Neurological causes of diaphragmatic paralysis in 11 alpacas (Vicugna pacos)

Abstract

Background: Diaphragmatic paralysis is a relatively uncommon medical condition in animals not reported in alpacas.

Objectives: Describe the signalment, physical examination, diagnostic testing, clinical, and histopathologic findings related to diaphragmatic paralysis in alpacas.

Animals: Eleven alpacas with spontaneous diaphragmatic paralysis.

Methods: A retrospective study examined medical records from a 10-year period and identified 11 alpacas with confirmed diaphragmatic paralysis admitted to Washington State University and Colorado State University Veterinary Teaching Hospitals between September 2003 and October 2009.

Results: The 11 alpacas ranged in age from 2 to 12 months. Fluoroscopic imaging confirmed the presence of bilateral diaphragmatic paralysis in the 7 alpacas that were imaged. Arterial blood gas analyses showed hypercapnea, hypoxemia, and low oxygen saturation. Seven alpacas died or were euthanized between 2 and 60 days after onset of respiratory signs. Histopathologic examination of tissues found phrenic nerve degeneration in the 6 alpacas that were necropsied and additional long nerves examined demonstrated degeneration in 2 of these animals. Two animals had spinal cord lesions and 2 had diaphragm muscle abnormalities. No etiologic agent was identified in the alpacas.

Conclusions and clinical importance: The etiology for diaphragmatic paralysis in these alpacas is unknown. A variety of medical treatments did not appear to alter the outcome.

Figure 1

The image on the left is a normal radial nerve. The image on the right is from the distal phrenic nerve of an alpaca diagnosed with diaphragmatic paralysis. Note severe swelling and vacuolation of axons. Both sections are stained with Bielchowsky stain. × 200, bar = 40 μm.

Figure 2

An ultrastructural image of the distal phrenic nerve of an alpaca with diaphragmatic paralysis shows several degenerate axons within a nerve bundle. Myelin sheaths are in various stages of degeneration with vesicular splitting and coiling of myelin lamellae. Affected axons vary from intact to vacuolated and degenerate with loss of neurofilaments and collapse. Uranyl acetate and lead citrate (scale 5.0 μm. Bar = 5,000 nm).