Changes

Also known as: heartworm disease.

[[Image:Dirofilaria immitus.jpg|thumb|right|250px|''Dirofilaria immitis'' - Courtesy of the Laboratory of Parasitology, University of Pennsylvania School of Veterinary Medicine]]

Do not confuse with: ''Angiostrongylus vasorum'', angiostrongylosis.

Also known as: '''Heartworm Disease — Dirofilariasis

Beware confusing with: ''[[Angiostrongylus vasorum]]'', [[angiostrongylosis]].

[[Image:Dirofilaria immitus.jpg|thumb|right|150px|''Dirofilaria immitus'' - Courtesy of the Laboratory of Parasitology, University of Pennsylvania School of Veterinary Medicine]]

''Dirofilaria immitis'' is a nematode parasite that causes heartworm disease in dogs, cats and ferrets. Heartworm

disease is transmitted by mosquito bites and there are more than 70 species of mosquito that are able to transmit infection; Aedes, Anopheles and Culex are the most common vector species. Heartwoem disease has been reported in many countries with temperate and is particularly prevalent in the USA, Canada, and southern Europe. The introduction of the PETS travel scheme has increased the concern over Dirofilariasis in the UK.

''Dirofilaria immitis'' is a nematode parasite that causes heartworm disease in dogs, cats and ferrets. Heartworm disease is transmitted by [[Culicidae|mosquito]] bites and there are more than 70 species of mosquito that are able to transmit infection; ''Aedes, Anopheles'' and ''Culex'' are the most common vector species. Heartworm disease has been reported in many countries with temperate climate and is particularly prevalent in the USA, Canada, and southern Europe. The introduction of the PETS travel scheme has increased the concern over Dirofilariasis in the UK.

Dirofilarias does have zoonotic potential: infected mosquitos can transmit ''Dirofilaria immitis'' to humans, but the infection does not become patent. The infective larvae instead reach the lungs, become encapsulated, and die causing granulomatous reactions called "coin lesions" in the process. These are only imporant because they may be confused with neoplastic metastasis to the lungs on radiography¹.

''Dirofilaria'' does have zoonotic potential: infected mosquitos can transmit ''D. immitis'' to humans, but the infection does not become patent. The infective larvae instead reach the lungs, become encapsulated, and die causing granulomatous reactions called "coin lesions" in the process. These are only important because they may be confused with neoplastic metastasis to the lungs on radiography¹.

==Life Cycle==

==Life Cycle==

 

''Dirofilaria immitis'' adults reach maturity and sexually reproduce in the '''pulmonary arteries''' and '''right ventricle'''. Adult males are around 15cm in length, and females are around 25cm¹. After mating, female worms release larvae known as microfilariae (or L1) into the circulation. When a mosquito takes a blood meal from the infected dog or cat, microfilariae are ingested. Mosquitoes are true intermediate hosts for ''Dirofilaria immitis'', since microfilariae require a period of maturation to L2 then L3 in the vector. The duration of this development depends upon environmental conditions. For example, maturation at 30°C takes around 8 days, but when temperatures are down to 18°C, this takes around one month². Below 14°C, development is halted and resumes when temperatures rise. In cooler climates, this means that transmission of heartworm disease to new canine or feline hosts can only occur in warmer months.  

''Dirofilaria immitis'' adults reach maturity and sexually reproduce in the pulmonary arteries and right ventricle. Adult males are around 15cm in length, and females are around 25cm¹. After mating, female worms release larvae known as microfilariae (or L1) into the circulation. When a mosquito takes a blood meal from the infected dog or cat, microfilariae are ingested. Mosquitos are true intermediate hosts for ''Dirofilaria immitis'', since microfilariae require a period of maturation to L2 then L3 in the vector. The duration of this development depends upon environmental conditions. For example, maturation at 30°C takes around 8 days, but when temperatures are down to 18°C, this takes around one month². Below 14°C, development is halted and resumes when temperatures rise. In cooler climates, this means that transmission of heartworm disease to new canine or feline hosts can only occur in warmer months.  

Once matured, L3 in the mosquito migrate to the labium, from which they erupt onto the host's skin as the mosquito feeds. Larvae then migrate into the bite wound and, as most dogs are highly susceptible to heartworm disease, most L3 then establish infection. It takes 2-3 days for L3 to moult to L4, which remain in the subcutaneous tissues for up to two months before becoming young adults (L5) and migrating to the pulmonary arteries.  

Once matured, L3 in the mosquito migrate to the labium, from which they erupt onto the host's skin as the mosquito feeds. Larvae then migrate into the bite wound and, as most dogs are highly susceptible to heartworm disease, most L3 then establish infection. It takes 2-3 days for L3 to moult to L4, which remain in the subcutaneous tissues for up to two months before becoming young adults (L5) and migrating to the pulmonary arteries.  

==Pathogenesis==

==Pathogenesis==

Sequelae to heartworm infection include pulmonary thromboembolism, which can either occur due to the death and metastasis of adult worms, or due to platelet aggregation induced by the parasite. In severe cases, live nematodes can migrate to the right ventricle, right atrium and caudal vena cava. The resulting incompetence of the tricuspid valve, augmented by concurrent pulmonary hypertension, leads to signs of right-sided heart failure. Flow of erythrocytes through the mass of parasites formed can also cause haemolysis and thus haemoglobinaemia. This combination of acute right-sided heart failure and intravascular haemolysis is referred to as "caval syndrome", which in severe cases can also be characterised by thromboembolic events and [[Disseminated Intravascular Coagulation|disseminated intravascular coagulation]]. Due to the smaller numbers of adult worms, caval syndrome is less common in cats².

 

Sequelae to heartworm infection include pulmonary thromboembolism, which can either occur due to the death and metastasis of adult worms, or due to platelet aggregation induced by the parasite. In severe cases, live nematodes can migrate to the right ventricle, right atrium and caudal vena cava. The resulting incompetence of the tricuspid valve, augmented by concurrent pulmonary hypertension, leads to signs of right-sided heart failure. Flow of erythrocytes through the mass of parasites formed can also cause haemolysis and thus haemoglobinaemia. This combination of acute right-sided heart failure and intravascular haemolysis is referred to as "caval syndrome", which in severe cases can also be characterised by thromboembolic events and disseminated intravascular coagulation. Due to the smaller numbers of adult worms, caval syndrome is less common in cats².

In cats, heartworm disease generally causes a diffuse pulmonary infiltrate and an eosinophilic pneumonia². Adult worms may die and embolise to the lungs, resulting in severe haemorrhage and oedema of the affected lobe. Immature nematodes have also been known to migrate to sites other than the pulmonary arteries and heart such as the CNS, eye and subcutaneous tissues. These ectopic infections are far more common in cats than in dogs, suggesting that ''D. immitis'' is not well adapted to feline hosts.

In cats, heartworm disease generally causes a diffuse pulmonary infiltrate and an eosinophilic pneumonia². Adult worms may die and embolise to the lungs, resulting in severe haemorrhage and oedema of the affected lobe. Immature nematodes have also been known to migrate to sites other than the pulmonary arteries and heart such as the CNS, eye and subcutaneous tissues. These ectopic infections are far more common in cats than in dogs, suggesting that ''D. immitis'' is not well adapted to feline hosts.

==Signalment==

==Signalment==

''Dirofilaria immitis'' infection affects dogs more commonly than cats, and risk is greatest in outdoor animals. Dogs of any age may be affected, but infections are most common in 3 to 8 year old dogs, and medium and large breeds are over-represented^{1, 3}. In cats, there are no breed or age predispositions, but males are more frequently affected³. Ferrets may also contract dirofilariasis; there are no age or sex predilections¹.

''Dirofilaria immitis'' infection affects dogs more commonly than cats, and risk is greatest in outdoor animals. Dogs of any age may be affected, but infections are most common in 3 to 8 year old dogs, and medium and large breeds are over-represented^{1, 3}. In cats, there are no breed or age predispositions, but males are more frequently affected³. Ferrets may also contract dirofilariasis; there are no age or sex predilections¹.

===Clinical Signs===

===Clinical Signs===

Heartworm disease tends to develop slowly and gradually

In dogs, historical findings at the time of presentation can vary. Some animals are asymptomatic, or cough only occasionally. In countries where heartworm is endemic, animals may be routinely tested for dirofilariasis six months after the end of the high-risk season³. Therefore, positive laboratory testing may be the first indication of disease¹. More obvious signs may be seen depending on the severity of disease. Generally, the onset of heartworm disease is insidious, and clinical signs are related either to a high parasite burden, or to an allergic response to the parasite². Affected dogs most often show coughing, and dyspnoea/tachypnoea, exercise intolerance, loss of condition and syncope may also be seen. In severe cases the pulmonary vessels may rupture, leading to haemoptysis or epistaxis. There is a tendency for signs to only manifest during exercise, and so patients with a sedentary lifestyle may never show overt disease. Right-sided congestive heart failure may ensue when worm burden is high, and signs can include jugular distension, ascites, marked exercise intolerance and hepatomegaly. A systolic murmur is sometimes audible on cardiac auscultation.

and clinical signs are usually only present in cases

with a high worm burden and/or when the host has a

significant allergic response to the parasite. Frequently,

never show overt signs of heartworm disease. In dogs,

coughing is the most common clinical sign, followed by

tachypnoea and dyspnoea, exercise intolerance, chronic

weight loss and syncope. In sexvee cases, haemoptysis

can be present as a possible consequeince of pulmonary

vessel rupture. Jugular distension, hepatomegaly, ascites

and marked exercise intolerance are typical signs of

concurrent right-sided heart failure. In such patients, a

death is preceded by an acute respiratory crisis, probably

due to a parasitic embolism and obstruction of a major

pulmonary artery. When present, clinical signs of heartworm

These may include anorexia, lethargy, coughing, vomiting,

dyspnoea, syncope and collapse. In some cases, the respiratory

disease both in dogs and cats. This is characterised

frequently, disseminated intrav ascular coagulaktion1.

In dogs, infection should be identified by serologic testing prior to the onset of clinical signs; however, it should be kept in mind that HW antigenemia and microfilaremia do not appear until ~5 and 6.5 mo postinfection, respectively. When dogs are not administered a preventative and are not appropriately tested, clinical signs such as coughing, exercise intolerance, unthriftiness, dyspnea, cyanosis, hemoptysis, syncope, epistaxis, and ascites (right-sided CHF) are likely to develop. The frequency and severity of clinical signs correlate to lung pathology and level of patient activity. Signs are often not observed in sedentary dogs, even though the worm burden may be relatively high. Infected dogs experiencing a dramatic increase in activity, such as during hunting seasons, may develop overt clinical signs. Canine HW disease can be classified by physical examination, thoracic radiographs, urinalysis, and PCV.  

A classification system for the presentation of heartworm disease exists¹, outlined in the table below.

{| class="wikitable collapsible"

{| class="wikitable collapsible"

  |-

  |-

  |<center>'''Class 1'''</center>

  !width="8%"|<center><u>'''Class '''</u></center>  

  |asymptomatic to mild HW disease, with no clinical or radiographic signs and no laboratory abnormalities. Subjective signs such as loss of condition, decreased exercise tolerance, or occasional cough might be seen.

  !width="92%"|<center><u>'''Clinical Signs'''</u></center>

  |-

  |-

  |<center>'''Class 2'''</center>  

  |<center>'''Class I'''</center>

  |derate HW disease, characterized by an occasional cough and mild-to-moderate exercise intolerance. A slight loss of condition, increased lung sounds, and mild to moderate radiographic changes, such as right ventricular enlargement, are present. Laboratory results may show anemia and proteinuria.

  |'''Asymptomatic or mild disease'''

*Weight loss, reduced exercise tolerance or an occasional cough may be seen.  

*No radiographic signs or laboratory abnormalities.

  |-

  |-

  |<center>'''Class 3'''</center>  

  |<center>'''Class II'''</center>  

  |severe disease variably characterized by anemia, weight loss, exercise intolerance, tachypnea at rest, severe or persistent coughing, dyspnea, hemoptysis, syncope, and ascites. Severely abnormal radiographs may show right ventricular hypertrophy, enlargement of the main pulmonary artery, and diffuse pulmonary densities. Laboratory results indicate marked anemia, thrombocytopenia, and proteinuria. Electrocardiographic evidence of right ventricular hypertrophy is often present.

  |'''Moderate disease'''

*Animal coughs occasionally and shows mild-to-moderate exercise intolerance.  

*Radiography may show mild-to-moderate changes, e.g. right ventricular enlargement.  

*Anaemia and proteinuria may be present.  

  |-

  |-

  |<center>'''Class 4'''</center>  

  |<center>'''Class III'''</center>  

  |lso known as the caval syndrome, is characterized by sudden onset with collapse, hemoglobinuria, and respiratory distress. If surgery is not immediately instituted, this syndrome is usually fatal.

  |'''Severe disease'''

*Radiographs appear abnormal: right ventricular hypertrophy, enlargement of the main pulmonary artery, and diffuse pulmonary densities. ECG often shows right ventricular hypertrophy.

|'''Caval syndrome'''

*Sudden onset of collapse, haemoglobinuria, and respiratory distress.  

*Usually fatal without immediate surgery.

  |-

  |-

  |}

  |}

nfected cats may be asymptomatic or exhibit intermittent coughing, dyspnea, vomiting, lethargy, anorexia, or weight loss. The symptoms often resemble those of feline asthma. In general, signs are most prevalent during periods when worms die, including when young adult worms arrive in the lungs. Antigen tests in cats are negative during the early eosinophilic pneumonitis syndrome, although antibody tests may be positive. Subsequently, clinical signs often resolve and may not reappear for months. Cats harboring mature worms may exhibit intermittent vomiting, lethargy, coughing, or episodic dyspnea. HW death can lead to acute respiratory distress and shock, which may be fatal and appears to be the consequence of pulmonary thrombosis.

 

In cats, most infections are asymptomatic. However, sudden death can occasionally occur. This may be preceded by an acute respiratory crisis, thought to be due to parasitic thromboembolism and obstruction of a major pulmonary artery^{1, 2}. When clinical signs are less acute, they are vague and may include anorexia, weight loss and lethargy. Intermittent coughing and dyspnoea can appear similar to feline asthma. Syncope may also occur, and cats may vomit. The cause of this vomiting is undetermined³.

 

In dogs, thoracic radiography provides good information on disease severity and is useful for screening dogs showing clinical signs compatible with ''D. immitis'' infection¹. However, thoracic radiograph do not necessarily reflect the current worm burden: radiographic signs of advanced disease can persist long after an infection has run its course⁴. Conversely, dogs with high burdens may be inactive and thus show few clinical signs or radiographic changes. Radiographic signs are mild-to-moderate in class II disease, but become more obvious in class III infections. The main pulmonary artery is enlarged^{1, 4}, and the caudal lobar vessels appear tortuous¹. Ill-defined, fluffy infiltrates are apparent, and often surround the caudal lobar vessels. Right-sided cardiomegaly may be appreciated, and pleural and peritoneal effusions can be noted in right-sided congestive heart failure⁴.

 

Cardiac changes on thoracic radiography are less common in cats than dogs. The caudal lobar veins are enlarged (greater than 1.5 times the width of the ninth rib), and the pulmonary arteries are blunted and tortuous^{3, 5}. Patchy parenchymal infiltrates may be seen in the region of vessels in animals showing respiratory signs^{1, 3}. Enlargement of the main pulmonary artery cannot normally be seen in cats, as it has a relatively midline position and is thus obscured by the cardiac silhouette^{1, 5}. Right-sided cardiomegaly is not considered a typical finding in the cat⁵.

===Diagnostic Imaging===

===Echocardiography===

In dogs, echocardiography is relatively unimportant as a diagnostic tool. Worms observed in the right heart and vena cava are associated with high-burden infection with or without caval syndrome. Severe, chronic pulmonary hypertension causes right ventricular hypertrophy, septal flattening, underloading of the left heart, and high-velocity tricuspid and pulmonic regurgitation. The ECG of infected dogs is usually normal. Right ventricular hypertrophy patterns are seen when there is severe, chronic pulmonary hypertension and are associated with overt or impending right-sided CHF (ascites). Heart rhythm disturbances are usually absent or mild, but atrial fibrillation is an occasional complication in dogs with Class III disease.

Echocardiography is more important in cats than dogs because of the increased difficulty of diagnosis and the fact that this test can have a high sensitivity depending on operator experience¹. Specificity is 100%⁵, and the test can help exclude or confirm other primary cardiac diseases such as hypertrophic cardiomyopathy³. Worms can be visualised as parallel hyperechoic lines¹, and are seen in the right atrium and ventricle and main pulmonary artery^{1, 3, 5}.

In cats, worms can usually be imaged on echocardiography. Parallel hyperechoic lines, which are an image from the heartworm cuticle, may be seen in the right heart and pulmonary arteries. High worm burdens may be associated with worms in the right heart. Echocardiography is more important in cats than dogs because of the increased difficulty of diagnosis and the high sensitivity of the test in experienced hands.  

The ECG of infected dogs is usually normal. Right ventricular hypertrophy patterns may be seen in chronic ,severe pulmonary hypertension and are associated with impending or apparent right-sided congestive heart failure⁴. Arrhythmias do not normally occur, buy atrial fibrillation is is occasionally seen in Class III disease.

n dogs, thoracic radiography provides the most information on disease severity and is a good screening tool for dogs with clinical signs compatible with dirofilariasis. Class III infections are characterized by a large main pulmonary artery segment and dilated, tortuous caudal lobar pulmonary arteries. If the latter are ≥1.5 times the diameter of the 9th rib at their point of superimposition, then severe pathology is present. Right ventricular enlargement may also be seen. Fluffy, ill-defined parenchymal infiltrates of variable extent often surround the caudal lobar arteries, usually worst in the right caudal lobe, in advanced disease. The infiltrate may improve with cage confinement with or without anti-inflammatory dosages of a corticosteroid.

Electrocardiography is less useful in the cat, as involvement of the heart chambers does not occur as frequently as in the dog⁵.

In cats, cardiac changes are less common. The caudal lobar arteries normally appear relatively large, but are larger still with heartworm infection. Patchy parenchymal infiltrates may also be present in cats with respiratory signs. The main pulmonary artery segment usually is not visible due to its relatively midline location.

===Laboratory Tests===

===Laboratory Tests===

In addition to special diagnostic tests in both cats and dogs, a CBC, chemistry profile, urinalysis, and particularly thoracic radiographs are indicated. Laboratory data are often normal. Eosinophilia and basophilia are common and together suggest occult dirofilariasis or allergic lung disease. Eosinophilia surges as the L5 arrive in the pulmonary arteries. Subsequently, eosinophil counts vary but are usually high in dogs with immune-mediated occult infections, especially if eosinophilic pneumonitis develops (<10% of total infections).

In both dogs and cats, '''routine haematology, biochemistry and urinalysis''' should be performed. Most parameters are usually within normal limits, but an anaemia can often be seen. Eosinophilia and basophilia are also common^{1, 3}. Eosinophilia peaks as L5 enter the pulmonary arteries and subsequently varies. An inflammatory leukogram is possible³. Hyperglobulinaemia due to antigenic stimulation is an inconsistent finding^{1, 3}. Right-sided heart failure or immune-complex glomerulonephritis can lead to hypoalbuminaemia and, very occasionally, nephrotic syndrome¹. Because of this, it is possible for urinalysis to reveal proteiunuria^{1, 3}. Haemoglobinaemia and haemoglobinuria are associated with caval syndrome³.

Hyperglobulinemia may be present in dogs and cats due to antigenic stimulation. Hypoalbuminemia in dogs is associated with severe immune-complex glomerulonephritis or right-sided CHF. Serum ALT and alkaline phosphatase are occasionally increased, but do not correlate well with abnormal liver function, efficacy of adulticide treatment, or risk of drug toxicity. Urinalysis may reveal proteinuria that can be semiquantitated by a urine protein:creatinine ratio. Occasionally, severe glomerulonephritis or amyloidosis can lead to hypoalbuminemia and nephrotic syndrome. Dogs with hypoalbuminemia secondary to glomerular disease also lose antithrombin III and are at risk for thromboembolic disease. Hemoglobinuria is associated with Class III disease when RBC are lysed in the pulmonary circulation by fibrin deposition. Heparin therapy (75-100 U/kg, SC, tid) is indicated. Hemoglobinuria is also a classic sign of the vena caval syndrome.  

 

[[Image:dirofilariasis.jpg|right|thumb|200px|Dirofilariasis. Courtesy of T. Scase]]

There are several methods for the specific demonstration of ''Dirofilaria immitis'' in the animal. Firstly, direct '''microscopic examination''' allows rapid identification of microfilariae in a drop of fresh blood, as their movements can vigorously displace the surrounding red blood cells². Despite being quick, simple and inexpensive, this test is not sufficiently sensitive to provide a definitive diagnosis, particularly when there is a low concentration of microfilariae in the bloodstream. '''Filtration methods''' therefore exist to facilitate the microscopic demonstration of microfilariae^{2, 3}. These include the '''modified Knott's test''', which involves haemolysis, centrifugation and staining with methylene blue before direct examination. Tests such as this are more sensitive than merely examining a drop of blood, and the morphology of microfilariae can be clearly seen. However, sensitivity in comparison to other methods is still low and so microfilarial identification tests are often reserved for confirmation of weak positive antigen tests and determination of microfilarial status prior to treatment with a microfilaricide³. Cats frequently lack circulating microfilariae, and so direct microscopic examination is of little use in this species.

[[Image:dirofilariasis 2.jpg|right|thumb|200px|'''Dirofilariasis'''. Courtesy of T. Scase]]

Tests exist to detect ''D. immitis'' antigens. '''ELISAs''' specific for proteins released from the reproductive tract of adult female worms are available for in-house use². Sensitivity and specificity are excellent, but small worm burdens and the presence of immature female- or male-only infections can give low antigen titres hence false negatives. This is especially common in cats. '''Specific agglutination and immunochromatography''' techniques are also available for use in dogs. Any antigen test performed in the first six months of infection may give false negative results as levels of circulating antigen are initially low while female worms mature. '''In-house tests''' are also available to detect antibody against ''Dirofilaria immitis''. The presence of antibodies confirms exposure, but does not necessarily provide information about current infection. These tests are therefore most useful for ruling out infection. ''D. immitis'' antibody tests have a low specificity² and so have largely been superceded by tests for antigen.

'''PCR-based tests''' are highly sensitive and specific for the diagnosis of immature and adult heartworms, and are especially useful in unconventional (e.g. wildlife) hosts². At present, these tests are not widely available for the diagnosis of ''Dirofilaria immitis''.

Available antigen detection tests are very sensitive and specific. To determine when testing might become useful, it is advisable to add a predetection period to the approximate date on which infection may have been possible. A reasonable interval is 7 mo. There is generally no need to test a dog for antigen or microfilariae prior to ~7 mo of age. The level of antigenemia is directly related to the number of mature female worms present. At least 90% of dogs harboring ≥3 adult females will test positive. In general, strong-quick positive reactions correlate with relatively high worm burdens. For low-burden suspects, commercial laboratory-based microwell titer tests are the most sensitive.

===Pathology===

===Pathology===

On post-mortem examination, the right side of the heart is found to be enlarged. There is proliferation of the pulmonary arterial myointima, as well as pulmonary thromboembolism and haemorrhage. If right-sided congestive heart failure was present in life, the hepatomegaly and hepatic congestion will be seen.

On post-mortem examination, ''Dirofilaria immitis'' worms are apparent in the pulmonary artery and possibly the right side of the heart. The right side of the heart is found to be enlarged and there is proliferation of the pulmonary arterial myointima. Pulmonary thromboembolism and haemorrhage may be seen. If right-sided congestive heart failure was present in life, hepatomegaly and hepatic congestion will be apparent.

==Treatment==

==Treatment==

Decisions in the treatment of heartworm disease are dependent on the severity of infection. A scheme exists to classify patients in terms of disease severity². Class one patients have subclinical heartworm disease, and carry an excellent prognosis following treatment wiht adulticidal drugs. Class two animals show mild to moderate clinical signs and similar radiographic changes. These animals may respond positively to treatment. Dogs with class 3 disease have severe clinical signs, such as persistent coughing, dyspnoea, right-sided heart failure or haemoptysis, and these are reflected by severe radiographic signs. These cases have a high risk of pulmonary thromboembolism and so prognosis is guarded and the benefits of adulticidal treatment should be considered carefully.  

In '''caval syndrome''', surgery is the treatment of choice. Worms are removed from the right side of the heart and the main pulmonary artery using flexible crocodile or basket-type retrieval forceps². This procedure is complex and requires general anaesthesia and fluoroscopic imaging, but reduces the risk of thromboembolism following subsequent adulticidal treatment. Symptomatic and supportive therapy to stabilise the patient should be continued for around one month after surgery before adulticidal treatment is administered³.

Even low grade infections in cats may result in pulmonary thromboembolism with adulticidal treatment, and spontaneous remission is seen in some cats. Because of this, symptomatic treatment (cage rest, oxygen supplementation, fluid therapy, bronchodilators and dexamethasone) may be more appropriate in sick cats, and clinically well cats can merely be monitored regularly for remission. Adulticidal treatment should only be considered in cats that fail to respond to supportive treatments but are in a stable condition.

'''No drugs are specifically approved for microfilaricidal treatment''' of ''Dirofilaria immitis'', and successful elimination of adult worms should result in the demise of circulating microfilariae four to six weeks later². '''Single doses of ivermectin, milbemycin oxime, moxidection or selamectin''' are, however, effective at removing microfilariae from the circulation. The sudden death of large numbers of microfilariae may invoke an anaphylactic response, and oral prednisolone may be administered with microfilaricides to help prevent this.

Heartworm prophylaxis should be implemented in all cats and dogs living in or visiting areas in which ''Dirofilaria immitis'' is endemic. Ivermectin or milbemycin oxime can be given ''per os'' on a monthly basis, and selemectin spot-on is effective when applied each month. If animals have already been exposed to ''Dirofilaria immitis'' it may be wise to perform an antigen test before starting treatment. In endemic countries, routine antigen testing six months after the end of the previous heartworm season will detect infections that have slipped through the net, and enable treatment during the mild, early stages of disease³.

 

 

In mildly symptomatic  or asymptomatic animals, the course of dirofilariasis is usually uneventful following treatment and the prognosis is excellent³. Animals with severe infection carry a guarded prognosis with a higher risk of complications.

|literature search = [http://www.cabdirect.org/search.html?rowId=1&options1=AND&q1=%22Dirofilaria+immitis%22&occuring1=title&rowId=2&options2=AND&q2=&occuring2=freetext&rowId=3&options3=AND&q3=&occuring3=freetext&x=21&y=6&publishedstart=2000&publishedend=yyyy&calendarInput=yyyy-mm-dd&la=any&it=any&show=all Dirofilaria immitis publications since 2000]

|full text = [http://www.cabi.org/cabdirect/FullTextPDF/2010/20103181752.pdf '''A review of American heartworm society guidelines for the management of heartworm infections in cats.''' Guerrero, J.; The North American Veterinary Conference, Gainesville, USA, Small animal and exotics. Proceedings of the North American Veterinary Conference, Orlando, Florida, USA, 16-20 January 2010, 2010, pp 1173-1176, 1 ref.]

licensed for use in the UK). Melarsomine is less nephrotoxic

and has a higher efficacy. Melarsomine is injected

dose of 2-5 mg/kg, repeated after 24 hours. However,

to kill just a proportion of worms and hence minimise

the risk of pulmonary thromboembolism. If the patient

remains stable, the standard adulticidal protocol can be

administered one month later. In the week following the

administration of melarsomine, the likelihood of pulmonary

If adulticidal treatment is declined by the owner,

further infection and may kill some adult nematodes.

physical removal of worms from the right side of the

or basket-type retrieval forceps. This procedure is

complex, requires general anaesthesia and fluoroscopic

imaging, but may reduce the risk of thromboembolism

following subsequent adulticidal treatment.

No drugs are specifically approved for microfilaricidal treatment of ''Dirofilaria immitis'', and successful elimination of adult worms should results in the demise of circulating microfilariae four to six weeks later². Single doses of ivermectin, milbemycin oxime, moxidection or selamectin are, however, effective at removing microfilariae from the circulation. The sudden death of large numbers of microfilariae may invoke an anaphylactic response, and oral prednisolone may be administered with microfilaricides to help prevent this.

[http://www.cabi.org/cabdirect/FullTextPDF/2006/20063226177.pdf ''' Heartworm of dog - its aetiopathogenesis, diagnosis, treatment and prevention.''' Kundu, P.; Intas Pharmaceuticals Ltd, Ahmedabad, India, Intas Polivet, 2006, 7, 1, pp 106-110, 16 ref.]

Heartworm prophylaxis should be implemented in all cats and dogs living in or visiting areas in which ''Dirofilaria immitis'' is endemic. In the UK, milbemycin oxime and selamectin are licensed for the prevention of heartworm disease and should be administered on a monthly basis as they are capable of killing migrating larvae up to week six post-infection. In the event of non-compliance or a missed dose, it may be necessary to test the animal for ''Dirofilaria immitis'' six months later if they are likely to have been exposed to infection during the time they were unprotected. Drugs that persist in the long term, such as injectable moxidectin, can help overcome this issue.

|Vetstream = [https://www.vetstream.com/canis/search?s=nematode Nematodes]

In mildly symptomatic  or asymptomatic animals, the course of dirofilariasis is usually uneventful following treatment and the prognosis is excellent³. Animals with severe infection carry a guarded prognosis with a higher risk of complications.

|book = Arthropod-borne Infectious Diseases of the Dog and Cat

|author = Susan E. Shaw, Michael J. Day

==Links==

==Links==

==References==

==References==

#Ferasin, L (2004) Disease risks for the travelling pet: Heartworm disease, ''In Practice'', '''26(6)''', 350-357.

#Ferasin, L (2004) Disease risks for the travelling pet: Heartworm disease, ''In Practice'', '''26(6)''', 350-357.

#Tilley, L P and Smith, F W K (2004) '''The 5-minute Veterinary Consult (Fourth Edition)''',''Blackwell''.

#Tilley, L P and Smith, F W K (2004) '''The 5-minute Veterinary Consult (Fourth Edition)''',''Blackwell''.

#Ridyard, A (2005) Heartworm and lungworm in dogs and cats in the UK, ''In Practice'', '''27(3)''', 147-153.

#Ridyard, A (2005) Heartworm and lungworm in dogs and cats in the UK, ''In Practice'', '''27(3)''', 147-153.

 

#Venco, L (2007) Heartworm (Dirofilaria immitis) disease in dogs. ''Dirofilaria immitis and D. repens in dog and cat and human infections'', 117-125.  

 

 

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[[Category:Filarioidea]]

[[Category:Filarioidea]]

[[Category:Dog_Nematodes]]

[[Category:Dog_Nematodes]]

[[Category:Cat_Nematodes]]

[[Category:Cat_Nematodes]]

[[Category:To_Do_-_Parasites]]

[[Category:Zoonoses]]

[[Category:Cardiovascular Diseases - Dog]]

[[Category:Respiratory Parasitic Infections]]

 

[[Category:Expert_Review]]

[[Category:Respiratory Parasitic Infections]]

[[Category:Cardiology Section]]

[[Category:To_Do_-_Lizzie]]