SUMMARYThe mutation lg of phage P2 has been located on the genetic map of P2 to the right of, and closely linked to, the del2 deletion, probably within tail gene F. The lg mutation causes larger burst sizes, compared with the wild type, especially at high incubation temperatures. The frequency of defective particles is lower in preparations of P2 lg than in those of wild type P2. It seems that the mutation lg improves the efficiency of particle assembly.

Campylobacter jejuni/coli is the leading bacterial cause of diarrhoea in humans in both developing and developed countries. Epidemiological studies show that most cases of campylobacteriosis are the result of the consumption of undercooked, contaminated poultry meat. Although campylobacteriosis is largely a self-limiting disease with low mortality, a specific treatment is required for patients infected with strains resistant to clinically important antibiotics and for patients who develop neurological symptoms or bacteremia in course of infection. Despite intensive efforts to improve an on-farm biosecurity practice over the past decade, about 70% of EU broiler chicken flocks remain Campylobacter-positive at slaughter. Control of spreading the Campylobacter infection in flocks of chickens by biosecurity actions turned out rather ineffective. The most efficient strategy to decrease the number of human Campylobacter infections may be to implement an immunoprophylactic method, namely, the protective vaccination of chickens. The publication presents the current state of knowledge on anti-Campylobacter immunoprophylaxis in poultry. 1. Campylobacteriosis – epidemiological data, disease symptoms. 2. Campylobacteriosis – source of infection. 3. Campylobacteriosis – prophylaxis. 4. Immunization of chicken. 4.1. Passive immunization. 4.2, Campylobacter Whole-cell Vaccines. 4.3. Subunit vaccines. 5. Strategies for developing modern subunit vaccines. 5.1 Searching for antigen. 5.2. The choice of a carrier. 6. Modulation of immune response. 7. The route of antigen administration. 8. Summary