Six isolates of Mycoplasma synoviae, identified as WVU 1853, K1968, K1858, 92D8034, F10-2AS, and FMT, were compared for pathogenicity in broiler chickens. Specific-pathogen-free chickens were inoculated, in two groups of 20, with each isolate by footpad or eyedrop inoculation at 1 day of age and were examined at necropsy 7, 14, 28, and 42 days postinoculation. Specimens were taken for histopathology, culture, polymerase chain reaction assay, and hemagglutination-inhibition serology. Isolates were grouped according to pathogenicity on the basis of differences in lesion development and tissue distribution in the respiratory system, other viscera, and the skeletal system. K1968 (pathogenic) induced lesions in all sites examined in both the footpad and eyedrop inoculation groups. It was detected in all sites following footpad inoculation and in all sites except viscera following eyedrop inoculation. WVU 1853, K1858, and 92D8034 (moderately pathogenic) induced lesions and were detected in all sites following footpad inoculation. With eyedrop inoculation, lesions were identified only in upper and lower respiratory sites, and organisms were detected only in upper respiratory sites. F10-2AS (moderately pathogenic) was similar; however, footpad inoculation failed to induce visceral lesions or permit organism detection in any site. F10-2AS was detected in upper and lower respiratory tissues following eyedrop inoculation. FMT (mildly pathogenic) induced only upper respiratory lesions when either footpad or eyedrop inoculation was used, and detection was restricted to upper respiratory sites following eyedrop inoculation. These results are useful in comparative evaluations of the virulence of other M. synoviae isolates and form a basis for characterization of virulence factors of M. synoviae.

Mycoplasma synoviae (MS) species-specific primers selected from the 16S rRNA sequence were evaluated by polymerase chain reaction (PCR). The MS primers were MS-1 (5'-GAAGCAAAATAGTGATATCA-3') and MS-2 (5'-GTCGTCTCCGAAGTTAACAA-3'). Analysis of cultures of avian mycoplasmas using the MS PCR indicated 100% specificity and sensitivity: 55 individual isolates of MS tested PCR-positive, and 44 isolates of eight other species of avian mycoplasmas tested PCR-negative. The MS PCR will detect 100 colony-forming units of MS. Analysis of 122 flock data sets indicated a sensitivity for the MS PCR test of 82% and a specificity of 100% as determined by comparison with culture, serology (serum plate test, hemagglutination-inhibition, enzyme-linked immunosorbent assay), epizootiology, and history.

Five hundred sixty-nine Salmonella were isolated out of 4745 samples from poultry products, poultry, and poultry environment in 1999 and 2000 from the Pacific northwest. These Salmonella were identified to their exact source, and some were serogrouped, serotyped, phage typed, and tested for antibiotic sensitivity. Food product samples tested included rinse water of spent hens and broilers and chicken ground meat. Poultry environment samples were hatchery fluff from the hatcheries where eggs of grandparent broiler breeders or parent broiler breeder eggs were hatched and drag swabs from poultry houses. Diagnostic samples were of liver or yolk sac contents collected at necropsy from the young chicks received in the laboratory. Of these samples tested, 569 were Salmonella positive (11.99%). Ninety-two Salmonella were serogrouped with polyvalent somatic antisera A-I and the polymerase chain reaction. Somatic serogroups B and C comprised 95.25% of all the Salmonella. Out of a total of 569 positive samples, 97 isolates of Salmonella were serotyped. A total of 16 serotypes and an unnamed Salmonella belonging to serogroup C1 were identified. The Salmonella serotypes were heidelberg (25.77%); kentucky (21.64%); montevideo (11.34%); hadar and enteritidis (5.15% each); infantis, typhimurium, ohio, and thompson (4.12% each); mbandaka and cerro (3.09% each); senftenberg (2.06%); berta, istanbul, indiana, and saintpaul (1.03% each); and an unnamed monomorphic Salmonella (2.06%). Ninety-two Salmonella were tested for drug sensitivity with nine different antimicrobials. All of the 92 Salmonella were resistant to erythromycin, lincomycin, and penicillin except one sample (S. berta), which was moderately sensitive to penicillin. All of the tested Salmonella were susceptible to sarafloxacin and ceftiofur. The percentages of Salmonella susceptible to sulfamethoxazole-trimethoprim, gentamicin, triple sulfa, and tetracycline were 97.83%, 92.39%, 86.96%, and 82.61%, respectively.

An epidemiological study of the prevalence of mycoplasmal conjunctivitis in the house finch (Carpodacus mexicanus) was conducted in Auburn (Alabama, USA) between March 1998 and February 1999. Clinical disease was observed in 4% of the 1,214 finches trapped and examined. This rate is comparable to the average annual prevalence observed in this population since 1996, although the prevalence of clinical disease observed in the peak months of September through November was lower than in previous years. Clinically ill birds were observed in all months of the study. To estimate the prevalence of recovering and asymptomatic, infected birds, we tested a subset of 334 house finches serologically for exposure to Mycoplasma gallisepticum (MG) using the serum plate agglutination (SPA) assay. The prevalence of clinical disease in this subsample was slightly higher (7%) than in the entire sample, reflecting the fact that the serological survey was initiated in the late summer when the prevalence of MG infection peaks in our study population and a sampling bias for symptomatic birds. The serological survey indicated that 13% of this subpopulation had been exposed to MG. We also tested 46 of 334 finches by polymerase chain reaction (PCR) to detect MG in seropositive, asymptomatic birds. Use of the PCR in conjunction with the SPA detected six asymptomatic, infected birds that may represent potential carriers or birds in the early stages of infection. The decreasing prevalence of clinical disease observed during the peak months suggests a changing host-parasite relationship. Continued surveillance of this population, employing both clinical observation and serological analysis will be useful in characterizing these changes over time.

Abstract. Beginning in summer 1977 and continuing through four consecutive seasons, we examined lame limb joints from 106 partially fattened cattle and 28,235 pairs of occipital condyles from fully fattened cattle for osteochondrosis. Of the 106 lame cattle, nine (8.5%) had characteristic lesions, usually in their stifle joints, and of the 28,235 atlanto-occipital joints, 1063 (3.8%) had lesions on their condyles.Slices of affected articular cartilage and subjacent bone were studied radiographically and histologically. Radiographs showed subchondral defects and epiphyseal "cyst-like" lesions, and histologic sections showed disarrayed and degenerated chondrocytes. Splits occurred along osteochondral junctions or in adjacent cartilage or bone. Some bone trabeculae had been replaced by fibrous tissue that, in some areas, extended deep into epiphyses.Osteochondrosis, a degenerative change in articular and growth plate cartilage of rapidly growing animals, is characterized clinically by prolonged limb lameness, and anatomically by disarray of chondrocytes, inadequate provisional calcification of cartilage, failure of endochondral ossification, retention of cartilage, and splits in cartilage and bone [3].Beginning in summer 1977 and continuing through four consecutive seasons, we examined small samples of limb joints and large samples of atlanto-occipital joints from slaughtered cattle for arthropathies and found this disease. Materials and MethodsMost cattle were Hereford, Angus, Charolais, and their crosses. Steers predominated. Their ages at slaughter ranged from 15 to 18 months. All had been fed high concentrate rations in feedlots of eastern Colorado, western Nebraska or western Kansas. They were slaughtered at one of three companies under federal inspection. Cattle with osteochondrosis were of two categories: those with limb joint lesions and lameness, and those with atlanto-occipital joint lesions and no recognized clinical signs. Some had become lame during the fattening period and were slaughtered prematurely for recovery of value. All others had been fattened through 90 to 140 days.During each of the four seasons, a sample of at least 25 lame cattle and a sample of nearly 529

Pigeon circovirus was identified by polymerase chain reaction (PCR) in young pigeons belonging to 12 different lofts. Viral DNA was extracted from formalin-fed, paraffin-imbedded tissues containing primarily bursa and occasionally liver and spleen with a commercial kit. PCR primers were selected from a published sequence for columbid circovirus and evaluated in a PCR assay. The histopathologic examination of various tissues revealed basophilic globular intracytoplasmic inclusions in the mononuclear cells of the bursa of Fabricius and occasionally in the spleen characteristic for a circovirus. Transmission electron microscopy of a few bursas of Fabricius revealed virus particles measuring 18-21 nm. All the samples were negative by PCR for psittacine beak and feather disease (PBFD) virus and chicken infectious anemia virus. The primers for both pigeon circovirus and PBFD virus did not react in PCR with the chicken anemia virus DNA. Most of the circovirus-infected pigeons had concurrent infections of Escherichia coli, Salmonella, Pasteurella, Aspergillus, candidiasis, nematodiasis, or capillariasis.

A new facility was designed to hold 1.8 million birds in 10 houses; chickens were placed in five of the houses, and the remaining five houses were under construction when this outbreak occurred. An increase in mortality was reported in five houses; however, mortality in house 7 was quite high. Well-fleshed birds were suddenly found dead without a significant drop in egg production. The middle and distal intestines were distended with gas, congested, thin walled, atonic, and bluish or pale in color with sloughed mucosa in some places. Necrotic enteritis was diagnosed as the cause of increased mortality. The ingesta in the crop occasionally contained flies. The 4-wk mortality in house 7 was 6.55% with a loss of 10,898 chickens. The 4-wk mortality rate in the other houses ranged from 0.54% to 1.98%. The houses affected with necrotic enteritis were treated for coccidiosis with amprolium because low numbers of the oocysts were present in the intestinal specimens of some of the chickens. Household bleach was added to the water at a dilution of one part bleach to 1040 parts water to control bacterial contamination. The fly (Musca domestica) population was out of control. Clostridium perfringens was isolated from the alcohol-washed macerated flies caught from houses 4 and 7. Dead flies were often seen in the feed troughs. The chickens may possibly have had C. perfringens infection as a result of consumption of dead flies or their secretions/excretions. The alcohol-washed, macerated, clarified fly extract from the affected houses caused death in 11 inoculated mice and paralysis in one mouse. Similarly, illness and mortality were present in four mice inoculated with clarified intestinal contents. The bacterium isolated on anaerobic culture was identified as C. perfringens by polymerase chain reaction. The disease was brought under control after straw was added and mixed in with the litter. As a result, the litter temperature increased, causing a decrease in the fly population. This study suggests that flies in the poultry houses acted as mechanical transmitters of C. perfringens and that the development of necrotic enteritis was by ingestion of bacteria present in the flies and their secretions/excretions.

Abstract. Of 30,444 larynges from fattened cattle at three companies, 3,985 (13.1%) had contact ulcers or ulcer scars in the mucous membranes over the vocal processes and medial angles of the arytenoid cartilages. The incidence was higher in cattle fed during fall than in cattle fed during other seasons. We hypothesize: 1. that some feedlot cattle develop acute mucositis from mixed infections with species of Pasteurella, Haemophilus, Mycoplasma, and viruses in the nose, pharynx, and larynx; 2. that reflex coughing and swallowing accelerate the rate of larynx closure; and 3. that the closures erode the swollen membrane over the vocal processes and medial angles of the arytenoid cartilages and thus produce primary contact ulcers.Laryngeal ulcers, either unilateral or bilateral, develop in mucous membranes over the arytenoid cartilages. These lesions, apparently benign and lacking clinical manifestations, have received slight attention in science laboratories and infrequent mention in veterinary literature. In acute stages, however, they may inhibit eating, retard weight gain, and acquire infections, and thus cause economic losses to producers, packers, and consumers.Beginning in summer 1977 and continuing through four consecutive seasons, we examined larynges from fattened cattle at slaughter. This report enumerates and describes the ulcers. Materials and MethodsThis investigation was conducted at three eastern Colorado meat packing establishments: Companies 1, 2, and 3. Each company killed about 2,000 cattle per work day throughout the year. All operations were conducted under federal inspection.Most cattle were Herefords, Angus, Charolais, and their crosses. They had been fed for 90 to 140 days on high-concentrate rations in feedlots in eastern Colorado, western Nebraska. and western Kansas. Their ages at slaughter ranged from 15 to 18 months. Most carcasses were graded good or choice. Soon after arriving at a feedlot, most cattle were vaccinated against infectious bovine rhinotracheitis and leptospirosis, implanted with anabolic pellet, and 667