Date Published: April 15, 2019
Publisher: Public Library of Science
Author(s): Sylvia L. Parmentier, Kristina Maier-Sam, Klaus Failing, Achim D. Gruber, Michael Lierz, Petr Heneberg.
The apicomplexan parasite Sarcocystis calchasi (Coccidia: Eimeriorina: Sarcocystidae) is the causative agent of Pigeon Protozoal Encephalitis (PPE) and infects birds of the orders Columbiformes, Piciformes and Psittaciformes. Accipiter hawks (Aves: Accipitriformes) are the definitive hosts of this parasite. Infections of S. calchasi have been detected in Germany, the United States and Japan. However, the prevalence of the parasite in racing pigeon flocks has not yet been determined. Here, the first cross-sectional prevalence study to investigate S. calchasi in pigeon racing flocks was accomplished including 245 pigeon flocks across Germany. A total of 1,225 muscle biopsies, were taken between 2012 and 2016 and examined by semi-nested PCR for S. calchasi DNA targeting the ITS gene. Additionally, a questionnaire on construction of the aviary as well as management and health status of the flock was conducted. In 27.8% (95% C.I. = 22.3–33.8%) of the flocks, S. calchasi DNA was detected in at least one pigeon. Positive flocks were located in 15 out of 16 federal states. A significant increase of infected racing pigeons was seen in spring. Half-covered or open aviary constructions showed a trend of increase of the prevalence rate, while anti-coccidian treatment and acidified drinking water had no effects. The high prevalence and the geographical distribution of S. calchasi suggest a long-standing occurrence of the parasite in the German racing pigeon population. For pigeons presented with neurological signs or other symptoms possibly related to PPE, S. calchasi should be considered as a potential cause throughout Germany.
In 2006 several racing pigeons (Columba livia f. domestica) (Aves: Columbiformes) from different racing pigeon flocks in the area of Berlin, Germany, developed clinical signs of diarrhoea, polyuria, opisthotonus, torticollis, and paralysis . Histopathology revealed varying degrees of multifocal to coalescing, granulomatous and necrotizing encephalitis and myositis with sarcosporidian cysts . A new Sarcocystis species, Sarcocystis calchasi (S. calchasi) (Coccidia: Eimeriorina: Sarcocystidae) was identified and described as the causative agent of Pigeon Protozoal Encephalitis (PPE) . Like all Sarcocystis species [3,4], S. calchasi has a heteroxenous two-host life cycle . In addition to the racing pigeon, the intermediate host spectrum includes the Common Wood Pigeon (Columba palumbus) , the White-winged Dove (Zenaida asiatica), the Eurasian Collared Dove (Streptopelia decaoto) , and various psittacine species [7,8]. DNA of S. calchasi was also detected in the European Green Woodpecker (Picus viridis), and the Great Spotted Woodpecker (Dendrocopos major) . Accipiter hawks (Aves: Accipitriformes) were confirmed as the definitive hosts of S. calchasi [10,11]. Infections of S. calchasi have been recorded in Germany, the United States of America, and Japan [2,12–14], suggesting a worldwide distribution of the parasite.
In the present study an almost country-wide occurrence of S. calchasi in the racing pigeon population was demonstrated. However, the prevalence regarding the federal states differed substantially. In Saxony, where all flocks were tested negative, a low pigeon breeder density with a mean of 0.1 B/km2 is present. In regions with a low pigeon population, Accipiter hawks may not prey regularly on pigeons and use other avian and non-avian species [20–22,24,33]. The higher the density of breeders, as seen, the more likely is a steady contact over time between Accipiter hawks and racing pigeons which is demonstrated for example in North-Rhine Westphalia with a high density of breeders (average 0.8 B/km2) and a high prevalence of S. calchasi (36.4%). The notion that the prey preference of the Accipiter hawks is essential for the occurrence of S. calchasi in the local pigeon population is supported by the fact that all positive flocks were located in the same area for at least three years, which allowed for an adaptation of the raptor to the local feeding source. A similar conclusion was drawn by Parmentier et al.  regarding the population density of the common wood pigeon which was determined as natural reservoir of S. calchasi. Therefore, the occurrence of S. calchasi in racing pigeons and wood pigeons may be dependent on the prey preferences of the local Accipiter hawks.
In a high proportion of sampled racing pigeon flocks DNA of S. calchasi was detected, with overall 27.8% of flocks affected, ranging regionally between 0% to 52%. Those flocks were located in 12 out of 13 non-city federal states in Germany. An ongoing spreading was not detected. This suggests a long-lasting parasite-host-relationship between racing pigeons and Accipiter hawks in the country. While acidification of drinking water may not be effective to prevent the infection, a fully covered roof is recommended as are other constructional details that help to impede defecation of Accipiter hawks into the aviary. It seems essential that testing for S. calchasi is included in common diagnostic procedures in birds with symptoms possibly associated with PPE.