Mastitis is an important animal health disease which constitutes a serious problem for the dairy industry in New Zealand. Mastitis reduces milk yield and quality, necessitates the use of antibiotic therapy, with associated risks of contaminating the raw milk supply, and imposes a serious economic burden, currently estimated at NZ$300 million per year. Mastitis is caused by a variety of infectious agents. In the New Zealand context, with cattle grazing on pasture, Streptococcus uberis is a major bacterial pathogen, responsible for a significant proportion of clinical cases, especially during early lactation and the dry period. Other pathogens of significance include Staphylococcus aureus, Streptococcus dysgalactiae and Escherichia coli, as well as so-called 'minor pathogens', namely coagulase-negative staphylococci(CNS). Current strategies aimed at reducing cases of mastitis include improved hygiene in the farm environment, particularly with regards to the health and cleanliness of teats. Once mastitis occurs, antibiotic therapy is a favoured option, and as a prophylactic tool, in the form of dry-cow therapy, has also shown value. Prevention of mastitis using immunological tools such as vaccines lags behind the major vaccine breakthroughs that have been achieved in preventing and/or reducing the severity of numerous infectious diseases in animals. In this review, the current state of research in the area of development of vaccines against mastitis is summarised, with particular emphasis on bacteria important to the dairy farming industry in New Zealand. Few, if any, effective vaccines have been designed to prevent or mitigate intramammary infections. It is argued that novel approaches must be considered to search for vaccine candidates, and vaccines need to be designed and constructed within the special framework of their uses, in the mammary gland which offers a unique immunological environment. In addition, effective vaccines against mastitis due to Strep. uberis may be more likely to emerge from strategies that target the cell-mediated arm of the immune response rather than strategies that target specific antibody responses.