Eosinophilic cerebrospinal fluid pleocytosis associated with neural Angiostrongylus vasorum infection in a dog

Abstract

A 1-year-old, female intact Pug dog was presented to the Small Animal Teaching Hospital of the University of Liverpool with a 4-week history of progressive multifocal intracranial signs. Magnetic resonance imaging (MRI) detected multiple hemorrhagic lesions in the brain. The Baermann and zinc sulfate flotation tests with centrifugation, performed on fecal samples, were positive for lungworm larvae and an antigenic test confirmed Angiostrongylus vasorum infection. Anthelmintic treatment was started with a consequent marked clinical improvement. Seventy days later, the dog was clinically normal, and no larvae were detected on the Baermann test. Repeat MRI of the brain revealed marked improvement of the hemorrhagic lesions. Cerebrospinal fluid analysis (CSF) showed marked eosinophilic pleocytosis, and anthelmintic treatment was restarted. A follow-up CSF analysis 4 months after the first presentation revealed resolution of the eosinophilic pleocytosis. This is the first case report of marked eosinophilic pleocytosis associated with neural A vasorum infection in a dog. The CSF eosinophilic pleocytosis persisted for several weeks after treatment, even in the absence of concurrent clinical signs and with a negative A vasorum Baermann test. K E Y W O R D S brain hemorrhage, canine angiostrongylosis, central nervous system, CSF, eosinophils, larval migration 1 | CASE PRESENTATION A 1-year-old female intact Pug dog was referred to the Neurology Service at the Small Animal Teaching Hospital (SATH), the University of Liverpool, for investigation of progressive truncal swaying, ataxia, right-sided head tilt, altered mentation, right eye exophthalmia, and conjunctival hyperemia. Clinical signs started 4 weeks prior to referral. The dog had always lived in the United Kingdom (UK), had never traveled abroad, and the vaccination status was up to date; however, no ectoparasite or endoparasite (including lungworm) prevention was given. The dog had free access to the outdoors where the dog could encounter wild animals. A CBC (LaserCyte Dx; IDEXX Laboratories,Westbrook, ME, USA) performed 6 days prior to referral revealed a mild leukocytosis (18.64 × 10 9 /L; RI 5.50-16.90) due to a mild neutrophilia (12.92 × 10 9 /L; RI 2-12) and mild monocytosis (3.16 × 10 9 / L; RI 0.30-2.00). Basophils were minimally increased (0.11 × 10 9 /L; RI 0.00-0.10), but the blood smear was not reviewed. The serum biochemistry profile (Catalyst Dx; IDEXX Laboratories) revealed mildly increased urea (12.4 mmol/L; RI 2.5-9.6), marginally increased ALP (227 IU/L; 23-212), and moderate hyperproteinemia (93 g/L; 52-82) due to moderate hyperglobulinemia (63 g/L; 25-45).Abstract presented in the 31st Annual Symposium of the ESVN-ECVN,

Further studies of neuroangiostrongyliasis (rat lungworm disease) in Australian dogs: 92 new cases (2010–2020) and results for a novel, highly sensitive qPCR assay

“…Canine NA is becoming more common as a cause of neurologic disease in eastern Australia, especially in Sydney and particularly in young dogs, rivalling more established entities such as meningitis of unknown origin (formerly granulomatous meningoencephalitis), aseptic suppurative meningitis, cryptococcosis, toxoplasmosis and neosporosis (Parzefall et al, 2014) as causes of inflammatory CNS disease. In the UK and Europe, ectopic A. vasorum infections can give rise to neurologic signs associated with eosinophilic pleocytosis in dogs, although such reports are currently rare (Negrin et al, 2008;Alcoverro et al, 2019). Veterinarians have a role to play in recommending measures that safely control rodent and mollusc numbers in urban and suburban settings, while the regular monthly administration of products containing the long-acting macrocyclic lactone moxidectin is likely to be effective against the development of NA based on extrapolation from A. vasorum prophylaxis (Helm et al, 2010).…”

Large T‐cell extradural lymphoma with concurrent marked cerebrospinal fluid eosinophilia in a dog

“…2 In contrast, CSF eosinophilia secondary to lymphoma is rarely reported, with CSF eosinophilia occurring most often with idiopathic, parasitic, or fungal etiologies. [4][5][6][7][8] Eosinophilia or regional eosinophilic infiltration is associated with lymphoma in dogs. [9][10][11][12][13] Intestinal T-cell lymphoma can be associated with regional eosinophilic infiltration 10 and hypereosinophilia.…”

“…68% of dogs with CNS lymphoma were diagnosed by CSF assessment, including 71% of T‐cell lymphoma cases 2 . In contrast, CSF eosinophilia secondary to lymphoma is rarely reported, with CSF eosinophilia occurring most often with idiopathic, parasitic, or fungal etiologies 4‐8 . Eosinophilia or regional eosinophilic infiltration is associated with lymphoma in dogs 9‐13 .…”

Persistent marked cerebrospinal fluid eosinophilia in a dog with primary central nervous system histiocytic sarcoma

“…A higher degree of CSF eosinophilia can be seen with infection by Angiostrongylus cantonenesis , which affects people and dogs in Southeast Asia, the tropical Pacific Islands, and Australia 3 . Other pathogens occasionally reported to cause CSF eosinophilia in dogs include Cryptococcus neoformans , Neospora caninum , Baylisascaris procyonis migrating larvae, Prototheca sp., Angiostrongylus vasorum , and Toxoplasma gondii 1,4–7 …”

“…3 Other pathogens occasionally reported to cause CSF eosinophilia in dogs include Cryptococcus neoformans, Neospora caninum, Baylisascaris procyonis migrating larvae, Prototheca sp., Angiostrongylus vasorum, and Toxoplasma gondii. 1,[4][5][6][7] Most commonly, CSF eosinophilia is due to eosinophilic meningoencephalitis (EME) of unknown etiology, also called idiopathic eosinophilic meningoencephalitis or eosinophilic MUO. 1,7-9 A minimum of 10% of eosinophils in CSF is required criterion for the diagnosis, with cases reported to have 12%-100% eosinophils, with most cases having >75% eosinophils.…”