Natural Habitat

The moraxellae are commensals on the mucous membranes of man and other mammals. The reservoir of M. bovis is thought to be the conjunctiva or nasopharynx of asymptomatic cattle over two years of age. The Moraxella species are susceptible to desiccation and do not survive well away from the animal host. Transmission is by direct contact or via flying insects.

Pathogenesis and Pathogenicity

Moraxella bovis, the cause of infectious bovine keratoconjunctivitis, is the major animal pathogen in the genus. The pathogenicity of M bovis strains depends on the production of type IV pili and a cytotoxin, in addition to other putative virulence factors (Table 29.1). The cytotoxin is a haemolysin and belongs to the repeat-in-toxin family of toxins (Angelos et al. 2001). Strains which are not haemolytic or lack pili are apathogenic for cattle. In addition to the pili, which have a major role in attachment of the organism, filamentous-haemagglutinin-like proteins may be important in the infectivity of the organism (Kakuda et al. 2006). Other enzymes which may play a role in tissue destruction include fibrinolysins, proteases and phospholipases. Acquisition of iron through transferrin and lactoferrin-binding proteins may contribute to virulence also.

Predisposing environmental factors are implicated in infectious bovine keratoconjunctivitis. These include irritation to the eyes by ultra-violet light (in sunlight), dust, long vegetation and flies. The incidence of the disease is highest in the summer months. Concurrent infections by such agents as Mycoplasma bovoculi, Listeria monocytogenes, Chlamydophila pecorum, bovine herpesvirus 1, bovine adenoviruses and the nematode Thelazia species may complicate the disease. Young animals under two years of age are most commonly affected and in a typical outbreak of disease about 60% of the young cattle may be affected while only about 20% of the older animals are affected.

The early signs of infectious bovine keratoconjunctivitis are lacrimation, blepharospasm and conjunctivitis. Later an ulcer develops on the cornea. Corneal opacity and oedema surround the ulcer and in severe cases vascularization of the cornea occurs from the limbus to the ulcer. The corneal opacity then involves the entire cornea. In the healing stage, granulation tissue forms on the ulcer floor and a characteristic red cone of granulation tissue will project from the cornea (Fig. 29.1). The granulation tissue and the ulcer itself will eventually regress leaving a white corneal scar. The scar may or may not be permanent. Mild cases are similar, but ulcers resolve without vascularization occurring and most eyes become clinically normal in two to three weeks.