Canine parvovirus

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This article is about canine parvovirus type 2. For canine parvovirus type 1, see canine minute virus.
Canine parvovirus 2
EM of canine parvovirus
EM of canine parvovirus
Virus classification
Group: Group II (ssDNA)
Family: Parvoviridae
Genus: Parvovirus
Species: Canine parvovirus 2

Canine parvovirus (CPV) is a contagious virus affecting dogs. The disease is highly infectious and is spread from dog to dog by direct or indirect contact with feces. It can be especially severe in puppies.

Contents

[edit] History

CPV is a relatively new disease that appeared in the late 1970s. It was first recognized in 1978 and spread worldwide in one to two years.[1] The virus is very similar to feline panleukopenia (also a parvovirus); in fact, they are 98% identical, differing only in two amino acids in the capsid protein VP2.[2] It is also highly similar to mink enteritis, and the parvoviruses of raccoons and foxes.[3] The early belief was that the feline panleukopenia mutated into CPV; however, this has never been proven. The current prevalent theory is that CPV mutated from an unidentified parvovirus (similar to feline parvovirus (FPV)) of some wild carnivore.[4] Interestingly, a strain of CPV2b (strain FP84) has been shown to cause disease in a small percentage of domestic cats, although vaccination for FPV seems to protect against it.[5] CPV, however, cannot lead to disease in cats and does so only mildly in mink and raccoons. Thus it is a virus almost exclusively affecting canines.[3]

Two additional strains of canine parvovirus CPV2a and CPV2b were identified in 1979 and 1984 respectively.[4] Most cases of canine parvovirus are believed to be of these two strains, which have replaced the original strain, thus making the present day virus different from the virus originally discovered[6][3] though indistinguishable by most routine tests. A third type, CPV2c (a Glu-426 mutant), has been discovered in Italy, Vietnam, and Spain.[7]

[edit] Viral Structure and Pathology

CPV is a non-enveloped single-stranded DNA virus. The name comes from the Latin parvus, meaning small, as the virus is only 20 to 26 nm in diameter. It has an icosahedral symmetry. The genome is about 5000 nucleotides long.[8] CPV continues to evolve, and the success of new strains seems to depend on extending the range of hosts affected and improved binding to its receptor, the canine transferrin receptor.[9] CPV has a high rate of evolution, possibly due to a rate of nucleotide substitution that is more like RNA viruses such as Influenzavirus A.[10] In contrast, FPV seems to evolve only through random genetic drift.[11]

Canine parvovirus affects dogs, wolves, foxes, and other canids. CPV2a and CPV2b have been isolated from a small percentage of symptomatic cats and is more common than feline panleukopenia in big cats.[12] It does not transmit to birds, or humans; although each species has its own parvovirus. Canine parvovirus cannot be spread to species outside of the canid family and other carnivores, but it can be spread by them (for example, a bird comes in contact with feces and then the dog's environment, or a cat goes to the groomers and returns with an exposed pet carrier).

[edit] Infection

There are two forms of CPV: intestinal and cardiac. Puppies are most susceptible. Most dogs that are infected, however, (more than 80 percent) will show no symptoms.[13] With severe disease, dogs can die within 48 to 72 hours with no treatment. In the more common, less severe form, mortality is about 10 percent.[2] Certain breeds, such as Rottweilers, Doberman Pinschers, Labrador Retrievers, and Pit bull terriers as well as other black and tan colored dogs may also be more susceptible to CPV [14] Along with age and breed, factors such as a stressful environment, as well as concurrent infections with bacteria, parasites, and canine coronavirus increase a dog's risk of severe infection.[13]

[edit] Intestinal form

Dogs become infected through oral contact with CPV in feces, infected soil, or fomites carrying the virus. Following ingestion, the virus replicates in the lymphoid tissue in the throat, and then spreads to the bloodstream. From there, the virus attacks rapidly dividing cells, notably those in the lymph nodes, intestinal crypts, and the bone marrow. There is depletion of lymphocytes in lymph nodes and necrosis and destruction of the intestinal crypts.[15] Bacteria that normally live in the intestines then cross into the bloodstream and cause sepsis. Dogs with CPV are also at risk for intussusception, a condition where part of the intestine prolapses into another part.[13] Three to four days following infection, the virus is shed in the feces for up to three weeks, and the dog may remain an asymptomatic carrier and shed the virus periodically.[16]

[edit] Cardiac form

This form is less common and affects puppies infected in utero or shortly after birth until about 8 weeks of age.[13] The virus attacks the heart muscle and the puppy often dies suddenly or after a brief period of breathing difficulty. On the microscopic level, there are many points of necrosis of the heart muscle that goes alongside mononuclear celular infiltrate. The formation of excess fibrous tissue (fibrosis) is often evident in surviving dogs. Myofibers are the site of viral replication within cells.[3] The disease may or may not be accompanied with the signs and symptoms of the intestinal form. However, this form is now rarely seen due to widespread vaccination of breeding dogs.[16]

Even less frequently, the disease may also lead to a generalized infection in neonates and cause lesions and viral replication and attack in other tissues other than the gastrointestinal tissues and heart, but also brain, liver, lungs, kidneys, and adrenal cortex. The lining of the blood vessels are also severely affected, which lead the lesions in this region to hemorrhage.[3]

[edit] Signs and symptoms

Dogs that develop the disease show symptoms of the illness within 3 to 10 days. The symptoms include lethargy, vomiting, fever, and diarrhea (usually bloody). Diarrhea and vomiting result in dehydration and secondary infections can set in. Due to dehydration, the dog's electrolyte balance can become critically unbalanced. Because the normal intestinal lining is also compromised, blood and protein leak into the intestines leading to anemia and loss of protein, and endotoxins escaping into the bloodstream, causing endotoxemia. There is a distinct odor that the dogs produce, which is in the later stages of the infestation. The white blood cell level drops, further weakening the dog. Any or all of these factors can lead to shock and death.[13]

[edit] Diagnosis

Diagnosis is made through detection of CPV in the feces by either an ELISA or hemagglutination test, or through electron microscopy. Clinically, the intestinal form of the infection can sometimes be confused with the likes of coronavirus or another form of enteritis. Parvovirus, however, is more serious and the presence of bloody diarrhea, a low white blood cell count, and necrosis of the intestinal lining also point more towards parvovirus, especially in an unvaccinated dog. The cardiac form is typically easier to diagnose, such that its symptoms are highly unique.[3]

[edit] Treatment

Survival rate depends on how quickly CPV is diagnosed and how aggressive the treatment is. Treatment for severe cases that are not caught early usually involves extensive hospitalization, due to the severe dehydration and damage to the intestines and bone marrow. A CPV test should be given as early as possible if CPV is suspected in order to begin early treatment and increase survival rate if the disease is found.

Home treatment using IV fluids is sometimes an effective option, but hospitalization may be required. Treatment ideally consists of IV fluids and colloids, antinausea injections (antiemetics) such as metoclopramide, dolasetron, ondansetron and prochlorperazine, and antibiotic injections such as cefoxitin, metronidazole, timentin, or enrofloxacin.[17] IV fluids are administered and antinausea and antibiotic injections are given subcutaneously, intramuscularly, or intravenously. The fluids are typically a mix of a sterile, balanced electrolyte solution, with an appropriate amount of B-complex vitamins, dextrose and potassium chloride. Analgesic medications such as buprenorphine are also used to counteract the intestinal discomfort caused by frequent bouts of diarrhea.

In addition to fluids given to achieve adequate rehydration, each time the puppy vomits or has diarrhea in a significant quantity, an equal amount of fluid is administered intravenously. The fluid requirements of a patient are determined by their body weight, weight changes over time, degree of dehydration at presentation and surface area. The hydration status is originally determined by assessment of clinical factors like tacky mucous membranes, concentration of the urine, sunken eyes, poor skin elasticity and information gathered in bloodwork.

A blood plasma transfusion from a donor dog that has already survived CPV is sometimes used to provide passive immunity to the sick dog. Some veterinarians keep these dogs on site, or have frozen serum available. There have been no controlled studies regarding this treatment. [17] Additionally, fresh frozen plasma and human albumin transfusions can help replace the extreme protein losses seen in severe cases and help assure adequate tissue healing.

Once the dog can keep fluids down, the IV fluids are gradually discontinued, and very bland food slowly introduced. Oral antibiotics are administered for a number of days depending on the white blood cell count and the patient's ability to fight off secondary infection. A puppy with minimal symptoms can recover in 2 or 3 days if the IV fluids are begun as soon as symptoms are noticed and the CPV test confirms the diagnosis. However, even with hospitalization, there is no guarantee that the dog will survive.

[edit] Unconventional treatments

There is no specific antiviral treatment for CPV. However, there have been anecdotal reports of oseltamivir (Tamiflu) reducing disease severity and hospitalization time in canine parvovirus infection. The drug may limit the ability of the virus to invade the crypt cells of the small intestine and decrease gastrointestinal bacteria colonization and toxin production.[18] There is also anecdotal evidence suggesting that colloidal silver is effective at treating CPV although currently regulatory authorities are discouraging its use due to potential toxicity issues and lack of demonstrated efficacy. ref (http://www.tga.gov.au/docs/html/csilver.htm) Lastly, recombinant feline interferon omega (rFeIFN-ω), produced in silkworm larvae using a baculovirus vector, has been demonstrated by multiple studies to be an effective treatment.[19][20][21][22]

[edit] Prevention and decontamination

Prevention is the only way to ensure that a puppy or dog remains healthy since the disease is extremely virulent and contagious. It is also extremely hardy and has been found to be present in feces or other organic material such as soil even after a year, surviving even extremely cold and hot temperatures. The only household disinfectant that kills the virus is bleach.[13]

It is extremely important to vaccinate puppies and adult dogs against CPV. Weaning puppies should receive initial vaccination of a modified live virus low passage high titer vaccine by a licensed veterinarian at 8 weeks of age, then every 3 to 4 weeks until 15 or 16 weeks. Puppies are initially protected through passive immunity from nursing. These maternal antibodies wear off before the puppy's immune system is mature enough to fight off CPV infection. Maternal antibodies also interfere with vaccination for CPV and can cause vaccine failure. Thus puppies are generally vaccinated in a series of shots, extending from the earliest time that the immunity derived from the mother wears off until after that passive immunity is definitely gone.[23] Older puppies (16 weeks or older) should receive 3 vaccinations 3 to 4 weeks apart. [14] The duration of immunity of vaccines for CPV has been tested for all major vaccine manufacturers in the United States and has been found to be at least three years after the initial puppy series and a booster 1 year later.[24]

A dog that successfully recovers from CPV is still contagious for up to 2 months, so the dog must be kept away from other dogs and puppies. Neighbours and family members with dogs should be notified of infected animals so that they can ensure that their dogs are vaccinated and tested.[citation needed]

[edit] See also

[edit] References

  1. ^ Carmichael L (2005). "An annotated historical account of canine parvovirus". J. Vet. Med. B Infect. Dis. Vet. Public Health 52 (7-8): 303–11. PMID 16316389. 
  2. ^ a b Carter, G.R.; Wise, D.J. (2006). Parvoviridae. A Concise Review of Veterinary Virology. Retrieved on 2006-06-11.
  3. ^ a b c d e f Jones, T.C.; Hunt, R.D.; King, N.W. (1997). Veterinary Pathology. Blackwell Publishing. 
  4. ^ a b Hirayama K, Kano R, Hosokawa-Kanai T, Tuchiya K, Tsuyama S, Nakamura Y, Sasaki Y, Hasegawa A (2005). "VP2 gene of a canine parvovirus isolate from stool of a puppy". J. Vet. Med. Sci. 67 (1): 139–43. doi:10.1292/jvms.67.139. PMID 15699614. 
  5. ^ Gamoh K, Senda M, Inoue Y, Itoh O (2005). "Efficacy of an inactivated feline panleucopenia virus vaccine against a canine parvovirus isolated from a domestic cat". Vet. Rec. 157 (10): 285–7. PMID 16157570. 
  6. ^ Martella V, Cavalli A, Decaro N, Elia G, Desario C, Campolo M, Bozzo G, Tarsitano E, Buonavoglia C (2005). "Immunogenicity of an intranasally administered modified live canine parvovirus type 2b vaccine in pups with maternally derived antibodies". Clin. Diagn. Lab. Immunol. 12 (10): 1243–5. doi:10.1128/CDLI.12.10.1243-1245.2005. PMID 16210491. 
  7. ^ Decaro N, Martella V, Desario C, Bellacicco A, Camero M, Manna L, d'Aloja D, Buonavoglia C (2006). "First detection of canine parvovirus type 2c in pups with haemorrhagic enteritis in Spain". J. Vet. Med. B Infect. Dis. Vet. Public Health 53 (10): 468–72. PMID 17123424. 
  8. ^ ICTVdB Management (2006). 00.050.1.01. Parvovirus. In: ICTVdB - The Universal Virus Database, version 4. Büchen-Osmond, C. (Ed), Columbia University, New York, USA [1]
  9. ^ Truyen U (2006). "Evolution of canine parvovirus--a need for new vaccines?". Vet. Microbiol. 117 (1): 9–13. doi:10.1016/j.vetmic.2006.04.003. PMID 16765539. 
  10. ^ Shackelton L, Parrish C, Truyen U, Holmes E (2005). "High rate of viral evolution associated with the emergence of carnivore parvovirus". Proc. Natl. Acad. Sci. U.S.A. 102 (2): 379–84. doi:10.1073/pnas.0406765102. PMID 15626758. 
  11. ^ Horiuchi M, Yamaguchi Y, Gojobori T, Mochizuki M, Nagasawa H, Toyoda Y, Ishiguro N, Shinagawa M (1998). "Differences in the evolutionary pattern of feline panleukopenia virus and canine parvovirus". Virology 249 (2): 440–52. doi:10.1006/viro.1998.9335. PMID 9791034. 
  12. ^ Recent Advances in Canine Infectious Diseases, Carmichael L. (Ed.) International Veterinary Information Service, Ithaca NY (www.ivis.org), 2000; A0106.0100
  13. ^ a b c d e f Ettinger, Stephen J.;Feldman, Edward C. (1995). Textbook of Veterinary Internal Medicine, 4th ed., W.B. Saunders Company. ISBN 0-7216-6795-3. 
  14. ^ a b Nelson, Richard W.;Couto, C. Guillermo (1998). Small Animal Internal Medicine, 2nd ed., Mosby. ISBN 0-8151-6351-7. 
  15. ^ Lobetti, Remo (2003). Canine Parvovirus and Distemper. Proceedings of the 28th World Congress of the World Small Animal Veterinary Association. Retrieved on 2007-04-22.
  16. ^ a b Canine Parvovirus. The Merck Veterinary Manual (2006). Retrieved on 2007-04-22.
  17. ^ a b Macintire, Douglass K. (2004). Management of Severe Parvoviral Enteritis. Proceedings of the Western Veterinary Conference. Retrieved on 2007-06-26.
  18. ^ Macintire, Douglass K. (2006). Treatment of Parvoviral Enteritis. Proceedings of the Western Veterinary Conference. Retrieved on 2007-06-09.
  19. ^ Ishiwata K, Minagawa T, and Kajimoto T. (1998). "Clinical effects of the recombinant feline interferon-ω on experimental parvovirus infection in beagle dogs.". J. Vet. Med. Sci. 60 (8): 911–7. doi:10.1292/jvms.60.911. 
  20. ^ Martin V, Najbar W, Gueguen S, Grousson D, Eun HM, Lebreux B, Aubert A. (2002). "Treatment of canine parvoviral enteritis with interferon-omega in a placebo-controlled challenge trial". Vet. Microbiol. 89: 115–127. doi:10.1016/S0378-1135(02)00173-6. 
  21. ^ De Mari K, Maynard L, Eun HM, Lebreux, B.. "Treatment of canine parvoviral enteritis with interferon-omega in a placebo-controlled field trial". Vet. Rec. 152: 105–8. 
  22. ^ Kuwabara M, Nariai , Horiuchi , Nakajima Y, Yamaguchi Y, Horioka I, Kawanabe M, Kubo Y, Yukawa M, Sakai T.. "Immunological effects of recombinant feline interferon-ω (KT80) administration in the dog.". Microbiol. Immunol. 50 (8): 637–641. 
  23. ^ Oh J, Ha G, Cho Y, Kim M, An D, Hwang K, Lim Y, Park B, Kang B, Song D (2006). "One-step immunochromatography assay kit for detecting antibodies to canine parvovirus". Clin. Vaccine Immunol. 13 (4): 520–4. doi:10.1128/CVI.13.4.520-524.2006. PMID 16603622. 
  24. ^ Schultz R (2006). "Duration of immunity for canine and feline vaccines: a review". Vet. Microbiol. 117 (1): 75–9. doi:10.1016/j.vetmic.2006.04.013. PMID 16707236. 

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