Centennial Review: History and husbandry recommendations for raising Pekin ducks in research or commercial production.

By some accounts, ducks were domesticated between 400 and 10,000 yr ago and have been a growing portion of the poultry industry for decades. Ducks specifically, and waterfowl in general, have unique health, housing, nutrition and welfare concerns compared to their galliform counterparts. Although there have been many research publications in regards to health, nutrition, behavior, and welfare of ducks there have been very few reviews to provide an overview of these numerous studies, and only one text has attempted to review all aspects of the duck industry, from breeders to meat ducks. This review covers incubation, hatching, housing, welfare, nutrition, and euthanasia and highlights the needs for additional research at all levels of duck production. The purpose of this review is to provide guidelines to raise and house ducks for research as specifically related to industry practices.

Serum ovotransferrin as a biomarker of inflammatory diseases in chickens.

Infectious and metabolic disorders are common in poultry and cause stress, poor performance, and mortality that results in considerable economic loss. Identifying the nature of stress in chickens will assist the development of appropriate measures to improve health and welfare. Acute phase proteins are hepatic proteins, the blood concentrations of which change significantly in the event of many health problems including inflammation and physical injuries. Thus, acute phase proteins are used as nonspecific diagnostic markers for various health disorders. Our previous studies showed that serum ovotransferrin (OVT) is an acute phase protein in chickens. Therefore, in the present study, we investigated whether OVT concentration can be a marker of physiological stress using sera from chickens with different infectious and metabolic disorders. A competitive enzyme immunoassay was developed to measure serum OVT concentrations. The results show that with experimentally induced pulmonary hypertension syndrome and tibial dyschondroplasia, there were no significant changes in OVT levels compared with matched controls. In contrast, when chickens were infected with microbes such as the bacterium Escherichia coli, or protozoan parasites such as Eimeria maxima and Eimeria tenella, there was a significant increase in the levels of OVT in the serum. Chickens with spontaneous autoimmune vitiligo also showed a significant increase in blood OVT levels. These studies suggest that blood OVT concentration is modulated under inflammatory and microbial stress and can therefore be used as a diagnostic marker of infection and inflammation in chickens.

The effect of light intensity on the behavior, eye and leg health, and immune function of broiler chickens.

Broilers are typically raised commercially in dim lighting. It has been suggested that providing brighter light intensity could improve health and provide opportunities for more normal behavioral rhythms. We examined the effects of 3 photophase light intensities (5, 50, and 200 lx) on activity patterns, immune function, and eye and leg condition of broilers (n = 753; 6 replicate pens/treatment). Broilers were reared with one of these intensities from 1 to 6 wk of age; photoperiod consisted of 16L:8D with 1 lx intensity during the scotophase. Broilers reared with 5 lx were less active (P = 0.023) during the day than 50 or 200 lx and showed less (P < 0.0001) change in activity between day and night than 50 or 200 lx. There was no difference between treatments for final BW (2.30 +/- 0.02 kg) or for most immune parameters (IgG primary and secondary responses to keyhole limpet hemocyanin, B and T lymphocyte proliferation, plasma lysozyme, haptoglobin, NO, whole blood killing of Escherichia coli and Staphylococcus aureus), but there was a trend (P = 0.072) for a greater IgM response in 50 lx (6.21 titer) than 5 lx (5.78 titer), with 200 lx (5.92 titer) intermediate. There was no effect of light intensity on back-to-front (1.13 +/- 0.01 cm) or side-to-side (1.48 +/- 0.01 cm) diameter of the eyes or on corneal radii (0.82 +/- 0.01 cm), but 5 lx (2.33 +/- 0.07 g) had heavier eyes (P = 0.002) than 50 lx (2.09 +/- 0.04 g) or 200 lx (2.11 +/- 0.04 g). There were no differences in gait score, although 200 lx broilers had more hock and footpad bruising (P = 0.038) but fewer erosions (P = 0.006) than 5 or 50 lx. Increased daylight intensity had little effect on broiler health but resulted in more pronounced behavioral rhythms.

Evaluation of the effectiveness of two infectious bronchitis virus vaccine programs for preventing disease caused by a California IBV field isolate.

Infectious bronchitis virus CA99 serotype was isolated from several broiler flocks in Northern California. The virus caused late-onset respiratory disease and increased airsacculitis condemnation in affected flocks despite the use of an established infectious bronchitis virus vaccination program. An experimental study compared Holland/Arkansas and Massachusetts/Arkansas vaccination protocols to determine the efficacy of commercial infectious bronchitis virus vaccines in reducing respiratory disease and airsacculitis lesions found at processing that were associated with a CA99 field isolate. All vaccination groups were given Massachusetts/Connecticut strains of infectious bronchitis virus vaccines at age 1 day followed by vaccination with either Holland/ Arkansas or Massachusetts/Arkansas vaccine strains at 18 days of age. Birds were challenged at age 31 days with a CA99 field isolate. Gross pathology, histopathology, and virus isolation were evaluated. Chickens vaccinated with Holland/Arkansas had marginally better protection against CA99 challenge than chickens vaccinated with Massachusetts/Arkansas, although differences were not statistically significant.

Predation as a cause of neurologic signs and acute mortality in a pheasant flock.

A flock of approximately 15,000 ring-necked pheasants (Phasianus colchicus) was evaluated for a sudden increase in mortality and acute neurological signs after having been previously diagnosed 3 wk earlier with a chronic respiratory disease of undetermined etiology. Approximately 25 live birds were displaying neurological signs including circling, ataxia, and obtunded behavior and 50 birds were dead. Three birds with neurological signs were submitted for evaluation. Extensive subcutaneous hemorrhage over the head and penetrating puncture wounds through the skull and into the brain were found. Trauma from a wild predatory mammal, most likely the long-tailed weasel (Mustela frenata) that had invaded the pheasant house and expressed surplus killing behavior was determined to be the cause of the acute neurological signs and mortality. The relationship of the chronic respiratory disease to the predation episode was not determined but it is possible that pheasants with severe respiratory disease may have had increased susceptibility to predation.

Effect of infectious bursal disease virus insult on iron, copper, and zinc concentration in liver, bursa of Fabricius, spleen, pancreas, and serum of chickens.

The effect of a systemic disease on the dynamics of iron, zinc, and copper in chickens fed ad libitum was examined by infecting 10-day-old specific pathogen-free chickens with infectious bursal disease virus (IBDV). Liver, bursa of Fabricius, pancreas, spleen, and serum were sampled in 10 controls and 10 challenged chickens at 3-day intervals postinfection (PI) for 15 days. The samples were analyzed using atomic absorption spectroscopy. Serum levels were similar to that reported in the literature. Concentrations of iron and zinc did not change significantly in the pancreas, but there was an increase in copper in infected pancreatic tissue on days 9 and 15 PI. Iron concentration in the spleen showed a significant increase on days 6, 9, and 15 PI, whereas zinc was only significantly increased on day 15 PI. There was no significant change in copper concentrations in the spleens of infected chickens vs. controls. This finding is in line with previously reported data. The results showed that the liver was not a major tissue where iron and zinc were sequestered, as previous data have shown in mammals. Instead, the bursa of Fabricius had significantly increased levels of both iron and zinc in infected tissue vs. control tissue from 9 days PI on. Furthermore, the bursa had increased levels of copper in the latter portion of the study. These findings suggest that the bursa of Fabricius rather than the liver is the major organ for metallic ion sequestering during IBDV infection.

Reliability and validity of a modified gait scoring system and its use in assessing tibial dyschondroplasia in broilers.

1. The gait scoring system for broilers developed by Kestin et al. (Veterinary Record, 131: 190-194, 1992) has been widely used to evaluate leg problems. The many factors and measures associated with this scale have empirically established its external (biological) validity. However, published test-retest (within-observer) reliabilities are poor, and inter-observer reliabilities are unknown. We evaluated several modifications to this scale aimed at improving its objectivity and reliability. 2. Eighteen naïve observers scored a standardised video of birds exhibiting varying degrees of lameness, either using Kestin et al.'s system, or our modified system. 3. Test-retest reliability (0.906) for Kestin et al.'s system was higher than previously reported. Inter-rater reliability was also good (0.892). The modified system offered significantly better test-retest (0.948) and inter-rater reliabilities (0.943), without incurring costs in terms of time taken or difficulty of use. The systems were consistent, assigning individual birds the same score on average. 4. It is concluded that the modified system offers the advantages of reduced error within and between studies. 5. In a second experiment, we used our modified scoring system to examine the relationship between tibial dyschondroplasia (TD) and gait score in 267 selected broilers. 6. Neither the presence nor severity of TD affected gait score, suggesting that, at least in this strain of broilers, other leg problems like slipped tendons or torsional deformities had more influence on gait impairment than did TD.

Isolation of a reovirus from poult enteritis and mortality syndrome and its pathogenicity in turkey poults.

Poult enteritis and mortality syndrome (PEMS) is an acute, infectious intestinal disease of turkey poults, characterized by high mortality and 100% morbidity, that decimated the turkey industry in the mid-1990s. The etiology of PEMS is not completely understood. This report describes the testing of various filtrates of fecal material from control and PEMS-affected poults by oral inoculation into poults under experimental conditions, the subsequent isolation of a reovirus, ARV-CU98, from one of the PEMS fecal filtrates, and in vivo and in vitro studies conducted to determine the pathogenicity of ARV-CU98 in turkey poults. In order to identify a filtrate fraction of fecal material containing a putative etiologic agent, poults were challenged in two independent experiments with 220- and 100-nm filtrates of fecal material from PEMS-negative and PEMS-positive poults. The 100-nm filtrate was chosen for further evaluation because poults inoculated with this filtrate exhibited mortality and significantly lower (P < or = 0.05) body weight and relative bursa weight, three clinical signs associated with PEMS. These results were confirmed in a third experiment with 100-nm fecal filtrates from a separate batch of PEMS fecal material. In Experiment 3, body weight and relative bursa and thymus weights were significantly lower (P < or = 0.05) in poults inoculated with 100-nm filtrate of PEMS fecal material as compared with poults inoculated with 100-nm filtrate of control fecal material. Subsequently, a virus was isolated from the 100-nm PEMS fecal filtrate and propagated in liver cells. This virus was identified as a reovirus on the basis of cross-reaction with antisera against avian reovirus (FDO strain) as well as by electrophoretic analysis and was designated ARV-CU98. When inoculated orally into poults reared under controlled environmental conditions in isolators, ARV-CU98 was associated with a higher incidence of thymic hemorrhaging and gaseous intestines. In addition, relative bursa and liver weights were significantly lower (P < or = 0.05) in virus-inoculated poults as compared with controls. Virus was successfully reisolated from virus-challenged poults but not from control birds. Furthermore, viral antigen was detected by immunofluorescence in liver sections from virus-challenged poults at 3 and 6 days postinfection and virus was isolated from liver at 6 days postinfection, suggesting that ARV-CU98 replicates in the liver. In addition to a decrease in liver weight, there was a functional degeneration as indicated by altered plasma alanine aminotransferase and aspartate aminotransferase activities in virus poults as compared with controls. Although this reovirus does not induce fulminating PEMS, our results demonstrated that ARV-CU98 does cause some of the clinical signs in PEMS, including intestinal alterations and significantly lower relative bursa and liver weights. ARV-CU98 may contribute directly to PEMS by affecting the intestine, bursa, and liver and may contribute indirectly by increasing susceptibility to opportunistic pathogens that facilitate development of clinical PEMS.

Transactivation of latent Marek's disease herpesvirus genes in QT35, a quail fibroblast cell line, by herpesvirus of turkeys.

The QT35 cell line was established from a methylcholanthrene-induced tumor in Japanese quail (Coturnix coturnix japonica) (C. Moscovici, M. G. Moscovici, H. Jimenez, M. M. Lai, M. J. Hayman, and P. K. Vogt, Cell 11:95-103, 1977). Two independently maintained sublines of QT35 were found to be positive for Marek's disease virus (MDV)-like genes by Southern blotting and PCR assays. Sequence analysis of fragments of the ICP4, ICP22, ICP27, VP16, meq, pp14, pp38, open reading frame (ORF) L1, and glycoprotein B (gB) genes showed a strong homology with the corresponding fragments of MDV genes. Subsequently, a serotype 1 MDV-like herpesvirus, tentatively name QMDV, was rescued from QT35 cells in chicken kidney cell (CKC) cultures established from 6- to 9-day-old chicks inoculated at 8 days of embryonation with QT35 cells. Transmission electron microscopy failed to show herpesvirus particles in QT35 cells, but typical intranuclear herpesvirus particles were detected in CKCs. Reverse transcription-PCR analysis showed that the following QMDV transcripts were present in QT35 cells: sense and antisense meq, ORF L1, ICP4, and latency-associated transcripts, which are antisense to ICP4. A transcript of approximately 4.5 kb was detected by Northern blotting using total RNA from QT35 cells. Inoculation of QT35 cells with herpesvirus of turkeys (HVT)-infected chicken embryo fibroblasts (CEF) but not with uninfected CEF resulted in the activation of ICP22, ICP27, VP16, pp38, and gB. In addition, the level of ICP4 mRNA was increased compared to that in QT35 cells. The activation by HVT resulted in the production of pp38 protein. It was not possible to detect if the other activated genes were translated due to the lack of serotype 1-specific monoclonal antibodies.

Protective immunity to infectious bronchitis in broilers vaccinated against Marek's disease either in ovo or at hatch and against infectious bronchitis at hatch.

Two experiments were conducted using commercial broiler chickens to determine if Marek's disease (MD) vaccines HVT/SB-1 and HVT plus CVI-988 given either in ovo or at hatch adversely affected the efficacy of infectious bronchitis (IB) vaccines (Ark and Mass serotypes) given by eyedrop on the day of hatch. Nonvaccinated negative controls and controls that received only IB vaccines were included in each study. Birds were challenged with either infectious bronchitis virus (IBV) Mass-41 or IBV Ark-99 on either day 26 or 27 of age. Protection was assessed 5 days post-IBV challenged by virus isolation from the trachea. The day of hatch mean antibody titer to IBV was 12,668 +/- 4704 and 2503 +/- 3243 by enzyme-linked immunosorbent assay in experiments 1 and 2, respectively. In each study, nonvaccinated controls had a significantly higher (P < or = 0.05) incidence (88%-100%) of IBV challenge virus isolation than did controls vaccinated for IB but not for MD. Analysis of data from both studies showed that protection to IB in groups that received only IB vaccines at hatch ranged from 55.0% to 77.3%, whereas protection to IB in groups receiving both MD and IB vaccines ranged from 50.0% to 95.5%. In both experiments and within IBV challenge serotype, broilers given MD vaccines (in ovo or at hatch) and IB vaccines at hatch had protection rates to IBV challenges that were not significantly less (P < or = 0.05) than IB protection rates of groups that received only IB vaccines at hatch. Analysis of these data shows that administration of high-titered MD vaccines either in ovo or at hatch did not affect the efficacy of an IB vaccination (serotypes Ark and Mass) given by eyedrop at hatch.

Induction of matrix metalloproteinases and collagenolysis in chick embryonic membranes before hatching.

The membranes surrounding the chick embryo undergo striking morphological changes before hatching, which include structural degradation of the allantoic membrane. The fibrillar collagen content of the membranes declined by embryonic day (ED) 20 (the day of hatching). By ED 19, a 55-kDa matrix metalloproteinase (MMP) activity appeared in the extraembryonic fluid, and by ED 20 there was substantial 55-kDa MMP activity in embryonic membrane extracts. Reverse transcription-polymerase chain reaction was employed to clone a partial cDNA representing the chicken homologue of MMP-13, a 55- to 57-kDa enzyme. MMP-13 mRNA dramatically increased in abundance in embryonic membranes by ED 19, reaching a peak on ED 20. Introduction of the MMP inhibitor batimastat into the extraembryonic fluid prevented the structural changes in the embryonic membranes before hatching. We conclude that, like mammalian fetal membranes, chick embryonic membranes undergo terminal remodeling before hatching, in part as a result of increased MMP activity. The chicken egg system represents a novel in vivo model for exploring biochemical events leading to embryonic membrane remodeling prior to birth and to test inhibitors of MMPs for their ability to prevent collagenolysis and fetal membrane rupture.

Dietary fish oil or lofrin, a 5-lipoxygenase inhibitor, decrease the growth-suppressing effects of coccidiosis in broiler chicks.

Broiler chicks were fed a diet containing 4% of either corn oil or fish oil from 3 to 14 d of age. From Days 15 to 23, half of the chicks in each dietary treatment were fed Lofrin (an experimental 5-lipoxygenase inhibitor) at 33 micrograms/kg feed. The remaining chicks within each dietary treatment were the untreated controls. At 24 d of age, half of the chicks within each diet-Lofrin treatment group were each infected with 4.6 x 10(4) sporulated Eimeria tenella oocysts, resulting in a 2 x 2 x 2 factorial arrangement of treatments. Body weight gain, feed consumption, and feed conversion efficiency were determined throughout the study. At 27 d of age, blood, liver, and ceca were sampled. Plasma tumor necrosis factor and hemopexin, hepatic fatty acid composition, and cecal inflammatory cell infiltration were determined. Liver fatty acid composition tended to reflect that of the diet. Chicks fed fish oil had livers that were enriched in (n-3) polyunsaturated fatty acids (PUFA) at the expense of (n-6) PUFA. Chicks fed fish oil gained body weight more rapidly than those fed corn oil. Infection of chicks with Eimeria decreased body weight gain of chicks fed corn oil, but not of chicks fed fish oil. The addition of Lofrin to the corn oil diets abrogated the growth-suppressing effects of infection, although there was no Lofrin effect among chicks fed fish oil. There was a diet by Lofrin interaction in which Lofrin treatment of birds fed corn oil decreased feed consumption and increased feed conversion efficiency, but had no effect on chicks fed diets containing fish oil. Plasma hemopexin was greater, but tumor necrosis factor was lower, in chicks fed fish oil than in chicks fed corn oil. Eimeria infection significantly increased cecal inflammatory cell infiltration across all dietary treatments. There were no clear relationships between growth rate or efficiency and the severity of the inflammatory response to Eimeria infection, as indicated by hemopexin levels and cecal inflammatory scores. These results indicate that Lofrin or fish oil, both of which modify eicosanoid metabolism, attenuate the growth-depressing effects of an Eimeria tenella infection.

Pathogenicity of attenuated infectious bronchitis viruses for oviducts of chickens exposed in ovo.

A fixed effects, completely randomized factorial design was used to study the effect of infectious bronchitis virus (IBV) inoculation at two different exposure ages and three postinoculation (PI) durations on chick oviduct pathology. Maternal antibody-positive chicken embryos at 18 days of embryonation (ED) and newly hatched chicks were inoculated with an IBV vaccine (V-IBV) or with an IBV vaccine that had been serially passaged 21 times in chick kidney tissue culture (P-IBV). Hatchability of eggs inoculated with V-IBV at 18 ED was significantly lower (27%) than eggs that were not inoculated with IBV or were inoculated with P-IBV (45-58%, P < 0.01). Chicks from all treatment groups survived to 5 days after hatch. Pathologic changes in the oviduct were evaluated at 9, 18, and 27 days PI by light microscopy. Inoculation of V-IBV and P-IBV in the presence of maternal antibodies did not result in any oviduct pathology at 9, 18, and 27 days PI. Respiratory clinical signs, however, were observed in 61% and 5% of chicks inoculated with V-IBV at 18 ED and at hatch, respectively. Respiratory clinical signs were not observed in control birds, birds inoculated with P-IBV at 18 ED, or birds inoculated with P-IBV at hatch.

Efficacy of a novel infectious bursal disease virus immune complex vaccine in broiler chickens.

Two experiments were conducted to test the efficacy of a novel infectious bursal disease virus (IBDV) vaccine in broiler chickens with maternal IBDV immunity. The IBDV vaccine was formulated by mixing IBDV strain 2512 with bursal disease antibodies (BDA) to produce the IBDV-BDA complex vaccine. In Expt. I, 1-day-old Cobb x Cobb broiler chickens were vaccinated subcutaneously with either IBDV-BDA or commercial live intermediate IBDV vaccine (vaccine A) or were left unvaccinated. In Expt. 2, the vaccine A group was not included; instead, IBDV strain 2512 was included. Chickens were maintained in isolation houses. On day 28 (Expt. 1) and day 32 (Expt. 2) of age, chickens from each group were challenged with a standard USDA IBDV (STC strain) challenge. Challenged and unchallenged chickens were evaluated for their bursa/body weight ratios and antibody titers 3 days post-challenge. Bursae collected from Expt. 2 were examined histologically to evaluate bursal lesions and confirm gross examination. None of the unvaccinated chickens was protected against the challenge virus as evidenced by the presence of acute bursal lesions (edema/hemorrhage). All chickens receiving the IBDV-BDA complex or the IBDV strain 2512 (Expt. 2) were protected from the challenge virus as evidenced by no acute bursal lesions. Additionally, chickens receiving the IBDV-BDA complex vaccine or the IBDV strain 2512 had antibody titers to IBDV, indication the presence of an active immune response. In Expt. 1, chickens vaccinated with vaccine A and challenged had bursal lesions similar to those observed in the unvaccinated, challenged chickens. These chickens also showed no indication of active immunity against the virus. These results suggest that the 1-day-of-age-administered IBDV-BDA complex vaccine can induce active immunity and protection against a standard IBDV challenge in the face of variable levels of maternal IBDV immunity.

Lack of protection against avian cholera by vaccination with recombinant P6-like protein from Pasteurella multocida.

The gene encoding the P6-like protein of Pasteurella multocida was cloned in the baculovirus expression system. Baculovirus-expressed recombinant protein was used to parenterally immunize 6-wk-old Nicholas broad-breasted white turkeys. Turkeys developed significant antibody titers to the recombinant protein as measured by enzyme-linked immunosorbent assay. Two weeks after the last immunizing injection, vaccinated turkeys were placed in contact with turkeys infected with P. multocida strain P1059, as were nonvaccinated control birds. No differences occurred in percent mortality between the two groups. We conclude that parenterally administered recombinant P6-like protein does not protect turkeys from avian cholera.

Association between the Rfp-Y haplotype and the incidence of Marek's disease in chickens.

Certain haplotypes at the major histocompatibility (B) complex (Mhc) of the chicken provide an easily demonstrated influence on tumor formation following infections with Marek's disease virus (MDV). Recognition that there is a second histocompatibility complex of genes in the chicken, Rfp-Y, comprised of Mhc class I and class II genes, some of which are at least transcribed, evokes the question of whether this gene complex might also influence the outcome of MDV infections. To test this hypothesis, pedigree-hatched chicks in families from the original Rfp-Y-defining stock in which three Rfp-Y and two B system haplotypes are segregating were challenged with the RB1B strain of MDV. Birds with the Y3/Y3 genotype were found to have 2.3 times the risk of developing a tumor compared with birds with other Rfp-Y genotypes combined (P <0.02). Additionally, birds carrying the BR9/B11 genotype had 2.3 times the risk of tumor formation, relative to birds with the B11/B11 genotype (P <0.02). We found no evidence for an interaction between genotypes within the B and Rfp-Y systems. These data provide evidence that Rfp-Y haplotypes, as well as B haplotypes, can significantly influence the outcome of infection with MDV.

Determination of optimum formulation of a novel infectious bursal disease virus (IBDV) vaccine constructed by mixing bursal disease antibody with IBDV.

A novel vaccine against infectious bursal disease virus (IBDV) has been developed. The new vaccine was constructed by mixing bursal disease antibody (BDA) contained in whole antiserum with live IBDV before lyophilization. To establish various formulations of BDA and IBDV, several BDA doses between 5 units and 80 units of BDA/50 microliters were mixed with 100 EID50/50 microliters of IBDV suspension in Expt. 1; in Expt. 2, several IBDV doses between 10 EID50/50 microliters and 977 EID50/50 microliters of IBDV suspension were mixed with 24 units of BDA/50 microliters. Vaccine preparations were administered subcutaneously to the nape of 1-day-old specific-pathogen-free (SPF) chicks. Safety, potency, and immunogenicity of the different vaccine formulations were evaluated using bursal weight, bursal gross examination, and IBDV antibody titer. Some bursae were examined histologically to confirm gross examinations. Several vaccine formulations were safe and efficacious and met the safety, potency, and immunogenicity criteria. A vaccine construct of 100 EID50 mixed with 24 units of BDA was selected as the release dose. When administered at 1 day of age, the novel vaccine allows for delayed infection of the bursa until after days 6-8 of age in SPF chicks, while initiating potency and immunogenicity to an IBDV challenge. The addition of BDA to the IBDV results in a complex vaccine that allows for safer immunization in SPF birds than under administration of the vaccine virus without BDA.

Embryo vaccination of chickens with infectious bronchitis virus: histologic and ultrastructural lesion response and immunologic response to vaccination.

Chicken embryos 18 days of age and newly hatched chicks were vaccinated with an infectious bronchitis virus (IBV) vaccine (V-IBV) or with an IBV vaccine that had been serially passaged 40 times in chick kidney tissue culture (P-IBV). Immunologic and pathologic changes in the chicks were compared at selected intervals until the 35th day. Pathologic changes were evaluated by light, transmission, and scanning electron microscopy. Immunologic changes were assayed by a constant virus-diluting serum plaque-reduction test in chicken cell cultures, by 51Cr-release cytotoxicity assays, and by phytohemagglutination (PHA) responses. Embryos vaccinated with P-IBV and 1-day-old chicks vaccinated with V-IBV had similar transient lesions that were confined primarily to the trachea. Embryo vaccination and posthatch vaccination induced similar primary and secondary antibody responses in chicks. It was concluded that neither vaccination technique consistently influenced PHA response of whole blood cells or natural killer cell reactivity of spleen effector cells. Additionally, effector cells cytotoxic to IBV-infected target cells were not detected in chicks vaccinated as embryos or at hatch. The pathologic and immunologic effects of vaccination with P-IBV were comparable to those induced by conventional vaccination of chicks.

In ovo pathogenicity of Mycoplasma iners strain Oz.

Embryonating chicken eggs were inoculated with the type strain (PG30) of Mycoplasma iners and with an additional strain of this species designated Oz. Marked gross and histopathologic lesions were observed in the embryos inoculated with strain Oz but not in those infected with strain PG30. Gross lesions were manifested by an enlargement of one or more joints that often contained a caseous exudate, both in the joint space and periarticularly. In the order of frequency, the most common lesions were found in the following joints: tibiotarsal, distal humoral, proximal humoral, femoral, mandibular, tibiofemoral, and phalangial. Similar caseous foci were also seen in the liver and, rarely, in the heart. Histologically, the most prominent lesion found in the joints and viscera was a multifocal caseous necrosis accompanied by the formation of granulomas. Many joints had progression of the inflammatory cells outward from the joint spaces along the periosteal surfaces, and the articular cartilages contained erosions and focal necrosis.

Mycoplasma infection in a commercial goat dairy caused by Mycoplasma agalactiae and Mycoplasma mycoides subsp. mycoides (caprine biotype).

A commercial dairy goat herd of 600 animals experienced sudden onset of arthritis/polyarthritis, clinical mastitis, and sudden death in does. The offending infectious agents were Mycoplasma agalactiae and M. mycoides subsp. mycoides (caprine biotype). The disease syndrome began approximately 4 weeks following the 1) introduction into the herd of a lactating doe with no apparent clinical signs and 2) a breakdown of proper hygienic conditions in the milking parlor. Over a period of 3 weeks, 90 does (15%) either died or were culled because of arthritis/polyarthritis and mastitis. A management decision resulted in only the does affected with M. mycoides subsp. mycoides being submitted for necropsy; those affected with M. agalactiae, which were in a different "string," were not submitted for evaluation. Gross necropsy of the does affected with M. mycoides subsp. mycoides showed purulent discharges from the udders, enlarged supramammary lymph nodes, enlarged and firm spleens, and swollen livers. Microscopic findings were characterized by a loss of vascular integrity and diffuse fluid leakage in multiple organs. Antibiotic therapy with tylosin was attempted but was not successful. The outbreak was terminated following the removal or segregation of affected does and implementation of hygienic conditions in the milking parlor.