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Peer-reviewed veterinary case report

Canine neural angiostrongylosis cases and review in eastern Australia

By Lunn Julian A et al.·Published in Parasites & Vectors·2012·View original on DOAJ

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Original publication title: Twenty two cases of canine neural angiostronglyosis in eastern Australia (2002-2005) and a review of the literature

Species:
dog

Plain-English summary

A group of dogs in eastern Australia showed signs of weakness in their hind legs, neck pain, and other neurological issues due to a condition called neural angiostrongylosis, which is caused by a parasite. Many of these dogs were young and came from the same litters or kennels, suggesting a common source of infection, likely from eating slugs or snails. Treatment involved high doses of steroids and pain relief, and most dogs improved, although some were left with lasting nerve damage. This condition is important to recognize, as it can also affect humans and other animals in the area.

People also search for: dog hind leg weakness treatment · canine neural angiostrongylosis symptoms · dog neck pain causes · dog parasite treatment · how to care for a dog with nerve damage

Abstract

<p>Abstract</p> <p>Cases of canine neural angiostrongylosis (NA) with cerebrospinal fluid (CSF) evaluations in the peer-reviewed literature were tabulated. All cases were from Australia. A retrospective cohort of 59 dogs was contrasted with a series of 22 new cases where NA was diagnosed by the presence of both eosinophilic pleocytosis and anti-<it>Angiostrongylus cantonensis </it>immunloglobulins (IgG) in CSF, determined by ELISA or Western blot. Both cohorts were drawn from south east Queensland and Sydney. The retrospective cohort comprised mostly pups presented for hind limb weakness with hyperaesthesia, a mixture of upper motor neurone (UMN) and lower motor neurone (LMN) signs in the hind limbs and urinary incontinence. Signs were attributed to larval migration through peripheral nerves, nerve roots, spinal cord and brain associated with an ascending eosinophilic meningo-encephomyelitis. The contemporary cohort consisted of a mixture of pups, young adult and mature dogs, with a wider range of signs including (i) paraparesis/proprioceptive ataxia (ii) lumbar and tail base hyperaesthesia, (iii) multi-focal central nervous system dysfunction, or (iv) focal disease with neck pain, cranial neuropathy and altered mentation. Cases were seen throughout the year, most between April and July (inclusive). There was a preponderance of large breeds. Often littermates, or multiple animals from the same kennel, were affected simultaneously or sequentially. A presumptive diagnosis was based on consistent signs, proximity to rats, ingestion/chewing of slugs or snails and eosinophilic pleocytosis. NA was diagnosed by demonstrating anti-<it>A. cantonensis </it>IgG in CSF. Detecting anti-<it>A. cantonensis </it>IgG in serum was unhelpful because many normal dogs (20/21 lb dogs; 8/22 of a hospital population) had such antibodies, often at substantial titres. Most NA cases in the contemporary series (19/22) and many pups (16/38) in the retrospective cohort were managed successfully using high doses of prednisolone and opioids. Treatment often included antibiotics administered in case protozoan encephalomyelitis or translocated bacterial meningitis was present. Supportive measures included bladder care and physiotherapy. Several dogs were left with permanent neural deficits. Dogs are an important sentinel species for NA. Human cases and numerous cases in tawny frogmouths were reported from the same regions as affected dogs over the study period.</p>

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Original publication on DOAJ: https://doi.org/10.1186/1756-3305-5-70