Page 341 - Feline Cardiology

354 Section K: Heartworm Disease

on an infected animal and ingesting the parasite. Two
molts then occur to produce the infective L 3 stage. Larvae
development to the third stage usually requires 1 to 2.5 L3 Transient patency
weeks, depending on the ambient temperatures. 7-8 months post infection
Mosquitoes can survive the development of only low Molt to L4 within If worm(s) reach adult
numbers (<10) of larvae. Larvae development within the a few days stage, AG positive
mosquito requires an average daily temperature of at L4
least 57°F (14°C) (Nelson et al. 2007). The cooler the
temperature, the longer the time required for L 3 to
develop and vice versa. Therefore, transmission is 2 months AB response
unlikely to occur during the cold months of the year, post infection At risk for HARD begins to wane
even in most southern regions of the U.S. Peak months AB response begins
of heartworm transmission in the northern hemisphere Juvenile worms begin arriving
are July and August (Nelson et al. 2005). This is primar- in the pulmonary vasculature
75-90 days post infection
ily because the time required for development from L 1
to L 3 may exceed the life span (30 days) of the mosquito Figure 23.1. The life cycle of Dirofilaria immitis in the cat. The
when temperatures are moderately low. cycle is similar for dogs and cats until immature adults enter the
Third-stage larvae (L 3) infect the cat via the bite pulmonary artery (approximately 100 days postinfection). In dogs,
wound created when an infected mosquito feeds. Larvae the majority of juvenile worms mature to adults and live 5 to 7
years. In cats, most juvenile worms die shortly after arriving at the
migrate through the subcutaneous tissues and vascular pulmonary artery creating a significant inflammatory response.
adventitial tissues. During this time, 2 molts occur. Once Antibody response begins at 60 days after infection (whether a
the larvae enter the bloodstream, they are swept with the dog or cat); however it begins to wane as juvenile worms die in
circulation to the pulmonary arteries. There is very high the cat. Worms that survive to the adult stage require longer to
mortality of the young adults (L 5 ) because they reach the mature in cats (7–8 months vs 6 months in the dog).
feline lungs approximately 3 to 4 months postinfection,
and only a subset of the larvae ever mature to the adult
stage. Adult heartworms are typically sexually mature FeLV, yet in the same report it was noted that fewer than
Heartworm Disease (which is 1–2 months longer than is seen in the dog) cations (Nelson 2008a). Another study determined sero-
5% of cats in the United States are on preventative medi-
and able to reproduce by 7–8 months postnfection
prevalance of dirofilariasis, FeLV infection and FIV
(McCall et al. 1994). However, microfilarial counts are
infection in cats exported from the Gulf Coast region
usually very low and transient in the cat, seldom lasting
for longer than 1–2 months (McCall et al. 1994). See
following the 2005 hurricanes were 4.0%, 2.6%, and
Figure 23.1 for an illustration of the heartworm life cycle
in the cat. 3.6%, respectively (Levy et al. 2007).
Pathogenesis
Prevalence Acute lung injury is the major contributing factor to the
Heartworm infection is most common in tropical and initiation of clinical signs. It is hypothesized that the
subtropical climates. However, D. immitis infections arrival of fifth stage larvae in the lungs (typically 80–160
have been reported in cats in many areas of the world, days postinfection) and the death of adult worms are the
with the prevalence varying by geographic region. Most most likely stages of the life cycle to be associated with
commonly it has been reported at 5–20% of the rate for clinical signs in the cat. After an initial host response, the
the local dog population (Nelson 2008b). It has been signs may disappear or become subclinical. Interestingly,
suggested that this variation between the species reflects recent research has shown that D. immitis has evolved
willingness of the local species of mosquitoes to feed on various strategies to evade a host immune attack. These
both dogs and cats. Indoor and outdoor cats are affected include dramatically different surface properties of
with heartworm disease and one retrospective study the third and fourth larval stages and an acellular cuticle
demonstrated that 25% of cats diagnosed with adult (Litster and Atwell 2008) and suppression of pulmonary
heartworms were classified as entirely indoor cats intravascular macrophages by living heartworms (Dillon
(Nelson et al. 2007). Some studies have suggested that et al. 2008). It is hypothesized that these capabilities
male cats are at increased risk compared to females; could account for the reduction of clinical signs after
however, this pattern has not been conclusively docu- the initial, often marked, inflammatory response
mented. In one necropsy-based report, the heartworm following arrival of the L 5 stage in the lungs, as well as
infection rate in cats was greater than that for FIV or the acute signs that follow death of the heartworm(s) in