The effect of transportation vibration on the microbiological status of bottled mineral water.

BACKGROUND: Microbiological status and stability are important in mineral waters because of increased global demand. An increase in distribution and supply chains has led to prolonged periods of transportation, causing microbiological changes. Therefore, this study examines the effect of vibration on mineral water quality. Freshly bottled and previously sterilized mineral waters inoculated with microbes isolated from freshly bottled water were tested. The water samples were exposed to random vibration using ASTM (D4169) truck level I, II and III standard vibration protocol for truck transportation at 4 × 1 h at 22 ± 1 °C. After agitation their microbiological status was determined. RESULTS: Under the influence of low-intensity mechanical impact, the growth rate of autochthonous species in the freshly bottled natural mineral water tripled (µcontrol  = 0.036 h-1 , µvibrated  = 0.093 h-1 ) and that of allochthonous species doubled (µcontrol  = 0.035 h-1 , µvibrated  = 0.069 h-1 ). The latter was also observed in the case of high-intensity vibration (µcontrol  = 0.102 h-1 , µvibrated  = 0.200 h-1 ). The effect of the medium intensity of the standard was manifested in the delay in microbial growth. CONCLUSION: The impact of transportation vibrations on microbiological status changes in mineral water could be observed when subjected to vibration. The native and allochthonous species of mineral water respond differently to changes in intensity. © 2022 The Authors. Journal of The Science of Food and Agriculture published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.

Epstein-Barr virus (HHV-4) inoculation to rabbits by intranasal and oral routes results in subacute and/or persistent infection dissimilar to human disease.

OBJECTIVE: We report the infection of New Zealand white rabbits with Epstein-Barr virus (EBV). METHODS: EBV prepared in B95-8 (producer) cells was inoculated to rabbits by combined intranasal and oral routes. Blood and white blood cell (WBC) samples were taken before infection, then on days 8, 28 and 98 post-infection (p.i.). RESULTS: Administration of either 3 × 10(8) (group A, 11 rabbits) or 1 × 10(9) (group B, 10 rabbits) EBV DNA copies per animal induced subacute and/or persistent infection. The IgG antibodies in plasma were detected by ELISA as well as by immunoblot (IB). The IB bands showed mainly antibodies to the BZRF1/Zta transactivation polypeptide (69.2%), the p54 early protein (53.4%) and to the p23 capsid protein (35.8%). No anti-EBNA1 antibody was detected throughout. Viral DNA could be detected by PCR in WBCs and/or spleen of 7 out of 21 infected rabbits (30%), while 60-80% of them showed serologic response. The transiently present EBV DNA was accompanied by LMP1 antigen. CONCLUSIONS: Rabbits developed persistent EBV infection in the absence of EBNA1 antibodies and by the lack of typical infectious mononucleosis-like syndrome. The absence of EBNA1 antibody may reflect the lack of EBNA1 in B cells of EBV-inoculated rabbits.

Short communication: role of Mycoplasma arginini in mastitis caused by Streptococcus dysgalactiae.

We performed a comparative study on the development of mastitis induced by Mycoplasma arginini or Streptococcus dysgalactiae after challenging the cows. Mycoplasma arginini did not cause any clinical symptoms on its own, resulting in only a transient increase of somatic cell count (SCC; increase ranging from 0.5 × 10(6) to 0.8 × 10(6) cells/mL) and a slight decrease of milk production (10%) for 5 d. In contrast, Strep. dysgalactiae induced more severe clinical signs in animals and SCC increased to 1.60 × 10(6) to 2.11 × 10(6) cells/mL for 10 d. In addition, milk production decreased (22.9 to 27.0%) for 10 d. After 3 mo (2 mo after the first challenge), animals that were challenged previously with M. arginini were rechallenged with Strep. dysgalactiae. Severe clinical mastitis developed, with very high SCC (5.00 × 10(6) to 21.5 × 10(6) cells/mL), and a very significant reduction of milk production (28.6 to 68.7%), which lasted more than 4 wk, was observed. The severe clinical mastitis developed not only in cows inoculated with Strep. dysgalactiae andM. arginini in the same udder quarter but also in cows infected in the quarter previously not challenged with mycoplasma. Cows challenged first with Strep. dysgalactiae and rechallenged with M. arginini 2 mo later developed only slight changes in both SCC and milk production, similar to those when the cows were challenged with M. arginini alone. We conclude that M. arginini infection does not cause remarkable mastitis (characterized by decrease in milk production and increase of SCC) but it significantly predisposes animals to infection with Strep. dysgalactiae, leading to severe clinical mastitis.