Detection of antibodies to platelets and erythrocytes during infection with haemorrhage-causing Trypanosoma vivax in Ayrshire cattle.

Ayrshire cattle, which were infected with a stock of Trypanosoma vivax from Galana, Kenya, which produced haemorrhagic disease, were examined for the presence of antibodies to erythrocytes and platelets. Antibodies to normal erythrocytes and platelets were detected in the plasma of infected animals using the enzyme-linked immunosorbent assay (ELISA). The antibodies were detectable following the first peak of parasitaemia (10-15 days after infection) and antibody activity was maximal 30-35 days after infection. Plasma from cattle, taken 32 days after infection, precipitated radiolabelled proteins from autologous platelets and, less efficiently, from autologous erythrocytes. Fluorescence-activated cell sorter (FACS) assays demonstrated that erythrocytes and platelets from infected cattle bound IgM and IgG in vivo, and that both normal blood cell types could adsorb these antibodies following incubation in plasma from infected animals. Complement (C3) was similarly adsorbed to erythrocytes during infection. Antibodies adsorbed to infected erythrocytes could be eluted and the eluted antibodies bound to normal erythrocytes, as detected by immunofluorescence, but they did not react with the infecting trypanosome. It is hypothesised that although anti-blood cell antibodies may not be the primary cause of the severe anaemia and thrombocytopaenia which accompany the haemorrhagic syndrome, they could play an important role in the maintenance of these signs of disease, adversely affecting the outcome of T. vivax-associated haemorrhagic disease in the field.

Haemorrhagic lesions resulting from Trypanosoma vivax infection in Ayrshire cattle.

Infection of Ayrshire cattle with a stock of Trypanosoma vivax from the Galana Ranch, Kenya, resulted in an acute disease characterised by profound anaemia and haemorrhage, which reached maximum severity between 3 and 5 weeks after infection. Bleeding from the ears, nose and rectum occurred. At necropsy, petechial and ecchymotic haemorrhages were widespread, but were particularly severe in the gastrointestinal tract. In confirmation of the gross findings, congestion, haemorrhage and degenerative changes in most tissues and organs were found histologically. Thrombi were seen in the lymphatic vessels and clots of fibrin were present in the ventricles of the brain. The anaemia was a consequence of frank blood loss through haemorrhaging, exacerbated by erythrophagocytosis of deformed red blood cells, whose occurrence was indicative of microangiopathic changes. Animals were euthanised between 23 and 36 days after infection when they became recumbent with PCV values as low as 9%. There is no doubt that animals affected by this syndrome in the field would die within a few weeks of infection, if left untreated.

Chemical studies of the blood, and histological studies of the heart of broiler chickens dying from acute death syndrome.

Comparison of the blood and hearts of birds dying from Acute Death Syndrome and of normal healthy birds from seven different broiler chicken flocks revealed no consistent differences. Marked changes in serum levels of potassium, phosphorus, magnesium, sodium, and glucose were noted to occur after death in birds dying from Acute Death Syndrome and in control birds. Cellular infiltrations, found in the hearts of birds dying from Acute Death Syndrome an in control birds, were considered to be normal lymphoid foci and foci of ectopic hemopoiesis.

Pathogenicity and distribution of egg-drop syndrome-1976 virus (JPA-1) in inoculated laying hens.

Rhode Island Red laying hens that lacked hemagglutination-inhibition antibody were inoculated orally with the JPA-1 strain of adenovirus isolated from a flock affected with egg-drop syndrome-1976 in Japan and observed for 80 days. Inoculated hens laid abnormal eggs, such as shell-less, soft-shelled, and cracked eggs and those with loss of pigmentation, from 8 days postinoculation (PI). Fifteen out of 16 hens laid abnormal eggs. Egg-production rte fell from 94% to 50% between 13 and 16 days PI. When the abnormal eggs were excluded, egg production was 17%; then it recoverd slowly, reaching 67% by the end of the experiment. The virus was recovered from various organs of inoculated hens from 3 to 7 days PI. Fluorescent antigens of the virus were observed in the epithelial cells and desquamated cells from the epithelium of the uterus and isthmus 10 and 14 days PI.

Outbreaks of egg-drop syndrome-1976 in Japan and its etiological agent.

A condition similar to egg-drop syndrome-1976 (EDS-76) occurred in 14 broiler breeding flocks in 2 farms in Japan from December 1978 to January 1980, and it was diagnosed as EDS-76 by serologic and virological investigations. Egg production fell suddenly when the hens were 30 to 55 weeks of age, and the depression lasted 3 to 7 weeks. Production fell 6 to 25%. Depressed egg production was accompanied by the laying of shell-less, soft-shelled, and thin-shelled eggs associated with loss of egg-shell pigment. Eleven isolates of hemagglutinating adenovirus were isolated from cloacal swabs (10 isolates) and a uterus (1 isolate) of hens in one farm. One isolate, cloned and named JPA-1, had the same antigenicity in serologic tests and the same biological and physicochemical properties as the BC14 strain of EDS-76 virus.

A study of cartilaginous nodules in the lungs of domestic poultry.

A high incidence of cartilaginous nodules was found in the lungs of broiler chickens. The incidence was higher in broilers fed ad libitum than in broilers fed a restricted amount of food. A much lower incidence of nodules was found in leghorn-type chickens, turkeys, ducks, and geese. It was theorized that the nodules may develop from embolic chondrocytes arising from abnormal cartilage, but no correlation could be found between lesions in the cartilage of the broilers and the presence of nodules in their lungs.

Influence of diet on a retrovirus-induced obesity and stunting syndrome.

An avian retrovirus, RAV-7, causes a syndrome characterized by stunting, high mortality, and obesity. In this study, the influence of the lipid content of the diet on the RAV-7-induced syndrome was examined. Failure to gain weight, a measure of the stunting, was not influenced by fat content of the diet, but a slight increase in mortality was noted with a low-fat diet.

An epizootiological study of acute death syndrome and leg weakness in broiler chickens in western Canada.

In a survey of 51 broiler chicken flocks, the incidence of chickens dying from acute death syndrome and of those with skeletal deformities varied from 0.71 to 4.07% and from 0.46 to 4.08% among the flocks, respectively. The average incidence of those with skeletal deformities was 1.72%; 1.10% were culled in the field, and 0.62% were condemned or downgraded as carcasses. The major types of skeletal deformities were valgus deformation of the intertarsal joint (70%), varus deformation of the intertarsal joint (9%), tibial rotation (7%), and spondylolisthesis (14%). The strain and source of chickens and the management and nutritional practices were recorded for each flock. Statistical analyses were conducted in an attempt to identify factors that might correlate with the incidence of either chickens dying from acute death syndrome or those with skeletal deformities. Results of these analyses are discussed.

Effect of endogenous leukosis virus genes on response to infection with avian leukosis and reticuloendotheliosis viruses.

We examined the effect of the presence or absence of endogenous viral gene (ev) 3, which controls expression of group-specific viral and envelope antigens (gs+chf+ phenotype), and ev2, which controls the production of a complete subgroup E virus (V-E+ phenotype), on the response of chickens to RAV-1, an exogenous avian leukosis virus (ALV) with an antigenic relationship to endogenous virus. After inoculation at one day of age, the chickens lacking either ev gene expression had a lower frequency of virus isolations and higher frequency and titer of neutralizing antibodies than those expressing ev genes. This relationship was not seen in groups inoculated with chick syncytial virus (CSV), a reticuloendotheliosis-associated virus with no relationship to endogenous virus, but the ev2+ birds tended to yield more CSV isolations than the ev2- birds. We suggest that chickens expressing ev genes may be immunologically tolerant to antigens common to exogenous and endogenous viruses. In addition, ev3- birds inoculated with RAV-1 at one day of age or as embryos died at a high rate between 6 and 12 weeks of age with a non-neoplastic syndrome characterized by severe atrophy of lymphoid organs, an inflammatory reaction in the liver, and a lower immune response to particulate antigens.

Aortic atherosclerosis in nonlaying hens with fatty liver syndrome.

Ten laying hens with low plasma cholesterol levels and no signs of fatty liver syndrome were examined at necropsy. Liver coloration and deposition of body fat were not abnormal in such hens. Eleven nonlaying hens had signs of fatty liver syndrome. They were out of production for 1 to 3 months and had elevate plasma cholesterol levels. At necropsy, such hens had yellow livers, heavy deposits of body fat, and several involuted egg yolks, which were dark yellow. Intimal plaques were observed by light microscopy in the abdominal aortas of hens with low plasma cholesterol levels; the plaques contained little or no lipid and were composed of three or four rows of modified smooth-muscle cells. Aortic intimal plaques of hens with high plasma cholesterol levels were composed of 16 to 18 rows of modified smooth-muscle cells when examined by light microscopy. The plaques contained intracellular and extracellular lipid, indicating aortic atherosclerosis. Electron-microscopic observations of the abdominal aortas of both groups of hens were similar to light-microscopic observations, except that lipid, including cholesterol clefts, was seen both intracellularly and extracellularly in the thickened tunica intima of hens with high plasma cholesterol values. Thus, the presence of aortic atherosclerosis was confirmed by electron microscopy. It is suggested that the endogenous hypercholesterolemia and cessation of egg production, characteristic of severe fatty liver syndrome, originated from the reabsorption of involuted egg yolks and that such reabsorption caused the development of aortic atherosclerosis and deposition of excess body fat.

Zinc deficiency in pheasant chicks fed practical diets.

A disease syndrome characterized by abnormal feathering and varus deviation of the tarsometatarsus spontaneously occurred in pheasant chicks fed a practical commercially prepared diet. The addition of supplemental Zn to the commercial diet was effective in alleviating the clinical signs, even though the commercial mix had Zn levels that met the published pheasant chick requirement. Supplemental arginine was ineffective in reducing the severity of the clinical signs. Also, when the diet was mixed in a laboratory setting, pheasant chicks did not develop abnormal feathering and leg bones. Clinical signs caused by feeding the commercial mix were not reproduced by altering dietary calcium and phosphorus levels in the laboratory mix. Neither adding a pellet binder nor removing supplemental Zn from the lab mix produced as severe leg and feather deformities as the commercial mix. Thus, unidentified dietary factors are capable of causing a Zn-deficiency syndrome in pheasant chicks fed practical diets with analyzed Zn levels meeting the required levels.

Dietary induction of sudden death syndrome in broiler breeders.

Sudden death syndrome in broiler breeders at the point of lay was a serious problem in Australia for 18 months. This condition was reproduced by a combination of dietary and management practices. Chickens fed a diet low in potassium, phosphorus, protein, and energy had plasma potassium and phosphorus levels significantly lower than the levels seen in the controls. The plasma values of the test breeders were similar to levels seen in field cases. There was a significant difference (P less than 0.01) in the venous acid-base balance between the test chickens and controls. Test chickens were alkalotic and had a 6% mortality rate between 18 and 30 weeks of age.

Proventricular dilatation syndrome in large psittacine birds.

Proventricular dilatation was diagnosed in 16 psittacine birds. Signs included anorexia, lethargy, weight loss, and intermittent vomiting. The proventriculus in all birds was thin-walled and impacted with ingesta and occupied most of the body cavity. Microscopic changes in the proventriculus varied from none to an infiltration of lymphocytes, macrophages, and heterophils. There was no evidence of viral or bacterial infection or lead toxicity.

Swollen-head syndrome in broiler chickens.

Swollen-head syndrome is a disease seen in broiler chickens between 4 and 6 weeks of age in Southern Africa. It appears to be caused by a mixed coronavirus and Escherichia coli infection. The coronavirus appears to be of a hitherto unrecorded serotype. The disease is controlled by an attenuated live-virus vaccine and antibacterial medication.

Influence of endogenous viral (ev) gene expression and strain of exogenous avian leukosis virus (ALV) on mortality and ALV infection and shedding in chickens.

Two experiments were conducted to determine the influence of endogenous viral (ev) gene expression on the response of chicken to day-old inoculation with two laboratory and two field strains of avian leukosis virus (ALV). The ev2- and ev3-negative semi-congenic chickens had much higher mortality from a unique non-neoplastic syndrome (NNS) than ev2- and ev3-positive semi-congenic chickens after inoculation with ALV strain RAV-1. The three other ALV strains induced little NNS. All four strains of ALV induced higher incidences of neutralizing antibody and lower incidences of viremia in ev2- and ev3-negative chickens than ev2- and ev3-positive chickens. The semi-congenic ev2- and ev3-negative chickens were only slightly less likely to shed ALV in the cloaca. Chickens of line 0, an unrelated line lacking ev genes, had a much higher rate of antibody production and lower rate of viremia and shedding than the semi-congenic chickens. Surprisingly, line 0 failed to get NNS after RAV-1 inoculation. There were major differences among strains of ALV in induction of antibody response, viremia, and shedding in the cloaca. The two field strains of ALV tended to be less immunogenic than the laboratory strains. We conclude that both the genetics of the host, including variation in ev gene expression, and the strain of ALV can influence the probability of ALV shedding and congenital transmission after horizontal infection.

Studies of avian urolithiasis associated with an infectious bronchitis virus.

Avian urolithiasis syndrome was diagnosed in 14-to-25-week-old chickens from a multiple-age caged-layer complex housing more than 2.5 million chickens. Losses from this syndrome ranged from 0.5 to 1.0% per week. Seven-to-14-week-old pullets from this facility had multifocal renal tubular necrosis leading to interstitial fibrosis, tophus formation, and tubular dilation. A coronavirus was isolated in embryos inoculated with pooled samples of trachea, kidney, and cecal tonsil of 4-week-old pullets. This virus, identified as 85-209, was related to infectious bronchitis virus strain Florida 88 by hemagglutination-inhibition assay. Day-old specific-pathogen-free chicks were inoculated with fifth-embryo-passage amnioallantoic fluid containing this virus. These chicks developed histologic lesions of tracheitis at 5 to 7 days postinoculation. Half the chicks inoculated by eyedrop developed renal tubular necrosis after 7 days. Urolithiasis in the flock investigated was attributed to renal damage by this strain of infectious bronchitis virus occurring in 4-to-7-week-old pullets and progressing to segmental atrophy, hyperplasia, and ureteral stone formation in 14-to-25-week-old chickens.

The roles of the infectious bursal agent and several avian adenoviruses in the hemorrhagic-aplastic-anemia syndrome and gangrenous dermatitis.

The effect that breeder-flock immune status regarding the infectious bursal agent (IBA) and two avian adenoviruses (DPI-1 and DPI-2) has on the susceptibility of their commercially reared Delmarva broiler progeny to the hemorrhagic-aplastic-anemia syndrome and concurrent gangrenous dermatitis was determined. Lack of immunity to the IBA in breeder flocks was related to an increased susceptibility of progeny to anemia and dermatitis. Breeder-flock immunity to the two adenoviruses tested could not be related to the resistance or susceptibility of their progeny to the hemorrhagic-aplastic-anemia syndrome and gangrenous dermatitis.

Lesions of right heart failure and ascites in broiler chickens.

A naturally occurring cardiomyopathy in broiler chickens from a single Ontario farm was studied in order to define the morphologic changes. Gross and histologic features of affected birds were compared with those in age-matched control penmates. Body weight and weight and volume of individual cardiac chambers were measured. Histologic sections of 18 different tissues were examined, and lesions observed were scored subjectively. Affected birds were stunted and had marked right ventricular dilation and hypertrophy, atrial hypertrophy, ascites, pulmonary congestion and edema, and hepatic capsular fibrosis. Microscopic changes in the heart of affected birds were mild and did not suggest a specific cause of heart failure. Lungs had marked hypertrophy of parabronchial smooth muscle and collapse and apparent loss of associated air capillaries. Other histologic changes observed were thought to be the result of passive congestion of viscera caused by right heart failure and chronic debility. Although the specific etiology of this condition could not be determined, it was felt that this syndrome was unlikely to have been the result of any of the commonly recognized causes of congestive heart failure and ascites in broilers.

Delayed T-cell maturation and suppression of mitogen-induced blastogenesis in turkey poults fed cortisone acetate and furazolidone.

The effect of cortisone acetate (CA) on the immune response of control and furazolidone (FZ)-fed turkey poults was investigated. CA, fed at a dose of 500 mg/kg of ration beginning at 1 week of age, decreased mortality but had little effect on the development of FZ-induced cardiomyopathy. When poults were 2 weeks of age, the in vitro stimulation of lymphocytes by phytohemagglutinin (PHA) and concanavalin A (Con A) was significantly depressed (P less than or equal to 0.001 and P less than or equal to 0.05, respectively) in cortisone-treated poults. The time of the peak response of lymphocytes from poults 2-5 weeks of age to in vitro stimulation by PHA was significantly delayed (P less than or equal to 0.01) and the magnitude of the response was significantly depressed (P less than or equal to 0.001) in cortisone-treated poults compared with control poults. Cortisone treatment had no effect on time of peak response to Con A stimulation but significantly depressed (P less than or equal to 0.05) the magnitude of the response. Poults receiving FZ administered by gastric tube showed a peak response to PHA stimulation significantly (P less than or equal to 0.05) earlier and significantly (P less than or equal to 0.05) greater than did control poults.

Experimental reproduction of turkey syndrome 65 with Mycoplasma meleagridis and M gallisepticum and associated changes in serum protein characteristics.

Groups of one-day-old turkeys were infected with two isolates of Mycoplasma meleagridis and one of M gallisepticum. The experiment was terminated at three weeks of age when the incidence of TS65 in the three groups were 32, 24 and 82 per cent respectively. The development of TS65 in the M meleagridis-infected groups was not accompanied by dramatic falls of serum albumin levels thus invalidating the hypothesis that low serum albumin concentration is a primary factor in the development of TS65.