Parvo virus natural

Mini-outbreaks of parvovirus B19 infection occur about every 3 to 4 years. Since parvovirus B19 only infects humans, a person cannot get the virus from a dog or cat. Also, dogs and cats cannot get parvovirus B19 from an infected person. Pet dogs and cats can get infected with other parvoviruses that do not infect humans.

Pets can be vaccinated to protect them from parvovirus infection. Your healthcare provider can do a blood test to determine if you are susceptible or possibly immune to parvovirus B19 infection or if you were recently infected. This is not a routine test but can be performed in special circumstances. Talk to your healthcare provider. The blood test may be particularly helpful for pregnant women who may have been exposed to parvovirus B19 and are suspected to have fifth disease.

Introduction Most immunocompetent people with detectable specific human parvovirus B19 pvB19 antibodies do not recall ever having had any specific symptoms. Case presentation We report the case of a year-old Caucasian woman with no relevant past medical history who presented at an outpatient clinic with unexplained isolated joint pain that had been ongoing for six months.

Table 1 Patient biological and clinical evolution during medical follow-up. Open in a separate window. All biological analyses were performed on serum defibrinated plasma. Discussion Few prior studies have reported on the treatment of persistent isolated joint pains due to pvB19 infection. Conclusions Whilst we are aware that the negativity of the pvBPCR analysis and the clinical improvement of our patient may be independent and coincidental, we suggest a possible efficacy when high doses of ascorbic acid are used for treating persistent pvB19 infections.

Consent Written informed consent was obtained from the patient for publication of this case report and any accompanying images. Footnotes Competing interests The authors declare that they have no competing interests.

Contributor Information Aloys Lallement, Email: rf. References 1. Clinical manifestations of human parvovirus B19 in adults. Arch Intern Med. Cochrane Database Syst Rev. Vitamin C for preventing and treating the common cold. Phase 1 clinical trial to evaluate the safety, tolerability and pharmacokinetics of high-dose intravenous ascorbic acid in patients with advanced cancer.

Cancer Chemother Pharmacol. Mikirova N, Hunninghake R. Effect of high dose vitamin C on Epstein-Barr viral infection.

Med Sci Monit. Intravenous vitamin C in the treatment of shingles: results of a multicenter prospective cohirt study. Franssila R, Hedman K. Infection and musculoskeletal conditions: viral causes of arthritis.

Best Pract Res Clin Rheumatol. Human parvovirus B Further, based on VP2 gene sequences, it was revealed that the Indian isolates formed a separate lineage distinct from the South East Asian isolates and the canine parvovirus isolates in India appear to have evolved independently without any distinct geographical patterns of evolution [ 14 ].

Its presence in India supports the assumption that CPV-2c is reaching a worldwide distribution and provides new information to understand the evolution of antigenic variants of CPV-2 [ 59 ].

Canine parvovirus spreads through oral contact with infected faeces or contaminated surfaces e. The source of CPV infection is faecal waste from infected dogs.

It has been diagnosed wherever groups of dogs are found: dog shows, obedience trials, breeding and boarding kennels, pet shops, animal shelters, parks and playgrounds [ 6 ].

Dogs that are confined to a house or yard and are not in contact with other dogs have much less chance of exposure to CPV. CPV is hardy and can remain in faeces-contaminated ground for 5 months or more if conditions are favorable. The faeces of infected dogs contaminate the places such as Veterinary hospitals, pet shops, boarding kennels and commercial breeding establishments.

These contaminated premises serve as source of secondary infection to the susceptible canine population [ 38 ]. The virus enters the body through the mouth as the puppy cleans itself or eats food off the ground or floor. There is a 3—7 day incubation period before the puppy seems obviously ill. Upon entering into the body, it replicates to large numbers in the lymph nodes [ 86 ].

After a couple of days, significant amounts of virus have been released free into the bloodstream. Over the next 3—4 days, the viruses go to new organs containing the rapidly dividing cells like the bone marrow and the delicate intestinal cells and form large eosinophilic intranuclear inclusion bodies.

The virus causes most devastating effects in the gastro-intestinal tract. Canine parvoviral infections are characterized by a drop in white blood cell count due to the bone marrow infection. It is in the GI tract where the heaviest damage occurs.

The cells of the villi are relatively short-lived and are readily replaced by new cells. The source of the new cells is the rapidly dividing area at the foot of the villi called the Crypts of Lieberkuhn [ 50 , 67 ]. It is right at the crypt where the parvovirus strikes.

Without new cells coming from the crypt, the villus becomes blunted and unable to absorb nutrients and diarrhea results. The barrier separating the digestive bacteria from the blood stream breaks down. The diarrhea becomes bloody and bacteria can enter the body causing widespread infection. The virus kills one of two ways, diarrhea and vomiting lead to extreme fluid loss and dehydration until shock and death result. Loss of the intestinal barrier allows bacterial invasion of potentially the entire body.

Canine parvovirus CPV is the most dangerous and contagious virus that affects unprotected dogs. CPV infection is now considered most threatening to puppies between the time of weaning and 6 months of age. Diarrhoea occurs in dogs of any age but appears in serious proportions in pups. Dogs with enteritis act like they are in extreme pain.

Early symptoms are depression, loss of appetite, vomiting, high fever and severe diarrhea Fig. There is slight rise of temperature in the initial stage of the disease but gradually turn to subnormal level with advancement of vomiting and diarrhoea [ 42 ]. There is no consistent character of the stool, it may be watery, yellow in color or tinged with frank blood in severe cases. Rapid dehydration is a danger, and dogs may continue to vomit and have diarrhoea until they die, usually 3 days after onset of symptoms.

The course of illness is also highly variable depending on the infectious dose of the virus and clinical signs usually develop from 3 to 5 days following infection and typically persist for 5—7 days [ 25 ]. The morbidity and mortality vary according to the age of the animals, the severity of challenge and the presence of intercurrent disease problems. Puppies can die suddenly of shock as early as 2 days into the illness [ 86 ]. A case of canine parvovirus infection with severe diarrhea and vomiting undergoing treatment.

The second form of CPV is cardiac syndrome, or myocarditis, which can affect puppies under 3 months old [ 2 ]. The most dramatic manifestation of CPV-2 myocarditis is the sudden death in young pups usually about 4 weeks of age [ 51 ]. The collapsed dying pup may have cold extremities, pale mucosae and show gasping respiration or terminal convulsions.

Acute heart failure with respiratory distress occurs in pups between 4 and 8 weeks of age. Subacute heart failure occurs in older pups usually 8 weeks or more. They are tachypnoeic or dyspnoeic especially on exercise. The abdomen is swollen with hepatomegaly and ascitic fluid is blood tinged [ 11 ].

There is tachycardia, sometimes with arrhythmias and a weak pulse. Most animals die due to cardiogenic shock. However, if the animal survives it will suffer from chronic myocardial and circulatory complications [ 30 , 77 ].

There is no diarrhoea because the virus multiplies rapidly in muscle cells of the immature heart. The pathological changes produced by CPV reflect the requirement of the virus for dividing cells. The macroscopic lesions of CPV infection are highly variable and relatively non-specific. In the enteric disease, lesions may be distributed segmentally in the gastrointestinal tract.

The lesions usually affect the jejunum and ileum but not the duodenum and colon. Affected segments may be somewhat flaccid with subserosal hemorrhage or congestion [ 77 ]. The lumen of the intestine is often empty but may contain variable watery ingesta. The mucosal surface is often congested but devoid of exudates. Mesenteric lymph nodes are frequently enlarged and edematous. Multifocal petechial hemorrhages are often seen within the cortex of a cut section of affected lymph nodes during acute stage of the disease and leucopenia is also common.

Thymic cortical necrosis and atrophy are common findings in young dogs [ 16 , 30 , 77 ]. In cases of parvoviral myocarditis, gross lesions include cardiac enlargement with prominent dilatation of the left atrium and ventricle. The lungs often do not collapse when cut although white frothy fluid may be present in the trachea and bronchi. Evidence of pulmonary edema and passive congestion of the liver is often present, with the variable degree of ascites and pleural effusion.

The ventricular myocardium frequently contains visible white streaks associated with the presence of a cellular infiltrate. Some pups may die from chronic decompensating left sided heart failure weeks or months after some of their littermates died suddenly with acute myocarditis. Pulmonary hypertension and myocardial dilation with scarring is often regarded as the cause of delayed death [ 30 ]. Microscopic lesions associated with CPV infection are initially confined to areas of proliferating cell population.

In the enteric form of the disease, the early lesions consist of necrosis of the crypt epithelial cells [ 16 ]. Crypt lumenae are often dilated, lined by attenuated epithelium and filled with necrotic debris. There may be occasional intranuclear eosinophilic inclusion bodies in intact crypt epithelial cells.

The villi and lamina propria may collapse completely as a result of the loss of crypt epithelium and the failure to replace sloughed villous epithelial cells. These lesions may be extensive or diffuse.

Loss of digestive epithelium and absorptive surface area presumably results in diarrhoea caused by combined effect of maldigestion and malabsorption. Death may follow as a result of dehydration, electrolyte imbalance, endotoxic shock or secondary septicemia.

The regeneration of intestinal epithelial cells has been reported even in fatal cases. The remaining intestinal crypts are elongated and lined by hyperplastic epithelium with a high mitotic index.

The shortened villi are covered by immature epithelial cells and adjacent villi are often fused. Diffuse cortical necrosis of the thymus occurs in young dogs, with an associated loss in thymic mass. Later in the disease, there is evidence of regenerative lymphoid hyperplasia. The biological effects of these few genomic changes were enormous, in that CPV-2 acquired the canine host range, but lost the ability to replicate in cats [ 93 ].

FPV replicates in feline cells in vitro and in cats in vivo, but does not infect canine cells in vitro and shows only a restricted tissue spectrum in vivo. CPV-2 does replicate in canine and feline cells in vitro, but the in vivo replication is restricted to canides [ 37 , 94 ].

No feline host has ever been described to be susceptible to CPV-2, although it replicates to low titers in mink which is a mustelid, after experimental inoculation [ 68 ]. After its emergence CPV spread to most populations of domestic and wild carnivores. In , reports from Belgium and the Netherlands indicated that the virus had spread throughout the world infecting wild and domestic canids [ 92 , 94 ]. Clinical signs of parvovirus disease were observed in captive and free-ranging coyotes and DNA sequence analysis of the VP2 gene showed the virus to be CPV Raccoons, in contrast, were shown to be resistant to CPV-2 infection [ 93 ].

Serologic prevalence, infection or clinical signs of disease due to CPV viruses were found in jackals Canis aureus , Canis adustus , Canis mesomelas , grey foxes Urocyon littoralis , the San Joaquin kit fox, Asiatic raccoon dogs Nyctereutes procyonoides and the crab eating fox Cerdocyon thous in the Kenya [ 25 , 89 ].

CPV-2a and CPV-2b DNA sequences were recovered from six of nine cheetahs, as well as from one Siberian tiger, all showing clinical symptoms of parvovirus disease [ 88 ]. Since vaccination of domestic cats and dogs is very effective in preventing disease, parvovirus vaccination of all domestic and non-domestic carnivores at risk of infection is highly recommended. CPV-2c type viruses have been isolated from leopard cats but not from domestic cats in the same area. A presumptive diagnosis of CPV enteritis can be made based on the clinical signs such as depression, vomiting, diarrhoea, anorexia and fever.

The viral HA titer commonly ranges between and 10,, between PI days 4 and 7, or when the signs of enteritis commence. The HA activity generally ceases between PI days 7 and 9 [ 9 ]. Though it is less sensitive than virus isolation in A cell line, HA test on stool samples is rapid and simple to perform.

Although HA test is sensitive, relatively simple and inexpensive to perform, it has several disadvantages, including requirement of a continuous source of RBC, and the need to monitor the specificity of the low titred reactions with HA inhibition assay [ 17 , 53 ]. HI test has also been used most frequently for the detection of CPV [ 43 ]. HA test can be performed by employing erythrocyte from various species as swine, sheep, goat, poultry and dogs.

Among the erythrocyte of different species, pig RBCs showed the characteristic haemagglutination. Erythrocyte from other species does not give specific haemagglutination [ 17 , 43 ]. Apart from this, various buffer system have been evaluated for HA test such as normal saline solution 0. During acute illness, parvoviral virions are readily demonstrated in faeces by negative staining and use of electron microscopy [ 8 , 50 ]. The cell culture adapted virus will enable the biochemical and molecular characterization of the CPV isolates [ 2 , 6 ].

A canine cell line A deserves special mention because it has proved to be particularly useful for CPV isolation from field materials. This line proved to be particularly useful for isolation and growth of CPV because CPE were pronounced on initial culture or after one additional passage. The sizes of the plaques produced by CPV under methyl cellulose or agarose overlay media vary from 0.

Since the original tissues for culture were derived from an uncharacterized tumour, A cells should not be used for vaccine virus production [ 9 ]. This test is based on the antigen—antibody reactions with specific MAbs fixed on plastic, nitrocellulose membranes, latex or gold particles [ 96 ]. The tests are rapid, relatively cheap and can be performed in any veterinary clinic.

Recently the PCR technique has been increasingly used as a tool for the diagnosis of canine parvoviral infection [ 45 , 51 ]. It has been widely applied to provide rapid, sensitive and accurate diagnosis of the disease. The PCR can now be used to differentiate the different mutants of CPV-2 using the primers specific for particular mutants [ 71 ].

To increase the sensitivity and specificity of the reaction, the nested PCR has been employed [ 31 ]. Thus, the nested PCR seems to be a sensitive, specific and practical method for the detection of CPV in faecal samples [ 31 , 71 ]. A touch-down protocol was used which enabled the specific amplification of virion DNA from faeces after a fast and simple boiling pretreatment. The sensitivity of PCR was as high as 10 infectious particles per reaction which corresponds, to a titer of about 10 infectious particles per gram of unprocessed feces.

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