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Also known as: French Heartworm

Do not confuse with: Heartworm caused by Dirofilaria immitis


Angiostrongylosis is a clinical syndrome of dogs caused by infection with Angiostrongylus vasorum, the 'French heartworm' or 'lungworm'. The adult worms accumulate in the pulmonary arterial vessels and right heart chambers and release eggs and larvae into the pulmonary circulation. The adult worms obstruct blood flow through the pulmonary vasculature and lead to the development of pulmonary undercirculation, right ventricular hypertrophy and cor pulmonale. The adults also cause local pulmonary arteritis and thrombi are able to form against the inflamed vessel wall.

The eggs lodge in the small pulmonary capillaries and the L1 larvae hatch at this location. These larvae penetrate the capillaries and enter the pulmonary parenchyma to cause an interstitial pneumonia. This pneumonia is the major cause of the respiratory signs observed in infested animals but, in severely affected animals, pulmonary oedema may also develop. By an unknown mechanism, the presence of infection reduces the blood concentrations of factors V and VIII and causes thrombocytopathia and thrombocytopaenia. Affected animals therefore often suffer from some form of coagulopathy.


The lungworm is acquired when dogs eat slugs and snails infected with the L3 larvae. It is therefore crucial to establish whether the dog does eat slugs or snails. As foxes are also able to act as definitive hosts, areas with a dense population of foxes are likely to have a high lungworm prevalence. A. vasorum was traditionally considered to be a disease acquired by animals that had travelled to Europe but it is now being diagnosed in untravelled animals as far north in the UK as Scotland[1].


Clinical Signs

Clinical signs are mainly related to coagulopathies and the presence of worms, eggs and larvae in the pulmonary vasculature and parenchyma. They include:


  • Cutaneous bruising
  • Intra-cavitatory haemorrhage producing haemoabdomen or haemothorax[2]
  • Haematomas may form in the spinal cord and cause neurological signs

Pulmonary disease, manifesting as:

  • A soft productive moist cough
  • In severe cases, dyspnoea and tachypnoea may be observed
  • Sudden-onset dyspnoea and collapse may occur in animals with pulmonary thromboembolism

Right-sided congestive heart failure, manifesting as:

  • Jugular pulses or positive hepatojugular relfux
  • Hydrothorax or ascites usually composed of a modified transudate

Aberrent larval migration may result in neurological signs if they enter the cerebro-spinal fluid[3].

The results of a recent study indicate that the most common clinical signs observed in infected dogs are cough (65%), dyspnoea (43%), coagulopathy (35%) and collapse (26%)[4].

Laboratory Tests

Blood eosinophilia and basophilia may or may not be present. In one study, eosinophilia was detected in 21% of naturally infected dogs[5] Animals may or may not be thrombocytopaenic and anaemic and a case of concurrent immune-mediated thrombocytopaenia with A. vasorum infection has been reported[6].

Fructosamine concentration may be low in cases of A. vasorum infection and this finding may prompt examination of a faecal sample[5][7].

Coagulation times may be prolonged due to the consumptive coagulopathy.

Diagnostic Imaging

Plain radiographs of the chest may show enlargement of the right heart chambers and truncation of pulmonary arterial vessels. There may be an alveolar lung pattern due to pulmonary haemorrhage or pneumonia.

Ultrasonography may be used to show enlargements in heart chambers and the presence of worms in the pulmonary artery and right ventricle. Pulmonary hypertension should also be detectable by ultrasound based on the velocity of flow through the pulmonic valve.

Other Tests

The gold standard test is considered to be identification of L1 larvae in faeces. At least five faecal samples should be submitted for examination by the Baermann technique as excretion of the larvae is variable[8][9].


Histopathological examination of pulmonary samples may reveal golden pigment within macrophages (haemosiderin) and inflammation and scarring of alveolar walls. The remaining air spaces may be enlarged.


Oxygen should be administered to animals with dyspnoea by nasal catheter, flow by or mask and low dose aspirin can be administered to animals considered to be at risk of developing pulmonary thromboembolism.

Infection with Angiostrongylus vasorum may be treated easily with suitable anthelmintics. Ideally, four 5 day courses of a benzimidazole should be administered at a high dose rate over 1-2 months. Fenbendazole is widely available in the UK in a granule form and this is used most frequently in the treatment of A. vasorum. If infection is suspected but larvae cannot be detected in faeces, it may still be worth treating the animal.

Alternatively, an imidacloprid/moxidectin spot-on can be used as a single application but this was found to have a lower efficacy than fenbendazole in the clearance of infection[10].


With increasing awareness of the threat posed by A. vasorum and with increasing prevalence across the UK, preventative treatment is now used more widely. Suitable products include the spot-on of imidacloprid/moxidectin[11].


Animals affected by clinical disease may become severely ill but, if the infection is cleared, they usually suffer few adverse consequences.

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Angiostrongylosis publications


  1. Helm J, Gilleard JS, Jackson M, Redman E, Bell R. A case of canine Angiostrongylus vasorum in Scotland confirmed by PCR and sequence analysis. J Small Anim Pract. 2009 May;50(5):255-9.
  2. Sasanelli M, Paradies P, Otranto D, Lia RP, de Caprariis D. Haemothorax associated with Angiostrongylus vasorum infection in a dog. Vet Parasitol. 2009 Dec 23;166(3-4):326-32. Epub 2009 Sep 17.
  3. Negrin A, Cherubini GB, Steeves E. Angiostrongylus vasorum causing meningitis and detection of parasite larvae in the cerebrospinal fluid of a pug dog. J Small Anim Pract. 2008 Sep;49(9):468-71. Epub 2008 May 12.
  4. Chapman PS, Boag AK, Guitian J, Boswood A. Angiostrongylus vasorum infection in 23 dogs (1999-2002). J Small Anim Pract. 2004 Sep;45(9):435-40.
  5. 5.0 5.1 Willesen JL, Jensen AL, Kristensen AT, Koch J. Haematological and biochemical changes in dogs naturally infected with Angiostrongylus vasorum before and after treatment. Vet J. 2009 Apr;180(1):106-11. Epub 2007 Dec 20. Cite error: Invalid <ref> tag; name "one" defined multiple times with different content
  6. Gould SM, McInnes EL. Immune-mediated thrombocytopenia associated with Angiostrongylus vasorum infection in a dog. J Small Anim Pract. 1999 May;40(5):227-32.
  7. Willesen JL, Jensen AL, Kristensen AT, Kjelgaard-Hansen M, Jessen R, Koch J. Serum fructosamine concentrations in 59 dogs naturally Infected with Angiostrongylus vasorum. J Vet Med A Physiol Pathol Clin Med. 2006 Jun;53(5):266-9.
  8. McGarry JW, Morgan ER. Identification of first-stage larvae of metastrongyles from dogs. Vet Rec. 2009 Aug 29;165(9):258-61.
  9. Humm K, Adamantos S. Is evaluation of a faecal smear a useful technique in the diagnosis of canine pulmonary angiostrongylosis? J Small Anim Pract. 2010 Apr;51(4):200-3. Epub 2010 Mar 1.
  10. Willesen JL, Kristensen AT, Jensen AL, Heine J, Koch J Efficacy and safety of imidacloprid/moxidectin spot-on solution and fenbendazole in the treatment of dogs naturally infected with Angiostrongylus vasorum (Baillet, 1866). Vet Parasitol. 2007 Jul 20;147(3-4):258-64. Epub 2007 Jun 4.
  11. Schnyder M, Fahrion A, Ossent P, Kohler L, Webster P, Heine J, Deplazes P. Larvicidal effect of imidacloprid/moxidectin spot-on solution in dogs experimentally inoculated with Angiostrongylus vasorum. Vet Parasitol. 2009 Dec 23;166(3-4):326-32. Epub 2009 Sep 17.

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