Canis ISSN: 2398-2942

Dirofilaria immitis

Synonym(s): D. immitis, Heartworm

Contributor(s): Gad Baneth, Dwight Bowman

Introduction

Classification

Taxonomy

  • Superfamily: Filarioidea
  • Family: Onchocercidae
  • Genus: Dirofilaria
  • Species: immitis

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Clinical Effects

Epidemiology

Habitat

  • Adults in pulmonary arteries and heart Dirofilariasis: villous endoarteritis Dirofilariasis: canine heart. The flow of blood tends to keep the worms in the pulmonary arteries; they tend to appear in the heart only when present in very large numbers or in very small dogs. The worms will often be found at necropsy in the heart because the pumping action of the blood into the pulmonary vessels has ceased and the worms can move back towards the heart.
  • Larval stages in the dog develop in the subcutaneous tissues, connective tissue, and fascia. After the larvae molt to the young-adult stage, they migrate to the heart.
  • Microfilariae are found in the circulating blood.

Lifecycle

  • Dirofilaria immitis undergoes heteroxenous development, ie it utilizes two hosts in its life cycle. Sexual maturation occurs in the final host, the canid, and it is in the canid host that the transmission stages, the microfilariae, circulate in the blood. The mosquito that takes a blood meal from a dog becomes both the required intermediate host and the vector of disease transmission. The microfilariae cannot develop to adult worms unless they pass through a mosquito where they develop to infective third-stage larvae.
  • A female mosquito takes a blood meal from a dog (only female mosquitoes take blood meals, and they feed repeatedly because the blood is required by most mosquitoes for their eggs to develop within their ovaries). The microfilariae in mosquitoes under optimal temperatures develop in slightly less than two weeks to infective-stage larvae. The next time the mosquito feeds, the larvae are in the head and mouthparts of the mosquito, and they leave the mosquito and move onto the skin of the dog near the bite wound. Then, when the mosquito retracts her proboscis, the larvae enter the open hole to gain entry to the body of the canine host.
  • In the dog, the larvae undergo a molt from the third to fourth stage in the subcutaneous tissues around three days after infection. They then migrate around in the tissues and fascia of the dog, molt again sometime between the second to third months after infection to become young adults that then make their way to the pulmonary arteries. The worms are around 4-7 cm long when they get to the heart and lungs, but by about 5 months after infection they will be around 10-16 cm long. The prepatent period, ie from the initiation of infection until microfilariae appear in the blood, is about 7 months

Transmission

  • The only way for a dog to become infected is via the bite of a mosquito harboring infective-stage larvae.

Pathological effects

  • Pathology is due to the worms being present in the pulmonary arteries. These large worms, 12-31 cm long, live in the lumen of these vessels. They maintain their position by twisting and coiling against the vessel wall. The blood coursing through the artery causes the worms to bang with each heartbeat onto the intima of the vessel. Also, red blood cells that impact the worms in the vessels will rupture releasing their contents into the surrounding serum.
  • The constant impact of the worms on the vessel wall induces a villous proliferation on the intima. This proliferation, which can be millimeters tall, will cause stasis of the blood along the vessel wall, and results in further red blood cell rupture and thrombus formation. These thrombi then get carried down into the deeper parts of the lungs where they preclude smaller vessels.
  • The hemoglobin from the ruptured red blood cells accumulates in various histocytes and macrophages within the lung tissue, and the lungs will take on a brown appearance.
  • Worms that die, either spontaneously or after treatment, have nowhere to go other than deeper into the pulmonary vessels of the lungs where they slowly decompose and induce granulomatous reactions to the large mass of foreign tissue.
  • In heavy infections or small dogs, worms can appear in the right ventricle or atrium and interfere with the function of the pulmonary and tricuspid valves.
  • Worms can sometimes enter the vena cava where they will induce severe hemolysis that can appear as hematuria with concurrent ascites; this is termed caval syndrome Caval Syndrome. This is a condition that is often fatal without the surgical removal of the worms from the vena cava.
  • As lung perfusion diminishes, there will be pulmonary hypertension Pulmonary Arterial Hypertension (PHT) , that can lead to cor pulmonale Cor pulmonale with enlargement of the right ventricle. Such disease will be associated with shortness of breath, exercise intolerance, syncope, ascites, and other sequela.
  • In long-standing chronic cases, there is also the deposition of antigen-antibody complexes onto kidney glomeruli that may lead to renal disease.
  • Microfilariae, except after rapid killing with various microfilaricidal products, tend not to be very pathogenic in their own right although they are present sometimes in very high numbers in the circulating blood.

Other Host Effects

  • Adult worms can occasionally migrate to ectopic sites and cause complications either while still alive or after their death.
  • There is very little known about pathology induced by the larvae that migrate in the dog prior to their making their way to the lungs, it is assumed that the disease induced is minimal or not significant.
  • When large numbers of microfilariae are killed rapidly with either diethylcarbamazine or doses of macrocyclic lactones, there can be significant disease in the treated dog. The reaction is usually great upon the administration of the diethylcarbamazine which also appears to act as an immunopotentiator. These dogs will be depressed, may vomit, and may become comatose, and can on rare occasions die.

Host interaction

  • Dirofilaria immitis can cause significant disease in cats. In cats there are usually only one or a very few worms that develop to the adult stage. The antigen detection test detects female uterine antigen, so that if there is only one or more males present (with only one worm in a host, the chances are about 50/50 that it will be a male, both sexes seem to mature equally well in experimentally infected cats), the infection will not be diagnosed. Thus, some prefer to use antibody tests in cats. In cats, the worms, although few in number, can very commonly be detected by ultrasound of the heart; the worms look like paired lines. Cats can develop severe lung disease from the developmental stages, even if they do not develop patent infections. Also, cats can die of ectopic migration of the worm to non-pulmonary sites. Cats should be placed on heartworm preventive, especially in areas where there is a high risk to the dog population (or where large percentages of coyotes are infected in the surrounding environment).
  • Ferrets make excellent hosts for heartworms. Thus, ferrets should be placed on macrocyclic lactone preventive regimen.
  • Seals and sea lions in zoos in areas with heartworms should be on preventive.
  • People do develop zoonotic infections with canine heartworms. These infections are often without clinical signs. It is unclear how many cases occur annually, and how many people in the United States and other heartworm endemic areas actually are infected with heartworms or have antibodies indicating prior exposure.
  • In areas where dogs in a practice are on preventive, it may seem that there is an apparent lack of heartworms in an area if dogs are tested for infection. However, unowned or feral dogs in the neighborhood and any coyotes in the area may be serving as a major reservoir for any animals not on preventive therapy, including cats.

Control

Control via chemotherapies

  • Prevention is typically by the killing of third stage and fourth stage larvae in dogs through the monthly administration of macrocyclic lactones Control of canine cardiopulmonary dirofilariasis. These occur in varied formulations, administered orally, topically, and as injectable product. They may or may not have efficacy also against various other helminth and arthropod parasites of the dog and cat. Some are also formulated with other anthelmintic or products with activity against various arthropods to give them a broader spectrum of activity.
  • Prevention is also still performed by killing either the third-stage larvae or larvae molting from the third to fourth stage by the daily administration of diethylcarbamazine.
  • Treatment of infections with adult worms requires the administration of organic arsenical chemotherapeutic agent melarsomine dihydrochloride Melarsomine {4-[(4,6-diamino-1, 3, 5-triazon-2-yl) amino] phenyl-dithioarsenite of di (2-aminoethyl), dihydrochloride}.
  • Killing of the microfilaria in infected dogs is achieved by treatment with avermectins Selamectin at microfilaricidal doses.

Control via surgery

  • Some people choose to treat heartworms in cats by the surgical extraction of the worms; the melarsomine dihydrochloride is highly toxic to cats.
  • Some people choose to treat dogs by the surgical removal of worms tather than administer melarsomine dihydrochloride Melarsomine.
  • In the case of caval syndrome Caval Syndrome Caval syndrome: heartworm extraction , the surgical extraction of the worms from the vena cava with alligator forceps is often required to keep the dog alive.

Control via environment

  • Mosquito control is helpful, but it is mainly applied by communities to protect against the nuisance of mosquito bites on human inhabitants and to protect against mosquito-borne arboviruses.
  • Permethrin collars or topically applied permethrin Permethrin will prevent mosquitoes from biting and may even kill some mosquitoes that come in contact with dogs.

Vaccination

  • None available.

Diagnosis

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Further Reading

Publications

Refereed papers

  • Recent references from VetMed Resource and PubMed.
  • Fukunaga N, Morita T, Sawada M, Matsumoto K, Okamoto M, Uemura T, Haruna A, Shimada A (2005) Cerebral haemorrhage and necrosis due to the aberration of Dirofilaria immitis in a dog. J Jap Vet Med Assoc 58, 751-754.
  • Nelson C T, McCall J W, Rubin S B, Buzhardt L F, Doiron D W, Graham W, Longhofer S L, Guerrero J, Robertson-Plouch C, Paul A (2005) Guidelines for the diagnosis, prevention and management of heartworm (Dirofilaria immitis) infection in dogs. Vet Parasitol 133, 255-266 PubMed.
  • Theis J H (2005)  Public health aspects of dirofilariasis in the United States. Vet Parasitol 133, 157-180 PubMed.
  • Yoon H Y, Jeong S W, Kim J Y, Han H J, Jang H Y, Lee B, Namkung H S (2005) The efficacy of surgical treatment with flexible alligator forceps in dogs with heartworm infection. J Vet Clinics 22, 309-313.
  • Kang S S, Kim J H, Kwon Y B, Choi S H (2002) A harbor seal infection with Dirofilaria. J Vet Clinics 19, 92-94.
  • Theis J H, Gilson A, Simon G E, Bradshaw B, Clark D (2001) Case report: unusual location of Dirofilaria immitis in a 28-year old man necessitates orchiectomy. Am J Trop Med Hyg 64, 317-322 PubMed.
  • Narine K, Brennan B, Gilfillan I, Hodge A (1999) Pulmonary presentation of Dirofilaria immitis (canine heartworm) in man. Eur J Cardio-Thoracic Surg 16, 475-477.
  • McCall J W (1998) Dirofilariasis in the domestic ferret. Clin Tech Small Anim Pract 13, 109-112.
  • Lichtenfels J R, Pilitt P A, Kotani T, Powers K G (1985) Morphogenesis of developmental stages of Dirofilaria immitis (Nematoda) in the dog. Proc Helm Soc Wash 52, 98-113.
  • Beusse D O, Asper E D, Baucom J N, Searles S W (1977) Diethylcarbamazine citrate for prevention of heartworm (Dirofilaria immitis) in the California sea lion (Zalophus californianus). Vet Med Small Anim Clin 72, 470-471.

Other sources of information

  • Peregrine A S (2005) Rational Use of Diagnostic Tests. Chapter 133, Volume 1. In: Textbook of Veterinary Internal Medicine: Disease of the Dog and Cat. 6th edn. SJ Ettinger and EC Feldman, editors. Elsevier Saunders, St. Louis, MO, pages 489-492.
  • Bowman D D (2003) Helminths. In: Georgis' Parasitology for Veterinarians. 8th edn. Philadelphia, PA.W B Saunders. pp 216-222.
  • Anderson R C (2000) Nematode Parasites of Vertebrates, Their development and transmission. 2nd edn. CABI Publishing, Oxon , UK.
  • Knight D H & Lok J B (1995) Seasonal timing of heartworm chemoprophylaxis in the United States. Proceedings of the heartworm symposium '95, Auburn, Alabama, USA, 31 March 2nd April, 1995. pp 37-42.
  • Slocombe J O D, Bhartendu-Srivastava, Surgeoner G A (1995) The transmission period for heartworm in Canada. Proceedings of the heartworm symposium '95, Auburn, Alabama, USA, 31 March 2nd April, 1995. pp 43-48.
  • Soulsby E J L (1982) Helminths, Arthropods and Protozoa of Domesticated Animals. 7th Edn. Ballière Tindall, London.
  • Levine N D (1980) Nematode Parasites of Domestic Animals and of Man. 2nd edn. Burgess Publishing Co, Minneapolis, MN. pp 356-359, 386-395.

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