Background
Nocardiosis is an acute, subacute, or chronic infectious disease that occurs in cutaneous, pulmonary, and disseminated forms. Primary cutaneous nocardiosis manifests as cutaneous infection (cellulitis or abscess), lymphocutaneous infection (sporotrichoid nocardiosis), or subcutaneous infection (actinomycetoma). Pleuropulmonary nocardiosis manifests as an acute, subacute, or chronic pneumonitis, usually in immunocompromised hosts, although isolated cases have been reported in immunocompetent hosts. Disseminated nocardiosis may involve any organ; lesions in the brain or meninges are most common.
Pathophysiology
Members of the genus Nocardia are aerobic actinomycetes that are ubiquitous saprophytes in soil, decaying organic matter, and water. At least 30 species of the genus Nocardia have been identified, and at least 13 of these are reported to cause human disease. New Nocardia species continue to be identified.[1] Nocardia asteroides is responsible for most cases of Nocardia disease among humans in the United States; various other Nocardia species are dominant in other parts of the world. Nocardia species also cause infections in animals, including bovine mastitis and sporotrichoid nocardiosis in horses.
When observed microscopically, either in Gram-stained smears of clinical specimens or cultures or on histopathology in tissues, Nocardia organisms are branching, beaded, filamentous, gram-positive bacteria with a characteristic morphology to a trained observer.
High-power microscopic appearance of Nocardia. Image courtesy of CDC. Nocardia are typically weakly acid-fast after traditional staining and positive on modified acid-fast staining, but this is not invariable.
The cutaneous, lymphocutaneous, and subcutaneous forms of nocardiosis arise from local traumatic inoculation. These infections are not necessarily associated with immunocompromised host states, but dissemination from these sites of inoculation is more likely in immunocompromised hosts. Pleuropulmonary nocardiosis presumably arises from inhalation exposure. Disseminated nocardiosis results from hematogenous dissemination, usually from a pulmonary focus. Most persons with disseminated nocardiosis have underlying immunocompromising disease or are receiving immunosuppressive therapy.
Nocardiosis produces suppurative necrosis with frequent abscess formation at sites of infection.
Photomicrograph of tissue biopsy stained with Gomori methenamine silver demonstrating acute inflammatory response and organisms compatible with Nocardia.Disease manifestations of nocardiosis are determined by strain characteristics, inoculation site, tissue tropism, ability to survive initial neutrophilic leukocyte phagocytic attack, and the nature of the immune response. T-cell–mediated immunity is the principal protective immune response to nocardiosis.[2] Therefore, nocardiosis is most problematic in individuals with impaired T-cell–mediated immunity.
Epidemiology
Frequency
United States
In the 1970s, a survey estimated the incidence of nocardiosis in the United States at 500-1000 cases per year (0.4 cases per 100,000 population per year). However, with the increased prevalence of impaired cell-mediated immunity since then, the incidence of nocardiosis has likely also increased.[3]
Clusters of nocardiosis have been described in hospitalized patients, related to contaminated fomites from construction or contaminated hands of staff.[1]
International
No reliable estimates on the international frequency of nocardiosis are available.
Mortality/Morbidity
Nocardiosis has a variable prognosis, depending on the site of infection, extent of infection, and underlying host factors.[4]
- Cure rates with appropriate therapy are approximately 100% in skin and soft-tissue infections.
- Ninety percent of pleuropulmonary infections can be cured with appropriate therapy.
- The cure rate in disseminated nocardiosis falls to 63%, while only half of patients with brain abscess can be cured with therapy.
Race
Nocardiosis has no apparent racial predilection.
Sex
Nocardiosis is more common in males than in females, with a male-to-female ratio of 3:1. This difference may be related to exposure frequency rather than a gender difference in susceptibility.
Age
All ages are susceptible to nocardiosis. The mean age at diagnosis is in the fourth decade of life.
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| N asteroides | N farcinica | N nova | N brasiliensis | N transvalensis | N otitidiscaviarum | |
| Sulfamethoxazole | 96-99 | 89-100 | 89-97 | 99-100 | 90 | Variable |
| TMP-SMX | 100 | --- | --- | 100 | 88 | Variable |
| Amoxicillin-clavulanate | 53-67 | 47-71 | 3-6 | 65-97 | 30 | Resistant |
| Ceftriaxone | 94-100 | 0-73 | 100 | 88-100 | 50 | --- |
| Imipenem | 77-98 | 64-87 | 100 | 20-30 | 90 | Resistant |
| Amikacin | 100 | 100 | 100 | 100 | 82 | Susceptible |
| Minocycline | 78-94 | 20-96 | 89-100 | 75-90 | 54 | Susceptible |
| Linezolid | 100 | 100 | 100 | 100 | 100 | 100 |

