eMedicine Specialties > Pediatrics: General Medicine > Infectious Disease
Atypical Mycobacterial Infection
Updated: Jan 8, 2008
Introduction
Background
Atypical mycobacterial infection has been described in the medical literature since the mid 1950s.1,2 The development and introduction of a rapid radiometric mycobacterial detection system has advanced the field of mycobacteriology over the past 20 years. This method has allowed the distinction of Mycobacterium tuberculosis from other mycobacteria and enabled the performance of antimicrobial susceptibility testing of mycobacteria. The increased frequency of atypical mycobacterial infection stems from advances in the diagnostic procedures concerning the infection paired with the prevalence of mycobacterial disease in immunocompromised patients infected with the human immunodeficiency virus (HIV).
Nontuberculous mycobacteria (NTM) are classified based on their growth rates. Rapidly growing NTM are categorized into pigmented and nonpigmented species. Mycobacterium fortuitum complex is nonpigmented and includes the M fortuitum group and the Mycobacterium chelonae/abscessus group. The pigmented species are rarely associated in clinical disease and include Mycobacterium phlei, Mycobacterium aurum, Mycobacterium flavescens, Mycobacterium vaccae, Mycobacterium neoaurum, and Mycobacterium thermoresistible. Mycobacterium smegmatis may be either pigmented or nonpigmented.3,4,5,6
Pathophysiology
Atypical mycobacteria are obligate aerobes that can be found in the environment in soil, water, vegetables, and even in domestic animals and dairy products. Mycobacterium avium complex (MAC) and Mycobacterium scrofulaceum are associated with lymphadenitis in immunocompetent children. All nodes in the cervical chain can be affected, but the nodes of the submandibular region appear to be the most commonly involved.7 Disseminated infections are usually associated with HIV infection. Host immunity seems to play a major role because a low CD4+ lymphocyte count (fewer than 100 cells/μ L for adults and age-appropriate decreases in children) is associated with an increased frequency of disseminated MAC disease.
Some cytokines such as interleukin (IL)–1 alpha and IL-6 enhance extracellular growth of the organism. IL-6 also promotes intracellular growth of MAC, apparently by down-regulating membrane receptors for tumor necrosis factor (TNF)–alpha.8,9,10 Other cytokines, such as interferon (IFN)–gamma and IL-2, work in the other direction. IL-2 enhances lymphocyte proliferation and cytotoxic activity and upregulates production of IFN-gamma.11,12,13 Ongoing studies are establishing the additional roles of cytokines.
In immunocompromised patients, the intestinal tract is the primary route for MAC infection, followed by the respiratory tract as a secondary portal of entry.14,15 CD4+ lymphocytes but not CD8+ or gamma delta+ lymphocytes are required for host protection against MAC and dissemination through the intestinal route.16 Abnormal immune response to MAC colonization may cause invasion of the epithelial cells of the gastrointestinal tract, followed by disseminated disease.15 In one series of adult patients infected with HIV with positive respiratory or stool isolates, 75% developed mycobacteremia within a year (mean 6 mo) after the isolation. A preceding stool culture positive for isolates was present in 25-36% of the patients.15 Pulmonary disease in adults without acquired immunodeficiency syndrome (AIDS) may occur.
Disseminated MAC in children without HIV has been described in the literature. It is associated in some cases with IFN-gamma receptor ligand-binding deficiency, which is a recently identified autosomal recessive inherited disorder.17,18,19 Affected children show a severe and apparently selective susceptibility to weakly pathogenic mycobacteria (either Bacillus Calmette-Guérin or NTM.20 This condition has revealed the importance of IFN-gamma in the control of mycobacterial disease in humans. The importance of immune reconstitution produced by highly active antiretroviral therapy (HAART) in reducing susceptibility to MAC infection may provide clues to the critical role of the host immune defense and may establish the basis for the use of immunotherapy in disseminated MAC disease.
Frequency
United States
In the pre-HIV/AIDS era, pulmonary disease and lymphadenitis due to atypical mycobacteria were found all across the United States, with most cases located in the central and southern regions.21 Because infections by NTM were not reportable in the past, few systematically collected data about their frequency and distribution are available. Early in the HIV epidemic, MAC disease was quite common in patients with AIDS.22 However, frequency is decreasing among patients with HIV because of new treatment modalities, such as combination therapy with nucleoside reverse transcriptase inhibitors and protease inhibitors, as well as antimycobacterial prophylaxis.
International
Distribution of atypical mycobacterial infection is worldwide. Mycobacterium ulcerans, the agent of a chronic ulcerative skin infection called Buruli ulcer, is widespread in Ghana, Cote d'Ivoire, Senegal, Uganda, and most central African countries.23,24
Mortality/Morbidity
Disseminated MAC disease is the second most common opportunistic infection in children with HIV infection after Pneumocystis carinii pneumonia. In the era before HAART, the frequency of disseminated MAC disease varied with age, history of prior opportunistic infections, and immunologic studies.25 Disseminated MAC infection may occur in children with HIV and adolescents who are severely immunocompromised after starting antiretroviral therapy.26
A review of 58 deaths from a cohort monitored during a 7-year period in the pre-HAART era, with a mean age of 4.43 years, has shown that MAC was the most common isolate at the time of death, followed by P carinii pneumonia.27 The risk increases in children infected with HIV with a CD4+ cell count fewer than 750/µL who are younger than 1 year; with a cell count fewer than 500/mL in children aged 1-2 years; with a cell count fewer than 75/µL in children aged 2-6 years; and with a cell count of 50/µL in children older than 6 years, the same threshold as in adults infected with HIV.28,29,30 Atypical mycobacterial infection has been described in children with cystic fibrosis (CF). Although MAC is more common in the United States in the population with CF, M abscessus and M avium are reported to be more common in Europe.31,32
Race
Atypical mycobacterial infection has no racial predilection.
Sex
Both sexes are affected with equal frequency.
Age
MAC and M scrofulaceum are associated with lymphadenitis in immunocompetent children aged 1-5 years.7 Although disseminated MAC disease rarely occurs during the first year of life, its frequency increases with age and declining CD4+ lymphocyte count in children infected with HIV.33,34,35
Clinical
History
Suppurative cervical or submandibular lymphadenopathy that produces or does not produce systemic symptoms is the most common presentation of atypical mycobacterial infection caused by M avium-intracellulare and M scrofulaceum in the immunocompetent pediatric host. In a cohort of children infected with HIV prospectively monitored by Hoyt et al in 1992, recurrent and persistent fever and chronic anemia were the most common signs and symptoms, followed by chronic diarrhea and a history of recurrent abdominal pain with disseminated M avium complex (MAC) disease34,36,37
Weight loss, failure to gain weight, and wasting syndrome are part of the long-term presentations of disseminated MAC disease in immunocompromised children. Other signs and symptoms include leukopenia, hepatosplenomegaly, and persistent generalized lymphadenopathies. Ulcerative lesions of the colon and mesenteric disease with abscess formation have been reported.37,38,39 Primary cutaneous infections with MAC are rare; most cases are caused by dissemination, with manifestations including scaling plaques, crusted ulcers, ecthymalike lesions, verrucous ulcers, inflammatory nodules, panniculitis, pustular lesions, and draining sinuses.40
Buruli ulcer is a chronic ulcerative skin disease, caused by M ulcerans, that mostly affects the limbs. The lack of acute inflammatory response is typical and is likely due to an immunosuppressive toxin called mycolactone, which is produced by mycobacteria.24,23 Buruli ulcer mainly affects children living in humid areas of the tropical rain forest. Following a microinjury, the organism penetrates the skin. A subcutaneous nodule develops a few weeks later, followed by necrosis of the subcutaneous fat and finally by a large dermal ulceration. Constitutional symptoms are normally absent.
Atypical mycobacteria may cause skeletal infections. A large outbreak of spinal infections after discovertebral surgery was reported in 2001.41 Tenosynovitis, multifocal osteomyelitis, septic arthritis, protracted carpal tunnel syndrome, and spondylitis implicating M chelonae, Mycobacterium kansasii, MAC, or Mycobacterium xenopi have been described in the literature.42,43,44,45,46 Keratitis and endophthalmitis after intravitreous injection of steroids or other ophthalmoscopic procedures secondary to M chelonae invasion have been reported. Although most of those infections secondary to atypical mycobacteria have been described in the adult population, cases of cutaneous mycobacteriosis manifesting as cellulitis, skin abscess, or sporotrichoid lesions secondary to M chelonae abscessus and M kansasii have been reported.
Catheter-related infections are the most common nosocomial nontuberculous mycobacterial infections encountered. The fast-growing atypical mycobacteria, such as M fortuitum, cause most catheter-related infections. Patients with long-term central intravenous catheters are most susceptible. However, infections have occurred in patients with peritoneal and shunt catheters. Local catheter site drainage; tunnel infections; and mycobacteremia, with or without fever, are the usual manifestations, but granulomatous hepatitis and, sometimes, pulmonary infiltrates have been observed. Case reports of atypical mycobacterial infection in transplant patients due to M chelonae and M xenopi have been described in the medical literature.47,48
Physical
Immunocompetent children with adenitis secondary to MAC present with suppurative adenitis that may or may not produce constitutional symptoms such as fever. Fistula may be present with coalescence of involved cervical or mandibular nodes. In immunocompromised children with HIV/AIDS, no pathognomonic signs are present. Physical examination may reveal that a debilitated patient has a history of failure to gain weight, chronic fatigue, chronic diarrhea, and recurrent abdominal pain. Hepatosplenomegaly may be present. Early during disseminated MAC disease, some patients may not have fever and may not appear acutely or chronically ill.49
Causes
Numerous atypical mycobacterial infections are known. The most common forms of diseases are chronic pulmonary disease resembling tuberculosis (occurring mainly in adults), cervical adenopathy in children, skin and soft tissue infections, and disseminated disease in immunocompromised persons.7,15 Lymphadenitis is the most common manifestation in children.7,21 However, progressive immunodeficiency due to infection with HIV appears to be the most significant factor for disseminated MAC disease.50,15,51
A unique MAC syndrome that develops in patients with AIDS in the first 1-2 months following the initiation of HAART has been described by 3 groups of investigators.52,53,54,55 The symptom consists of fever and focal MAC lymphadenitis, with a blood culture negative for mycobacteria in most cases. The symptom is also known as immune reconstitution syndrome. It may occur in patients who already had subclinical MAC disease that becomes unmasked by HAART. The atypical mycobacteria observed in children are M avium-intracellulare complex, M scrofulaceum, and, rarely observed in children with AIDS, M kansasii.
Mycobacterium marinum is the causative agent of swimming pool granuloma. However, both rapidly growing and slow-growing species of NTM have been implicated in chronic granulomatous infections. Those infections mostly involve tendon sheaths, bursae, bones, and joints after direct inoculation through accidental trauma, surgical incisions, or puncture wounds.3,56 Tenosynovitis of the hand secondary to MAC and M marinum has been described. Osteomyelitis of the sternum caused by M abscessus has been found in clustered and sporadic outbreaks. M fortuitum and M chelonae strains, also known as the rapidly growing organisms, have occasionally been implicated in wound, soft tissue, pulmonary, and middle ear infections.57,7
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 Overview: Atypical Mycobacterial Infection |
| Differential Diagnoses & Workup: Atypical Mycobacterial Infection |
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| References |
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Further Reading
Keywords
atypical mycobacteria, mycobacterial disease, mycobacterial infection, Mycobacterium tuberculosis, M tuberculous, nontuberculous mycobacteria, NTM, lymphadenitis, Mycobacterium avium complex infection, disseminated MAC disease, MAC infection, HIV-associated infections, human immunodeficiency virus, highly active antiretroviral therapy, HAART, interferon-gamma, IFN-gamma, opportunistic infections, Buruli ulcer, IFN-gamma receptor ligand-binding deficiency, Mycobacterium phlei, Mycobacterium aurum, Mycobacterium flavescens, Mycobacterium vaccae, Mycobacterium neoaurum, Mycobacterium thermoresistible, Mycobacterium smegmatis, Mycobacterium scrofulaceum, Bacillus Calmette-Guérin, AIDS, pulmonary disease, Mycobacterium ulcerans, Buruli ulcer, cystic fibrosis, CF
