Page 232 - Small Animal Internal Medicine, 6th Edition

204 PART I Cardiovascular System Disorders

pulmonary arteries, and most die from an acute host inflam- in more than half of symptomatic cats, including tachypnea,
matory reaction involving pulmonary intravascular mac- paroxysmal cough, and/or increased respiratory effort.
VetBooks.ir rophage activation. These specialized phagocytic cells are Other client complaints include lethargy, anorexia, weight
loss, vomiting (including hemoptysis), syncope, neuro-
located in the pulmonary capillary beds of cats but not dogs.
Activation of these macrophages by the presence of the para-
to eating, is common and may be the only sign in some
sites leads to acute eosinophilic and neutrophilic inflamma- logic signs, or sudden death. Vomiting, usually unrelated
tion, and proliferative lesions in the pulmonary arteries, as infected cats. Severe clinical signs usually are associated with
well as in lung tissue and bronchioles. Increased pulmonary the arrival of immature worms in the pulmonary arteries
vascular permeability can promote edema formation, and (HARD) or with the death of one or more adult worms. The
the more extensive alveolar type 2 (surfactant-producing) sudden onset of neurologic signs, with or without anorexia
cell hyperplasia seen in cats (compared with dogs) also can and lethargy, is common during aberrant worm migration.
interfere with alveolar O 2 exchange. This initial HARD phase Such signs include seizures, dementia, apparent blindness,
can mimic signs of feline allergic airway disease (asthma) and ataxia, circling, mydriasis, and hypersalivation. Only rarely
can lead to acute respiratory distress in cats 3 to 9 months do cardiopulmonary and neurologic signs coexist. Although
after infection. Although many cats recover, this phase is HWs can cause marked pulmonary disease, some cats have
fatal in others. Sudden death can occur. no clinical signs.
In cats that survive, the acute inflammation subsides and Auscultation might reveal pulmonary wheezes or crackles,
any remaining worms continue to mature. Vascular injury muffled lung sounds (either from pulmonary consolidation
leads to myointimal proliferation, muscular hypertrophy, or pleural effusion), tachycardia, and sometimes a cardiac
luminal narrowing, tortuosity, and thrombosis in affected gallop sound or murmur. Pleural effusion or ascites caused
pulmonary arteries. Because HWD in cats usually involves by right-sided CHF, as well as syncope, are less common in
only a few worms and worm life span is relatively short, cats than in dogs with HWD. Pneumothorax occurs rarely.
pulmonary arterial lesions tend to be localized; as a result, There are sporadic reports of caval syndrome in cats.
clinically relevant pulmonary hypertension, secondary RV
hypertrophy, and right-sided CHF are uncommon in cats. In Diagnosis
cats that do develop CHF, pleural effusion (modified transu- Definitive diagnosis is more difficult in cats than dogs. A
date or chylous), ascites, or both can develop. As in dogs, the combination of serologic testing, thoracic radiographs, and
bronchopulmonary collateral circulation helps protect echocardiography is used. Microfilaria testing is only occa-
against pulmonary infarction. sionally helpful.
The host often tolerates mature HWs, but dying and
degenerating worms cause recrudescence of pulmonary TESTS FOR HEARTWORM DISEASE
inflammation and thromboembolism that can be fatal. IN CATS
Disease is most severe in the caudal lung lobes. Caudal lobar Serologic tests
arterial obstruction can be caused by villous proliferation, Antigen tests. The HW Ag tests are highly specific in
thrombi, or dead HWs. Adult worms are more likely to detecting adult (female) HW infection, but their sensitivity
obstruct the pulmonary arteries of cats (compared with depends on the sex, age, and number of worms; therefore Ag
dogs) by virtue of their relative size. tests often are negative in cats. Ag test results are negative
Vomiting is common in cats with HWD. The mechanism during the first 5 months of infection, the time period when
for this may involve central stimulation (of the chemorecep- clinical signs from HARD are common. Ag tests can be vari-
tor trigger zone) by inflammatory mediators. Antiinflamma- ably positive at 6 to 7 months; infections with mature female
tory doses of a glucocorticoid often control this sign. worms should be detected after 7 months. Feline-specific Ag
tests are reported to have increased sensitivity for detecting
Clinical Features HWD in cats compared with canine tests. False-negative
Most reported cases have occurred in cats 3 to 6 years of HW Ag test results are more likely in cats because worm
age, although cats of any age are susceptible. Although burden is typically low; also, a longer time is required for cats
outdoor lifestyle is a risk factor for HW exposure in cats, to become Ag-positive. Up to 50% of cats with mature HWs
those living strictly indoors account for approximately 25% could have a negative Ag test, and acute death and severe
of feline HW infections. Unlike in dogs, haircoat length does clinical signs can occur in Ag-negative cats. False-negative
appear to affect HW prevalence in cats; longhaired cats are tests can occur because of Ag-Ab complexation, similar to
infected less frequently than shorthaired cats. Many exposed dogs; heating the samples before testing can improve test
cats could clear the infection without ever showing clinical accuracy in cases with a high index of suspicion for HWD.
signs. Some clinicians have noted an increase in feline HWD Occasionally, a positive Ag test result occurs, but no worms
diagnosis during fall and winter, presumably after infection are found on postmortem examination. Spontaneous worm
in the spring, but others have found fewer cases in the latter death, worms overlooked during pulmonary evaluation, and
part of the year. ectopic infection are likely reasons for this finding. Postmor-
Clinical signs are variable and can be transient or non- tem diagnosis is difficult if the worms are located in distal
specific. Respiratory signs mimicking feline asthma occur pulmonary arteries or aberrant sites.