Florida Veterinarian Ebook Continuing Education

virus (Lorentzen & Caola, 2008). Given that antigen-positive heartworm tests are literally “the tip of the iceberg” in feline heartworm infections, this data suggests that the incidence of feline heartworm infection is likely far greater than the incidence of feline leukemia virus and feline immunodeficiency virus.

While the facts above may come as a surprise to many veterinarians, they again emphasize the need for veterinarians to place a greater emphasis on the prevention and treatment of feline heartworm disease. This condition is just as important to feline patients as feline leukemia virus and feline immunodeficiency virus and is deserving of a similar level of attention.

PATHOPHYSIOLOGY

The life cycle of Dirofilaria immitis in cats is very similar to the life cycle observed in dogs, although there are key differences in the duration of specific life stages and the later stages of the life cycle. The primary difference between canine and feline heartworm infection lies in the pathophysiology of the infection and Heartworm transmission and life cycle The basic heartworm life cycle, as traditionally described in dogs (Heartworm Life Cycle, 2018), is as follows: ● A mosquito bites the dog, introducing L3 larvae into the subcutaneous tissue. ● The L3 larvae mature for 3-4 days in the dog’s tissues. ● The L3 larvae molt to L4 larvae. ● The L4 larvae migrate to the bloodstream, a process which takes 45-65 days. ● At the time they arrive in the bloodstream, the L4 larvae are in the process of developing into immature adults. ● Immature adults reach maturity over a period of approximately 4-5 months (Note: adult heartworms are typically present 6-7 months after the initial infection.). ● Mature adults remain in the bloodstream for 5-7 years, producing large numbers of microfilariae. ● Microfilariae live in the circulation for 1-2 years. ● Microfilariae in the circulation are ingested by a feeding mosquito. ● In the mosquito, microfilariae pass through the L1 and L2 stages, maturing into L3 larvae after approximately 10-14 days. ● The L3 larvae can reinfect a new host, when the mosquito delivers a bite. In cats, the same stages are followed but the timelines differ: ● A mosquito bites the cat, introducing L3 larvae into the subcutaneous tissues. Heartworm disease and its effects on the infected cat As illustrated by the Dirofilaria immitis life cycle outlined above, larval and immature heartworms begin to reach the pulmonary vasculature of an infected cat several months after infection. Unlike in dogs, where a significant degree of the clinical signs associated with heartworm disease are attributable to the adult heartworms, cats infected with heartworms develop significant pulmonary damage early in the course of heartworm infection, before the heartworms have even reached adulthood (Stannard, 2015). In fact, many cats that develop clinical signs attributable to heartworm infection may not even experience a progression of their worms into adulthood (Atkins, 2015). The arrival of immature worms in the pulmonary vasculature and subsequent death of some of these immature worms leads to an acute parenchymal and vascular inflammatory response known as heartworm-associated respiratory disease, or HARD (American Heartworm Society, 2014; “A Roundtable Discussion,” 2008). HARD can be regarded as the first phase of feline heartworm disease and is the major cause of morbidity in feline heartworm disease (“A Roundtable Discussion,” 2008). On histopathology, cats affected with HARD demonstrate a number of significant changes within the lungs. These histopathological changes include occlusive medial hypertrophy of small pulmonary arterioles and a number of inflammatory changes associated with the vessels and bronchi (American Heartworm Society, 2014). Eosinophilic inflammation of the

how larval and adult heartworms affect their host. Although cats typically carry very low worm burdens, they respond to heartworm infections with significantly more inflammation than what is typically seen in dogs. This results in different clinical signs and different outcomes of infection.

● The L3 larvae spend 3-4 days in the cat’s tissues. ● The L3 larvae molt to L4 larvae. ● The L4 larvae migrate to the bloodstream, a process which takes 2 months. ● At the time they reach the bloodstream, the L4 larvae are in the process of developing into immature adults. ● Immature adults reach maturity over a period of approximately 4-6 months (Note: adult heartworms are typically present 7-8 months after the initial infection.). ● Mature adults remain in the bloodstream for 2-4 years, but rarely produce circulating microfilariae. Therefore, infected cats rarely serve as a source of infection for mosquitoes and play little role in the transmission of heartworm disease (Heartworm Life Cycle, 2018). Heartworms are transmitted by as many as 10 to 12 unique mosquito species, found across the United States. These species can differ significantly in their preferred habitat, times of day that they are most active, feeding preferences, and other behavioral and ecological factors. Some of these mosquito species even prefer to spend time around doors and windows, in an effort to gain entry indoors to feed on humans and pets (American Heartworm Society, 2016). Observed differences in the behaviors and physiology of different mosquito species makes prevention challenging, adding a layer of complexity to heartworm disease transmission and management. pulmonary parenchyma, vasculature, and air spaces can lead to pulmonary edema and impaired oxygen exchange, contributing to clinical signs of disease (Atkins, 2015). After the initial inflammatory stage of HARD, many of the heartworm larvae may die off. If the heartworms do survive to adulthood, the amount of inflammation seen within the lungs may decrease even more dramatically. This can be regarded as the second stage of feline heartworm disease. Adult heartworms suppress the activity of pulmonary vascular macrophages, which are a major component of the feline reticuloendothelial system; this suppression inhibits inflammatory changes within the surrounding tissues, reducing signs of inflammation within the lungs (ESDA, 2017). During the second stage of heartworm disease, a reduction in clinical signs may be seen along with a reduction in histopathologic changes (American Heartworm Society, 2014). This relatively quiescent period may persist for a couple of years, during which time the cat may be completely asymptomatic for heartworm infection. Not all adult heartworm infections are asymptomatic, however. Live adult heartworm infection can have mechanical effects within the heart. Cats do not develop caval syndrome in the manner that dogs do, but adult worms may lead to tricuspid regurgitation and an audible heart murmur. While right ventricular hypertrophy, pulmonary hypertension, and right heart failure can occur, they are uncommon (American Heartworm

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