Faculty of Veterinary Sciences, University of Agriculture Faisalabad, Pakistan
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International Journal of Molecular Veterinary Research, 2015, Vol. 5, No. 2 doi: 10.5376/ijmvr.2015.05.0002
Received: 16 Mar., 2015 Accepted: 05 Jun., 2015 Published: 16 Jun., 2015
This is an open access article published under the terms of the
Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Anwar A. , Abbas G., Rasheed I., 2015, Canine Parvovirus-2 in a young German shepherd dog---A Case Report, International Journal of Molecular Veterinary Research, 5(2) 1-3 (doi: 10.5376/ijmvr.2015.05.0002)
Canine parvovirus (CP) is a life threatening disease in young dogs. Lack of proper immunization and mismanagement are the key factors associated with its occurrence. The disease manifests itself in cardiac and intestinal form, however, intestinal form is more frequently observed. The present case report describes Canine parvovirus in 4 month old Germen shepherd dog diagnosed on the basis of history, clinical signs, biochemical parameters and significant post mortem examination.
Canine parvovirus (CP) is highly contagious viral disease affecting mostly young dogs up to six months of age (Pollock and Carmichael, 1983) but a few new genotypes can also infect cats (Mccaw and Hoskins. 2006). The disease spreads from one dog to another by fecal-oral route. Diarrhea, vomiting and intestinal hemorrhages are the prominent manifestations of this disease resulting in loss of body fluids (Carmichael, 1994). Nevertheless, acute myocarditis has also been observed (Panda et al., 2009). The virus replicates in cardiac muscle fibers producing extensive fibrosis of myocardium (Jones et al., 1997). However, this form is less likely to be observed due to effective immunization of female dogs. Secondary infections caused by enteric bacteria commonly Salmonella, Clostridia and Campylobacter further spoil the conditionby producing endotoxemia. Inappropriate immunization of pups and lack of maternal antibodies are the main causes of incidence of CP (Muzaffar et al., 2006).
Case study
A 4 months old German shepherd dog weighing 10 kg was referred to University Medical Teaching Hospital (VMTH) with the complaint of diarrhea and vomiting from last 2 days. The dog was previously vaccinated against parvo, distemper, leptospira, rabies, hepatitis and adenovirus (Hexadog®; Merial ). The dog was on parasitic control program consisting of a commercially available suspension product containing pyrantel pamoate (Zentel®;). Physical examination revealed moderate dehydration (skin tenting time 4 sec; Normal < 2secc), elevated rectal temperature (40.1oC: Normal 39oC), heart rate (103 bpm; Normal 70 to 120 bpm), respiration rate (20 bpm; Normal 18 to 34 bpm) and pale mucous membranes (CRT >3sec; Normal < 2 sec). The hematological results depicted moderate leucopenia characterized by lymphopenia and neutropenia. Along with this, the serum profile of dog revealed hyponatremia (110mmol/L; Normal 142-152mmol/L), hypochloremia (87mmol/L; Normal 110-124mmol/L), hypoglycemia(3.3mmol/L; Normal 4.2-6.6mmol/L) and hypoalbuminemia (15g/dL; Normal 23-31g/dL). A fecal examination was also conducted but no parasitic involvement was seen. Based on the physical, hematological and fecal examination, it appeared to be a case of Canine Parvovirus (CP). For further affirmation of the diagnosis, a CPV-2 Test Kit (SensPERT®) was employed to detect the presence of CPV antigen in the feces of dog. As anticipated, the results were positive. To correct the hydration status, the dog was instituted with ringer lactate-D (Ringer-D® 20ml/kg) along with potassium chloride (New-K-Tab® 25mEq/L). For the prevention of secondary infections, ceftriazone Na (Oxidil® 20 mg/kg, IV, bid) was administered. Along with this, metoclopramide (Maxolon® 0.3 mg/kg) was given intravenously to control emesis. Next day, the physical examination of dog was carried out and slight improvement regarding its health was observed and the previous medication was repeated. Irrespective of the treatment, the dog died and a postmortem examination was conducted for further investigation of disease.
Necropsy findings
Gross necropsy findings were significant regarding depletion of bone marrow, hyperemia of enteric blood vessels and congestion of mesenteric lymph nodes. Intestine was hemorrhagic, dilated and filled with watery contents. Pancreas and liver were also hemorrhagic. Moreover, lungs were heavy and edematous with focal congestion (Figure 1~4).
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Figure 1 Hyperemia of enteric blood vessels
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Discussion
Canine Parvovirus-2 (CPV-2) is small, nonenveloped, single stranded DNA virus with incubation period of 3-7 days (Muzyczka and Berns, 2001). CPV-2 is the main culprit known to cause acute infectious gastroenteritis in young dogs (Appel et al., 1979; Morais and Costa, 2007). The incidence of CPV in Pakistan is about 21.33% (Ahmed and Rabbani, 1999). The disease is highly contagious and young dogs of all breeds are susceptible to it, but the incidence and severity of disease depends upon age, breed, stress level and immunity status of animal. The disease mostly affects the dog breeds including German shepherds, Labrador retrievers and Doberman pinschers particularly at early age (Hoskins. 1998). Canine Parvovirus has two forms; intestinal and myocardial. The most obvious clinical sign in intestinal form is diarrhea that leads to dehydration and critical electrolytic imbalances. The intestinal wall gets hemorrhagic followed by loss of blood and protein causing anemia and hypoproteinemia respectively. It is reported that young dog infected with CPV are at high risk of intussusception (Ettinger et al., 1995). Secondary infections by enteric bacteria may elicit a systemic inflammatory response syndrome (SIRS) leading to acute respiratory distress and endotoxemia. However, the cardiac form is also observed (Panda et al., 2009). The virus causes necrosis of cardiac muscles followed by pulmonary edema and the dog dies due to apnea. Usually if dog is kept untreated, it dies within 3 days (Muzaffar et al., 2006). For the prevention and control of CPV, modified live vaccines are administered at the age of six to eight weeks with booster dose annually and 3 years thereafter. Nevertheless, in pregnant and clostrum deprived canines, inactivated vaccines are preferred. The foremost cause of CPV vaccine failure in pups is high level of circulating maternal antibodies that decrease the efficacy of immunization. However, the disease can be prevented by adopting preventive measures and making people aware of the importance of vaccination protocols.
Mccaw D.L., and Hoskins J.D., 2006, Canine viral enteritis, Infec dis of the dog and cat, 3rd Ed., Editor: Greene C.E. Saunders Elsevier, St Louis, USA. Pp.63-70
Carmichael L.E., 1994, Canine parvovirus type -2. An evolving pathogen of dogs, Ann. Vet. Med., 135: 459-464
Muzaffar A.K., Rabbani M., Muhammad K., Murtaza N and Nazir J., 2006, Isolation and characterization of canine parvovirus, Int. J. Agri. Biol., 8: 898-900
Muzyczka N., Berns K.I., 2001, Parvoviridae: The Viruses and Their Replication. In: Knipe, D.M., Howley, P.M. (Eds.), Fields Vorology. 4th Ed. Lippincott Williams & Wilkins, Philadephia, PA, pp.2327-2359
Appel M.J.G., Cooper B.J., Greisen H., Scott F.W and Carmichael L.E.,1979, Canine viral enteritis. I. Status report on corona and parvo–like viral enteritides, Cornell Vet., 69: 123-133
Jafri S.A and Rabbani M., 1999, Prevalence of canine diseases in Lahore area, Pakistan Vet. J., 19: 40-42
Hoskins JD., 1997, Update on canine parvoviral enteritis, Vet. Med., 92: 694-709
Ettinger., Stephen J., Feldman., Edward C., 1995,Textbook of Veterinary Internal Medicine(4th ed.). W.B. Saunders Company. ISBN0-7216-6795-3
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