Botulism in chickens associated with elevated iron levels.

Clostridium botulinum type C toxicosis was diagnosed by the mouse inoculation test in two outbreaks of botulism in commercial broiler and roaster chickens. One case involved 7-wk-old commercial roaster chickens, and the other involved 15-day-old commercial broiler chickens. A definitive point source for preformed C. botulinum exotoxin was not identified in either case investigation. Elevated iron concentrations in the drinking water and/or feed may have presented a significant risk factor that may have resulted in intestinal proliferation of C. botulinum and subsequent botulism.

Histopathology and epidemiology of condemnations due to squamous cell carcinoma in broiler chickens in North Carolina.

Squamous cell carcinoma (SCC) lesions were confirmed by histopathology in 94% of 176 carcasses condemned for SCC during 8-hour shifts at four different processing plants. Lesions in the remaining carcasses were diagnosed as focal ulcerative dermatitis. SCC lesions were confined to the skin; no metastasis or invasion of underlying muscle was present. Monthly prevalence of SCC condemnations at processing was obtained from two plants for a 1-year period and from two additional plants for 3-year periods. Overall study prevalence of SCC varied between 0.03% and 0.09% of total condemnations. Servicemen were found not to have an effect on SCC condemnations for the only company that had these data available. Chronological trends were evaluated for SCC condemnations. A trigonometric model predicted 6-month cycles for one processing plant over a 3-year period. The same model was used to describe 6-month cycles present in the last 12 months of a 3-year observation period in a different processing plant. Chronologic trends were evaluated qualitatively for the two other processing plants.

Salt toxicosis in commercial turkeys.

Salt toxicosis was confirmed in a flock of 20,000 thirteen-week-old tom turkeys experiencing an increase in mortality. Clinical signs included polydipsia, diarrhea, ataxia, incoordination, tremors that progressed to depression, sternal and lateral recumbency accompanied by torticollis, and death. Mortality over a 5-day period was 6.7%. Necropsy lesions included pallor and dehydration of pectoral muscles, hepatic congestion, and fluid-filled small and large intestines. Microscopic lesions consisted of bilaterally symmetrical areas of necrosis within the cerebral hemispheres accompanied by vascular congestion and edema, as well as hyalinization of the glomerular capillary walls of the kidney and eosinophilic granular casts in the renal tubules. Average salt concentration in the feed from affected houses with 8.04%.

Decreased egg production in turkeys experimentally infected with eastern equine encephalitis virus or Highlands J virus.

Turkey breeder hens were experimentally infected with strains of eastern equine encephalitis (EEE) virus or Highlands J (HJ) virus previously isolated from turkey hens experiencing decreased egg production. Depression and inappetance were observed on day 1 postexposure (PE) in hens inoculated with either EEE virus or HJ virus, and egg production fell in each virus-inoculated group from approximately 75% to less than 20% within 2-3 days PE. Egg production remained depressed (less than 20%) for 15 days in EEE-virus-inoculated hens and for 7 days in HJ-virus-inoculated hens. EEE virus and HJ virus were recovered from various tissues on days 1-5 PE, and virus was detected in eggs laid on days 2-5 PE. The findings of this study confirm that EEE virus and HJ virus are potential causes of decreased egg production in turkey breeder hens.

Egg-production drop in turkeys associated with alphaviruses: eastern equine encephalitis virus and Highlands J virus.

Alphaviruses were isolated from tracheas of turkey breeders in two North Carolina flocks experiencing a severe drop in egg production. Highlands J virus was isolated from one of the breeder flocks, in which production decreased by as much as 72.6% in selected houses over a 48-to-96-hour period. Eastern equine encephalitis virus was isolated from the second breeder flock, which experienced an egg-production drop of 44.5%. Clinical signs in both flocks were similar, with inactivity and the egg-production drop being the only clinical signs observed. Eggs from affected breeders were small and white, and a few were soft-shelled. Sera collected from the flocks 2 to 3 weeks after production began dropping confirmed the presence of antibodies to the viruses recovered. In the first flock, egg production failed to return to above 50%, although heat stress may have played a role in production recovery. The second flock was taken out of production and recycled.

Cerebral encephalomalacia in commercial turkeys.

A flock of 9 1/2-week-old commercial tom turkeys experienced high mortality after consuming a complete feed containing an unidentified toxic substance. Initially, turkeys were found dead. Clinically, the birds were calm and still but became hyperexcitable with noise. A small percentage of birds exhibited torticollis, opisthotonos, circling, ataxia, and blindness. Findings at necropsy and upon microscopic examination were bilaterally symmetrical areas of necrosis of the cerebral hemispheres in the area of the neostriatum that were well demarcated from the surrounding normal neuropil. A feeding trial with the suspect feed in twelve 4-week-old turkey hens induced clinical disease and gross and microscopic brain changes similar to those observed in the field case. Analyses for the following substances in the suspect feed were either negative or within acceptable limits: salt, selenium, furazolidone, monensin, amprolium, 3-nitro-4-hydroxyphenylarsonic acid, aflatoxin, deoxynivalenol, zearalenone, T-2 toxin, ochratoxin, fumonisin, organophosphates, chlorinated hydrocarbons, and carbamates. The toxic component of the feed remains unidentified.

Experimental infection of young turkeys with eastern equine encephalitis virus and highlands J virus.

Depression, somnolence, and increased mortality were observed in 2-week-old turkeys inoculated intramuscularly with either eastern equine encephalitis (EEE) virus or Highlands J (HJ) virus. Mortality rates in EEE virus- and HJ virus-inoculated turkeys were 7/30 (23%) and 9/30 (27%), respectively; no sham-inoculated controls died. Both EEE virus- and HJ virus-inoculated turkeys developed viremia that lasted 2 days; peak mean titers were 5.5 and 3.2 log10 plaque-forming units per ml of blood, respectively. Pathologic changes in both EEE virus- and HJ virus-inoculated turkeys consisted primarily of multifocal necrosis in the heart, kidney, and pancreas, and lymphoid necrosis and depletion in the thymus, spleen, and bursa of Fabricius. The findings indicate that EEE virus and HJ virus are pathogenic for young turkeys.

High mortality of domestic turkeys associated with Highlands J virus and eastern equine encephalitis virus infections.

High mortality occurred in two flocks of commercial turkey hens placed in southern North Carolina in fall 1991. Daily mortality peaked at 3.19% in Flock 1 and 3.79% in Flock 2. Clinical signs included restlessness, somnolence, vocalization, and acute death. Gross lesions included atrophy of the bursa of Fabricius, thymus, and spleen, and watery intestinal contents. Microscopic changes included moderate to marked lymphocyte necrosis and depletion in the bursa, thymus, and spleen, widely scattered necrosis of pancreatic acinar cells, and mild villous atrophy and fusion in the jejunum and ileum with cuboidal to low columnar epithelial cells covering the villous tips. In Flock 1, at 27 days of age, reovirus and picornavirus particles were detected in the feces. One week later, togavirus-like particles were observed in fecal contents, and two of seven serum samples showed seroconversion to Highlands J virus. Eleven days later, five of six serum samples were positive for antibodies against Highlands J virus, with a fourfold increase in the geometric mean titer. In Flock 2, seroconversion to eastern equine encephalitis virus was observed in four of 10 serum samples 11 days after the onset of clinical signs. Based on the above observations, it is suspected that these alphaviruses were the cause of the clinical syndrome.

Marek's disease virus isolates with unusual tropism and virulence for ocular tissues: clinical findings, challenge studies and pathological features.

Outbreaks of Marek's disease (MD) were diagnosed in two flocks from the same company. Clinical signs, mainly blindness (>90%), but also depression, mild paralysis, and 11 to 12% mortality by 20 weeks of age were observed. MD virus, serotype 1 was isolated. The isolates were designated NC-1 (flock 1) and NC-2 (flock 2). Challenge experiments were conducted with these isolates and with two reference MD virus strains (JM/102W and Md5) in unvaccinated, turkey herpesvirus- (HVT) vaccinated and bivalent- (HVT and SB-1) vaccinated chickens. Blindness, gross ocular lesions and tumour formation were observed in a high proportion of all groups challenged with NC-1 and NC-2 when compared with chickens challenged with JM/102W and Md5. In chickens challenged with isolates NC-1 and NC-2, corneal changes included oedema, midstromal cellular infiltration consisting of macrophages, lymphocytes, plasma cells and lesser numbers of heterophils, collagen degeneration and keratic precipitates consisting primarily of macrophages covering the central endothelium. Eosinophilic intranuclear inclusion bodies were present in mononuclear cells infiltrating the cornea. Changes in the uveal tract consisted of inflammatory cell infiltrates similar to those present in the cornea. Retinal lesions included disruption of the retinal pigmented epithelium, inflammatory cell infiltration in the subretinal space, photoreceptor degeneration and in severely affected eyes, necrosis of retinal cellular elements. Pecten changes consisted of necrosis and mononuclear cell infiltration. Intranuclear inclusion bodies were abundantly present in cells of the retina's ganglion and inner nuclear cell layers. The unusual clinical manifestation of MD, the unusual tropism and virulence of NC-1 and NC-2 for ocular tissues and the incomplete protection afforded by conventional vaccination suggest that these isolates may be new pathotypes.

Effects of poult source on turkey production parameters.

Flock records from a commercial turkey company were analyzed to determine if poult source affected flock performance. Comparisons were made between flocks supplied by two hatcheries (X and Y) reared on the same farms and among flocks reared on different farms. Flocks from hatchery X had significantly better livability and feed-conversion ratios than flocks from hatchery Y. Although not statistically significant, flocks from hatchery X tended to grade better at processing (percent grade A) and have lower condemnations than flocks from hatchery Y. Season significantly affected livability and feed conversion of all flocks regardless of hatchery source.

Effects of CGA-72662 (Larvadex) in turkeys during rearing and reproduction.

Turkeys were fed CGA-72662 (Larvadex) at treatment levels of 0, 500, 1,000, and 2,000 mg/kg diet from hatch to 16 wk of age, when the 500 mg/kg level was reduced to 250 mg/kg because of a significant reduction in feed intake. All diets continued through 40 wk of age. Body weight, feed consumption, livability, egg production, fertility, hatchability, and progeny performance were examined. Turkeys fed a treatment level of 2,000 mg CGA-72662/kg diet exhibited reduced growth rate and feed consumption prior to sexual maturity and decreased fertility and poult weight after sexual maturity. Necropsies suggested that the kidney was the primary site of lesions at the 1,000 and 2,000 mg/kg diet treatment levels. The kidneys were characterized as enlarged, nodular, and cystic, containing urate deposits and areas of necrosis. These data indicate that dosage levels of CGA-72662 at 250 mg/kg diet produced no deleterious effects on growth, feed consumption, egg production, fertility, hatchability, livability, or progeny performance.

Monensin toxicity in turkey breeder hens.

High mortality in two flocks of 1900 turkey breeder hens accidentally fed 280 g monensin/ton of complete feed is described. Mortality attributed to the poisoning was 76% in flock 1 and 18% in flock 2. Clinically, turkeys were found dead, exhibited respiratory distress with wings extended laterally, had fine tremors, or showed posterior paresis and inability to rise. The most striking finding at necropsy was the almost complete absence of gross lesions. Some turkeys had severely congested lungs; however, many did not. A few birds had pale streaks within the adductor muscles of the legs. Microscopic lesions included myofiber degeneration and necrosis of skeletal and myocardial muscle. Serum phosphorus, lactate dehydrogenase, and creatine phosphokinase were markedly elevated, whereas potassium, chloride, and calcium values were lowered.

Cryptosporidiosis and turkey viral hepatitis in turkeys.

Cryptosporidiosis and turkey viral hepatitis were diagnosed in 25-day-old turkeys with increased mortality, enteritis, and stunting. Necropsy lesions included foul-smelling, tan-colored, loose feces in the terminal small intestines and ceca. The small intestines and ceca were congested. Multiple white to gray foci were present in the liver and pancreas. Mortality attributed to these conditions was estimated at 4.9%. Microscopic lesions included necrosis with accumulations of macrophages in the liver and pancreas. Bile-duct hyperplasia was present in the livers. Microscopic intestinal lesions consisted of mild to moderate atrophy of the villi of the distal small intestine (ileo-cecal junction) with infiltration of the lamina propria by mononuclear cells. Cryptosporidia were identified and appeared to be attached to villous epithelial cells of the terminal small intestines. Cryptosporidium sp. oocysts were also confirmed by fluorescent microscopic examination of feces stained auramine O. Reovirus was isolated on chicken embryo liver cells from affected livers.

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.

Diseases of pigeons.

This article contains the most common bacterial, viral, protozoan, mycotic, and parasitic diseases of pigeons encountered by the practicing veterinarian. Emphasis is placed on etiology, transmission, clinical signs, postmortem lesions, treatment, and control to aid the veterinarian in assessing clinical conditions.

A necrotizing pneumonia in lambs caused by pseudorabies virus (Aujesky's disease virus).

An outbreak of pseudorabies occurred in sheep housed with swine in the same building. Although the sheep and swine were not in physical contact, the lambs and ewes were exposed to air from the sows' section. Three dead lambs were submitted to the Iowa State University Veterinary Diagnostic Laboratory for necropsy. Grossly there were pulmonary congestion and multifocal pulmonary hemorrhages. Microscopic lesions were severe acute multifocal necrotizing bronchopneumonia with necrotizing vasculitis and intranuclear inclusion bodies within the neurons of the parabronchial ganglia. Bacterial cultures were negative for pathogenic agents; pseudorabies virus was isolated from ovine brain tissue. Viral antigen was demonstrated in the neurons of the parabronchial ganglia by immunoperoxidase staining. Electron microscopy revealed nucleocapsids in the parabronchial ganglionic neurons which contained basophilic intranuclear inclusion bodies. Viral DNA prepared from the ovine pseudorabies virus isolate was found by restriction endonuclease analysis to be related to the Indiana Funkhauser strain of pseudorabies virus.

Studies on the use of a long-acting oxytetracycline in turkeys: serum levels and tissue residues following injection.

Forty 6-week-old large white commercial turkeys were injected subcutaneously with a long-acting oxytetracycline formulation (69 mg/lb). The turkeys were divided into four groups of 10 birds each, and the birds in each group were bled twice at different times between 4 and 144 hours postinjection (PI) to determine serum levels of oxytetracycline. Two additional groups of turkeys were also given the long-acting oxytetracycline formulation mixed with either neomycin or a bacterin for Pasteurella multocida to determine if either of these compounds interfered with absorption of the oxytetracycline. Serum levels of oxytetracycline were 5.38 micrograms/ml, 1.59 microgram/ml, and 0.93 microgram/ml at 24, 48, and 72 hours PI, respectively, following an average dose of 69 mg/lb of body weight. These levels are all considered therapeutic. There appeared to be no interference with absorption of oxytetracycline when mixed with either neomycin or the bacterin. Tissue residues of oxytetracycline in the muscle, liver, and kidney were within tolerance levels by 3 weeks PI.

Studies on the use of a long-acting oxytetracycline in turkeys: efficacy against experimental infections with Alcaligenes faecalis and Pasteurella multocida.

A group of 2-week-old turkey poults was inoculated with a pathogenic strain of Alcaligenes faecalis. One week later, half the group was injected with a long-acting oxytetracycline formulation. Poults were examined post-mortem on days 3, 5, and 10 post-treatment. Swabs were taken of the trachea, sinus, and lung of each poult. Poults were observed closely for clinical signs, and appropriate tissues were taken for histopathology. Results showed no evidence of therapeutic effect on A. faecalis infection in vivo, even though the organism was highly sensitive in vitro. Six-week-old turkeys were inoculated intramuscularly with 3.7 X 10(3) organisms of the P-1059 strain of Pasteurella multocida. Immediately following inoculation, half the group was treated with the long-acting oxytetracycline. Ninety percent of the untreated poults were dead 72 hours postinoculation, whereas none of the treated turkeys died. No evidence of any clinical disease was observed in the treated group during the 8-day observation period. The long-acting oxytetracycline product was highly efficacious in preventing disease caused by experimental inoculation with the P-1059 strain of P. multocida.