The poultry red mite, Dermanyssus gallinae, a potential vector of Erysipelothrix rhusiopathiae causing erysipelas in hens.

Erysipelas is a bacterial disease caused by Erysipelothrix rhusiopathiae, which may infect swine as well as several other species of mammals and birds, including domestic fowl. In poultry, erysipelas may cause sudden high mortality due to septicemia. This communication describes the first isolation of E. rhusiopathiae from the haematophagous poultry red mite, Dermanyssus gallinae DeGeer (Acari: Dermanyssidae), that was collected on three farms where hen erysipelas was diagnosed. The bacteria were isolated from the integument as well as from the interior of the mites. Serotypes 1a and 1b of E. rhusiopathiae found in the mites corresponded with those isolated from the diseased birds. These findings imply that D. gallinae is a potential vector of E. rhusiopathiae. The current lack of effective measures to control D. gallinae causes recurring mite problems in poultry facilities once afflicted by this parasite. Consequently, mites containing E. rhusiopathiae may act as reservoir hosts of this bacterium, allowing it to persist in the poultry house between flock cycles as a source of infection for the replacement pullets. The zoonotic potentials of both E. rhusiopathiae and D. gallinae should also be considered.

Health of laying hens in an aviary system over five batches of birds.

Mortality and health were studied in laying hens kept in an aviary system on a practical scale. All management inputs were done by university staff. Five batches of birds (trials) during a period of 6 years with approximately 4,700 birds per trial were included in the study. The aviary was a three-tiered "Marielund" system divided into 4 pens. Three hybrids, reared on litter with access to perches, were used; Lohmann Selected Leghorn (LSL), Lohmann Brown (LB) and an experimental cross (SLU-1329). The hens were not beak-trimmed. The stocking density was 17 hens/m2 ground floor. Mortality varied between pens and between batches, ranging from normal rates of 3.4% to 7.8%, except in LSL in Trial 2 and LB in Trial 3 where it was much higher (15.6% and 20.9%, respectively). The dominating causes of total mortality were salpingitis and cannibalism. Coccidiosis and lymphoid leucosis contributed significantly to mortality in Trial 2. An infestation with fowl mites (Dermanyssus gallinae) occurred in Trial 1. Feather loss was most severe in LB. Keel bone deviations were recorded at increasing levels by age. Foot abscesses occurred more frequently at 35 weeks than at 55 weeks. LSL was more severely affected than LB and SLU-1329.

Effect of antibiotic growth promoters and anticoccidials on growth of Clostridium perfringens in the caeca and on performance of broiler chickens.

The effects of the growth promoters avoparcin and avilamycin and the ionophore anticoccidials maduramicin, narasin and monensin on the growth of Clostridium perfringens (Cp) in the caeca and on performance of broiler chickens were tested in 2 experiments. The supplements were fed as single feed additives or in some combinations. No clinical signs or lesions caused by coccidia were observed in any of the studies. All supplements had an antibacterial effect on Cp and improved growth rate significantly. Carcass yield of birds fed growth promoters avilamycin or avoparcin was significantly higher compared with birds fed anticoccidials. These data indicate that, what concerns bird performance, during good hygienic conditions supplementation with antibiotic growth promoters may not be necessary when the diet is supplemented with an anticoccidial with antibacterial effects.

Nivalenol in Swedish cereals--occurrence, production and toxicity towards chickens.

Nivalenol has been analysed in Swedish cereals between 1987 and 1990 and it was found in oats (35% of all samples), barley (13%) and wheat (4%), with a high yearly variation. The highest concentration was 4700 micrograms/kg. Nivalenol-producing strains of Fusarium poae were isolated from contaminated samples. Feeding nivalenol to chicks produced no toxic effects at concentrations below 5 mg/kg and only small effects at 6 and 12 mg/kg.

Effects of feeding nivalenol-contaminated diets to male broiler chickens.

In two feeding trials the effect of nivalenol (NIV) on male broiler chickens was studied. A commercial starter diet was provided for ad libitum consumption throughout the whole experiment. The NIV was added to the feed when the birds were 7 d old. Growth and feed consumption were thereafter registered every 5th d during 20 d. In the first trial birds were offered feed containing 0, .5, 2.5, or 5 ppm NIV. The only variable that significantly differed from the control was the concentration of uric acid in plasma, which was increased by 94 and 66%, respectively, in treatment groups 2.5 and 5 ppm. In the second trial, NIV-concentrations of 0, 3, 6, and 12 ppm were used. The weight gain for the 20-d period was decreased by 11% with 6 and 12 ppm. During this period these birds showed a decrease of about 6% in feed consumption and feed conversion efficiency. Gizzard erosions were found in 33% of the birds fed 12 ppm NIV and in 8% of those fed 3 or 6 ppm. No such erosions were found in the control birds. Relatively, the liver weights in the 12 ppm group were reduced more than total body weights. No effects on relative organ weights were found when bursa, spleen, and gizzard were compared to control. In the blood, no change compared to control was found in hematocrit or in the plasma concentration of glucose, calcium, cholesterol, triglycerides, and uric acid, or in the plasma activity of aspartate amino transferase, alanine amino transferase, or gamma glutamyl transpeptidase.

Factors affecting the incidence of necrotic enteritis, caecal carriage of Clostridium perfringens and bird performance in broiler chicks.

Two trials were conducted to study the effects of a competitive exclusion (CE) product BROILACT and the anticoccidial narasin on the incidence of necrotic enteritis (NE), the numbers of Clostridium perfringens (CP) in the caeca of broiler chicks and the performance of the birds. In trial 1 the effects of type of protein and partial replacement of a narasin containing diet with whole wheat were also studied. All groups of chicks were studied up to the point of slaughter at 43 days of age and after evisceration in a processing plant to determine slaughter yield. In trial 1, statistically significant results included the following: CE-treatment reduced total mortality, and incidence of NE, on diet containing animal but not vegetable protein. Caecal carriage of CP was also reduced, while slaughter yield increased. Narasin reduced caecal carriage of CP and increased both growth rate and slaughter yield in both trials. Whole wheat replacement improved feed conversion but reduced bird growth rate. In trial 2, both CE-treatment and narasin influenced feed intake, CE-treatment significantly only at days 22 and 44. Narasin improved feed conversion until 5 weeks of age and CE-treatment did so until 22 days of age. In both trials, there was also an interaction effect indicating that CE-treatment increased slaughter yield for birds that were not fed narasin.

Blue wing disease of chickens: experimental infection with a Swedish isolate of chicken anaemia agent and an avian reovirus.

Isolates of an avian reovirus and chicken anaemia agent (CAA) from a field case of blue wing disease (BWD) in Sweden were inoculated into groups of SPF, one-day-old chicks as follows: Expt 1, an organ suspension from the field case; Expt 2, a selected non-purified reovirus isolate grown in chicken embryo liver cells. Expt 3, a plaque-purified reovirus strain; Expt 4, the CAA isolate from the organ suspension and Expt 5, a combination of reovirus (from Expt 3) and CAA (from Expt 4). The inoculations were given intraperitoneally. In a sixth experiment the isolates were given intramuscularly. The chicks in Expts 1, 2, 5 and 6 became ill after two weeks, and several birds died or were killed when moribund between 13 and 22 days of age. These birds had lesions similar to those found in field cases of BWD, i.e., atrophy of the thymus and the bursa of Fabricius and petechial haemorrhages in the skin. All of them had atrophie bone marrow. The chicks inoculated with the cloned reovirus strain (Expt 3) or CAA alone (Expt 4), did not show any apparent signs of disease. In Expt 4, lesions were found in the thymus, bursa of Fabricius, and bone marrow but to a less severe degree. In Expts 1, 2 and 5 both the reovirus and the CAA were successfully reisolated.

Gizzard erosions as a cause of mortality in White Leghorn chickens.

Increased mortality connected with gizzard erosions has been observed in several flocks of White Leghorn chicks in Sweden. Bacterial infection of the gizzard wall was a common finding in chicks that had died from the disease. Infection with Clostridium perfringens is supposed to be the main cause of mortality, but the primary cause of the gizzard lesions has not been established.