Acetate uptake by isolated perfused guinea-pig mammary glands was approximately l·0 mg g−1 h−1 when perfusate acetate concentrations were in the physiological range (5–11 mg/100 ml plasma). At perfusate concentrations below this range (mean 3·62 mg/100 ml plasma) the uptake was not significantly different, but in one experiment in which the mean acetate concentration was 14·5 mg/100 ml plasma the uptake was markedly elevated. Radioactivity from Na [1-14C]acetate was incorporated into CO2 and milk and tissue fat, being largely present in C16 and C18 fatty acids. The guinea-pig is atypical of non-ruminants and similar to ruminants in respect of the blood concentration and mammary utilization of acetate.

Small numbers of Escherichia coli were infused into both lactating and non-lactating udders. Twelve of the 17 lactating quarters infused became infected, and all 12 showed clinical symptoms of udder disease. The 5 lactating quarters which did not become infected all had pre-infusion somatic cell counts > 300000 cells/ml milk, whilst all the quarters which became infected had cell counts < 300000 cells/ml milk. E. coli was subsequently recovered from only 6 of the 16 non-lactating quarters infused. In only 2 of these quarters did clinical infection follow, both quarters being in a cow infused 2 d before calving. The remaining 4 quarters from which E. coli was recovered were all negative within 5 d of infusion. These differences in susceptibility are discussed, particularly with reference to the frequent occurrence of coliform mastitis at and shortly after calving.

The effects of supplementing a basal diet, in which the low level of fatty acids limited milk production, with soya oil, a palm oil/palmitic acid mixture and tallow, on the yield of milk and of its constituents, and on the composition of the milk, are reported. The yields of milk and milk fat were greatly increased by all the oil-supplemented diets; the mean daily yield of solids-not-fat (SNF) was also increased, but supplementation with soya oil caused the yield of crude protein (CP) to decrease, whereas the other fat-rich concentrate mixtures gave the same mean yield of protein as did the low-fat, control diet. All 3 oil-supplemented diets lowered the proportion of CP in the milk, but the SNF content was unchanged by any treatment. Dietary soya oil tended to lower the proportion of fat in the milk, whilst the palm oil/palmitic acid mixture raised it, with the tallow exerting no effect. The results are discussed in relation to previous work in which these dietary oils have been used, but in which the intake of fatty acids from the control diets did not limit milk production to the extent reported here.

The effects on the fatty acid composition of milk fat of feeding various oil-enriched diets (soya oil, red palm oil/palmitic acid and tallow) to dairy cows receiving a fat-deficient basal diet are reported. It was found that a linear relation was obtained between the dietary intake of C18 fatty acids and their output in milk fat. A similar relation, applicable only to the oil-rich diets, was found for the C16 acids. The significance of these relations is discussed. Fatty acid compositions and yields are discussed and compared with literature examples in which similar oil-rich diets were fed, but in which the low amount of fat in the basal diet did not markedly depress milk yield. The proportion of trans-isomer in the octadecenoic acid was found to increase appreciably on feeding soya oil, and to a lesser extent with dietary tallow. A linear relation between the 18:0 and 18:1 contents of milk fat was found, and its significance is discussed.

The carotene and immunoglobulin concentrations in colostra and milks of 6 Jersey, 4 Friesian and 6 Jersey × Friesian cows were determined during the first 21 d of lactation. Carotene concentrations of between 50 and 300 μg/g milk fat were found at first milking and these declined to normal concentrations, in the range 9–21 μg/g milk fat, by the eighth to tenth day of lactation. Immunoglobulin concentrations at first milking were in the range 4–40 g/l milk and decreased to normal concentrations, in the range 0·3–0·5 g/l, by the fifth to seventh day of lactation. For both substances the data from each cow's milk fitted an exponential decay model. The fractional rates of decrease in concentration of carotene were 0·19–0·57/d and of immunoglobulin were 0·40–0·73/d. Breed-group differences were observed in both carotene and immunoglobulin concentrations in milks after the fourteenth day of lactation. In Jersey milks, the average carotene and immunoglobulin concentrations were respectively 18·5 μg/g milk fat and 0·32 g/l of milk, while in Friesian milks the concentrations were respectively 11·4 μg/g milk fat and 0·46 g/l milk. There was also a difference between breed groups in the daily rates of decrease of the immunoglobulin concentrations. The average rate of decrease for the Friesians was about 1·5 times the rate for the Jerseys.

Factors contributing to the initiation of lipid oxidation in cow's and mare's milk containing high levels of polyunsaturated fatty acids were studied. Addition of H2O2 just after milking, in slight excess of the stoichiometric amounts required to destroy ascorbic acid, delayed the development of oxidized flavours in cow's milk high in linoleic acid. Hydrogen peroxide treatment followed by the addition of α- or γ-tocopherols prevented lipid oxidation in cow's milk even when 0·1 mg Cu/l milk was added. When used separately in the presence of Cu these treatments were ineffective as was butylated hydroxyanisole treatment.

The lipid and ascorbic acid in mare's milk were remarkably stable to oxidation. Addition of 0·05 or 0·1 mg Cu/l, ethylenediamine tetraacetic acid, neocuproine, or H2O2 had very little effect on the loss of ascorbic acid and lipid oxidation in mare's milk.

Assay procedures were developed for a number of enzymes in milk which apparently originate from leucocytes. The enzymes studied were acid phosphatase, N-acetyl-β-D-glucosaminidase, β-glucuronidase, arylsulphatase, α-mannosidase, and catalase. Quarter-milk samples were analysed for enzyme activity and results compared with the electronic cell count and the Wisconsin Mastitis Test. All enzymes measured except acid phosphatase and α-mannosidase showed good correlation with the electronic cell count. Of the other 4 enzymes tested, β-glucuronidase and arylsulphatase were unsuitable as diagnostic aids owing to the lengthy incubation periods required in their assay procedures. The assay of catalase, which involved the measurement of the initial rate of release of O2 using an O2 analyser apparatus, was rapid, sensitive and reasonably reliable, if fresh milk samples were used. The assay procedure for N-acetyl-β-D-glucosaminidase was considered to be the most reliable, simple and rapid enzymic method for estimating the number of somatic cells in milk.

A method is described for the quantitative estimation of a mixture of whey proteins by spectrophotometric scanning of the stained protein bands following polyacrylamide-gel electrophoresis. The incorporation of β-lactoglobulin A as an internal standard improves the accuracy of the technique. The method has been used to measure residual native whey proteins in milk after heating. Results are presented for whey protein denaturation in skim-milk after heat treatment at 130 and 140 °C for various periods of time.

Addition of isolated κ-casein to milk reduced the destabilizing influence of forewarming, while the addition of isolated β-lactoglobulin (β-lg) to the κ-casein-enriched systems resulted in a loss in stability on forewarming. This effect was ascribed mainly to a β-lg:κ-casein interaction. Some individual milks were unaffected by forewarming while others were markedly destabilized by the same treatment. Addition of Ca2+ + Mg2+ and interchanging of milk sera by dialysis influenced stability.

It is concluded that milks which are destabilized by forewarming generally give a type A response (minimum in the pH–heat stability curves) and that preheat-stable milks generally give a type B curve (no minimum).

The autolysin of Streptococcus cremoris had the specificity of an endo-N-acetylmuramidase as it hydrolysed the linkage between N-acetylmuramic acid and N-acetylglucosamine. The enzyme had no amidase or endopeptidase action. It reached highest activity in the exponential phase of growth and in the electron microscope seemed to fragment the coccal wall at the equatorial ring.

Electron microscopy showed that a varying proportion of cells of Streptococcus cremoris NCDO 924 grown in autoclaved skim-milk possessed a layer of extracellular material attached to the cell wall. Occasional filamentous extensions of this layer made contact with neighbouring casein micelles. The same surfacestaining material persisted during the production of cheese-curd, but after maximum scald it was predominantly filamentous in appearance. These filaments made frequent contact with the adjacent curd matrix and with milk-fat globules. Str. cremoris NCDO 1986 produced similar surface material when in curd, but not when grown in skim-milk. In all situations, the extracellular material stained with colloidal iron hydroxide, ruthenium red and periodic acid–thiosemicarbazide–silver proteinate, indicating that it was largely composed of an acidic carbohydrate. It is suggested that this carbohydrate facilitates the adhesion of starter bacteria to the cheese-curd matrix and that during the initial stages of syneresis this serves to prevent their expulsion from the curd with the whey.

Some strains of commercial cheese starters were obtained in higher yield after batch culture in whey-based media supplemented with soy peptones than in those supplemented with papain digested skim-milk. The soy peptones contained a greater proportion of small peptides than did the skim-milk digest. Also the average size of peptides was lower (3·4–3·9 residues) in soy preparations than in the milk digest (6·8). Small peptides isolated from the soy peptones were utilized by growing starters more completely than the equivalent peptides isolated from the papain digested milk. These observations may account for the difference in cell yields with soy and milk-digest peptones.

The number of starter bacteria in Cheddar cheese was increased approximately 2 or 8 times by supplementing the normal starter inoculum with starter-cell suspensions which had been incubated with lysozyme in the absence of salt. Lysozyme-treated cells were also introduced into chemically acidified cheese in an attempt to achieve ripening in the absence of a normal starter culture. The added starters did not interfere with normal cheese-making by producing acid. The lysozyme-treated starter cells were lysed when the curd was salted and lysis was detected by the release of cell-free DNA and an intracellular marker enzyme (dipeptidase) into the cheese matrix. Free amino acid concentrations in maturing cheeses were increased up to 3 times compared with control cheeses. The intensity of Cheddar flavour was not increased in starter cheeses by the presence of additional lysozyme-treated starter and no Cheddar flavour developed in chemically acidified cheese containing the lysozyme-treated cells. It is concluded that intracellular starter enzymes play no direct part in flavour formation, but produce breakdown products from which Cheddar flavour compounds may be formed by other unknown mechanisms.

A method is described for determining H2S, methanethiol and dimethyl sulphide in Cheddar-cheese headspace. Cheeses ranging in age from 2 to 12 months were analysed using a gas chromatograph equipped with a photometric detector. These cheeses were presented to a trained flavour panel for the assessment of quality and intensity of Cheddar cheese flavour.

An attempt is made to correlate the concentration of sulphur compounds in the headspace with the average flavour scores. The results suggest that the flavour intensity of the cheese is related to the concentration of methanethiol in the headspace.