Heartworm disease

What it is

Heartworm disease is caused by Dirofilaria immitis, a filarial nematode transmitted by mosquitoes of the genera Culex, Aedes and Anopheles. The mosquito ingests microfilariae when it bites an infected dog; inside the mosquito they develop into infective larvae (L3), which it deposits when it bites another animal. The larvae migrate through the tissues for several months, moult, and the immature worms reach the pulmonary arteries through the veins, especially those of the caudal lobes, where they mature. Adults can live for years and, when males and females are present, release microfilariae into the blood.

The worms and their endosymbiotic bacterium Wolbachia damage the endothelium and cause proliferative endarteritis: the intima thickens with villous proliferations, the arteries dilate, become tortuous and lose elasticity, and thrombi form. Over time pulmonary hypertension and right-sided heart failure develop. Death of the worms, spontaneous or due to treatment, causes pulmonary thromboembolism.

It is common in warm, humid areas of the Americas, southern Europe, Asia, Africa and Australia, and is spreading into central and eastern Europe.

It is a vector-borne zoonosis: people are infected by mosquito bites, never by direct contact with the dog. D. immitis does not reach adulthood in people: the worm dies and lodges in a branch of the pulmonary artery, where it forms a pulmonary nodule that can be mistaken for a tumour on radiographs. Dirofilaria repens, which in the dog lives in the subcutaneous tissue and is usually asymptomatic, causes subcutaneous and ocular nodules in people and is the species responsible for most human cases in Europe. Controlling infection in dogs reduces the source for mosquitoes and, with it, the risk to people.

Who it affects

Dogs of any age that live in or travel to endemic areas and do not receive prevention, especially those that spend a lot of time outdoors. Working, hunting and guard dogs are more exposed. Cats are infected less often (see the section on the cat), as are ferrets and wild canids such as the fox and the coyote.

Anatomy involved

• Heart: pulmonary hypertension forces the right ventricle to work against greater resistance, so it hypertrophies and dilates (cor pulmonale), with tricuspid regurgitation and right-sided heart failure. In heavy infections worms also occupy the right ventricle and atrium. In caval syndrome, a mass of worms moves into the right atrium and the tricuspid valve, obstructs flow and causes intravascular haemolysis.
• Great vessels: in caval syndrome the worms can extend into the caudal vena cava, and right-sided heart failure distends this vessel and congests the liver, with ascites.
• Lungs: the lobar pulmonary arteries are dilated, tortuous and truncated; around them there is periarterial inflammation, eosinophilic pneumonitis, thrombosis, infarcts and fibrosis. Lesions are most severe in the caudal lobes and worsen with exercise and after the worms die.

Clinical signs

Many infected dogs have no signs at first. Later, chronic cough, exercise intolerance, dyspnoea, weight loss and syncope appear; in advanced disease, ascites and right-sided heart failure. After the worms die there may be pulmonary thromboembolism with acute dyspnoea, fever and haemoptysis. Caval syndrome is an emergency: sudden collapse, pale mucous membranes, haemoglobinuria, a tricuspid murmur and shock. Guidelines classify dogs by disease severity, from mild to severe, plus caval syndrome.

Diagnosis

• Antigen test: detects proteins from adult female worms and is the test of choice in the dog. It only becomes positive several months after infection and can be negative when there are few females or only males. Annual testing is recommended in endemic areas.
• Microfilaria detection (modified Knott's test or filtration): confirms infection and requires differentiation from Dirofilaria repens and Acanthocheilonema reconditum. Many infected dogs have no microfilariae.
• Thoracic radiographs: dilated, tortuous lobar pulmonary arteries, right heart enlargement and a pulmonary pattern, which help to assess severity.
• Echocardiography: assesses pulmonary hypertension and the right heart and can show the worms, as parallel hyperechoic lines, in the pulmonary artery or the right heart.

Treatment and prevention

Treatment follows the guidelines of the American Heartworm Society (AHS) and the European Society of Dirofilariosis and Angiostrongylosis (ESDA). The dog is stabilised first and strict exercise restriction is imposed throughout treatment, because exercise worsens thromboembolism. A macrocyclic lactone is given, which kills migrating larvae and reduces microfilariae, together with doxycycline for several weeks against Wolbachia, which reduces the lung pathology associated with worm death. Then the only approved adulticide, melarsomine, is used with the three-injection protocol: one injection and, one month later, two injections 24 hours apart. Glucocorticoids help control pulmonary inflammation. Success is checked with an antigen test months later. Prolonged use of macrocyclic lactones and doxycycline without melarsomine ("slow-kill" protocols) kills adults more slowly while the disease keeps progressing and may favour resistance; the guidelines reserve it for when melarsomine is unavailable or contraindicated. Caval syndrome is treated by extracting the worms through the jugular vein.

Prevention is simple and effective: macrocyclic lactones (ivermectin, milbemycin oxime, moxidectin or selamectin) given orally or topically every month, or sustained-release injectable moxidectin, all year round or throughout the mosquito season depending on the area. They act on larvae acquired in the preceding weeks, so late doses leave infections uncovered. Populations of D. immitis resistant to macrocyclic lactones have been confirmed in the United States, so strict compliance, annual testing, the use of mosquito repellents and elimination of microfilariae in positive dogs are emphasised.

In the cat

The cat is an unsuitable host: it is infected less often than the dog, harbours few worms, which live for a shorter time, and almost never has microfilariae. Even so, the disease can be severe, and it also affects indoor cats, because mosquitoes enter homes.

• Lungs: the arrival of immature worms in the pulmonary arteries and their death trigger an intense inflammatory reaction in the arteries, bronchioles and alveoli, called heartworm-associated respiratory disease (HARD). It occurs even if no worm reaches adulthood. Death of adult worms can cause acute lung injury and thromboembolism, sometimes fatal.
• Heart: worms lodge in the pulmonary arteries and sometimes in the right heart, but, unlike in the dog, right-sided heart failure is uncommon.

Signs resemble those of feline asthma: cough, dyspnoea and open-mouth breathing; intermittent vomiting is also common, and some cats die suddenly without previous signs. Diagnosis is difficult: antigen tests are less sensitive than in the dog, because cats have few worms, sometimes only males or only immature ones, and antibody tests indicate exposure but not active infection. Both tests are combined with thoracic radiographs (dilated caudal pulmonary arteries and a bronchointerstitial pattern) and echocardiography, which can show the worms. There is no safe adulticide treatment in the cat and melarsomine is not used in this species; signs are treated with glucocorticoids and oxygen therapy when needed. That is why monthly prevention with macrocyclic lactones is the key measure for cats in endemic areas.

Key studies

• Anvari et al. (2020), systematic review and meta-analysis of 193 studies on prevalence in dogs worldwide. Pooled prevalence was 10.91% (95% CI 10.18–11.65), with significant differences between countries. It relies on published studies with very different populations and methods.
• Jacobson et al. (2026), randomised clinical trial in 168 dogs with class 1 or 2 disease treated with sustained-release moxidectin, doxycycline, prednisone and melarsomine in two or three injections. Efficacy was 95.3% with two doses and 98.8% with three, with no significant difference, and survival was 100%, with few complications. The sample size was not enough to demonstrate non-inferiority and it only included dogs with mild or moderate disease; guidelines still recommend the three-dose protocol.
• Santiwattanatarm et al. (2026), systematic review and meta-analysis of 14 studies with 358 dogs, mostly with mild or moderate disease, treated with topical moxidectin and doxycycline without melarsomine. The adulticidal effect increased over time: in comparative studies antigen conversion to negative was similar to melarsomine from 9 months onward, and in before-after studies it reached 99% at 12 months (95% CI 99–100%; moderate certainty). Comparative data were scarce, complications were variably reported and there was risk of bias; it is an alternative when melarsomine cannot be used, not a general substitute.
• Curry et al. (2025), genetic surveillance of 310 microfilaraemic blood samples from client-owned dogs, from 45 clinics in 22 US states. Based on genetic markers associated with resistance, 35.8% of infections were susceptible, 31.0% resistant and 33.2% mixed, and resistant infections appeared outside the endemic Lower Mississippi River Valley, as far north as Michigan. These are genetic markers, not efficacy tests in dogs, samples came only from infected dogs and the study was funded by a parasiticide manufacturer.
• Berdoulay et al. (2004), comparison of serological tests in 380 cats from an endemic area, with necropsy as the reference. Antigen tests detected 79.3% to 86.2% of infections and were highly specific; most false negatives were cats with a single male worm. Antibody tests detected 62.1% to 72.4%, with more false positives (1.4–19.1%), and combining both increased sensitivity. The tests evaluated are two decades old.
• Hattendorf and Lühken (2025), systematic review of D. immitis and D. repens infections in mosquitoes and mammals in Europe. Both species share mosquitoes of the genera Aedes, Anopheles and Culex as potential vectors; most published D. immitis infections were in dogs, while those of D. repens were mainly in people. Over the last 20 years both have spread to many more countries, especially in central Europe. Only PubMed was searched and it depends on what has been published.