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The production of muramidase-released protein (MRP), extracellular protein factor (EF) and hemolysin (suilysin) by 101 Canadian field strains of Streptococcus suis capsular type 2 is described. Most strains (72%) isolated from diseased pigs were MRP-EF- and only 1 strain was MRP+EF+. This strain was also the only 1 to produce the hemolysin. Thirteen strains (15%) were MRP+ EF- and only 3 strains were MRP* EF-. All the strains isolated from clinically healthy pigs as well as a bovine and 2 human isolates had a MRP-EF- phenotype. In addition, 7 strains (8%) had a MRPS phenotype, which had so far been described for S. suis capsular type 1. In conclusion, most Canadian field isolates of S. suis capsular type 2 tested in this study do not produce the virulence-related proteins described so far for this bacterial pathogen.

To determine whether the virulence of Streptococcus suis type 2 is associated with the phenotype of the strain, we infected newborn germfree pigs with 10 strains of S. suis type 2 categorized by three phenotypes. In an earlier study, the phenotypes were distinguished by the presence or absence of the muramidase-released protein (MRP) and an extracellular factor (EF) and were designated MRP + EF +, MRP+ EF- and MRP - EF -. Pigs were first inoculated with Bordetella bronchiseptica to predispose them to infection and were then intranasally inoculated with the streptococci. Strains of the MRP+ EF + phenotype induced fever and increased the number of polymorphonuclear leukocytes in blood. Specific clinical signs of disease such as nervous disorders and lameness were also observed. At necropsy bacteriologic and pathologic examination disclosed meningoencephalitis, polyserositis, and polyarthritis. Strains of the MRP + EF- phenotype induced only nonspecific clinical signs of disease such as recumbency, lack of appetite, and fever; only slight pathologic changes were detected in the serosae. The four strains of the MRP- EF- phenotype induced no signs of disease. These findings indicate that the 110-kDa EF and, to a lesser degree, the 136-kDa MRP may be associated with the virulence of the bacterium. The results demonstrated that S. suis type 2 strains producing both MRP and EF are pathogenic for pigs.

Bulk milk samples of 227 at random selected herds and quarter milk samples of 10336 cows ofthese herds were collected once. Bulk milk somatic cell counts (BMSCCs), which are estimatedevery four weeks, being part of the Dutch Milk Quality Control Programme, were used to calculatethree derivative cell counts: the C3 count, the Cl3 count and the Ci8 count. The correlationof these counts with the prevalence of mastitis in herds was determined. Correlation coefficientsvaried from 0.42 to 0.62. BMSCC and the C3 were neither highly sensitive (maximum sensitivity 75%) nor predictive (maximum predictive value 70 %) in identifying herds with a high prevalenceof mastitis. At the cell count threshold C = 500, 55-76 % herds with a high prevalence ofsubclinical mastitis were not detected by the C3. Thirty-six percent of the herds with a C3 exceedingthe threshold of C = 500 and 42 % of the herds with a C3 exceeding the threshold of c =400 could not be classified as mastitis problem herds. Both BMSCC and C3 had higher sensitivitybut lower specificity and predictive value at a threshold of C = 400 than at the threshold of c= 500. BMSCC and the C3 could reasonably specifically (84-99 %) diagnose herds with a lowprevalence of mastitis. Because of their low sensitivity and predictive value it would not be justifiedto assume a high prevalence of subclinical mastitis on farms based on BMSCC and the C3,without further evidence. Direct bulk milk cell counts and their derivatives appeared unsuitablein determining the prevalence of mastitis in individual herds.

Summary Since 1983 some pig breeding and fattening farms in the Netherlands have been faced with a considerable mortality in pigs due to Streptococcus suis type 2 infections. The most predominant clinical feature of S. suis type 2 infection is meningitis, although sudden deaths often occur. It was noted that some affected farms had imported breeding stock from the United Kingdom. Tonsils of slaughter pigs were collected from herds with and without a history of S. suis type 2 infections. Bacteriological examination was done by using an elective‐selective medium. No significant difference was found in carrier rates of S. suis type 2 between clinically healthy and affected herds (38% vs. 45%). A cohort study was carried out by regular bacteriological examination of tonsil biopsies on a farm with a high incidence of streptococcal meningitis. Twenty‐seven percent of the pigs were carriers of S. suis type 2 at nine weeks of age. Possible methods for disease control are discussed.

The purpose of the national mastitis survey was to collect information on the prevalence and causes of bovine subclinical mastitis in the Netherlands. Milk samples were collected once from 10 336 cows in a stratified random selection of herds (n = 227) in the Netherlands during the years 1985-1986. Results showed that 84.2 % of the cows were free from mastitis. Ten per cent of all udder quarters were infected, and 3.7 % of these were infected with Staphy(ococcus aureus, the main udder pathogen. Statistical analysis based on a 'split-plot' model was used to analyse the effect of herd factors and animal factors on somatic cell counts (SCC). Several factors significantly influenced SCC: breed, season, geographical region, type of housing, and the use of teat disinfection. The effect of herd and animal factors on SCC of milk samples of individual cows was calculated as deviation from the geometric mean cell count of the standard cow (222 000/ml) and presented as the excpected SCC per cow. The interaction of parity x stage of lactation x infection status also significantly influenced SCC. On the basis of expected SCC of uninfected cows correction factors were calculated for individual cows with various parities and at various stages of lactation. We conclude that the use of these correction factors can improve the analysis of SCC in the diagnosis of mastitis.

The heat resistance of Listeria monocytogenes suspended in milk was determined with a plate pasteurizer and glass capillary tubes. The reduction of the, number of Listeria obtained by the plate pasteurizer was ,,;5 log 10 units at 64.0 °C for 10 s and 6-7 log 10 units at 67.0 °C for 10 s. The heat resistance of freely suspended and phagocyted Listeria was investigated with glass capillary tubes. The surviving Listeria were determined with and without resuscitation at 4 °C. Using the resuscitation method it appeared that phagocytosis did increase the heat resistance of one of the two tested Listeria strains by factor 2. With the resuscitation method up to 30 times more Listeria could be recovered than without resuscitation. The estimated decimal reduction times for the most heat-resistant strain was about 17 sat 64.0 °C and 8 sat 66.0 °C. Incubation tests of L. monocytogenes in raw and HTST-pasteurized milk (15 s 72 °C) at 4 and 7 °C showed some injury of Listeria during the first 1-2 days. Thereafter growth commenced. In intensively pasteurized milk (30 min 98 °C) Listeria was not injured. Gouda and Maasdam types of cheese were made from Listeria-contaminated milk. During the manufacture Listeria was concentrated in the curd by factor 10, and a limited growth occurred. During 6 weeks of ripening at 13 °C the number of Listeria was almost constant.