Induction of acquired cellular resistance in mice with viable and macrophage-processed Listeria monocytogenes

Intracutaneous immunization of mice with 10(5) or 10(6) viable listeria resulted in acquired cellular resistance (ACR) of short duration (7 days). The period during which viable Listeria monocytogenes had to be present in order to induce ACR was estimated by killing the listeria at different times after immunization by injecting the bactericidal antibiotic amoxycillin. The killing of listeria within 6 h after injection prevented the induction of A CR completely, between 6 and 12 h partially, while survival of listeria within animals for at least 18 h was required for the induction of complete protection. To determine whether multiplication of viable listeria was a prerequisite for the induction of ACR, the bacteriostatic antibiotic minocycline was injected for four days after immunization. Induction of ACR was only possible if the dose of viable listeria was large enough to permit a proportion of the listeria to escape bacteriostasis. Interaction of peritoneal macrophages of normal mice and viable listeria yielded a supernatant which induced specific ACR in normal recipient mice. No ACR could be induced with supernatant obtained from normal macrophages after digestion of killed listeria. A reduced level of ACR was obtained with supernatant collected after interaction of macrophages from immune mice and viable listeria. The immunogenic material present in the supernatant of normal macrophages after interaction with viable listeria is thermolabile, has a molecular weight of over 300,000, and is not affected by treatment with DNase, RNase, or trypsin.     

Influence of ascorbic acid on the adverse effect of feeding a diet containing excess tyrosine to chicks

1. The effects of dietary or parenteral administration of ascorbic acid on the adverse effects of excess dietary tyrosine were investigated with young male White Leghorn chicks in a 2‐week experiment.

2. Addition of 10 g ascorbic acid/kg to the control diet (without excess tyrosine) produced no beneficial effects on performance. Excess dietary tyrosine caused depressions in all measures of performance.

3. Adding 0.1, 1, 10 or 20 g ascorbic acid/kg to the diet containing excess tyrosine tended to improve performance.

4. Subcutaneous injection of 50 mg ascorbic acid/bird d to chicks receiving excess tyrosine brought about a significant improvement in body‐weight gain.

5. The elevation of plasma free tyrosine caused by excess dietary tyrosine decreased as dietary ascorbic acid increased.

6. Ascorbic acid can alleviate, though not completely counteract, the adverse effect of excess dietary tyrosine.     

Book reviews

Research and Development in Relation to Farm Animal Welfare, contributions by B. A. Baldwin, J. R. Bareham, I. J. H. Duncan, R. Ewbank, D. C. Hardwick and K. Vestergaard, Animal Management, 11, Series Edited by D. W. Fölsch. Birkhauser Verlag, Basel, 1981. ISBN‐3–7643–1241–6.

First European Symposium on Poultry Welfare. Edited by L. Yding S0RENSEN. Published by the Danish Branch of World's Poultry Science Association. 1981. 238pp. D.Kr.90. ISBN 87–88162–00–1.     

Relationship between energy and protein intakes and laying characteristics in individually‐caged broiler breeder hens

1. Individually‐caged broiler hens, which had been reared on an advised rationing programme, were fed allowances of 1.88, 1.61, 1.32 or 1.13 MJ apparent metabolisable energy/bird d at four different protein intakes (27, 23, 19.5 or 16.5 g crude protein per bird d) from 21 to 60 weeks of age.

2. Age at first egg, body‐weight gain and egg production were affected by energy allowance. Birds on the lower energy allowances came into lay later than birds on the higher energy allowances and at a lower body weight.

3. Body‐weight gain decreased with decreasing energy allowance. The decrease in egg output in response to decreasing energy allowance resulted from more birds ceasing to lay and fewer birds laying on more than 3 d per week. Similar changes in the distribution of rates of lay were observed on each treatment as the flock aged.

4. The relationship between body‐weight gain and egg number on each treatment was negative from 21 to 36 weeks, but became less consistent with age.

5. Protein intake had little effect on body weight. At the lowest energy allowance, egg number and egg weight decreased with increasing protein allowance. This effect was not observed on the higher energy allowances.     

Effect of injecting amino acids into the egg on embryonic and subsequent growth in the domestic fowl

1. The growing embryo uses about 1% of the total protein available in the egg during the first week of incubation.

2. Injecting the growing embryo with amino acids equivalent to the amount of protein used resulted in higher weight of chicks at all stages up to 56 d.     

Gastrointestinal colonization by salmonellae and pathogenic Escherichia coli in monoxenic and holoxenic chicks and poults

Chicks monocolonized by either salmonellae or pathogenic strains of Escherichia coli had persistent and undiminished colonization of all levels of the gastrointestinal tract and frequently had bacteremia during test periods ranging to 35 days. Poults monocolonized by salmonellae or Arizona hinshawii 7:"1,7,8 developed a similar pattern of colonization. Conventionally reared chicks and poults had rather variable colonization by these pathogens, and it was most persistent in the ceca. Groups treated with a native protective microflora were infrequently colonized. Differences in colonization are explainable by lack of competing bacteria in the monocolonized group and by various degrees of protection provided by microflora colonizing the other groups.     

Oat cells in the pathology of ovine pneumonia-pleurisy

Light microscope observations on oat cells in the ovine pneumonia-pleurisy complex are presented. This study is based on the experimental production of the disease by viruses and Pasteurella haemolytica. Oat cells appeared only in necrotic lesions associated with large numbers of P. haemolytica in the pneumonic lung. It is suggested that oat cells originate from blood monocytes, which transform into the oat shape when developing in the necrotic, hypoxic environment created by P. haemolytica. They were not, however, observed to be phagocytic. Oat cells are characteristic of pneumonic pasteurellosis but are not pathognomonic because they can also be found in extrapulmonary locations and in other pathological conditions of the lungs.     

Selenium deficiency, the drug metabolising enzymes and mycotoxicoses in sheep

An examination was made of the relationship in Romney sheep between selenium deficiency and (i) the state of the liver drug metabolising enzyme system, (ii) subclinical liver damage, (iii) susceptibility to facial eczema, and (iv) susceptibility to ryegrasss staggers. The microsomal electron transport detoxifying enzymes based on cytochrome P-450 were unaffected by Se deficiency, suggesting that these enzymes are uninduced on ryegrass/clover pastures. Selenium deficiency had no effect on sporidesmin-induced liver damage, which makes it unlikely that peroxidative events countered by Se-dependent glutathione peroxidase (E.C.1.11.10) have a major role in the mechanism of sporidesmin toxicity. Selenium deficiency did appear to suppress the development of photosensitisation. There was no major effect on ryegrass staggers and no deficiency-induced subclinical liver damage.     

Stimulation of the titre of a sheep serum factor that is related to the sheep complement system

Serum from most sheep subjected to a single jugular bleeding, repeated bleeding or an intraperitoneal injection of yeast and repeated bleeding, showed an increase in the titre of a serum component called serum factor. Serum factor reached a peak titre 2 to 5 days after treatment started. For some sheep, the titre was elevated for a 9- to 12-day period whereas for others the titre dropped markedly on day 7 followed by a rise on day 9. Serum factor reacts with sheep erythrocytes sensitised with rabbit antibody (sheep E-rabbit A). Serum factor can be detected on sheep E-rabbit A using guinea-pig antiserum that reacts with sheep complement (C). Serum factor is inactivated by heating at 56 degrees C for 30 minutes, but is only partially inactivated at 50 degrees C for 30 minutes. The reaction of serum factor with sheep E-rabbit A is inhibited by chelators of Ca++ and/or Mg++. Serum factor appears to be related to the sheep C system. Preliminary results suggest it may he a component of the classical pathway of sheep C, possibly the second component, C2.