Rotavirus replication in colostrum-fed and colostrum-deprived pigs

A porcine rotavirus isolate was titrated in neonatal colostrum-fed and colostrum-deprived pigs. The stock rotavirus suspension had a titer of 10(-6.5)/ml and was in its fifteenth cell culture passage in MA-104 cells. Fourteen colostrum-fed pigs were orally inoculated with dilutions of the stock virus suspension ranging from undiluted to 10(-5). These pigs did not develop notable clinical signs during the 7-day experimental trial and no pathologic changes were found in intestine, liver, lung, kidney, spleen, or brain. However, rotavirus was detected in feces of the colostrum-fed pigs, using virus isolation and electron microscopic techniques. Rotavirus was also isolated from lung, brain, or spleen of 4 of 12 of these pigs. Sixteen colostrum-deprived pigs were orally inoculated with dilutions of the stock virus suspension ranging from 10(-1) to 10(-8). Diarrhea developed in 10 of 12 pigs that were given up to the 10(-6) dilution. Seven of these 12 pigs died because of the severity of diarrhea. Pigs that died of rotavirus-induced diarrhea had severe villus loss in the jejunum and ileum. Villi of the small intestine of colostrum-deprived pigs that survived the severe diarrhea were within normal limits at the end of the 7-day trial. The colostrum-deprived pigs that were inoculated with a dilution less than 10(-6) and survived past 96 hours underwent seroconversion. Rotavirus was detected by virus isolation and electron microscopy in the feces of all colostrum-deprived pigs that survived beyond 18.5 hours after inoculation. Virus was isolated from lungs, brain, or spleen of 12 of 16 colostrum-deprived pigs.     

Intestinal permeability in pigs during rotavirus infection.

Macromolecular permeability of the small intestine was tested in four 3-week-old gnotobiotic pigs inoculated with porcine rotavirus strain RV277 (group A). Pigs were administered 125I-labeled polyvinylpyrrolidone (molecular weight [mol wt], 40,000) orally 1 day before and 2 and 24 hours after virus inoculation, and blood samples were obtained every 6 hours. Eight hours after rotavirus inoculation, pigs had watery diarrhea. Increased permeation of 125I-labeled polyvinylpyrrolidone was not observed after clinical signs of infection had developed. Serum total protein and urea nitrogen concentrations increased slightly at the end of the study, probably as a consequence of dehydration. Differences in blood glucose concentration were not seen. At 48 hours after viral inoculation, macromolecular permeability was tested morphologically by injecting horseradish peroxidase (mol wt, 40,000) into the jejunal lumen just distally to the ligamentum colicoduodenale. After an incubation period of 20 minutes, small segments of jejunum were obtained for stereomicroscopic, histologic, and ultrastructural investigations. Moderate hyperregenerative villus atrophy was found. Ultrastructural changes of the villus epithelium were minor, and increased macromolecular permeation was not observed.     

Inoculation of neonatal gnotobiotic dogs with a canine rotavirus

Neonatal gnotobiotic dogs were inoculated orally with a rotavirus isolated from a pup with fatal diarrhea, and in the gnotobiotic dogs, diarrhea was observed between postinoculation hours (PIH) 20 and 24. The diarrhea persisted through PIH 154, and inoculated pups had clinical signs of dehydration after PIH 24. Negative-contrast electron microscopy of the feces from inoculated pups revealed rotavirus particles from PIH 12 through 154. Using an indirect-fluorescent antibody test, serum rotavirus antibody was detected in inoculated pups by PIH 96. In the duodenum, jejunum, and ileum of inoculated pups, group-specific rotaviral antigen was observed within absorptive villus epithelial cells and mononuclear cells in the villus lamina propria with an indirect-fluorescent antibody test. Fluorescence was seen in the small intestine of inoculated pups killed by PIH 12 and was present in intestines of pups killed through PIH 154. Rotaviral antigen was also seen in the mesenteric lymph nodes of a few inoculated pups killed at PIH 48.     

Lack of an effect of a commercial vaccine adjuvant on the development of postweaning multisystemic wasting syndrome (PMWS) in porcine circovirus type 2 (PCV2) experimentally infected conventional pigs

The objective of this study was to evaluate the effect of a commercial vaccine adjuvant on the clinical and pathological outcome of PCV2 experimentally infected 8 to 9-week-old conventional pigs. Forty-four pigs were divided into four groups: non-infected control pigs, pigs that received a vaccine adjuvant, pigs inoculated with PCV2, and pigs inoculated with PCV2 together with the vaccine adjuvant. Infection was monitored until 69 days post-inoculation (PI). Some PCV2 inoculated pigs had hyperthermia, but no other clinical signs were recorded. No characteristic PMWS gross or microscopic lesions were observed in any of the pigs. PCV2 DNA was detected in lymphoid tissues by in situ hybridisation in 6 PCV2 inoculated pigs on day 69 PI. All PCV2 inoculated pigs seroconverted between days 21 and 49 PI, shortly after viremia detection. Moreover, viremia was detected between days 7 and 69 PI using PCR. A peak of the virus load was detected by real-time quantitative PCR between days 14 and 21 PI. There were no significant differences in the proportion of PCV2 positive serum and in the viral load between PCV2 and PCV2 + adjuvant inoculated pigs. Although PMWS was not reproduced in neither PCV2 nor PCV2 + adjuvant inoculated pigs, viremia detection and seroconversion indicated that all PCV2 inoculated pigs developed a chronic long-term asymptomatic infection. An increase of PCV2 replication was not observed in pigs inoculated with the adjuvant. These results indicate that the principle of immunostimulation may not be applicable under the experimental conditions used, suggesting that not all adjuvants used in commercial vaccines are capable of triggering mechanisms for PMWS development.     

Diagnosis of swine influenza with an immunofluorescence technique using monoclonal antibodies

Direct diagnosis of swine influenza infection by an indirect immunofluorescence technique using anti-nucleoproteine monoclonal antibody was compared with virus isolation. Five 8-week-old pigs were inoculated with 2 x 10(7) EID50 of strain A H1N1Sw/4115/85. Clinical signs developed in only three pigs. Antigen was detected in nasal epithelial cells obtained from all animals the first day after inoculation; the antigen was detected in one pig 6 days after the infection. Fluorescence was present in the nucleus, nucleolus and cytoplasm of infected cells. The indirect immunofluorescence test was specific and as sensitive as virus isolation in embryonated eggs, allowing a rapid diagnosis that could be achieved within hours.     

Specific mucosal IgA immunity in turkey poults infected with turkey coronavirus

The objective of this study was to elucidate the kinetics and magnitudes of specific IgA antibody responses in intestines of turkey poults infected with turkey coronavirus (TCV). Turkey poults were orally inoculated with TCV at 10 days of age. Intestinal segment cultures were administered for duodenum, jejunum, and ileum and the IgA antibody responses were analyzed at 1, 2, 3, 4, 6, or 9 weeks post-infection (PI) in two different experiments. The kinetics of virus-specific IgA antibody responses in duodenum, jejunum, and ileum were similar: gradually increased from 1 week PI, reached the peak at 3 or 4 weeks PI, and declined afterward. The virus-specific IgA antibody responses in duodenum, jejunum, and ileum showed negative correlation with duration of TCV antigen in the corresponding locations of intestine with Spearman's correlation coefficient of -0.85 (p=0.034), -0.74 (p=0.096), and -0.75 (p=0.084), respectively. Moreover, the virus-specific IgA antibody responses in serum were positively correlated with that of duodenum (coefficient=0.829, p=0.042), jejunum (coefficient=0.829, p=0.042), and ileum (coefficient=0.771, p=0.072) segment cultures, suggesting that the induction of specific IgA response in serum was predictive of an IgA response in intestine. The results indicate that intestinal mucosal IgA antibodies to TCV are elicited in turkeys following infection with TCV. The local mucosal antibodies may provide protective immunity for infected turkeys to recover from TCV infection.     

Specificity of the indirect enzyme-linked immunosorbent assay for detection of pseudorabies virus antibodies in pigs exposed to bovine herpesvirus-1

Six 5-week-old pigs were inoculated intranasally (IN) with 10(7.6) TCID50 of bovine herpesvirus-1 (BHV-1). Three of the pigs also were inoculated IV with a similar dose of BHV-1. Clinical responses were not observed in these 6 pigs before oronasal challenge exposure with 10(7.8) TCID50 of virulent pseudorabies virus (PRV) at postinoculation day 42. Two pigs inoculated IN with BHV-1 and challenge exposed with PRV remained healthy, whereas the remaining 4 pigs developed severe clinical signs of pseudorabies and were moribund at postinoculation day 50 (8 days after challenge exposure). Anti-BHV-1 antibodies were demonstrable by ELISA in all 6 pigs and by serum neutralization (SN) in 5 pigs before challenge exposure with PRV. Anti-PRV antibody was not detected by ELISA or SN before challenge exposure to PRV. After challenge exposure to PRV, pigs with humoral antibody to BHV-1 responded anamnestically, and anti-PRV antibody activity was demonstrable by ELISA and SN in the 2 surviving pigs.     

Studies on the age resistance of swine to group A rotavirus infection.

To determine whether swine become naturally age resistant to group A rotavirus infection, colostrum-deprived, rotavirus-naive newborn pigs that were raised in isolation (n = 34) were studied. Neonatal pigs and pigs 1, 2, 4, 6, 8, 10, and 12 weeks of age were inoculated orally with group A porcine rotavirus or mock inoculum and euthanatized at 24, 31, or 48 hours post-infection. Nine sections of small intestine, cecum, and colon were harvested and immunohistochemically examined for evidence of rotavirus replication within enterocytes. Infectivity was semiquantified by intestinal segment, and a composite score was obtained for each animal. In pigs inoculated at 1 week of age, enterocyte infection was mild and scattered; all other pigs became infected regardless of age or region of intestine, and older animals that became infected had infectivity scores similar to those of younger animals. In a second more limited study, pigs raised in the same isolation environment (n = 11) but previously exposed to virus and demonstrating rotavirus serum antibody had a much lower degree of enterocyte infection at 8, 10, and 12 weeks of age (2, 4, and 6 weeks, respectively, after initial exposure to virus). Age resistance to clinical rotavirus disease in swine is due to factors other than an age-dependent development of resistance of enterocytes to infection, at least through 12 weeks of age.     

Pathogenesis of porcine enteric calicivirus-like virus in four-day-old gnotobiotic pigs

Eighteen 4-day-old gnotobiotic pigs were orally inoculated with porcine enteric calicivirus-like virus (C strain). Seven additional gnotobiotic pigs served as noninoculated controls. Mild diarrhea developed in all inoculated pigs by postinoculation day (PID) 3 and persisted for 3 to 7 days. Severe diarrhea developed in 2 inoculated pigs between PID 4 and 5. Twelve inoculated and 7 control pigs were euthanatized over a 7-day period. Small intestinal mucosal smears were stained with a fluorescein-conjugated anti-porcine enteric calicivirus-like virus serum. Immunofluorescence was observed in villous epithelial cells (primarily in the duodenum or jejunum) of all inoculated pigs, except for 1 pig euthanatized at PID 7. Villus length was determined in histologic sections of the small intestinal specimens from control and inoculated pigs. Statistically significant (P less than 0.01) villus atrophy was found in the duodenum and/or jejunum of inoculated pigs at PID 3 to 7. These observations were confirmed by scanning electron microscopy, which revealed shortening, blunting, fusion, or absence of villi in the duodenum and jejunum of inoculated pigs at PID 3 to 7. Lesions were not seen in control pigs. Calicivirus-like particles were detected by immune electron microscopy in the large intestinal contents and feces of inoculated pigs from PID 1 to 7.     

猪肠道碱性氨基酸转运载体(CAT1)mRNA表达的组织特异性和发育性变化

本研究旨在探讨不同品种猪肠道碱性氨基酸转运载体（CAT1）mRNA表达的组织特异性和发育规律。试验选取1、7、26、30、60、90和150日龄长白和蓝塘公猪各5头（同一品种同一日龄且体重接近）,共70头,测体重后屠宰,采集十二指肠、空肠、回肠和结肠组织样品。以18S基因为内标,用实时荧光定量RT-PCR法（SYBR Green Ⅰ试剂盒）检测CAT mRNA在60日龄长白猪十二指肠、空肠、回肠和结肠表达的组织特异性,以及在长白和蓝塘猪不同日龄其十二指肠、空肠、回肠表达的发育性变化。结果显示：60日龄长白猪CAT1 mRNA的表达丰度从十二指肠到回肠呈逐渐升高的趋势,到结肠开始下降,回肠极显著高于其他3个肠段（P〈0．01）,十二指肠最低;十二指肠和空肠CAT mRNA的表达在1～26d（即哺乳期）都呈上升的趋势,随后都开始有所下降;蓝塘猪十二指肠CAT1 mRNA的表达丰度在150d时显著低于其他各个阶段（P〈0．05）,而长白猪90和150d都显著低于其他各阶段（P〈0．05）;空肠CAT1 mRNA的表达在26～150d各阶段都差异不显著,而26d显著高于1和7d（P〈0．05）;1～60d长白和蓝塘猪回肠CAT1 mRNA的表达都呈逐渐上升的趋势,60d后都显著下降（P〈0．05）。两品种猪不同日龄时十二指肠和空肠CAT1 mRNA的表达量都没有显著差异（P〉0．05）;长白猪回肠CAT mRNA表达在26d时显著高于蓝塘猪（P〈0．05）;在90和150d时,长白猪都显著低于蓝塘猪（P〈0．05）,其他各阶段没有显著差异。结果说明,CAT mRNA在不同肠段及不同发育阶段的表达存在明显的差异,这可能与肠腔中氨基酸的浓度和氨基酸的需要水平及相关激素水平有关。     

Development of γδ T cell subset responses in gnotobiotic pigs infected with human rotaviruses and colonized with probiotic lactobacilli

γδ T cell responses are induced by various viral and bacterial infections. Different γδ T cells contribute to activation and regulation of the inflammatory response and to epithelial repair. How γδ T cells respond to rotavirus infection and how the colonization of probiotics influences the γδ T cell response were unknown. In this study, we evaluated by multicolor flow cytometry the frequencies and distribution of total γδ T cells and three major subsets (CD2-CD8-, CD2+CD8- and CD2+CD8+) in ileum, spleen and blood of gnotobiotic (Gn) pigs at early (3-5 days) and late phases (28 days) after rotavirus infection. The Gn pigs were inoculated with the virulent human rotavirus Wa strain and colonized with a mixture of two strains of probiotics Lactobacillus acidophilus and Lactobacillus reuteri. In na?ve pigs, the highest frequency of total γδ T cells was found in blood, followed by spleen and ileum at the early age (8-10 days old) whereas in older pigs (32 days of age) the highest frequency of total γδ T cells was found in ileum and spleen followed by blood. Rotavirus infection significantly increased frequencies of intestinal total γδ T cells and the putatively regulatory CD2+CD8+ γδ T cell subset and decreased frequencies of the putatively proinflammatory CD8- subsets in ileum, spleen and blood at post-infection days (PID) 3 or 5. The three γδ T cell subsets distributed and responded differently after rotavirus infection and/or lactobacilli colonization. The CD2+CD8+ subset contributed the most to the expansion of total γδ T cells after rotavirus infection in ileum because more than 77% of the total γδ T cells there were CD2+CD8+ cells. There was an additive effect between lactobacilli and rotavirus in inducing total γδ T cell expansion in ileum at PID 5. The overall effect of lactobacilli colonization versus rotavirus infection on frequencies of the CD2+CD8+ γδ T cell subset in ileum was similar; however, rotavirus-infected pigs maintained significantly higher frequencies of CD8- subsets in ileum than lactobacilli-colonized pigs. The dynamic γδ T cell responses suggest that γδ T cell subsets may play important roles in different stages of immune responses after rotavirus infection and probiotic colonization. The knowledge on the kinetics and distribution patterns of γδ T cell subsets in na?ve pigs and after rotavirus infection or lactobacilli colonization provides the foundation for further mechanistic studies of their functions.     

Correlation of tissue infection and serologic findings in pigs fed Toxoplasma gondii oocysts

Each of thirteen 6-week-old pigs was inoculated per os with 10,000 sporulated oocysts of Toxoplasma gondii. By postinoculation day (PID) 13, pigs were seropositive by the indirect fluorescent antibody test. Beginning on PID 13 and every 7 days thereafter through PID 97, 1 pig was killed and 6 tissues were examined for T gondii. Of the 13 pigs, 11 were infected, including the 1st pig killed on PID 13, although none of the pigs had gross lesions of toxoplasmosis. Tissues harboring T gondii most frequently were the heart and brain; organisms were detected less frequently in the longissimus muscles, diaphragm, and liver. Toxoplasma gondii was not detected in the bronchial lymph nodes. There was good correlation between antibody and presence of T gondii in these pigs. One additional pig, maintained as a noninfected control, remained seronegative and had no evidence of infection when killed on PID 97.     

Does Porcine Reproductive and Respiratory Syndrome Virus Potentiate Classical Swine Fever Virus Infection in Weaner Pigs?

Fifteen 6-week-old crossbred weaners weighing about 12 kg each were randomly divided into three groups of five animals each. One group of pigs was inoculated first with porcine reproductive and respiratory syndrome (PRRS) virus and then 3 days later with CSF virus. The second group received classical swine fever (CSF) virus, while the third group was inoculated with PRRS virus only. The aim of the experiment was to determine whether a primary PRRS virus infection influences the clinical outcome of experimentally induced CSF in young pigs. The PRRS virus infected weaners developed mild respiratory symptoms and recovered completely. All five weaners which were inoculated with CSF virus only showed severe clinical signs typical of the acute form of CSF. One pig had to be killed 15 days post-inoculation (p.i.); the remaining four died between the 18th and 22nd day p.i. The clinical course of the animals inoculated with both viruses was slightly different from that of the pigs that received only CSF virus. Four out of five pigs from the PRRS/CSF group became febrile and viraemic earlier than the animals which received CSF virus only. These pigs had to be killed 15–17 days post CSF virus inoculation. One animal in this group survived the acute phase of CSF and recovered completely. It was concluded that the observed divergences of the clinical courses would not have been noticed under field conditions. Therefore these findings cast doubt on the relevance of PRRS virus infection potentiating significantly the clinical outcome of CSF in young pigs.     

Porcine reproductive and respiratory syndrome virus: routes of excretion

This study was conducted to delineate potential sites of exit and duration of shedding of porcine reproductive and respiratory syndrome virus (PRRSV). Two experiments of 6 pigs each were conducted. Pigs were farrowed in isolation, weaned at 7 days of age, and housed in individual HEPA filtered isolation chambers. In each experiment, 3 pigs served as controls and 3 were inoculated intranasally with PRRSV (ATCC VR-2402) at 3 weeks of age. In a first experiment, on days 7, 14, 21, 28, 35, and 42 post inoculation (PI), pigs were anesthetized and intubated. The following samples were collected: serum, saliva, conjunctival swabs, urine by cystocentesis, and feces. Upon recovery from anesthesia, the endotracheal tube was removed, rinsed, and the rinse retained. In the second experiment, the sampling schedule was expanded and serum, saliva, and oropharyngeal samples were collected from day 55 to day 124 PI at 14 day intervals. Virus was isolated in porcine alveolar macrophages up to day 14 from urine, day 21 from serum, day 35 from endotracheal tube rinse, day 42 from saliva, and day 84 from oropharyngeal samples. No virus was recovered from conjunctival swabs, fecal samples, or negative control samples. This is the first report of isolation of PRRSV from saliva. Virus-contaminated saliva, especially when considered in the context of social dominance behavior among pigs, may play an important role in PRRSV transmission. These results support previous reports of persistent infection with PRRSV prolonged recovery of virus from tonsils of swine.     

An experimental model for subclinical edema disease (Escherichia coli enterotoxemia) manifest as vascular necrosis in pigs.

An experimental model for subclinical edema disease was developed in weanling pigs. In multiple experiments, 3-week-old pigs were weaned, then inoculated intragastrically with 10(10) colony-forming units of an SLT-IIv-positive strain of Escherichia coli originally isolated from a pig with edema disease (principals). Control pigs were inoculated with a nonpathogenic E coli strain. Of 39 principals, 8 developed clinical edema disease within 14 days after inoculation. However, 20 of 21 principals that did not develop clinical signs of edema disease, but were submitted for necropsy examination at 14 days after inoculation, had characteristic vascular lesions of edema disease. Vascular lesions, found principally in ileum and brain, consisted of segmental necrosis of myocytes in the tunica media of small arteries and arterioles. None of the pigs inoculated with a nonpathogenic strain of E coli developed edema disease or vascular lesions. None of the principals necropsied at 2 days after inoculation had vascular lesions. Development of vascular lesions by 14 days after inoculation was used as the end point for detecting subclinical edema disease in the model.     

Evaluation of protective immunity in pigs following oral administration of an avirulent live vaccine of Lawsonia intracellularis

OBJECTIVE: To evaluate the efficacy of an orally administered avirulent live vaccine to protect pigs against challenge exposure with virulent Lawsonia intracellularis. ANIMALS: 108 weaned 3-week-old pigs (35 in experiment 1 and 73 in experiment 2). PROCEDURE: 2 experiments were conducted. On day 0, vaccinates were orally administered vaccine via drench or in drinking water, whereas challenge-control pigs were administered cultured medium. On day 21, pigs were challenge exposed with a virulent heterologous isolate of L. intracellularis. Clinical observations, weights, seroconversion, and fecal excretion of L. intracellularis were measured until day 42. At study termination, pigs were euthanatized and examined for L. intracellularis-specific lesion development of the ileum and colon. RESULTS: Pigs receiving a single dose of vaccine were protected when challenge exposed with virulent L. intracellularis (at least 10(77) TCID50/dose). In experiment 1, vaccinates had significantly less fecal excretion (47% and 40% for days 35 and 42, respectively), compared with challenge-control pigs. In experiment 2, vaccinates had significantly less fecal excretion (50% and 58% for days 35 and 42, respectively), compared with challenge-control pigs. Significant reductions in lesion development were evident in the ileum of vaccinated pigs (70% and 56% at day 42 for experiments 1 and 2, respectively), compared with challenge-control pigs. CONCLUSIONS AND CLINICAL RELEVANCE: Oral administration by drench or via drinking water of an avirulent live vaccine against L. intracellularis resulted in substantial protection against proliferative enteropathy among vaccinates and offers a better way to reduce stress of pigs during vaccine administration.     

Passive protection against porcine epidemic diarrhea (PED) virus in piglets by colostrum from immunized cows.

The effects of hyperimmune cow colostrum (HCC) on experimentally induced porcine epidemic diarrhea (PED) were investigated in piglets. In experiment 1, four 2-day-old piglets fed HCC containing an antibody titer of 1:512 and another four piglets fed unimmune cow colostrum (UCC) were orally inoculated with 10LD50 of PED virus. The piglets were given colostrum three times a day at 4 hr intervals. Half of the piglets fed HCC showed diarrhea and recovered, and all piglets survived. In contrast, all piglets fed UCC developed diarrhea and three of them died. In experiment 2, 2-day-old piglets fed HCC containing antibody titers of 1:512, 1:128 and 1:32, and UCC were inoculated with PED virus, and survival rates after challenge were 100, 75, 50 and 0 %, respectively. In experiment 3, 1-day-old piglets fed HCC with 1:512 antibody titer or UCC were inoculated and necropsied at 24, 48 and 72 hr after the inoculation for pathological examination. Piglets fed HCC remained healthy and PED virus antigen was not detected in the epithelial cells of the small intestine, and the length of the villi in small intestine was normal. On the other hand, in piglets fed UCC, villous atrophy and PED virus antigen were observed in epithelial cells of the jejunum and ileum from 24 hr. It was concluded that oral administration of HCC to piglets was effective in preventing PED virus infection and reduced their mortality.     

Adenovirus enteritis in pigs

Experimental transmissions were done with adenovirus strain 6618 in hysterectomy-produced colostrum-deprived pigs. After an incubation period of 3 to 4 days, all inoculated animals had diarrhea. Histopathologically, many intranuclear inclusion bodies were present on short villi of the terminal parts of jejunum and ileum. With electron microscopy, the inclusion bodies were observed to contain numerous adenovirus particles. Immunoperoxidase-positive cells were seen on short villi of the terminal parts of jejunum and ileum. Adenovirus particles also were detected by negative staining of intestinal contents. In 1 pig (naturally occurring infection), adenovirus enteritis was studied by the aforementioned techniques. Similar intestinal lesions as described in the experimental pigs were observed.     

Bordetella bronchiseptica and toxigenic type D Pasteurella multocida as agents of severe atrophic rhinitis of swine

Bordetella bronchiseptica and toxigenic type-D Pasteurella multocida were cultured from pigs in each of five herds diagnosed as having severe atrophic rhinitis (AR). B. bronchiseptica alone, P. multocida alone, or both organisms isolated from four herds were inoculated intranasally into 1-week-old gnotobiotic pigs which were necropsied 4 weeks post-inoculation (PI). Nasal turbinate atrophy in B. bronchiseptica-inoculated pigs was moderate to severe, while P. multocida-inoculated pigs had slight to severe atrophy. Pigs inoculated with both organisms had moderate to complete turbinate atrophy. P. multocida was reisolated at necropsy from all pigs receiving the organism except those having no turbinate damage. B. bronchiseptica and P. multocida from a fifth herd were simultaneously inoculated into six naturally farrowed 6-day-old SPF pigs. Necropsy performed 4 weeks PI revealed severe to complete turbinate atrophy. Nasal turbinates were normal for control pigs in both experiments.