History and exam
Key diagnostic factors
common
presence of risk factors
Strong risk factors include cell-mediated immunocompromise, structural pulmonary disease, malignancy, or chemotherapy.
cough with purulent sputum
Pulmonary infection is the most frequent clinical presentation of nocardiosis, accounting for approximately two-thirds of cases. No specific sign or symptom is associated with pulmonary involvement, and the clinical presentation can be acute, sub-acute, or chronic. Fever, cough, and purulent expectoration are typically seen. Radiographic features include consolidation, nodules, or cavities on chest x-ray. Pleural effusion and empyema are also common.[21]
fever
Typical presenting symptom of pulmonary nocardiosis.
Other diagnostic factors
common
headache
Due to raised intracranial pressure from brain abscess(es).
nausea and vomiting
Due to raised intracranial pressure from brain abscess(es).
confusion
Due to raised intracranial pressure from brain abscess(es).
depressed consciousness
Due to raised intracranial pressure from brain abscess(es).
cutaneous ulcers or abscesses
One half of cases of pulmonary nocardiosis involve body sites other than the lungs. Approximately 20% of patients with disseminated infection present solely with extra-pulmonary disease, and the most frequently affected body sites are the central nervous system, skin, and soft tissues.[8]
Risk factors
strong
solid organ and haematopoietic stem cell transplant recipients
Deficient cell-mediated immunity makes these patients highly susceptible to Nocardia species infections.[21]Nocardia is a well-recognised, though rare, cause of cutaneous, pulmonary, and disseminated infection in solid organ transplant and haematopoietic stem cell transplant recipients.[22][23][24][25][26]
The frequency of Nocardia infections in this patient group varies between 0.04% and 3.50%, and these infections have mostly been reported in heart, kidney, liver, lung, and stem cell transplant recipients.[9][10][27]
It is uncommon for Nocardia infection to occur within the first month of organ transplantation. Independent risk factors for Nocardia infection among organ transplant recipients include treatment with high-dose corticosteroids, high levels of calcineurin inhibitors, and a history of cytomegalovirus infection.[28]
Trimethoprim/sulfamethoxazole prophylaxis in the first 6 months after transplantation for the prevention of Pneumocystis jiroveci pneumonia may reduce the rate of Nocardia infections, although breakthrough infections in patients receiving this therapy have been described, particularly with lower doses.[29]
HIV-positive and low CD4 T-cell count (<100 cells/mm³)
Patients with low CD4 T-cell count (<100 cells/mm³) are at risk of developing nocardiosis, due to deficient cell-mediated immunity.[30]
Although nocardiosis incidence is low among patients with AIDS (between 0.1% and 0.4%), it is associated with high morbidity and mortality.[20][31]
Most infections have pulmonary involvement or are disseminated.[32]
Trimethoprim/sulfamethoxazole prophylaxis for prevention of Pneumocystis jiroveci pneumonia in patients with <200 CD4 T cells/mm³ may reduce the rate of nocardiosis.[29] Because the clinical presentation may be very similar, nocardiosis diagnosis can be delayed or even misdiagnosed in HIV-positive patients clinically suspected of having tuberculosis.[33]
The outcome is poor with delayed diagnosis.[32]
immunosuppression
Systemic use of corticosteroids causes selective suppression of cellular immunity.[34] Many case reports describe prolonged use of systemic corticosteroids as a major predisposing factor for pulmonary and disseminated nocardiosis. Corticosteroid therapy is frequently associated with other predisposing conditions such as pulmonary diseases, autoimmune diseases, or transplantation.[35]
Use of anti-tumour necrosis factor drugs for several conditions, such as inflammatory bowel disease, has also been linked to the development of nocardiosis.[36]
structural pulmonary disease
Bronchiectasis and other structural lung abnormalities, such as cystic fibrosis, have been reported as important risk factors for colonisation by Nocardia species.[37] Patients with these clinical conditions are frequently on corticosteroid therapy and thus even more susceptible to invasive nocardiosis.
weak
agricultural work
Patients with primary cutaneous nocardiosis are frequently agricultural workers in whom the entry portal is skin and soft tissues. Infection follows any puncture or other traumatic, direct introduction of Nocardia.[20]
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