Abstract

Sarcocystosis as a cause of avian mortality is well known in captive collections. In one zoological collection, the disease appeared with regularity during the late autumns of 2006–2010 and decimated a parakeet (Melopsittacus undulatus) and cockatiel (Nymphicus hollandicus) aviary. Sarcocystosis had been diagnosed previously in this collection in lorikeets (Trichoglossus haematodus) and generated the first report of the disease in a thick-billed parrot (Rhynchopsitta pachyrhyncha).¹ In the present cases, deceased birds had good condition with ample food in the gastrointestinal tract. Most deaths were peracute and birds reported as almost dropping in mid-flight. Principal gross necropsy findings were severely congested lungs. Histopathology confirmed pneumonitis with Sarcocystis sp. organisms in the lungs and occasionally in other tissues. A small percentage of birds presented with neurologic signs and survived with treatment of ponazuril (Marquis 15%, Bayer HealthCare, LLC, Shawnee Mission, KS) at 20 mg/kg PO SID x 30 days, although neurologic deficits were not reversible. Deaths occurred sporadically: one a day, then none for 2–3 days then two dead, and none for 2–3 days. Males and females and all age classes were affected. Mortality rate over the season reached 50%. By end November to early December or January, the epidemic had ceased. During the remainder of the year deaths were rarely attributed to sarcocystosis. Other disease conditions detected in this population were liver abscesses, bacterial hepatitis, gastrointestinal nematodes, and aspergillosis but none of these were significant causes of mortality. Other species in the aviary, doves (Streptopelia sp.), pigeons (Columba livia) and golden pheasants (Chrysolophus pictus) were not affected.

Preliminary genetic sequencing of a portion of the ribosomal RNA genes has indicated that the involved Sarcocystis species present is not Sarcocystis falcatula, but it may be closely related. Evidence of genetic variation between Sarcocystis specimens collected from different host species and at different times has been detected at this institution. If Sarcocystis falcatula is not the causative agent of this disease, elements of this parasite’s life cycle need re-examination. The accepted opossum (Didelphis virginiana) host and cockroach (Periplaneta americana) transmission model may not be accurate at this location. Novel Sarcocystis species and hosts are being described so the likelihood of other species is real.² Use of oral ponazuril for treatment or prophylaxis has not yielded consistent results in this collection supporting a different sensitivity of the target parasite. Considering that treatment of a peracute disease is generally not feasible, disease control must focus on defining and seeking strategies to interrupt the lifecycle of this possibly novel parasite. Current strategy is the development of genetic probes sufficiently robust to identify this Sarcocystis sp. through its lifecycle in definitive and dead-end hosts.

Literature Cited

1.  Smith, J.H., T.M. Craig, E.A. Dillard, P.J.G. Neill, and L.P. Jones. 1990. Naturally occurring apicomplexan acute interstitial pneumonitis in thick-billed parrots (Rhynchopsitta pachyrhyncha). J. Parasit. 76(2): 285–288.

2.  Dubey, J.P., B.M. Rosenthal and C.A. Speer. 2001. Sarcocystis lindsayi n. sp. (Protozoa: Sarcocystidae) from the South American opossum, Didelphis albiventris from Brazil. J. Eukaryot. Microbiol. 48(5): 595–603.