust™ Plus Chewable Tablets (ivermectin/pyrantel) (Sergeant's) 
    • ProHeart® 6 (moxidectin) (Zoetis) 
    • Revolution® (selamectin) (Zoetis) 
    • Sentinel® Flavor Tabs® (milbemycin oxime/lufenuron) (Virbac) 
    • Sentinel® Spectrum® Chewables (milbemycin oxime/lufenuron/praziquantel) (Virbac) 
    • Trifexis® (milbemycin oxime/spinosad) (Elanco) 
    • Tri-Heart® Plus Chewable Tablets (ivermectin/pyrantel) (Intervet/Merck Animal Health) 

Treatment

The goals of treatment are to address the clinical condition of the animal, to eliminate adult heartworms that cause disease, and to eliminate microfilariae that are infectious to mosquitoes that can vector the infection to other hosts, including back to the treated dog. 

  • Stabilize dogs presenting with clinical heartworm disease. Any or all of the following may be medically indicated: 
    • corticosteroid therapy 
    • fluid therapy 
    • diuretics 
    • vasodilators 
    • positive inotropic agents 
  • Dogs receiving a macrocyclic lactone should be maintained on preventive if it is already being administered.  If a dog is not receiving a macrocyclic lactone preventive, administration of preventive should be instituted as soon as any severe medical condition has been stabilized.  The purpose of preventive use is to kill recent infections of new larvae that can be transmitted by additional infected mosquitoes, preventing the development of additional adult heartworms. Treatment with melarsomine for removal of adult worms will not kill newly introduced larvae. 
  • CAPC recommends treating infected dogs with adulticide promptly, as soon as medically practical.  Delaying treatment while maintaining dogs on preventives may contribute to selection for resistance, allows pathology to progress, and, when treatment is delayed for several months, could lead to more infected dogs remaining untreated if practical concerns interfere with completing an extended treatment protocol.  No experimental studies have been conducted to determine if delaying treatment while maintaining dogs on preventives improves clearance of worms with subsequent adulticide treatment. 
  • Infected dogs are staged by veterinarians into one of three classes based on clinical signs: asymptomatic or mild disease (stage 1), moderate disease (stage 2), or severe disease (stage 3). 
    • For Stage 1 and 2 dogs, melarsomine dihydrochloride (2.5 mg/kg) can be administered intramuscularly twice over a 24-hour period, followed by at least 1 month of strict exercise restriction.  This treatment regimen will kill greater than 90% of the worms present and clear a similar percentage of dogs of their infections.  The treatment can be repeated for dogs that remain antigen-positive 4 months after the previous treatment. 
    • The prescribed method for treating Stage 3 dogs is to administer melarsomine dihydrochloride (2.5 mg/kg) intramuscularly once, followed in 1 month (or longer if the dog’s condition dictates) by two intramuscular injections (2.5 mg/kg each) 24 hours apart. Any excitement or exercise beyond slow walking for should be restricted for at least 1 month following each set of injections. This treatment regimen will kill up to 98% of the worms present. 
    • The greater efficacy obtained using the 3-injection regimen developed for Stage 3 dogs also makes this approach the treatment of choice for Stage 1 and 2 dogs.  Other, off-label regimens for administration of melarsomine dihydrochloride are not recommended. 
    • Melarsomine is not effective against heartworms younger than 4 months of age.  Because infected mosquitoes can bite dogs over a period of months, heartworms of different ages can be present within a given season.  Thus, melarsomine treatment may not be completely efficacious in all situations, which may necessitate additional therapy or alternate therapeutic strategies. 
    • All melarsomine-treated dogs should be antigen tested 4-6 months after therapy to determine if infection has been cleared. 
  • Adulticidal therapy using long-term macrocyclic lactone administration - the "slow kill" method - is not recommended, especially in light of resistance.  Repeated macrocyclic lactone administration to infected dogs increases the proportion of circulating microfilariae that possess resistance markers (i.e., application of long-term drug pressure will select for survival of drug-resistant microfilariae).
    • Depending on the macrocyclic lactone used, as many as 20% of adult heartworm-infected dogs will continue to have circulating microfilariae for at least a year or longer when receiving monthly preventative.  
    • In a recent study, false-negative antigen test results were observed for approximately half of dogs managed with slow-kill protocols, presumably because of antigen-antibody complex formation.  Antigen test results from dogs on slow-kill may not be a reliable indicator of infection status. 
    • Although the “slow-kill” method should be avoided, if it is the only medically acceptable option, microfilariae should be eliminated prior to exposure to preventive doses of macrocyclic lactones and dogs should be maintained on a mosquito repellent. 
    • Topical moxidectin/imidacloprid is label approved in dogs for removal of microfliariae when used monthly. 
  • Post-adulticide microfilaricidal treatment 
    • Microfilariae present after treatment should be cleared from the circulation.  Microfilariae can persist for more than a year in the presence of very high levels of some macrocyclic lactones, and these microfilariae put other dogs at risk of infection (or re-infection) with potentially resistant phenotypes. 
    • Advantage Multi® Topical Solution for Dogs (imidacloprid + moxidectin) (Bayer Animal Health) is approved for the removal of circulating microfilariae in heartworm positive dogs. 
  • Additional considerations for adulticide and microfilaricidal therapy 
    • Wolbachia 
      • Most filarial nematodes, including D. immitis, harbor obligate, intracellular, gram-negative bacteria belonging to the genus Wolbachia (a rickettsial symbiont). 
      • Although more research is needed, initial data suggest treatment of dogs with doxycycline prior to adulticide therapy may i) reduce the gross pulmonary pathology that occurs as a result of thromboembolic shower of dead worm fragments, ii) decrease the number of microfilariae after adulticide therapy, and iii) interfere with the ability of the microfilariae to develop into infective larvae in mosquito vectors.  Importantly, further investigations are needed to test each of these hypotheses. 

Public Health Considerations

  • Dirofilaria immitis is of public health concern even though the number of reported cases is small. 
  • More than 100 human cases of pulmonary dirofilariasis have been reported in the United States in the last fifty years. 
  • Human heartworm Infections have also been recorded in the eye, skin, testicle, and elsewhere. 
  • Human dirofilariasis results in nodular inflammation of the lungs. 
    • Pulmonary nodules are usually solitary and form around dead immature heartworms. 
    • Nodules are often mistaken for lung tumors or tuberculosis, resulting in unnecessary surgery. 
  • Prevention is best accomplished through mosquito abatement programs (including screening outdoor kennels), and by using mosquito repellents, wearing protective clothing, and remaining indoors during mosquito feeding periods. 
    • Reducing the prevalence of heartworm infection in the definitive canine host will also reduce the risk of D. immitis transmission to people

Selected References

  • Blagburn BL, Carmichael J, Kaminsky R, Schenker R, Kaplan R, Moorhead A, Prichard R, Geary T, Bourguinat C, Malone J, Bowman DD.    2013.   Resistance and heartworm preventives: historical perspective and overview of research.  ABSTRACT 28, 58th Annual Meeting of the American Association of Veterinary Parasitologists, Chicago, IL, July 20-23.
 
  • Blagburn BL, Dillon AR, Arther RG, Butler JM, Newton JC.  2011. Comparative efficacy of four commercially available heartworm preventive products against the MP3 laboratory strain of Dirofilaria immitisVet Parasitol. 176(2-3):189-94.
Bowman DD. 2012. Heartworms, macrocyclic lactones, and the specter of resistance to prevention in the United States. Parasit Vectors. 5:138.
 
  • Bowman DD, Atkins CE. 2009. Heartworm biology, treatment, and control. Vet Clin North Am Small Anim Pract. 39(6):1127-58
 
  • Lee AC, Montgomery SP, Theis JH, Blagburn BL, Eberhard ML. 2010. Public health issues concerning the widespread distribution of canine heartworm disease. Trends Parasitol. 26(4):168-73.
 
  • Little SE, Munzing C, Heise SR, et al. 2014. Pre-treatment with heat facilitates detection of antigen of Dirofilaria immitis in canine samples.  Veterinary Parasitol. 203(1-2):250-2. 
Heartworm for Cat Last updated: 2015-07-01

Synopsis

CAPC Recommends

 

  • Testing cats for heartworm with antigen or antibody test prior to starting them on preventive. 

  • Protecting all cats from heartworm infection by using preventives year round. 

  • Maintaining infected cats on preventives to protect them from acquiring additional heartworms, and closely monitoring their health status, providing symptomatic care as needed.

Life Cycle and Stages


  • Microfilariae (300 to 322 µm by 6.8 to 7.0 µm) are ingested by female mosquitoes when they feed on infected canids. (Felids are seldom microfilaremic; consequently, they are less likely sources of microfilariae for mosquitoes). After development through two molts (approximately 2 weeks), infective L3 larvae are present in mosquito mouth parts. Development may require a longer period at cooler temperatures. 
  • Third-stage larvae (L3) are 1,000 µm by 40 µm. They are deposited by mosquitoes on the skin surface during subsequent feeding(s) and then enter the new host via the mosquito bite wound. Most L3 larvae molt to fourth-stage larvae (L4) within 1 to 3 days in the subcutaneous, adipose, and muscle tissues. 
  • The final molt to the juvenile worm occurs approximately 2 months (50 to 70 days) after infection. 
  • Juvenile worms (1 to 3 cm in length) enter the vascular system and are carried to the heart and pulmonary arteries; they arrive as early as 70 days after infection. Most feline infections are aborted at this time, resulting in inflammation in the pulmonary vessels, pulmonary parenchyma, and airways. In a small percentage of infections, further development to mature adult worms and mating may occur. Because of the typically small worm burdens in cats (often one to three worms), single-sex infections (i.e., male or female only) are common. 
  • Maturation to adult worms occurs at about 6 months; development and release of microfilariae occurs about 7 or 8 months after initial infection. 
  • As noted previously, microfilaremia is infrequent (typically less than 20% of naturally infected cats) and short-lived; the number of circulating microfilariae typically is low. Microfilariae are seen in small numbers in experimentally infected cats and persist no more than a few weeks to months. 
  • Mature heartworms in cats are smaller than those in dogs; 12-month-old female worms in cats average 21 cm in length, compare with longer than 26 cm in dogs. 
  • Adult heartworms are believed to live for 2 to 4 years in cats. 
800X600 Heartworm Feline Life Cycle

Heartworm Life Cycle in Cats

Disease

  • Heartworm disease in the cat may involve some or all of the following: 
    • Pulmonary arterial, bronchial, and alveolar disease—Heartworm Associated Respiratory Disease (HARD)—is associated with the death of developing juvenile worms. Cats may present with cough, dyspnea, and/or wheezing. 
    • Death of adult heartworms (if present) can potentiate HARD signs. Sudden death occurs in approximately 10 to 20% of diagnosed cases. Pathogenesis is unclear, but a condition (similar to acute respiratory distress syndrome [ARDS]) caused by the release of antigenic moieties from injured or dying adult worms is suspected. 
    • Vomiting unrelated to eating may be present. 
    • Pulmonary thromboemboli (fragments from dead adult worms) may cause acute vascular and interstitial inflammatory events that lead to dyspnea and death. 
    • Hematological abnormalities may include anemia, hyperglobulinemia, basophilia, and eosinophilia. 
    • Neurological signs may indicate aberrant migration of the worm to the brain, eye, or spinal cord.

Prevalence

  • Geographic prevalence of feline heartworm infection (adult worms) generally follows canine infections, but infection occurs at approximately 10% of the prevalence rate for dogs (see map below for canine prevalence). Cats are infected with juvenile worms at a much higher rate than with adult worms; estimates based on necropsy and antibody studies suggest that cats are infected with juvenile worms at an infection rate similar to that of dogs. The greatest number of cases is seen in the southeastern U.S., the Mississippi River Valley, and Texas. 
  • A study involving more than 2,000 largely asymptomatic cats was conducted in 19 states comprising 21 geographic regions (see figure below). For pet cats (excepting North Carolina, which surveyed shelter animals), the nationwide exposure rates (i.e., percentage of cats that were antibody-positive) were approximately 12%. Many of these cats were from areas not highly endemic for heartworm infection. Results do not confirm mature heartworm infection but imply infection with immature worms and increased risk of HARD. 
  • A second study of 25,000 cats tested nationwide reported a 15.9% antibody positive rate. 

Click here to view our Prevalence Maps and to sign up for updates on reported cases in your area

800X600 Heartworm Feline Map

American Heartworm Society.  The severity of heartworm incidence as shown in this map is based on the average number of cases per reporting clinic.  She remote regions of the United States lack veterinary clinics, therefore we have no reported cases from these areas.

800X600 Heartworm Feline Map Antigen Study

Necropsy-based data (percentage infected) for cats with adult heartworms in shelters is shown in this figure

800X600 Heartworm Feline Map Percent Antibody

Results from a study involving more than 2,000 largely asymptomatic cats.  CNJ = central New Jersey, NNJ = northern New Jersey, LL = Long Island, New York.  Source:  Miller and Atkins, American Heartworm Symposium, 1998

Host Association and Transmission Between Hosts

  • More than 70 species of mosquito are capable of transmitting D. immitis. However, only about 22 species are common and important vectors. 
  • Differences in biological behavior and host preferences by mosquitoes can affect the epidemiology of heartworms in a particular location. 
  • Transmission can occur anytime infected mosquitoes are active and feeding. 
  • Although L3 larvae taken from mosquitoes that had fed on experimentally infected cats were capable of infecting puppies, the infrequency, low numbers, and transient nature of microfilaremia in cats support that in many cases, cats are a dead-end host for D. immitis. 

Site of Infection and Pathogenesis

  • In dogs, adult heartworms reside largely in the pulmonary arteries. However, if numerous worms are present, worms may be found in the right ventricle and pulmonary trunk. In cats, the relative size of the adult heartworm is such that it is much more likely that a portion of the worm can be observed in the right side of the heart. 
  • Migration of immature heartworms to other anatomic sites can occur in cats, sometimes resulting in death. 
  • Pulmonary intravascular macrophages—the primary component of the cat’s reticuloendothelial system—have been implicated in the unique pulmonary pathology found in cats. 

Diagnosis

  • Because of potentially lower worm burden, single-sex infections, and infrequency of microfilaremia, heartworm infection is more difficult to diagnose in cats than in dogs. 
  • Microfilariae identification 
    • Fewer than 20% of cats with mature heartworm infection are microfilaremic. Because of the frequent absence of microfilariae, microfilarial testing (e.g., direct smear, microhematocrit tube, modified Knott test, millipore filter test) is less useful in the cat than in the dog. Nevertheless, a positive microfilariae test confirms active adult heartworm infection in the cat. 
  • Hematological testing 
    • Eosinophilia (and possibly basophilia), although nonspecific, can support a diagnosis of heartworm infection. Eosinophilia, often transient, is most frequently observed 4 to 7 months after infection. 
  • Antibody tests (available as both send-off and point-of-care tests) do not require the presence of circulating antigen produced by mature female worms for a positive test result. Different antibody tests may detect migrating larvae of different ages. If an exposed cat eliminates the infection at the juvenile worm stage, HARD may still result. 
    • Antibody testing may not be effective for diagnosis of feline heartworm disease. Approximately 15 to 25% of cats with adult infection are antibody-negative. Conversely, 80 to 90% of antibody-positive cats do not harbor mature heartworms. 
    • Depending on the preventive product used, up to 30% of cats on preventives that are exposed to heartworms will convert to an antibody-positive state without mature infection or heartworm-related disease. 
    • In a limited number of experimental studies, 50% of experimentally infected cats with confirmed pulmonary pathologic lesions (HARD) seroconverted to a negative antibody status within 8 months after infection. Within 16 months after infection, 100% of experimentally infected cats (HARD) were negative for detectable antibodies. However, after initial infection and induction of HARD lesions, these cats were restricted from further potential exposure to heartworm-infected mosquitoes. 
    • Positive antibody tests may or may not support heartworms as a cause of respiratory signs or lesions. Additionally, a negative antibody test does not rule out current or previous infection. 
  • Antigen testing 
    • Antigen testing is available as both send-off and point-of-care tests. 
    • Only mature female worm infections (typically 7 to 8 months post-infection) are detected. Rarely, in experimental infections, female heartworms may be detected as early as 6 months after infection. A positive antigen test indicates that the cat harbors mature female heartworms or that mature female heartworms were present but died recently. 
    • One third of adult heartworm infections in cats consist only of male worms and will not be detected using available antigen tests. 
    • Studies of naturally infected cats examined at necropsy have shown that some antigen tests are capable of detecting a single mature female heartworm. 
    • A negative antigen test does not conclusively rule out adult heartworm infection nor will it detect juvenile worms often responsible for pulmonary disease (HARD). 
    • Serum samples from cats may be false negative on antigen tests, particularly early in infection, presumably due to formation of antigen-antibody complexes.  Heat treatment of these samples prior to testing has been shown to destroy the complexes, allowing detection of antigen. 
    • Although helpful when a diagnosis of heartworm is suspected but the initial antigen test is negative, routine heat treatment of all samples prior to testing is not recommended.  Heat treatment of serum will destroy antibody, rendering results of subsequent feline antibody tests invalid.

Radiography

  • The most common radiographic findings in feline heartworm disease are enlargement of the right caudal lobar artery and a bronchointerstitial inflammatory pattern in the caudal lung lobes. 
800X600 Heartworm Feline Radiograph

Photo courtesy of Dr. Clarke Atkins, North Carolina State University

Echocardiography

  • Ultrasound in the hands of a skilled ultrasonographer may detect 68% of naturally infected cats. However, the caudal pulmonary arteries must be examined to their point of bifurcation within the lung fields. 

Treatment

  • At present, removal of adult worms from cats using melarsomine dihydrochloride is not recommended. 
  • Early data indicate that concurrent ivermectin and doxycycline therapy for Wolbachia reduces inflammation associated with worm death in dogs. It is not yet known whether this same result can be achieved in cats. 
  • Surgical removal of heartworms via the jugular vein can be performed. However, deaths have been reported during the use of this procedure. In addition, jugular venotomy is expensive and requires the use of a fluoroscope for anatomic guidance. 
  • Microfilaricidal therapy is not recommended in cats. 
  • At present, no specific therapy is recommended for asymptomatic cats with confirmed heartworm infections. However, infected cats cats with symptomatic feline dirofilariasis should be treated with corticosteroids in decreasing dosages to minimize dyspnea, coughing, and wheezing caused by death of either juvenile (HARD) or adult worms. Antileukotrienes also may be beneficial in reducing the risks associated with adult worm death. Bronchodilators may be useful if there is radiographic evidence of air-trapping. Specific therapies should be used if vomiting and neurological signs are present. 
  • Emergency treatment of symptomatic cats may include parenteral corticosteroid therapy, oxygen therapy via an oxygen cage or nasal insufflation, and furosemide in ARDS-like cases. If available, ventilator therapy may be utilized. Xanthine bronchodilators (theophylline or aminophylline) may be used to dilate bronchioles and support the muscles of respiration. 

Prognosis

  • The published life expectancy for cats with adult dirofilariasis is 1.5 years (median). 
  • For cats surviving acute disease beyond day 1, the median survival is 4 years. 
  • Current information suggests that more than 80% of cats diagnosed with heartworm infection survive the infection. 

Control and Prevention

  • All cats, regardless of their lifestyle, should be on year-round heartworm prevention.  Available preventives for cats include oral ivermectin, topical moxidectin/imidacloprid, and topical selamectin.  Topical moxidectin/imidacloprid is also approved for use in ferrets. 
  • Although cats housed indoors have a lower risk for heartworm infection, studies have shown that 25 to 30% of heartworm-infected cats were characterized by their owners as “strictly” indoor cats. Furthermore, certain mosquitoes that typically are found indoors will feed on cats. 
  • Available broad-spectrum feline heartworm preventives are also label-approved for other important feline internal or external parasites. 
  • Available preventives for cats include: 
    • HEARTGARD® Chewables for Cats (ivermectin)(Merial) 
    • Advantage Multi®  Topical Solution for Cats (imidacloprid/moxidectin) (Bayer Animal Health)* 
    • Interceptor® Flavor Tabs® for Dogs & Cats (milbemycin oxime)(Elanco) 
    • Paradyne® (selamectin) (Zoetis) 
    • Revolution® (selamectin)(Zoetis) 

*Note: this product additionally has a label claim for prevention of heartworm disease in ferrets 

Public Health Considerations

  • Because cats typically are amicrofilaremic, heartworm-infected cats pose little to no public health risk. 

Selected References

  • Bowman DD, Atkins CE. 2009. Heartworm biology, treatment, control. Vet Clin North Am Small Anim Pract. 39(6):1127-58
 
  • Lee AC, Aktkins CE. 2010 Understanding feline heartworm infection: disease, diagnosis, and treatment. Top Companion Anim Med Nov 25 (4):224-230
 
  • Little SE, Raymond MR, Thomas JE, et al. 2014. Heat treatment prior to testing allows detection of antigen of Dirofilaria immitis in feline serum. Parasit Vectors Jan 13;7:1
 
  • Maia FC, McCall JW, Valdimero AS, Jr. et al. 2011 Structural and ultrastructual changes in the lungs of Felis catus (Linnaeus, 1758) experimentally infected with D. immitis (Leidy, 1856). Vet Parasitol. 176(4):304-12 

Synopsis

CAPC Recommends

 

  • Testing cats for heartworm with antigen or antibody test prior to starting them on preventive. 

  • Protecting all cats from heartworm infection by using preventives year round. 

  • Maintaining infected cats on preventives to protect them from acquiring additional heartworms, and closely monitoring their health status, providing symptomatic care as needed.

Life Cycle and Stages


  • Microfilariae (300 to 322 µm by 6.8 to 7.0 µm) are ingested by female mosquitoes when they feed on infected canids. (Felids are seldom microfilaremic; consequently, they are less likely sources of microfilariae for mosquitoes). After development through two molts (approximately 2 weeks), infective L3 larvae are present in mosquito mouth parts. Development may require a longer period at cooler temperatures. 
  • Third-stage larvae (L3) are 1,000 µm by 40 µm. They are deposited by mosquitoes on the skin surface during subsequent feeding(s) and then enter the new host via the mosquito bite wound. Most L3 larvae molt to fourth-stage larvae (L4) within 1 to 3 days in the subcutaneous, adipose, and muscle tissues. 
  • The final molt to the juvenile worm occurs approximately 2 months (50 to 70 days) after infection. 
  • Juvenile worms (1 to 3 cm in length) enter the vascular system and are carried to the heart and pulmonary arteries; they arrive as early as 70 days after infection. Most feline infections are aborted at this time, resulting in inflammation in the pulmonary vessels, pulmonary parenchyma, and airways. In a small percentage of infections, further development to mature adult worms and mating may occur. Because of the typically small worm burdens in cats (often one to three worms), single-sex infections (i.e., male or female only) are common. 
  • Maturation to adult worms occurs at about 6 months; development and release of microfilariae occurs about 7 or 8 months after initial infection. 
  • As noted previously, microfilaremia is infrequent (typically less than 20% of naturally infected cats) and short-lived; the number of circulating microfilariae typically is low. Microfilariae are seen in small numbers in experimentally infected cats and persist no more than a few weeks to months. 
  • Mature heartworms in cats are smaller than those in dogs; 12-month-old female worms in cats average 21 cm in length, compare with longer than 26 cm in dogs. 
  • Adult heartworms are believed to live for 2 to 4 years in cats. 
800X600 Heartworm Feline Life Cycle

Heartworm Life Cycle in Cats

Disease

  • Heartworm disease in the cat may involve some or all of the following: 
    • Pulmonary arterial, bronchial, and alveolar disease—Heartworm Associated Respiratory Disease (HARD)—is associated with the death of developing juvenile worms. Cats may present with cough, dyspnea, and/or wheezing. 
    • Death of adult heartworms (if present) can potentiate HARD signs. Sudden death occurs in approximately 10 to 20% of diagnosed cases. Pathogenesis is unclear, but a condition (similar to acute respiratory distress syndrome [ARDS]) caused by the release of antigenic moieties from injured or dying adult worms is suspected. 
    • Vomiting unrelated to eating may be present. 
    • Pulmonary thromboemboli (fragments from dead adult worms) may cause acute vascular and interstitial inflammatory events that lead to dyspnea and death. 
    • Hematological abnormalities may include anemia, hyperglobulinemia, basophilia, and eosinophilia. 
    • Neurological signs may indicate aberrant migration of the worm to the brain, eye, or spinal cord.

Prevalence

  • Geographic prevalence of feline heartworm infection (adult worms) generally follows canine infections, but infection occurs at approximately 10% of the prevalence rate for dogs (see map below for canine prevalence). Cats are infected with juvenile worms at a much higher rate than with adult worms; estimates based on necropsy and antibody studies suggest that cats are infected with juvenile worms at an infection rate similar to that of dogs. The greatest number of cases is seen in the southeastern U.S., the Mississippi River Valley, and Texas. 
  • A study involving more than 2,000 largely asymptomatic cats was conducted in 19 states comprising 21 geographic regions (see figure below). For pet cats (excepting North Carolina, which surveyed shelter animals), the nationwide exposure rates (i.e., percentage of cats that were antibody-positive) were approximately 12%. Many of these cats were from areas not highly endemic for heartworm infection. Results do not confirm mature heartworm infection but imply infection with immature worms and increased risk of HARD. 
  • A second study of 25,000 cats tested nationwide reported a 15.9% antibody positive rate. 

Click here to view our Prevalence Maps and to sign up for updates on reported cases in your area

800X600 Heartworm Feline Map

American Heartworm Society.  The severity of heartworm incidence as shown in this map is based on the average number of cases per reporting clinic.  She remote regions of the United States lack veterinary clinics, therefore we have no reported cases from these areas.

800X600 Heartworm Feline Map Antigen Study

Necropsy-based data (percentage infected) for cats with adult heartworms in shelters is shown in this figure

800X600 Heartworm Feline Map Percent Antibody

Results from a study involving more than 2,000 largely asymptomatic cats.  CNJ = central New Jersey, NNJ = northern New Jersey, LL = Long Island, New York.  Source:  Miller and Atkins, American Heartworm Symposium, 1998

Host Association and Transmission Between Hosts

  • More than 70 species of mosquito are capable of transmitting D. immitis. However, only about 22 species are common and important vectors. 
  • Differences in biological behavior and host preferences by mosquitoes can affect the epidemiology of heartworms in a particular location. 
  • Transmission can occur anytime infected mosquitoes are active and feeding. 
  • Although L3 larvae taken from mosquitoes that had fed on experimentally infected cats were capable of infecting puppies, the infrequency, low numbers, and transient nature of microfilaremia in cats support that in many cases, cats are a dead-end host for D. immitis. 

Site of Infection and Pathogenesis

  • In dogs, adult heartworms reside largely in the pulmonary arteries. However, if numerous worms are present, worms may be found in the right ventricle and pulmonary trunk. In cats, the relative size of the adult heartworm is such that it is much more likely that a portion of the worm can be observed in the right side of the heart. 
  • Migration of immature heartworms to other anatomic sites can occur in cats, sometimes resulting in death. 
  • Pulmonary intravascular macrophages—the primary component of the cat’s reticuloendothelial system—have been implicated in the unique pulmonary pathology found in cats. 

Diagnosis

  • Because of potentially lower worm burden, single-sex infections, and infrequency of microfilaremia, heartworm infection is more difficult to diagnose in cats than in dogs. 
  • Microfilariae identification 
    • Fewer than 20% of cats with mature heartworm infection are microfilaremic. Because of the frequent absence of microfilariae, microfilarial testing (e.g., direct smear, microhematocrit tube, modified Knott test, millipore filter test) is less useful in the cat than in the dog. Nevertheless, a positive microfilariae test confirms active adult heartworm infection in the cat. 
  • Hematological testing 
    • Eosinophilia (and possibly basophilia), although nonspecific, can support a diagnosis of heartworm infection. Eosinophilia, often transient, is most frequently observed 4 to 7 months after infection. 
  • Antibody tests (available as both send-off and point-of-care tests) do not require the presence of circulating antigen produced by mature female worms for a positive test result. Different antibody tests may detect migrating larvae of different ages. If an exposed cat eliminates the infection at the juvenile worm stage, HARD may still result. 
    • Antibody testing may not be effective for diagnosis of feline heartworm disease. Approximately 15 to 25% of cats with adult infection are antibody-negative. Conversely, 80 to 90% of antibody-positive cats do not harbor mature heartworms. 
    • Depending on the preventive product used, up to 30% of cats on preventives that are exposed to heartworms will convert to an antibody-positive state without mature infection or heartworm-related disease. 
    • In a limited number of experimental studies, 50% of experimentally infected cats with confirmed pulmonary pathologic lesions (HARD) seroconverted to a negative antibody status within 8 months after infection. Within 16 months after infection, 100% of experimentally infected cats (HARD) were negative for detectable antibodies. However, after initial infection and induction of HARD lesions, these cats were restricted from further potential exposure to heartworm-infected mosquitoes. 
    • Positive antibody tests may or may not support heartworms as a cause of respiratory signs or lesions. Additionally, a negative antibody test does not rule out current or previous infection. 
  • Antigen testing 
    • Antigen testing is available as both send-off and point-of-care tests. 
    • Only mature female worm infections (typically 7 to 8 months post-infection) are detected. Rarely, in experimental infections, female heartworms may be detected as early as 6 months after infection. A positive antigen test indicates that the cat harbors mature female heartworms or that mature female heartworms were present but died recently. 
    • One third of adult heartworm infections in cats consist only of male worms and will not be detected using available antigen tests. 
    • Studies of naturally infected cats examined at necropsy have shown that some antigen tests are capable of detecting a single mature female heartworm. 
    • A negative antigen test does not conclusively rule out adult heartworm infection nor will it detect juvenile worms often responsible for pulmonary disease (HARD). 
    • Serum samples from cats may be false negative on antigen tests, particularly early in infection, presumably due to formation of antigen-antibody complexes.  Heat treatment of these samples prior to testing has been shown to destroy the complexes, allowing detection of antigen. 
    • Although helpful when a diagnosis of heartworm is suspected but the initial antigen test is negative, routine heat treatment of all samples prior to testing is not recommended.  Heat treatment of serum will destroy antibody, rendering results of subsequent feline antibody tests invalid.

Radiography

  • The most common radiographic findings in feline heartworm disease are enlargement of the right caudal lobar artery and a bronchointerstitial inflammatory pattern in the caudal lung lobes. 
800X600 Heartworm Feline Radiograph

Photo courtesy of Dr. Clarke Atkins, North Carolina State University

Echocardiography

  • Ultrasound in the hands of a skilled ultrasonographer may detect 68% of naturally infected cats. However, the caudal pulmonary arteries must be examined to their point of bifurcation within the lung fields. 

Treatment

  • At present, removal of adult worms from cats using melarsomine dihydrochloride is not recommended. 
  • Early data indicate that concurrent ivermectin and doxycycline therapy for Wolbachia reduces inflammation associated with worm death in dogs. It is not yet known whether this same result can be achieved in cats. 
  • Surgical removal of heartworms via the jugular vein can be performed. However, deaths have been reported during the use of this procedure. In addition, jugular venotomy is expensive and requires the use of a fluoroscope for anatomic guidance. 
  • Microfilaricidal therapy is not recommended in cats. 
  • At present, no specific therapy is recommended for asymptomatic cats with confirmed heartworm infections. However, infected cats cats with symptomatic feline dirofilariasis should be treated with corticosteroids in decreasing dosages to minimize dyspnea, coughing, and wheezing caused by death of either juvenile (HARD) or adult worms. Antileukotrienes also may be beneficial in reducing the risks associated with adult worm death. Bronchodilators may be useful if there is radiographic evidence of air-trapping. Specific therapies should be used if vomiting and neurological signs are present. 
  • Emergency treatment of symptomatic cats may include parenteral corticosteroid therapy, oxygen therapy via an oxygen cage or nasal insufflation, and furosemide in ARDS-like cases. If available, ventilator therapy may be utilized. Xanthine bronchodilators (theophylline or aminophylline) may be used to dilate bronchioles and support the muscles of respiration. 

Prognosis

  • The published life expectancy for cats with adult dirofilariasis is 1.5 years (median). 
  • For cats surviving acute disease beyond day 1, the median survival is 4 years. 
  • Current information suggests that more than 80% of cats diagnosed with heartworm infection survive the infection. 

Control and Prevention

  • All cats, regardless of their lifestyle, should be on year-round heartworm prevention.  Available preventives for cats include oral ivermectin, topical moxidectin/imidacloprid, and topical selamectin.  Topical moxidectin/imidacloprid is also approved for use in ferrets. 
  • Although cats housed indoors have a lower risk for heartworm infection, studies have shown that 25 to 30% of heartworm-infected cats were characterized by their owners as “strictly” indoor cats. Furthermore, certain mosquitoes that typically are found indoors will feed on cats. 
  • Available broad-spectrum feline heartworm preventives are also label-approved for other important feline internal or external parasites. 
  • Available preventives for cats include: 
    • HEARTGARD® Chewables for Cats (ivermectin)(Merial) 
    • Advantage Multi®  Topical Solution for Cats (imidacloprid/moxidectin) (Bayer Animal Health)* 
    • Interceptor® Flavor Tabs® for Dogs & Cats (milbemycin oxime)(Elanco) 
    • Paradyne® (selamectin) (Zoetis) 
    • Revolution® (selamectin)(Zoetis) 

*Note: this product additionally has a label claim for prevention of heartworm disease in ferrets 

Public Health Considerations

  • Because cats typically are amicrofilaremic, heartworm-infected cats pose little to no public health risk. 

Selected References

  • Bowman DD, Atkins CE. 2009. Heartworm biology, treatment, control. Vet Clin North Am Small Anim Pract. 39(6):1127-58
 
  • Lee AC, Aktkins CE. 2010 Understanding feline heartworm infection: disease, diagnosis, and treatment. Top Companion Anim Med Nov 25 (4):224-230
 
  • Little SE, Raymond MR, Thomas JE, et al. 2014. Heat treatment prior to testing allows detection of antigen of Dirofilaria immitis in feline serum. Parasit Vectors Jan 13;7:1
 
  • Maia FC, McCall JW, Valdimero AS, Jr. et al. 2011 Structural and ultrastructual changes in the lungs of Felis catus (Linnaeus, 1758) experimentally infected with D. immitis (Leidy, 1856). Vet Parasitol. 176(4):304-12