INTRODUCTION — Nocardiosis is an uncommon gram-positive bacterial infection caused by aerobic actinomycetes in the genus Nocardia. Nocardia spp have the ability to cause localized or systemic suppurative disease in humans and animals [1-5]. Nocardiosis is typically regarded as an opportunistic infection, but approximately one-third of infected patients are immunocompetent [5]. (See "Microbiology, epidemiology, and pathogenesis of nocardiosis", section on 'Immunocompromise'.)
The major clinical manifestations and diagnosis of nocardiosis will be reviewed here. Two characteristics of nocardiosis are its ability to disseminate to virtually any organ, particularly the central nervous system, and its tendency to relapse or progress despite appropriate therapy.
The classification of nocardiosis is based upon the location and extent of disease and includes pulmonary, central nervous system, cutaneous, and disseminated disease [2,6]. Although there are no pathognomonic signs or symptoms of nocardiosis, it should be suspected in any patient who presents with brain, soft tissue, or cutaneous lesions and a concurrent or recent pulmonary process. Nocardia colonization of the lower respiratory tract in patients with no clinical disease has also been described [7].
This topic will review the clinical manifestations and diagnosis of Nocardiosis. The microbiology, epidemiology, pathogenesis, and treatment of Nocardia infection are discussed separately. (See "Microbiology, epidemiology, and pathogenesis of nocardiosis" and "Treatment of nocardiosis".)
RISK FACTORS — The risk of nocardial infection is increased in immunocompromised patients, particularly those with defects in cell-mediated immunity [4]. In a literature review of over 1000 cases, 64 percent of patients with nocardiosis were immunocompromised [5]. (See "Microbiology, epidemiology, and pathogenesis of nocardiosis", section on 'Immunocompromise'.)
The causes of immunocompromise have included solid organ or hematopoietic cell transplantation, glucocorticoid therapy, HIV infection (especially if the CD4 count is <100 cells/mm3), malignancy (most often after recent chemotherapy or glucocorticoid therapy), and diabetes mellitus [5,8-12]. Chronic lung disease and alcoholism are additional risk factors for pulmonary nocardiosis [11].
In a matched case-control study of organ transplant recipients, independent risk factors for nocardiosis were receipt of high-dose glucocorticoids, history of cytomegalovirus disease, and high levels of calcineurin inhibitors [8].
SITES OF INFECTION — Data on the sites of nocardial infection come from multiple sources [5,13,14]. In one review of 1050 cases of nocardiosis, the following sites were affected [5]:
●Systemic (≥2 sites involved) – 32 percent; among patients with systemic disease, 44 percent had central nervous system (CNS) involvement
●Pulmonary (only) – 39 percent
●CNS (only) – 9 percent
●Cutaneous or lymphocutaneous – 8 percent
●Single-site extrapulmonary (eg, eyes, bone) – 12 percent
Pulmonary — The lungs are the primary site of nocardial infection in more than two-thirds of cases [3,15]. Nocardia spp are not normally found in the respiratory tract; as a result, isolation of Nocardia from the sputum is almost always indicative of infection. There are reports in which a respiratory nocardial isolate has been considered a non-pathogen (ie, colonizer), but these are uncommon [7,16]. Most pulmonary infections are primary, but Nocardia can spread to the lung from other sites, such as the skin [17].
The onset of pulmonary nocardiosis may be acute, subacute, or chronic and is not distinguished by any specific signs or symptoms. Fever, night sweats, fatigue, anorexia, weight loss, dyspnea, cough, hemoptysis, and pleuritic chest pain have all been described [2-4,6,11,18].
Pulmonary nocardiosis may mimic or present as an exacerbation of a known or underlying lung disease. This has been described with chronic obstructive pulmonary disease [19] and pulmonary sarcoidosis [20]. The presence of such coexisting disease may delay the diagnosis of nocardial infection. Also, if the underlying disease is treated with glucocorticoids, this therapy may predispose or increase the severity of the nocardial infection.
Although 20 percent of extrapulmonary Nocardia infections occur in the absence of pulmonary disease, up to 50 percent of all pulmonary cases disseminate to sites outside the lungs [14], most commonly the brain [6]. In addition, complications such as empyema, mediastinitis, pericarditis, and superior vena cava syndrome can occur following contiguous spread of nocardial infection from a lung, pleural, or cutaneous focus [21-23].
Imaging findings — A multitude of imaging findings have been demonstrated in pulmonary nocardiosis, including single or multiple nodules, lung masses (with or without cavitation), reticulonodular infiltrates, interstitial infiltrates, lobar consolidation, subpleural plaques, and pleural effusions (image 1 and image 2) [5,24]. As a result, nocardiosis has frequently been misdiagnosed initially as tuberculosis (since upper lobe involvement is common and Nocardia spp are weakly acid fast), invasive fungal disease, and malignancy [2]. (See 'Pulmonary nocardiosis' below.)
Central nervous system — Nocardia appears to have special tropism for neural tissue [5,6], as illustrated in the retrospective review of 1050 cases of nocardiosis cited above in which the CNS was involved in approximately 20 percent of cases overall and in 44 percent of disseminated cases [5]. Isolated CNS disease has been reported, but this probably represents dissemination from a resolved or transient pulmonary or cutaneous infection (image 3) [2].
The hallmark of CNS nocardiosis is formation of a parenchymal abscess that can occur in any region of the brain [5,25,26]. Signs and symptoms of nocardial brain abscess are diverse and nonspecific. Patients may present with fever, headache, meningismus, seizures, and/or focal neurologic deficits [5,27]. (See "Pathogenesis, clinical manifestations, and diagnosis of brain abscess".)
In some patients, typically those with intact immune systems, CNS nocardiosis remains clinically silent, at times persisting for years before a diagnosis is made [5]. CNS nocardiosis can present with symptoms suggesting a mass lesion without any symptoms typically associated with infection [28,29]. In such patients, nocardial brain abscess may be erroneously diagnosed as a primary or metastatic neoplasm prior to biopsy.
Nocardial meningitis is an infrequent manifestation of CNS nocardiosis and can occur with or without an associated brain abscess [30]. In a case series of 28 episodes of nocardial meningitis, the clinical presentation was consistent with subacute or chronic meningitis characterized by fever (68 percent), meningismus (64 percent), headache (55 percent), and associated brain abscess (43 percent) [31]. The cerebrospinal fluid typically demonstrates a neutrophilic pleocytosis, hypoglycorrhachia, and elevated protein concentration, findings that are characteristic of bacterial meningitis. (See "Cerebrospinal fluid: Physiology and utility of an examination in disease states".)
Cutaneous — Four patterns of cutaneous disease have been observed:
●Primary cutaneous
●Lymphocutaneous
●Cutaneous involvement from a disseminated focus
●Mycetoma
It may be prudent to assume that immunocompetent patients with cutaneous disease who do not have a clear history of antecedent trauma at the site of their infection, a mycetoma, or a sporotrichoid (lymphocutaneous) pattern of lesions have disseminated disease until proven otherwise.
Primary cutaneous — When the skin is the primary site of nocardiosis, the infection results from direct inoculation of organisms into the skin, often during gardening or farming; in some cases, this occurs via puncture by a thorn or splinter [3,5]. Inoculation can also occur via trauma, surgery, a vascular catheter, an insect bite [32], or an animal scratch or bite.
Nocardiosis is an uncommon cause of skin infection and is clinically indistinguishable from lesions produced by common pyogenic bacteria such as Staphylococcus aureus and group A Streptococcus. Since most superficial skin infections are treated without a bacteriologic diagnosis, the true incidence of nocardial skin infection may be underestimated.
Manifestations of primary cutaneous nocardiosis include ulcerations, pyoderma, cellulitis, nodules, and subcutaneous abscesses [33,34]. Cellulitis presents with pain, swelling, erythema, and warmth at the affected site, typically without associated drainage; cellulitis caused by Nocardia spp rarely disseminates to bone, muscles, or joints [1,4]. The diagnosis of nocardiosis as the etiologic agent of skin lesions will be delayed if a culture is not obtained [35]. (See "Cellulitis and skin abscess: Epidemiology, microbiology, clinical manifestations, and diagnosis".)
Lymphocutaneous — The lymphocutaneous form of nocardiosis occurs when a primary nocardial skin infection involves the regional lymphatics, producing a nodular lymphangitis. A clinical picture identical to the lymphocutaneous syndrome caused by Sporothrix schenckii develops; this type of cutaneous involvement has been termed "sporotrichoid nocardiosis" [36-39]. (See "Lymphangitis", section on 'Nodular lymphangitis' and "Clinical features and diagnosis of sporotrichosis".)
Cutaneous manifestations of disseminated nocardiosis — Disseminated nocardiosis presents with cutaneous skin lesions in approximately 2 percent of cases; these lesions may be the first sign of the disease (picture 1) [40]. Primary and secondary skin lesions cannot be distinguished based upon their appearance.
Mycetoma — A mycetoma is a chronic cutaneous infection that can be caused by fungi (eumycetoma) or members of the Actinomycetales order of bacteria, such as Nocardia spp (actinomycetoma) [6]. N. brasiliensis is the most common species of Nocardia to cause mycetoma [6]. (See "Eumycetoma".)
After the organism is inoculated into the skin, most commonly on the feet, legs, or back, a pyogenic response ensues with formation of a painless nodule at the site of entry. As the nodule enlarges, a chronic inflammatory response occurs. Indurated lesions develop in an indolent fashion, with sinus tract formation exuding granules composed of clumped organisms. The enlarging granulomatous mass can remain localized or can extend, eventually involving muscle and bone. Once extension has occurred, mycetomas are frequently unresponsive to antimicrobial therapy.
Disseminated infection — Disseminated nocardiosis is defined as two noncontiguous sites of involvement that may or may not include a pulmonary focus [2]. Nocardia can disseminate from a pulmonary or cutaneous focus to virtually any organ [3,41]. Although dissemination is presumed to result from hematogenous spread, identifying Nocardia in blood cultures is uncommon due in part to their fastidious nature [41]. To maximize the yield of Nocardia, blood cultures should be incubated for approximately four weeks. (See 'Culture techniques and incubation' below.)
Bacteremia — Nocardia bacteremia produces severe disease but is a rare occurrence. A systematic review identified 138 cases from the years 1999 to 2018; 81 percent of patients were immunocompromised, most commonly by corticosteroids, malignancy, and transplantation [42].
The presentation and risk factors for infection are similar to those in patients who are nonbacteremic; the only unique risk factor for bacteremia is an endovascular foreign body [41,43]. As an example, in one report, 10 of 17 cases of Nocardia bacteremia in cancer patients were associated with a central venous catheter [44]. In a literature review of 36 cases of Nocardia bacteremia, approximately 30 percent had concomitant bacteremia with other pathogens, mostly gram-negative organisms [41].
Methods to maximize the yield of Nocardia on blood cultures are discussed below. (See 'Culture techniques and incubation' below.)
Other sites — The most commonly involved sites (other than pulmonary, CNS, and cutaneous) are bone, heart valves (primarily prosthetic valves), joints, and kidneys [5,6,45,46]. In addition, numerous other sites of involvement have been reported including the sinuses, eyes, spleen, liver, adrenal glands, pancreas, thyroid gland, paravertebral and epidural space, prostate, and testicles; Nocardia spp can also cause epidural abscess, postsurgical mediastinitis, implantable defibrillator pocket infection, and retroperitoneal and psoas abscesses [2,3,6,47-62]. When the original focus of infection cannot be identified, the patient is presumed to have resolved pulmonary or cutaneous disease.
Primary infection can also result from inoculation of organisms into the eye, resulting in keratitis and endophthalmitis [6,63-66]. Nocardia endophthalmitis after cataract surgery is an aggressive disease with poor visual outcomes in most patients [64]. (See "Bacterial endophthalmitis".)
DIFFERENTIAL DIAGNOSIS — Although there are no pathognomonic signs or symptoms of nocardiosis, it should be suspected in any patient who presents with brain, soft tissue, or cutaneous lesions and a concurrent or recent pulmonary process.
Nocardiosis has a broad range of clinical presentations and can present similarly to several other infections as well as malignancy. Many patients with nocardiosis are immunocompromised, necessitating empiric therapy upon presentation while a diagnosis is sought. The differential diagnosis varies with the site of infection.
Pulmonary nocardiosis — The differential diagnosis of pulmonary nocardiosis includes the following disorders:
●Fungal infection (eg, Aspergillus spp, zygomycosis [mucormycosis], Cryptococcus neoformans)
●Mycobacterial infection (eg, M. tuberculosis, M. avium intracellulare complex, M. kansasii)
●Bacterial infection (eg, Rhodococcus equi and gram-negative bacilli such as Pseudomonas aeruginosa and Klebsiella pneumoniae)
●Malignancy (eg, primary lung cancer, lung metastases)
(See "Approach to the immunocompromised patient with fever and pulmonary infiltrates".)
CNS nocardiosis — The differential diagnosis of central nervous system (CNS) nocardiosis includes the following disorders:
●Other causes of bacterial brain abscess, including anaerobic bacteria
●Fungal infection (eg, Aspergillus spp, Cryptococcus neoformans, Coccidioides immitis, zygomycosis [mucormycosis])
●Parasitic infection (eg, toxoplasmosis, cysticercosis)
●Malignancy (eg, primary CNS lymphoma, CNS metastases)
(See "Pathogenesis, clinical manifestations, and diagnosis of brain abscess".)
Cutaneous nocardiosis — The differential diagnosis of cutaneous nocardiosis includes the following disorders:
●Fungal infection (eg, Aspergillus spp, Cryptococcus spp, Scedosporium apiospermum/Pseudallescheria boydii, Sporothrix schenckii)
●Nontuberculous mycobacterial infection (particularly the rapidly growing nontuberculous mycobacteria, Mycobacterium chelonae and M. fortuitum, and the intermediately growing mycobacterium M. marinum)
●Bacterial infection (eg, Erysipelothrix rhusiopathiae and Francisella tularensis)
●Parasitic infection (eg, cutaneous leishmaniasis)
(See "Fever and rash in immunocompromised patients without HIV infection".)
DIAGNOSIS — A definitive diagnosis of nocardiosis requires the isolation and identification of the organism from a clinical specimen. Delay in establishing the correct diagnosis is common due to the nonspecific and diverse clinical presentation of nocardiosis and the inherent difficulty in cultivating Nocardia. The mean time from the development of symptoms to diagnosis has, in different studies, ranged from 42 days to 12 months [11,67].
Appropriate specimens — The difficulty in establishing a diagnosis of nocardiosis may be related to the inadequacy of specimens obtained by noninvasive means. In one case series, 44 percent of pulmonary infections required an invasive procedure to establish the diagnosis of nocardiosis [67]. When an invasive procedure is performed, cultures are positive in 85 to 90 percent of specimens [68].
Even when adequate specimens are obtained, recovery of Nocardia in the laboratory can be difficult. Thus, when Nocardia infection is suspected, the clinical laboratory should be notified so that specific media and staining procedures can be performed on submitted samples. Certain sputum decontamination solutions have been shown to be toxic to Nocardia spp, particularly sodium hydroxide, N-acetylcysteine, and benzalkonium chloride [2,6]. These solutions should be avoided when isolation of Nocardia is attempted. Examination of clinical specimens for Nocardia should include macroscopic examination for granules, which, when found, can be crushed for microscopic examination [1].
Gram stain — Nocardia spp appear as delicate, filamentous, sometimes beaded [1], branching gram-positive rods in clinical specimens (picture 2).
Modified acid-fast staining — In the proper clinical setting, a presumptive diagnosis of nocardiosis can be made if partially acid-fast filamentous branching rods are visualized in clinical specimens. The value of direct examination of specimens cannot be overemphasized, since early diagnosis and treatment of nocardiosis have been associated with improved clinical outcomes in some patient groups [18,69].
The acid-fast nature of Nocardia is most reliably demonstrated when organisms are stained with the modified acid-fast (Kinyoun) stain (picture 3) or the auramine-rhodamine fluorescent stain. The Kinyoun method substitutes 1% sulfuric acid for acid alcohol as a decolorizer, which allows the less tenaciously acid-fast Nocardia to retain fuchsin [6]. The acid-fast staining property of Nocardia is often lost in older cultures.
The acid-fast reaction and the aerial branching of mycelial-like structures extending from the agar surface are simple tests that differentiate Nocardia from other aerobic and anaerobic actinomyces. (See "Microbiology, epidemiology, and pathogenesis of nocardiosis".)
Culture techniques and incubation — Most routine aerobic bacterial, fungal, and mycobacterial culture media can support Nocardia growth. However, selective media, such as buffered charcoal yeast extract (the media used for the isolation of Legionella spp) and modified Thayer-Martin agar may be beneficial in decreasing the overgrowth of other organisms in specimens derived from nonsterile sites [2,6]. Nocardia can also be cultured on Mycobacterium culture media, such as Lowenstein-Jensen (LJ) media [70]. In our experience, approximately 20 percent of Nocardia are isolated on such media.
In routine aerobic cultures, Nocardia spp have variable colonial morphology, from chalky white to pigment-producing orange, yellow, or brown colonies [1], and usually require 5 to 21 days for growth [3,5,71]. To maximize the yield of Nocardia, blood cultures should be incubated for approximately four weeks. Since most routine fluid or tissue cultures are discarded at 48 to 72 hours, laboratory personnel must be notified when nocardiosis is suspected in order to ensure an adequate incubation period.
Although Nocardia spp can be recovered in most blood culture systems, this rarely occurs despite frequent hematogenous dissemination [41,42]. Most cases of bacteremia are associated with endovascular devices, such as central venous catheters [41,43,44]. Thus, blood cultures should be considered for patients with endovascular devices who remain febrile despite appropriate therapy or have evidence of embolic disease. Blood cultures should be held for up to two to four weeks, with blind subculture to selective media [71]. Communication by the clinician with the laboratory is essential to maximize the yield of Nocardia from blood cultures. (See 'Bacteremia' above.)
Polymerase chain reaction testing — Polymerase chain reaction (PCR) testing provides more accurate and rapid results for the diagnosis of nocardiosis than the conventional methods, but it is not available in many clinical laboratories. The sensitivity and specificity of a 16S rRNA-based PCR assay were examined using 18 samples (eg, skin biopsies, abscess material, sputum, and bronchoalveolar lavage fluid) from patients with nocardiosis diagnosed by conventional cultures and 20 clinical samples from patients with confirmed tuberculosis as negative controls [72]. All specimens from patients with nocardiosis were positive, whereas none of the 20 control samples were positive, confirming the sensitivity and specificity of the primers and PCR protocol. Sequencing allowed identification to the species level.
Speciation — Methods of speciation have undergone improvement. It is now clear that, with previously used biochemical techniques for Nocardia speciation, misidentification was common and that molecular methods, such as 16S ribosomal RNA (rRNA) gene analysis, are more accurate [73]. 16S rRNA gene analysis and other molecular techniques, such as restriction fragment length polymorphisms and multilocus sequence analysis, are therefore the preferred methods for speciation [13,14,74-79]. (See "Microbiology, epidemiology, and pathogenesis of nocardiosis", section on 'Taxonomy'.)
There are increasing reports of Nocardia identification using matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF) technology [80-84]. However, success rates are variable and may depend on modification of the standard extraction method and expansion of the currently available databases [81]. This may be improved with future expansion of the MALDI-TOF databases and/or modification of the bacterial processing methods.
Histopathology — Histopathology of tissue specimens most often shows necrosis [85-87] with abscess (including microabscess) formation. There may be a mixed cellular infiltrate of polymorphonuclear leucocytes [86,88], lymphocytes [86,88], plasma cells [88,89], and hemosiderin-laden macrophages [88,89]. Granulomas with central necrosis mimicking tuberculosis have been described in lung and pleural tissue [86,90], but these findings occur infrequently [88]. Organisms can sometimes be seen on histologic stains, including methenamine silver and the Grocott stain [85,87,90].
Susceptibility testing — In vitro susceptibility studies have shown that different Nocardia species and strains often have markedly different susceptibility patterns, underlining the importance of obtaining speciation and susceptibility testing of all clinical isolates [2,4,71,91-95]. This is particularly important because most patients with nocardiosis are immunocompromised, the central nervous system (CNS) is frequently involved, and there is a high mortality rate of untreated or inadequately treated infection. As an example, identification of N. farcinica is important because this species characteristically demonstrates resistance to third-generation cephalosporins and is often resistant to imipenem [4,71]. Furthermore, trimethoprim-sulfamethoxazole (TMP-SMX) intolerance is common, which can necessitate switching to alternative agents. Antibiotic susceptibility patterns in the different Nocardia spp are discussed separately. (See "Treatment of nocardiosis", section on 'Antibiotic susceptibility'.)
The optimal method for antimicrobial susceptibility testing, as recommended by the Clinical and Laboratory Standards Institute (CLSI, formerly the National Committee for Clinical Laboratory Standards [NCCLS]) is the microdilution method [96]. As recommended by CLSI, the following drugs are tested by microdilution: amikacin, amoxicillin-clavulanate, ceftriaxone, ciprofloxacin, clarithromycin, imipenem, linezolid, minocycline (which also predicts doxycycline susceptibility), sulfamethoxazole or trimethoprim-sulfamethoxazole, and tobramycin [96]. However, the microdilution method is not available in many laboratories. The E-test method of susceptibility testing has also been considered by some experts to be an appropriate alternative method for susceptibility testing of Nocardia [1,13,97,98].
Despite the availability of these techniques in hospital laboratories, the minimum inhibitory concentration (MIC) of antimicrobials can be difficult to interpret. Isolates of Nocardia may therefore be sent to a reference laboratory for precise identification and confirmation of susceptibility testing [2]. Reference laboratories that perform Nocardia spp culture and susceptibility testing include:
●The Mycobacteria/Nocardia Research Laboratory, The University of Texas Health Science Center
●The University of Pennsylvania Health System
●ARUP Laboratories, University of Utah
Imaging studies — Nocardia spp have a propensity to cause brain infection. Thus, the presence of any symptoms indicative of CNS disease warrants brain imaging (computed tomography or magnetic resonance imaging) to exclude the presence of a brain abscess (image 4). In addition, all immunocompromised patients with cutaneous and/or pulmonary nocardiosis, even those without symptoms of CNS involvement, should undergo brain imaging. Immunocompetent patients with pulmonary nocardiosis should also undergo radiographic evaluation to exclude CNS infection. Immunocompetent patients with primary cutaneous nocardiosis only rarely have disseminated disease, and the decision regarding brain imaging should be made on an individual basis.
SUMMARY
●Clinical manifestations
•Nocardiosis is caused by an aerobic actinomycete in the genus Nocardia, an unusual gram-positive bacteria. Nocardial infection most often occurs in immunocompromised patients. (See 'Introduction' above.)
•The most common disease sites are the lung, central nervous system (CNS), and skin. There are no pathognomonic signs or symptoms for nocardiosis. It should be suspected in any patient who presents with brain, soft tissue, or cutaneous lesions and a concurrent or recent pulmonary process. (See 'Introduction' above.)
•The lungs are the primary site of nocardial infection in more than two-thirds of cases. The onset of pulmonary nocardiosis may be acute, subacute, or chronic and is not distinguished by any specific signs or symptoms. (See 'Pulmonary' above.)
•Radiographic findings of lung involvement are variable and include single or multiple nodules, lung masses (with or without cavitation), reticulonodular infiltrates, interstitial infiltrates, lobar consolidation, subpleural plaques, and pleural effusions (image 1 and image 2). (See 'Pulmonary' above.)
•CNS disease accounts for approximately 20 percent of Nocardia cases and most commonly results from dissemination of infection from a pulmonary or cutaneous site. The hallmark of CNS nocardiosis is formation of a parenchymal abscess that can occur in any region of the brain. (See 'Central nervous system' above.)
•Four patterns of cutaneous disease occur: primary cutaneous, lymphocutaneous, cutaneous involvement from a disseminated focus, and mycetoma. (See 'Cutaneous' above.)
•Most cutaneous disease results from the direct inoculation of organisms into the skin from trauma. (See 'Primary cutaneous' above.)
•Disseminated nocardiosis is defined as two or more noncontiguous sites of involvement that may or may not include a pulmonary focus. (See 'Disseminated infection' above.)
●Diagnosis
•A definitive diagnosis of nocardiosis requires the isolation and identification of the organism from a clinical specimen. (See 'Diagnosis' above.)
•Establishing a diagnosis of nocardiosis is problematic since an invasive procedure is often required to obtain an adequate specimen and recovery of Nocardia in the laboratory is difficult because of its slow growth. (See 'Appropriate specimens' above.)
•In the proper clinical setting, a presumptive diagnosis of nocardiosis can be made if partially acid-fast filamentous branching rods are visualized in clinical specimens. (See 'Modified acid-fast staining' above.)
•Nocardia in routine aerobic cultures usually require 5 to 21 days for growth. (See 'Culture techniques and incubation' above.)
•Polymerase chain reaction provides more accurate and rapid results for the diagnosis of nocardiosis than the conventional methods, but it is not available in many clinical laboratories. (See 'Speciation' above.)
•Precise speciation and susceptibility testing of clinical isolates is important because resistance patterns vary by species. (See 'Speciation' above.)
•Nocardia isolates are often sent to a reference laboratory for precise identification and susceptibility testing. (See 'Susceptibility testing' above.)
•Because of the propensity for Nocardia spp to cause central nervous system infection, brain imaging should be performed in all immunocompromised patients and in all patients with pulmonary nocardiosis. (See 'Imaging studies' above.)
