Quick review of the life cycle: Adult worms live in the pulmonary arteries and RHS heart and lay eggs. L1 larvae hatch and migrate through the pulmonary parenchyma before being coughed up, swallowed and excreted in the faeces. They mature from Ll to infective L3 in snails and slugs. Once ingested, L3 penetrate the gastric wall and enter the lymphatics which carries them into the pulmonary arteries where they mature into adults. The prepatent period is approximately 42 days.
The most common clinical signs are cardiorespiratory in nature (cough, dyspnoea and exercise intolerance) due to inflammation in the pulmonary parenchyma caused by the migrating L1larvae however some dogs develop haemostatic dysfunction that can lead to a variety of bleeding manifestations, sometimes in the absence of respiratory signs. The underlying cause of bleeding in these patients is not fully understood but it appears that the haemostatic system may be affected at multiple different sites even in the same animal. The most commonly seen signs are haematomas, petecchiation, ecchymoses, oral mucosaI membrane bleeding, scleral bleeding, epistaxis, pulmonary haemorrhage and wound bleeding following trauma or surgery and, more rarely, haemothorax, haemoabdomen, haematuria and intracranial and spinal cord haemorrhage. In the referral practice setting in endemic areas, a fatal outcome among A.vasorum positive dogs with clinical bleeding is reported in the range of 12.5-33.3% (Willesen etal. 2022).
It was previously thought that immune complex deposition caused by the infection may trigger haemostasis leading to a consumption of platelets and coagulation factors resulting in a low grade or chronic DIC however more recent studies have suggested that downregulation of proteins important for physiological haemostasis may result in the formation of a less stable blood clot. Furthermore, this may be combined with hypofibrinogenaemia and hyperfibrinolysis increasing the instability of the clot. Acquired van Willebrand syndrome has been detected in a few cases and it has been speculated that an acquired thrombocytopathy may be present but evidence for this is lacking.
Ideally, TEG or ROTEM would be used in cases of A.vasorum infection to determine if a patient is hypo or hypercoagulable but this is not widely available at this time.
Treatment of haemostatic abnormalities should be tailored to the individual case but may include:
- Serial monitoring of PT and aPTT and fresh frozen plasma administered if these become prolonged.
- Thrombocytopaenia is usually mild to moderate and rarely requires specific therapy.
- Packed red blood cell transfusion if haemodynamically unstable with ongoing haemorrhage.
- Use oftranexamic acid to treat hyperfibrinolysis. This should ideally be done after TEG but, given the high risk of catastrophic ongoing haemorrhage in these cases, may need to be considered in a setting where TEG is not available.