Foot pad dermatitis develops at an early age in commercial turkeys

1. A field experiment was conducted to identify the macroscopic and histological changes associated with the development of foot pad dermatitis (FPD) in growing turkeys. Two affected and two unaffected turkeys were sampled weekly from 1 to 8 and at 10 and 21 weeks of age. 2. At one week old, birds with external signs of FPD (surface skin discolouration) showed abnormal cellular changes of the foot pad integument. As the flock aged the reactions intensified, with one sample exhibiting a fully developed macroscopic lesion at 3 weeks. 3. Major pathological changes had occurred by 6 weeks and all turkeys with external signs of lesions had fully developed microscopic inflammatory cellular lesions. From 6 weeks of age onwards lesions were increasingly numerous and became more overtly necrotic. 4. Externally normal foot pads showed microscopic evidence of lesions after the turkeys reached 4 weeks. 5. We conclude that FPD lesions become severe over a short period of time and at a very early age.     

Femoral fractures in a young male Turkey breeder flock

Twenty-two 32-to-35-wk-old male turkeys from a commercial breeding flock were presented to the California Veterinary Diagnostic Laboratory System, Fresno Branch, with a clinical complaint of lameness and increased mortality. Necropsy findings included a unilateral, closed oblique fracture involving the femur in 12 birds. Ten complete femoral fractures had periosteal new bone adjacent to and bridging the fracture. Periosteal callus formation, in this case, suggested that preexisting lesions preceded complete fracture of the femur. Factors such as selection for heavy body weight, lack of exercise, and handling might have contributed to the development and promotion of complete fractures.     

Suspected Reticuloendotheliosis in Turkeys with Cutaneous Lesions Reminiscent of Fowl Pox

Twelve turkeys from a flock of 2,500 had cutaneous lesions somewhat resembling fowl pox. Lymphoid-like tumors were evident in livers and spleens. Closer examination of cutaneous lesions, and histopathological examinations indicated skin lesions were also infiltrative and not unlike reticuloendotheliosis. Electron micrographs revealed the presence of C-type virus particles.     

Skeletal muscle lesions in turkeys associated with the feeding of monensin

The feeding of monensin as a coccidiostat in three separate flocks of turkeys was associated with increased mortality, posterior paresis, and a skeletal muscle myopathy. Mortality attributed to the disease was 1.65%, 1.86%, and 4.80% in the three flocks. Samples of monensin-supplemented feed fed to the flocks when showing clinical signs contained 88, 85, and 106 g/ton of complete feed, respectively. Clinically, the turkeys showed posterior paresis, inability to rise, incoordination, reluctance to move, and leg trembling and weakness. Necropsy findings included consistent lesions of pallor within the type I muscles of the legs, wings, and backs. Microscopic lesions included myofiber degeneration and necrosis with massive cellular proliferation interpreted as sarcolemmal nuclei proliferation. Occasional axonal degeneration with loss of axons was present in peripheral nerves embedded in the damaged musculature. In the youngest flock, multifocal areas of acute coagulation necrosis of the myocardium were also present. These outbreaks occurred following intake of monensin in the complete feed at levels considered therapeutic; however, no associated predisposing clinical condition, drug/toxin interaction, or excessive monensin levels in the feed could be demonstrated.     

Pasteurella multocida recovered from live turkeys: prevalence and virulence in turkeys

Swabs of the oropharynges of 801 live turkeys (621 meat birds and 180 breeders), collected from 15 flocks that had experienced an outbreak of fowl cholera and from 12 non-outbreak flocks, were screened for the presence of Pasteurella multocida. Turkeys from outbreak flocks were sampled within 2 to 9 weeks of the outbreak. Forty-nine isolates of P. multocida were recovered from turkeys in 11 of the outbreak flocks, and none were recovered from turkeys in non-outbreak flocks. Isolation rates varied from 0 to 72% of turkeys sampled in a flock. Nineteen isolates were tested for virulence by injecting them intravenously into turkeys, and 14 were lethal. Results demonstrated that for purposes of disease control, meat birds in fowl-cholera-outbreak flocks should be considered carriers of potentially virulent P. multocida for the life of the flock.     

Interaction of ionophore and vitamin E in knockdown syndrome of turkeys

Monensin and vitamin E concentrations, as well as histopathology of skeletal muscles and myocardium, were evaluated in broad-breasted white turkeys kept in commercial facilities. Turkeys with knockdown syndrome had myopathy of skeletal muscles, but no lesions in the myocardium. Generally, concentration of monensin in serum was highest in turkeys diagnosed with knockdown syndrome given more than 90 mg/kg of monensin in the diet, followed by turkeys diagnosed with knockdown syndrome given <90 mg/kg of monensin in the diet, healthy turkeys fed a diet that contained <90 mg/kg of monensin, and finally healthy turkeys fed a diet free of monensin (not detectable). However, the concentration of monensin was highly variable within each group, and the median was lower than the average. Vitamin E concentrations in the livers varied from low-normal to below normal and were statistically higher in healthy turkeys fed a diet free of monensin than in the livers of birds from the 3 groups exposed to monensin. This suggests that the concentration of monensin in serum positively correlates to the severity of clinical signs and pathology and to the amount of monensin in the feed. Although the methodology developed to detect serum monensin concentrations is beneficial and accurate for case investigations, it is recommended that several samples from each flock be evaluated because of variation within a flock. The current study also suggests that monensin in the feed could induce lower concentrations of vitamin E in the liver of turkeys and can predispose the turkeys to knockdown syndrome.     

Conium maculatum (poison hemlock) toxicosis in a flock of range turkeys

Five 20-week-old tom turkeys from a flock of range turkeys were presented for examination; the flock had a history of salivation, tremors, paralysis, and increased mortality. Necropsy revealed numerous seeds identified as seeds from Conium maculatum (poison hemlock) within the crop, proventriculus, and gizzard. Histopathologic alterations were limited to catarrhal enteritis. Clinical signs of Conium maculatum toxicosis abated after the turkeys were removed from their range, which was infested with poison hemlock.     

Cartilage lesions associated with shaky-leg lameness in turkeys

Shaky-leg lameness is a poorly defined, mild to very severe, painful lameness occurring mainly in 10-to-18-week-old fast-growing male turkeys. Since there are no significant gross or microscopic lesions in early or uncomplicated cases, the cause of the lameness is likely soft-tissue (muscle or tendon) pain. A case history of a flock problem of shaky-leg lameness is described, and it is suggested that stiffness and inactivity secondary to footpad dermatitis in these turkeys was responsible for the severe shaky-leg lameness in the flock. The cartilage lesion described is an avascular lesion and appeared to be the result of inactivity rather than the cause of lameness in these turkeys.     

A case of salinomycin intoxication in turkeys

A flock of 4287 heavy hybrid turkey hens were accidentally fed broiler premix containing salinomycin sodium and suffered a 34.5% death loss. Measures taken to ensure food safety for the remaining flock and consumer food safety included feed record studies, on-farm veterinary consultation, diagnostic laboratory studies, and CgFARAD and CFIA consultation. The remaining turkeys were processed 3 weeks after the initial toxicosis with no evidence of lesions that would render the product unfit for human consumption.     

Recurrent transient paresis in a turkey flock.

Recurring episodes of extreme leg weakness and associated mortality were documented in a turkey flock at 8 to 15 weeks of age. Flock mortality attributed to posterior paresis was approximately 12%, or 4800 of 40,000 turkeys. Four of six open-confinement units were affected. Gross and histological examinations revealed no significant lesions. Immunology and virology were uninformative. There were no significant differences in serum chemistry between clinically affected and normal turkeys. Testing of feed, water, soil, and tissues revealed no common toxicants. Isolation and supportive care for affected turkeys, both in the laboratory and in the field, frequently resulted in full recovery. Injection of a test group of affected turkeys with Type C botulism antitoxin appeared to enhance recovery. However, repeated attempts to detect botulism toxin in serum, liver, or cecal contents using mouse bioassay procedures were unsuccessful.     

Prevalence of skin lesions in turkeys at slaughter

1. The aims of this study were (i) to evaluate the prevalence of welfare-related cutaneous lesions in turkeys at the end of the rearing period and (ii) to study the correlations between lesions.

2. The percentage of lesions in each flock was determined by observation at the slaughterhouse. Sixty flocks were investigated in 13 slaughterhouses between April and July 2006.

3. All flocks showed a high proportion of turkeys with footpad lesions, with 40·7% of turkey flocks having severe footpad dermatitis. A significant number of feet had swelling of the footpad and deviated toes (60·0% and 21·4% respectively). Arthritis was observed in 25·4% of the carcases and an average of 30·1% had breast buttons on the keel.

4. Positive correlations were found between evidence of feather pecking and arthritis, toe deviations and swelling of the footpad. Deviated toes, swelling of the feet and feather pecking were negatively linked to the most severe scratches (P? 5. A method is proposed to assess turkey welfare at the slaughterhouse based on several criteria: footpad lesions, arthritis, severe scratches, deviated toes, swelling of the footpad and breast buttons.     

Dermal necrosis caused by Pasteurella multocida infection in turkeys

Severe dermal necrosis caused by Pasteurella multocida Serotype 1 was diagnosed in three dressed turkey carcasses and two live turkeys from a commercial flock. The dressed carcasses were among several condemned at a processing plant. The isolate, P. multocida Serotype 1, produced progressive dermal necrosis when experimentally inoculated into injured skin of turkeys. The organism was reisolated from the dermal lesions. The turkey houses were found to be infested by mice; the skin injury and infection with P. multocida probably originated from mouse bites.     

Ulcerative cholecystitis produced by 3-nitro-4-hydroxy-phenylarsonic acid toxicosis in turkey poults

Naturally occurring ulcerative cholecystitis was present in a flock of 21-day-old turkey hens that were accidentally given at least 0.004% 3-nitro-4-hydroxy-phenylarsonic acid (3-NITRO) in their water for 2 days. Similar lesions were reproduced by administering 0.002% 3-NITRO to 2-day-old turkey poults for 6 days. Turkeys 31 days old were given up to 0.004% 3-NITRO in their water for 6 days, but no gall bladder ulcers were present in these poults. The toxicity to turkeys of 3-NITRO in the water appears to be age-dependent.     

Late clinical expression of lameness related to associated osteomyelitis and tibial dyschondroplasia in male breeding turkeys.

A sudden outbreak of lameness related to transport stress is described in a flock of male breeding turkeys. Most of the affected turkeys exhibited obvious unilateral leg disorders. All were affected with tibial or metatarsal dyschondroplasia with at least one lesion associated with a large focus of necrosis. By histological examinations, bone lesions showed the typical feature of osteomyelitis. The inflammatory bone lesions appeared at only single isolated sites and were always associated with obvious sequestra of dyschondroplastic retained cartilage. Osteomyelitis seems to be an unexpected acute complication of previous dyschondroplasia in relation with different breeding stress situations. The resulting pain of the associated lesions could be the main cause of clinical expression of lameness. The pathogenesis of the phenomenon remains uncertain.     

Infectious sinusitis in turkeys at Ibadan, Nigeria

Thirty out of 70 imported broad-breasted white turkeys with severe sinusitis were both culturally and serologically positive for Mycoplasma gallisepticum. Infectious sinusitis due to M. gallisepticum was therefore diagnosed. A low mortality of 5.7% of the total flock was recorded. This appears to be the first published report on M. gallisepticum isolation in turkeys in Nigeria.     

Mycoplasma gallisepticum infection in wild-type turkeys living in close contact with domestic fowl

Mycoplasma gallisepticum was isolated from 2 wild-type turkeys (Meleagris gallopavo) and 1 domestic turkey living in close contact on a farm in Tehama County, California. Sinusitis was detected in 2 of 14 wild-type turkeys and in 1 of 12 feral broad-breasted bronze turkeys, but in none of several chickens on the premises. The entire mixed flock was captured, sinus aspirates were collected from affected birds, and blood samples were obtained from all birds for serologic testing. Blood samples also were obtained from 10 domestic turkeys on adjacent premises from which breeding stock had been borrowed. The M gallisepticum isolated from sinus aspirates was typed and inoculated into susceptible chickens, resulting in airsacculitis. California wild turkeys with and without histories of exposure to domestic fowl and wild turkeys shipped into California from Texas for release were tested for antibodies to M gallisepticum, using the plate agglutination test. Evidence of M gallisepticum infection was not found in wild turkeys at any location other than the original premises.     

Salinomycin poisoning in point-of-lay turkeys

Salinomycin poisoning occurred in a flock of 700 point-of-lay turkeys; 400 birds died over 7 days as a result of consuming feed contaminated with 50 ppm salinomycin. No gross lesions were detected. Histologic evidence of a myopathy was most readily detected in leg muscles of turkeys 5 to 7 d after ingesting salinomycin. Feeding trials were undertaken and individual susceptibility to the drug was found to vary greatly. In affected birds the plasma concentrations of creatine kinase (CK) and aspartate aminotransferase (AST) were found to be in the range of 500,000 to 2,500,000 IU/l and 9000 to 25,000 IU/l, respectively. The marked increase in the plasma activities of these enzymes preceded histological evidence of segmental muscle necrosis.     

Effect of dietary protein deficiency on the performance of turkeys and chickens

Two field occurrences of protein-deficiency disease were reported in turkeys and chickens. The disease caused unthriftiness, poor growth, and the exhibition of pica in flocks of 15-week-old pedigree large white turkeys, and it resulted in a sharp drop (18%) in egg production in a flock of 60-week-old white leghorn layers. In each case, the disease was cured by replacing the protein-deficient diet with a protein-sufficient one.     

Respiratory disease (rhinotracheitis) of turkeys in Brittany, France. III. Interaction of multiple infecting agents

A candidate breeder flock of turkeys was studied during and after an outbreak of rhinotracheitis. Laboratory studies revealed the presence of three pathogens during the acute phase of the disease. These agents were hemorrhagic enteritis virus (HEV), paramyxovirus type 2 (PMV2), and chlamydia. Twenty-five turkeys in the flock were individually identified, and blood samples from these birds were collected for serological studies each week for 21 weeks. The serological results revealed high titers for HEV and chlamydia but very low titers for PMV2.