Biomedical subjects
Publications and source records attributed to R B Truscott.
A slow-spreading infection due to a strain of Mycoplasma gallisepticum was detected serologically in a flock which remained free of clinical symptoms. The strain was shown to be tylosin resistant. Serological studies indicated that vertical transmission occurred.
The clearance of (51)Cr-labelled Pseudomonas endotoxin from the blood was studied in calves in a nontolerant and in an endotoxin-tolerant state. Calves were rendered tolerant to the toxic effects of the endotoxin by four daily intravenous injections of endotoxin at the dose rate of 5 microg/kg body weight. Clearance of a small amount of (51)Cr-endotoxin from the blood of nontolerant calves was almost complete within three minutes of injection and was not significantly faster in tolerant calves. The lungs and liver were the major organs involved in clearance of endotoxin from the blood. The (51)Cr label was slowly excreted by the kidneys. Neither platelets nor leukocytes were demonstrated to participate in endotoxin clearance in calves. (51)CrCl(3) was injected into control calves. Relative to the distribution and loss of labelled endotoxin, the (51)CrCl(3) was cleared slowly from the blood, was distributed uniformly throughout the body and was excreted rapidly.
A toxin which is lethal for two week old chicks has been recovered from strains of Escherichia coli O78:K80 of bovine and avian origin and from avian isolates of serogroups O2, O45 and O109. The toxin is heat-labile, antigenic, high in protein, inactivated by pronase, trypsin, amylase, and pancreatic lipase. The toxin may be precipitated by ammonium sulfate or TCA treatment from the supernatant obtained by repeated centrifugation of sonicated cells. Considerable purification has been obtained by column chromatography using Sepharose 6B.
Turkey hens were vaccinated six times with Salmonella typhimurium endotoxin prior to and during their egg production cycle. The resultant poults possessed a significant degree of immunity to challenge with S. typhimurium.
Chicks two, three and four weeks of age respond well serologically to endotoxin given intravenously, with the older chicks giving a better response. The induced immunity against live organism challenge produced by homologous endotoxin from Escherichia coli or Salmonella typhimurium is specific between these two organisms, however, cross-immunity occurs between E. coli 045 and E. coli 0109 and between Salmonella enteritidis and S. typhimcrium and further, endotoxins from different organisms may be combined to provide immunity against the homologous organisms. Endotoxoid administered to chicks rendered them more susceptible to live organism challenge for five days, following which some immunity developed.
Lead acetate administered intravenously in a mixture with endotoxin preparations potentiates the toxic effect of endotoxin for 14-21 day old meat strain chicks. A dose of 2.8 mg of lead acetate/100 g body weight is more effective with endotoxin than a dose of 2.5 mg; however, a dose of 3.0 mg or greater is toxic alone. The degree of potentiation appears to be at least 1000 fold and permits toxicity determinations using endotoxin levels ranging from 0.125 microg to 250 microg/chick. Endotoxin preparations made using NaCl, TCA or phenol-water extraction procedures, possessed toxic activity for chicks when tested by this method.
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Necrotic enteritis was consistently reproduced when enough active broth culture of Clostridium perfringens type A was infused intraduodenally. Typical lesions of necrotic enteritis were seen as early as 5 hr after infusion was begun. The histologic lesions observed at 1 hr were characterized by edema in the lamina propria and desquamation of epithelial cells. Large numbers of clostridia were seen among these sloughed cells. Coagulation necrosis of the tips of villi became evident at 3 hr and was marked at 5 hr. Many clumps of clostridia were obvious among the necrotic tissue. At 8 and 12 hr the necrotic lesions extended to involve most of the villus structures. Morphologically abnormal erythrocytes were evident in the visceral organs at 12 hr.
Necrotic enteritis was produced in 4-week-old chickens with bacteria-free crude toxins of Clostridium perfringens. Typical gross lesions could be seen as early as 3 hr after intraduodenal infusion of toxin was begun. Early microscopic lesions were observed at 20 minutes, progressing with time to involve most of the mucosa. Death was related to the amount of toxin administered. Because systemic absorption of toxin is likely, acutely affected birds may die from toxemia.
The intraduodenal administration of large numbers of Clostridium perfringens cells harvested from broth cultures and resuspended in PBS or fresh sterile thioglycollate broth produced a very mild form of necrotic enteritis. Administering an appropriate number of cells in culture supernatant, however, produced typical field-type disease. Alpha toxin was shown to be the significant toxin recoverable from broth-culture supernatant fluids. Requirements to produce the disease are minor intestinal damage and sufficient numbers of toxigenic C. perfringens in the intestine.
Multivalent antigen preparations of sonicated lyophilized cells derived from up to 6 different salmonella serotypes were added in decreasing levels to broiler feed throughout the broiler's life. Several preliminary experiments challenging chicks via contaminated feed with some of the homologous serotypes showed that salmonellae were cleared more rapidly from treated chicks than from untreated controls and that fewer isolations of salmonellae were made from their ceca.