The aetiology and pathogenesis of ovine foot-rot: I. A histological study of the bacterial invasion

Abstract

Tissues from the feet of a number of sheep with natural or experimental foot-rot were examined histologically to elucidate the invasive and pathogenic role of each of the bacterial forms demonstrable in the lesion. Cocco-bacilli and diphtheroids were relatively superficial in location and did not appear to participate directly in the infection. Spirochaetes and motile fusiforms penetrated more deeply, but grew mainly in tissue already destroyed by the pathogenic process. They did not invade alone into fresh tissue. Spirochaetes were not detectable in artificial cases until typical foot-rot had developed, even when the disease was induced with natural infective material containing them. It is concluded that spirochaetes and motile fusiforms are probably not essential to the pathogenesis of foot-rot. Like F. necrophorus they are derived from the environment and do not have to be transferred with F. nodosus. F. nodosus and F. necrophorus were the only organisms to be seen penetrating fresh epidermal tissue. In early lesions F. nodosus was predominant at the point of separation where it was often the sole invader. However, there was little associated tissue response and, although F. nodosus is essential to foot-rot, its role in the destructive process is uncertain. There was usually severe inflammation and destruction in response to invasion by F. necrophorus, which thus undoubtedly contributes to the severity of foot-rot. The ability of F. nodosus to cause foot-rot without the assistance of F. necrophorus appears doubtful. Under conditions that permitted the artificial reproduction of foot-rot, a superficial invasion by F. necrophorus always preceded the growth of F. nodusus in the lesion. The establishment of F. nodosus was followed by deeper penetration of F. necrophorus, recognizable histologically and also by an allergic acceleration of the inflammatory response in sheep vaccinated against F. necrophorus. It was confirmed that the separation of horn is caused by inflammatory destruction of the epidermal matrix, a process described in histological detail. There was no evidence of separation due to a direct bacterial attack on the horn itself.