Clinical study on air in epidural hematomas

Twenty 2nd specific pathogen-free pigs were divided into 4 groups: Group A were infected with porcine reproductive and respiratory syndrome (PRRS) virus at 6 weeks of age and treated with available swine erysipelas and swine fever combined vaccine (vaccinated) at 7 weeks of age; Group B were vaccinated at 7 weeks of age and infected with PRRS virus at 8 weeks of age; Group C were vaccinated at 7 weeks of age: Group D were neither vaccinated nor infected with PRRS virus. All pigs were challenged to Erysipelothrix rhusiopathiae C42 strain at 10 weeks of age. No clinical signs appeared after vaccination of group A and B pigs, thus confirming that the safety of the vaccine was not influenced by infection with PRRS virus. None of the pigs in Groups A and C developed erysipelas after challenge exposure to E. rhusiopathiae. In contrast, fever and/or urticaria appeared transiently in all pigs of Group B after challenge exposure. At the time of challenge exposure to E. rhusiopathiae, the PRRS virus titer was high in sera of Group B, but was low in those from Group A. However, vaccination of pigs with attenuated E. rhusiopathiae was effective in dual infection with PRRS virus and E. rhusiopathiae, because the clinical signs were milder and the E. rhusiopathiae strain was less recovered from these pigs compared to pigs of group D.     

Metabolism of the carcinogen N-hydroxy-N-2-fluorenylacetamide by rat peritoneal neutrophils

A thymidine kinase (TK), inverted repeat, glycoprotein I (gI) and glycoprotein X (gpX) gene-deleted modified live virus pseudorabies vaccine was evaluated for safety in swine and for efficacy in protecting swine against challenge with pseudorabies virus (PRV). Safety was evaluated by inoculating pregnant gilts intravenously and 3-day-old pigs intracerebrally with the vaccine. Efficacy was evaluated by 1) vaccinating 3-day-old pigs with a minimal protective dose intranasally and then challenging with PRV 3 weeks postvaccination or 2) vaccinating weaned pigs with a standard field dose intramuscularly and then challenging with PRV 4 weeks postvaccination. The pigs vaccinated intranasally remained clinically normal following vaccination and challenge with PRV. The pigs vaccinated intramuscularly remained clinically normal following vaccination, but mild respiratory signs were seen in some of the vaccinated pigs following challenge with PRV. Humoral immune response was evaluated with enzyme-linked immunosorbent assays (ELISAs) and a serum virus neutralization test. All of the intramuscularly vaccinated pigs became gI and gpX positive on differential ELISAs following challenge. All of the intranasally vaccinated pigs were seropositive on the indirect gI ELISA following challenge, but not all of the pigs were seropositive on the blocking gI ELISA or the gpX ELISA 3 weeks postchallenge.     

Inoculation experiments with Bordetella bronchiseptica strains in SPF pigs

The progeny of 9 SPF gilts fed a balanced ration (Table I) was used in an inoculation experiment with field strains of Bordetella bronchiseptica isolated in herds suffering atrophic rhinitis. Acute rhinitis was produced within a week after intranasal inoculation of B. bronchiseptica into 1 to 11-day-old piglets. Coughing occurred in some of the exposed pigs, but signs of pneumonia did not develop. A few pigs were killed at intervals of 1 to 3 weeks after exposure. These pigs all showed histological lesions in the turbinate and B. bronchiseptica was recovered from various parts of the respiratory tract. Pigs killed 3 weeks after inoculation showed advanced turbinate atrophy (Tables II and III). Among inoculated litter mates reared to slaughter weight, only one developed clinical signs (slight) of atrophic rhinitis, and a tendency towards an elimination of the B. bronchiseptica infection from the accessible part of the nasal cavity was noticed during the growth period. By examination of nasal swabs collected when the pigs were 10 to 13 weeks old, Mycoplasma flocculare was isolated as well from pigs inoculated with B. bronchiseptica as from the control pigs. The growth rate of the experimental pigs was high and no difference in feed consumption or feed conversion occurred between the exposed pigs and the control pigs. By post mortem examination of the snouts from the pigs slaughtered at approx. 85 kg live weight, severe atrophic rhinitis was not found. Approximately one third (32%) of the exposed pigs showed slight atrophic rhinitis lesions (Table IV). The results are discussed and it is concluded that the isolated B. bronchiseptica strains are pathogenic in young pigs and able to induce turbinate atrophy 2 to 3 weeks after inoculation. Turbinate atrophy induced in pigs a few weeks old, may apparently restore completely or almost completely during the growth period. Under the provided experimental conditions, infection with B. bronchiseptica did not result in the development of a lasting, growth-retarding atrophic rhinitis.     

Cross-protection experiments in pigs vaccinated with Actinobacillus pleuropneumoniae subtypes 1A and 1B

Cross-protection experiments were conducted to determine whether antigenic differences located within the lipopolysaccharides (LPS) of Actinobacillus pleuropneumoniae subtypes 1A and 1B were important with respect to the efficacy of whole cell, formalin-inactivated bacterins. Based on clinical signs, lung lesions scores and mortality rates, pigs immunized with A. pleuropneumoniae subtype 1A were partially protected against severe challenge with both subtypes 1A and 1B. In contrast, 1B vaccinated pigs were not protected against severe challenge with subtype 1A but were partially protected against 1B challenge. Cross-reactive serum antibody levels were measured with an ELISA using outer membranes of subtype 1A or 1B as the coating antigen. Serum antibodies were detected against both subtypes within 2 weeks after the first immunization. Antibody levels increased with time and were generally higher against the homologous subtype coating antigen. We conclude that antigenic variation within a capsular serotype, due to antigenic variation within LPS, can result in the failure of whole cell bacterins to provide protection against challenge with the same capsular serotype. This lack of cross-protection within a capsular serotype provides partial explanation for vaccination failures observed under field conditions.     

Pathogenicity of Haemophilus parasuis serovars 4 and 5 in contact-exposed pigs

The pathogenicities of Haemophilus parasuis strains SW124 (serovar 4) and Nagasaki (serovar 5) were examined by contact-exposure of specific pathogen-free (SPF) pigs. Ten pigs were divided into three groups. Two of four pigs in the first group were inoculated intranasally (IN) with 2 x 10(8) CFU of strain SW124, and the other two pigs were mingled with these IN-exposed ones. All the four pigs were subclinically infected in this group. The four pigs of the second group were likewise exposed to strain Nagasaki (two IN-inoculated pigs with 3 x 10(8) CFU of strain Nagasaki). All four pigs in this group died of Gl?sser's disease. Two pigs kept as controls showed neither abnormality nor positive H. parasuis isolation.     

Contribution of passive immunity to porcine respiratory coronavirus to protection against transmissible gastroenteritis virus challenge exposure in suckling pigs

OBJECTIVE: To determine the ability of porcine respiratory coronavirus (PRCV) infections to induce passive immunity in suckling pigs to transmissible gastroenteritis virus (TGEV) challenge exposure. DESIGN AND ANIMALS: 4 TGEV seronegative sows and their litters (group A) served as controls, whereas 2 other groups (B and C) of sows (also TGEV seronegative) were oronasally inoculated with live PRCV during 1 or 2 subsequent pregnancies, respectively. PROCEDURE: Effectiveness of passive immunity provided to pigs via colostrum and milk was assessed after TGEV challenge exposure, and TGEV antibody responses in colostrum and milk were analyzed. RESULTS: Mortality in the 3 groups of young pigs correlated with severity of clinical signs of TGEV infection and was highest in control litters (86% in group-A pigs) and lowest in litters of sows inoculated with PRCV in 2 subsequent pregnancies (14% in group-C pigs). Virus-neutralization and IgA and IgG TGEV antibody titers of milk collected from sows at challenge exposure had significant positive correlation with litter survival. Significantly higher numbers of TGEV-specific IgA and IgG antibody-secreting cells were found in group-A pigs than in group-C pigs, suggesting that high titer of maternal antibodies (induced in group-C sows multiply exposed to PRCV) may interfere with active antibody responses. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that, in PRCV-infected pig herds, multiple exposures of pregnant sows are associated with higher IgA and IgG antibody titers to TGEV in milk, and these titers contribute to protection against TGEV infection.     

Observations on the epidemiology of porcine parvovirus

Evidence presented suggests that porcine parvovirus is highly stable and infective. Introduction of virus to susceptible herds results in 100% infection rate within the following 3 months. Active immunity is associated with high persistent levels of haemagglutination-inhibitating (HI) antibody (greater than 256), piglets suckling immune sows acquiring HI titres between 10,000 and 40,000. Loss of passive immunity, measured by HI, occurs in a majority of pigs between 14 and 26 weeks of age (mean 21 weeks), whilst an average of 25% (2-47%) of pigs lose HI titres between 26 and 36 weeks of age. Susceptibility to challenge with virus does not occur until 3-5 weeks following loss of HI titres. In endemically infected herds 98-100% of adult pigs show serological evidence of active immunity. A significant proportion of gilts may not be actively immune to porcine parvovirus at the time of first service, and subsequent infection may occur while these gilts are pregnant.     

Interaction of Mycoplasma hyopneumoniae and Pasteurella multocida infections in swine

To investigate the interaction between Mycoplasma hyopneumoniae and Pasteurella multocida infection, 32 pigs were randomly assigned by litter, sex, and weight to 4 treatment groups. Group-1 pigs were inoculated with M hyopneumoniae and allowed to recover from M hyopneumoniae infection. Group-2 pigs were vaccinated against M hyopneumoniae and then inoculated with M hyopneumoniae. Group-3 pigs were inoculated with M hyopneumoniae and developed clinical signs of mycoplasmosis. Group-4 pigs had never been exposed to M hyopneumoniae. All pigs were initially seronegative for M hyopneumoniae. All pigs were subsequently inoculated with P multocida and euthanatized 2 weeks later. Pasteurella multocida was isolated only from the lungs of group-3 pigs, and these pigs had a significantly higher median percentage of lung surface area affected by pneumonia than did pigs in the other groups. For group-3 pigs, percentage of lung surface area affected by pneumonia was positively correlated with the number of P multocida colonies isolated. We concluded that P multocida is not a primary respiratory pathogen in pigs, but that M hyopneumoniae infection can render the lungs susceptible to P multocida colonization and infection. Pigs recovered from or vaccinated against infection with M hyopneumoniae were resistant to P multocida infection.     

Effect of maternally acquired Aujeszky's disease (pseudorabies) virus-specific antibody in pigs on establishment of latency and seroconversion to differential glycoproteins after low dose challenge

This study investigated whether (1) passively immune pigs could become latently infected after challenge with low doses of wild type pseudorabies virus (PRV) and (2) if seroconversion to PRV could be consistently detected using two commercially available differential diagnostic ELISAs. Three litters of piglets with passively acquired PRV serum neutralizing (SN) antibody (geometric mean titers 47.03 to 95.10) were challenged at 6 to 12 days of age with 236 to 500 TCID50 of Shope strain virus; pigs were vaccinated at 11 weeks of age with a commercially available genetically engineered vaccine (TK- gE- gG- Iowa S62 strain PRV). Vaccination was intended to reduce the risk of reactivation of latent infection resulting in spread of virulent PRV infection to previously uninfected pigs during the experiment. Vaccination at this age also approximated common field practices in infected herds. After 15 weeks, all challenged pigs were seropositive on the PRV glycoprotein (g or gp) E differential ELISA but were seronegative on the gG differential ELISA. All three challenge groups had pigs that were latently infected as evidenced by the detection of PRV DNA by polymerase chain reaction (PCR) assay of their trigeminal ganglia (TG). There was a significant inverse relationship observed for age at challenge and the proportion of PCR positive pigs in the group 15 weeks postchallenge (p = 0.0004). This trend was independent of the passively acquired PRV SN antibody titers at challenge. In this study, passively acquired antibody did not provide protection against establishment of latent infection in piglets after exposure to low doses of virulent PRV. These latent infections were detected serologically by only one of two available differential diagnostic ELISA.     

Aerosol exposure of pigs to viable or inactivated Actinobacillus pleuropneumoniae serotype 9 induces antibodies in bronchoalveolar lining fluids and serum, and protects against homologous challenge

A dose-defined nose-only inhalation system for pigs was used to study the immunogenic and protective potentials of a single aerosol application of viable or killed Actinobacillus pleuropneumoniae serotype 9. Respiratory volumes were measured for each pig to calculate inhaled individual doses. Eight pigs inhaled 107 CFU A. pleuropneumoniae CVI 13261 reference strain for serotype 9. Another eight pigs received an identical dose of killed actinobacilli. After three weeks the pigs and nonexposed controls were challenged with 108 CFU of the homologous strain by aerosol. Bronchoalveolar lavage (BALF) in pigs was performed during the experiment to obtain lavage samples for assessment of local antibodies. Isotype-specific antibody responses in serum and BAL fluids were measured by ELISAs based on whole-cell antigens. The protective efficacy of aerosol immunization was evaluated by clinical and post-mortem examinations. The controls developed fever and severe pleuropneumonia, whereas previously exposed pigs had less fever and less extensive gross pulmonary lesions. After the first aerosol exposure pulmonary IgM, and IgG antibodies reactive with A. pleuropneumoniae increased significantly in both aerosol exposed groups. IgA in BALF and serum concentrations of each Ig class were significantly increased in the group exposed to viable bacteria when compared to the non-exposed controls. After aerosol challenge a pronounced increase of systemic and pulmonary IgA, IgM, and IgG antibodies was detected in both exposure groups. Aerosol application of whole-cell A. pleuropneumoniae bacterins induced similar protective effects against aerosol challenge infection as administration of an identical dose of viable bacteria. Inhalation of A. pleuropneumoniae may lead to asymptomatic carriers in some pigs that could spread the disease under field conditions.     

Altered cytokine production and impaired antimycobacterial immunity in protein-malnourished guinea pigs

Protein malnutrition leads to multiple detrimental alterations of host immune responses to mycobacterial infection. In this study, we demonstrated that splenocytes from low-protein (LP) guinea pigs vaccinated 6 weeks previously with attenuated Mycobacterium tuberculosis H37Ra failed to control the accumulation of virulent M. tuberculosis H37Rv in cocultured autologous peritoneal macrophages, despite the fact that they were able to control the accumulation of virulent tubercle bacilli in cocultured syngeneic peritoneal macrophages from normally nourished guinea pigs as successfully as did those from high-protein (HP) counterparts. Vaccine-induced growth control of virulent M. tuberculosis H37Rv in these cocultures appeared to be mediated by CD4 lymphocytes but not CD8 cells. Tuberculin (purified protein derivative [PPD])-induced lymphoproliferation was markedly impaired in vaccinated LP guinea pigs, and the depletion of CD4 lymphocytes significantly decreased lymphocyte proliferation whereas CD8 cell depletion did not. Protein malnutrition also impaired the abilities of cells from vaccinated LP guinea pigs to produce cytokines, including interferon, tumor necrosis factor alpha (TNF-alpha) and transforming growth factor beta (TGF-beta), in response to PPD, despite the demonstration of higher serum levels of TNF-alpha and TGF-beta after an intravenous injection of PPD into LP guinea pigs. In contrast, peritoneal macrophages from protein-malnourished guinea pigs produced a higher level of TGF-beta 4 days after infection in vitro with M. tuberculosis H37Rv than did those from protein adequate controls. These results suggest that dietary protein malnutrition impairs vaccine-induced resistance to M. tuberculosis, in part, by altering the cytokine profile to favor macrophage deactivation.     

The persistence of genetic homogeneity among Trypanosoma brucei rhodesiense isolates from patients in north-west Tanzania

The decrease in titer of PRV antibodies in serum was evaluated at 10, 37, 67, 109 and 173 days of age in 16 non-vaccinated pigs and 43 pigs vaccinated at 3, 67 and 80 days of age with a modified live TK/gIII gene deleted pseudorabies virus (PRV) vaccine. Serum samples were analyzed for antibodies to PRV by the serum-virus neutralization test (SN), a commercial competitive ELISA (CELISA), and the CELISA OMNIMARK PRV differential (OMD) diagnostic kit. At 10 days of age, all pigs had SN titers > or = 1:4 and were CELISA+/OMD+, indicating circulating antibodies to field strains of PRV. At 109 days, all non-vaccinated pigs had SN titers < 1:4. Forty-five percent of vaccinated pigs had SN titers > or = 1:4, 56% were CELISA positive and most were CELISA+/OMD-, indicating antibodies due to vaccination. At 24 weeks of age, all pigs had SN titers > or = 1:4 and were CELISA+/OMD+ due to exposure to field strains. Although circulating maternal antibodies interfere with the development of active immunity, vaccination at 3 days of age resulted in detectable antibodies by 67 days of age, and a limited immune response could be measured at 109 days of age.     

Experiences with a vaccine being developed for the control of swine dysentery

A prototype vaccine that is being developed for the control of swine dysentery (SD) was tested in two groups of experimental pigs. Vaccination induced high circulating antibody titres against the aetiological agent, Serpulina (Treponema) hyodysenteriae. Pigs in the first trial were vaccinated twice before being challenged orally with the bacteria. Five of 6 unvaccinated animals developed dysentery within a fortnight of challenge, but only 1 of 6 vaccinated pigs showed signs of disease at this time. Unexpectedly, 1 mo after challenge, the surviving unvaccinated pig and 2 remaining healthy vaccinated animals succumbed to the disease. The reason for the development of this late-onset form of dysentery was not clear. In the second trial, 8 pigs were vaccinated 3 times. Only 2 of these animals (25%) developed severe dysentery after being mixed with infected pigs, whereas 7 of 8 (88%) unvaccinated control pigs in the same pen became diseased. The late-onset form of dysentery was not observed. The prototype vaccine for SD provided a useful level of protection, and could be used in programs to control the disease in Australia.     

Immune response of sows vaccinated with attenuated transmissible gastroenteritis virus (TGEV) and recombinant TGEV spike protein vaccines and protection of their suckling pigs against virulent TGEV challenge exposure

OBJECTIVE: To compare recombinant transmissible gastroenteritis virus (TGEV) spike protein, (SP) R2-2, with attenuated live virus (ALV) vaccine in sows during late pregnancy. ANIMALS: 13 TGEV-seronegative sows and their pigs. PROCEDURE: At prepartum weeks (PPW) 6 and 4, sows of groups 1 and 2 received ALV via the oral/intranasal (O/IN) route. At PPW 2, group-1 sows received ALV IM and group-2 sows received SPR2-2 IM. Group-3 sows received SPR2-2 IM at PPW 4 and ALV O/IN at PPW 2. Sows of group 4 (negative controls) were inoculated O/IN with mock-infected ST cell fluids at PPW 6 and 4 and IM with Sf9 cell lysates at PPW2 (n = 2), or IM with Sf9 cell lysates at PPW4 and O/IN with mock-infected ST cell fluids at PPW2 (2). Serum, colostrum, and milk samples were tested for antibody to TGEV, and a lymphoproliferative (LP) assay was done on blood mononuclear cells. Suckling pigs were challenge exposed with virulent TGEV. RESULTS: Sows of groups 1 and 2 had higher IgG and significantly higher antibody titers in colostrum; their pigs had significantly higher serum antibody titer. At challenge exposure of their pigs, LP responses of group-2 sows were significantly higher than those of sows in the other 3 groups. Mean pig mortality ranged from 43 (group 2) to 92% (group 4). Significant negative correlations were observed among litter mortality and sow LP response, colostral titer, and pig serum titer at time of challenge exposure. CONCLUSIONS: In sows vaccinated twice with attenuated live TGEV, the recombinant SPR2-2 administered IM may be comparable to ALV administered IM as a booster. Vaccination failed to provide complete protection to suckling pigs after challenge exposure.     

Comparison among strains of porcine reproductive and respiratory syndrome virus for their ability to cause reproductive failure

OBJECTIVE: To compare the virulence of selected strains of porcine reproductive and respiratory syndrome virus (PRRSV) relative to reproductive performance of pregnant gilts. DESIGN: 16 pregnant gilts (principals) were exposed oronasally to 4 strains (vaccine strain RespPRRS, field strains VR-2385, VR-2431, and NADC-8, 4 gilts/strain) of PRRSV on or about day 90 of gestation, 4 pregnant gilts (controls) were kept under similar conditions, except for exposure to PRRSV. Samples and specimens obtained from gilts, pigs (before ingestion of colostrum), and fetuses were tested for PRRSV and homologous antibody. ANIMALS: 20 pregnant gilts. PROCEDURE: The virulence of each strain of PRRSV was evaluated mainly on the clinical status of the corresponding litters at farrowing. RESULTS: Most gilts remained clinically normal throughout the study and farrowed normally at or near the expected farrowing time. All virus strains crossed the placenta of principal gilts to infect fetuses in utero. The number of late-term dead fetuses (which appeared to be the best measure of relative virulence) ranged from 0 for litters of control gilts and gilts exposed to strain RespPRRS, to 38 for gilts exposed to strain NADC-8. All principal gilts became viremic and developed antibody against PRRSV. All strains persisted in alveolar macrophages of at least some principal gilts for at least 7 weeks after exposure. CONCLUSION: Strains of PRRSV vary in virulence. CLINICAL RELEVANCE: The effects of PRRSV on reproductive performance are strain dependent and this should be considered in making a tentative diagnosis on the basis of clinical observations.     

Immune responses and protective efficacy of recombinant baculovirus-expressed glycoproteins of equine herpesvirus 1 (EHV-1) gB, gC and gD alone or in combinations in BALB/c mice

Baculovirus-expressed glycoproteins of EHV-1 gB, gC and gD alone or in combination evoked antibody responses and protected vaccinated mice against a challenge with EHV-1. gB, gD, gB + gC, gB + gD and gC + gD elicited very high levels of ELISA antibodies while gC and gC + gD elicited high levels of virus neutralising antibodies. Western blotting demonstrated that the antibodies produced were not only specific for the baculovirus-expressed glycoproteins gB, gC and gD, but also highly specific for each EHV-1 glycoprotein. Vaccination of mice with gB or gD prevented clinical signs of infection in mice challenged with EHV-1 and all vaccinated groups of mice except controls showed a rapid clearance of virus from the lungs and a reduction in lesions characteristic of herpesviruses in the lungs post-challenge. Notably, the lungs of mice vaccinated with gB, gD or gB + gD and challenged with EHV-1 showed prominent peribronchiolar and perivascular aggregations of mononuclear cells, predominantly lymphocytes. Immunocytochemical staining of these sections showed large numbers of T cells, suggesting an active role for these cells at the site of virus replication post-challenge.     

Experimentally induced infections bovine keratoconjunctivitis: effectiveness of a pilus vaccine against exposure to homologous strains of Moraxella bovis

A study was conducted to determine whether vaccination with sonicated pili of Moraxella bovis would protect cattle from subsequent infection and disease when experimentally challenged by exposure to homologous cultures of M bovis. Some calves were intramuscularly inoculated 2 times with pili of M bovis suspended in water, and others were subcutaneously inoculated 2 times with pili of M bovis suspended in oil; 21 days were allowed between inculations. Controls were nonvaccinated calves. Fourteen days after the last inculation, all calves were exposed to virulent homologous cultures of M bovis. The results indicated that vaccination with sonicated pili of M bovis may induce protective immunity against homologous strain challenge exposure. Vaccines in oil that were injected subcutaneously protected to a greater extent than did vaccines in water that were injected intramuscularly. The development of inflammatory nodules at the site of inoculation was associated with resistance to infection and disease. Only 1 of the vaccinated calves that resisted disease lacked precipitating antibodies against sonicated pili at the time of the challenge exposure. This calf had antibodies 2 weeks later.     

13C-urea breath test for diagnosis of experimental Helicobacter pylori infection in barrier born pigs

Previous studies with Helicobacter pylori infected barrier born pigs indicate that the infection has a patchy distribution, resulting in false negative culture results on endoscopic biopsy specimens. This study aimed to adapt the 13C-urea breath test as used in humans to diagnose H pylori infection in barrier born pigs. The breath test was also performed after bismuth as a single treatment and after triple therapy (bismuth, ampicillin, metronidazole). In control pigs the median excess of 13CO2 in expired air was 2.2 (range 0-12 n = 22) ppm. The infected pigs (n = 4) showed consistently high values (median 23 range 14-43) when examined on four occasions (n = 16) four to 10 weeks after inoculation. Biopsy specimens for culture had lower sensitivity than the breath test. No reduction in excess 13CO2 was seen after three days' single bismuth treatment, but after two weeks' triple therapy the breath test results had returned to normal. This suppression was temporary only, however, as the breath test was positive again four weeks after stopping treatment. In conclusion, the 13C-urea breath test is a simple and reliable test for determining H pylori infection and monitoring treatment effects in barrier born pigs. Because the test can be performed in awake pigs anaesthesia and gastroscopy are unnecessary.     

Cross-protection between Actinobacillus pleuropneumoniae biotypes-serotypes in pigs

Four groups of hysterectomy-derived and colostrum-deprived pigs were intranasally inoculated with an Actinobacillus pleuropneumoniae biotype 1-serotype 2 strain (producing RTX toxins ApxII and ApxIII. 6 pigs), an A. pleuropneumoniae biotype 1-serotype 10 strain (producing ApxI. 5 pigs), an A. pleuropneumoniae biotype 2-serotype 2 strain (producing ApxII, 5 pigs) or saline (controls, 7 pigs). All pigs were exposed to A. pleuropneumoniae biotype 1-serotype 2 endobronchial challenge. After challenge, severe clinical signs were observed in all control pigs, one pig immunized with the A. pleuropneumoniae biotype 1-serotype 10 strain and two pigs immunized with the A. pleuropneumoniae biotype 2-serotype 2 strain. These pigs died within 36 h after challenge and 20 to 50% of the lungs were macroscopically affected. In the other pigs, clinical signs were mild or absent and no or only small, focal lung lesions were observed when euthanized at 48 h after challenge. At the time challenge neutralizing antibodies against ApxI only. ApxII only and both ApxII and III were present in sera of pigs immunized with the A. pleuropneumoniae biotype 1-serotype 10 strain, the A. pleuropneumoniae biotype 2-serotype 2 strain and the A. pleuropneumoniae biotype 1-serotype 2 strain, respectively. These results indicate that immune mechanisms other than Apx neutralizing antibodies were involved in partial cross-protection of pigs immunized against A. pleuropneumoniae biotype 1-serotype 10 and challenged with the A. pleuropneumoniae biotype 1-serotype 2.     

Marked increases in neuronal nitric oxide synthase (nNOS) mRNA and NADPH-diaphorase histostaining in adrenal cortex after immobilization stress in rats

The immunoprophylaxis of mycoplasmal pneumonia of swine (MPS) caused by Mycoplasma hypopneumoniae was investigated for the first time in fattening pigs in Croatia. The incidence of MPS was monitored in pigs weighing on average 27.5 kg (12 weeks old) after immunization with a M. hyopneumoniae vaccine. Of 350 pigs in each group, in the nonvaccinated group 55 animals (15.7%) were affected by pneumonia and 11 (3.1%) died of consequences of pneumonia, whereas in the vaccinated group 20 pigs (5.7%) were affected by pneumonia without any death due to the infection. In the nonvaccinated group 44% more pigs were individually treated with antibiotic, and these animals received in-feed therapy for more than 1/4 of the fattening period. Vaccinated pigs gained weight faster, at the rate of 0.745 kg/day (or 82 g/day more) than control animals. The mean score of lung lesions due to M. hyopneumoniae was 10.51 in the control pigs and only 0.54 in the vaccinated animals. The total tissue alterations on lungs due to M. hyopneumoniae, Pasteurella multocida and/or Actinobacillus pleuropneumoniae expressed as the mean-score were 13.21 in the control group and 2.98 in the vaccinated group. According to the results of evaluation of the M. hyopneumoniae vaccine in the field, the vaccine appeared to provide an adequate immunity in fattening pigs but was less effective when administered to younger pigs at 1-3 weeks of age.