Boxer with Angiostrongylus Vasorum

Bridget, a two-year-old, female, neutered boxer was presented to our Internal Medicine team following a two-week history of very mild lethargy and cough that had progressed to acute onset, marked depression and weakness.

This case highlights that Angiostrongylus vasorum (Lung Worm) should be considered as a differential diagnosis in cases of unexplained bleeding even if respiratory findings are mild.

Bridget's owners usually treated her with Nex Gard Spectra as a broad spectrum, prophylactic anti-parasitic but were overdue in administering the most recent dose. On clinical examination, her mucous membranes were pale but cardiovascular parameters were stable. She was ambulatory but with depressed mentation without any other neurological deficits. Haematology and biochemistry revealed a mild-moderate, non-regenerative anaemia and a moderate thrombocytopenia. PT and aPTT were within reference limits. An Angiodetect SNAP test displayed a strong positive result. The degree of the haematological findings did not explain the extent of her altered mental status and an intracranial bleed was suspected.

Whilst thoracic radiographs showed a very mild bronchial pattern, lung pathology on CT was more pronounced and consistent with parasitic pneumonia and arteritis:

  • Diffuse multifocal pulmonary parenchymal changes (patchy ground glass attenuation and mild to moderate irregular bronchial wall thickening) with a subtly peripheral distribution. Multifocal moderate to marked dilation of several small pulmonary arteries peripherally.

CT also confirmed that there was haemorrhagic infarct and associated oedema in the left frontal lobe of the brain.

Supportive treatment was instigated with:

  • Maintenance intravenous fluids.
  • Mannitol 0.Smg/kg intravenously over 20mins as there was concern over raised intracranial pressure. Her mentation had worsened in the hours after admission, her blood pressure had risen to 160-170 mmHg and her PLR had become more sluggish.
  • Levetiracetam 20 mg/kg every 8 hours intravenously as a minimally sedative anti-seizure therapy.
  • Dexamethasone 0.2mg/kg every 24 hours intravenously at an anti-inflammatory dose to treat secondary inflammation in the brain.
  • Paracetamol l0mg/kg intravenously.
  • Fenbendazole S0mg/kg orally every 24 hours started on the day of admission once her neurological signs had improved and she was able to sit up and swallow.
  • Tranexamic acid lOmg/kg every 8 hours orally

ScieraI bleeding was noted on the following day but there was no other ongoing haemorrhage in her case.

She remained hospitalised for 5 days to monitor for ongoing bleeding and to allow for recovery of heme urological signs. She was discharged with a 21-day course offenbendazole and a tapering dose of prednisolone and levetiracetam. She is currently doing well and getting back to her usual playful Boxer self.

How does A. vasorum cause bleeding and how should we treat it?

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.

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