Adiposity, plasma insulin, leptin, lipids, and oxidative stress in mature light breed horses.

BACKGROUND: Increased blood insulin levels are associated with an increased risk of pasture-associated laminitis in equids. OBJECTIVE: To determine the relationship between plasma insulin, leptin, and lipid levels, and measures of oxidative stress with adiposity in mature light breed horses. ANIMALS: 300 randomly selected light breed horses, aged 4-20 years. METHODS: A random sample of horses (140 mares, 151 geldings, and 9 stallions) was drawn from the VMRCVM Equine Field Service practice client list. Evaluations occurred June 15 - August 15, 2006, with all sampling performed between 0600 and 1200 hours. Concentrate feed was withheld for at least 10 hours before sampling. Plasma was analyzed for insulin, glucose, leptin, triglycerides, nonesterified fatty acids, and measures of oxidative stress. Body condition score was determined as the average of 2 independent investigators. RESULTS: Overconditioned and obese horses had higher plasma insulin (P < .001) and leptin (P < .01) levels than optimally conditioned horses. Obese horses had higher triglyceride levels (P = .006) and lower red blood cell gluthathione peroxidase activities (P = .001) than optimally conditioned horses. CONCLUSIONS AND CLINICAL IMPORTANCE: Maintaining horses at a BCS <7 might be important for decreasing the risk of pasture-associated laminitis.

Prevalence of overconditioning in mature horses in southwest Virginia during the summer.

BACKGROUND: The prevalence of obesity in horses in the eastern United States is not well documented. OBJECTIVE: To determine body condition and risk factors for obesity in horses in Southwest Virginia during summer. ANIMALS: A sample of 300 mature (4-20 years old), light breed horses (140 mares, 151 geldings, and 9 stallions) from the VMRCVM Equine Field Service practice equine database. The horses were from 114 farms and 138 owners. METHODS: Horses were evaluated over a 60-day period in this cross-sectional, prospective study. A questionnaire was completed for each horse. Body condition score (BCS) was assigned using a scale of 1 (emaciated) to 9 (obese) by 2 independent scorers. Morphometric measurements included average neck circumference (ANC), girth, body length, and height at the withers. Horses were categorized based on BCS as underconditioned (BCS < 4), optimal condition (BCS 4-6), overconditioned (BCS 7), and obese condition (BCS 8-9). RESULTS: Five horses (1.7%) were underconditioned, 142 horses (47.3%) were optimally conditioned, 97 horses (32.3%) were overconditioned, and 56 (18.7%) were obese. Estimated body weight (EBW) (r = 0.14, P = .015), body mass index (BMI) (r = 0.46, P < .001), and neck circumference to height ratio (NCHR) (r = 0.50, P = .001) increased with increasing BCS. CONCLUSIONS AND CLINICAL IMPORTANCE: The prevalence of overconditioned and obese horses in this population was higher than reported in previous studies and indicates that obesity might be an emerging problem in horses.

Influence of age on surfactant isolated from healthy horses maintained on pasture.

BACKGROUND: Surfactant alterations are described in horses after exercise, anesthesia, and prolonged transport, in horses with recurrent airway obstruction, and in neonatal foals. The effect of horse age or bronchoalveolar lavage fluid (BALF) sample characteristics on surfactant is unknown. OBJECTIVES: To evaluate surfactant phospholipid composition and function in healthy horses, and to investigate the influence of age and BALF sample characteristics on surfactant. ANIMALS: Seventeen healthy horses 6-25 years of age maintained on pasture year-round. METHODS: BALF was collected by standard procedures and was assessed for recovery volume, nucleated cell count (NCC), and cytology. Cell-free BALF was separated into crude surfactant pellet (CSP) and surfactant supernatant (Supe) by ultracentrifugation. Phospholipid and protein content were determined from both fractions. CSP phospholipid composition was analyzed by high-performance liquid chromatography with an evaporative light scatter detector. Surface tension of CSP was evaluated with a pulsating bubble surfactometer. Regression analysis was used to evaluate associations between age, BALF sample characteristics, and surfactant variables. RESULTS: Results and conclusions were derived from 15 horses. Increasing age was associated with decreased phospholipid content in CSP but not Supe. Age did not affect protein content of CSP or Supe, or surfactant phospholipid composition or function. Age-related surfactant changes were unaffected by BALF recovery percentage, NCC, and cytological profile. CONCLUSIONS AND CLINICAL IMPORTANCE: Older horses have decreased surfactant phospholipid content, which might be because of age-related pulmonary changes. Surfactant composition is unaffected by BALF sample characteristics at a BALF recovery percentage of at least 50%.

Ophthalmic examination findings in a colony of Screech owls (Megascops asio).

OBJECTIVE: To report ophthalmic findings in the Screech owl (Megascops asio). Sample population Twenty-three, apparently healthy adult captive Screech owls in Maryland. PROCEDURES: OU of all owls underwent complete ophthalmic examination. One randomly assigned eye of each bird was measured by phenol red thread tear test (PRT), and the other eye by Schirmer tear test (STT). TonoVet rebound tonometry and TonoPen-XL applanation tonometry were performed in each eye to measure IOP. Conjunctival swabs were cultured from one eye of 10 birds, corneal diameter was measured in OU of eight birds, and streak retinoscopy was performed on OU of seven birds. Ten birds were anesthetized, and A-scan ultrasonography using a 15-MHz probe was performed to obtain axial intraocular measurements. RESULTS: Ophthalmic abnormalities were noted in 24/46 (52%) of eyes. Median STT result was < or = 2 mm/min, ranging < or = 2-6 mm/min, and mean +/- SD PRT was 15 +/- 4.3 mm/15 s. Mean +/- SD IOP were 9 +/- 1.8 mmHg TonoVet-P, 14 +/- 2.4 mmHg TonoVet-D, and 11 +/- 1.9 mmHg TonoPen-XL. Coagulase negative staphylococcal organisms were cultured from all conjunctival swabs. Mean +/- SD corneal dimensions were 14.5 +/- 0.5 mm vertically and 15.25 +/- 0.5 mm horizontally. All refracted birds were within one diopter of emmetropia. Mean +/- SD axial distance from the cornea to the anterior lens capsule was 4.03 +/- 0.3 mm, from cornea to the posterior lens capsule was 10.8 +/- 0.5 mm, and from cornea to sclera was 20.33 +/- 0.6 mm. CONCLUSIONS: This study reports ophthalmic examination findings in Screech owls, and provide means and ranges for various ocular measurements. This is the first report of rebound tonometry and PRT in owls.

Curli production and genetic relationships among Escherichia coli from cases of bovine mastitis.

Curli are adhesive surface structures produced by some Escherichia coli and Salmonella strains that bind host proteins and activate inflammatory mediators. In this study, 61 E. coli isolates from 36 clinical cases of bovine mastitis were characterized using enterobacterial repetitive intergenic consensus-PCR and screened for their ability to produce curli. Effect of curli production on case recovery, based on a return to precase milk yield, was investigated for a subset of 43 isolates from 20 quarters of 19 cows. Thirty-five (57%) of 61 isolates were curli positive. Fifty-eight of the 61 isolates clustered into 2 clonal groups at 52% genetic similarity. Genetically diverse E. coli isolates were simultaneously cultured from individual cases. Twenty-three isolates from 13 cows were clustered in clonal group I, of which 5 cases (38%) were curli positive; 35 isolates from 22 cows were clustered in clonal group II, of which 15 cases (68%) were curli positive. No association was found between genetic similarity and phenotypic curli expression of isolates from cows with clinical E. coli mastitis cases. Phenotypic curli expression in isolates did not affect recovery of cows' milk yield to premastitis production levels.

Effects of porcine circovirus type 2 (PCV2) maternal antibodies on experimental infection of piglets with PCV2.

To determine the effects of porcine circovirus type 2 (PCV2) maternal antibodies on and response to experimental PCV2 infection, 24 piglets were divided into four groups on the basis of the enzyme-linked immunosorbent assay titers of PCV2 maternal antibodies: group A (n = 6; sample/positive [S/P] ratio, <0.2), group B (n = 5; S/P ratio, >0.2 to <0.5), and groups C (n = 8) and D (n = 5) (S/P ratio, >0.5). Piglets in groups A, B, and C were inoculated with PCV2 at day 0 and challenged with PCV2 at day 42. Group D piglets were not exposed to PCV2 at day 0 but were challenged at day 42. Before challenge, seroconversion to PCV2 antibodies occurred in five of six group A piglets, and the antibody level rose above the cutoff level in one of five group B piglets. Viremia was detected in five of six, four of five, and two of eight pigs in groups A, B, and C, respectively. After challenge, PCV2 DNA was detectable from 7 to 21 days postchallenge in the sera from six of six, four of five, three of eight, and five of five pigs in groups A, B, C, and D, respectively. The results indicated that protection against PCV2 infection conferred by maternal antibodies is titer dependent: higher titers are generally protective, but low titers are not.

Systematic pathogenesis and replication of avian hepatitis E virus in specific-pathogen-free adult chickens.

Hepatitis E virus (HEV) is an important human pathogen. Due to the lack of a cell culture system and a practical animal model for HEV, little is known about its pathogenesis and replication. The discovery of a strain of HEV in chickens, designated avian HEV, prompted us to evaluate chickens as a model for the study of HEV. Eighty-five 60-week-old specific-pathogen-free chickens were randomly divided into three groups. Group 1 chickens (n=28) were each inoculated with 5 x 10(4.5) 50% chicken infectious doses of avian HEV by the oronasal route, group 2 chickens (n=29) were each inoculated with the same dose by the intravenous (i.v.) route, and group 3 chickens (n=28) were not inoculated and were used as controls. Two chickens from each group were necropsied at 1, 3, 5, 7, 10, 13, 16, 20, 24, 28, 35, and 42 days postinoculation (dpi), and the remaining chickens were necropsied at 56 dpi. Serum, fecal, and various tissue samples, including liver and spleen samples, were collected at each necropsy for pathological and virological testing. By 21 dpi, all oronasally and i.v. inoculated chickens had seroconverted. Fecal virus shedding was detected variably from 1 to 20 dpi for the i.v. group and from 10 to 56 dpi for the oronasal group. Avian HEV RNA was detected in serum, bile, and liver samples from both i.v. and oronasally inoculated chickens. Gross liver lesions, characterized by subcapsular hemorrhages or enlargement of the right intermediate lobe, were observed in 7 of 28 oronasally and 7 of 29 i.v. inoculated chickens. Microscopic liver lesions were mainly lymphocytic periphlebitis and phlebitis. The lesion scores were higher for oronasal (P=0.0008) and i.v. (P=0.0029) group birds than for control birds. Slight elevations of the plasma liver enzyme lactate dehydrogenase were observed in infected chickens. The results indicated that chickens are a useful model for studying HEV replication and pathogenesis. This is the first report of HEV transmission via its natural route in a homologous animal model.

Two amino acid mutations in the capsid protein of type 2 porcine circovirus (PCV2) enhanced PCV2 replication in vitro and attenuated the virus in vivo.

Porcine circovirus type 2 (PCV2) is the primary causative agent of postweaning multisystemic wasting syndrome (PMWS) in pigs. To identify potential genetic determinants for virulence and replication, we serially passaged a PCV2 isolate 120 times in PK-15 cells. The viruses harvested at virus passages 1 (VP1) and 120 (VP120) were biologically, genetically, and experimentally characterized. The PCV2 VP120 virus replicated in PK-15 cells to a titer similar to that of the PK-15 cell line-derived nonpathogenic PCV1 but replicated more efficiently than PCV2 VP1 with a difference of about 1 log unit in the titers. The complete genomic sequences of viruses at passages 0, 30, 60, 90, and 120 were determined. After 120 passages, only two nucleotide mutations were identified in the entire genome, and both were located in the capsid gene: the mutations were located at nucleotide positions 328 (C328G) and 573 (A573C). The C328G mutation, in which a proline at position 110 of the capsid protein changed to an alanine (P110A), occurred at passage 30 and remained in the subsequent passages. The second mutation, A573C, resulting in a change from an arginine to a serine at position 191 (R191S), appeared at passage 120. To experimentally characterize the VP120 virus, 31 specific-pathogen-free pigs were randomly divided into three groups. Ten pigs in group 1 received phosphate-buffered saline as negative controls. Each pig in group 2 (11 pigs) was inoculated intramuscularly and intranasally with 10(4.9) 50% tissue culture infective doses (TCID(50)) of PCV2 VP120. Each pig in group 3 (10 pigs) was similarly inoculated with 10(4.9) TCID(50) of PCV2 VP1. Viremia was detected in 9 of 10 pigs in the PCV2 VP1 group with a mean duration of 3 weeks, but in only 4 of 11 pigs in the PCV2 VP120 group with a mean duration of 1.6 weeks. The PCV2 genomic copy numbers in serum in the PCV2 VP1 group were significantly higher than those in the PCV2 VP120 group (P < 0.0001). Gross and histopathologic lesions in pigs inoculated with PCV2 VP1 were more severe than those inoculated with PCV2 VP120 at both day 21 and 42 necropsies (P = 0.0032 and P = 0.0274, respectively). Taken together, the results from this study indicated that the P110A and R191S mutations in the capsid of PCV2 enhanced the growth ability of PCV2 in vitro and attenuated the virus in vivo. This finding has important implications for PCV2 vaccine development.

A chimeric porcine circovirus (PCV) with the immunogenic capsid gene of the pathogenic PCV type 2 (PCV2) cloned into the genomic backbone of the nonpathogenic PCV1 induces protective immunity against PCV2 infection in pigs.

Porcine circovirus type 2 (PCV2) is associated with postweaning multisystemic wasting syndrome in pigs, whereas PCV1 is nonpathogenic. We previously demonstrated that a chimeric PCV1-2 virus (with the immunogenic capsid gene of PCV2 cloned into the backbone of PCV1) induces an antibody response to the PCV2 capsid protein and is attenuated in pigs. Here, we report that the attenuated chimeric PCV1-2 induces protective immunity to wild-type PCV2 challenge in pigs. A total of 48 specific-pathogen-free piglets were randomly and equally assigned to four groups of 12 pigs each. Pigs in group 1 were vaccinated by intramuscular injection with 200 microg of the chimeric PCV1-2 infectious DNA clone. Pigs in group 2 were vaccinated by intralymphoid injection with 200 microg of a chimeric PCV1-2 infectious DNA clone. Pigs in group 3 were vaccinated by intramuscular injection with 10(3.5) 50% tissue culture infective doses (TCID(50)) of the chimeric PCV1-2 live virus. Pigs in group 4 were not vaccinated and served as controls. By 42 days postvaccination (DPV), the majority of pigs had seroconverted to PCV2 capsid antibody. At 42 DPV, all pigs were challenged intranasally and intramuscularly with 2 x 10(4.5) TCID(50) of a wild-type pathogenic PCV2 virus. By 21 days postchallenge (DPC), 9 out of the 12 group 4 pigs were viremic for PCV2. Vaccinated animals in groups 1 to 3 had no detectable PCV2 viremia after challenge. At 21 DPC the lymph nodes in the nonvaccinated pigs were larger (P < 0.05) than those of vaccinated pigs. The PCV2 genomic copy loads in lymph nodes were reduced (P < 0.0001) in vaccinated pigs. Moderate amounts of PCV2 antigen were detected in most lymphoid tissues of nonvaccinated pigs but in only 1 of 36 vaccinated pigs. Mild-to-severe lymphoid depletion and histiocytic replacement were detected in lymphoid tissues in the majority of nonvaccinated group 4 pigs but in only a few vaccinated group 1 to 3 pigs. The data from this study indicated that when given intramuscularly in pigs, the attenuated chimeric PCV1-2 live virus, as well as the chimeric PCV1-2 infectious DNA clone, induces protective immunity against PCV2 infection and could potentially serve as an effective vaccine.

A model to estimate the optimal sample size for microbiological surveys.

Estimating optimal sample size for microbiological surveys is a challenge for laboratory managers. When insufficient sampling is conducted, biased inferences are likely; however, when excessive sampling is conducted valuable laboratory resources are wasted. This report presents a statistical model for the estimation of the sample size appropriate for the accurate identification of the bacterial subtypes of interest in a specimen. This applied model for microbiology laboratory use is based on a Bayesian mode of inference, which combines two inputs: (ii) a prespecified estimate, or prior distribution statement, based on available scientific knowledge and (ii) observed data. The specific inputs for the model are a prior distribution statement of the number of strains per specimen provided by an informed microbiologist and data from a microbiological survey indicating the number of strains per specimen. The model output is an updated probability distribution of strains per specimen, which can be used to estimate the probability of observing all strains present according to the number of colonies that are sampled. In this report two scenarios that illustrate the use of the model to estimate bacterial colony sample size requirements are presented. In the first scenario, bacterial colony sample size is estimated to correctly identify Campylobacter amplified restriction fragment length polymorphism types on broiler carcasses. The second scenario estimates bacterial colony sample size to correctly identify Salmonella enterica serotype Enteritidis phage types in fecal drag swabs from egg-laying poultry flocks. An advantage of the model is that as updated inputs from ongoing surveys are incorporated into the model, increasingly precise sample size estimates are likely to be made.

Effects of feeding supplemental fat to beef cows on cold tolerance in newborn calves.

Our objectives were to examine the effects of added fat in late-gestation cow diets on neonatal response to cold. In Exp. 1, pregnant fall-calving heifers received control (n = 5), safflower seed (n = 5), or whole cottonseed (n = 5) diets. The hay-based, isonitrogenous, and isocaloric diets, fed for 47 d prepartum, contained 1.5, 4.0, and 5.0% fat for control, safflower, and whole cottonseed diets, respectively. At calving, calf BW and vigor score, as well as fat, lactose, and IgG in colostrum were not affected (P > 0.30) by diet. Heifers fed the safflower diet tended to have greater colostral solids (P < 0.10) than heifers fed the control or whole cottonseed diets. At 6.5 h of age, calves were placed in a 5 degrees C cold room for 90 min. Calf vigor, shivering, body temperature, and blood samples were taken every 15 min. During cold stress, calf body temperature decreased 0.7 degrees C (P < 0.03). Across all diets, shivering and serum glucose concentrations increased (P < 0.05), whereas calf vigor and cortisol concentrations decreased (P < 0.02) during cold exposure. In Exp. 2, pregnant spring-calving cows (n = 98) received a control (n = 47) or whole cottonseed (n = 51) supplement. Hay-based diets fed for 68 d prepartum contained 2.0 and 5.0% fat for control and whole cottonseed diets, respectively. Calf BW, vigor, shivering, dystocia score, time to stand, time to nurse, serum glucose concentrations, and serum IgG were not affected (P > 0.50) by diet. Between 30 and 180 min, body temperature of calves from dams fed the whole cottonseed supplement decreased (P < 0.05) more than calves from dams fed the control supplement. Serum glucose concentrations in calves were not affected by diet (P > 0.30). Serum cortisol concentrations tended (P < 0.09) to be greater for calves from dams fed whole cottonseed than control calves. When ambient temperature was < 6 degrees C, calves born to dams fed whole cottonseed had greater (P < 0.05) BW, tended (P < 0.1) to stand earlier, and had greater serum IgG concentrations. We conclude that calves from dams fed high-fat diets containing safflower or whole cottonseed respond similarly to cold stress, but these responses may not be consistent with greater cold resistance. In addition, high-fat dietary supplementation of late-gestation cows may only be beneficial during calving seasons with prolonged cold weather.

Heterogeneity and seroprevalence of a newly identified avian hepatitis e virus from chickens in the United States.

We recently identified and characterized a novel virus, designated avian hepatitis E virus (avian HEV), from chickens with hepatitis-splenomegaly syndrome (HS syndrome) in the United States. Avian HEV is genetically related to but distinct from human and swine HEVs. To determine the extent of genetic variation and the seroprevalence of avian HEV infection in chicken flocks, we genetically identified and characterized 11 additional avian HEV isolates from chickens with HS syndrome and assessed the prevalence of avian HEV antibodies from a total of 1,276 chickens of different ages and breeds from 76 different flocks in five states (California, Colorado, Connecticut, Virginia, and Wisconsin). An enzyme-linked immunosorbent assay using a truncated recombinant avian HEV ORF2 antigen was developed and used to determine avian HEV seroprevalence. About 71% of chicken flocks and 30% of chickens tested in the study were positive for antibodies to avian HEV. About 17% of chickens younger than 18 weeks were seropositive, whereas about 36% of adult chickens were seropositive. By using a reverse transcription-PCR (RT-PCR) assay, we tested 21 bile samples from chickens with HS syndrome in California, Connecticut, New York, and Wisconsin for the presence of avian HEV RNA. Of the 21 bile samples, 12 were positive for 30- to 35-nm HEV-like virus particles by electron microscopy (EM). A total of 11 of the 12 EM-positive bile samples and 6 of the 9 EM-negative bile samples were positive for avian HEV RNA by RT-PCR. The sequences of a 372-bp region within the helicase gene of 11 avian HEV isolates were determined. Sequence analyses revealed that the 11 field isolates of avian HEV had 78 to 100% nucleotide sequence identities to each other, 79 to 88% identities to the prototype avian HEV, 76 to 80% identities to chicken big liver and spleen disease virus, and 56 to 61% identities to other known strains of human and swine HEV. The data from this study indicated that, like swine and human HEVs, avian HEV isolates are genetically heterogenic and that avian HEV infection is enzoonotic in chicken flocks in the United States.

Pathogenic and fecal Escherichia coil strains from turkeys in a commercial operation.

The biochemical phenotypes and antimicrobial susceptibility patterns of 105 clinical Escherichia coli isolates from flocks with colibacillosis in a turkey operation were compared with 1104 fecal E. coli isolates from 20 flocks in that operation. Clinical isolates and 194 fecal isolates with biochemical phenotypes or minimum inhibitory concentrations for gentamicin and sulfamethoxazole similar to clinical isolates were tested for somatic antigens and the potential virulence genes hylE, iss, tsh, and K1. The predominant biochemical phenotype of clinical isolates contained 21 isolates including 14 isolates belonging to serogroup 078 with barely detectable beta-D-glucuronidase activity. Thirty-five fecal isolates had biochemical phenotypes matching common phenotypes of clinical isolates. Sixty-six (63%) clinical isolates exhibited intermediate susceptibility or resistance to gentamicin and sulfamethoxazole compared with 265 (24%) fecal isolates (P < 0.001). Seventy-seven clinical isolates reacted with O-antisera, of which 51 (66%) belonged to the following serogroups: O1, O2, O8, O25, O78, O114, and O119. In comparison, 8 of 35 (23%) fecal isolates subtyped on the basis of biochemical phenotype belonged to these serogroups and four of 167 (2%) fecal isolates subtyped on the basis of their antimicrobial resistance patterns belonged to these serogroups. Iss, K1, and tsh genes were detected more often among clinical isolates than these fecal isolates (P < 0.05). In summary, a small subgroup of E. coli strains caused most colibacillosis infections in this operation. These strains existed at low concentration in normal fecal flora of healthy turkeys in intensively raised flocks. The data suggest that colibacillosis in turkey operations may be due to endogenous infections caused by specialized pathogens.

Prevalence of antibodies to hepatitis E virus in veterinarians working with swine and in normal blood donors in the United States and other countries.

Hepatitis E virus (HEV) is endemic in many developing and some industrialized countries. It has been hypothesized that animals may be the source of infection. The recent identification of swine HEV in U.S. pigs and the demonstration of its ability to infect across species have lent credence to this hypothesis. To assess the potential risk of zoonotic HEV infection, we tested a total of 468 veterinarians working with swine (including 389 U.S. swine veterinarians) and 400 normal U.S. blood donors for immunoglobulin G anti-HEV. Recombinant capsid antigens from a U.S. strain of swine HEV and from a human HEV strain (Sar-55) were each used in an enzyme-linked immunosorbent assay. The anti-HEV prevalence assayed with the swine HEV antigen showed 97% concordance with that obtained with the human HEV antigen (kappa = 92%). Among the 295 swine veterinarians tested from the eight U.S. states (Minnesota, Indiana, Nebraska, Iowa, Illinois, Missouri, North Carolina, and Alabama) from which normal blood donor samples were available, 26% were positive with Sar-55 antigen and 23% were positive with swine HEV antigen. In contrast, 18% of the blood donors from the same eight U.S. states were positive with Sar-55 antigen and 17% were positive with swine HEV antigen. Swine veterinarians in the eight states were 1.51 times more likely when tested with swine HEV antigen (95% confidence interval, 1.03 to 2.20) and 1.46 times more likely when tested with Sar-55 antigen (95% confidence interval, 0.99 to 2.17) to be anti-HEV positive than normal blood donors. We did not find a difference in anti-HEV prevalence between veterinarians who reported having had a needle stick or cut and those who had not or between those who spent more time (> or = 80% of the time) and those who spent less time (< or = 20% of the time) working with pigs. Similarly, we did not find a difference in anti-HEV prevalence according to four job categories (academic, practicing, student, and industry veterinarians). There was a difference in anti-HEV prevalence in both swine veterinarians and blood donors among the eight selected states, with subjects from Minnesota six times more likely to be anti-HEV positive than those from Alabama. Age was not a factor in the observed differences from state to state. Anti-HEV prevalence in swine veterinarians and normal blood donors was age specific and paralleled increasing age. The results suggest that swine veterinarians may be at somewhat higher risk of HEV infection than are normal blood donors.

Ataxia and paresis with equine herpesvirus type 1 infection in a herd of riding school horses.

An outbreak of neurologic disease associated with serologic evidence of equine herpesvirus type 1 (EHV-1) infection occurred in a herd of 46 riding school horses. Ataxia and paresis were observed in 14 geldings and 5 barren mares. Eight affected horses had distal limb edema, 1 horse had a head tilt, and 3 others had urinary incontinence. Other clinical signs included fever, depression, and inappetance in 30 horses. Seven horses with neurologic signs were treated with acyclovir. Serum neutralizing antibody titers against EHV-1 increased 4-fold between acute and convalescent samples or exceeded 1:256 in 19 of 44 horses, confirming recent infection. A significantly greater proportion of horses that seroconverted were mares (P = .014). Of the 19 horses exhibiting ataxia and paresis, 17 made a complete recovery, 1 made a partial recovery, and 1 was euthanized.

Exposure of swine to Trichinella spiralis antigen as determined by consecutive ELISAs and western blot.

Exposure of swine to Trichinella spiralis was evaluated using a combination of 3 consecutive enzyme-linked immunosorbent assays (ELISAs) based on larval T. spiralis excretory-secretory antigen as screening test and western blot analysis as confirmatory test. Ninety-three of 32,693 domestic swine sera collected in Georgia over a 5-yr period contained antibodies specific to T. spiralis (prevalence of exposure = 0.28%). The highest prevalence (0.52%) of exposure to T. spiralis was in samples from stockyards and salebarns. Prevalence of exposure in samples from cull sows from 1 slaughter house was 0.38% compared with 0.17% in samples obtained from farms. Pepsin-HCl digestion of diaphragms from 49 swine from 6 seropositive farms revealed 0.01 larvae/g in 4 swine from 3 farms. Determination of T. spiralis infection status of farms appears to be accurately determined with this combination of exploratory ELISAs and confirmatory western blot analysis.

Macrophage inhibitory factor-A3 derived from Mycobacterium avium serovar 2 inhibits candidacidal activity of murine peritoneal macrophages.

Macrophage inhibitory factor-A3 (MIF-A3), a fraction derived from Mycobacterium avium serovar 2 inhibited candidacidal activity in macrophages from C57BL/6, C57BL/10, C3H/HeJ and A/J strains of mice. Inhibition of candidacidal activity was demonstrated at MIF-A3 concentrations ranging from 100-400 micrograms/ml in macrophages without additional stimulators (exception C3H/HeJ macrophages) and in macrophages additionally stimulated with 200 U/ml interferon-gamma, 100 ng/ml phorbol myristate acetate and 0.4 ng/ml E. coli lipopolysaccharide from all mouse strains tested. The decreased candidacidal effect produced by MIF-A3 was dose-dependent and appeared greatest in macrophages treated with phorbol myristate acetate and lipopolysaccharide. This effect was neutralized by the addition of goat anti-MIF-A3 antiserum. Macrophages from the Bcgs mouse strains (C57BL/6 and C57Bl/100 were more sensitive to the effect(s) of MIF-A3 than macrophages from the Bcgr mouse strains (C3H/HeJ and A/J).

Protection of pigs by vaccination of pregnant sows against eastern equine encephalomyelitis virus.

Serum-virus neutralizing antibodies were detected in serum and colostrum of sows vaccinated during pregnancy with commercially available vaccines against eastern equine encephalomyelitis virus (EEEV), and antibodies were detected in serum from nearly all pigs from vaccinated sows following colostrum uptake. Serum-virus neutralizing antibody (SVN) test titers were measured in colostrum and pigs at the next farrowing, and additional vaccination of sows prior to the third farrowing led to elevated SVN titers in serum, colostrum and all pigs. Six pigs from vaccinated sows challenged at 8 to 9 days of age with 1 x 10(6) TCID50 EEEV did not develop the high temperatures or signs of central nervous system disease that 6 pigs from non-vaccinated sows developed. Virus was isolate from blood and oropharyngeal swabs from all pigs from non-vaccinated sows with blood virus titers as high as 9.3 x 10(4) TCID50, while only low levels of virus were detected in blood and oropharyngeal swabs from pigs from vaccinated sows. Virus was also isolated from tonsils collected at necropsy from 3 pigs from non-vaccinated and 1 pig from vaccinated sows. Vaccination of pregnant sows leads to development of maternal antibodies that are transmitted via colostrum to pigs and are protective against clinical EEEV related disease after experimental challenge with EEEV. In addition, vaccination prevents amplification of virus in infected pigs and could result in protection of animals and farm labor in the environment of infected pigs.