Clinical signs are generally not observed in immunocompetent hosts, although the host response to P. aeruginosa infection varies among inbred mouse strains. Some immunocompromised mice and rats may develop hunched posture, apathy, dullness, shortness of breath, ruffled coat, emaciation, circling movements around their longitudinal axis, and oblique head posture, and some of them will die. Clinical disease is due to invasion of deep tissues, resulting in hematogenous spread of the bacteria to multiple organs. Entry into the vascular system may be facilitated by pseudomonal proteases and bradykinin generated in infectious foci. Pathologic lesions are found in affected tissues and consist of multifocal necrosis, abscess formation, and suppuration.
Lesions are often most severe in the lungs.
Vegetative lesions may be found on heart valves of animals with infected indwelling vascular catheters. Much of what is known of the cell biology of P. aeruginosa infections comes from experimentally induced infections. Studies of immune responses to P. aeruginosa present evidence of both humoral and cellular contributions to immunity, which is enhanced by vitamin B2 and IL-1. Macrophages and neutrophils are important effector cells, with neutrophil accumulation mediated through CD11 and CD18 cells. Also, inbred mouse strains differ in susceptibility.