Cleavage of huntingtin by apopain, a proapoptotic cysteine protease, is modulated by the polyglutamine tract.

Apoptosis has recently been recognized as a mode of cell death in Huntington disease (HD). Apopain, a human counterpart of the nematode cysteine protease death-gene product, CED-3, has a key role in proteolytic events leading to apoptosis. Here we show that apoptotic extracts and apopain itself specifically cleave the HD gene product, huntingtin. The rate of cleavage increases with the length of the huntingtin polyglutamine tract, providing an explanation for the gain-of-function associated with CAG expansion. Our results show that huntingtin is cleaved by cysteine proteases and suggest that HD might be a disorder of inappropriate apoptosis.

Lessons learned from three avian influenza simulation exercises in the southwest of France.

The Southwest of France raises different species of poultry. These production activities present structural vulnerabilities to severe infectious diseases such as highly pathogenic avian influenza. Indeed, many farms have free-range flocks, multi-age and multi-species productions, while being located near wild bird migratory corridors. These factors may partly explain the H5 virus epidemics that occurred between 2015 and 2021. Their serious economic and technical consequences and psychological impact have generated solidarity, collective learning and operational cohesiveness among all poultry professionals. Consequently, a decision was made to conduct annual simulation exercises for a major health event in order to maintain a high level of vigilance and responsiveness within different poultry sectors. Three exercises took place, in 2017, 2018 and 2019, in semi-real conditions (real dates and compressed time) and according to different scenarios. They took place outside an epidemic context and have in common to focus on the initial phase of the crisis (suspicions, results of preliminary analyzes), which is critical to assess the reactivity of industry personnel in order to mitigate infectious disease spread. The preparation of the simulation exercises was based on a common methodology. They were created by an organizing team and each included up to 60 people (industry personnel, observers and auditors). These simulations highlighted several critical points: poultry professionals have detailed knowledge of the field, but this information can only be effectively obtained and used if there is already a poultry industry decision-making structure in place (with good networking); there is a need (1) for better information sharing within the industry; (2) to develop an assistance structure for producers directly involved in a crisis; and (3) to increase collaboration with State services in peacetime. Finally, several technical issues were raised regarding control zones; blocking poultry movements; production site quarantine; depopulation strategies; self-financing capacity of the poultry industry in the absence of governmental involvement; and enhanced mapping tools with real-time traceability of animal transportation.

Canadian experiences with avian influenza: a look at regional disease control--past, present, and future.

Over the past 5 yr, the poultry industry in Canada has had a few H5 or H7 avian influenza (AI) epidemics. An analysis of these outbreaks by government officials highlighted the need to establish a better partnership between those responsible for controlling the disease and public health officials responsible for protecting the public and those participating in eradication efforts. These officials also agreed that compensations had to be reviewed, that national biosecurity standards needed to be established to better prevent AI, that a national mortality disposal plan was needed, and finally that the current emergency disease management protocols had to be reviewed. Industry representatives stressed the need for early detection and reporting; for more effective tools for decision making, including using local expertise for trace-back activities and quick interventions; for better communications within industry, but mainly between industry and governmental authorities at the federal, provincial, and municipal levels; and finally, for better planning to minimize the impact of eradication efforts on poultry production and for the recovery following the epidemic. These observations triggered a series of initiatives. A National Office of Animal Biosecurity was created by federal authorities, with the mandate to establish national biosecurity standards. A Canadian Animal Health Surveillance Network was also put in place to improve the capacity of early detection of the disease and to increase the surge capacity of the Canadian laboratory system. Wildlife and commercial poultry AI surveillance programs have also been put in place. Provincial poultry grower organizations have established AI control and eradication plans that are increasing their ability to intervene early and to assist government authorities once AI is confirmed in the field. This includes the creation of industry incident command centers with emphasis on confidentiality agreements between government and industry organizations and effective grower assistance before, during, and after an epidemic.

Experimental infection of chickens and turkeys with Mycoplasma gallisepticum reference strain S6 and North Carolina field isolate RAPD type B.

During an epidemic of mycoplasmosis in chicken and turkey flocks in North Carolina between 1999 and 2001, isolates of Mycoplasma gallisepticum (MG) from affected flocks were characterized by random amplification of polymorphic DNA (RAPD), and eight distinct RAPD types were identified. MG RAPD type B accounted for more than 90% of the isolates and was associated with moderate-to-severe clinical signs and mortality. The virulence of MG RAPD type B for chickens and turkeys was compared with sham-inoculated negative controls and MG S6 (a virulent strain)-inoculated positive controls. Clinical signs occurred in chickens and turkeys inoculated with either MG RAPD type B or MG S6. However, they were not as frequent or severe as those seen in naturally affected flocks, and there was no mortality in the experimental groups. Based on gross and microscopic findings, MG RAPD type B was equal to or more virulent than MG S6. All MG-inoculated birds were culture and PCR positive at 7 and 14 days postinoculation (PI). Among serological tests, the serum plate agglutination test was positive for the majority of chickens and turkeys (58%-100%) infected with either strain of MG at both 7 and 14 days PI. The hemagglutination inhibition test was negative for all birds at 7 days PI and positive for a few chickens (8%-17%) and several turkey sera (40%-60%) at 14 days PI. Only a single serum was positive by enzyme-linked immunosorbent assay (an MG S6-infected turkey) at 14 days PI.

Purification and catalytic properties of human caspase family members.

Members of the caspase family of cysteine proteases are known to be key mediators of mammalian inflammation and apoptosis. To better understand the catalytic properties of these enzymes, and to facilitate the identification of selective inhibitors, we have systematically purified and biochemically characterized ten homologues of human origin (caspases 1 - 10). The method used for production of most of these enzymes involves folding of active enzymes from their constituent subunits which are expressed separately in E. coli, followed by ion exchange chromatography. In cases where it was not possible to use this method (caspase-6 and -10), the enzymes were instead expressed as soluble proteins in E. coli, and partially purified by ion exchange chromatography. Based on the optimal tetrapeptide recognition motif for each enzyme, substrates with the general structure Ac-XEXD-AMC were used to develop continuous fluorometric assays. In some cases, enzymes with virtually identical tetrapeptide specificities have kcat/Km values for fluorogenic substrates that differ by more than 1000-fold. Using these assays, we have investigated the effects of a variety of environmental factors (e.g. pH, NaCl, Ca2+) on the activities of these enzymes. Some of these variables have a profound effect on the rate of catalysis, a finding that may have important biological implications.

Cell death attenuation by 'Usurpin', a mammalian DED-caspase homologue that precludes caspase-8 recruitment and activation by the CD-95 (Fas, APO-1) receptor complex.

Apoptotic cell suicide initiated by ligation of CD95 (Fas/APO-1) occurs through recruitment, oligomerization and autocatalytic activation of the cysteine protease, caspase-8 (MACH, FLICE, Mch5). An endogenous mammalian regulator of this process, named Usurpin, has been identified (aliases for Usurpin include CASH, Casper, CLARP, FLAME-1, FLIP, I-FLICE and MRIT). This protein is ubiquitously expressed and exists as at least three isoforms arising by alternative mRNA splicing. The Usurpin gene is comprised of 13 exons and is clustered within approximately 200 Kb with the caspase-8 and -10 genes on human chromosome 2q33-34. The Usurpin polypeptide has features in common with pro-caspase-8 and -10, including tandem 'death effector domains' on the N-terminus of a large subunit/small subunit caspase-like domain, but it lacks key residues that are necessary for caspase proteolytic activity, including the His and Cys which form the catalytic substrates diad, and residues that stabilize the P1 aspartic acid in substrates. Retro-mutation of these residues to functional caspase counterparts failed to restore proteolytic activity, indicating that other determinants also ensure the absence of catalytic potential. Usurpin heterodimerized with pro-caspase-8 in vitro and precluded pro-caspase-8 recruitment by the FADD/MORT1 adapter protein. Cell death induced by CD95 (Fas/APO-1) ligation was attenuated in cells transfected with Usurpin. In vivo, a Usurpin deficit was found in cardiac infarcts where TUNEL-positive myocytes and active caspase-3 expression were prominent following ischemia/reperfusion injury. In contrast, abundant Usurpin expression (and a caspase-3 deficit) occurred in surrounding unaffected cardiac tissue, suggesting reciprocal regulation of these pro- and anti-apoptotic molecules in vivo. Usurpin thus appears to be an endogenous modulator of apoptosis sensitivity in mammalian cells, including the susceptibility of cardiac myocytes to apoptotic death following ischemia/ reperfusion injury.

Validation of a poultry biosecurity survey.

A questionnaire for farm managers was designed, to obtain information regarding biosecurity on Ontario commercial broiler chicken and turkey operations, and then pre-tested. The questions that could be validated were verifiable by seeing the facility, by using farm records or by interviewing technical personnel other than the survey respondent. The survey was validated using a convenience sample of 24 farms from two companies. For 15 questions with dichotomous responses, the sensitivity ranged from 16.7 to 100%; the specificity ranged from 0 to 100%. For example, fences and gates seen during the farm visit were not accurately reported on the survey (poor sensitivity). Chance-corrected agreement was low (kappa < 0.4) for 34 questions, fair to good (0.4 < kappa < 0.8) for 25 questions, and excellent (kappa > 0.8) for seven questions. The percent agreement for questions where only one of the possible options was observed on validation ranged from 60.9 to 100%. Five questions with continuous numeric variables were analysed. A difference was observed (P < 0.1) between the survey and validation data for three questions regarding the number of birds, the bird sources and the downtime between flocks. In spite of pre-testing, the lack of clear wording and the absence of definitions for technical terms appeared to reduce validity. Response bias seems to be an issue with biosecurity surveys. The value of validating questionnaires before their use in epidemiologic research is confirmed.

The relation of egg specific gravity to the incidence of spontaneous cardiomyopathy in tom turkeys.

The specific gravity and weight of eggs were determined for two groups of 600 eggs each, originating from Nicholas and British United Turkey of America (BUTA) turkey breeder flocks. A total of 137 Nicholas and 190 BUTA toms hatched from these eggs were used for the experiment. At days 21, 33, 40, 47, 56, and 61, toms that showed retarded growth were euthanatized, along with a corresponding number of normal birds. Both groups were measured for body weight, heart weight, separate weights of left and right ventricles, and combined atrial weight. At market age, the remaining toms were weighed, and the hearts were checked at processing for lesions characteristic of spontaneous turkey cardiomyopathy (STC). STC was found in 10.2% of Nicholas and 8.4% of BUTA toms. No correlation could be found between specific gravity of eggs and incidence of STC. Body weights of affected toms were reduced during the growing period. At processing, 2.8% of toms had lesions of STC, and mean body weight was 1298 g lower than average. The ratios of combined atrial weight:body weight, right ventricular weight:body weight, left ventricular weight:body weight, and total heart:body weight were significantly higher at all times in affected toms than in controls, and the differences were the greatest at 3 weeks of age.

Impact of stocking density, breed, and feathering on the prevalence of abdominal skin scratches in broiler chickens.

Associations between abdominal skin scratches and stocking density, strain of birds, and degree of feathering were investigated in a clinical trial. Four hundred eighty 1-day-old male broiler chicks from two different strains (A and B) were assigned to four groups: 1) high density (0.07 m2/bird) and strain A, 2) high density and strain B, 3) normal density (0.14 m2/bird) and strain A, and 4) normal density and strain B. Birds were examined for scratches and feathering at 28, 35, and 42 days of age. Two outcomes were considered for scratches: presence (yes/no) and severity (severe [if a deep cut or at least three superficial cuts were present]/not severe). Only the examination at 35 days of age was blind. The outcome "scratches" was significantly associated with stocking density at all ages (P < or = 0.0001), strain A at 28 days of age (P = 0.0480), and poor feathering at 35 days of age (P < or = 0.0001). The outcome "severe scratches" was significantly associated with stocking density at 35 (P = 0.0003) and 42 days of age (P = 0.0021), strain A at 35 (P = 0.0089) and 42 days of age (P = 0.0306), and poor feathering at 35 days of age (P = 0.0018). Stocking density, strain of birds, and degree of feathering could be considered as potential risk factors for abdominal scratches in broiler chickens.

Farm management risk factors associated with cellulitis in broiler chickens in southern Ontario.

A mail survey of 171 farms with broiler chicken flocks processed in a single processing plant in southern Ontario was conducted during the period July-August 1993 as part of a retrospective study. The population farm prevalence of cellulitis was 31/10,000 birds. The survey provided information about the management of broiler chickens in southern Ontario and allowed investigation of the association between cellulitis and management risk factors. Univariate and multivariate analyses were performed to examine the relationship between a binary outcome (high/low prevalence) and management risk factors using logistic regression. Cellulitis was positively associated (P < or = 0.05) with male and mixed (males and females) flocks, use of straw as litter, certain feed companies, use of zinc bacitracin as a growth promoter, and other diseases diagnosed at the processing plant. Total down time was negatively associated with cellulitis.

High mortality and growth depression experimentally produced in young turkeys by dual infection with enteropathogenic Escherichia coli and turkey coronavirus.

Six-day-old turkeys were inoculated with turkey coronavirus (TCV) and an enteropathogenic Escherichia coli (EPEC) (isolate R98/5) that were isolated from poult enteritis and mortality syndrome (PEMS)-affected turkeys. Turkeys inoculated with only R98/5 did not develop clinically apparent disease, and only mild disease and moderate growth depression were observed in turkeys inoculated with only TCV. Turkeys dually inoculated with TCV and R98/5 developed severe enteritis with high mortality (38/48, 79%) and marked growth depression. R98/5 infection resulted in attaching/effacing (AE) intestinal lesions characteristic of EPEC: adherence of bacterial microcolonies to intestinal epithelium with degeneration and necrosis of epithelium at sites of bacterial attachment. AE lesions were more extensive and were detected for a prolonged duration in dually inoculated turkeys compared with turkeys inoculated with only R98/5. An apparent synergistic effect in dually inoculated turkeys was indicated by increased mortality, enhanced growth depression, and enhanced AE lesion development. The results suggest that TCV promoted intestinal colonization by R98/5; however, R98/5 did not appear to alter TCV infection. The present study provides a possible etiologic explanation for PEMS.

Enhancement of enteropathogenic Escherichia coli pathogenicity in young turkeys by concurrent turkey coronavirus infection.

In a previous study, turkey coronavirus (TCV) and enteropathogenic Escherichia coli (EPEC) were shown to synergistically interact in young turkeys coinfected with these agents. In that study, inapparent or mild disease was observed in turkeys inoculated with only TCV or EPEC, whereas severe growth depression and high mortality were observed in dually inoculated turkeys. The purpose of the present study was to further evaluate the pathogenesis of combined TCV/EPEC infection in young turkeys and determine the role of these agents in the observed synergistic interaction. Experiments were conducted to determine 1) effect of EPEC dose, with and without concurrent TCV infection, and 2) effect of TCV exposure, before and after EPEC exposure, on development of clinical disease. Additionally, the effect of combined infection on TCV and EPEC shedding was determined. No clinical sign of disease and no attaching and effacing (AE) lesions characteristic of EPEC were observed in turkeys inoculated with only EPEC isolate R98/5, even when turkeys were inoculated with 10(10) colony forming units (CFU) EPEC (high dose exposure). Only mild growth depression was observed in turkeys inoculated with only TCV; however, turkeys inoculated with both TCV and 10(4) CFU EPEC (low dose exposure) developed severe disease characterized by high mortality, marked growth depression, and AE lesions. Inoculation of turkeys with TCV 7 days prior to EPEC inoculation produced more severe disease (numerically greater mortality, significantly lower survival probability [P < 0.05], increased frequency of AE lesions) than that observed in turkeys inoculated with EPEC prior to TCV or simultaneously inoculated with these agents. Coinfection of turkeys with TCV and EPEC resulted in significantly increased (P < 0.05) shedding of EPEC, but not TCV, in intestinal contents of turkeys. These findings indicate that TCV infection predisposes young turkeys to secondary EPEC infection and potentiates the expression of EPEC pathogenicity in young turkeys.

Escherichia coli cellulitis: experimental infections in broiler chickens.

The objectives of this study were to evaluate the role of trauma to the skin in development of Escherichia coli cellulitis and to compare the abilities of three cellulitis isolates (O78, O115, O21,83), one airsacculitis isolate (untypable) and one fecal isolate (O86) of E. coli to induce cellulitis in broiler chickens. Forty-eight 4-week-old commercial broiler chickens were housed in groups of six in eight battery cages. For five groups, the skin on the left side of the abdominal region of chickens was traumatized by scratching with a 22-gauge needle, then contaminated with a swab dipped in a broth culture of one of the five E. coli isolates. For chickens in the remaining three groups, an avian cellulitis culture (O115, O21,83) or sterile broth was applied to intact skin. The experiment was duplicated. All birds were euthanatized 10-13 days postinoculation. No lesion developed in chickens in which the skin had not been traumatized. Among the traumatized birds, cellulitis isolates induced characteristic lesions of cellulitis in 86% of the birds, whereas airsacculitis and fecal isolates induced lesions in 42% and 8% of birds, respectively. Severe or moderate gross pathologic changes were found in 86% and microscopic pathologic changes were found in 88% of birds inoculated with cellulitis isolates; the corresponding percentages for the airsacculitis isolate were 25% and 17%. This study demonstrated that trauma to the skin is necessary for initiating disease and that strains of E. coli of serotypes epidemiologically associated with cellulitis are highly virulent in experimental infection.

Characteristics of Escherichia coli isolates from avian cellulitis.

The purpose of this study was to characterize Escherichia coli isolates from avian cellulitis, particularly with respect to the occurrence of potential virulence factors. At slaughter, five broilers with lesions of cellulitis were selected from each of 20 farms from among the broilers processed. One hundred E. coli isolates from the lesions were characterized with respect to serotype; biotype; drug susceptibility; plasmid profile; ability to produce aerobactin, colicin, colicin V, and hemolysin; and cytotoxicity for Vero cells and chicken fibroblasts. The same properties were determined from a collection of 25 E. coli from the feces of chickens. Serotyping showed that, among the cellulitis isolates, 23 belonged to O group 78, 14 belonged to O2, eight belonged to O115, and seven belonged to O(21.83); 25 were untypable. Isolates from a single farm typically belonged to three to five O groups. More than half of the fecal isolates were untypable, and the rest were distributed among seven O groups. Biotype, drug-resistance pattern, and plasmid profile could not be used as markers of avian cellulitis E. coli. No plasmid was detected in 12% of cellulitis isolates and 48% of fecal isolates. No isolate was hemolytic or showed cytotoxic effects. Aerobactin was produced by 90% of cellulitis isolates, and colicin was produced by 85% of these isolates; the corresponding percentages for the fecal isolates were 16% and 40%. Production of colicin V was detected in 21% of cellulitis isolates and 24% of fecal isolates.(ABSTRACT TRUNCATED AT 250 WORDS)

Prevalence of enteropathogenic Escherichia coli in naturally occurring cases of poult enteritis-mortality syndrome.

Enteropathogenic Escherichia coli (EPEC) previously were identified in poult enteritis-mortality syndrome (PEMS)-affected turkeys and associated as a cause of this disease. In the present study, the prevalence of EPEC in PEMS-affected turkeys was examined retrospectively with archived tissues and intestinal contents collected from 12 PEMS-affected turkey flocks in 1998. Formalin-fixed intestinal tissues were examined by light and electron microscopy for attaching and effacing (AE) lesions characteristic of EPEC, and frozen (-75 C) intestinal contents were examined for presence of EPEC. Escherichia coli isolates were characterized on the basis of epithelial cell attachment, fluorescent actin staining (FAS) test, and presence of E. coli attaching/effacing (EAE), shigalike toxin (SLT) type I, SLT II, and bundle-forming pilus (BFP) genes by polymerase chain reaction procedures. EPEC isolates were examined for pathogenicity and ability to induce AE lesions in experimentally inoculated young turkeys. AE lesions were identified by light microscopy in Giemsa-stained intestines from 7 of 12 PEMS-affected turkey flocks. Lesions consisted of bacterial microcolonies attached to epithelial surfaces with epithelial degeneration at sites of attachment and inflammatory infiltration of the lamina propria. Electron microscopy confirmed the identity of AE lesions in six of seven flocks determined to have AE lesions by light microscopy. EPEC were identified in 4 of 12 flocks on the basis of the presence of EAE genes a nd absence of SLT I and SLT II genes; all isolates lacked BFP genes. EPEC isolates produced AE lesions and variable mortality in turkeys coinfected with turkey coronavirus. In total, EPEC were associated with 10 of 12 (83%) naturally occurring PEMS cases on the basis of identification of AE lesions and/or EPEC isolates. These findings provide additional evidence suggesting a possible role for EPEC in the pathogenesis of PEMS.

Description of cellulitis lesions and associations between cellulitis and other categories of condemnation.

A total of 110 broiler flocks processed in a single processing plant in southern Ontario were studied for purposes of describing the cellulitis lesions and investigating possible associations between cellulitis and other categories of condemnation at the processing plant. Two hundred and ninety-five carcasses condemned for cellulitis were examined. They came from 65 of the 110 flocks. The lesions tended to be unilateral with most carcasses (87%) having one lesion. The majority of the lesions (92%) were located on the abdomen. Almost 65% of the lesions were large (> or = 8.1 cm2), and 27% were medium (2.1-8.0 cm2). On the basis of gross appearance, 69% of the lesions were classified as severe, 26% moderate, and 5% mild. Of 149 lesions examined histologically, 74% were classified as chronic, 21% ongoing, and 5% mild-acute. Condemnation data from the 110 broiler flocks were analyzed using Poisson regression. Simple relationships were examined between a count outcome (number of cellulitis-condemned carcasses per flock) and other categories of condemnation and average bird weight. Cellulitis was significantly associated with average bird weight (P = 0.0018), Escherichia coli-related conditions (SEROSITIS; P < or = 0.0001), ascites (P = 0.0004), cyanosis (P < or = 0.0001), valgus varus deformity (P < or = 0.0001), REJECT (combined carcass condemnations for bruising, mutilation, and contamination; P = 0.0003), and the interaction terms "average bird weight and ascites" (AVWT*ASCIT; P < or = 0.0001) and "average bird weight and cyanosis" (AVWT*CYAN; P < or = 0.0001). Average bird weight, SEROSITIS, ascites, cyanosis, valgus varus deformity, and AVWT*ASCIT were the only significant factors after adjusting for clustering. No association was observed between cellulitis and emaciation and dead on arrival. Variables significantly associated with cellulitis in the multivariate analysis could be considered as potential predictors. These predictors may share common risk factors predisposing broiler chickens to cellulitis.

A prospective study of cellulitis in broiler chickens in southern Ontario.

This study investigated the associations among cellulitis and hatchery, farm, and abattoir factors. Forty-four broiler flocks from 24 farms located in southern Ontario were followed from hatching to processing. Poisson regression was used to analyze the data. Cellulitis as a count outcome (CELLCOUNT) was significantly associated (P < or = 0.05) with the hatchery of origin, strain of birds, farm size, type of litter, lighting system, total down time, prevalence of abdominal scratches, Escherichia coli-related conditions (SEROSITIS), ascites, and valgus varus deformity. However, only farm size, abdominal scratches, SEROSITIS, ascites, and valgus varus deformity were significant (P < or = 0.05) after adjusting for clustering. No significant associations were found between cellulitis and source of eggs, sex, average bird weight, feed company, growth promoter, or stocking density. Factors significantly associated with cellulitis in this study could be considered as potential risk factors for cellulitis in broiler chickens in southern Ontario.

Mortality patterns associated with poult enteritis mortality syndrome (PEMS) and coronaviral enteritis in turkey flocks raised in PEMS-affected regions.

Poult enteritis mortality syndrome (PEMS) is an economically devastating disease. To date, many questions about the syndrome remain unanswered, including its cause, transmission of causative agent(s), and control methods. Turkey coronavirus (TCV) infection has been associated with some outbreaks of PEMS, with areas having a higher prevalence of TCV infection also experiencing an increased incidence of PEMS. This study was designed to establish mortality patterns for flocks experiencing excess mortality and TCV infection in PEMS-affected regions and to delineate the possible role of TCV in PEMS-affected flocks. Fifty-four commercial turkey flocks on farms in areas with and without a history of TCV infection were monitored for weekly mortality and for antibodies to TCV. Flocks were chosen on the basis of placement dates and were monitored from day of placement until processing. All flocks were tested for TCV by an indirect fluorescent antibody assay. PEMS status was determined with the use of the clinical definition of mortality greater than 2% during any 3-wk period from 2 wk of age through the end of brooding due to unknown cause. Of the 54 flocks, 24 remained healthy, 23 experienced PEMS, and 7 tested positive for TCV but did not experience PEMS. Ten flocks experienced PEMS and tested positive for TCV, whereas 13 flocks experienced PEMS and did not test positive for TCV. Four health status groups were evident: healthy, PEMS positive, TCV positive, and PEMS + TCV positive. Distinct mortality patterns were seen for each of the four health status groups. Whereas TCV was associated with PEMS in 43% of PEMS cases, 13 cases (57%) of PEMS did not involve TCV. Additionally, 7 out of 17 cases of TCV (41%) did not experience excess mortality (PEMS) at any time during brooding of the flock. The results of this study indicate that TCV can be associated with PEMS but is neither necessary nor sufficient to cause PEMS.

Poult enteritis complex.

Poult enteritis complex (PEC) is a general term that encompasses the infectious intestinal diseases of young turkeys. Some diseases, such as coronaviral enteritis and stunting syndrome, are relatively well characterised, while others, such as transmissible viral enteritis, poult growth depression and poult enteritis mortality syndrome, remain ill-defined. All forms of PEC are multifactorial, transmissible and infectious. Salient clinical features include stunting and poor feed utilisation that result from enteritis. In the more severe forms, runting, immune dysfunction and mortality are reported. Gross and microscopic lesions of enteritis are present in all forms but tend to be non-specific. Other lesions may be present, depending on the agents involved. The basic pathogenesis involves the following: a) alteration of the intestinal mucosa, generally by one or more viruses infecting enterocytes; b) inflammation; c) proliferation of secondary agents, usually bacteria. Non-infectious factors interplay with infectious agents to modulate the course and severity of disease. Diarrhoea is believed to be primarily osmotic because of maldigestion and malabsorption, but may also have a secretory component. Transmission is primarily faecal-oral. No public health significance is recognised or suspected. Prevention is based on eliminating the infectious agents from contaminated premises and preventing introduction into flocks. This is accomplished by an effective cleaning, disinfection and biosecurity programme. All-in/all-out production or separate brooding and finishing units are helpful. Control may require regional co-ordination among all companies producing turkeys, especially if the production is highly concentrated, and a quarantine programme for more severe forms of PEC. No vaccines or specific measures for controlling the organisms involved in PEC are available. Treatment is supportive for the viral component, while antibiotics, especially those with efficacy against Gram positive bacteria, may help to reduce the impact to bacterial infections. Evidence suggests that PEC occurs wherever turkeys are raised commercially, but this is not well documented and distribution of the various organisms that have been associated with PEC is largely unknown. The disease causes enormous economic loss, mostly from failure of the turkey to reach its genetic potential.

Changes in the susceptibility of Actinobacillus pleuropneumoniae to antimicrobial agents in Quebec (1981-1986).

An important reduction in the in vitro efficacy of spectinomycin and chloramphenicol was recorded between 1981 and 1986 against the causal agent of porcine pleuropneumonia Actinobacillus. Antimicrobial susceptibility tests were carried out by use of Kirby-Bauer disk diffusion technique on a total of 723 isolates of Actinobacillus pleuropneumoniae. Results did not agree with those of other reports in which a constant susceptibility to any of the antimicrobial agents tested was reported with serotype 2 isolates. The ability to acquire drug resistance may differ from one serotype to another.