Feline Heart Worms

8/4/2019 Feline Heart Worms

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If dogs not previously exposed to heartworms are infected with

100 L3 larvae, about 75 adult worms develop in almost 100 % of

dogs .

If cats not previously exposed to heartworms are infected with 100

L3 larvae, about 3-10 adult worms develop in about 75% of cats.

Thus the cat is a susceptable, but resistant host. Anywhere

heartworm disease has been found in the dog, it has been observed

in cats


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Less infective larvae survive to become adults, but most cats can be

infected if exposed to L3 larvae.

Remember, the average mosquito can only transmit a maximum of 10infective larvae, therefore an experimental infection with 100 L3 would

represent 10 - 20 mosquitoes all biting a cat at the same time.

Infective larvae in the cat are poorly oriented therefore ectopic sites for

the adult (brain, subcutaneous tissue, abdomen) are more common thanin the dog.

The worm burden is less in the cat (range usually 1-9 worms) compared

to the dog, but up to 20 adults have been experimentally induced in a cat.

Although the adult worms reach significant size in the cat, (female > 21

cm, male > 12 cm), their development seems to be slower in the cat than

the dog.

Experimentally, the male cat is easier to infect and the worm burden

tends to be higher when exposed to the same number of L3 larvae as in

female cats.
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The average time from infective larvae being introduced into the cat

until the development of circulating microfilaria in experimental

infections is about 8 months and occasionally longer in the catcompared to the typical 5 to 6 1/2 months in the dog. Since the

microfilaremia is transient and in very low numbers , the use of

concentration tests are recommended and a negative test does not

rule-out heartworm disease (see "Diagnosis" below). Microfilaremia is

uncommon (< 20% of spontaneous clinical cases), inconsistent and

transient when present.

Infective larvae developed in about 1% ofAnopheles spp. andAedes spp. mosquitos that fed on cats with patent infections. Thus the

cat is a potential but insignificant source as a reservoir for the

parasite.
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after transplantation and after L3 infections would indicate that the cat

does not harbor the adult as long and spontaneous recovery is much more

likely in the cat than in the dog. A shortened longevity would contributeto an underestimation of the incidence of heartworm disease in the cat

based on routine necropsy examination of the general population. A

gradual decrease in the number of adult worms found in the heart has

been noted when cats are chronologically studied. Thus the cat is asusceptible but resistant host forDirofilaria immitis with a more

transitory disease than in the dog.

There is a high mortality of the L5 as they first reach the lungs, 3-4

months after infection. An acute reaction is often noted at this time.

Evidence supports the premise that adult heartworms in the cat have a

relatively short life span (probably less than 2 years) compared to thedog (approximately 5 years). Survival of adult worms


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The life cycle would then dictate that for a cat to becomeinfected, a mosquito must bite a species of animal with apatent infection (usually a dog) and then after properclimate conditions, bite a cat. The feeding pattern of themosquito determines which cat get infected.

Some species of mosquitoes will readily feed on both dogs and cats,

others prefer only one species. The incidence of heartworms in cats is

very high in some areas (18%) and may reflect the willingness of aspecies of mosquito in the area to feed on both dogs and cats.


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Typical of the reaction of the cat, the smaller

arteries develop severe muscular hypertrophy .

The host's response to the parasite is intense asdemonstrated by enlarged pulmonary arteries

within 1 week of transplantation.
http://pth21l.gif/


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The cause of the acute crisis in the cat is lunginjury resulting in respiratory distress. Often thisis associated with the death of an adultheartworm. The lung can become acutelyedematous and respiratory failure, not heartfailure, becomes the life threatening event. Theinflammatory lung changes are much like theeffects of a bee sting on a persons finger, theresulting swelling of the tissues make the lungunable to function.


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This cat had demonstrated no clinical signs before

a fatal crisis. Obvious the subclinical disease had

been chronic.
http://pth15.gif/


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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.

Obstruction of blood flow, especially to the caudal

pulmonary arteries causes acute signs and the lung

lobe involved becomes hemorrhagic with areas of

edema.


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The hallmark of the disease in the cat is the acute

lung injury resulting in a generalized respiratoryfailure. 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 explainmany 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 intenseinflammation and "asthma- like" symptoms may

develop. The cat has a specialized macrophage

(designed to envelop and digest foreign materials) inthe capillary beds of the lung that are not present in the

dog.


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The parasite seems to be able to suppress the

immune function. However, at the time of wormdeath, the lungs become extremely inflamed and

the specialized macrophages may become key

players in the intense reaction. The result is anon-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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Clinical DiseaseThere is no age predilection toDirofilaria immitis infection

in cats and a wide age range of clinically infected cats isreported (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.

A higher incidence in males compared to females in

experimental and clinical cases may represent a sex

susceptibility.


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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


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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.


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History: The most common historical complaints in cats with

clinical signs are coughing, dyspnea, vomiting, lethargy,

anorexia, and weight loss. Vomiting and respiratory signs arethe predominate complaints in chronic clinical cases, although

it is unusual for an infected cat to exhibit both symptoms

concurrently.

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.
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. 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 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 duringdiagnostic screening.


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Physical Examination: The physical examination is usually

normal inDirofilaria 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
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DiagnosisThere are 3 serologic methods which have been used

for feline heartworm disease. Rapid advances are

constantly changing these assays.

1) IFA for microfilarial antibody2) ELISA for adult antibody

3) Adult antigen detection by ELISA and colloid gold


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The IFA test (detecting antibodies to microfilarial cuticular

antigen) is diagnostic in about 33% of positive cases, but the

presence of immature or sterile worms, worms of only one

sex, or the absence of host response to antigen does not

produce a diagnostic titer.

A ib d T i Th ELISA (d i f li


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Antibody Testing: The ELISA test (detecting feline

antibodies to adult heartworm antigen) shows promise and

initial concerns related to false positives from cross-reactivity

have not been detected. The use of the ELISA (as adaptedfrom the canine ELISA) in the cat to confirm a clinical

diagnosis has been very helpful and false positives from cross-

reactivity have not been observed. The canine methods for

measuring dog antibodies to heartworms cannot be used on catserum.

Additionally, the death of adult heartworms may produce

a strong antibody response after release of large

amounts of antigen. Some of the highest titers are

associated with severe clinical signs in cats where the

worms have died and the disease may be resolving.


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Antigen Testing: Heartworm antigen detection testsutilizing blood or serum have been successful in dogs

and have been positive in cats within days of

transplantation of mature adult worms from dogs intocats. Since the antigen being detected seems to be

derived primarily from the adult female reproductive

tract, immature infections, a low worm burden, a male

infection, or sexually immature worms may not produce

enough antigen to be detected. The elimination of the

adult parasite will also cause a negative antigen test.

Cats may develop positive antigen tests 6 months afterthe experimental introduction of large numbers of

infective larvae.


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However, clinical cats and experimentally infected cats

with active heartworm disease and high antibody titers

can be negative on antigen testing. The low number and

slow maturation of adult worms in clinical infections and

the clinical signs associated with immature worms make

it prudent to consider a positive antigen test diagnosticbut not to rule out heartworms based on a negative

antigen test. Most cats with heartworm disease are

antigen negative.


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Tracheal Cytology: The finding ofeosinophils on a trachealwash is common in heartworm disease, asthma and parasitic

lung diseases. In feline heartworms, the presence of

eosinophils on the wash seems to occur 4-7 months after L3

infection and often may not be present later in the infectioneven when adult worms are present. Tracheal cytology typical

of chronic inflammation may be present after the eosinophilic

reaction resolves.
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Feline Heart Worms