Concentrations of estrogen (ER) and progesterone (PR) receptors were measured by radioreceptor assay in tumor (n = 319) and normal (n = 166) mammary tissue from 248 bitches. Correlations between ER and PR and between receptor expression in tumor and normal mammary tissue from the same bitches were evaluated. The influence of tumor, clinical, or hormonal variables on receptor expression also was studied. Approximately 80% of tumor and 95% of normal mammary tissue expressed detectable concentrations of ER, PR, or both. Direct correlation was found between ER and PR concentrations in normal and tumor tissues. Median ER concentrations were significantly higher (46 +/- 47 fmol/mg of cytosolic protein vs 27 +/- 24 fmol/mg of cytosolic protein; P = 0.0002) in normal than in tumor tissue. On the other hand, PR concentrations were significantly higher (57 +/- 52 fmol/mg vs 77 +/- 99 fmol/mg; P = 0.03) in tumors (especially benign tumors) than in normal tissue. Poorly differentiated malignant tumors expressed lower concentrations of receptors than did benign or well differentiated malignant tumors. The ER and PR concentrations decreased with increasing size of the lesion. Hormonal status of the bitch significantly (P < 0.05) influenced receptor expression in normal tissue: bitches in the luteal phase of the estrous cycle had higher concentrations of ER (69 +/- 62 fmol/mg) than did ovariectomized bitches (24 +/- 19 fmol/mg) or bitches in anestrus (38 +/- 45 fmol/ mg) or the follicular phase (13 +/- 7 fmol/mg). For PR, higher concentrations were observed in normal tissue during anestrus than during pseudopregnancy or in bitches treated with medroxyprogesterone acetate. Similar, but nonsignificant, variations were seen in tumor tissue except in medroxyprogesterone acetate-treated bitches in which PR concentrations were high in tumors and low in normal tissue from the same bitches.

To compare the effects of milk stasis and milk flow on Brucella abortus infection of the mammary gland under the same systemic conditions, primiparous goats (n = 5) were inoculated IV with B abortus on the day of parturition, and suckling by their neonates was restricted to one mammary gland. Goats were euthanatized and necropsied at 3 weeks after inoculation, and milk, mammary glands, and supramammary lymph nodes were evaluated by bacteriologic, histologic, and immunoenzymatic staining techniques. Nonnursed mammary glands had high titers of brucellae in milk, moderate interstitial mastitis, and brucellar antigen in macrophages located primarily in alveolar and ductal lumina. Brucellae often filled the macrophage cytoplasm. In contrast, nursed mammary glands had fewer brucellae in milk, minimal inflammatory changes, and no detectable brucellar antigen in histologic sections. Hyperplastic changes were only seen in supramammary lymph nodes draining nonnursed mammary glands; these contained more brucellae than lymph nodes draining nursed mammary glands. These studies show that milk stasis may be the sole cause of increased susceptibility of nonnursed mammary glands to B abortus infection.

Bovine mammary glands were inoculated intracisternally with a streptomycin-resistant (SR) strain of Corynebacterium bovis to determine the number of colony-forming units (CFU) required to induce colonization and to maintain persistence of C bovis colonization throughout lactation and involution. Streptomycin resistance was used as a strain marker. Uninfected quarters in cows during midlactation were challenge exposed with successively higher numbers of SR C bovis until all quarters became colonized. Inoculum containing 790 CFU of SR C bovis established colonization in only 7 of 38 quarters. Colonization persisted in only 4 of these quarters by 23 days after inoculation. Eleven quarters were reinoculated with higher numbers of SR C bovis, and all became colonized by the time challenge-exposure inoculum contained 8 X 10(4) CFU. Colonization persisted throughout the 93-day experimental period. Somatic cell counts were significantly (P less than 0.01) higher in SR C bovis-colonized quarters after inoculation than before. Sixteen additional quarters were inoculated with a mean number of 8 X 10(4) CFU of SR C bovis 7 days before suppression of lactation. All quarters became colonized, and SR C bovis was shed during the experimental period; throughout the nonlactating and peripartum periods, high numbers of SR C bovis in pure culture were shed from 13 of 16 quarters.

Intramammary devices (IMD) were abraded with medium-grade emery cloth or were left smooth. One IMD of each type was inserted into a mammary quarter of each of 5 lactating cows. The remaining 2 quarters served as controls. Quarter foremilk, bucket milk, and stripping milk samples were collected for 3 consecutive days at 2 weeks after IMD insertion, and milk somatic cell counts (SCC) were determined. Milk samples also were collected immmediately after and 0.5, 1,2,4,6,8, and 11 hours after milking. All quarters were challenge exposed with 250 colony-forming units of Streptococcus uberis at 2 months after IMD insertion. Foremilk and stripping milk samples were collected for bacteriologic culture and SCC at the next 10 milkings. Mean foremilk, bucket milk, and stripping milk SCC (X 10(6) cells/ml) were 0.18, 0.07, and 0.91, respectively, for quarters with abraded IMD; 0.06, 0.05, and 0.43, respectively, for quarters with smooth IMD; and 0.03, 0.03, and 0.15, respectively, for control quarters. Mean SCC after milking ( X 10(6) cells/ml) for the various intervals were 0.70, 1.29, 0.70, 0.97, 1.15, 1.17, 0.77, and 0.85 for quarters with abraded IMD; 0.43, 0.62, 0.61, 0.45, 0.64, 0.60, 0.31, and 0.26 for quarters with smooth IMD; and 0.15, 0.24, 0.15, 0.19, 0.15, 0.15, 0.14, and 0.06 for control quarters. After challenge exposure, 2 of 5 of the quarters with abraded IMD, 4 of 5 of the quarters with smooth IMD, and 8 of 9 of control quarters became infected. Results indicated that abraded IMD increased SCC in stripping milk to concentrations that provided 60% protection against challenge exposure with S uberis.

Twelve biotinylated lectins and an avidin-biotin-peroxidase method were used to detect and localize specific carbohydrate residues on formalin-fixed, paraffin-embedded female canine mammary gland sections. Histologic sections from 3 lactating and 7 nonlactating mixed-breed dogs (age 5.6 +/- 0.35 years) were incubated with Arachis hypogea agglutinin (peanut agglutinin; PNA), Concanavalia ensiformis agglutinin (conA), Dolichos biflorus agglutinin (DBA), Glycine max agglutinin (SBA), Griffonia simplicifolia agglutinin-I (GS-I), Lens culinaris agglutinin (LCA), Lycopersicon esculentum agglutinin (LEA), Phytolacca americana mitogen (pokeweed mitogen; PWM), Ricinus communis agglutinin-I and-II (RCA-I and -II), Triticum vulgaris (WGA), and Ulex europaeus agglutinin-I (UEA-I). Each lectin had a specific binding pattern, except SBA and DBA. In nonlactating glands, PNA, conA, LEA, and UEA-I stained duct cells in a linear-binding pattern, with a mean percentage of positive ducts per section of 28.7 (+/- 0.6), 65.7 (+/- 0.3), 100 (+/- 0), and 8.4 (+/- 0.2), respectively. Strong apical, lateral, basal, and cytoplasmic positivity on duct cells was seen after incubation of the sections with RCA-I, RCA-II, and WGA in all ducts. In acinar cells, the binding pattern and the staining distribution of all the lectins studied were similar to those in duct cells. However, for PNA, conA, and UEA-I, the mean percentage of positive lobules per section was 33.7 (+/- 0.9), 62 (+/- 0.5), and 10.5 (+/- 0.2), respectively. In glands from lactating dogs, conA and UEA-I did not stain. The cytoplasm of all myoepithelial cells was moderately stained with RCA-I, RCA-II, and WGA. Endothelial cells stained with GS-I, PWM, RCA-I, RCA-II, WGA, conA, and LCA. The extracellular matrix, especially the periacinar and periduct regions, and the interstitial fibroblasts were positive for LCA, RCA-I, RCA-II, and WGA. Peripheral unmyelinated nerve fibers of the nipple were strongly positive for GS-I, PWM, RCA-1, RCA-II, and WGA. Some of the lectins used (ie, PNA, conA, UEA-I, GS-I, PWM, and LEA) appear to have selective staining of mammary gland structures that seems to be correlated with various physiologic functions. The contrasting binding pattern of lectins specific for the same sugar indicates a lack of knowledge of interactions between lectins and carbohydrate residues in tissue sections.

Streptococcal species isolated from dairy cows with clinical mastitis were obtained from mastitis research workers in Florida, Louisiana, New York, Vermont, Washington, and West Virginia. Seventy-one streptococcal isolates were tested, including 39 strains of Streptococcus agalactiae, 21 strains of S dysgalactiae, and 11 strains of S uberis. The minimal inhibitory concentration of erythromycin, lincomycin, oxytetracycline, penicillin, spectinomycin, streptomycin, and tetracycline was determined for each isolate. Differences were not detected among strains with respect to geographic origin. None of the strains was resistant to penicillin. Lincomycin was the next most effective antimicrobial, with only 2 resistant strains of each streptococcal species. There were no differences among the streptococcal species with respect to resistance to either penicillin or lincomycin. Streptococcus uberis was more likely to be resistant to erythromycin than were S agalactiae and S dysgalactiae (P < 0.02). Streptococcus agalactiae and S uberis had similar distributions for resistance to oxytetracycline, tetracycline, spectinomycin, and streptomycin. Strains of S dysgalactiae were more likely to have intermediate resistance to oxytetracycline and streptomycin than were strains of S agalactiae and S uberis, which were highly resistant to oxytetracycline and streptomycin (P < 0.001). Differences were not detected among the streptococcal species with respect to resistance to spectinomycin. Resistance to multiple antimicrobials was observed in all streptococcal species tested. Although S dysgalactiae appeared to have a greater percentage of strains (73%) that were resistant to multiple antimicrobials than did S agalactiae (31%) or S uberis (45%), differences were not statistically significant.

An intramammary device (IMD) was adapted for use in ewes; this device was made of abraded poly. ethylene material (1.7 mm in diameter, 47 mm long) and formed a 15-mm-diameter loop in the gland cistern. The IMD was inserted in 1 gland in each of 43 ewes. A significant (P < 0.0001) increase in milk somatic cell count (SCC) was observed in glands provided with an IMD. This increase was attributable to an increase in neutrophil numbers and was observed during the first 12 weeks after insertion. The IMD had a protective effect against experimentally induced staphylococcal mastitis (Staphylococcus aureus and S epidermidis), although different milk SCC were required for protection from each bacterial species in most ewes (10(6) and 2 X 10(5) cells/ml, respectively). Histologic studies revealed that the IMD induced local squamous metaplasia in the glandular part of the lactiferous sinus. Erythrocytes were found in milk from glands provided with an IMD throughout the studied period (35 days of the 45-day lactation) and, in some cases, blood clots were observed during the first 2 weeks of lactation. Glands with IMD also had lower milk production and quality at 30 and 32 days of lactation. Eight ewes with IMD were studied throughout a subsequent lactation. Milk from the IMD-containing glands had an increase in SCC, as in the previous lactation period; did not contain blood clots or erythrocytes; and had normal composition (similar to that in glands without the IMD).

Blood and urine chemical values at parturition in clinically normal Holstein cows (n = 12) were compared with the same values in Holstein cows developing udder edema (n = 12). There was no statistically significant mean difference between the 2 groups for the serum and urine chemical data. Furosemide (500 mg) given IV caused a significant increase in serum calcium and sodium, urine chloride, potassium, and sodium, and fractional excretional ratio of chloride, potassium, and sodium. There was a significant mean decrease in the serum potassium, urine creatinine, osmolality, pH, and specific gravity. Hydrochlorothiazide (250 mg) given IV caused a significant mean increase in serum chloride, urine chloride, potassium, and sodium, and fractional excretion ratio of chloride, potassium, and sodium. There was a significant mean decrease in serum potassium and sodium, urine osmolality, pH, and specific gravity. Acetazolamide (500 mg) given IV caused a significant mean increase in blood urea nitrogen, serum chloride and glucose, urine sodium, and fractional excretion ratio of sodium, while causing a significant mean decrease in serum potassium, sodium, and phosphorus, and urine creatinine. Dextrose (500 g) given IV as a 50% solution caused a statistical mean increase in serum glucose, urine chloride, potassium, and sodium, and fractional excretion ratio of chloride and potassium. A statistical mean decrease occurred in the packed cell volume, blood urea nitrogen, serum calcium, potassium, sodium, and phosphorus, urine creatinine, osmolality, and pH.