Effects of dietary soybean meal concentration on growth and immune response of pigs infected with porcine reproductive and respiratory syndrome virus.

An experiment was conducted to determine the effects of dietary soybean meal (SBM) concentration on the growth performance and immune response of pigs infected with porcine reproductive and respiratory syndrome virus (PRRSV). Four experimental treatments included a 2 × 2 factorial arrangement of 2 dietary SBM concentrations, 17.5% (LSBM) or 29% (HSBM), and 2 levels of PRRSV infection, uninfected sham or PRRSV infected. Sixty-four weanling pigs of split sex (21 d of age, 7.14 ± 0.54 kg) were individually housed in disease containment chambers. Pigs were provided a common diet for 1 wk postweaning before being equalized for BW and sex and allotted to 4 treatment groups with 16 replicate pigs per group. Pigs were fed experimental diets for 1 wk before receiving either a sham inoculation (sterile PBS) or a 1 × 10 50% tissue culture infective dose of PRRSV at 35 d of age (0 d postinoculation, DPI). Pig BW and feed intake were recorded weekly, and rectal temperatures were measured daily beginning on 0 DPI. Blood was collected on 0, 3, 7, and 14 DPI for determination of serum PRRSV load, differential complete blood cell counts, and haptoglobin and cytokine concentrations. Infection with PRRSV increased (P < 0.01) rectal temperatures of pigs throughout the infection period, with no influence of dietary SBM concentration. Pigs in the PRRSV-infected group had lower (P < 0.01) ADFI and G:F from 0 to 14 DPI compared with uninfected pigs. In the PRRSV-infected group, pigs fed HSBM tended to have improved ADG (P = 0.06) compared with pigs fed LSBM, whereas there was no influence of SBM concentration on growth of pigs in the uninfected group. At 14 DPI, PRRSV-infected pigs fed HSBM had a lower serum PRRSV load (P < 0.05), a higher (P = 0.02) hematocrit value, and a tendency for greater hemoglobin concentration (P = 0.09) compared with pigs fed LSBM. Serum haptoglobin and tumor necrosis factor-α concentrations of PRRSV-infected pigs were lower (P < 0.05) in pigs fed HSBM at 3 and 14 DPI, respectively, than in pigs fed LSBM. Overall, increasing the dietary SBM concentration modulated the immune response and tended to improve the growth of nursery pigs during a PRRSV infection.

Dietary plant extracts improve immune responses and growth efficiency of pigs experimentally infected with porcine reproductive and respiratory syndrome virus.

A study was conducted to evaluate the effects of 3 different plant extracts on growth performance and immune responses of weaned pigs experimentally infected with porcine reproductive and respiratory syndrome virus (PRRSV). A total of 64 weaned pigs (7.8 ± 0.3 kg BW), free of PRRSV, were randomly allotted to 1 of 8 treatments in a 2 × 4 factorial arrangement with a randomized complete block design. Pigs were blocked by initial BW. Sex and ancestry were equalized across treatments. The first factor was with or without PRRSV challenge (intranasal dose; 10(5) 50% tissue culture infective dose). The second factor was represented by 4 diets: a nursery basal diet (CON), 10 mg/kg capsicum oleoresin (CAP), garlic botanical (GAR), or turmeric oleoresin (TUR). Pigs were housed in disease containment chambers for 28 d [14 d before and after the inoculation (d 0)]. Blood was collected on d 0, 7, and 14 to measure the total and differential white blood cells (WBC), and serum was collected to measure viral load by quantitative PCR, PRRSV antibody titer, tumor necrosis factor-α (TNF-α), IL-1ß, C-reactive protein (CRP), and haptoglobin (Hp) by ELISA. In the unchallenged group, all piglets were PRRSV negative during the overall period postinoculation. All data were analyzed using PROC MIXED of SAS. The PRRSV challenge decreased (P < 0.01) ADG, ADFI, and G:F from d 0 to 14. Feeding TUR improved G:F of the PRRSV-infected pigs from d 0 to 14. The numbers of WBC and neutrophils were decreased (P < 0.05) by PRRSV on d 7 but increased (P < 0.05) by PRRSV on d 14, indicating the PRRSV-infected pigs undergo a stage of weak immune responses. Feeding GAR increased (P < 0.05) B cells and CD8+ T cells of PRRSV-infected pigs compared with the CON. Furthermore, the PRRSV challenge increased (P < 0.05) serum viral load, TNF-α, and IL-1ß on d 7 and serum viral load, CRP, and Hp on d 14, but feeding plant extracts to PRRSV-infected pigs reversed (P < 0.05) this increase. Infection with PRRSV increased (P < 0.05) rectal temperature of pigs on d 7, 9, and 11, but PRRSV-infected pigs fed plant extracts had lower rectal temperature (P < 0.05) than pigs fed the CON, indicating feeding plant extracts delayed the fever caused by PRRSV infection. In conclusion, results indicate that supplementation with plant extracts reduces the adverse effects of PRRSV by improving the immune responses of pigs, and the 3 plant extracts tested here show different effects. Supplementation with TUR improved feed efficiency of pigs challenged with PRRSV.

Mannan oligosaccharide increases serum concentrations of antibodies and inflammatory mediators in weanling pigs experimentally infected with porcine reproductive and respiratory syndrome virus.

Mannan-containing products are capable of modulating immune responses in animals. However, different products may have diverse immunomodulation. The experiment was conducted to examine effects of mannan oligosaccharide (Actigen; ACT) on growth performance and serum concentrations of antibodies and inflammatory mediators in weanling pigs (Sus scrofa) experimentally infected with porcine reproductive and respiratory syndrome virus (PRRSV). A total of 32 PRRSV-negative pigs (3 wk old) were randomly assigned from within blocks to 1 of 4 treatments in a 2 by 2 factorial arrangement [2 types of diet: control (0%) and ACT addition (0.04%); and with and without PRRSV] in a randomized complete block design. Pigs were blocked by initial BW within sex. Ancestry was equalized across treatments. Pigs (8/treatment) were kept individually in each pen. After 2 wk of an 8-wk period of feeding the treatments, pigs received an intranasal inoculation of PRRSV or sham medium at 5 wk of age. Infection by PRRSV decreased ADG, ADFI, and G:F throughout the experiment (P < 0.01). Actigen did not affect ADG (P = 0.450), but decreased (P = 0.047) ADFI from 28 to 42 days postinoculation (DPI). During that time, ACT improved G:F in infected pigs but not in sham controls (interaction, P = 0.009). Dietary ACT did not affect viremia in infected pigs (P > 0.05), but increased PRRSV-specific antibody titer at 35 DPI (P = 0.042). Infection with PRRSV induced the febrile responses of pigs from 3 to 10 DPI (P < 0.001) with return to normal at 14 DPI. During the experimental period, the rectal temperature of pigs was found slightly elevated by ACT (P = 0.045). Infected pigs had greater serum concentrations of IL-1ß, tumor necrosis factor (TNF)-α, IL-12, interferon (IFN)-γ, IL-10, and haptoglobin (Hp) than sham controls (P < 0.001). These results indicate that PRRSV stimulated secretion of cytokines involved in innate, T-helper 1, and T-regulatory immune responses. Actigen tended to decrease the serum TNF-α concentration regardless of PRRSV (P = 0.058). The ACT × PRRSV interaction was significant for IL-1ß (P = 0.016), IL-12 (P = 0.026), and Hp (P = 0.047), suggesting that infected pigs fed ACT had greater serum concentrations of these mediators than those fed the control. The increases in IL-1ß and IL-12 may favorably promote innate and T-cell immune functions in infected pigs fed ACT. Feeding ACT may be useful as ACT is related to increased PRRSV antibody titers and G:F in infected pigs at certain times during infection.

Mannan oligosaccharide modulates gene expression profile in pigs experimentally infected with porcine reproductive and respiratory syndrome virus.

This study characterized gene expression in peripheral blood mononuclear cells (PBMC) and bronchoalveolar lavage fluid (BALF) cells from control- or mannan oligosaccharide (MOS)-fed pigs with or without porcine reproductive and respiratory syndrome virus (PRRSV) at d 7 postinfection (PI). Weaned pigs (3 wk old) fed 0 or 0.2% MOS (Bio-Mos) diets were intranasally inoculated with PRRSV or a sterile medium at 5 wk of age. Total RNA (3 pigs/treatment) was extracted from cells. Double-stranded cDNA was amplified, labeled, and further hybridized to the Affymetrix GeneChip Porcine Genome Array consisting of 23,937 probe sets representing 20,201 genes. Microarray data were analyzed in R using packages from the Bioconductor project. Differential gene expression was tested by fitting a mixed linear model equivalent to a 2 × 2 factorial ANOVA using the limma package. Dietary MOS and PRRSV changed the expression of thousands of probe sets in PBMC and BALF cells (P < 0.05). The MOS × PRRSV interaction altered the expression of more nonimmune probe sets in PBMC (977 up, 1,128 down) than in BALF cells (117 up, 78 down). The MOS × PRRSV interaction (P < 0.05) for immune probe sets in PBMC affected genes encoding key inflammatory mediators. In uninfected pigs, gene expression of IL-1α, IL-6, myeloid differentiation factor 88, Toll-like receptor (TLR) 4, major histocompatibility complex (MHC) II, and dead box polypeptide 58 increased in PBMC of MOS-fed pigs (P < 0.05). This suggests that MOS enhances disease resistance in pigs and supports the fact that MOS induced a rapid increase in leukocytes at d 3 and 7 PI. Within infected pigs, however, MOS reduced the expression of IL-1ß, IL-6, IL-8, macrophage inflammatory protein (MIP)-1α, MIP-1ß, monocyte chemotactic protein (MCP)-1, and TLR4 genes in PBMC (P < 0.05). This finding may explain why fever was ameliorated in infected pigs fed MOS by d 7 PI. The expression of IL-1ß, IL-6, MIP-1ß, MCP-1, and TLR4 genes was confirmed by quantitative real-time reverse-transcription PCR. In BALF cells of infected pigs, MOS reduced the gene expression of TLR4, MHCII, and molecules associated with the complement system, but increased the gene expression of MHCI. In short, MOS regulated the expression of nonimmune and immune genes in pig leukocytes, perhaps providing benefits by enhancing the immune responses of the pigs to an infection, while preventing overstimulation of the immune system.

Mannan oligosaccharide improves immune responses and growth efficiency of nursery pigs experimentally infected with porcine reproductive and respiratory syndrome virus.

This study was conducted to determine whether the ingestion of mannan oligosaccharide (MOS, Bio-Mos) alters the immune response of nursery pigs challenged with porcine reproductive and respiratory syndrome virus (PRRSV). A total of 64 pigs (3 wk old), free of PRRSV, were used in 2 separate but similar experiments conducted sequentially. Pigs were blocked by initial BW. Sex and ancestry were equalized across treatments. Pigs were randomly assigned from within blocks to 1 of 4 treatments in a 2 × 2 factorial arrangement [2 types of diet: control (0%) and MOS addition (0.2%); 2 levels of PRRSV: with and without]. There were 8 replicate chambers of 2 pigs each. After 2 wk of a 4-wk period of feeding the treatments, pigs were intranasally inoculated with PRRSV or a sterile medium at 5 wk of age. The PRRSV challenge decreased ADG, ADFI, and G:F throughout the experiment (P < 0.001). Feeding MOS improved G:F of the pigs during d 7 to 14 (P=0.041) postinfection (PI). Serum concentrations of tumor necrosis factor (TNF)-α, C-reactive protein, and haptoglobin were increased by PRRSV (P < 0.001). The MOS × PRRSV interaction was significant for TNF-α at d 14 PI (P=0.028), suggesting that infected pigs fed MOS had less TNF-α than those fed the control. Dietary MOS increased serum IL-10 at d 14 PI (P=0.036). Further, MOS-fed pigs had greater numbers of white blood cells (WBC) at d 3 (P=0.048) and 7 PI (P=0.042) and lymphocytes at d 7 PI (P=0.023) than control-fed pigs. In contrast, PRRSV decreased (P < 0.01) WBC numbers until d 14 PI. Dietary MOS appeared (P=0.060) to increase the neutrophils in PRRSV-infected pigs at d 3 PI, but no (P=0.202) MOS × PRRSV interaction was found. Infection with PRRSV increased rectal temperature (RT) of pigs at d 3 PI (P < 0.001) and continued to affect the infected pigs fed the control diet until d 14 PI. The MOS × PRRSV interaction for RT was found at d 7 (P < 0.01) and 10 (P=0.098) PI, indicating that the infected pigs fed MOS had a decreased RT compared with those fed the control. This could explain why feed efficiency was improved by MOS. No effect (P > 0.05) of treatments on viremia or PRRSV-specific antibody was observed. These results suggest that MOS is associated with rapidly increased numbers of WBC at the early stage of infection and alleviates PRRSV-induced effects on G:F and fever. The results also indicate that the reduced intensity of inflammation by MOS may be related to changes in inflammatory mediator levels at the end of the acute phase.

Expression of inflammatory cytokines and Toll-like receptors in the brain and respiratory tract of pigs infected with porcine reproductive and respiratory syndrome virus.

The objective of this experiment was to evaluate the central and peripheral expression of selected pro-inflammatory cytokines and Toll-like receptors (TLRs) in pigs infected with porcine reproductive and respiratory syndrome virus (PRRSV). Twenty-four 8-week-old pigs were inoculated with either sterile medium or PRRSV. Pigs were monitored 14d after inoculation and then euthanized for tissue sample collection. PRRSV was detected in serum, lung and brain tissue of pigs given PRRSV but not in any tissue of pigs given medium. Infection with PRRSV increased serum levels of IL-1beta, IL-6, TNFalpha, and IFNgamma and elicited a mild transient fever and reduced growth performance. Infection by PRRSV also increased mRNA for the pro-inflammatory cytokines as well as mRNA for TLR3, TLR4, and TLR7 in the tracheobronchial lymph nodes. The TLR3, TLR4, TLR7 and most of the pro-inflammatory genes also were up-regulated in discrete brain areas of PRRSV-infected pigs. Collectively, the results indicate that following inoculation, PRRSV is present in the periphery and brain and that infection is associated with a peripheral and central pro-inflammatory response, fever, and reduced growth performance. The findings are interpreted to suggest the innate immune system of the brain is responsive to PRRSV infection.

Supplementing drinking water with Solutein did not mitigate acute morbidity effects of porcine reproductive and respiratory syndrome virus in nursery pigs.

The objective of this study was to determine whether providing nursery pigs drinking water supplemented with spray-dried animal plasma (Solutein, American Protein Corporation Inc., Ankeny, IA) would reduce the detrimental impact of porcine reproductive and respiratory syndrome virus (PRRSV) infection. Sixty-four pigs were subjected to 1 of 4 treatment combinations (2 x 2 factorial arrangement) of Solutein [0 or 2.5% (wt/wt) in drinking water] and PRRSV (sterile medium or 5 mL of tissue culture infectious dose of high-virulence strain ATCC VR-2385). Pigs were provided the water treatments during a 1-wk period before inoculation as well as during a 2-wk period after inoculation. Growth performance was determined throughout the study, and several indicators of the immunological response to PRRSV and disease pathology were assessed in blood and tissue samples collected from pigs killed 7 or 14 d after inoculation. Before inoculation, pigs provided water supplemented with Solutein tended to eat less (P = 0.08) but tended to gain more BW (P = 0.13) than pigs provided tap water. Thus, Solutein markedly improved G:F (P < 0.01), after accounting for the DM provided by Solutein. Inoculation with PRRSV reduced ADG and ADFI (P < 0.01) irrespective of water treatment; however, the beneficial effects of Solutein on G:F persisted. Infection with PRRSV also reduced (P < 0.009) villus height and crypt depth in cranial, medial, and caudal segments of the small intestine and increased (P < 0.05) lung and spleen weight, the number of leukocytes in lung lavage fluid, and serum concentrations of interferon-gamma and IL-1beta regardless of water treatment. Collectively, these results indicate that supplementing water with spray-dried animal plasma improved feed efficiency but did not afford nursery pigs protection from the effects of PRRSV on growth and certain hematological traits.

Vitamin E supplementation does not mitigate the acute morbidity effects of porcine reproductive and respiratory syndrome virus in nursery pigs.

The objective of this study was to determine whether feeding a vitamin E-rich diet would benefit nursery pigs infected with porcine reproductive and respiratory syndrome virus (PRRSV). Sixty-four pigs were subjected to one of four treatment combinations (2 x 2 factorial) of dietary vitamin E (adequate or excess) and PRRSV (medium or inoculation with VR-2385 isolate P-129). Pigs were fed experimental diets during a 3-wk period before inoculation as well as during a 12-d period after inoculation. Growth performance was determined throughout the study, and lipid peroxidation in liver, glutathione peroxidase (GPX) activity in serum, circulating white blood cells, and serum interleukin-1beta (IL-1beta) and interferon-gamma (IFN-gamma) were determined in samples collected from pigs killed 4 or 12 d after inoculation. Infection by PRRSV (P < 0.001) induced a marked decrease in both ADFI and ADG, but neither the main effect of diet nor the diet x PRRSV interaction was significant. Neither diet nor PRRSV affected feed efficiency. At 12 d after inoculation, lipid peroxidation in liver and GPX activity in serum were lower in pigs fed excess vitamin E than in those fed adequate vitamin E (P < 0.01), suggesting that the diet high in vitamin E bolstered the antioxidant status of the pigs. However, PRRSV did not affect lipid peroxidation in liver or serum GPX activity, and the diet x PRRSV interaction was not significant. White blood cell counts were decreased and IFN-gamma, and IL-1beta were increased (P < 0.05) 4 and 12 d after inoculation in PRRSV-infected pigs, but neither diet nor the diet x PRRSV interaction was significant. Collectively, these results indicate that increasing antioxidant defenses by feeding high levels of vitamin E did not ameliorate the effects of PRRSV on decreased growth, leukopenia, and increased serum IL-1beta and IFN-gamma. Thus, feeding nursery pigs a diet high in vitamin E may not be useful for mitigating the acute morbidity effects of PRRSV infection.

Effect of formalin fixation on the immunohistochemical detection of PRRS virus antigen in experimentally and naturally infected pigs.

The purpose of this study was to determine the effect of formalin fixation on the immunohistochemical detection of porcine reproductive and respiratory syndrome (PRRS) viral antigen in lungs of experimentally and naturally infected pigs. In separate trials, five 24-day-old pigs and six 10-day-old pigs were housed as separate groups in isolation and inoculated intranasally with 10(5.5) TCID50 of an isolate of PRRS virus (PRRSV; P129). The older and younger pigs were euthanatized at 7 and 10 days post inoculation (dpi), respectively. At necropsy, all pigs had gross and microscopic lung lesions typical of PRRS, and PRRSV was isolated from all pigs. To insure uniform fixation, lungs from each pig were cut into 1-cm-thick slices and immersed into 10% neutral-buffered formalin. After fixation in formalin for 8 hours or 1, 2, 3, 5, 6, 8, 10, and 15 days, 3 lung sections from some or all pigs were processed for histological examination using routine methods. Immunohistochemical staining for PRRSV antigen was positive at the following times (days unless otherwise stated) after fixation (percentage of pigs staining positive for PRRSV in parentheses): 8 hours (100); 1 (100); 2 (100); 3 (80); 5 (33); and 6, 8, 10, and 15 (0-all negative). To further evaluate the effects of formalin fixation on PRRSV immunodetection, 31 field cases of PRRS were selected for immunohistochemistry (IHC). Over a 3-month period, submitted cases were selected from the Purdue University Animal Disease Diagnostic Laboratory, W. Lafayette, Indiana, for IHC if 1) the clinical history included respiratory disease, 2) PRRSV was isolated from lung and/or serum from the submitted pigs or tissues, 3) at least 1 section of lung fixed in 10% neutral-buffered formalin was submitted for IHC, and 4) the duration of fixation could be accurately determined from the case history. Of the 31 PRRSV-infected pig cases meeting the selection criteria, 23 were fixed in formalin for 4 days or less. Twenty-one of these 23 (91%) were positive by IHC. Two of 8 cases fixed for greater than 4 days (25%) were positive by IHC. In practical terms, 1-day shipping of fixed samples to a laboratory followed by routine tissue processing within a laboratory should not adversely affect immunohistochemical detection of PRRS viral antigen. But a delay in shipping or processing of more than 2 days could reduce or prevent the detection of PRRS viral antigen by IHC.

Growth performance and whole-body composition of pigs experimentally infected with Mycoplasma hyopneumoniae.

Mycoplasma hyopneumoniae (Mh) is the primary infectious pathogen responsible for enzootic pneumonia in pigs. Although Mh is thought to impair growth performance, whole-body composition, and fat and protein accretion in pigs with pneumonia have not been reported and the mechanism through which Mh reduces growth is unknown. The objectives of this study were to evaluate the effects of Mh on growth performance, whole-body composition, and protein and fat accretion in nursery pigs and to determine whether Mh infection increases the expression of interleukin (IL)-1beta, IL-6, and tumor necrosis factor-alpha (TNF-alpha). Sixty-four 2-wk-old Mh-free pigs were used (two trials) in a randomized complete block design. In each trial, two pigs were housed in each of 16 disease-containment chambers. At 4 wk of age, pigs were inoculated intratracheally with 3 mL of Mh broth (P5722-3, 10(7) cfu/mL) or sterile Friis culture medium. Clinical signs of disease and feed intake were monitored daily and body weight was determined weekly for 4 wk. Whole-body composition was determined from pigs killed 0, 14, and 28 d after inoculation, and the comparative slaughter technique was used to estimate protein and fat accretion. At death, gross lung lesions were quantified, and lung tissue was collected to verify the presence or absence of Mh, and to determine cytokine mRNA levels. Control pigs displayed no overt signs of infection and were Mh-negative and free of pulmonary lesions. Pigs inoculated with Mh showed pneumonic coughing (P < 0.005), were Mh-positive, and had pulmonary lesions that affected 4.5% (P < 0.01) and 14.1% (P < 0.001) of total lung surface area at 14 and 28 d, respectively, after inoculation. Ribonuclease protection assays revealed increased IL-1beta (P < 0.04) and TNF-alpha (P < 0.06) mRNA in lung tissue collected from a lesion site compared with tissue collected 10 cm from a lesion site or from control pigs. Interestingly, Mh did not depress weight gain or feed efficiency during any week of the 28-d study (P > 0.10). Moreover, Mh did not affect whole-body fat or protein accretion (P > 0.10). Thus, in spite of inducing disease and expression of inflammatory cytokines, Mh alone did not affect growth performance and whole-body composition of nursery pigs during the 4-wk experiment. The ability of pigs to contend with Mh may have resulted from the absence of other pathogens that generally co-exist with Mh under commercial conditions.

Ureteral diverticula in two dogs.

We describe ureteral diverticula in two dogs and briefly review the related literature. The diagnosis of this condition is radiographic and based on the excretory urographic observation of multiple ureteral outpouchings. Pathologically, ureteral transitional cell hyperplasia and mucinous metaplasia result in submucosal proliferation of the urothelium and the formation of crypts and small cysts. Ureteral diverticulosis in humans is associated with an increased risk of urothelial malignancies, such as transitional cell carcinoma of the urinary bladder. Clinically, both dogs were older, small breed neutered females. Both had a history of chronic urinary obstruction. One dog died during surgery to remove an adrenal mass, and the other was euthanized at the owner's request because of an inoperable bladder neoplasm. Histopathologic diagnosis of ureteral lesions confirmed the radiographic diagnosis of ureteral diverticula in both dogs.

High feline trypsin-like immunoreactivity in a cat with pancreatitis and hepatic lipidosis.

A 1.5-year-old domestic shorthair cat was examined because of vomiting and icterus. Clinicopathologic abnormalities included high alanine transaminase, alkaline phosphatase, and gamma-glutamyltransferase activities and high total bilirubin concentration. During abdominal ultrasonography, the left limb and body of the pancreas appeared hypoechoic, and a small quantity of peritoneal effusion was seen. The liver was diffusely hyperechoic, with echogenicity similar to that of the spleen, indicating hepatic lipidosis. Feline trypsin-like immunoreactivity was high, suggesting that the cat also had pancreatitis. The cat was treated with crystalloid fluids and was fed a protein-restricted diet via a percutaneous endoscopically placed gastrostomy tube. The cat's condition continued to deteriorate despite medical treatment, and it was euthanatized. Necropsy confirmed the clinical suspicion of acute pancreatitis and hepatic lipidosis. This case suggests that measurement of trypsin-like immunoreactivity may be useful in cats suspected of having pancreatitis.

Pulmonary and mediastinal metastases of a vaccination-site sarcoma in a cat.

Sarcomas at vaccination sites in cats were first reported in 1992. Recent retrospective studies have confirmed an association between these vaccination-site sarcomas (VSS) and feline leukemia virus (FeLV) and/ or rabies vaccines. In most cases, VSS are locally invasive fibrosarcomas that tend to recur but rarely metastasize. We report the mediastinal and pulmonary metastases of a VSS in a FeLV-and feline immunodeficiency virus-negative, 8-year-old, domestic short-haired cat. The primary sarcoma was removed from an interscapular vaccination site and diagnosed as a VSS 3 months prior to radiographic lesions suggestive of pulmonary and mediastinal metastases. At necropsy, there were multiple pulmonary and mediastinal nodules that histologically and ultrastructurally were fibrosarcomas, cytomorphologically similar to the VSS. In addition, immunohistochemical staining patterns of the VSS and metastatic sites were consistent with that described for VSS. Recent reports of pulmonary and mediastinal metastases of interscapular VSS emphasize the importance of early diagnosis and treatment of these tumors.

Dietary polyunsaturated fatty acids modulate responses of pigs to Mycoplasma hyopneumoniae infection.

Polyunsaturated fatty acids (PUFA) are immunomodulators, but few studies have examined how these dietary components influence infectious respiratory disease. Groups of nine pigs were fed casein and corn starch-based diets containing 10.5 g/100 g corn oil (CO), linseed oil (LO), menhaden oil (MO), linseed + corn oil (LC, 1:1) and menhaden + corn oil (MC, 1:1). As a methodological control, one group of pigs (n = 15) was fed a commercial ration (control diet; C). Pigs inoculated intratracheally with Mycoplasma hyopneumoniae after 4 wk of consuming the diets were killed 3 wk later. Gross lung lesions in MO-fed pigs were less (P < 0.05) than those in LC- and MC-fed pigs. Pigs fed MO had less peribronchial inflammation (P < 0.05) than all other groups. Gross lung lesions correlated negatively with basal in vitro alveolar macrophage tumor necrosis factor (TNF) production in pigs fed diets that contained negligible levels of (n-3) PUFA (C and CO). Basal macrophage TNF production did not correlate with lung lesion scores for diets containing more (n-3) PUFA than C or CO (LO, MO, LC and MC). For pigs fed the LO, MO, LC and MC diets, mean gross lung lesions increased as the mean ratio of (n-3):(n-6) PUFA in alveolar macrophage lipids decreased. Serum levels of alpha1 acid glycoprotein (AGP) were less (P < 0.05) in pigs fed MO, and there was a rise in mean lung lesions scores for each PUFA-fed group as mean AGP levels increased. These results indicate that dietary PUFA can affect disease pathogenesis and that the (n-3):(n-6) PUFA ratio may modulate the host response.

Porcine reproductive and respiratory syndrome virus does not exacerbate Mycoplasma hyopneumoniae infection in young pigs.

The purpose of this study was to determine if Porcine Reproductive and Respiratory Syndrome (PRRS) virus infection altered the severity of acute Mycoplasma hyopneumoniae (MH) infection in young pigs. Twenty five, 3-week-old male pigs were randomly assigned by litter and weight to one of 3 groups. Groups 1 (PRRS only, n = 5) and 2 (PRRS + MH, n = 10) were inoculated intranasally with PRRS virus (IN-5 isolate, 10(5) TCID50) and viremia in all pigs was confirmed by virus isolation from serum 3 days later. Group 3 (MH only, n = 10) was inoculated at the same time with virus free culture media. Seven days after virus inoculation, Groups 2 and 3 were inoculated intratracheally with MH (strain P-5722-3, 10(7) CCU). All pigs were euthanized and necropsied 28 days later, when maximum lesions of mycoplasmosis occurs. Pigs in group 1 did not cough and had no gross lung lesions, but were still viremic at necropsy. MH was isolated from all pigs in groups 2 (avg. log 5.2 +/- 1.3) and 3 (avg. log 5.1 +/- 1.5), but differences were not significant (P = 0.87). Similarly, there were no differences in average days coughing (8.9 +/- 2.8 v 11.2 +/- 4.5, P = 0.17), grossly pneumonic lung (16.5% v 17%, P = 0.91), or microscopic lung lesion scores (10.1 +/- 2.6 v 11.1 +/- 1.9, P = 0.35) between pigs in groups 2 and 3. Under these experimental conditions, PRRS virus infection did not increase the severity of experimental Mycoplasma hyopneumoniae infection in young pigs.

Dietary polyunsaturated fatty acid effects on immune cells of the porcine lung.

The effects of various dietary polyunsaturated fatty acids (PUFAs) on the function of immune cells of the porcine lung was studied. Groups of six pigs were fed diets containing 10.5% corn oil [CO; enriched in linoleic acid (18:2, n-6)], linseed oil (LO; enriched in alpha-linolenic acid (18:3, n-3)], menhaden oil (MO; enriched in eicosapentaenoic (20:5; n-3) and docosahexaenoic (22:6; n-3) acids], linseed + corn oil (1:1; LC), and menhaden + corn oil (1:1; MC) for 28-30 days. Basal levels of alveolar macrophage (m phi) tumor necrosis factor-alpha (TNF-alpha) production were higher (P < .05) for LC- and MC-fed pigs than for CO- and LO-fed pigs. Lipopolysaccharide (LPS)-stimulated LC and MC m phi s produced more TNF than m phi s from pigs fed CO, LO, and MO diets. Macrophages from pigs receiving the CO and LC diets had higher (P < .05) levels of leucine aminopeptidase than m phi s from the other dietary groups. Lipopolysaccharide did not increase m phi nitrite production over basal levels except in the MO diet group. However, LPS-stimulated m phi s from the CO, MO, and LC dietary groups produced more nitrite than m phi s from MC-fed pigs. Alveolar lymphocytes from pigs receiving the MC diet produced more T cell growth factors than LO and MO m phi s. Alveolar m phi s from the different dietary groups did not differ in their capacity for non-immune-mediated phagocytosis of fluorescent latex beads. These results indicate that dietary PUFAs can modulate some functions of porcine alveolar immune cells and that this may prove significant for host response to respiratory disease agents.

Characterization of infection with endemic porcine reproductive and respiratory syndrome virus in a swine herd.

Infection of 8-week-old pigs with endemic porcine reproductive and respiratory syndrome (PRRS) virus was detected on a farm that had an epidemic of PRRS in 1989. During the 2.5 years since the original epidemic, reproductive performance of the breeding herd had been within acceptable limits, but mortality had periodically exceeded one-fourth of the pigs in the nursery (195 died of 761 weaned, 25.6%). Investigators attempted to determine the age and humoral immune status of pigs infected with endemic PRRS virus on the farm. Serum obtained from 9 groups of 1- to 18-week-old pigs (10 pigs/group) was examined for PRRS virus by virus isolation. Serum was obtained from 8 sows that had farrowed within the preceding 24 hours. Serum from the sows was obtained weekly until litters were weaned at 3 weeks of age. Serum was obtained from 27 newborn pigs (3 to 4 newborn pigs from each of the 8 sows) prior to intake of colostrum and at weekly or biweekly intervals until the pigs were 20 to 21 weeks of age. Isolation of PRRS virus and indirect fluorescent antibody serologic testing were performed on these serum samples. In another study, serum was obtained for serologic testing from 10 sows in each of 6 parity groups. The PRRS virus was isolated from serum of only 3- to 12-week-old pigs. The 8 sows and their 27 pigs were seronegative for PRRS virus during the 3-week lactation period. By 10 weeks of age, 18 of the 27 suckling pigs were still alive and had seroconverted (titers > or = 1:20).(ABSTRACT TRUNCATED AT 250 WORDS)

Mice and rats (laboratory and feral) are not a reservoir for PRRS virus.

Porcine reproductive and respiratory syndrome (PRRS) is caused by an unclassified arterivirus. The syndrome was first reported in the USA in 1987 as epizootics of reproductive failure in sows and respiratory disease in nursery, growing, and fattening pigs. An enzootic form of the disease has now emerged, characterized by interstitial pneumonia and an increased incidence of secondary infections. Because the disease has now become enzootic on many farms, rodents were investigated as a possible reservoir for the infection. Wild rodents from an endemically infected farm were trapped, and virus isolation for PRRS virus (PRRSV) was attempted using porcine primary alveolar macrophage cultures. PRRSV was not isolated from serum and selected pooled tissues (thymus, lung, and spleen) of 14 feral mice and 2 feral rats. Also, transmission experiments were carried out on 3-week-old Balb/c mice and 12-week-old Fischer-344 rats to determine if these species were susceptible to infection. The rodents were inoculated intranasally, orally, and intraperitoneally with a virus proven to transmit PRRS to pigs. Virus isolations from selected pooled tissues (lung, spleen, thymus, and kidney) and from serum were negative, and there were neither gross nor microscopic lesions. Weight gains and white blood cell counts were not significantly different between treated and control groups. These results indicate that rodents are not susceptible to infection with PRRSV and therefore are probably not a reservoir for the disease.

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.

Growth and reproductive performance, during exposure to ammonia, of gilts afflicted with pneumonia and atrophic rhinitis.

From 2 to 4.5 months of age, 80 crossbred gilts were reared in a conventional grower unit where they were naturally exposed to mycoplasmal and bacterial pathogens that cause pneumonia and atrophic rhinitis. At 4.5 months of age, gilts were moved to environmentally regulated rooms (4.9 x 7.3 m) and assigned at random to 1 of 2 treatment groups: low aerial concentration of ammonia (4 to 12 ppm; mean, 7 ppm) or moderate aerial concentration of ammonia (26 to 45 ppm, mean, 35 ppm). Low concentration of ammonia was obtained by flushing of manure pits weekly, whereas moderate concentration of ammonia was maintained by adding anhydrous ammonia to manure pits that were not flushed. Gilts were weighed biweekly. Mean daily gain (MDG) was less (P < 0.01) for gilts exposed to moderate concentration of ammonia than for gilts exposed to low concentration of ammonia after 2 weeks in their respective environments. By 4 and 6 weeks, however, MDG was similar between the 2 treatment groups. After 6 weeks in these environments, 20 gilts from each treatment group were slaughtered, and prevalence and severity of lung lesions and snout grades were determined. At slaughter, body weight was greater (P < 0.01) in gilts exposed to low, rather than moderate, ammonia concentration (94.5 vs 86.8 kg; SEM, 3.3 kg). Percentage of lung tissue containing lesions (18 vs 12) and snout grade (2.8 vs 3.1) were similar between gilts exposed to low or moderate concentration of ammonia. The remaining 20 gilts in each treatment group were maintained in their respective environments, exposed daily to mature boars and bred at first estrus.(ABSTRACT TRUNCATED AT 250 WORDS)