Diagnosing parelaphostrongylosis in moose (Alces alces).

ABSTRACT: Thirty-six moose (Alces alces) reported as acting abnormally were examined in northwestern Ontario and adjacent northeastern Minnesota in 1986-2000. Thirty-four typically had little fear of humans, remained in an area for some time, and showed clinical signs of neuromotor incoordination including walking in circles, showing weakness and difficulty in rising, head tilted to one side, or standing with legs positioned wide apart. A definitive diagnosis of parelaphostrongylosis was confirmed in 15 (44%) of these by finding small numbers (2.5 [+ or -] 0.6; 1 - 9) of adult meningeal worms, Parelaphostrongylus tenuis, within the cranium; the meninges of 12, (excluding 3 unsuitable for examination), were cloudy in appearance. An additional 5 clinically abnormal animals had no visible P tenuis but presented with cloudy inflammation of the meninges. No evidence of infection other than typical neurological signs was found in 14 more, but examination was impossible or incomplete for 9 of these. One, however, had P. tenuis-like, dorsal-spined larvae in its feces and another tested positive for P. tenuis using the newly developed serological test (ELISA). Female animals predominated in the sample (21/34) and 10 were judged underweight. The remaining 2 moose in the sample, although aggressive toward humans, had no worms visible in the cranium and neither showed neuromotor signs or cloudy meninges; 1 tested using the ELISA was negative for P. tenuis. Moose with adult P. tenuis in the cranium were younger (1.8 [+ or -] 0.5 yr) than those abnormal animals without worms (5.2 [+ or -] 1.2 yr) (U = 20, P = 0.006). Five of 15 moose with adult worms in the cranium were passing small numbers of dorsal-spined larvae in their feces (0.1 - 2.8 larvae/gm). Sixty-five percent of animals exhibiting typical neuromotor clinical signs of moose sickness showed post-mortem evidence of parelaphostrongylosis. The diagnostic reliability of clinical signs would have been further increased by wider use of the P. tenuis ELISA. This is a convenient, commercially available test and potentially a valuable tool for investigating the level of P. tenuis exposure experienced by moose populations sharing range with infected white-tailed deer.

Key words: Alces, meningeal worm, moose disease, moose sickness, parelaphostrongylosis, Parelaphostrongylus tenuis

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Parelaphostrongylosis is a disease in moose (Alces alces) and other ungulates caused by a neurotropic nematode, Parelaphostrongylus tenuis, spread by white-tailed deer (Odocoileus virginianus) which is the parasite's normal host (see review by Lankester 2001). In extreme cases, infected moose may show a pronounced posterior weakness and have difficulty rising while those less affected may lack fear of humans or show only slight, transitory signs such as unsteady gait or stumbling over obvious obstacles. From experimental work (Lankester 2002), the severity of clinical signs is associated with parasite burden, the age of the infection, and possibly the host's immunological familiarity with the parasite. In the wild, only the most severely affected animals are likely to be reported. Yet, because of their large size, careful post-mortem examination of animals showing signs is a daunting task and may be abandoned. However, the extent to which a typical suite of recognizable neuromotor signs accurately predicts P. tenuis infection in moose has not been examined thoroughly.

The causative agent of parelaphostrongylosis has been known for many years but important aspects of its pathogenesis and impact on moose populations remain unclear. An early experiment demonstrated that when large numbers of infective larvae are given to calf moose, P. tenuis can cause a rapidly advancing, acute neurological disease (Anderson 1964). As well, naturally infected moose showing similarly severe signs were sometimes found to have only a single worm in the cranium, making it tempting to think that moose were particularly susceptible. The prevailing idea was that moose could survive only where they were almost totally isolated from contact with the parasite. However, study of contemporary moose populations sympatric with white-tailed deer confirm that the impact of parelaphostrongylosis on moose is likely more subtle and complex (Whitlaw and Lankester 1994a,b).

Moose currently persist in many areas of eastern North America where deer densities are held at modest levels by regulated hunting (Whitlaw and Lankester 1994b). When deer densities remain below 4-5/[km.sup.2], P. tenuis may cause only low, and marginally limiting mortality (Karns 1967, Lenarz and Kerr 1987, Whitlaw and Lankester 1994a, Dumont and Crete 1996, Gogan et al. 1997). However, there remains good reason to believe that P tenuis played a significant role historically in marked moose population declines (Whitlaw and Lankester 1994a) and could again with warming climate favoring increased deer numbers. The current and future impact of parelaphostrongylosis on moose populations may be underestimated because of our limited ability to conveniently and reliably identify exposed animals.

This paper describes the clinical manifestations of sick moose observed over a 14-year period in northeastem Minnesota and northwestern Ontario and the available diagnostic procedures and tools used to determine which had parelaphostrongylosis.