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Heartworm

Heartworm for Dog Last updated: Jul 28, 2020

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 microfilariae are present) as soon after diagnosis as medically practical.

View forecasts for Heartworm in your local area at https://petdiseasealerts.org.

Species

Dirofiliaria immitis

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. Also, developing larvae in mosquitoes can undergo developmental arrest in some mosquito species if they become inactive (overwinter) during cold weather. Larvae then resume development when mosquito development proceeds.
  • 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 and the blood vascular system 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 Capc Heartworm Lifecycle

Heartworm Lifecycle

Disease

  • Live heartworms in the dog induce pulmonary endothelial damage, villous proliferation, and activation and attraction of leukocytes and platelets. Dead and dying heartworms induce thrombosis, granulomatous, and villous inflammation.
  • 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.
  • Heartworms may induce glomerulonephritis and proteinuria secondary to antigen-antibody complex deposition.
  • Heartworms can be found at abnormal locations such as the eyes, central nervous system, peritoneal cavity, peripheral vasculature and skin.
  • Caval syndrome (CS) occurs in a small number of cases, and is usually associated with large numbers of adults in the pulmonary arteries
    • Worms present in the post cava and right atrium interfere with the function of the tricuspid valve. CS is a peracute life-threatening condition resulting in hemolytic anemia and right heart failure.
    • Additional 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 geographic expansion of heartworm infection is caused, in part, by increased efforts to re-locate and re-home dogs (see Drake and Parrish, 2019 in the reference section).

  • The greatest numbers of cases are seen in the southeastern U.S. and the Mississippi River Valley.  However, cases are appearing with increasing frequency in traditionally low prevalence areas such as California, Oregon, Washington and Colorado.

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

Hwrawdatamap2019Only

Raw reported heartworm prevalence rates for 2019

Heartworm Baseline Prevalence 2019 Only

Head-banging smoothed heartworm prevalence rates for 2019

Host Associations and Transmission Between Hosts

  • At least 25 species of mosquitoes were shown to harbor L3 larvae (see Ledesma and Harrington, 2011 in the reference section). Mosquito species capable of transmitting heartworms can be found in most geographical areas.
  • Key criteria for determining if mosquitoes are successful heartworm vectors include:
    • Presence of L3 larvae in wild caught mosquitoes.
    • Vector distribution overlaps areas of high heartworm prevalence in wildlife and domestic canids.
    • Feeding on susceptible vertebrate hosts in nature.
    • High feeding frequency on microfilaremic vertebrate reservoirs in nature.
    • Demonstrated development of L3 larvae in laboratory studies.
  • 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 many factors such as mosquito species, 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 exposed to high numbers of mosquitoes for long periods.
    • 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. Recent research supports that the diagnostic glycoprotein is produced by male worms but it may be complexed by antibody (see Gruntmeir et al, 2019 in the reference section).
    • A number of commercial antigen-capture diagnostic tests are available. Formats include well enzyme-linked immunosorbent assay (ELISA) tests, solid substratum ELISA tests, and immunochromatograhic (immunomigratory) tests.
  • Heartworm infection and/or disease is confirmed or ruled out in light of antigen detection, detection of microfilariae, radiography, echocardiography, and/or electrocardiography. These tests may also be used to identify and select 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 most available tests in dogs, it is better to accept than reject a positive test result. Because no test is 100% accurate, it is prudent to repeat positive tests using a different test platform or a test performed at a different site. Similarly, a negative test for an animal exhibiting clinical signs of heartworm disease or circulating D. immitis microfilariae, should be repeated.
      • 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 of antigen (see Little et al, 2014 in the reference section).
      • When a diagnosis of heartworm is suspected but the initial antigen test is negative, heat treatment is recommended. However, heat treatment of all samples prior to testing is not recommended at this time. Although it can improve antigen detection, heat treatment denatures antibodies and will render subsequent antibody detection assays invalid.
      • Mixing 2 or more samples prior to testing is not recommended. Mixing samples can block antigen detection through formation of antigen-antibody complexes or it can dilute circulating heartworm antigen below detectable limits.
    • Clinical pathological parameters
      • Changes in hemogram and chemistry panel are not uniquely diagnostic for heartworms.
      • Hematological changes associated with but not pathognomonic for heartworm infection include eosinophilia, basophilia, neutrophilia, nonregenerative anemia, and thrombocytopenia.
      • Biochemical changes may include elevated liver enzymes, azotemia, and hyperbilirubinemia.
      • Urinalysis may indicate proteinuria and albuminuria in advanced cases or CS.
    • 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.)
        • test used to detect microfilariae is not sensitive enough to detect low numbers.
    • 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 test (MKT)

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 table compares characteristics of D. immitis and A. reconditum. The number and type of motion of microfilariae can only be assessed in fresh blood samples. The shape and size of microfilariae are better determined using a Millipore filter test or a MKT.

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

Width: 4.7 to 5.8 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

Width: 6.7 to 7.0 µm

800X600 Heartworm Canine Microfilariae

Microfilariae of D. immitis (bottom) and A. reconditum (top) as they appear in a modified Knott test. In these preparations, the microfilariae of D. immitis have a greater length and are wider at midbody than those of A. reconditum (see table above).

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.

  • It is important to note that although some radiographic changes can be highly supportive of heartworm disease, particularly in the advanced stages, radiographs should always be combined with other diagnostic test results before assuming a definitive diagnosis.

20170117 Capc Image Bkgd F V1

Chest radiograph

Control and Prevention

  • Heartworm infection is prevented by the administration of macrocyclic lactone preventives as soon as possible, and by behaviorally limiting contact with mosquitoes. Use of products on dogs that repel mosquitoes, further reduces risk of heartworm infection.
  • Heartworm 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, oral, topical or injectable moxidectin, and topical selamectin (Visit CAPC’s “Parasite Product Applications” webpage).
  • RESISTANCE - Some heartworm isolates can develop to adults even in dogs receiving routine prophylaxis with any of the available macrocyclic lactones. However, efficacies against resistant heartworms may vary among available products and formulations.
    • Infected dogs must be treated promptly with an approved adulticide (see below) and non-infected dogs should be maintained on macrolide preventives year round to protect them from heartworm disease.
    • Annual antigen testing of dogs receiving preventives is important. 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 may be advised.
    • At this time, the geographic extent of these resistant heartworms is not known. Re-location of re-homed and rescued dogs that are not treated to removed adult heartworms and microfilariae increases the potential risk and rate of spread.
  • The more common heartworm preventives for dogs include:
    • Advantage Multi® Topical Solution for Dogs (imidacloprid/moxidectin) (Elanco)
    • HEARTGARD® Plus Chewables for Dogs (ivermectin/pyrantel) (Boehringer Ingelheim)
    • Interceptor® Flavor Tabs® for Dogs & Cats (milbemycin oxime) (Elanco)
    • InterceptorTM Plus (milbemycin oxime/praziquantel) (Elanco)
    • Iverhart Max® Chewable Tablets (ivermectin/pyrantel pamoate/praziquantel)  (Virbac)
    • Iverhart Plus® Flavored Chewables (ivermectin/pyrantel) (Virbac)
    • MilbeGuard® (milbemycin oxime) (CEVA)
    • ProHeart® 6 (moxidectin) (Zoetis)
    • ProHeart® 12 (moxidectin) (Zoetis)
    • Revolution® (selamectin) (Zoetis)
    • Sentinel® Flavor Tabs® (milbemycin oxime/lufenuron) (Virbac)
    • Sentinel® Spectrum® Chewables (milbemycin oxime/lufenuron/praziquantel) (Virbac)
    • Simparica TrioTM (sarolaner, moxidectin, pyrantel pamoate) (Zoetis)
    • Trifexis® (milbemycin oxime/spinosad) (Elanco)
    • Tri-Heart® Plus Chewable Tablets (ivermectin/pyrantel) (Merck Animal Health)

Treatment

The goals of treatment are to address the clinical condition of the animal and to eliminate adult heartworms, and microfilariae.

  • Any or all of the following may be medically indicated to stabilize dogs presenting with clinical heartworm disease:
    • corticosteroid therapy
    • fluid therapy
    • diuretics
    • vasodilators
    • positive inotropic agents
  • Dogs receiving a macrocyclic lactone should be maintained on preventive. If a dog is not receiving a macrocyclic lactone preventive, administration of preventive should be initiated as soon as any severe medical condition is stabilized.  The purpose of preventive use is to eliminate new larvae. Treatment with adulticide (melarsomine; see below) is for removal of adult worms and will not kill newly introduced larvae. Melarsomine dihydrochloride is an organo-arsenical adulticide that is available as an injectable product in two branded products (Immiticide (Boehringer Ingelheim); Diroban (Zoetis).
  • CAPC recommends treating infected dogs with adulticide as soon as is medically practical.  Delaying treatment while maintaining dogs on preventives may promote progression of disease.
  • Infected dogs may be placed by veterinarians into one of three disease 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 AND INCREASED SAFETY IN DOGS WITH EVIDENCE OF HIGH WORM BURDENS AND/OR SEVERE DISEASE OBSERVED WITH THE 3-INJECTION REGIMEN MAKES THIS APPROACH THE TREATMENT OF CHOICE FOR ALL HEARTWORM INFECTED DOGS. There is opinion that melarsomine is not effective against heartworms younger than 4 months of age. Because infected mosquitoes can continue to transmit heartworm over a period of many months, heartworms of different ages can be present in dogs. To address this, many veterinarians have also adopted a delay strategy involving a combination of doxycycline and preventive. Both are administered for 1 month followed by an additional month of prevention prior to administration of the first dose of melarsomine. The 3-injection protocol is then followed as discussed above. This strategy is thought to address the gaps discussed above between prevention and adulticide. However, there is alternative opinion that the delay can be reduced to 1 month without any compromise in efficacy (see Carretón et al, 2019 in the reference section). Other, off-label regimens for administration of melarsomine dihydrochloride are not recommended.
    • Melarsomine treatment may not be completely efficacious in all situations. This may necessitate additional therapy or alternate therapeutic strategies (see below).
    • All melarsomine-treated dogs should be antigen tested 6-7 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. However, recent research using a combination of topical moxidectin and doxycycline resulted in demonstrable efficacy. The combination regimen also will reduce or eliminate microfilariae. This decreases risks and concerns about resistance selection.
    • False-negative antigen test results have been observed for dogs treated with slow-kill protocols, presumably because of antigen-antibody complex formation. Consequently, antigen test results from dogs on slow-kill may not be a reliable indicator of infection status.
    • Although the “slow-kill” method is not the preferred heartworm treatment, if it is the only medically acceptable option, microfilariae should be eliminated as soon as possible, and dogs should be maintained on a mosquito repellent as discussed above.
    • Topical moxidectin/imidacloprid is label approved in dogs for removal of microfliariae when used monthly.
  • Post-adulticide microfilaricidal treatment
    • If microfilariae are present after treatment, they should be cleared from the circulation. Caution should be applied when treating dogs with high numbers of microfilariae. Rare anaphylaxis-like reactions have occurred a very few dogs. Microfilariae produced by certain heartworm isolates can persist for more than a year in the presence of high levels of some macrocyclic lactones., These microfilariae put other dogs at risk of infection (or re-infection). Veterinarians who experience difficulties removing microfilariae should consult a parasitologist or other heartworm specialist for advice.
  • Wolbachia pipientis
    • Many filarial nematodes, including D. immitis, harbor obligate, intracellular, gram-negative bacteria known as Wolbachia pipientis. The use doxycycline in regimens discussed above is intended to eliminate these co-habitant organisms.
    • Although research continues, current data indicate that treatment of dogs with doxycycline prior to adulticide therapy to eliminate Wolbachia will i)improve adulticidal and microfilaricidal efficacy ii) reduce the gross pulmonary pathologic changes that occurs as a result of dead and dying worms and fragments, , and iii) interfere with the ability of the microfilariae to develop into infective larvae in mosquito vectors.

Public Health Considerations

  • More than 100 human cases of pulmonary dirofilariasis have been reported in the United States in the last fifty years. Most cases occur in regions where heartworm is common in dogs (see Lee et al, 2010 in the reference section).
  • 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), 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 transmission of D. immitis to people.

Selected References

  • Bowman DD, Atkins CE. 2009. Heartworm biology, treatment, and control. Vet Clin North Am Small Anim Pract. 39(6):1127-58
  • Carretón E, Falcón-Cordón Y, Falcón-Cordón S, Marchón R, Maton JI, Montoya-Alonso JA. 2019. Variation of the adulticide protocol for the treatment of canine heartworm infection: Can it be shorter? Vet Parasitol. 272:54-56.
  • Drake J, Parrish RS. 2019. Dog importation and changes in heartworm prevalence in Colorado 2013-2017. Parasites and Vectors 12:207.
  • Gruntmeir J, Long M, Blagburn B, Walden H. 2019. Heat Treatment: Improved Detection of Male Only Dirofilaria immitis Infection and Overall Assessment of Antigen Detection in Necropsy Positive and Negative Sheltered Dogs in Florida, USA. Proceedings of the 16th Triennial Symposium American Heartworm Society, September 8-11, 2019, New Orleans, LA
  • 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.
  • Ledesma N, Harrington L. 2011. Mosquito vectors of dog heartworm in the United States: Vector status and factors influencing transmission efficiency. Topics in Comp Anim Med 26(4):178-185.
  • 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.
  • McCall JM, Hodgkins E, Varloud M, Mansour A, DiCosty U. 2017. Blocking the transmission of heartworm (Dirofilaria immitis) to mosquitoes (Aedes aegypti) by weekly exposure for one month to microfilaremic dogs treated once topically with dinotefuran-permethrin-pyriproxyfen. Parasites and Vectors 10 (Suppl 2):511:88-95.
  • McCall JM, Varloud M, Hodgkins E, Mansour A, DiCosty U, McCall S, Carmichael J, Carson B, Carter J. 2017. Shifting the paradijm in Dirofilaria immitis prevention: blocking transmission from mosquitoes to dogs using repellents/insecticides and macrocyclic lactone prevention as part of a multimodal approach. Parasites and Vectors 10 (Suppl 2):525):75-85.
  • Paterson T, Fernandez C, Burnett P, Lessey L, Hockley T, Schaper R. Heartworm Control in Grenada, West Indies: Results of a field study using imidacloprid 10% + moxidectin 2.5% (Advantage Multi®, Advocate®) spot-on and doxycycline for naturally acquired Dirofilaria immitis infections. Proceedings of the 27th Conference of the World Association for the Advancement of Veterinary Parasitology/64th American Association of Veterinary Parasitologists Annual Meeting, 7-11 July, 2019, Madison, WI, USA, Abstract OA06.08
  • Prichard R, Ballesteros C, Geary T, Keller K, Bourguinat C, Pulaski C. 2019. Macrocyclic Lactone Resistance in Dirofilaria immitis: Extent of resistance and investigation of the genomic changes underlying resistance. Proceedings of the 27th Conference of the World Association for the Advancement of Veterinary Parasitology/64th American Association of Veterinary Parasitologists Annual Meeting, 7-11 July, 2019, Madison, WI, USA, Abstract OA01.04
  • Starkey LA, Bowles JV, Blagburn BL. 2019. Comparison of acid vs. heat treatment for immune complex dissociation and detection of Dirofilaria immitis antigen in canine plasma. Proceedings of the 16th Triennial Symposium American Heartworm Society, September 8-11, 2019, New Orleans, LA, Pg 47.

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 microfilariae are present) as soon after diagnosis as medically practical.

View forecasts for Heartworm in your local area at https://petdiseasealerts.org.

Species

Dirofiliaria immitis

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. Also, developing larvae in mosquitoes can undergo developmental arrest in some mosquito species if they become inactive (overwinter) during cold weather. Larvae then resume development when mosquito development proceeds.
  • 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 and the blood vascular system 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 Capc Heartworm Lifecycle

Heartworm Lifecycle

Disease

  • Live heartworms in the dog induce pulmonary endothelial damage, villous proliferation, and activation and attraction of leukocytes and platelets. Dead and dying heartworms induce thrombosis, granulomatous, and villous inflammation.
  • 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.
  • Heartworms may induce glomerulonephritis and proteinuria secondary to antigen-antibody complex deposition.
  • Heartworms can be found at abnormal locations such as the eyes, central nervous system, peritoneal cavity, peripheral vasculature and skin.
  • Caval syndrome (CS) occurs in a small number of cases, and is usually associated with large numbers of adults in the pulmonary arteries
    • Worms present in the post cava and right atrium interfere with the function of the tricuspid valve. CS is a peracute life-threatening condition resulting in hemolytic anemia and right heart failure.
    • Additional 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 geographic expansion of heartworm infection is caused, in part, by increased efforts to re-locate and re-home dogs (see Drake and Parrish, 2019 in the reference section).

  • The greatest numbers of cases are seen in the southeastern U.S. and the Mississippi River Valley.  However, cases are appearing with increasing frequency in traditionally low prevalence areas such as California, Oregon, Washington and Colorado.

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

Hwrawdatamap2019Only

Raw reported heartworm prevalence rates for 2019

Heartworm Baseline Prevalence 2019 Only

Head-banging smoothed heartworm prevalence rates for 2019

Host Associations and Transmission Between Hosts

  • At least 25 species of mosquitoes were shown to harbor L3 larvae (see Ledesma and Harrington, 2011 in the reference section). Mosquito species capable of transmitting heartworms can be found in most geographical areas.
  • Key criteria for determining if mosquitoes are successful heartworm vectors include:
    • Presence of L3 larvae in wild caught mosquitoes.
    • Vector distribution overlaps areas of high heartworm prevalence in wildlife and domestic canids.
    • Feeding on susceptible vertebrate hosts in nature.
    • High feeding frequency on microfilaremic vertebrate reservoirs in nature.
    • Demonstrated development of L3 larvae in laboratory studies.
  • 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 many factors such as mosquito species, 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 exposed to high numbers of mosquitoes for long periods.
    • 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. Recent research supports that the diagnostic glycoprotein is produced by male worms but it may be complexed by antibody (see Gruntmeir et al, 2019 in the reference section).
    • A number of commercial antigen-capture diagnostic tests are available. Formats include well enzyme-linked immunosorbent assay (ELISA) tests, solid substratum ELISA tests, and immunochromatograhic (immunomigratory) tests.
  • Heartworm infection and/or disease is confirmed or ruled out in light of antigen detection, detection of microfilariae, radiography, echocardiography, and/or electrocardiography. These tests may also be used to identify and select 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 most available tests in dogs, it is better to accept than reject a positive test result. Because no test is 100% accurate, it is prudent to repeat positive tests using a different test platform or a test performed at a different site. Similarly, a negative test for an animal exhibiting clinical signs of heartworm disease or circulating D. immitis microfilariae, should be repeated.
      • 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 of antigen (see Little et al, 2014 in the reference section).
      • When a diagnosis of heartworm is suspected but the initial antigen test is negative, heat treatment is recommended. However, heat treatment of all samples prior to testing is not recommended at this time. Although it can improve antigen detection, heat treatment denatures antibodies and will render subsequent antibody detection assays invalid.
      • Mixing 2 or more samples prior to testing is not recommended. Mixing samples can block antigen detection through formation of antigen-antibody complexes or it can dilute circulating heartworm antigen below detectable limits.
    • Clinical pathological parameters
      • Changes in hemogram and chemistry panel are not uniquely diagnostic for heartworms.
      • Hematological changes associated with but not pathognomonic for heartworm infection include eosinophilia, basophilia, neutrophilia, nonregenerative anemia, and thrombocytopenia.
      • Biochemical changes may include elevated liver enzymes, azotemia, and hyperbilirubinemia.
      • Urinalysis may indicate proteinuria and albuminuria in advanced cases or CS.
    • 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.)
        • test used to detect microfilariae is not sensitive enough to detect low numbers.
    • 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 test (MKT)

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 table compares characteristics of D. immitis and A. reconditum. The number and type of motion of microfilariae can only be assessed in fresh blood samples. The shape and size of microfilariae are better determined using a Millipore filter test or a MKT.

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

Width: 4.7 to 5.8 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

Width: 6.7 to 7.0 µm

800X600 Heartworm Canine Microfilariae

Microfilariae of D. immitis (bottom) and A. reconditum (top) as they appear in a modified Knott test. In these preparations, the microfilariae of D. immitis have a greater length and are wider at midbody than those of A. reconditum (see table above).

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.

  • It is important to note that although some radiographic changes can be highly supportive of heartworm disease, particularly in the advanced stages, radiographs should always be combined with other diagnostic test results before assuming a definitive diagnosis.

20170117 Capc Image Bkgd F V1

Chest radiograph

Control and Prevention

  • Heartworm infection is prevented by the administration of macrocyclic lactone preventives as soon as possible, and by behaviorally limiting contact with mosquitoes. Use of products on dogs that repel mosquitoes, further reduces risk of heartworm infection.
  • Heartworm 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, oral, topical or injectable moxidectin, and topical selamectin (Visit CAPC’s “Parasite Product Applications” webpage).
  • RESISTANCE - Some heartworm isolates can develop to adults even in dogs receiving routine prophylaxis with any of the available macrocyclic lactones. However, efficacies against resistant heartworms may vary among available products and formulations.
    • Infected dogs must be treated promptly with an approved adulticide (see below) and non-infected dogs should be maintained on macrolide preventives year round to protect them from heartworm disease.
    • Annual antigen testing of dogs receiving preventives is important. 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 may be advised.
    • At this time, the geographic extent of these resistant heartworms is not known. Re-location of re-homed and rescued dogs that are not treated to removed adult heartworms and microfilariae increases the potential risk and rate of spread.
  • The more common heartworm preventives for dogs include:
    • Advantage Multi® Topical Solution for Dogs (imidacloprid/moxidectin) (Elanco)
    • HEARTGARD® Plus Chewables for Dogs (ivermectin/pyrantel) (Boehringer Ingelheim)
    • Interceptor® Flavor Tabs® for Dogs & Cats (milbemycin oxime) (Elanco)
    • InterceptorTM Plus (milbemycin oxime/praziquantel) (Elanco)
    • Iverhart Max® Chewable Tablets (ivermectin/pyrantel pamoate/praziquantel)  (Virbac)
    • Iverhart Plus® Flavored Chewables (ivermectin/pyrantel) (Virbac)
    • MilbeGuard® (milbemycin oxime) (CEVA)
    • ProHeart® 6 (moxidectin) (Zoetis)
    • ProHeart® 12 (moxidectin) (Zoetis)
    • Revolution® (selamectin) (Zoetis)
    • Sentinel® Flavor Tabs® (milbemycin oxime/lufenuron) (Virbac)
    • Sentinel® Spectrum® Chewables (milbemycin oxime/lufenuron/praziquantel) (Virbac)
    • Simparica TrioTM (sarolaner, moxidectin, pyrantel pamoate) (Zoetis)
    • Trifexis® (milbemycin oxime/spinosad) (Elanco)
    • Tri-Heart® Plus Chewable Tablets (ivermectin/pyrantel) (Merck Animal Health)

Treatment

The goals of treatment are to address the clinical condition of the animal and to eliminate adult heartworms, and microfilariae.

  • Any or all of the following may be medically indicated to stabilize dogs presenting with clinical heartworm disease:
    • corticosteroid therapy
    • fluid therapy
    • diuretics
    • vasodilators
    • positive inotropic agents
  • Dogs receiving a macrocyclic lactone should be maintained on preventive. If a dog is not receiving a macrocyclic lactone preventive, administration of preventive should be initiated as soon as any severe medical condition is stabilized.  The purpose of preventive use is to eliminate new larvae. Treatment with adulticide (melarsomine; see below) is for removal of adult worms and will not kill newly introduced larvae. Melarsomine dihydrochloride is an organo-arsenical adulticide that is available as an injectable product in two branded products (Immiticide (Boehringer Ingelheim); Diroban (Zoetis).
  • CAPC recommends treating infected dogs with adulticide as soon as is medically practical.  Delaying treatment while maintaining dogs on preventives may promote progression of disease.
  • Infected dogs may be placed by veterinarians into one of three disease 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 AND INCREASED SAFETY IN DOGS WITH EVIDENCE OF HIGH WORM BURDENS AND/OR SEVERE DISEASE OBSERVED WITH THE 3-INJECTION REGIMEN MAKES THIS APPROACH THE TREATMENT OF CHOICE FOR ALL HEARTWORM INFECTED DOGS. There is opinion that melarsomine is not effective against heartworms younger than 4 months of age. Because infected mosquitoes can continue to transmit heartworm over a period of many months, heartworms of different ages can be present in dogs. To address this, many veterinarians have also adopted a delay strategy involving a combination of doxycycline and preventive. Both are administered for 1 month followed by an additional month of prevention prior to administration of the first dose of melarsomine. The 3-injection protocol is then followed as discussed above. This strategy is thought to address the gaps discussed above between prevention and adulticide. However, there is alternative opinion that the delay can be reduced to 1 month without any compromise in efficacy (see Carretón et al, 2019 in the reference section). Other, off-label regimens for administration of melarsomine dihydrochloride are not recommended.
    • Melarsomine treatment may not be completely efficacious in all situations. This may necessitate additional therapy or alternate therapeutic strategies (see below).
    • All melarsomine-treated dogs should be antigen tested 6-7 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. However, recent research using a combination of topical moxidectin and doxycycline resulted in demonstrable efficacy. The combination regimen also will reduce or eliminate microfilariae. This decreases risks and concerns about resistance selection.
    • False-negative antigen test results have been observed for dogs treated with slow-kill protocols, presumably because of antigen-antibody complex formation. Consequently, antigen test results from dogs on slow-kill may not be a reliable indicator of infection status.
    • Although the “slow-kill” method is not the preferred heartworm treatment, if it is the only medically acceptable option, microfilariae should be eliminated as soon as possible, and dogs should be maintained on a mosquito repellent as discussed above.
    • Topical moxidectin/imidacloprid is label approved in dogs for removal of microfliariae when used monthly.
  • Post-adulticide microfilaricidal treatment
    • If microfilariae are present after treatment, they should be cleared from the circulation. Caution should be applied when treating dogs with high numbers of microfilariae. Rare anaphylaxis-like reactions have occurred a very few dogs. Microfilariae produced by certain heartworm isolates can persist for more than a year in the presence of high levels of some macrocyclic lactones., These microfilariae put other dogs at risk of infection (or re-infection). Veterinarians who experience difficulties removing microfilariae should consult a parasitologist or other heartworm specialist for advice.
  • Wolbachia pipientis
    • Many filarial nematodes, including D. immitis, harbor obligate, intracellular, gram-negative bacteria known as Wolbachia pipientis. The use doxycycline in regimens discussed above is intended to eliminate these co-habitant organisms.
    • Although research continues, current data indicate that treatment of dogs with doxycycline prior to adulticide therapy to eliminate Wolbachia will i)improve adulticidal and microfilaricidal efficacy ii) reduce the gross pulmonary pathologic changes that occurs as a result of dead and dying worms and fragments, , and iii) interfere with the ability of the microfilariae to develop into infective larvae in mosquito vectors.

Public Health Considerations

  • More than 100 human cases of pulmonary dirofilariasis have been reported in the United States in the last fifty years. Most cases occur in regions where heartworm is common in dogs (see Lee et al, 2010 in the reference section).
  • 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), 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 transmission of D. immitis to people.

Selected References

  • Bowman DD, Atkins CE. 2009. Heartworm biology, treatment, and control. Vet Clin North Am Small Anim Pract. 39(6):1127-58
  • Carretón E, Falcón-Cordón Y, Falcón-Cordón S, Marchón R, Maton JI, Montoya-Alonso JA. 2019. Variation of the adulticide protocol for the treatment of canine heartworm infection: Can it be shorter? Vet Parasitol. 272:54-56.
  • Drake J, Parrish RS. 2019. Dog importation and changes in heartworm prevalence in Colorado 2013-2017. Parasites and Vectors 12:207.
  • Gruntmeir J, Long M, Blagburn B, Walden H. 2019. Heat Treatment: Improved Detection of Male Only Dirofilaria immitis Infection and Overall Assessment of Antigen Detection in Necropsy Positive and Negative Sheltered Dogs in Florida, USA. Proceedings of the 16th Triennial Symposium American Heartworm Society, September 8-11, 2019, New Orleans, LA
  • 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.
  • Ledesma N, Harrington L. 2011. Mosquito vectors of dog heartworm in the United States: Vector status and factors influencing transmission efficiency. Topics in Comp Anim Med 26(4):178-185.
  • 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.
  • McCall JM, Hodgkins E, Varloud M, Mansour A, DiCosty U. 2017. Blocking the transmission of heartworm (Dirofilaria immitis) to mosquitoes (Aedes aegypti) by weekly exposure for one month to microfilaremic dogs treated once topically with dinotefuran-permethrin-pyriproxyfen. Parasites and Vectors 10 (Suppl 2):511:88-95.
  • McCall JM, Varloud M, Hodgkins E, Mansour A, DiCosty U, McCall S, Carmichael J, Carson B, Carter J. 2017. Shifting the paradijm in Dirofilaria immitis prevention: blocking transmission from mosquitoes to dogs using repellents/insecticides and macrocyclic lactone prevention as part of a multimodal approach. Parasites and Vectors 10 (Suppl 2):525):75-85.
  • Paterson T, Fernandez C, Burnett P, Lessey L, Hockley T, Schaper R. Heartworm Control in Grenada, West Indies: Results of a field study using imidacloprid 10% + moxidectin 2.5% (Advantage Multi®, Advocate®) spot-on and doxycycline for naturally acquired Dirofilaria immitis infections. Proceedings of the 27th Conference of the World Association for the Advancement of Veterinary Parasitology/64th American Association of Veterinary Parasitologists Annual Meeting, 7-11 July, 2019, Madison, WI, USA, Abstract OA06.08
  • Prichard R, Ballesteros C, Geary T, Keller K, Bourguinat C, Pulaski C. 2019. Macrocyclic Lactone Resistance in Dirofilaria immitis: Extent of resistance and investigation of the genomic changes underlying resistance. Proceedings of the 27th Conference of the World Association for the Advancement of Veterinary Parasitology/64th American Association of Veterinary Parasitologists Annual Meeting, 7-11 July, 2019, Madison, WI, USA, Abstract OA01.04
  • Starkey LA, Bowles JV, Blagburn BL. 2019. Comparison of acid vs. heat treatment for immune complex dissociation and detection of Dirofilaria immitis antigen in canine plasma. Proceedings of the 16th Triennial Symposium American Heartworm Society, September 8-11, 2019, New Orleans, LA, Pg 47.
Heartworm for Cat Last updated: Jul 28, 2020

Synopsis

CAPC Recommends

  • Annual wellness examinations for all cats. This may identify problems associated with heartworms and other parasites early enough to apply successful therapy.
  • Testing cats for heartworm with antigen and antibody test prior to placement on preventive.
  • Considering heat treatment (see diagnostic section) for all samples prior to antigen testing.
  • 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.

Species

Dirofilaria immitis

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 in mosquitoes 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 feeding(s). Larvae enter the host via the mosquitoe 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) arrive in the heart and pulmonary arteries as early as 70 days after infection. Most immature heartworms die before maturing to adults, resulting in inflammation in the pulmonary vessels, pulmonary parenchyma, and airways. However, in a small percentage of infections, 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 (see Genchi et al, 2008 in the reference section).
800X600 Heartworm Feline Life Cycle

Life cycle of heartworm in cats

Disease

  • Heartworm disease in the cat may take several forms:
    • The profile of heartworm disease can be quite different in cats compared to dogs. Research has demonstrated that experimental elimination of immature heartworms after their arrival in the lungs (70-120 days) creates clinical signs and pulmonary lesions similar to what is observed in naturally infected antibody positive, antigen-negative cats. Researchers named the experimentally induced disease heartworm-associated respiratory disease (HARD) to emphasize that the disease primarily targets the lungs and is associated with otherwise undetectable immature stages (see Dillon et al, 2017 in the reference section).
    • Cats with clinical HARD present with cough, dyspnea, and/or wheezing, all signs that are similar to other allergic and infectious respiratory disease. Interestingly, very little cardiac involvement is observed in cats with HARD aside from loss of right ventricular myocardial collagen (see Winter et al, 2017 in the reference section).
      • There is evidence that a corollary to experimental HARD is likely observed in cats naturally infected with heartworms (see Browne et al, 2005 in the reference section). These authors observed lesions very similar to those in experimental HARD in 50% of shelter cats that were positive for heartworm antibodies, but negative for adult worms in heartworm antigen.
    • 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, although none is specific for heartworm disease.
  • 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 2019 CAPC feline antibody prevalence data). 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. However, heartworm infections in cats are likely to occur anywhere that canine heartworm is present.
  • 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 percentage of cats that were antibody-positive was 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 more than 25,000 cats tested nationwide reported a 15.9% antibody positive rate (see Piche et al, 1998 in the reference section).

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

2019 Feline Hw Ab Map

Companion Animal Parasite Council. 2019 Feline Heartworm Ab Map.

800X600 Heartworm Feline Map Antigen Study

Figure from Atkins CE. 2017. Canine and Feline Heartworm Disease. In Textbook of Veterinary Internal Med, Ettinger SJ, Feldman ED, Côté, (eds), Elsevier, St Louis, Mo, pp: 1316-1344.

800X600 Heartworm Feline Map Percent Antibody

Figure from Atkins CE. 2017. Canine and Feline Heartworm Disease. In Textbook of Veterinary Internal Med, Ettinger SJ, Feldman ED, Côté, (eds), Elsevier, St Louis, Mo, pp. 1316-1344.

Host Association and Transmission Between Hosts

  • More than 25 species of mosquitoes were shown to harbor L3 larvae (see Ledesma and Harrington, 2011 in the reference section). However, it is not known whether all of these species can transmit heartworms to cats (see below). It is known that mosquitoe species capable of transmitting heartworms can be found in most geographical areas.
  • Key criteria for determining if mosquitoes are successful heartworm vectors include:
    • Presence of L3 larvae in wild caught mosquitoes.
    • Vector distribution overlaps areas of high heartworm prevalence in wildlife and domestic canids.
    • Feeding on susceptible vertebrate hosts (ie. cats) in nature.
    • High feeding frequency on microfilarmeic vertebrate reservoirs (principally dogs) in nature.
    • Demonstrated development of L3 larvae in laboratory studies.
  • As noted aboe, 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.
  • The infrequency, low numbers, and transient nature of microfilaremias in cats support that they are less likely than dogs to be a source of infections for other animals.

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 pathologic responses observed in the lungs of cats.

Diagnosis

  • Because of potentially fewer heartworms, 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 not specific for heartworm, 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 reference laboratory 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 infected cat eliminates the parasite at the juvenile worm stage, HARD may still result.
    • Antibody testing may not be effective for diagnosis of all forms 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. As mentioned above, symptomatic cats with a positive antibody response could be suffering from heartworm-associated respiratory disease (HARD).
    • Depending on the preventive product used, up to 30% of cats on preventives that are infected with L3 larvae will convert to an antibody-positive state without mature infection or heartworm-related disease.
    • In an experimental study, 50% of 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 (see Dillon et al, 2017 in the reference section).
    • 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 reference laboratory 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. Heat treatment of samples may allow earlier detection of heartworm antigen (see below). 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 likely be detected using available antigen tests. However, heat treatment of serum or plasma may enhance detection of male-only infections (see Gruntmeir et al, 2019 in the reference section).
    • 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.
    • 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 (see Little et al, 2014 in the reference section).
    • Given the increase in sensitivity of antigen tests in cats following heat treatment, in heartworm endemic areas, CAPC suggests heat treatment of all feline serum samples prior to testing for heartworm antigen.
    • 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 broncho-interstitial 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.
  • Although data indicate that concurrent administration of preventive and doxycycline 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 neither required nor recommended in cats because of the infrequency of microfilaremia.
  • 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. Anti-leukotrienes 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. Additional supportive therapies such as warmth, oxygen and fluids (conservatively) may be helpful during acute events. It has been suggested that Clopidogrel may have more relevant application in the cat than other anti-platelet medications. Additional 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

  • In a study of naturally infected cats with adult heartworms, 79% (34/43) survived the infection (see Genchi et al, 2008 in the reference section). In that study, the median survival time was 37 months.
  • In another report, for cats surviving acute disease beyond day 1, the median survival was >1400 days (see Atkins, 2007 in the reference section.

Control and Prevention

  • All cats, regardless of their lifestyle, should be on year-round heartworm prevention (see below).
  •  Available broad-spectrum feline heartworm preventives for are also label-approved for other important feline internal or external parasites.
  • Available preventives for cats include:
    • Advantage Multi®  Topical Solution for Cats (imidacloprid/moxidectin) (Elanco)*
    • Bravecto® PLUS (moxidectin/fluralaner) (Merck)
    • Centragard® (eprinomectin/praziquantel) (Boerhinger Ingelheim)
    • HEARTGARD® Chewables for Cats (ivermectin)(Boehringer Ingelheim)
    • Interceptor® Flavor Tabs® for Dogs & Cats (milbemycin oxime)(Elanco)
    • Revolution® (selamectin)(Zoetis)
    • Revolution® Plus (selamectin/sarolaner)(Zoetis)
  • 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.

Public Health Considerations

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

Selected References

  • Atkins C. 2017. Canine and Feline Heartworm Disease. In Textbook of Veterinary Internal Med, Ettinger SJ, Feldman EC, Côté E (eds), Elsevier, St Louis, MO pp. 1316-1344.
  • Bowman DD, Atkins CE. 2009. Heartworm biology, treatment, control. Vet Clin North Am Small Anim Pract. 39(6):1127-58
  • Browne LE, Carter TD, Levy JK, Snyder PS, Johnson CR. 2005. Pulmonary arterial disease in cats seropositive for Dirofilaria immitis but lacking adult heartworms in the heart and lungs. AJVR 66(9):1544-1549.
  • Dillon AR, Blagburn BL, Tillson M, Brawner W, Welles B, Johnson C, Cattley R, Rynders P, Barney S. 2017. Heartworm-associated respiratory disease (HARD) induced by immature adult Dirofilaria immitis in cats. Parasit Vectors 10(Suppl 2):209-224.
  • Genchi C, Venco L, Ferrari N, Motortarino M, Genchi M. 2008. Feline heartworm (Dirofilaria immitis) infection: A statistical elaboration of the duration of the infection and life expectancy in asymptomatic cats. Vet Parasitol 158:177-182.
  • Gruntmeir J, Long M, Blagburn B, Walden H. 2019. Heat treatment: Improved detection of male-only Dirofilaria immitis infection and overall assessment of antigen detection of necropsy positive and negative sheltered dogs in Florida, USA. Proceedings of the 16th Triennial Symposium American Heartworm Society, September 8-11, 2019, New Orleans, LA, Pg 46.
  • Ledesma N, Harrington L. 2011. Mosquito vectors of dog heartworm in the United States: Vector status and factors influencing transmission efficiency. Topics in Comp Anim Med 26(4):178-185.
  • 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
  • Piche CA, Cavanaugh MT, Donoghue AR, Radecki SV. 1998. Results of antibody and antigen testing for feline heartworm infection at Heska Veterinary Diagnostic Laboratories. In Recent Advances in Heartworm Disease: Symposium ’98, Seward L (ed), American Heartworm Society, Batavia, IL pp. 139-143.
  • Venco L, Marchesotti F, Manzocchi S. 2015. Feline heartworm disease: a ‘Rubik’s-cube-like’ diagnostic and therapeutic challenge. J Vet Cardiology 17: S190-S201.
  • Winter RL, Dillon AR, Cattley RC, Blagburn BL, Tilson DM, Johnson CM, Brawner WR, Welles EG, Barney S. 2017. Effect of heartworm disease and heartworm-associated respiratory disease (HARD) on the right ventricle of cats. Parasit Vectors 10(Suppl 2):209-224.

Synopsis

CAPC Recommends

  • Annual wellness examinations for all cats. This may identify problems associated with heartworms and other parasites early enough to apply successful therapy.
  • Testing cats for heartworm with antigen and antibody test prior to placement on preventive.
  • Considering heat treatment (see diagnostic section) for all samples prior to antigen testing.
  • 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.

Species

Dirofilaria immitis

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 in mosquitoes 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 feeding(s). Larvae enter the host via the mosquitoe 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) arrive in the heart and pulmonary arteries as early as 70 days after infection. Most immature heartworms die before maturing to adults, resulting in inflammation in the pulmonary vessels, pulmonary parenchyma, and airways. However, in a small percentage of infections, 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 (see Genchi et al, 2008 in the reference section).
800X600 Heartworm Feline Life Cycle

Life cycle of heartworm in cats

Disease

  • Heartworm disease in the cat may take several forms:
    • The profile of heartworm disease can be quite different in cats compared to dogs. Research has demonstrated that experimental elimination of immature heartworms after their arrival in the lungs (70-120 days) creates clinical signs and pulmonary lesions similar to what is observed in naturally infected antibody positive, antigen-negative cats. Researchers named the experimentally induced disease heartworm-associated respiratory disease (HARD) to emphasize that the disease primarily targets the lungs and is associated with otherwise undetectable immature stages (see Dillon et al, 2017 in the reference section).
    • Cats with clinical HARD present with cough, dyspnea, and/or wheezing, all signs that are similar to other allergic and infectious respiratory disease. Interestingly, very little cardiac involvement is observed in cats with HARD aside from loss of right ventricular myocardial collagen (see Winter et al, 2017 in the reference section).
      • There is evidence that a corollary to experimental HARD is likely observed in cats naturally infected with heartworms (see Browne et al, 2005 in the reference section). These authors observed lesions very similar to those in experimental HARD in 50% of shelter cats that were positive for heartworm antibodies, but negative for adult worms in heartworm antigen.
    • 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, although none is specific for heartworm disease.
  • 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 2019 CAPC feline antibody prevalence data). 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. However, heartworm infections in cats are likely to occur anywhere that canine heartworm is present.
  • 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 percentage of cats that were antibody-positive was 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 more than 25,000 cats tested nationwide reported a 15.9% antibody positive rate (see Piche et al, 1998 in the reference section).

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

2019 Feline Hw Ab Map

Companion Animal Parasite Council. 2019 Feline Heartworm Ab Map.

800X600 Heartworm Feline Map Antigen Study

Figure from Atkins CE. 2017. Canine and Feline Heartworm Disease. In Textbook of Veterinary Internal Med, Ettinger SJ, Feldman ED, Côté, (eds), Elsevier, St Louis, Mo, pp: 1316-1344.

800X600 Heartworm Feline Map Percent Antibody

Figure from Atkins CE. 2017. Canine and Feline Heartworm Disease. In Textbook of Veterinary Internal Med, Ettinger SJ, Feldman ED, Côté, (eds), Elsevier, St Louis, Mo, pp. 1316-1344.

Host Association and Transmission Between Hosts

  • More than 25 species of mosquitoes were shown to harbor L3 larvae (see Ledesma and Harrington, 2011 in the reference section). However, it is not known whether all of these species can transmit heartworms to cats (see below). It is known that mosquitoe species capable of transmitting heartworms can be found in most geographical areas.
  • Key criteria for determining if mosquitoes are successful heartworm vectors include:
    • Presence of L3 larvae in wild caught mosquitoes.
    • Vector distribution overlaps areas of high heartworm prevalence in wildlife and domestic canids.
    • Feeding on susceptible vertebrate hosts (ie. cats) in nature.
    • High feeding frequency on microfilarmeic vertebrate reservoirs (principally dogs) in nature.
    • Demonstrated development of L3 larvae in laboratory studies.
  • As noted aboe, 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.
  • The infrequency, low numbers, and transient nature of microfilaremias in cats support that they are less likely than dogs to be a source of infections for other animals.

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 pathologic responses observed in the lungs of cats.

Diagnosis

  • Because of potentially fewer heartworms, 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 not specific for heartworm, 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 reference laboratory 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 infected cat eliminates the parasite at the juvenile worm stage, HARD may still result.
    • Antibody testing may not be effective for diagnosis of all forms 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. As mentioned above, symptomatic cats with a positive antibody response could be suffering from heartworm-associated respiratory disease (HARD).
    • Depending on the preventive product used, up to 30% of cats on preventives that are infected with L3 larvae will convert to an antibody-positive state without mature infection or heartworm-related disease.
    • In an experimental study, 50% of 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 (see Dillon et al, 2017 in the reference section).
    • 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 reference laboratory 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. Heat treatment of samples may allow earlier detection of heartworm antigen (see below). 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 likely be detected using available antigen tests. However, heat treatment of serum or plasma may enhance detection of male-only infections (see Gruntmeir et al, 2019 in the reference section).
    • 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.
    • 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 (see Little et al, 2014 in the reference section).
    • Given the increase in sensitivity of antigen tests in cats following heat treatment, in heartworm endemic areas, CAPC suggests heat treatment of all feline serum samples prior to testing for heartworm antigen.
    • 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 broncho-interstitial 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.
  • Although data indicate that concurrent administration of preventive and doxycycline 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 neither required nor recommended in cats because of the infrequency of microfilaremia.
  • 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. Anti-leukotrienes 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. Additional supportive therapies such as warmth, oxygen and fluids (conservatively) may be helpful during acute events. It has been suggested that Clopidogrel may have more relevant application in the cat than other anti-platelet medications. Additional 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

  • In a study of naturally infected cats with adult heartworms, 79% (34/43) survived the infection (see Genchi et al, 2008 in the reference section). In that study, the median survival time was 37 months.
  • In another report, for cats surviving acute disease beyond day 1, the median survival was >1400 days (see Atkins, 2007 in the reference section.

Control and Prevention

  • All cats, regardless of their lifestyle, should be on year-round heartworm prevention (see below).
  •  Available broad-spectrum feline heartworm preventives for are also label-approved for other important feline internal or external parasites.
  • Available preventives for cats include:
    • Advantage Multi®  Topical Solution for Cats (imidacloprid/moxidectin) (Elanco)*
    • Bravecto® PLUS (moxidectin/fluralaner) (Merck)
    • Centragard® (eprinomectin/praziquantel) (Boerhinger Ingelheim)
    • HEARTGARD® Chewables for Cats (ivermectin)(Boehringer Ingelheim)
    • Interceptor® Flavor Tabs® for Dogs & Cats (milbemycin oxime)(Elanco)
    • Revolution® (selamectin)(Zoetis)
    • Revolution® Plus (selamectin/sarolaner)(Zoetis)
  • 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.

Public Health Considerations

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

Selected References

  • Atkins C. 2017. Canine and Feline Heartworm Disease. In Textbook of Veterinary Internal Med, Ettinger SJ, Feldman EC, Côté E (eds), Elsevier, St Louis, MO pp. 1316-1344.
  • Bowman DD, Atkins CE. 2009. Heartworm biology, treatment, control. Vet Clin North Am Small Anim Pract. 39(6):1127-58
  • Browne LE, Carter TD, Levy JK, Snyder PS, Johnson CR. 2005. Pulmonary arterial disease in cats seropositive for Dirofilaria immitis but lacking adult heartworms in the heart and lungs. AJVR 66(9):1544-1549.
  • Dillon AR, Blagburn BL, Tillson M, Brawner W, Welles B, Johnson C, Cattley R, Rynders P, Barney S. 2017. Heartworm-associated respiratory disease (HARD) induced by immature adult Dirofilaria immitis in cats. Parasit Vectors 10(Suppl 2):209-224.
  • Genchi C, Venco L, Ferrari N, Motortarino M, Genchi M. 2008. Feline heartworm (Dirofilaria immitis) infection: A statistical elaboration of the duration of the infection and life expectancy in asymptomatic cats. Vet Parasitol 158:177-182.
  • Gruntmeir J, Long M, Blagburn B, Walden H. 2019. Heat treatment: Improved detection of male-only Dirofilaria immitis infection and overall assessment of antigen detection of necropsy positive and negative sheltered dogs in Florida, USA. Proceedings of the 16th Triennial Symposium American Heartworm Society, September 8-11, 2019, New Orleans, LA, Pg 46.
  • Ledesma N, Harrington L. 2011. Mosquito vectors of dog heartworm in the United States: Vector status and factors influencing transmission efficiency. Topics in Comp Anim Med 26(4):178-185.
  • 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
  • Piche CA, Cavanaugh MT, Donoghue AR, Radecki SV. 1998. Results of antibody and antigen testing for feline heartworm infection at Heska Veterinary Diagnostic Laboratories. In Recent Advances in Heartworm Disease: Symposium ’98, Seward L (ed), American Heartworm Society, Batavia, IL pp. 139-143.
  • Venco L, Marchesotti F, Manzocchi S. 2015. Feline heartworm disease: a ‘Rubik’s-cube-like’ diagnostic and therapeutic challenge. J Vet Cardiology 17: S190-S201.
  • Winter RL, Dillon AR, Cattley RC, Blagburn BL, Tilson DM, Johnson CM, Brawner WR, Welles EG, Barney S. 2017. Effect of heartworm disease and heartworm-associated respiratory disease (HARD) on the right ventricle of cats. Parasit Vectors 10(Suppl 2):209-224.