Canine parvovirus type 2 (CPV2): Difference between revisions

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CPV2 is highly contagious and can be spread through direct contact, the [http://en.wikipedia.org/wiki/Fecal-oral_route/ fecal-oral route], or [http://en.wikipedia.org/wiki/Vector_(epidemiology)/ vectors] such as [http://en.wikipedia.org/wiki/Fomites/ fomites] <sup>6</sup> (Johnson 2014). Most frequently, the virus is spread by indirect contact with infected feces, as they are highly infectious, containing billions of CPV2 [http://en.wikipedia.org/wiki/Virion#Structure/ virions] per gram <sup>4</sup> (Decaro and Buonavoglia 2012). CPV2 is shed in the feces of infected dogs within 4-5 days prior to the onset of clinical symptoms, throughout the period of illness, and up to 3 weeks after clinical recovery <sup>6</sup> (Johnson 2014).
CPV2 is highly contagious and can be spread through direct contact, the [http://en.wikipedia.org/wiki/Fecal-oral_route/ fecal-oral route], or [http://en.wikipedia.org/wiki/Vector_(epidemiology)/ vectors] such as [http://en.wikipedia.org/wiki/Fomites/ fomites] <sup>6</sup> (Johnson 2014). Most frequently, the virus is spread by indirect contact with infected feces, as they are highly infectious, containing billions of CPV2 [http://en.wikipedia.org/wiki/Virion#Structure/ virions] per gram <sup>4</sup> (Decaro and Buonavoglia 2012). CPV2 is shed in the feces of infected dogs within 4-5 days prior to the onset of clinical symptoms, throughout the period of illness, and up to 3 weeks after clinical recovery <sup>6</sup> (Johnson 2014).


After initial infection, the virus replicates in the [http://en.wikipedia.org/wiki/Lymphatic_system/ lymphoid tissues] of the [http://en.wikipedia.org/wiki/Oropharynx/ oropharynx], [http://en.wikipedia.org/wiki/Mesenteric_glands/ mesentric lymph nodes] and [http://en.wikipedia.org/wiki/Thymus/ thymus] <sup>4</sup> (Decaro and Buonavoglia 2012), then spreads through the blood stream <sup>6</sup> (Johnson 2014) (Figure 1). CPV will infect and attack the rapidly dividing tissues or cells of the [http://en.wikipedia.org/wiki/Intestinal_crypt/ intestinal crypt], lymphopoietic tissue, and bone marrow  <sup>6</sup> [http://www.merckmanuals.com/vet/digestive_system/diseases_of_the_stomach_and_intestines_in_small_animals/canine_parvovirus.html/: <sup>1</sup>] (Johnson 2014, Aiello et al.  2012). The viral attack on the intestinal crypt epithelium results in massive [http://en.wikipedia.org/wiki/Lysis/ lysis] and [http://en.wikipedia.org/wiki/Necrosis/ necrosis] of [http://en.wikipedia.org/wiki/Enterocytes/ enterocytes], which impairs the [http://en.wikipedia.org/wiki/Absorptive_capacity/ absorptive capacity], [http://en.wikipedia.org/wiki/Cell_turnover/ cell turnover] at the villi tips, and results in the onset of [http://en.wikipedia.org/wiki/Diarrhea/ diarrhea] [http://www.merckmanuals.com/vet/digestive_system/diseases_of_the_stomach_and_intestines_in_small_animals/canine_parvovirus.html/: <sup>1</sup>]<sup>4</sup> (Aiello et al.  2012, Decaro and Buonavoglia 2012). In addition, the virus infects [http://en.wikipedia.org/wiki/White_blood_cells/ white blood cells] (WBCs), in the bone marrow and lymphopoetic tissues, inducing [http://en.wikipedia.org/wiki/Lymphopenia/ lymphopenia] and [http://en.wikipedia.org/wiki/Neutropenia/ neutropenia], often resulting in the secondary infections [http://www.merckmanuals.com/vet/digestive_system/diseases_of_the_stomach_and_intestines_in_small_animals/canine_parvovirus.html/: <sup>1</sup>]<sup>4</sup> (Aiello et al.  2012, Decaro and Buonavoglia 2012).  In 2-3 week-old puppies, often lacking [http://en.wikipedia.org/wiki/Antibodies/ antibodies] obtained from their mother, CPV2 can replicate in cardiac cells, without signs of enteritis, and result in fatal [http://en.wikipedia.org/wiki/Myocarditis/ myocarditis] [http://www.merckmanuals.com/vet/digestive_system/diseases_of_the_stomach_and_intestines_in_small_animals/canine_parvovirus.html/: <sup>1</sup>]<sup>4</sup> (Aiello et al.  2012, Decaro and Buonavoglia 2012) (Aiello et al. 2012, Decaro and Buonavoglia 2012).  
After initial infection, the virus replicates in the [http://en.wikipedia.org/wiki/Lymphatic_system/ lymphoid tissues] of the [http://en.wikipedia.org/wiki/Oropharynx/ oropharynx], [http://en.wikipedia.org/wiki/Mesenteric_glands/ mesentric lymph nodes] and [http://en.wikipedia.org/wiki/Thymus/ thymus] <sup>4</sup> (Decaro and Buonavoglia 2012), then spreads through the blood stream <sup>6</sup> (Johnson 2014) (Figure 1). CPV will infect and attack the rapidly dividing tissues or cells of the [http://en.wikipedia.org/wiki/Intestinal_crypt/ intestinal crypt], lymphopoietic tissue, and bone marrow  <sup>6</sup> [http://www.merckmanuals.com/vet/digestive_system/diseases_of_the_stomach_and_intestines_in_small_animals/canine_parvovirus.html/: <sup>1</sup>] (Johnson 2014, Aiello et al.  2012). The viral attack on the intestinal crypt epithelium results in massive [http://en.wikipedia.org/wiki/Lysis/ lysis] and [http://en.wikipedia.org/wiki/Necrosis/ necrosis] of [http://en.wikipedia.org/wiki/Enterocytes/ enterocytes], which impairs the [http://en.wikipedia.org/wiki/Absorptive_capacity/ absorptive capacity], [http://en.wikipedia.org/wiki/Cell_turnover/ cell turnover] at the villi tips, and results in the onset of [http://en.wikipedia.org/wiki/Diarrhea/ diarrhea] [http://www.merckmanuals.com/vet/digestive_system/diseases_of_the_stomach_and_intestines_in_small_animals/canine_parvovirus.html/: <sup>1</sup>]<sup>4</sup> (Aiello et al.  2012, Decaro and Buonavoglia 2012). In addition, the virus infects [http://en.wikipedia.org/wiki/White_blood_cells/ white blood cells] (WBCs), in the bone marrow and lymphopoetic tissues, inducing [http://en.wikipedia.org/wiki/Lymphopenia/ lymphopenia] and [http://en.wikipedia.org/wiki/Neutropenia/ neutropenia], often resulting in the secondary infections [http://www.merckmanuals.com/vet/digestive_system/diseases_of_the_stomach_and_intestines_in_small_animals/canine_parvovirus.html/: <sup>1</sup>]<sup>4</sup> (Aiello et al.  2012, Decaro and Buonavoglia 2012).  In 2-3 week-old puppies, often lacking [http://en.wikipedia.org/wiki/Passive_immunity/ maternally derived antibodies] (MDA), CPV2 can replicate in cardiac cells, without signs of enteritis, and result in fatal [http://en.wikipedia.org/wiki/Myocarditis/ myocarditis] [http://www.merckmanuals.com/vet/digestive_system/diseases_of_the_stomach_and_intestines_in_small_animals/canine_parvovirus.html/: <sup>1</sup>]<sup>4</sup> (Aiello et al.  2012, Decaro and Buonavoglia 2012).
 
Puppies between the age of 4 and 12 weeks are the most susceptible to CPV2 infection, as this is when the MDA typically wanes <sup>4</sup> (Decaro and Buonavoglia 2012), while unvaccinated young (6 week to 6 month-old) dogs also remain vulnerable [http://www.merckmanuals.com/vet/digestive_system/diseases_of_the_stomach_and_intestines_in_small_animals/canine_parvovirus.html/: <sup>1</sup>] (Aiello et al. 2012). Some breeds, such as Rottweilers, Doberman Pinschers, American Pit Bull Terriers, English Springer Spaniels and German Shepherd dogs are also thought to be at higher risk to CPV2 infection [http://www.merckmanuals.com/vet/digestive_system/diseases_of_the_stomach_and_intestines_in_small_animals/canine_parvovirus.html/: <sup>1</sup>] (Aiello et al. 2012).


<b>Symptoms</b>
<b>Symptoms</b>


The appearance of clinical symptoms of CPV2 infection generally surfaces within 3-7 days of infection [http://www.merckmanuals.com/vet/digestive_system/diseases_of_the_stomach_and_intestines_in_small_animals/canine_parvovirus.html/: <sup>1</sup>] (Aiello et al. 2012).
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<b>Diagnostics</b>
<b>Diagnostics</b>
[[Image:Parvo_lab_work.jpeg|thumb|450px|right|Figure 2. CPV2 laboratory work. Adapted from <sup>6</sup> (Johnson 2014).]]
[[Image:Parvo_lab_work.jpeg|thumb|450px|right|Figure 2. CPV2 laboratory work. Adapted from <sup>6</sup> (Johnson 2014).]]
The most commonly used diagnostic tool is an in-house enzyme linked immunosorbent assay ELISA test <sup>6</sup> (Johnson 2014).
Laboratory blood tests can also contribute to diagnosis but are not definitive, and thus should only be used in conjunction with other tests. <sup>6</sup> (Johnson 2014) (Figure 2).


<b>Treatment and Prognosis</b>
<b>Treatment and Prognosis</b>

Revision as of 16:14, 1 April 2014

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Canine parvovirus type 2 (CPV2) is a highly contagious virus that causes acute gastroenteritis in domestic dogs (Canis familiaris) 6 (Johnson 2014). CPV2 is a non-enveloped, single-stranded DNA virus belonging to the Parvoviridae family and genus parvovirus, along with feline panleukopenia virus (FPLV) and other parvoviruses of carnivores 4 (Decaro and Buonavoglia 2012). A wide range of species are affected by viruses of the Parvoviridae family, however CPV2 does not cross species lines 4 (Decaro and Buonavoglia 2012).

Canine parvovirus (CPV) was first isolated in 1978 7 (Appel et al. 1979, in Truyen 2006), however further studies on the rate of CPV molecular evolution indicate that the virus likely emerged 10 years earlier 7 (Shackelton et al. 2005, in Truyen 2006). The exact origin of CPV2 is not known, although it is thought to have originated as a host range variant from FPLV or other parvoviruses 4 (Decaro and Buonavoglia 2012). Since the original type CVP2 was discovered, several antigenic variants-- CPV2a, CPV2b, and CPVc--have replaced it entirely and have become distributed throughout the canine population worldwide 4.

Structure and Function in Relation to Variant Evolution

Parvoviruses are small (18-26 nm in diameter), non-enveloped viruses, that are made up of single-stranded DNA consisting of 5,000-5,200 nucleotides 4 (Decaro and Buonavoglia 2012). As these viruses contain a small DNA molecules with limited genetic information, they must replicate in the cell nuclei and most require rapidly dividing cells in the synthesis (S) phase of the cell cycle for optimal replication 4 (Decaro and Buonavoglia 2012). This makes tissues with high replication rates--like those of fetuses and neonates, in addition to the hematopoietic and epithelial tissues in adults--targets of parvovirus infection 4 (Decaro and Buonavoglia 2012).

CPV is able to infect canine cells by binding to the canine transferrin receptor (TfR). Studies have shown that the virus strain CPV2 binds to higher levels of TfR on cells than other parvovirus strains, and that canine TfR expressing cells were infected more efficiently by CPV2b variants in comparison to the original CPV2 type 5 (Hueffer et al. 2003). The adaptation of CPV to dogs led to the natural global replacement of CPV2 by the CPV2a variant, and later by the CPV2b strain, through the addition of a point mutation 5 (Hueffer et al. 2003). As CPV is a relatively new virus that continues to evolve and produce new antigenic types, the more predominant mutants are selected for by their ability to bind to the TfR and by extending host range, in newer antigenic types, to include both dogs and cats 7 (Truyen 2006).

Pathogenesis and Symptoms

Figure 1. Flow-chart of CPV2 pathogenesis in dogs. Adapted from IDEXX Laboratories, Inc.

Pathogenesis

CPV2 is highly contagious and can be spread through direct contact, the fecal-oral route, or vectors such as fomites 6 (Johnson 2014). Most frequently, the virus is spread by indirect contact with infected feces, as they are highly infectious, containing billions of CPV2 virions per gram 4 (Decaro and Buonavoglia 2012). CPV2 is shed in the feces of infected dogs within 4-5 days prior to the onset of clinical symptoms, throughout the period of illness, and up to 3 weeks after clinical recovery 6 (Johnson 2014).

After initial infection, the virus replicates in the lymphoid tissues of the oropharynx, mesentric lymph nodes and thymus 4 (Decaro and Buonavoglia 2012), then spreads through the blood stream 6 (Johnson 2014) (Figure 1). CPV will infect and attack the rapidly dividing tissues or cells of the intestinal crypt, lymphopoietic tissue, and bone marrow 6 1 (Johnson 2014, Aiello et al. 2012). The viral attack on the intestinal crypt epithelium results in massive lysis and necrosis of enterocytes, which impairs the absorptive capacity, cell turnover at the villi tips, and results in the onset of diarrhea 14 (Aiello et al. 2012, Decaro and Buonavoglia 2012). In addition, the virus infects white blood cells (WBCs), in the bone marrow and lymphopoetic tissues, inducing lymphopenia and neutropenia, often resulting in the secondary infections 14 (Aiello et al. 2012, Decaro and Buonavoglia 2012). In 2-3 week-old puppies, often lacking maternally derived antibodies (MDA), CPV2 can replicate in cardiac cells, without signs of enteritis, and result in fatal myocarditis 14 (Aiello et al. 2012, Decaro and Buonavoglia 2012).

Puppies between the age of 4 and 12 weeks are the most susceptible to CPV2 infection, as this is when the MDA typically wanes 4 (Decaro and Buonavoglia 2012), while unvaccinated young (6 week to 6 month-old) dogs also remain vulnerable 1 (Aiello et al. 2012). Some breeds, such as Rottweilers, Doberman Pinschers, American Pit Bull Terriers, English Springer Spaniels and German Shepherd dogs are also thought to be at higher risk to CPV2 infection 1 (Aiello et al. 2012).

Symptoms

The appearance of clinical symptoms of CPV2 infection generally surfaces within 3-7 days of infection 1 (Aiello et al. 2012).

Diagnostics and Treatment

Diagnostics

Figure 2. CPV2 laboratory work. Adapted from 6 (Johnson 2014).

The most commonly used diagnostic tool is an in-house enzyme linked immunosorbent assay ELISA test 6 (Johnson 2014).

Laboratory blood tests can also contribute to diagnosis but are not definitive, and thus should only be used in conjunction with other tests. 6 (Johnson 2014) (Figure 2).

Treatment and Prognosis

Prevention and Control

Further Reading

An annotated historical account of canine parvovirus (Carmichael 2005) reviews the evolution of CPV2 and its variants in order to provide a better understanding of the manifestation of the disease.

References

1. Aiello SE, Moses MA, Steigerwald MA eds. 2012. Canine Parvovirus. In: The Merk Veterinary Manual Online.

2. Decaro N, Elia G, Martella V, Camploo M, Desario C, Camero M, Francesco C, Lorusso E, Lucente MS, Narcisi D, et al. 2006. Characterisation of the canine parvovirus type 2 variants using minor groove binder probe technology. Journal of Virological Methods 133:92–99.

3. Decaro N, Desario C, Addie DD, Martella V, Vieria MJ, Elia G, Zicola§ A, Davis C, Thompson G, Thiry§ E, et al. 2007. Molecular epidemiology of canine parvovirus, Europe. Emerging Infectious Diseases 13:1222–1224.

4. Decaro N, Buonavoglia C. 2012. Canine Parvoviral Enteritis. In: Gavier-Widen D, Duff JP, Meredith A, editors. Infectious Diseases of Wild Mammals and Birds in Europe. Somerset, NJ: Wiley-Blackwell. p. 182–184.

5. Hueffer K, Parker JSL, Weichert WS, Geisel RE, Sgro J-Y, Parrish CR. 2003. The natural host range shift and subsequent evolution of canine parvovirus resulted from virus-specific binding to the canine transferrin receptor. Journal of Virology 77:1718–1726.

6. Johnson A. 2014. Canine Parvovirus Type 2 (CPV-2). In: Small Animal Pathology for Veterinary Technicians. Wiley-Blackwell. p. 10–13.]

7. Truyen U. 2006. Evolution of canine parvovirus: a need for new vaccines? Veterinary Microbiology 117:9–13.


Edited by Casey Sprague, a student of Nora Sullivan in BIOL168L (Microbiology) in The Keck Science Department of the Claremont Colleges Spring 2014.