Dog Heartworm
Dog heartworm, Dirofilaria immitis. is an important filarial nematode infection of dogs and canids primarily, but can occur in other mammals and occasionally in humans. It usually occupies the pulmonary arteries and the right ventricle of the heart. Dog heartworm is transmitted by mosquitoes.
BIOLOGY
D. immitis is a filarial nematode in the superfamily Filarioidea (order Spirurida, class Chromadorea). The males are 12-20cm in length and 0.7-0.9 mm in diameter, with a spirally coiled posterior end. The females are 25-31 cm in length and 1.0-1.3mm in diameter. D. immitis was first found in the United States, but it occurs globally, with a tendency for increased prevalence in humid warm regions conducive to abundant mosquito populations. In the United States, the prevalence can be as great as 45% in dogs within 150 miles of the Gulf of Mexico coast, Atlantic coast north to New Jersey, and Mississippi River and its tributaries. The prevalence elsewhere in the United States is generally less than 5%. Although dogs are the primary host, D. immitis has been found in coyotes, wolves, dingoes, foxes, sea lions, harbor seals, wolverines, ferrets, and cats. The number of nematodes per dog is variable, ranging from a single nematode to as many as 250. Cats are less tolerant, with maximum parasite loads of 1-2 nematodes. D. immitis can persist for 5-7 years in dogs and 2-3 years in cats.
Mature female nematodes reproduce ovoviparously, and the microfilaria are released from the uterus of the worm via the vaginal opening into the host blood. Microfilaria are 220-330 |im in length and 5-7 |im in width. Under laboratory conditions, over 60 species of mosquitoes are competent hosts for D. immitis. When mosquitoes take a blood meal, microfilaria are ingested and reside in the mosquito midgut briefly and then migrate to the Malpighian tubules, where they enter the cells and shorten. After a short developmental period, the juvenile nematodes leave the cells day 6- 7 postinfec-tion and enter the lumen of the tubules where the first molt (day 10) takes place, with the formation of the second-state juveniles (J2). After further growth and differentiation, the J2 molts (days 10- 14 postinfection) to the infective stage (J3), which reaches a length of 1.3 mm. The J3 migrate through the hemocoel to the proboscis sheath of the mosquito. Development of the juvenile stages ceases if ambient temperatures decline below 15°C, which constitutes a constraint on the distribution of D. immitis. When the infected mosquito takes a blood meal, the J3 escape from the proboscis sheath, dropping onto the host in a droplet of hemolymph; they enter the host through the wound made by the piercing mouthparts of the mosquito. The J3 enter the subcutaneous tissue where they undergo the third molt to the fourth-stage juveniles, which reside in subcutaneous tissues or muscle of the abdomen or thorax for about 60 days, at which time the last molt to the adult stage occurs. The nematodes are now 12-15 mm long and enter the pulmonary arteries and attain lengths of 3.2- 11 cm by 85 – 120 days postinfection. Fertilized females can be found 120 days postinfection, and microfilaria enter the blood 6-9 months postinfection. Microfilaria can survive in the blood for 2.5 years. Wolbachia, a group of intracellular rickettsial-like organisms, have been recognized as endosymbionts in D. immitis. Host treatment with tetracycline leads to the loss of the endosymbi-onts and a concomitant reduction in survival and reproduction of D. immitis.
HOST PATHOLOGY
Usually no signs of infection are present in dogs until 8-9 months postinfection. Symptoms are generally related to the intensity of infection. The presence of 25 worms may be tolerated by the dog, with no signs of disease. Symptoms such as reduced exercise tolerance and coughing increase significantly when the nematode burden doubles and serious symptoms appear, such as dyspnea (difficulty in breathing), hepatomegaly (enlargement of the liver), syncope (temporary loss of consciousness), and ascites (fluid accumulation in the abdomen). At this level, death may occur. Pathogenesis is related primarily to inflammation of pulmonary arteries and lungs induced by the adult stage of D. immitis although current evidence suggests that Wolbachia metabolic products/antigens contribute significantly to the pathogenesis of heartworm infections. This chronic inflammatory process in combination with the physical obstruction by the nema-todes of blood flow leads to pulmonary hypertension and heart failure. Diagnosis depends on an accurate history, recognition of symptoms, and diagnostic procedures such as microfilarial detection, serology, clinical laboratory tests, radiology, ultrasonography, and angiography. Microfilaria are detected through concentration of the microfilaria from a small quantity of blood by the Knott’s test or filtration. In some dog heartworm infections (occult heartworm infection), microfilaria are not detectable and diagnosis relies on serology and other diagnostic tools.
MANAGEMENT
Treatment is effective. The goal is elimination of the primary disease agent, the adults. An arsenical drug is currently approved for use in dogs, melarsomine hydrochloride (Immiticide; Merial), but pretreat-ment with ivermectin (Stromectol®; Merck) to reduce heartworm mass is recommended. Treatment requires concomitant restriction of exercise and use of anti-inflammatory support to reduce the possibility of pulmonary thromboembolism from the dead heartworms. Microfilaria are eliminated by secondary treatment with ivermectin or milbemy-cin. Prevention of heartworm infection is safer and more economical than treatment and is accomplished readily by routine administration of diethylcarbamazine citrate (daily in the diet) or one of the macrolide anthelminthics (monthly treatment; ivermectin, milbemycin oxime, moxidectin, selamectin) initiated before the transmission season.
