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[Parvovirus enteritis in dogs based on autopsy statistics 1978-1985].

The occurrence of canine parvovirus enteritis was monitored in post mortem record from 1978-1985. In a total of 7,615 canine necropsies 654 cases of parvovirus enteritis were diagnosed. The number of cases rose considerably in 1980, accounting for about 10% of the total of canine necropsies since then. Seasonal distribution of cases shows a maximum in November, December, and January and a minimum in June, July and September. In German shepherds and Yorkshireterriers parvovirus enteritis is diagnosed with significantly higher frequency than in other breeds. 80% of all cases of parvovirus enteritis necropsied were diagnosed up to the age of 6 months.

Age Factors↗

Attempts to isolate parvovirus from human acute non-bacterial gastro-enteritis cases.

It has been suggested that the causative agent of human acute non-bacterial gastro-enteritis, based on morphology, buoyant density in caesium choloride, resistance to acid, and reactions to ether and heat, may be a parvovirus. Using conditions optimal for parvovirus multiplication, attempts were made to isolate a parvovirus from such specimens. Results were negative indicating that the agent is not a parvovirus.

Acute Disease↗

[Parvovirus infection in pigs: incidence and prevention. The Diessen Group Veterinarian Practice].

A trial is reported, which was carried out to find an answer to two questions: to which extent do Parvovirus-infections occur and what is the effect of a single porcine Parvovirus vaccination? Parvovirus was found to be enzootic on the farms included in the trial, whereas a singled vaccination was shown to be effective with regard to the prevention of lesions due to porcine Parvovirus infections.

Animal Husbandry↗

Successful experimental challenge of dogs with canine parvovirus-2.

Withholding food from dogs for 24 hours prior to, and for 48 hours following oral challenge with a gut mucosal homogenate of canine parvovirus-2, was a successful means of reproducing gastroenteric signs of canine parvovirus-2 infection. Twenty-one of 24 dogs, which had previously received various vaccine preparations of mink enteritis virus or were unvaccinated, and which were starved at challenge, developed soft or liquid feces with large or without large clots of mucus. Altered feces were most frequent on postexposure day 11. Seven dogs passed frank blood in their stools on one or more occasions and seven dogs vomited sporadically. Pyrexia was noted in 71.6% of the dogs on postexposure day 6 and lymphopenia was detected on postexposure day 5 or 6 in 50% of the dogs monitored. In contrast, four dogs not starved at the time of challenge remained free of gastrointestinal signs apart from one dog which passed a soft stool with scant mucus on one day, postexposure day 6. Also four dogs vaccinated with a killed canine parvovirus-2 vaccine preparation and subsequently starved at the time of challenge, remained clinically healthy. Apart from these last mentioned four dogs, all others shed canine parvovirus-2 in their feces following challenge.

Animals↗

Radiographic appearance of canine parvovirus enteritis.

Sixty dogs with serologically proved parvovirus infection were radiographically evaluated for signs of gastrointestinal disease. Patient grouping was based on duration of illness, which correlated generally with severity of clinical signs. Early in the disease, the radiographic appearance usually was normal. As the disease progressed, abnormal gas and fluid distention of the small bowel became evident. Contrast radiographic findings usually were normal early in the disease but became abnormal as the disease progressed. Vomiting of the contrast agent, delayed gastrointestinal transit time, flocculation, and abnormal bowel patterns were observed frequently. It was concluded that noncontrast radiographic features of canine parvovirus enteritis often were similar to those identified in other gastrointestinal disorders and, therefore, were not always specific for the disease. Results of contrast radiography, however, were highly specific for parvovirus enteritis. Intestinal contrast examination was believed to be a reliable means of differentiating parvovirus enteritis from clinically similar disorders and in ruling out primary or secondary intestinal obstruction. The duration of illness was correlated with the number, severity, and nature of radiographic signs.

Animals↗

[Parvovirus B19 infection and pregnancy].

Parvovirus B19 was identified in 1975. It causes infections megalerythemia in adults associated with skin eruptions and joint pain (about 50% of the adult population is immunized). The risk of contamination in case of an epidemia is high in school teachers and school personnel. In 1984, the parvovirus B19 was implicated as the cause of fetal anasarca. The risk of transplacental contamination is estimated at 33% in case of maternal infection. Pregnant women with parvovirus B19 infection and confirmed serology should have an echography every 15 days. Fetal anasarca can be complicated by in utero fetal death related to erythroid stem-cell anaemia. The diagnosis of fetal infection is based on PCR techniques on fetal blood. Symptomatic antenatal treatment with in utero transfusion was proposed as early as 1988. This method does not however appear to be necessary in all cases as the outcome in several reports of untreated fetuses was delivery of a normal child. There is the possibility of myocardial damage caused by parvovirus B19 which would make in utero transfusion difficult and limit its beneficial effect. Finally associated thrombopenia is often severe and increased fetal risk.

Erythema Infectiosum↗

[The temperature stability of bovine parvovirus].

The stability of the bovine Parvovirus, strain Haden against moist heat in the temperature range 75 to 90 degrees C was tested. It was found that the resistance depended largely on the medium (distilled water, water of standardized hardness (WSH), plasm) in which the viruses were suspended during heating. In WSH the resistance was highest. When heated in plasm, the viruses were inactivated in two phases. From the temperature dependence of the D-values, z-values of 5,6 for distilled water and 8,2 for WSH were found. It is recommended to use the Parvovirus for the evaluation of chemo-thermic and thermic disinfection procedures in view of virucidal effectiveness. The usual pasteurizing procedures fail to inactivate the Parvovirus. To eliminate Parvoviruses from blood products, other methods are, therefore, necessary.

Animals↗

Infectious bill atrophy syndrome caused by parvovirus in a co-outbreak with duck viral hepatitis in ducklings in Taiwan.

In October 1989, an epizootic duckling disease with high mortality occurred in Taiwan. The disease was characterized by droopiness, inappetence, ataxia, ruffled feathers, and watery diarrhea. Affected ducklings were lame, were unable to stand, showed opisthotonos, and often died 3 or 4 days after the onset of the disease. Tolerant maturing ducklings displayed atrophic upper bills with a protruding tongue and became stunted as they reached maturity. No diagnostic histopathologic lesions were found in these ducklings. Fourteen parvovirus isolates, 33 duck viral hepatitis virus (DVHV) isolates, two adenovirus isolates, and two reovirus isolates were obtained and identified from more than 500 sick ducklings in the epizootic. The epizootic was diagnosed as a co-outbreak of duck parvovirus infections and duck viral hepatitis. The high mortality in ducklings and the bill atrophy syndrome were reproduced in ducklings by inoculating the parvovirus isolates alone. The epizootic was controlled by an emergency immunization program of ducklings with sera collected from recovered ducks or a bivalent inactivated vaccine composed of local DVHV and parvovirus isolates.

Animals↗

Comparison of the inactivation of canine and bovine parvovirus by freeze-drying and dry-heat treatment in two high purity factor VIII concentrates.

The inactivation of bovine parvovirus (BPV) and canine parvovirus (CPV) by freeze-drying and terminal dry-heat treatment at 80 degrees C for 72 h has been investigated in two high purity factor VIII concentrates. In one product, CPV was slightly more resistant to freeze-drying compared to BPV, i.e. 0.7 vs. 1.4 log. However, BPV was substantially more resistant to heat-treatment compared to CPV, i.e. 1.3 vs. > 3.1 log inactivation after 72 h at 80 degrees C. In a second product, CPV was also slightly more resistant to freeze-drying than BPV, i.e. 0.2 vs. 1.3 log inactivation. However, heat-treatment gave essentially similar inactivation for both viruses, i.e. 2.8-3.4 log after 72 h at 80 degrees C. In conclusion, the resistance of these parvovirus models is dependent both on the type of virus and on the specific product involved.

Animals↗

A putative nucleoside triphosphate-binding domain in the nonstructural protein of B19 parvovirus is required for cytotoxicity.

Cytotoxicity secondary to B19 parvovirus infection is due to expression of the viral nonstructural protein. Nonstructural proteins of many parvoviruses contain a well-conserved nucleoside triphosphate (NTP)-binding motif, which has been shown to be essential for a variety of protein functions. We show here that cytotoxicity of the B19 parvovirus nonstructural protein was abolished by single mutations of amino acids within the NTP-binding domain, especially within the A motif, implicating NTP-binding in virus-induced cell death.

Amino Acid Sequence↗

Persistent parvovirus B19 related anemia of seven years' duration in an HIV-infected patient: complete remission associated with highly active antiretroviral therapy.

A human immunodeficiency virus (HIV)-infected individual was first diagnosed with red blood cell aplasia due to B19 parvovirus infection in late 1989. Over the subsequent seven-year period, he received a total of 119 units of red blood cells (RBCs) and intravenous immunoglobulin every 2-3 weeks. In 1996 combination antiretroviral treatment with a protease inhibitor was initiated. He received four more units during the following two months and then required no more transfusions for the subsequent 24 months of follow-up. His CD4 count progressively increased and DNA polymerase chain reaction for parvovirus B19 became undetectable. Aggressive antiretroviral treatment may effectively diminish transfusion requirements among HIV-infected individuals with pure RBC aplasia resulting from parvovirus B19 infection.

Adult↗

Seroprevalence of parvovirus B19 NS1-specific IgG in B19-infected and uninfected individuals and in infected pregnant women.

Parvovirus B19 is the causative agent of erythema infectiosum in children, but the virus is associated with an increasing range of different diseases. These include acute and chronic arthritis, hydrops fetalis in pregnant women, aplastic anemia, and thrombocytopenia. The host's immune response is directed against the viral structural proteins VP1 and VP2. This study investigated the presence of IgG against the viral nonstructural protein NS1 using Western blot. Serum panels from healthy individuals, B19-infected pregnant women, and various disease groups were tested. The disease groups included patients with symptoms that may be linked to parvovirus B19 infection. The results showed that IgG against the NS1 protein was present in 22% of healthy individuals with past B19 infection. In cases of persistent or prolonged B19 infections, the prevalence of NS1-specific antibodies was as high as 80%. It is concluded that NS1-specific IgG may be used as an indicator of chronic or more severe courses of parvovirus B19 infections.

Adolescent↗

Fetal hydrops secondary to human parvovirus infection in early pregnancy.

Parvovirus B19 infection has been associated with fetal anaemia, hydrops, and in some cases demise. Most of the reported cases of fetal hydrops were detected in second-trimester fetuses. We report a series of three cases in which human parvovirus infection was associated with hydropic changes at an earlier gestational age. Spontaneous resolution of hydrops occurred in all fetuses. A greater understanding of the natural history of human parvovirus infection is needed prior to deciding on the mode of therapy (conservative management versus in utero fetal therapy).

Adult↗

Parvovirus B19 as a cause of chronic anemia in rhabdomyosarcoma.

BACKGROUND: Several reports have been published of anemia due to infection by parvovirus in patients receiving chemotherapy for leukemia. However, parvovirus B19 has not been previously identified as a cause of chronic anemia in children with solid tumors. METHODS: A child with rhabdomyosarcoma developed chronic anemia, with need for regular blood transfusions during chemotherapy. An infectious etiology was sought. RESULTS: B19 viremia and an absent antibody response was present during the period of chronic anemia during chemotherapy. After completion of chemotherapy, the viremia cleared, IgM and IgG antibody to B19 virus were detected, and the anemia resolved. CONCLUSIONS: Parvovirus must be considered as a cause of anemia in patients undergoing chemotherapy for solid tumors as well as leukemia.

Anemia, Aplastic↗

Similarities of specificity and cofactor dependence in serum antiphospholipid antibodies from patients with human parvovirus B19 infection and from those with systemic lupus erythematosus.

OBJECTIVE: To assess the phospholipid specificity and immunoglobulin isotype of antiphospholipid (aPL) antibodies in patients with acute parvovirus B19 infection. METHODS: Specificity of aPL and isotype distribution in the negatively charged phospholipids, cardiolipin and phosphatidyl serine, and in the neutral phospholipid, phosphatidyl ethanolamine, were measured in the sera of patients with acute parvovirus B19 infections (n = 12), in those with other acute viral infections (n = 10), and in those with syphilis (n = 15) by enzyme-linked immunosorbent assays. The dependence of anticardiolipin (aCL) binding on the presence of beta 2-glycoprotein I (beta 2-GPI) as a binding cofactor was assessed in these same groups, and was compared with sera from systemic lupus erythematosus (SLE) patients (n = 11) with raised aCL antibody reactivity. RESULTS: Antibodies against any of the 3 phospholipids were found in all 3 groups of patients with infections (B19 in 11 of 12 patients, other viral infections in 8 of 10 patients, and syphilis in 14 of 15 patients). B19 patients' sera contained predominantly IgG antibodies against the negatively charged phospholipids, cardiolipin and phosphatidyl serine, and differed in their specificity and isotype distribution from those found in the other 2 patient groups. B19-associated aCL increased their binding to antigen in the presence of beta 2-GPI as a binding cofactor, similar to aCL found in SLE patients, but unlike antibodies from patients with other viral infections or from those with syphilis. CONCLUSION: The results show the remarkable similarity in specificity of aPL antibodies between B19-infected patients and SLE patients, and raise the question of whether parvovirus infection may be a trigger for the development of aPL antibodies in autoimmune diseases.

Antibodies, Anticardiolipin↗

Cytodiagnosis of parvovirus B19 infection from ascites fluid of hydrops fetalis: report of a case.

The cytologic changes in the smears of fetus ascites fluid with parvovirus B19 infections are described. Cytology revealed the ground-glass appearance of the nuclei having a perinuclear halo, and the nuclear chromatin was spread as a thin rim around the inclusion. Subsequently, monoclonal antibodies for parvovirus B19 were applied to identify the specific antigen in the Papanicolaou-destained specimens. Positive staining reaction products were found throughout the cytoplasm of cells. Similar phenomena were confirmed in paraffin-embedded tissue sections of many organs in autopsy materials. It is hoped that recognition of those virus-infected cells in the body cavity fluid of the fetus will be helpful in making a diagnosis of hydrops fetalis associated with parvovirus B19 infections of the pregnant woman.

Adult↗

Carrier cell-mediated delivery of oncolytic parvoviruses for targeting metastases.

Over the last few years, naturally occurring or genetically manipulated oncolytic viruses gained increasing attention as novel therapeutics for cancer treatment. The present work provides proof of principle that an organotropic cell-based carrier system is suitable to deliver oncolytic parvoviruses to a tissue known to be a target for the formation of metastases. Carrier cells were inactivated by gamma-irradiation after infection, which was found not to affect the production and release of parvoviruses that were capable of lysing cocultured target neoplastic cells. Although systemically administered parvovirus H-1 showed a pronounced therapeutic effect against the development of established Morris hepatoma (MH3924A) lung metastases, the carrier cell strategy offered a number of advantages. Infected carriers were able to sustain H-1 virus expression for 6 days in the lungs of rats affected by metastatic disease and to reduce the spreading of the virus to peripheral organs. Compared to direct virus injection, the carrier cell protocol led to an improved therapeutic effect (metastases suppression) and a lesser generation of virus-neutralizing antibodies. These data support the use of carrier cells to deliver oncolytic viruses and/or viral vectors locally in tumors and, more particularly, metastases.

Animals↗

Autonomous parvovirus vectors: preventing the generation of wild-type or replication-competent virus.

The preferential expression of autonomous parvoviruses in tumour cells and their oncolytic activity has attracted attention to the potential use of these viruses as vectors for cancer gene therapy. Moreover, they are non-pathogenic in adult animals and they seem to be associated with low or no immunogenicity. Other interesting features are their episomal replication and high stability. Vectors derived from the autonomous parvoviruses MVM(p) or H1 express proteins that can directly or indirectly interfere with tumour development. They retain cis- and trans-acting sequences required for viral DNA amplification; the transgene replaces part of the capsid coding genes. Their development has been hampered by low titres and contamination with replication-competent virus (RCV) that is generated through homologous recombination with helper plasmids. Several approaches have been used to avoid recombination between vectors and helpers. In most instances, reducing the homology up- or downstream of the transgene in either the vector or the helper did not significantly affect RCV production. However, completely eliminating homology downstream of the transgene, splitting VP genes on different helpers or pseudotyping vectors resulted in the production of RCV-free stocks. Although VP-containing particles could sometimes be identified in these stocks by in situ hybridisation, they did not amplify and are therefore not true RCV. The integration of capsid-coding sequences into packaging cells also reduced contamination by RCV and allowed for the amplification of vectors through serial infections. Great progress has been made recently towards the generation of truly RCV-free stocks of vectors derived from autonomous parvoviruses H1 and MVMp. Combining these new vectors with a new packaging cell line should greatly facilitate their development.

Animals↗