Necrotizing enteritis in suckling pigs (Clostridium perfringens type C enterotoxemia). II. Toxin formation, heat and drug resistance of Clostridium perfringens strains isolated from suckling pigs and broilers with necrotizing enteritis]

Nineteen Clostridium perfringens Type C strains and ten foreign control strains of subtypes C1, C3, and C4 were tested for their toxin formation and spore resistance to heat. The 19 Type C strains had been isolated from unweaned piglets in the context of necrotising enteritis outbreaks in the GDR. The Clostridium perfringens Type C strains formed beta-toxin, but they failed to form epsilon-toxin or gamma-toxin, alpha-toxin was successfully recorded from 15 of the 19 strains tested from unweaned piglets. The minor-lethal toxin fractions were also tested, with delta-toxin being recorded from all strains, non-alpha-delta-theta-toxin from six, theta-toxin from five, and K-toxin from one. Tests for delta-toxin, lambda-toxin, and mu-toxin were negative. The Clostridium perfringens Type C strains isolated in the GDR from unweaned piglets with necrotising enteritis were, basically, identical with those described in Denmark by von Hogh (1967) with regard to toxin formation. Clostridium perfringens strains cultured in broilers with necrotising enteritis were characterised by regular toxin production in the context of alpha, theta, delta as well as non-alpha-delta-theta. They failed to form beta, epsilon, gamma and lambda, while mu-toxin was formed by them quite irregularly. They, consequently, are Type A strains. Resistance to chloramphenicol and/or oxytetracycline was exhibited by 78.5 per cent of 237 tested Clostridium perfringens strains which had been isolated from unweaned piglets and broilers with necrotosing enteritis. Multiple resistance was recorded from 33.9 per cent. All strains were susceptible to penicillin, nitrofurantoin, and erythromycin.     

THE PATHOGENESIS OF INFECTIOUS AVIAN ENCEPHALOMYELITIS

Infectious avian encephalomyelitis virus (IAEV) maternal antibody was detected in the serum of chickens for up to 21 days following hatching. This antibody protected chickens against clinical IAE after intracerebral inoculation with van Roekel strain or oral administration of the NSW-1 strain of IAEV. Maternal antibody to IAEV also protected testosterone bursectomised chickens against the development of clinical disease. IAEV maternal antibody also influeced the pattern of virus excretion in faeces and serological responsiveness. This influence on antibody responses persisted beyond the time that IAEV maternal antibody could be detected. The importance of IAEV maternal antibody on the strategy of vaccination against IAE is discussed.     

Indirect solid-phase microradioimmunoassay for detection of pseudorabies virus antibody in swine sera.

An indirect solid-phase microradioimmunoassay (IRIA) was developed for detection and quantitation of antibodies to pseudorabies virus (PRV) in swine serum. Qualitative results of the IRIA compared closely with results of the serum neutralization test (NT) and the microimmunodiffusion test (MIDT). The IRIA was more sensitive than the NT for detection of antibodies to PRV in swine serum. The IRIA result is expressed numerically. With the IRIA and NT, antibody to PRV was first detectable in 3 experimentally infected pigs at 9 days after inoculation. With MIDT, antibody was detected in the 3 experimentally infected pigs at 9 days after inoculation. With the MIDT, antibody was detected in the 3 experimentally infected pigs at 7, 8, and 9 days after inoculation. The IRIA results are obtainable within a few hours; the NT and MIDT require 48 hours for completion.     

Effect of the proteinase inhibitor aprotinin in the management of hemorrhagic shock in the dog.

Aprotinin, a proteinase inhibitor, was evaluated as a pharmacologic aid in dogs subjected to lethal hemorrhagic shock. Survival time, hemodynamic changes, and plasma enzyme analysis were measured as criteria for drug effects. Mixed-breed dogs (n = 14) were divided into 2 groups of 7 each: nontreated dogs in shock (group 1) and aprotinin-treated dogs in shock (group 2). One of 7 dogs in group 1 and 2 of 7 dogs in group 2 survived. Survival time, for the remaining dogs in group 1 (190 min, n = 6) and group 2 (188 min, n = 5) were not significantly different. There was no significant difference in mean arterial pressure, mean pulmonary arterial pressure, cardiac output, or left ventricle systolic pressure associated with aprotinin treatment at any time after hemorrhagic shock. There was no significant difference in plasma lactic acid, aspartate aminotransferase, alanine aminotransferase, creatine phosphokinase, alpha-amylase, and beta-glucuronidase associated with treatment at any time; however, there were significant (P less than 0.05) increases with time. The gastrointestinal tract was the site of most obvious lesions found at necropsy. Lesions varied considerably in extent and severity without apparent correlation to the treatment regimen. These experiments did not show beneficial effects of aprotinin in dogs subjected to hemorrhagic shock, but neither did they completely rule out some valuable actions that may have been obscured by the type of model used.     

An invasive procedure for in utero fetal electrocardiology: recording of fetal electrocardiograms by applying electrodes through the uterus.

An in utero technique was developed that allows direct access to the canine fetus for experimentation. This procedure reduces the need for fetal manipulation and umbilical blood flow compromise and reduces fetal fluid loss. In pregnant bitches, uterine horns could be delivered through a ventral midline incision. By manipulating the fetal membranes, and positioning the fetuses through them, electrodes could be inserted subcutaneously in the fetuses. Electrocardiograms satisfactory for interpretation were obtained from as many as 4 fetuses in a bitch for periods up to postoperative week 3.     

Studies on the avian shell gland during egg formation: The effect of acetazol‐amide on the transfer of ions to the albumen 1

1. Twenty‐five laying hens were fed on a diet containing 100 mg acetazolamide/kg in order to determine the effects of a decrease in the activity of carbonic anhydrase on the transfer of minerals to the egg albumen.

2. Treatment with acetazolamide decreased the rate of shell formation by 44%; reduced the concentrations of water and Na+ in the albumen at the beginning of the plumping stage but increased the accumulation of water during plumping; increased the concentration of Cl‐ in the albumen after the 6‐h stage without any appreciable change in K+ and Ca²⁺ concentrations.

3. The computed relationships between the concentrations of different ions also showed that the transfer of water and Na+ were linked during egg formation, that a water‐independent, acetazolamide‐sensitive reabsorption of Na+ occurred after the 10‐h stage and that Na+ and Cl‐moved simultaneously up to 14 h but with the ratio of Cl‐ to Na+ three times higher in the treated group.

4. It is concluded that acetazolamide impairs the transfer of Na+ and Cl‐ between the albumen and the extracellular fluid and that secretion of Ca²⁺ into the uterine lumen seems to depend on Na+ and Cl‐ reabsorption.     

Requirement of the hen for sulphur‐containing amino acids

1. The sulphur amino acid requirements of White Leghorn‐type laying hens were determined in two 52‐week experiments using diets based on maize and soyabean meal providing from 5.0 to 6.5 g sulphur amino acids/kg, 12.35 MJ ME/kg and 8.6 to 8.8 g lysine/kg. There were six replicates of 15 individually‐caged hens each per treatment.

2. A requirement of approximately 775 to 800 mg sulphur amino acids /hen d, of which about 390 to 440 mg was methionine, was found for a maximum of 80 to 83 eggs/100 hen d. There were indications that the requirement for maximum egg production was less than that for maximum efficiency of food utilisation.

3. Diets containing 138 g protein/kg supplemented with methionine and lysine supported production and food utilisation as effectively as a diet containing 167 g protein/kg.     

The effect of delaying the onset of laying in pullets with a low‐calcium diet on subsequent egg production

1. A low‐calcium diet (0.5 g calcium/kg) was used to prevent the onset of laying in young pullets.

2. It was fed at 16 weeks of age to five separate groups (groups 2 to 6) each of 50 to 60 birds.

3. Group 2 was fed on a normal layers’ diet at 23 weeks of age, group 3 at 27 weeks, group 4 at 31 weeks, group 5 at 35 weeks and group 6 at 55 weeks while the control group (group 1) of similar size to groups 2 to 6 was subjected to a normal commercial treatment for laying stock.

4. In all the experimental groups the onset of sexual maturity occurred normally, but only one or two eggs were laid before laying ceased under the influence of the treatment.

5. Laying re‐started when the hens were fed on a normal diet and production rapidly rose to a high level.

6. Groups 1, 2 and 3 differed little in the total number of eggs produced up to 72 weeks of age.

7. In all experimental groups there were fewer very small, small and medium eggs than in the control group.

8. It is suggested that the use of a low‐calcium diet before the onset of lay may have advantages which could be exploited on a commercial scale.