A 7-year-old lesser panda (Ailurus fulgens fulgens) had been showing signs of intermittent inappetence, lethargy, mild ataxia, and occasional head tremors for several weeks. The symptoms seemed to be very mild and sporadic, with improvement between episodes, which slowly began to increase in frequency. One month after onset, a head tilt to the left was noticed. The animal was examined under anesthesia and was discovered to be in poor body condition, weighing 4.2 kg, and demonstrated muscle atrophy of the rear limbs, more pronounced on the right. The animal developed rear limb paresis 1 week after this initial examination, demonstrating minimal motor function and muscle tone.
Complete blood count, serum chemistries, heartworm antigen levels, and skull radiographs at the time of initial exam showed no abnormalities. Serum was tested for evidence of Toxoplasma gondii IgG and IgM, Neospora caninum, Sarcocystis neurona, Babesia canis, Blastomyces, Histoplasma, Aspergillus, Coccidioides, and Leptospira spp. No significant abnormalities were found. Antigen levels of Cryptococcus were slightly elevated (1:16), and serum neutralization titers for canine distemper virus (CDV) were significantly increased (1:6144). Magnetic resonance imaging (MRI) was performed, and cerebrospinal fluid (CSF) was collected. The MRI of the brain revealed increased water density on T1/T2 images as well as no contrast enhancement in the periaquaductal gray matter. Differentials for these findings include inflammation, thiamine deficiency, a vascular accident, or a minor neoplastic lesion. Protein levels in the CSF were increased (43 mg/dl), making inflammation a likely cause. Cerebrospinal fluid was negative for evidence of S. neurona and T. gondii IgG and IgM. Viral neutralization titers for CDV in the CSF were negative.
Multi-drug therapy was initiated with dexamethasone 1.3 mg IV BID, enrofloxacin 45 mg PO BID, clindamycin 150 mg IV BID, doxycycline 25 mg PO BID, and thiamine 300 mg SC BID. The symptoms progressed and became more severe despite intensive therapy. Eventually, ventroflexion of the neck, vertical nystagmus and difficulty with mastication and swallowing became evident. The animal became dyspneic with abdominal breathing and increased bilateral lung sounds. Radiographs revealed congestion around the base of the heart and the large vessels. Due to the worsening clinical signs, the animal was euthanatized.
A review of the animal’s records revealed that it had been vaccinated once subcutaneously with a modified-live canine distemper vaccine (FerVac™-D, United Vaccines, Inc., Madison, Wisconsin 53713 USA) 3 years previously. One month after vaccination, the animal exhibited signs of decreased appetite, mild diarrhea, and head tremors, which improved with treatment. Two years after vaccination, the animal was again showing signs of inappetence and weight loss. Mild neutrophilia and an interstitial pattern on thoracic radiographs were discovered. The animal again improved, although very rare and short episodes of head tremors were observed by keepers throughout the next year until the fatal episode described above began, 3 years after the vaccine was given.
Postmortem findings included perivascular, lymphocytic encephalitis, lymphoid depletion of the lymph nodes and spleen, interstitial neutrophilic pneumonia, and suppurative hepatitis. Immunohistochemistry of brain tissue revealed scattered neurons that stained strongly positive for morbillivirus. Brain and heart sections were negative for West Nile virus on immunohistochemistry.
In order to determine whether the CDV infection was caused by a wild strain or the vaccine, a morbillivirus phosphoprotein (P) gene fragment was amplified by RT-PCR from frozen brain tissue. This gene contains several highly preserved areas and varies among the different morbilliviruses, and to a lesser extent among different species, geographic areas, and wild vs. vaccine strains of the virus.1,2 A sequence of the P gene was derived from the brain sample, as well as from a sample of the vaccine, and both were found to be not only similar, but identical, confirming that the vaccine strain caused the infection in this animal.
This panda was housed in an outdoor wire mesh enclosure and contact to animals carrying the canine distemper virus, including feral dogs and raccoons, was possible for the entire extent of its 3-year stay at the zoo. However, after extensive PCR testing of the panda tissue and the vaccine product itself, it was determined that the strain of virus was not wild, but rather vaccine induced. This is the first report of a lesser panda showing clinical signs and succumbing to canine distemper virus several years after vaccination with a modified live product.
We thank Ronald O. Schueler, DVM, Veterinary Neurology and Rehabilitation Center, Catonsville, MD 21228 for his assistance with this case.
1. Harder T.C., M. Kenter, H. Vos, K. Siebelink, W. Huisman, G. van Amerongen, C. Orvell, T. Barrett, M.J. Appel, A.D. Osterhaus. 1996. Canine distemper virus from diseased large felids: biological properties and phylogenetic relationships. J Gen Virol. 77 ( Pt 3):397–405.
2. Harder, T.C.; M. Kenter; M.J.G. Appel; M.E. Roelke-Parker; T. Barrett; A.D. Osterhaus. 1995. Phylogenetic evidence of canine distemper virus in Serengeti lions. Vaccine. 13: 6, 521–523.