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Biomedical subjects

C Riddell

Publications and source records attributed to C Riddell.

At least 73 records · Page 4Linked to original sources
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Viral hepatitis in domestic geese in Saskatchewan.

Up to 25% mortality occurred in goslings between 8 and 28 days of age in three sequential hatches from a closed breeder flock on a single farm. The birds died suddenly with minor ascites, subcutaneous and myocardial hemorrhages, and pale, mottled livers with petechial hemorrhages. Liver necrosis associated with intranuclear inclusion bodies was seen on histology. Virus particles were found on examination of the inclusion bodies with an electron microscope. Liver homogenates caused variable mortality 7 to 17 days postinoculation in goose embryos, some of which had hepatic necrosis and intranuclear inclusion bodies. Experimental goslings inoculated with material from these infected embryos died from hepatitis.

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Toxicity of dimetridazole in waterfowl.

Dimetridazole at a concentration of 1.0 g/l in drinking water caused mortality in both ducklings and goslings. When given to goslings at a concentration of 0.5 g/l, the drug caused growth depression and nervous signs characterized by excess activity, abnormal head attitudes, and ataxia.

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Pathology of the skeleton and tendons of broiler chickens reared to roaster weights. I. Crippled chickens.

The incidence of cripples among broiler chickens kept until 74 days of age was greatest in chickens fed ad libitum and kept in batteries. The incidence was lower in chickens kept in floor pens and was reduced by feed restriction. Crippling was due to long-bone distortion, rupture of the gastrocnemius tendon, and spondylolisthesis. Long-bone distortion was the most common defect and could be divided into valgus and varus deformation. The former was more important in chickens less than 7 weeks of age, and the latter was more important in older chickens. Tibial dyschondroplasia was found in some chickens with long-bone distortion, and the possible significance of this abnormal cartilage as a cause of long-bone distortion is discussed.

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Pathology of the skeleton and tendons of broiler chickens reared to roaster weights. II. Normal chickens.

Broiler chickens were raised to 74 days of age under different feeding and housing regimens. Conformation, growth plates and tendon strength were studied in clinically normal chickens of various ages. A change with age from slight valgus deviation of the metatarsal bones to varus deviation was recorded. Separation of the proximal femoral epiphysis from the femur on disarticulation of the coxofemoral joint was a common post-mortem artifact. It was more common in chickens on full feed than in chickens fed a restricted amount of feed. Two distinct growth-plate abnormalities were recognized. Dyschondroplasia was most common in the proximal tibiotarsus and was almost completely absent in chickens fed a restricted amount of feed. Eosinophilic streaks were found in growth plates of the proximal femur and the thoracic vertebral bodies. The incidence of these streaks was not affected by feed restriction. It is suggested that these streaks represent microscopic tears in growth plates exposed to shear forces and that they may be similar to osteochondrosis in mammals. The tensile strength of the flexor digitus perforatus and perforans tendon to the third digit increased with age. It was not affected by housing or feeding regimen, but the ratio of tensile strength over body weight was less in chickens fed ad libitum than in those fed a restricted amount of feed.

Age Factors↗
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Studies on the pathogenesis of staphylococcal osteomyelitis in chickens. I. Effect of stress on experimentally induced osteomyelitis.

A single strain of Staphylococcus aureus was used to study the pathogenesis of osteomyelitis in chickens. The disease was consistently reproduced in 6-week-old broiler chickens when 1 X 10(5) or more organisms were given intravenously. Severe feed restriction, debeaking, and single or multiple injections of corticosteroids delayed the appearance and decreased the severity of lesions due to staphylococcal infection. This increased resistance was associated with increased numbers of circulating heterophils and monocytes. No correlation between the presence of tibial dyschondroplasia and osteomyelitis was found.

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Studies on the pathogenesis of staphylococcal osteomyelitis in chickens. II. Role of the respiratory tract as a route of infection.

Groups of 6-week-old broiler chickens were exposed to Staphylococcus aureus by aerosol, intratracheal or intravenous (control) inoculation. No lesions were produced by aerosol. A single dose of up to 5 X 10(10) organisms given intratracheally failed to produce any lesions. Single or repeated doses of 5 X 10(11) organisms given intratracheally resulted in osteomyelitis in a low proportion of chickens.

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Rickets in turkey poults.

Fifteen outbreaks of rickets were diagnosed in turkey poults in Saskatchewan between 1978 and 1981. No relationship to farm, source of poults, or source of feed was apparent. Most outbreaks started when the poults were between 10 and 14 days of age, and they had recovered by 28 days of age. Losses varied from 1% to 14% of poults started. Skeletal lesions were characteristic of a vitamin D or calcium deficiency. On the basis of chemical analyses, adequate levels of calcium and phosphorus and proper amounts of vitamin premixes were present in the feed, but in five outbreaks biological feed tests implicated feed as a causative factor. The severity of rickets in poults fed defective feeds was markedly reduced by providing the poults with extra vitamin D in the drinking water or by injection. Two premixes used in different feeds contained adequate available vitamin D on the basis of biological testing. In some of the outbreaks, the rickets may have resulted from inadequate distribution of vitamin D in the feed, destruction of vitamin D during feed processing, or some unknown factor in the feed interfering with vitamin D utilization.

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Cecal and hepatic granulomas of unknown etiology in chickens.

One hundred and seventy-nine outbreaks of cecal and hepatic granulomas were diagnosed in small flocks of 3-to-7-month-old chickens in Saskatchewan between 1968 and 1981. The lesions were generally found at slaughter in the autumn. Outbreaks were widely distributed in farming areas in the province. The granulomas were either rough or smooth and were commonly confined to the liver and ceca but were also found in some outbreaks in the spleen, lung, mesentery, heart, kidney, and pancreas. The cause of the granulomas is unknown. Most granulomas were sterile on the basis of routine bacterial culture, but either Escherichia coli or a mixed flora of bacteria was isolated from some others. Acid-fast organisms and fungal elements have never been demonstrated using special histological stains.

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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.

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Effect of infection with hemorrhagic enteritis virus on susceptibility of turkeys to Escherichia coli.

The present study was designed to investigate hemorrhagic enteritis virus (HEV) as a predisposing factor influencing the susceptibility of young turkeys to Escherichia coli infections. In addition, the pathologic changes caused by administration of E. coli by various routes were compared. Following oral infection with HEV, groups of turkeys were inoculated with various doses of pathogenic E. coli by intravenous (IV), intra-air sac (IA), or intratracheal (IT) routes. A synergistic effect was observed in birds that were exposed to a combined HEV-E. coli challenge, resulting in higher mortality than that caused by either pathogen alone. This synergy was more evident when the bacteria were administered by the IT route than when it was administered by the two other routes. Turkeys infected with HEV and then inoculated IT with E. coli O78 had higher mortality (61%) and higher occurrence of gross body lesions (74%) than birds given E. coli alone (0% mortality and 16% gross lesions). After E. coli inoculation by the IA and IT routes, lesions observed were mainly pericarditis, perihepatitis, lung and air-sac lesions, splenic enlargement, and occasional arthritis. The incidence of lesions was affected by HEV exposure. In contrast, IV inoculation with E. coli O78 usually resulted in arthritis, and its incidence was independent of previous HEV exposure. The synergistic effect between HEV and E. coli administered IT can be used as a challenge model for testing E. coli vaccines.

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Studies on the pathogeneis of tibial dyschondroplasia in chickens. IV. Some features of the vascular supply to the growth plates of the tibiotarsus.

Several features of the vascular supply to the growth plates of the tibiotarsus were compared in two strains of broiler chickens selected for a high and low incidence of tibial dyschondroplasia. No difference was found between the two strains in the area of the proximal growth plate of the tibiotarsus or in the distance of the nutrient foramen from the same growth plate. Vascular tunnels invading the zone of hypertrophy were significantly fewer in the proximal growth plate than in the distal growth plate, and tunnels invading the zone of hypertrophy of each growth plate were also fewer in the high-incidence chickens than in the low-incidence chickens.

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Esophagitis due to a herpesvirus associated with mortality in a psittacine aviary.

In a disease outbreak at a psittacine aviary, eight Pionus sp. and Amazon parrots became sick. Three of four Amazon parrots died with severe esophagitis, and epithelial intranuclear inclusion bodies containing herpesvirus were prominent. Focal liver necrosis with rare hepatocyte intranuclear inclusion bodies were found in two of the dead Amazon parrots.

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Experimental reproduction of Escherichia coli cellulitis and septicemia in broiler chickens.

Experimental reproduction of avian cellulitis was conducted by subcutaneous inoculation of 25-day-old broiler chickens with a field isolate of serogroup O78 Escherichia coli. Development of the cellulitis lesion occurred as early as 24 h post-infection. Reproduction of cellulitis occurred in 98% of inoculated birds, and E. coli was isolated from > 75% of cellulitis lesions. In addition to cellulitis, other lesions, including pericarditis, airsacculitis, osteomyelitis, arthritis, and perihepatitis, occurred in > 80% of birds inoculated with E. coli. Bacteremia occurred as early as 6 h post-infection and dramatically declined by 5 days post-infection. Seventeen of 59 (29%) birds inoculated with E. coli developed a fatal infection between 1 and 6 days post-infection, and bacteria were isolated from lesions in 98% birds. In contrast, E. coli was not isolated from lesions in birds that survived until days 7-14 post-infection. Birds that survived with cellulitis and other lesions until day 14 post-infection had a significantly lower body weight compared with the control group. This avian model of cellulitis and other lesions will be useful for studying the development of vaccination strategies for E. coli in broilers.

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