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At least 217 records · Page 12Linked to original sources
PubMed1990

[Seroprevalence of human parvovirus B 19 antibodies (Sticker's disease/erythema infectiosum) in the DRG population].

We tested 638 human sera of all age groups (patients and blood donors) from the northern area of the G.D.R. and found 216 cases (33.9%) of specific parvovirus B19 antibodies (IgG) by antibody capture ELISA. The seroprevalence rose to 36.7% when the 18 parvo B19-IgM- and/or parvo B19-DNA-positive results were included. The antibody prevalence was 24.9 (27.8% resp.) in the 0-10 years group and increased continuously in the following age groups up to 61.1% (69.4% resp.) in the 51-60 years group. 50% of the newborn infants showed parvo B19-IgG-antibodies in the cord blood (of maternal origin). No sex differences in seroprevalence were observed. Parvovirus B19 is obviously very prevalent in the G.D.R. population. The main immunization occurs in the first 30-40 years of life but infection with parvo B19 at a later age is also well documented. Hence it follows that 35-45% of all G.D.R. females of reproductive age are susceptible to a parvovirus B19 infection.

Adolescent↗
PubMedDate not supplied

[Maternofetal infection by parvovirus associated with antenatal meconium peritonitis].

A case of meconium peritonitis associated with materno-fetal infection by human B19 parvovirus is reported. The meconium peritonitis was recognized by ultrasonography at 25 weeks of pregnancy and was confirmed after delivery. Postnatal "opaque index" of the small bowel revealed multiple stenosis. Evolution was favorable and did not require surgery. Diagnosis of B19 parvovirus materno-foetal infection was documented on specific IgM antibodies and viral DNA in the maternal serum and specific IgM antibodies in the infant's serum. Thus, B19 parvovirus appears to be responsible for non lethal fetopathies.

Antibodies, Viral↗
PubMed1990

[Pure red cell aplasia induced by B19 parvovirus during allogeneic bone marrow transplantation].

We report a patient who had abrupt onset of pure red cell aplasia (PRCA) induced by B19 parvovirus during allogeneic bone marrow transplantation (BMT). A 14-year-old girl with APL in complete remission was admitted in February 1988, for the purpose of BMT. She was received marrow from HLA identical sister on March 17, 1988 (day 0). She received 120 mg/kg cyclophosphamide and 12 Gy total body irradiation for conditioning of BMT. For graft-versus-host disease (GVHD) prophylaxis she was given cyclosporine and short term methotrexate. She did not develop acute GVHD after BMT, but on the day 28 a bone-marrow aspirate revealed findings of PRCA. During this course the number of white blood cell and platelet favorably recovered. B 19 parvovirus DNA was detected in the serum of the day 30 and day 42. Antihuman B 19 parvovirus (HPV) antibody titers were increased: the values of anti-HPV IgM were suddenly elevated and those of anti-HPV IgG were elevated. Serum on the day 42 inhibited erythroid progenitors (CFU-E, BFU-E) but not inhibited myeloid progenitors (CFU-C). A reticulocyte count recovered on the day 50. As the patient was HPV-IgG negative prior to BMT and the donor was HPV-IgG seronegative, the source of infection may be platelet transfusion (day 7 through 14).

Adolescent↗
PubMed1990

Excretion of porcine parvovirus through the genital tract of boars.

The putative binding of porcine parvovirus (PPV) to semen components in vitro was examined along with the shedding pattern of PPV in oronasally infected boars. Porcine parvovirus DNA was determined to be bound to spermatozoa that had been incubated in vitro with PPV and washed to remove loosely adherent virus. To determine whether PPV was shed in the semen, four 8-month-old boars, seronegative for PPV, were inoculated oronasally with a virulent strain of PPV. Prior to virus inoculation, a catheter was surgically implanted in the vas deferens for the purpose of collecting cauda epididymal semen free of extrinsic contamination. Epididymal semen specimens were collected prior to inoculation and daily thereafter for 21 days. A fifth boar was inoculated oronasally with PPV, but semen was collected by electroejaculation twice weekly for an equal period of time. Reproductive glands and semen specimens from all boars were examined by nucleic acid hybridization for the presence of viral DNA. All boars seroconverted to PPV, as evidenced by serum antibody titers ranging from 512 to 8,192 hemagglutinating inhibition units/50 microliters. Porcine parvovirus DNA was detected in epididymal semen of 3 of 4 catheterized boars on postinoculation days 5 through 9, but not in semen obtained by electroejaculation. Viral DNA was consistently detected in tissue samples collected on postinoculation days 8 and 21 from the scrotal lymph nodes (4 of 5 boars) and epididymides (3 of 5 boars).

Animals↗
PubMed1989

Parvovirus infection in pregnancy.

A case is presented of serologically proved parvovirus infection leading to intrauterine death of the hydropic fetus at 20 weeks' gestation. Although serologic studies of the population indicate that 30-50% of women are susceptible to parvovirus infection, the prevalence of parvovirus infection in pregnancy and the consequences of such an infection are not well understood. A review of reported cases in the world literature indicates a high risk to the fetus once the virus crosses the placenta.

Adult↗
PubMed1989

[Parvovirus infections in humans].

The Human Parvovirus (HPV) like other Parvovirus is a single strand DNA virus with autonomous replication which measures 23mm. Infection with this virus is followed by a non-specific viral syndrome during the prodrome, leading to viremia, which may be followed by arthropathy and/or different kind of rash including the syndrome called erythema infectiosum. It has also been related to an increase in the number of spontaneous abortion in pregnant women with acute infection; and it is the etiology of the aplastic crisis in patients with hemolytic anemias. Many other Parvovirus serologically different from HPV are present in stools and are responsible for acute infectious non bacterial gastroenteritis in people more than 5 years old.

Female↗
PubMed1989

Hepatic disease associated with intrauterine parvovirus B19 infection in a newborn premature infant.

A hydropic premature infant with intrauterine growth retardation died at 4 days of age and was found at necropsy to have advanced liver disease. Clinical and serologic findings in mother and infant were consistent with recent parvovirus B19 infection. Parvovirus can cause fetal liver disease in animals, and some instances of congenital hepatic dysfunction in man may be due to intrauterine parvovirus B19 infection.

Female↗
PubMed1987

[The growth of attenuated strains of canine parvovirus, mink enteritis virus, feline panleukopenia virus, and rabies virus on various types of cell cultures].

The growth characteristics were studied in the attenuated strains of canine parvovirus CPVA-BN 80/82, mink enteritis virus MEVA-BN 63/82 and feline panleucopenia virus FPVA-BN 110/83 on the stable feline kidney cell line FE, and in the attenuated canine distemper virus CDV-F-BN 10/83 on chicken embryo cell cultures (KEB) and cultures of the stable cell line VERO. When the FE cultures were infected with different parvoviruses in cell suspension at MOI 2-4 TKID50 per cell, the first multiplication of the intracellular virus was recorded 20 hours p. i. In the canine parvovirus, the content of intracellular and extracellular virus continued increasing parallelly until the fourth day; then, from the fourth to the sixth day, the content of extracellular virus still increased whereas that of intracellular virus fell rapidly. In the case of the mink enteritis virus the release of the virus into the culture medium continued parallelly with the production of the cellular virus until the sixth day. In the case of the feline panleucopenia virus the values concerning free virus and virus bound to cells were lower, starting from the second day p. i. When KEB or VERO cultures were infected in cell suspension with the canine distemper virus at MOI about 0.004 per 1 cell, the replicated intracellular virus was first recorded in the KEB cultures five hours after infection but in the VERO cultures only 20 hours after infection, with a timely release of the virus into the culture medium in both kinds of tissue. In the KEB and VERO cultures the highest values of infection titres were recorded on the fourth day p. i., the course of virus multiplication on the cells being parallel with its release into the culture medium.

Animals↗
PubMed1985

Equine parvovirus: initial isolation and partial characterization.

A viral agent was isolated from the fetal liver of an aborted equine fetus. The isolate hemagglutinated red blood cells from guinea pig, rhesus monkey and rooster. By hemagglutination inhibition tests, the isolate was shown to be antigenically distinct from parvoviruses of bovine and canine origin. Specific hemagglutination inhibiting antibody against the viral isolate was exhibited by 26 of 136 horse sera tested. The isolated virus showed properties compatible with those of an autonomous parvovirus including size, morphology, stability to ether treatment and heating to 56 degrees C, the presence of a 5300 base DNA genome, characteristic protein composition and density (1.405 g/mL). The virus was classified as an equine parvovirus.

Abortion, Veterinary↗
PubMed1985

Prenatal and preweaning deaths caused by pseudorabies virus and porcine parvovirus in a swine herd.

Sequential outbreaks of pseudorabies virus and porcine parvovirus infections were documented at a swine farm in southern Minnesota. Data for the prevalence of mummified fetuses born and the preweaning mortality were recorded over a 3-year-period. The farm was a farrow-to-finish facility, with breeding females housed in 4 groups according to their stage of pregnancy. The herd consisted of approximately 130 breeding females in December 1981, and expanded to 220 females during the 12 months of 1982. Excluding the outbreaks, the mean preweaning mortality was 20.43% (SE 1.59) and the number of mummified fetuses per litter was 0.19 (SE 0.01). An outbreak of porcine parvovirus infection caused the preweaning mortality and number of mummified fetuses to increase to 50% and 4.10 per litter, respectively. Two outbreaks of pseudorabies 27 months apart, caused the preweaning mortality to increase to 95% and 82%, and the number of mummified fetuses to increase to 0.96 and 1.25 mummified fetuses per litter, respectively. The increase in mummification was observed 1 month after the increase in preweaning mortality caused by pseudorabies virus infections, whereas the increase in mummification and preweaning mortality was simultaneous with porcine parvovirus infections.

Animals↗
PubMedDate not supplied

[Auto-immune hemolytic anemia revealed by erythroblastopenia linked to a parvovirus infection].

In a 12 year-old boy presenting with auto-immune hemolytic anemia of the IgG type, human parvovirus infection was responsible for acute erythroblastopenia. Aplastic crisis quickly and spontaneously recovered but auto-hemolysis was durable. Human parvovirus induced erythroblastopenia has only been reported in patients with constitutional hemolytic anemia. On the other hand, in this case, human parvovirus infection revealed the auto-immune hemolytic anemia.

Anemia, Hemolytic, Autoimmune↗
PubMed1987

On the pathogenesis of spontaneous parvovirus infection.

The internal organs of 21 beagles spontaneously infected with parvovirus were examined histologically and in 10 of the dogs immunofluorescence examination was also performed. The study showed that the pathological process had started in the small intestine and from there the viral agent had spread through the regional lymph nodes into the other lymphatic and the haemopoietic organs causing there depletion predominantly of lymphocytes and arrest of haemopoiesis. Four dogs displayed conspicuous oedema of the media of the arterioli in the liver. In the cytoplasm of probably Kupffer's cells specific fluorescence was present in all the 10 dogs examined. On the other hand neither viral antigen nor histological changes were found in kidneys. Our observations suggest that spontaneous infection of dogs with parvovirus takes place per os. Parvovirus is not eliminated from the organism with urine.

Animals↗
PubMed1986

[Acute parvovirus B 19-induced erythroblastopenia and hereditary spherocytosis. Apropos of 1 pediatric case and review of the literature].

Authors report a new case of acute erythroblastopenia linked to a parvovirus B 19 infection by a 10 years old boy suffering from an hereditary spherocytosis. Aurillac antigen or parvovirus B 19 is one of the smallest virus to be known. It has been well demonstrated in vitro that the virus inhibits especially erythropoiesis but mechanism remains unclear. Systematic vaccination of all children at risk with congenital or acquired chronic haemolytic anaemia should be in the near future the best prophylaxis of parvovirus B 19 infections.

Acute Disease↗
PubMed1978

Demonstration of parvovirus in Canadian swine and antigenic relationships with isolates from other countries.

A Canadian isolate of porcine parvovirus, isolated from cultured pig thyroid cells, was shown to be antigenically indistinguishable from a British (59e/63) and a German (G10/1) strain when treated by the modified direct complement-fixation, the hemagglutination-inhibition and the fluorescent antibody tests. These tests also revealed that antibodies to parvoviruses were detectable in a large proportion of the conventionally raised pigs in the provinces of Quebec and Ontario. Cell cultures, prepared from tissues collected in a slaughterhouse, were often found to be infected with parvovirus. In cell cultures the infection was demonstrated more effectively by immunofluorescence than by the hemagglutination test.

Animals↗
PubMed1979

Prenatal infection following maternal exposure to porcine parvovirus on either the seventh or fourteenth day of gestation.

Intranasal and oral exposure of two gilts to porcine parvovirus on either the seventh or 14th day of gestation resulted in prenatal infection. Normal appearing fetuses and necrotic remnants of what were believed embryos and extraembryonic membranes were found when the gilts were necropsied seven weeks after exposure. The presence of masses of porcine parvovirus antigen throughout necrotic tissues of six of seven embryos, but not in any of the nine normal appearing fetuses suggested that embryonic death was due to porcine parvovirus.

Animals↗
PubMed1984

Aplastic crisis and other effects of the human parvovirus infection.

Human parvovirus infections are common, provoke aplastic crises in patients with congenital haemolytic anaemia and cause fifth disease. An unknown proportion of the infections are subclinical. Parvoviraemia occurs in the early acute stage of infection and specific IgM can be detected during recovery. Most patients commencing an aplastic crisis are viraemic, but fifth disease arises after the viraemia. Serological tests for HPV, available at a small but increasing number of laboratories, will soon be complemented by tests for HPV DNA sequences present in blood, marrow and at other sites. Human parvovirus infection is occasionally fatal in patients with severe forms of congenital haemolytic anaemias and further study may reveal other unusual serious consequences of this ubiquitous infection. Short-term protection of vulnerable patients may be achievable with normal immunoglobulin, but there are still considerable obstacles to the preparation and use of a human parvovirus vaccine.

Adolescent↗
PubMed1981

[Removal of polio- and parvovirus in sewage-sludge by lime-treatment (author's transl)].

Lime (CaO) applied as conditioner for dewatering municipal sewage sludge in filter-presses is suitable to disinfect sewage sludge with respect to virus. A pH-rise to more than 12 followed by release of ammonia inactivates Polio- and Bovine Parvovirus. Addition of 3 kg CaO and more per m3 of raw sludge inactivates Poliovirus within 30 minutes. 7.5 kg CaO per m3 of anaerobically digested sludge are required to inactivate Polio-virus within 5 days and Bovine Parvovirus within 24 hours. Parvovirus seems to be more sensitive against free ammonia than Poliovirus, but less sensitive against high pH-values.

Calcium↗
PubMed1982

Field evaluation of a canine parvovirus vaccination program, using feline origin modified live virus vaccine.

Antibody titers measured by hemagglutination inhibition testing were determined in previously vaccinated dogs at the time of booster vaccination and 2 weeks later. All vaccines consisted of modified live panleukopenia virus. The booster injection was administered approximately 6 months after the initial parvovirus vaccination series was given. Fecal and serum specimens were collected immediately before and 2 weeks after administration of the booster vaccine for hemagglutination and hemagglutination inhibition testing, respectively. All dogs were privately owned and were from the Columbus, Ohio, area but were from environments with various exposure potentials to canine parvovirus. Results of hemagglutination (HA) testing on feces were negative in all dogs before and after booster vaccination. Therefore, these vaccinations did not interfere with interpretation of HA testing of feces. Results of serum hemagglutination inhibition (HI) testing indicated that 50% of the dogs had serum titers less than 1:80 prior to vaccination and that, of these dogs, 65.2% still had serum titers less than 1:80 2 weeks after the booster vaccination. Only 10.9% of all dogs had a marked increase in serum HI titer after the booster vaccination, indicating that overall serologic response to vaccination was poor. High HI titers (greater than or equal to 1:640) were associated with exposure to other dogs and cats in the neighborhood or to dogs suspected of having had parvovirus infection.

Animals↗