The general pulmonary pathology in the cat is similar
to that of the dog. Muscular hypertrophy, villous endarteritis, and
cellular infiltrates of the adventitia
are 
typically
more severe in the caudal pulmonary arteries. Typical of the reaction of
the cat, the smaller arteries develop severe muscular hypertrophy . The
host's response to the parasite is intense as demonstrated by enlarged
pulmonary arteries within 1 week of transplantation.
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The cause of the acute crisis in the cat is lung injury resulting
in respiratory distress. Often this is associated with the death of an
adult heartworm. The lung can become acutely edematous and respiratory
failure, not heart failure, becomes the life threatening event. The inflammatory
lung changes are much like the effects of a bee sting on a persons finger,
the resulting swelling of the tissues make the lung unable to function.
This cat had demonstrated no clinical signs before a fatal crisis. Obvious the subclinical disease had been chronic. |
Embolization
of pulmonary arteries can be a contributing factor to initiation of clinical
signs. Although pulmonary hypertension does occasionally occur, right axis
EKG changes, radiographic evidence of right sided hypertrophy, and right
sided heart failure are infrequent. Indicating that severe cor
pulmonale is uncommon in the heartworm cat. Although in chronic
cases perivascular reaction
and evidence of thrombus formation with recanalization are noted, it would
appear in the cat that cardiac changes are minimal.. 
Obstruction
of blood flow, especially to the caudal pulmonary arteries causes acute
signs and the lung lobe involved becomes hemorrhagic with areas of edema.
If the cat survives the initial embolic lesion, recanalization around the
obstruction occurs 
rapidly
and the lung is markedly improved within days. The result of the acute
lung injury is a Type
II alveolar cell hypertrophy. Post-caval
syndrome with ascites and
right sided heart failure will occur in rare cases with very high worm
burdens. Hemglobinurea has
not been a consistent finding is these heartworm cats. Poor venous return
and tricuspid insufficiency
rather than cor pulmonale are considered the pathogenic mechanism of this
syndrome in cats.
The hallmark of the disease in the cat is the acute lung injury resulting in a generalized respiratory failure. The inflammation is observed even in lung lobes not associated with embolization. Thus the disease is not a simple obstructive disease associated with blocking of blood flow. The lesions are acute and inflammatory; expecially associated with dead worms.
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Because the cat is a resistant but susceptible host as compared to the dog, the increased immunologic response of the cat to the parasite would help explain many of the clinical signs. As the parasite first arrives in the lungs as early as 100 days after being infected by a mosquito, the lung responses with intense inflammation and "asthma- like" symptoms may develop. The cat has a specialized macrophage (designed to envelop and digest foreign materials) in the capillary beds of the lung that are not present in the dog. After the mature parasite develops, the clinical signs may be intermittent or absent. The parasite seems to be able to suppress the immune function. However, at the time of worm death, the lungs become extremely inflamed and the specialized macrophages may become key players in the intense reaction. The result is a non-functioning lung and an acute respiratory distress syndrome. This reaction can occur as the result of even a single worm burden.
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There is no age predilection to Dirofilaria immitis
infection in cats and a wide age range of clinically infected cats is reported
(6 month - 17 yrs). Indoor and outdoor cats are both represented and indoor
cats have a high incidence of positive antibody
titers suggesting a successful early infection. (AAVP
abstract on clinical study.)A higher incidence in males compared to
females in experimental and clinical cases may represent a sex susceptibility.
Feline leukemia virus infection is not a predisposing
factor and heartworms are not a common incidental finding at necropsy of
cats with FeLV. The arrival of immature heartworms in the lungs and death
of adults, are most likely to be associated with clinical signs. The initial
arrival (as early as 100 days after infection) of the L5 in the distal
pulmonary arteries induces a diffuse pulmonary infiltrate and signs typical
of "eosinophilic pneumonitis."
Clinical Signs: The initial clinical signs associated with early infections occur most frequently in the late Fall and early Winter months (4-7 months after the exposure). At this time, because the worms are immature, antigen tests are usually negative. After the initial host response, the signs may abate and become subclinical for a period of time. However, the subsequent death of adult heartworms causes additional severe signs. Infected cats may die acutely, exhibit chronic signs, or be asymptomatic (Table 1). Based on cardio-pulmonary changes and experimental studies, most heartworm cats even with severe heartworm disease are asymptomatic once the infection becomes established.
In the acute cases, death may be so rapid as to preclude diagnosis or treatment. Sudden death has been attributed to circulatory collapse and respiratory failure from acute pulmonary arterial infarction and acute lung injury. Acute collapse may occur with or without previous clinical signs. Cats which die from heartworms can be clinically normal 1 hour before death. All cats with peracute death in heartworm endemic areas should be examined for heartworm disease. In acute cases as few as 1 worm has been found accompanied by severe pulmonary congestion, infarction and edema. The worms in the acute syndrome are not always found embolizing the main pulmonary arteries.
History: The most common
historical complaints in cats with clinical signs are coughing, dyspnea,
vomiting, lethargy, anorexia, and weight loss. Vomiting and respiratory
signs are the predominate complaints in chronic clinical cases, although
it is unusual for an infected cat to exhibit both symptoms concurrently.
(AAVP abstract on clinical study.) Vomiting tends
to be sporadic. The etiology of vomiting in
heartworm cats is unknown although the release of inflammatory
mediators from the lungs which stimulate the chemoreceptor
trigger zone has been hypothesized. The vomitus generally contains
food or foam and is rarely bile stained. Retching and severe paroxysmal
vomiting is a rare historical findings. Heartworm disease in endemic areas
should be included in the differential
diagnosis of chronic emesis
in the cat. The most common respiratory complaints are coughing and intermittent
dyspnea. Hemoptysis is occasionally
noted. The coughing can be in severe paroxysmal attacks. Periods of normalcy
(days to weeks ) is often seen between episodes. Based on historical data,
the coughing is usually temporarily corticosteroid responsive with exacerbation
during therapy. The clinical presentation, radiographic pattern, and response
to therapy often lead to a tentative diagnosis of bronchial
asthma. 
The
dyspnea may be a result of acute emboli formation especially associated
with worm death. On occasion, occlusion of a pulmonary artery (right caudal
being the most common) is accompanied by a radiographic appearance of lung
lobe consolidation and the development of life-threatening acute
dyspnea. The non-specific clinical signs are consistent with many feline
diseases. Anorexia and/or lethargy can be the only presenting signs in
heartworm cats. In these cases, heartworm disease is often an incidental
finding on thoracic radiographs during diagnostic screening. Cats with
worms found in abnormal locations may have signs attributable to local
pathology. Neurological signs are uncommon but can occur in infected cats
with or without worms in the CNS.
Physical Examination: The physical examination is usually normal in Dirofilaria immitis infected cats. A systolic murmur over the tricuspid valve area and occasionally a gallop rhythm can be present, but as a general rule are uncommon. Harsh lung sounds (dry rales) are the most frequent abnormal auscultatory finding and can be present in cats without respiratory signs. Ascites, exercise intolerance, and signs of right sided heart failure are rare. There does not seem to be a correlation between the clinical signs, physical findings, and radiographic findings.
Clinical Pathology:
Routine complete blood counts may demonstrate a mild anemia
(23-33% Hct), occasionally nucleated
RBC's, , and
basophilia (rare). Anemia is present in
about one-third the infected cats and is non-regenerative,
as in heartworm positive dogs. 
Peripheral
eosinophilia, present in about
one-third of client cats at the time of diagnosis, is an inconsistent finding
even on serial samples in the same cat and is dependent on the stage of
the infective larvae. The eosinophilia occurs 4-7 months post-infection
and intermittently thereafter. The absence of eosinophilia does not exclude
a diagnosis of feline heartworms.
Cytology of bronchial alveolar lavage fluid may contain eosinophils without the presence of a peripheral eosinophilia. As in the dog, the presence of basophilia is highly suggestive of heartworm disease.
Blood chemistries and urinalysis
are usually normal. Although hyperglobulinemia
does occur in some heartworm cats, it is neither consistent nor predictable
and should not be used to rule out feline heartworm disease. Normal serum
globulins and normal electrophoresis
are found in cats that are heartworm positive based on Knott's
tests, IFA tests and/or
antigen tests. Experimental infections produced via L3 larvae or transplantation
of adults usually result in a microfilaremia of short duration and low
numbers. Thus, a positive blood test for microfilariae is unlikely but
diagnostic for heartworm disease. The odds of identifying a heartworm infection
are increased by repeated testing (3-4 tests) and using larger quantities
of blood (5 ml) for each test. Concentration tests such as Knott tests
or milipore filter techniques
are best.
Even with repetitive testing, occult
heartworms represent over 80% of feline heartworm disease.
In North & South America, the only filarial disease
of cats is heartworms, therefore any microfilaria observed should be considered
D immitis.
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