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Genetically distant American Canine distemper virus lineages have recently caused epizootics with somewhat different characteristics in raccoons living around a large suburban zoo in the USA

John A Lednicky1*, Jean Dubach2, Michael J Kinsel3, Thomas P Meehan4, Maurizio Bocchetta5, Laura L Hungerford6, Nicolene A Sarich1, Kelley E Witecki1, Michael D Braid1, Casandra Pedrak1 and Christiane M Houde1

Author Affiliations

1 Department of Pathology, Loyola University Medical Center, Maywood, Illinois 60153, USA

2 Animal Molecular Genetics, Brookfield Zoo, Brookfield, Illinois 60513, USA

3 Zoological Pathology Program, University of Illinois at Urbana-Champaign, Loyola University Medical Center, Maywood, Illinois 60513, USA

4 Department of Animal Health, Veterinary Services, Brookfield Zoo, Brookfield, Illinois 60513, USA

5 Cancer Immunology Program, Cardinal Bernardin Cancer Center, Department of Pathology, Loyola University Medical Center, Maywood, Illinois 60513, USA

6 Department of Epidemiology and Preventive Medicine, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA

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Virology Journal 2004, 1:2  doi:10.1186/1743-422X-1-2

Published: 2 September 2004

Abstract

Background

Mortality rates have differed during distemper outbreaks among free-ranging raccoons (Procyon lotor) living around a large Chicago-area zoo, and appeared higher in year 2001 than in 1998 and 2000. We hypothesized that a more lethal variant of the local Canine distemper virus (CDV) lineage had emerged in 2001, and sought the genetic basis that led to increased virulence. However, a more complex model surfaced during preliminary analyses of CDV genomic sequences in infected tissues and of virus isolated in vitro from the raccoons.

Results

Phylogenetic analyses of subgenomic CDV fusion (F) -, phosphoprotein (P) -, and complete hemagglutinin (H) – gene sequences indicated that distinct American CDV lineages caused the distemper epizootics. The 1998 outbreak was caused by viruses that are likely from an old CDV lineage that includes CDV Snyder Hill and Lederle, which are CDV strains from the early 1950's. The 2000 and 2001 viruses appear to stem from the lineage of CDV A75/17, which was isolated in the mid 1970's. Only the 2001 viruses formed large syncytia in brain and/or lung tissue, and during primary isolation in-vitro in Vero cells, demonstrating at least one phenotypic property by which they differed from the other viruses.

Conclusions

Two different American CDV lineages caused the raccoon distemper outbreaks. The 1998 viruses are genetically distant to the 2000/2001 viruses. Since CDV does not cause persistent infections, the cycling of different CDV lineages within the same locale suggests multiple reintroductions of the virus to area raccoons. Our findings establish a precedent for determining whether the perceived differences in mortality rates are actual and attributable in part to inherent differences between CDV strains arising from different CDV lineages.