Signs and Their Pathogenesis

The pathogenicity of Nocardia spp. is influenced by the strain and growth phase of the organism, and host susceptibility. Virulent Nocardia strains are facultative intracellular pathogens that inhibit phagosome-lysosome fusion, neutralize phagosomal acidification, resist oxidative burst, secrete superoxide dismutase, and alter lysosomal enzymes within neutrophils and macrophages.¹⁷ These effects are partly related to the content and structure of mycolic acids within the bacterial cell wall, which vary among strains and throughout the growth phase. Filamentous log-phase cells in the environment can be highly resistant to phagocytosis. Some strains have a greater propensity to invade the central nervous system (CNS).^19,20

The normal host response to infection is characterized by an initial pyogenic inflammatory response, but a cell-mediated immune response is necessary to destroy the organisms. Diminished host resistance, especially impaired cell-mediated immunity (CMI), is a primary factor in susceptibility to nocardiosis and the extent to which dissemination occurs.

Cutaneous-subcutaneous nocardiosis, the most common form in cats (>75% of affected cats), is characterized by slow and progressive circumferential spread of a nonhealing, draining wound (Figure 43-2). Lesions are typically subacute to chronic. Infections of feeding tube sites can also occur.²¹ Mycetoma-like lesions in the inguinal area resemble those described for rapidly growing mycobacterial infections (see Chapter 44), with multiple draining sinuses. These may result from contamination of “raking” injuries inflicted by the hindlimbs during fighting behavior,⁸ or contamination of traumatic wounds from penetrating plant material. Cutaneous-subcutaneous nocardiosis was documented in 8 of 9 dogs from Brazil⁶ but represents the minority of canine nocardiosis cases in California and Australia.^8,9 Dogs with cutaneous involvement typically develop draining wounds and masses, often on the head and limbs. Osteomyelitis can occur in association with cutaneous lesions.

The pathogenesis of pulmonary or disseminated nocardiosis is similar to that of the deep mycoses. Branching nocardial filaments fragment into small, unicellular particles that are aerosolized and inhaled, possibly in dust. Once within the lung, Nocardia spp. proliferate in the face of immune suppression, which leads to formation of intrapulmonary masses or pneumonia, hilar lymphadenopathy, and/or extrapulmonary masses and pyothorax (Figure 43-3, A). Pulmonary nocardiosis is the most common form of nocardiosis in humans and also occurs in dogs and less commonly in cats. In dogs, it can have a peracute onset characterized by tachypnea, hemoptysis, hypothermia, collapse, and death; however, subacute to chronic clinical signs are more common.22–25 Co-infection with CDV is occasionally reported.^6,26,27 Disseminated nocardiosis occurs when organisms in the lung erode into blood vessels and spread systemically, with abscess formation in a variety of organs. This results in signs of lethargy, fever, inappetence, and signs that relate to the location of the infectious process. Disseminated disease occurs in cats as well as in dogs. The most frequently involved extrathoracic organs after dissemination are skin and subcutaneous tissue, kidney, liver, spleen, lymph nodes, CNS, eye, bone, and joints. In dogs and cats, CNS lesions can result in seizures or neurologic signs that relate to the local effects of abscesses or granulomas in the brain, meninges, or spinal cord (see Figure 43-3, B). CNS involvement is common in human nocardiosis. Peritoneal nocardiosis has rarely been reported in cats, possibly as a result of penetrating wounds to the abdomen.^8,28

Physical Examination Findings

Physical examination findings in animals with cutaneous-subcutaneous disease consist of chronic, sometimes crusted, ulcerated, nonhealing draining wounds, and in cats may involve the extremities, inguinal area, flank, head, bridge of the nose, and neck (see Figure 43-2). Animals with pulmonary or systemic involvement may have a thin body condition, lethargy, and fever. Tachypnea and cough may be present, and lung sounds may be increased (with bronchopneumonia) or decreased (with pyothorax). Involvement of the liver, spleen, and lymph nodes may result in hepatomegaly, splenomegaly, and/or peripheral or abdominal lymphadenomegaly. Ophthalmic examination may reveal chorioretinitis. Bone or joint infection results in focal limb swelling and lameness. Animals with CNS involvement may show mental obtundation, anisocoria, decreased menace and pupillary light responses, head tilt, nystagmus, decreased gag reflexes, and/or delayed or absent placing reactions.

Laboratory Abnormalities

Diagnostic Imaging