A possible regulatory function for bacterial outer surface components in fireblight disease

Both the wild-type isolate of Erwinia amylovora (Burrill) Winslow and a noncapsulated avirulent form, mutant S, when in contact with pear fruit slices, induced electrolyte leakage and grew rapidly. A capsulated form of the mutant S, induced by growing it in d-galactose medium, was found to have reduced capacity to cause leakage and grew less rapidly. Loss of capsule by the pre-capsulated mutant occurred simultaneously with increased leakage of pear electrolytes and bacterial growth. Another capsulated avirulent form, mutant P, did not induce electrolyte leakage from pear tissue and failed to grow. In mixed inocula, the capsulated mutant P partially inhibited the action and growth of both the wild-type and the non-capsulated mutant S on pear tissue. Prevention of contact between bacterial inoculum of the wild-type for the non capsulated mutant S, and the pear tissue by means of a membrane filter, also prevented loss of electrolytes and bacterial growth. Cell-free fluids from cultures of bacteria in artificial media or from inoculated pear tissue suspensions, failed to cause loss of electrolytes from healthy pear slices. Wild-type bacteria isolated from infected apple plants contained a proportion of cells wholly or partly deficient in outer surface components, in contrast to bacteria grown in culture, which were more uniformly coated. It is suggested that host damage is caused by contact with partially or wholly noncapsulated virulent bacteria and that the amount of damage is regulated by the properties of the outer coat of the pathogen. It is also suggested that the regulation of host damage is a requisite for infection and the progress of the disease.