Twenty two cases of canine neural angiostrongylosis in eastern Australia (2002-2005) and a review of the literature

Abstract

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- Angiostrongylus cantonensis 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- A. cantonensis IgG in CSF. Detecting anti- A. cantonensis IgG in serum was unhelpful because many normal dogs (20/21 pound 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. Electronic supplementary material The online version of this article (doi:10.1186/1756-3305-5-70) contains supplementary material, which is available to authorized users.

Eosinophilic meningoencephalomyelitis in an orangutan (Pongo pygmaeus) caused byAngiostrongylus cantonensis

“…The only case previously documented in Florida occurred in 2004, where a case of fatal A. cantonensis meningoencephalitis was diagnosed in a white-handed gibbon (Hylobates lar) from Zoo Miami (formerly Miami Metrozoo) (Duffy et al 2004). Other species reported with clinical disease from this parasite include humans, non-human primates, dogs, horses, opossum, mice, birds, and various other zoo animals (Gardiner et al 1990;Alicata 1991;Carlisle et al 1998;Kim et al 2002;Duffy et al 2004;Gelis et al 2011;Lunn et al 2012). Also known as the rat lungworm, A. cantonensis is a nematode that normally lives in the right ventricle and pulmonary artery of various species of rat, the definitive host (Alicata 1991).…”

“…Signs of infection are related to migration of the larvae and associated multifocal eosinophilic inflammation. Symptoms can include headache, fever, malaise, nausea, neck stiffness, paraesthesias, urine and fecal retention, cranial nerve and ascending limb paralysis, seizures, coma, and death (Hochberg et al 2007;Diaz 2009;Ramirez-Avila et al 2009;Lunn et al 2012;Wang et al 2012). In humans, the disease is most often self-limiting with 2-8 weeks of severe headache and malaise (Hochberg et al 2001).…”

Molecular and pathological studies on Angiostrongylus species in southeast Queensland

“…Once the larvae have migrated to the nervous system through intestinal veins, they physically damage the CNS tissue as a consequence of migration and cause eosinophilia in CSF by releasing antigens. The eosinophilic cell infiltrate increases the CSF pressure and leads to a variety of neurological signs in the patient 41 . T-cell populations, cytokines, immunoglobulins, matrix metalloprotienases and eosinophils are important components in the host cellular response to infection with A. cantonensis 89 .…”

“…Pups and adolescent dogs are more commonly infected and show some attraction to slugs 63 . The combination of this exploratory behaviour by younger dogs, as well as accidental ingestion of slugs that may contaminate dog food left outside the house are likely sources of infections of domestic dogs 41 . In addition, the infection of the two toddlers in Sydney also occurred during the autumn and winter period (Morton et al 2013), thus supporting a seasonal prevalence.…”

“…Apart from the indication of a broad rat survey, it has been proposed that dogs can be used as sentinels for disease transmission in the urban and peri-urban areas 41 . Lunn and colleagues noted that the majority (64%) of dogs diagnosed with neural angiostrongyliasis in Sydney occurred between the autumn and winter months from April to July.…”