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Fungal infection of the lung results in an acute to chronic active, pyogranulomatous pneumonia.
Etiology
Cryptococcus neoformans, Histoplasma capsulatum, Coccidioides immitis, Blastomyces dermatiditis, Pneumocystis jiroveci, Aspergillus spp, Candida spp, and other less common fungi have been identified as causative agents of mycotic pneumonia in domestic animals (also see Fungal Infections). Often these agents are found in immunocompromised hosts, but they can cause disease in healthy individuals as well. Infection is typically caused by inhalation of spores, which can lead to hemolymphatic dissemination. Pulmonary tissues and secretions are an excellent environment for these organisms. The source of most fungal infections is believed to be soil-related rather than horizontal transmission. Considering the high rate of exposure to these pathogens in certain environments, there are unresolved questions on the epidemiology of the condition, including individual susceptibility, pathogenicity of organisms, the immune response of the host, and concurrent disease. Blastomyces and Histoplasma are prevalent in the Mississippi and Ohio River valleys, whereas Coccidioides is found in the southwestern USA and northwestern Mexico. Cryptococcus is often associated with accumulation of pigeon excreta.
Clinical Findings
Mycotic pneumonia is more commonly seen in small animals. Blastomyces infections typically occur in young, male, large-breed dogs. In cats, Cryptococcus has a predilection for the nasal cavity, where it causes a granulomatous rhinitis and sinusitis. Acute, fulminant clinical presentations do occur but are rare, and the most common course of disease is chronic. A short, moist cough is characteristic. A thick, mucoid to mucopurulent nasal discharge may be present. As the disease progresses, dyspnea, emaciation, and generalized weakness become increasingly evident. Respiration may become abdominal, resembling that of a diaphragmatic hernia (see Diaphragmatic Hernia). On auscultation, harsh respiratory sounds are heard. In advanced cases, breath sounds are decreased or almost inaudible. Tracheobronchial lymphadenopathy can cause extrinsic airway compression. Neutrophilic leukocytosis or neutropenia with a left shift, nonregenerative anemia, and periodic fever can occur, possibly concurrent with bacterial infections. Radiography shows enlargement of tracheobronchial lymph nodes and variable, nodular to linear, interstitial infiltrates.
Lesions
Multifocal to coalescing lesions of granulomatous to pyogranulomatous inflammation are present in the lungs. Abscess formation and cavitation may be seen in conjunction with yellow or gray areas of necrosis. Causative organisms are present within macrophages or areas of intense inflammation. Dissemination to other organ systems (eg, skin, eyes, peripheral lymph nodes, bones, CNS, male genitalia, oral cavity, nasal cavity) may occur.
Diagnosis
A tentative diagnosis of mycotic pneumonia can be made if an animal with chronic respiratory disease exhibits the clinical signs described and does not respond to antibiotic therapy. Definitive diagnosis requires laboratory confirmation. Radiography may be useful. Serology can provide a presumptive diagnosis. Some antigens (eg, histoplasmin, blastomycin) have been developed and are an aid in diagnosis. Cytologic examinations of the sputum or exudates from sites of extrapulmonary inflammation may reveal the etiologic agent. The clinical diagnosis can be confirmed at necropsy by appropriate microbiology and histopathology. Special stains can be used to highlight the organisms.
Treatment
There is no entirely satisfactory method of treating systemic mycotic infections. Amphotericin may be helpful but is undesirably nephrotoxic. Ketoconazole, and several newer antifungal agents such as itraconazole and fluconazole, show better, but variable, results against fungal pathogens in companion animals. Protracted therapy, at least 2 mo beyond clinical resolution, is usually necessary for elimination of the infection.
Last full review/revision March 2012 by Neil W. Dyer, DVM, MS, DACVP
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