Heartworms cause disease which is severe and can be fatal to infected dogs. This disease affects many systems and can cause many signs. The most common sign of heartworm disease however, is “NO SIGN AT ALL.” Most of the dogs that we diagnose with heartworm disease are healthy in appearance and action. They are dogs that may have been on an inconsistent heartworm preventive program or stray pets that appear healthy. The following is a description of the progression of heartworm disease. The cause of this progression is usually associated with four factors. 1) Increased numbers of adult heartworms; 2) Exercise or activitiy of the affected pet. An active pet with 15 heartworms will have more severe disease than a sedate or inactive pet of the same size with 50 heartworms; 3) Reaction of the lung tissue to the presence of the heartworms. A pet with as few as one heartworm can die if there is allergic reaction in the lungs; 4) The size of the pet. Adult heartworms are the same size regardless of the size of the animal and the smaller animals such as small breed dogs, cats and ferrets are more likely to die from heartworms than large breed dogs.
Adult heartworms cause disease by disturbance of the blood circulation through the lungs. The presence of adult heartworms in the arteries will cause changes in the vessel wall to develop within days. This occurs because of the physical presence of the heartworms in the vessel. This reaction gains in severity as the number of heartworm adults increases. Additional changes in the blood vessel walls also contribute to heartworm disease. These changes are reactions to the chemicals and waste products produced by the heartworm. These discharges from the heartworm cause the blood vessel walls to respond with immune mediated cellular infiltration (white blood cell invasion). White blood cells (lymphocytes, neutrophils, monocytes) move into the blood vessel wall to neutralize the foreign substances liberated by the heartworms. This cellular reaction leads to the release of inflammatory mediators from the white blood cells causing subsequent tissue damage and inflammation. This reaction compromises blood flow through the blood vessel. Compromised blood flow leads to turbulence and activation of platelets and clot formation. Thickening of the blood vessel wall also occurs (villus hyperplasia) that causes uneven blood flow. These factors result in reduced transfer of oxygen and carbon dioxide to and from the red blood cells and blood. The cellular infiltration and inflammation also cause reduced compliance (stretching) of the arteries. This reduced compliance will lead to pulmonary hypertension (high blood pressure). High blood pressure causes fluid to leak out of the blood vessels of the lungs flooding the air filled spaces (alveoli). Fluid filled alveoli cause bronchoconstriction (narrowing of the airways) which stimulates coughing.
As the hypertension continues, the right side of the heart is forced to pump the blood to the lungs at increasingly higher pressures resulting in dilation of the right heart and main pulmonary artery. This back pressure causes sludging of blood flow from the liver and abdominal organs resulting in fluid leakage from the surface vessels of the congested liver and internal organs. This fluid leakage accumulates in the abdomen and is called ascites. Fluid in the abdomen causes problems by pressing on the diaphragm reducing its motion and further compromising respiratory function. The effects of reduced blood flow from the abdominal organs include reduced metabolism in the liver, reduced digestion by the intestines and reduced blood filtration by the kidneys. Microangiopathic hemolytic anemia is a condition that can develop in the smaller vessels of the lungs, whereby small fibrin strands in arterioles cut (“clothes line”) the red blood cells as they traverse the vessels, resulting in anemia. The general condition of the patient deteriorates; resulting in loss of body weight, poor hair coat, reduced resistance to infection and reduced exercise tolerance and generalized debility. Other signs include coughing, rapid respiration, anemia, and severe ulcerative dermatitis. The heart will continue to dilate until the valve leaflets do not touch causing a murmur to develop along with the poor blood flow. The main pulmonary artery will also continue to bulge and may develop an aneurysm. Acute death may result from splitting of the main pulmonary artery or tearing of the right heart during exercise of a severely affected dog. The pulmonary hypertension and reduced compliance of the pulmonary vasculature will eventually cause bleeding into the airways, and subsequent bleeding from the mouth or nose. Activation of the coagulation mechanisms may result in disseminated intravascular coagulation (D.I.C.). This occurs when the tissue damage in the lungs is severe. This damage causes activation of clotting factors and subsequent clot formation. If the reaction is severe enough or chronic enough to use all the clotting factors then excessive bleeding is seen. The dog will likely bleed to death into his lungs. It is not uncommon to have a client find their heartworm positive dog laying in a pool of blood one morning.