depending on the severity of infection, potentially leading to the production of massive numbers of microfilariae (Blagburn, 2013). Microfilariae are the first larval stage (L1) of heartworms, produced approximately six to seven months after heartworm infection. These larvae are released from the female adult heartworm and circulate in the peripheral blood. Microfilariae are approximately 300 µm long by 7 µm wide. They circulate through the bloodstream all day, but they are found in higher numbers during the evening, a pattern referred to as incomplete nocturnal periodicity (Blagburn, 2013). These microfilariae can live for approximately two years in the circulatory system, waiting to be ingested by a mosquito.
When a susceptible mosquito vector bites a dog with circulating microfilariae, these microfilariae may be ingested. Once in the mosquito’s gut, microfilariae migrate to the malphigean tubules (part of the mosquito excretory system), where they will remain as they undergo two molts to the infective L3 larval stage. Once in the L3 stage, these infective larvae will migrate to the mouthparts, where they can infect a new canine host. Microfilariae are only infectious after they have undergone two molts within the mosquito. Direct transmission of microfilariae will not produce infection with adult heartworms. Although puppies can be infected with microfilariae transplacentally, these microfilariae will not mature into adult heartworms (Blagburn, 2013).
PATHOPHYSIOLOGY
The clinical signs of heartworm disease are caused by both the heartworms themselves, and the host immune response to the heartworms. Upon arriving to the heart, adult heartworms create mechanical irritation and inflammation within the heart and vessels. Live heartworms also produce vasoactive substances that exacerbate and perpetuate vessel damage. Inflammation within the pulmonary vessels leads to pulmonary hypertension, increasing the cardiac workload and contributing to right ventricular hypertrophy. Over time, signs of right heart failure may also be observed (Companion Animal Parasite Council, 2016). Clinical signs of heart failure may include cough, hemoptysis, dyspnea, exercise intolerance, and weight loss. On physical exam, ascites, jugular venous distension, and arrhythmias may also be noted. In addition to local effects within the heart and lungs, heartworm disease can also have systemic effects. As cardiac output begins to decrease, organ perfusion decreases; therefore, signs of liver disease, and kidney disease may be observed (Blagburn, 2013). Furthermore, the immune reaction to heartworms may lead to antigen-antibody complex deposition in the kidneys, resulting in glomerulonephritis and proteinuria (Companion Animal Parasite Council, 2016). In some situations, ectopic infections at aberrant sites may also develop due to aberrant worm migration. In these cases, heartworms migrate to the central nervous system, eye, peritoneal cavity, systemic circulation, or skin. The effects of these ectopic infections vary, depending on the specific tissues affected (Companion Animal Parasite Council, 2016). In dogs with severe heartworm infection, adult heartworms have the potential to interfere with the function of the tricuspid
valve, obstructing blood flow and interfering with closure of the valve. Clinical signs of caval syndrome include a sudden onset of severe lethargy, pale mucous membranes, dyspnea, and weakness. Physical exam often reveals a systolic murmur consistent with tricuspid regurgitation, palpable jugular pulses, and liver congestion. Hemoglobinuria often develops, and the diagnosis is confirmed by echocardiographic visualization of heartworms within the tricuspid orifice and vena cava. Without appropriate treatment, caval syndrome is typically fatal within 24-48 hours. The severity of heartworm disease can be graded on the following scale (Blagburn, 2013): ● Mild/moderate : Clinical signs include mild weight loss, exercise intolerance, and intermittent cough. Thoracic radiographs may reveal mild radiographic changes, including right ventricular enlargement, interstitial lesions, and perivascular densities. Laboratory abnormalities may include mild anemia (PCV between 20-30%) and mild proteinuria. ● Severe : Clinical signs include severe muscle wasting, fatigue/ lethargy, persistent cough, dyspnea, and ascites. Thoracic radiographs reveal more dramatic changes, including significant right ventricular enlargement, pulmonary arterial enlargement, and prominent pulmonary densities. Laboratory abnormalities may include significant anemia (PCV<20%) and pronounced proteinuria. ● Caval syndrome : Clinical signs include sudden onset of severe lethargy and weakness. Physical exam findings commonly include a heart murmur over the tricuspid valve and palpable jugular pulses. Urinalysis typically reveals hemoglobinuria.
DIAGNOSIS
There are two primary methods of detecting heartworm infection in dogs. One method involves searching for microfilariae. This testing can be performed using a number of different procedures, including the Modified Knott's test, filter test (Difil ® Test), a direct smear of anticoagulated blood, or an examination of the buffy coat in a capillary tube of blood. The other test, which is more reliable and more commonly utilized, involves testing for heartworm-specific antigen or antibodies. Antigen test Heartworm antigen testing is the most commonly utilized canine heartworm test. This test detects a protein that is secreted by adult female heartworms of the species D. immitis . Current heartworm antigen tests identify the majority of “occult” infections (consisting of adult heartworms without circulating microfilaria), consisting of at least one adult female worm. Furthermore, these tests are nearly 100% specific (American Heartworm Society, 2014). It is important to note that antigen tests rely on detecting proteins released by female adult worms. There is currently no available test that can detect infections consisting of only adult male worms. Although false-negative and false-positive antigen tests are uncommon, they can occur. For this reason, all unexpected
positive results should be verified with additional testing. The test can first be repeated on an in-house antigen test, but if an unexpected positive test is repeatable on an in-house test, samples should be sent to a reference laboratory for confirmation. Additional tests that can be used for confirmation include concentration tests for microfilariae, thoracic radiography to detect signs of heartworm disease, or ultrasonographic visualization of worms (American Heartworm Society, 2014). False negative heartworm tests are uncommon, but can occur. Most commonly, false negative tests are observed in light infections, all-male infections, or when testing is performed too early after exposure (before the female worms have matured to adulthood). Recently, however, an additional cause of false negative heartworm antigen tests has been identified. In some cases, antigen-antibody complexes can form in heartworm- positive dogs, interfering with the heartworm antigen test’s ability to bind to heartworm antigens. Studies have shown that heat-treating serum can destroy the antigen-antibody complexes, allowing heartworm antigen to be accurately detected in these dogs. One study, conducted in the southern United States, showed that 7.1% of randomized shelter dogs initially testing negative on heartworm antigen tests were positive after heating the sample (Velasquez, 2014). Research
Page 59
Book Code: VFL1524
EliteLearning.com/Veterinarian
Powered by FlippingBook