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Biomedical subjects

W L Mengeling

Publications and source records attributed to W L Mengeling.

At least 91 records · Page 5Linked to original sources

Antibody response of pigs to inactivated monovalent and bivalent vaccines for porcine parvovirus and pseudorabies virus.

Groups of pigs vaccinated with an inactivated bivalent vaccine containing porcine parvovirus (PPV) and pseudorabies virus (PRV) developed geometric mean titers (GMT) of humoral antibody for each of the viruses as high or slightly higher than those of other groups of pigs that were vaccinated with inactivated monovalent vaccines containing one or the other of the same viruses. An increase in GMT after challenge exposure of vaccinated pigs to live virus indicated that vaccination did not prevent virus replication. However, an indication that replication was less extensive in vaccinated pigs was provided by the following. Although neither vaccinated nor nonvaccinated (control) pigs had clinical signs after exposure to the live PPV, the effect of vaccination was evident by the fact that GMT were higher in nonvaccinated pigs after exposure than they were in vaccinated pigs. Conversely, all pigs exposed to live PRV had clinical signs, but these signs varied between mild-to-moderate and transient for vaccinated pigs to severe and fatal for nonvaccinated pigs.

Animals↗

Evaluation of a modified live-virus vaccine for the prevention of porcine parvovirus-induced reproductive disease in swine.

Each of 5 gilts was vaccinated IM with modified live-virus (MLV) vaccine for porcine parvovirus (PPV), and 5 gilts were used as nonvaccinated controls. Vaccinated gilts developed hemagglutination-inhibiting (HI) antibodies to PPV (titer of 320 to 1,280) by 2 weeks after vaccination. All gilts wee bred, and at about 40 days of gestation their immunity was challenged by intranasal and oral administration of a virulent strain of PPV. Gilts were killed at about 84 days of gestation and their litters were examined. Litters from vaccinated gilts comprised 59 live and 2 dead fetuses. Neither the virus nor antibodies to the virus were detected in any of the fetuses. In contrast, litters from nonvaccinated gilts comprised 25 live and 29 dead fetuses, and PPV was isolated from all dead and 9 live fetuses. Viral antigen was detected by direct immunofluorescence in the lungs of all PPV-infected fetuses, and 7 of the live infected fetuses had HI antibodies. Modified live virus did not cause transplacental fetal infection in 3 seronegative gilts inoculated at about 40 days of gestation. All 3 gilts had antibodies to PPV (80 to 640) when killed at about 84 days of gestation, and neither HI antibodies nor PPV were detected in any of the 20 live and 1 dead fetuses from these gilts. Modified live virus replicated in the tissues of fetuses of 2 gilts inoculated in utero. Seven of 8 fetuses inoculated with MLV died and were infected. These results demonstrated the efficacy of MLV vaccine for the prevention of PPV-induced reproductive disease in swine. Although MLV did not cross the placental barrier in pregnant animals, its pathogenicity for porcine fetuses after direct in utero inoculation indicates that its use should be limited to nonpregnant animals.

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Response of conventionally raised weanling pigs to experimental infection with a virulent strain of porcine parvovirus.

Conventionally raised 6-week-old pigs were inoculated intranaslly and orally with porcine parvovirus. The pigs remained clinically normal for up to 17 days. They were viremic between 2 and 6 days after inoculation and had detectable hemagglutination-inhibiting titers to porcine parvovirus at 5 or 6 days after inoculation. Virus was isolated from multiple tissues of pigs killed between 3 and 17 days after inoculation. Viral antigen was demonstrated mainly in lymphoid tissues of these pigs. Gross and microscopic examination of tissues failed to reveal any notable pathologic changes. The numbers of thymus- and bone marrow-derived lymphocytes did not differ significantly in inoculated and noninoculated control pigs, and the response of peripheral blood lymphocytes to selected mitogens was not altered by infection.

Animals↗

Effect of vaccinal and passive immunity on experimental infection of pigs with porcine parvovirus.

One group of 5 pigs was vaccinated twice at 6 and 8 weeks of age with an inactivated porcine parvovirus (PPV) vaccine. A 2nd group of 5 pigs was passively immunized at 9 weeks of age, and a 3rd group of 5 pigs served as nonimmunized controls. The immunity of all pigs was challenged with live PPV at 10 weeks of age. Four vaccinated pigs with hemagglutinating-inhibiting (HI) antibody titer of 160 to 640 and 3 passively immunized pigs with HI titer of 80 to 160 were resistant to PPV infection. Neither infective virus nor viral antigen was detected in their tissues. However, virus replicated in tissues of 1 vaccinated and 2 passively immunized pigs with HI titers of 80, and viral antigen was detected in their lymphoid tissues. There was a 4-fold increase of HI titer in 1 passively immunized pig. Viremia and viral excretion were not detected in any of the vaccinated or passively immunized pigs. In contrast, PPV replicated in the tissues of nonimmunized pigs; both virus and viral antigen were detected in their tissues, and they produced HI antibodies to PPV. All nonimmunized pigs developed viremia and shed virus in oral secretions and feces. Our data show that a high level of humoral antibodies is required for protection from PPV infection.

Animals↗

Replication of porcine parvovirus in peripheral blood lymphocytes, monocytes, and peritoneal macrophages.

Porcine peripheral blood lymphocytes (PBL), peripheral blood monocytes, and peritoneal macrophages were examined for their ability to support porcine parvovirus (PPV) replication. The cell cultures were infected with the NADL-2 strain of PPV at 0.1 multiplicity of infection. PBL cultures were stimulated with the following phytomitogens: phytohemagglutinin M, concanavalin A, and pokeweed mitogen. Unstimulated PBL cultures infected with PPV and uninfected PBL stimulated with phytomitogens served as controls. All cultures were examined daily for PPV-specific immunofluorescence and hemagglutinin. PPV replicated in PBL cultures stimulated with all phytomitogens. Both viral hemagglutinin in culture fluids and nuclear immunofluorescence in cells were detected. In contrast, unstimulated PBL did not support viral replication; however, PPV antigen was detected in the cytoplasm. PPV persisted in unstimulated PBL for 21 days (duration of the experiment) without replication, but replicated each time with the addition of phytohemagglutinin M at 0, 3, 7, 14, and 21 days after infection. Uninfected PBL stimulated with phytomitogens lacked both viral hemagglutinin and immunofluorescence. Simultaneous detection of lymphocyte surface marker and viral antigens in pokeweed mitogen-stimulated PBL revealed that both T and non-T cells (B and null cells) are able to support PPV replication. Peripheral blood monocytes and peritoneal macrophages phagocytized PPV but did not support virus replication.

Animals↗

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.

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Efficacy of an inactivated virus vaccine for prevention of porcine parvovirus-induced reproductive failure.

Gilts vaccinated IM either once (4 gilts) or twice (2 gilts) with an acetylethyleneimine-inactivated porcine parvovirus (PPV) vaccine before they were bred were subsequently exposed intranasally and orally to virulent PPV at about the 40th day of gestation (from 37 to 43 days). At 2 weeks after vaccination, all had hemagglutination-inhibiting (HI) titers for PPV (from 20 to 80) which decreased by the time the immunity was challenged with virulent virus (from 10 to 40), but increased thereafter (from 160 to 1,280). Titers of singly and doubly vaccinated gilts were similar throughout the experiment. The gilts were killed at about the 84th day of gestation (from 80 to 87 days), and their litters were examined. Litters were comprised of 68 live fetuses and 1 dead fetus (7 to 14 fetuses/litter). Neither viral antigen, PPV, nor homologous HI antibody was found in any of the fetuses. In addition, 4 gilts were kept in contact with the vaccinated gilts and were treated similarly except for vaccination. These 4 gilts remained free of HI antibody until after they were exposed to virulent PPV during gestation. At the time the gilts were killed the titers were 1,280 to 2,560. Their litters were comprised of 11 live fetuses and 26 dead fetuses (8 to 11 fetuses/litter). Virus was isolated from fetuses of all litters. Viral antigen was found in 24 of the dead fetuses and 10 of the live fetuses. All infected live fetuses also had HI antibody for PPV. The 2 boars used to breed vaccinated and nonvaccinated gilts (usually each gilt was bred to each of the 2 boars), but not exposed to virulent PPV, remained free of HI antibody for PPV.

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Antigenic relationship of the feline infectious peritonitis virus to coronaviruses of other species.

Utilizing the direct and indirect fluorescent antibody procedure, the antigenic relationship of the feline infectious peritonitis virus (FIPV) to 7 other human and animal coronaviruses was studied. FIPV was found to be closely related to transmissible gastroenteritis virus (TGEV) of swine. Transmissible gastroenteritis virus and FIPV were in turn antigenically related to human coronavirus 229E (HCV-229E) and canine coronavirus (CCV). An interesting finding in the study was that the 8 coronaviruses selected for this study fell into one of two antigenically distinct groups. Viruses in each group were antigenically related to each other to varying degrees, but were antigenically unrelated to coronaviruses of the second group. The first antigenically related group was comprised of mouse hepatitis virus, type 3 (MHV-3), hemeagglutinating encephalomyelitis virus 67N (HEV-67N) of swine, calf diarrhea coronavirus (CDCV), and human coronavirus 0C43 (HCV-OC43). The second antigenically related group was comprised of FIPV, TGEV, HCV-229E and CCV.

Antigens, Viral↗

Development and evaluation of a microimmunodiffusion test for detection of antibodies to pseudorabies virus in swine serum.

A microimmunodiffusion test (MIDT) was developed for the detection of pseudorabies virus (PRV) antibodies in swine serum. The optimal medium for the MIDT was determined to contain 0.69% agarose in 0.05 M tris buffer (pH 7.2) with 0.025% sodium azide and no NaCl. The PRV antigen prepared by (NH4)2SO4 precipitation of viral fluids (42.5 g/100 ml), dialyzed against distilled water, and concentrated to approximately 100-fold of the original volume with polyethylene glycol (mol wt 20,000) provided a good reproducible antigen. The sensitivity of the MIDT was compared with the microtitration procedure of the virus-neutralization (VN) test by assaying 2,203 swine serums for PRV antibodies. An equal percentage of serums was positive in both tests; 419 had VN titers of greater than or equal to 4, and 421 were MIDT positive. Serums (314) that had VN titers of greater than or equal to 16 were all positive by the MIDT. Of serum samples with a VN titer of 8 (53), 50 were MIDT positive, a 94% correlation, and of 52 serums that had VN titers of 4, 36 were MIDT positive, a 69% correlation. In addition, 8 serums that had titer of less than 4 by VN test were positive by MIDT. Seventy-one serum samples were too cytotoxic, markedly hemolyzed, or contaminated to evaluate properly in the VN test; of these serums, 13 were MIDT positive. The MIDT is an accurate, rapid, economical, and sensitive diagnostic test for the detection of PRV antibodies in swine serums.

Animals↗

A skin test for pseudorabies virus infection in swine.

Heat-inactivated pseudorabies virus caused cutaneous delayed-type hypersensitive reactions when injected intradermally on the dorsolateral aspect of the thorax and tips of the ears of pigs previously exposed to the homologous virus. The reaction induced by subcutaneous injection in the lower eyelid was more easily administered and evaluated. Nonexposed control pigs did not react to the antigen and exposed and control pigs did not react when injected with a cell control antigen prepared in a similar manner. A positive response was detectable as early as seven days after exposure, reached near maximal levels by 28 days, and remained at similar levels for at least 90 days.

Animals↗

Pathogenicity of field isolants of hemagglutinating encephalomyelitis virus for neonatal pigs.

The pathogenicity of hemagglutinating encephalomyelitis virus isolated from the brain of each of 5 pigs with clinical signs and microscopic lesions of encephalomyelitis (1 pig from each of 5 naturally infected herbs) was tested under experimental conditions. Each isolant was administered intranasally to 5 neonatal pigs. Clinically affected pigs developed either an acute or chronic form of illness, commencing 4 to 8 days after exposure. Listless, inappetence, and vomiting were clinical signs common to both forms. Additional signs of the acute form were paddling, muscle tremors, and hyperesthesia. Additional signs of the chronic form were loss of condition and either loss of weight or failure to gain weight at a rate similar to nonaffected littermates.

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Reproductive disease experimentally induced by exposing pregnant gilts to porcine parvovirus.

Porcine parvovirus (PPV) was administered intravenously or intranasally and orally between the 22nd and the 81st days of gestation to 20 pregnant gilts that were free of hemagglutination-inhibiting (HI) antibody for PPV. Gilts were exposed to 1 or both of 2 strains (NADL-7, NADL-2) of PPV and were killed 21 or more days later. Fetal and maternal fluids and tissues collected at necropsy were tested for PPV, viral antigen, and HI antibody. Transplacental infection occurred with 11 of 12 gilts given the mixture of strains NADL-7 and NADL-2 and with the 1 gilt given strain NADL-7 alone, but not with any of the 7 gilts given strain NADL-2 alone. The 8 noninfected litters were comprised of 74 fetuses of which 73 were alive and 1 was dead. The 12 infected litters were comprised of 91 fetuses of which 62 were alive (31 infected) and 29 were dead (26 infected). Virus was isolated from all of the 57 infected fetuses. Viral antigen was detected in tissues of 50 fetuses, including 5 live fetuses and 24 dead fetuses that were laden with antigen. All dead fetuses with a high concentration of viral antigen in their tissues were members of litters of gilts that were exposed to PPV no later than the 42nd day of gestation. Antibody was detected in serums (HI titers 10 through 1,280) of 27 of the 31 live infected fetuses and in serum (HI titer 10) of 1 fetus for which infection was not demonstrated. All serums collected from gilts at necropsy contained antibody (HI titers 320 through 2560) for PPV, but with the exception of isolating virus from 1 uterine lymph node, neither virus nor antigen was detected in maternal tissues.

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Fetal mummification associated with porcine parvovirus infection.

A crossbred gilt farrowed 2 mummified fetuses at term, but subsequently developed uterine inertia and became listless. The remaining 5 fetuses of the litter (4 mummified and 1 normal appearing) were collected by hysterectomy. Porcine parvovirus (PPV) was isolated from tissues of the mummified fetuses, and masses of viral antigen were detected throughout the same tissues when cryostat sections were examined by immunofluorescence microscopy. Serum from the normal-appearing fetus of this litter had a hemagglutination inhibition (HI) titer for PPV of 320. The finding of antibody (HI titer of 1,280) in serum collected from the gilt on the day of farrowing, but not in serum collected 67 days before, indicated initial exposure to PPV during gestation.

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Pathogenesis of in utero infection: experimental infection of five-week-old porcine fetuses with porcine parvovirus.

Injection of porcine parvovirus (PPV) into the allantoic fluid of 3 or 4 fetuses of each of 4 litters of PPV-immune gilts early in gestation (34 to 36 days) resulted in fetal maceration and mummification. A high concentration of virus demonstrated in many tissues of fetuses collected 1 week after initial intraallantoic exposure indicated extensive viral replication. Progressively lesser amounts of virus were isolated from tissues of macerated and mummified fetuses collected after longer intervals; however, direct examination of many of the same tissues by immunofluorescence microscopy revealed masses of viral antigen throughout. Abortion was not a sequela of infection of fetuses of immune gilts nor was either virus or viral antigen ever demonstrated in maternal tissues, including those contiguous with infected fetuses. Intrauterine transmission of PPV from fetuses exposed by intraallantoic injection of virus was only confirmed for 2 of the 18 littermate controls that were tested.

Allantois↗

Experimentally induced infection of neonatal swine with porcine parvovirus.

One-day-old pigs were exposed to porcine parvovirus (PPV) and killed at postinoculation day (PID) 3 or 7. Signs of illness and lesions were not seen. Hemagglutination-inhibition (HI) antibodies for PPV were present in the serums of pigs killed on PID 7. As detected by viral isolation and immunofluorescence, PPV was mainly located in rapidly proliferating tissues. Heaviest concentration of viral antigen was in the germinal centers of lymph nodes and lightest concentration of antigen was in the central nervous system.

Administration, Intranasal↗

Pathogenesis of in utero infection: experimental infection of eight- and ten-week-old porcine fetuses with porcine parvovirus.

Selected numbers of fetuses in each of 4 pregnant gilts were exposed to a porcine parvovirus by injecting the virus into the allantoic fluid at gestation day 56 or 70. The fetuses were examined on postexposure day 7 or 14. When pregnancy was terminated, 2 of 15 exposed fetuses were dead. Several fetuses tested at post-exposure day 14 had hemagglutination-inhibiting antibodies to porcine parvovirus. Virus was detected most frequently and in highest concentration in the parenchymatous organs of thorax and abdomen of fetuses exposed on gestation day 56. A small amount of antigen was in neurons and capillary endothelium of cerebral and cerebellar cortexes.

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