Heartworm disease continues to be researched, and new aspects of the disease and its management are discovered every year.
We now have an arsenal of test kits and prophylactics to choose from, and it can be confusing to know which to purchase. We
tend to mold ourselves to the product instead of molding the product to the individual patient. This article should help you
tailor the heartworm diagnostic, therapeutic, and prophylactic options to each of your canine and feline patients.
CANINE HEARTWORM DISEASE
Dogs, coyotes, and wolves are the natural hosts for the spread and development of Dirofilaria immitis. Mosquitoes can transmit infective larvae two to two and a half weeks after ingesting blood from infected dogs.1,2 The development of microfilariae into the infective third-stage larvae (L3) (in the mosquito) requires average daily temperatures
greater than 57 F (13.9 C), and transmission is unlikely if the average daily temperature for any 30-day period is less than
65 F (18.3 C).3 So transmission probability varies within the United States depending on the region and ambient seasonal temperature. Dogs
housed outside are four to five times more likely to be infected, and thick coats do not reduce the probability of heartworm
infections.4 Infective L3 enter a dog's skin through a mosquito bite. After three or four months, the larvae molt into young adults (L5),
enter the circulatory system, and eventually travel to the pulmonary arteries.2 Microfilariae (L1) can be seen in the circulatory system six or seven months after the infective L3 enter a susceptible host.
The severity of canine heartworm disease depends on the number of adult heartworms. Dogs with large worm burdens are more
likely to develop severe pulmonary hypertension.5 Heartworms in the pulmonary arteries lead to rapid division of the arterial endothelial smooth muscle cell layer and production
of collagen (pulmonary arteritis).5 Caudal lobar arteries are predominantly affected (Figure 1).2 This vascular endothelial disease is reversible if the heartworm burden is reduced within four to six weeks of developing
an adult heartworm infestation.6
Figure 1: A necropsy specimen of a lung from a dog with heartworm disease. Note the dilated caudal lobar artery with endothelial
Clinical signs and prognosis based on classification
Most dogs with small heartworm burdens are asymptomatic. Coughing secondary to edema (vasculitis) and arteriolar inflammation
is the most common clinical sign. Dyspnea associated with parenchymal disease of the caudal lung lobes is also common.2,5 Exercise dramatically increases pulmonary arterial pressure, and exercise intolerance is common with more severe disease.2 If the disease progresses, right-sided congestive heart failure may develop. Physical examination results associated with
right-sided congestive heart failure include an abdominal fluid wave (ascites) and decreased lung sounds in the ventral thorax
(pleural effusion). Jugular pulses may be present because of increased right atrial pressures. Dyspnea may develop secondary
to hypoxemia, and a split second heart sound may occur because of pulmonary arterial hypertension.2
The prognosis for dogs with heartworm disease depends on the severity of the infestation. Class 1 heartworm disease patients
have no abnormal physical examination findings or radiographic changes and have an excellent prognosis.
Class 2 patients have mild clinical signs, such as an occasional cough with or without exercise intolerance. Thoracic radiographs
show mild pulmonary artery enlargement with mixed alveolar-interstitial lesions (Figure 2). Most Class 2 patients have a good prognosis with proper treatment.
Figure 2: A thoracic radiograph of a dog with heartworm disease. The caudal lobar artery (arrows) is dilated.
Class 3 patients have a poorer prognosis. These patients present with persistent coughing, severe exercise intolerance, weight
loss, cachexia, and often right-sided congestive heart failure. Thoracic radiographs show severe pulmonary artery enlargement,
right ventricular enlargement, and diffuse pulmonary infiltrates. After heartworm adulticide treatment, recommended adjunctive
treatment in Class 3 patients is strict cage rest and oxygen therapy and possibly anti-inflammatory drugs or anticoagulant
Caval syndrome is present in patients with Class 4 heartworm disease in which the worm burden is so severe (50 to > 200 worms)
that the worms drop back into the heart from the pulmonary artery. Worms may extend from the right ventricle across the tricuspid
valve and even back into the venae cavae. Patients with caval syndrome present with dyspnea, tachypnea, tachycardia, pale
mucous membranes, weakness, and often collapse.9 They are usually anemic and hemoglobinuric because erythrocytes fracture as blood is forced through the mass of worms across
the tricuspid valve. Class 4 patients are not candidates for adulticide treatment, and surgical extraction of the heartworms
is required (Figure 3).10
Figure 3: Surgical extraction of heartworms through jugular venotomy in a dog with caval syndrome.