Pathogenesis of canine parvovirus-2 in dogs: histopathology and antigen identification in tissues

Carman, P S; Povey, R.C.

doi:10.1016/s0034-5288(18)31817-4

Cited by 25 publications

(18 citation statements)

References 28 publications

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“…Canine parvovirus 2, belonging to the genus Protoparvovirus, was first identified in dogs in the 1970s as a major cause of viral enteritis in young dogs and has subsequently become endemic among dogs worldwide (Hoelzer and Parrish, 2010). Canine parvovirus 2 targets rapidly proliferating cells, like those in intestinal crypts and lymphoid organs, causing necrosis of crypt epithelia and depletion of lymphoid organs such as spleen, thymus, lymph node and bone marrow (Carman and Povey, 1985;. Furthermore conspicuous villous shortening and atrophy as well as syncytial giant cell representing crypt regeneration are among typical histological changes (Osterhaus et al, 1980).…”

Section: Introductionmentioning

confidence: 99%

Novel canine bocavirus strain associated with severe enteritis in a dog litter

Bodewes

Lapp²,

Hahn³

et al. 2014

Veterinary Microbiology

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Bocaviruses are small non-enveloped viruses with a linear ssDNA genome, that belong to the genus Bocaparvovirus of the subfamiliy Parvovirinae. Bocavirus infections are associated with a wide spectrum of disease in humans and various mammalian species. Here we describe a fatal enteritis associated with infection with a novel strain of canine bocavirus 2 (CaBoV-2), that occurred in a litter of German wirehaired pointers. Necropsy performed on three puppies revealed an enteritis reminiscent of canine parvovirus associated enteritis, accompanied with signs of lymphocytolytic disease in bone marrow, spleen, lymph nodes and thymus. While other major causes of enteritis of young dogs, including canine parvovirus, were excluded, by random PCR in combination with next-generation sequencing, a novel CaBoV-2 strain was detected. Phylogenetic analysis of the genome of this novel canine bocavirus strain indicated that this virus was indeed most closely related to group 2 canine bocaviruses. Infection with canine bocavirus was confirmed by in situ hybridization, which revealed the presence of CaBoV-2 nucleic acid in the intestinal tract and lymphoid tissues of the dogs. In a small-scale retrospective analysis concerning the role of CaBoV-2 no additional cases were identified. The findings of this study provide novel insights into the pathogenicity of canine bocaviruses.

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Section: Introductionmentioning

confidence: 99%

Novel canine bocavirus strain associated with severe enteritis in a dog litter

Bodewes

Lapp²,

Hahn³

et al. 2014

Veterinary Microbiology

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“…Animals also can be infected by most parenteral routes. Virus is isolated between 1 and 3 days after infection from the tonsil, retropharyngeal lymph nodes, thymus, and mesenteric lymph nodes, and after approximately 3 days virus is also recovered from the intestinal-associated lymphoid tissues and Peyer's patches (Csiza et al, 1971a;Carlson and Scott, 1977;Carlson et al, 1978;Macartney et al, 1984b;Carman and Povey, 1985a;Meunier et al, 1985a). Virus spreads systemically through a plasma viraemia, resulting in widespread infection of the lymphoid tissues including the thymus and all lymph nodes.…”

Section: Older Animalsmentioning

confidence: 99%

“…Panleukopenia is very uncommon in CPV infections, although a relative lymphopenia is often observed (Figure 2). Dogs infected with CPV develop relative lymphopenia, and some animals develop neutropenia, but total leukocyte counts are generally not markedly affected (Robinson et al, 1980a; Carmichael et al, 1981;Pollock, 1982;Macartney et al, 1984a;Carman and Povey, 1985a).…”

Section: Cpvmentioning

confidence: 99%

“…In FPV and CPV infections of cats and dogs the bone marrow may be severely affected, with a marked decrease in cellularity. Most animals show decreased numbers of myeloid, erythroid and megakaryocytic cells ( Figure 3) (Hammon and Enders, 1939a,b;Lawrence et al, 1940;Robinson et al, 1980a;Boosinger et al, 1982;Macartney et al, 1984a;Carman and Povey, 1985a). Individual animals differ in both the extent of the depletion and the effects on individual cell types.…”

Section: Bone Marrowmentioning

confidence: 99%

“…Intestinal infections appear very similar for all the carnivore parvoviruses. FPV or CPV infect the rapidly dividing epithelial cells in the crypts of the intestinal villi of the ileum and jejunum between 3 and 5 days after inoculation, and virus is found throughout the epithelium of those portions of the intestine 4-8 days after infection ( Figure 6) (Carlson and Scott, 1977;Carlson et al, 1977;Carman and Povey, 1985a;Meunier et al, 1985a;Uttenthal et al, 1990). T h e degree and the severity of the infection are in part determined by the rate of turnover of the intestinal epithelial cells.…”

Section: Intestinal Infectionmentioning

confidence: 99%

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3 Pathogenesis of feline panleukopenia virus and canine parvovirus

Parrish¹

1995

Baillière's Clinical Haematology

131

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Feline panleukopenia virus (FPV) and canine parvovirus (CPV) are autonomous parvoviruses which infect cats or dogs, respectively. Both viruses cause an acute disease, with virus replicating for less than seven days before being cleared by the developing immune responses. The viruses have a broad tropism for mitotically active cells. In neonatal animals the viruses replicate in a large number of tissues, and FPV infection of the germinal epithelium of the cerebellum leads to cerebellar hypoplasia, while CPV may infect the hearts of neonatal pups, causing myocarditis. In older animals the virus replicates systemically, primarily in the primary and secondary lymphoid tissues, and also in the rapidly replicating cells of the small intestinal epithelial crypts. A transient panleukopenia or relative lymphopenia is often observed after FPV or CPV infection, respectively. Whether the reduction in cell numbers in vivo is due to virus replicating in and killing cells, or due to other indirect effects, is not known. However, FPV kills both erythroid and myeloid colony progenitors in in vitro bone marrow cultures, and it has been suggested that virus replication in the myeloid cells in vivo could lead to the reduced neutrophil levels seen after FPV infection of cats.

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