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Disseminated Mycobacterium abscessus infection with idiopathic CD4+ T-lymphocytopenia: a case report and review of the literature

Journal of Medical Case Reports volume 18, Article number: 645 (2024) Cite this article

Abstract

Background

Idiopathic CD4+ T lymphocytopenia is a rare immune dysfunction disease that is usually found after opportunistic infections. Mycobacterium abscessus is a rapidly growing mycobacterium that can cause pulmonary infections, lymphadenitis, skin and soft tissue infections, disseminated infections, among others, as a conditional pathogenic bacterium.

Case presentation

We present the case of a 43-year-old Chinese woman who developed disseminated Mycobacterium abscessus infection due to idiopathic CD4+ T lymphocytopenia. The patient exhibited symptoms including skin infections, lymphadenitis, and bacteremia. A tailored multidrug therapy was initiated, guided by drug susceptibility testing. Within a month of treatment, the patient’s fever resolved, and she exhibited a significant recovery and was discharged.

Conclusions

Cases of clinical idiopathic CD4+ T lymphocytopenia with Mycobacterium abscessus infection are not common. Clinicians should be vigilant and accurately identify Mycobacterium abscessus as an opportunistic pathogen when dealing with immunocompromised patients, in particular with idiopathic CD4+ T lymphocytopenia.

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Introduction

Mycobacterium abscessus (MBA) is an emerging pathogen that has increasingly garnered attention in the fields of medicine and microbiology. M. abscessus belongs to the rapidly growing mycobacteria (RGM) complex, first proposed by Moore and Frerichs in 1953 [1] and is one of the most extensively antibiotic-resistant and pathogenic RGM, including subtypes of M. abscessus subsp. massiliense, M. abscessus subsp. abscessus,, and M. abscessus subsp. Bolletii [2, 3]. In 1992, the M. abscessus group strains acquired recognition as important human pathogens associated to significantly higher mortality rates than any other RGM [1]. MBA can initiate soft tissue and skin infections after injury or surgery, disseminated infections in immunocompromised individuals, and pulmonary infections in patients with structural lung disease [4, 5]. It primarily presents as chronic infection, with clinical symptoms being varied and nonspecific, often manifesting as recurrent or chronic cough. However, reports of bloodstream infections caused by this pathogen are rare. Patients with idiopathic CD4+ T-lymphocytopenia (ICL) are often susceptibility to opportunistic infections. ICL is a clinically rare condition that presents with symptoms similar to those of acquired immune deficiency syndrome (AIDS), despite the absence of human immunodeficiency virus (HIV) infection [6]. It is characterized by a deficiency of CD4+ T cells in peripheral blood, leading to an increased risk of severe opportunistic infections. Currently, the etiology, pathogenesis, and clinical manifestations of ICL remain unclear. There are no specific therapeutic interventions for this disease, with management primarily focused on symptomatic treatment of opportunistic infections. Clinically, the majority of patients are diagnosed following the occurrence of opportunistic infections, with the most common pathogens being human papillomavirus (29%), Cryptococcus (24%), and molluscum contagiosum (9%), followed by nontuberculous mycobacterial infections (5%) [7].

In this report, we describe a case of disseminated infection caused by MBA in a patient with ICL, which presented as skin infection, lymphadenitis, and bloodstream infection.

Case report

A 43-year-old Chinese female was admitted to our hospital with a prolonged fever and fatigue that lasted 3 months. Erythema nodosum was detected in both lower extremities. Her medical history included anemia, leukocytopenia, and recurrent upper respiratory tract infections. She had no history of diabetes mellitus, tumor, long-term corticoid use, or autoimmune disorders.

Laboratory tests revealed a lower leukocyte count (2.16 × 109/L; reference range [4–10] × 109/L) and pronounced lymphocytopenia (0.15 × 109/L; reference range [0.8–4] × 109/L). Immunophenotyping of lymphocytes demonstrated a marked decrease of CD8 + T lymphocytes (55 cells/µL; reference range 320–1250 cells/µL), CD4+ T lymphocytes (55 cells/µL; reference range 450–1440 cells/µL), NK lymphocytes (25 cells/µL; reference range 150–1100 cells/µL), and CD19 + B lymphocytes (1.5 cells/µL; reference range 90–560 cells/µL). The antibodies for HIV and hepatitis C virus (HCV), as well as the surface antigen for hepatitis B virus (HBV-Ag), were all negative. To detect early HIV infection, p24 antigen was tested, and the antigen was negative. Serum levels of C-reactive protein (CRP) were significantly increased (CRP > 193 mg/L; reference range < 8 mg/L), along with an increase in procalcitonin (PCT) (PCT = 0.44 ng/mL; reference range ≤ 0.05 ng/mL); the erythrocyte sedimentation rate (ESR) was elevated (ESR > 140 mm/h; reference range 0–20 mm/h), indicating heightened inflammation. Four weeks later, repeat testing was conducted for leukocyte count, lymphocyte subset counts, serum levels of CRP, PCT, and ESR, as well as HIV antibodies. However, no noteworthy changes were observed in these repeated tests.

Ultrasound of the neck showed multiple enlarged lymph nodes in the bilateral supraclavicular. Contrast-enhanced computed tomography (CECT) of her chest, abdomen, and pelvis displayed bilateral superior pulmonary infection, retroperitoneal lymphadenectasis swelling, and retroperitoneal merging (Fig. 1).

Fig. 1
figure 1

Contrast-enhanced computed tomography of the abdomen, showing the swollen lymph nodes

Full size image

A skin biopsy on the left leg (Fig. 2) revealed an abscess formation, positive for acid-fast bacilli. A biopsy of the right supraclavicular lymph node showed coagulation necrosis and acid-fast bacilli positive. M. abscessus complex was identified by polymerase chain reaction-reverse dot blotting (PCR-RDB).

Fig. 2
figure 2

Hematoxylin and eosin analysis of a biopsy specimen of the left leg skin (hematoxylin and eosin staining, 10 ×). The abscess formation was detected

Full size image

A blood sample was drawn from the patient for blood culture testing, and a positive result was obtained. Matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (Bruker MALDI-TOF MS, score value 2.043) was employed to identify the positive MBA culture. Antimicrobial susceptibility testing was conducted using the broth microdilution method in accordance with the guidelines outlined in the Clinical and Laboratory Standards Institute (CLSI) M24-A2 [8]. Table 1 presents the minimum inhibitory concentration (MIC) values for 13 drugs, adhering meticulously to the stringent guidelines set forth by the CLSI and World Health Organization (WHO) for interpretation. According to the results of drug susceptibility testing, and given that cefoxitin and imipenem are the only β-lactam antibiotics recommended for treating MBA infections [9], a multidrug treatment regimen was formulated for the patient. This regimen comprised clarithromycin 500 mg orally twice daily, amikacin 400 mg daily, and cefoxitin 2 g every 8 hours in combination with imipenem/cilistatin 1 g every 8 hours intravenously. After 1 week of treatment, the patient’s fever resolved, but treatment was monitored and continued for over 2 years.

Table 1 Determination of the minimum inhibitory concentration (MIC) of Mycobacterium abscessus by broth microdilution method
Full size table

Discussion

ICL is defined by a decrease in CD4+ T lymphocytes (CD4+ T-cell counts fewer than 300 cells/µL or < 20% total T-cells) with no serologic evidence of HIV infection and no defined immunodeficiency or therapy related to T-cell depletion [10]. Other diverse immune defects have been labeled in some ICL patients, such as depletion of CD8+ T cells, B cells, or NK cells, or all three types of cells [10]. Patients with CD8+ T cells less than 180 cells/µL had a higher risk of critical opportunistic infections and death [6], and low B cells level or even absence has been presented in some patients [11, 12]. B-lymphocytes are important to prevent infections from MBA [13]. ICL is exceptionally rare, occurring sporadically worldwide without any apparent gender predilection. Most of the initially stated ICL patients were adults, although it has successively been described in a small quantity of children, adolescents, and older adults [14,15,16]. Most patients were identified when opportunistic infections occurred and had not been detected in a potentially immunosuppressive state. Very few cases have been reported in the same family. The male/female ratio was 1.8:1 [17]. No evidence was revealed of new transmissible agents that cause lymphocytopenia [18]. It cannot be ruled out that ICL may be caused by decreased clonal ability of bone marrow or failure of successful maturation of bone marrow stem cells [19]. This may result from decreased interleukin-2 and increased tumor necrosis factor-alpha in the internal milieu [20]. If the CD4+ T cell cytopenia is very low, i.e., < 100 cells/µL, and there is a presence of recalcitrant infections, then treatment with interleukin-2 is warranted [21].

The patient in this case exhibited recurrent fever, generalized lymphadenopathy, and rash, as well as a history of repeated respiratory infections, necessitating an assessment for potential immune deficiency. Consequently, we evaluated the patient’s T-lymphocyte subsets and found that the peripheral blood CD4+ T-lymphocyte count remained consistently below 300 cells/µL, with further reductions in CD8 + T cell and B cell levels. Additionally, the patient tested negative for anti-HIV antibodies, effectively ruling out AIDS. Throughout the patient’s prior treatment, no immunosuppressive agents had been administered beyond standard antibacterial medications, thereby aligning the clinical presentation with the diagnostic criteria for ICL. CD4+ T cells play a critical role in the immune response against mycobacterial infections and other parasitic or viral infections. As a result, ICL patients are susceptible to a range of opportunistic infections; indeed, 87.6% of them had at least one infection. Cryptococcal infection was the most common one, then mycobacteria or candida infections, followed by varicella zoster virus (VZV) infections [7].

MBA, as an opportunistic pathogen, is recognized as the most virulent species among RGM and can colonize certain sites in the human body, leading to infections in immunocompromised patients [22]. MBA lung disease represents the most common site for nontuberculous mycobacterial (NTM) infections and is frequently observed in patients with underlying pulmonary conditions, such as bronchiectasis [23]. Moreover, disseminated MAB disease is often associated with immunosuppression. Disseminated MBA infection has at least one of the following characteristics: affected organs > 1, involvement of at least two groups of lymph nodes, or positive assay of blood culture for bacteria [24]. Previous reports indicated that immunosuppression such as AIDS, organ transplantation [25, 26], and corticosteroid treatment of autoimmune diseases are risk factors [27, 28].

MBA can invade the human body through various routes, including the skin and respiratory tract, and its clinical course is reminiscent of tuberculosis, with symptoms that closely resemble those of pulmonary tuberculosis—such as fever, night sweats, fatigue, cough, and hemoptysis [29, 30]. The radiological findings can also be similar, rendering misdiagnosis based solely on clinical symptoms and imaging studies quite common. It is very difficult to distinguish lymphadenitis from lymphoma by radiograph. In this case, computed tomography (CT) revealed retroperitoneal lymphadenectasis and suspicious lymphoma; the maximum standard uptake value (SUV) in positron emission tomography-CT (PET-CT) was 3.3. The manifestation, characteristics of radiograph, and pathology are similar between nontuberculous mycobacteria and tuberculosis mycobacteria. Pathogens are difficult to obtain, delayed diagnosis is common, and the time to diagnose is usually > 12 weeks [31]. In our case, the determined diagnosis took 14 weeks.

For suspected disseminated mycobacterium infections, the best way is to explore infection-associated pathogens [32]. Acid-fast bacilli smear of tissue and mycobacterium culture are essential methods, including blood culture. However, as the former can be nonspecific and not diagnostic, the latter may be more specific and hold greater diagnostic value [33]. When the culture from isolated mycobacterium forms visible, brown, smooth, and flat colonies on the solid medium within 7 days, and the colony morphology is different from Mycobacterium tuberculosis or does not respond to standard antituberculosis therapy, and the bacteria isolates are resistant to antibiotics [34], molecular biology methods should be considered for differential diagnosis, and correct specimen collection and technical processing should be carried out in accordance with the guidelines.

To date, the treatment of MBA remains challenging, with only a limited number of drugs available for therapeutic use. Clarithromycin is the cornerstone of MBA treatment [35]. It is frequently susceptible to clarithromycin and amikacin, inconsistently susceptible to cefoxitin and imipenem, and resistant to other antimicrobial drugs [36]. The MBA isolates were susceptible to clarithromycin (92.5%), amikacin (95%), cefoxitin (32.5%), moxifloxacin (22.5%), imipenem (12.5%), and tigecycline (100%) [26]. However, acquired resistance has occurred rapidly owing to erm and rll gene mutation [37]. It is recommended to have all clinical isolates tested for antibiotic susceptibility. Wang et al. reported a case of disseminated cutaneous MBA infection in a patient with low peripheral blood CD4+ T cell levels, which significantly improved after 6 months of treatment with rifampicin, isoniazid, ofloxacin, clarithromycin, and thymosin, resulting in normalization of peripheral blood CD4+ T cell levels [38]. Colomba et al. described the first case of disseminated M. abscessus subsp. bolletii infection in a patient with immunocompromising conditions [39]. Contrary to previous reports, the isolated M. abscessus subsp. bolletii exhibited moderate resistance to clarithromycin, while remaining sensitive to cefoxitin and imipenem. The in vitro drug susceptibility model is not completely related to the clinical response, and the measurement of antibiotic MIC cannot ensure that the therapeutic effect can be predicted. Therefore, treatment of MBA infection usually requires prolonged (> 6 months) use of multiple antibacterial drugs [40]. For disseminated infections, it is recommended to use clarithromycin or azithromycin in combination with amikacin, cefoxitin, or imipenem [27]. Early treatment failure is significantly related to macrolide resistance, immunosuppression, and kidney diseases [4]. Standard antituberculosis drugs such as isoniazid and ethambutol should not be used in RGM; they are more expected to cause side effects [41]. This patient received a standard antituberculosis regimen for 2 weeks, which exacerbated symptoms. If MBA lung disease is misdiagnosed as pulmonary tuberculosis, it not only delays the treatment of MBA infection but also may expose the patient to adverse reactions from antituberculosis medications. Therefore, differential diagnosis between MBA and Mycobacterium tuberculosis is crucial, and a comprehensive identification of pathogens and antibiotic susceptibility testing is key to effective diagnosis and treatment.

This report did not evaluate the prognostic factors of MBA infection, bacteremia, and immunosuppressant use, which may be related to the poor prognosis [27].

Conclusion

A rare cause of disseminated M. abscessus infection, besides HIV infection, long-term use of hormone therapy, and organ transplantation, may be in patients with ICL. Patients with ICL who are faced with opportunistic infections require clinical attention; it is necessary to further study the pathogenic mechanism and treatment strategy of patients with ICL.

Data availability

All data generated or analyzed during this study are included in this published article.

Abbreviations

MBA:

Mycobacterium abscessus

RGM:

Rapidly growing mycobacterium

HIV:

Human immunodeficiency virus

HCV:

Hepatitis C virus

HBV-Ag:

Hepatitis B surface antigen

CRP:

C-reactive protein

ESR:

Erythrocyte sedimentation rate

PCT:

Procalcitonin

MIC:

Minimum inhibitory concentration

ICL:

Idiopathic CD4+ T-lymphocytopenia

VZV:

Varicella zoster virus

AIDS:

Acquired immune deficiency syndrome

SUV:

Standard uptake value

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Acknowledgements

We thank all patients for participating in the study and all local health staff for their assistance in sample and data collection.

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Authors and Affiliations

  1. Department of Laboratory Medicine, Guangming District People’s Hospital, Shenzhen, 518106, China

    Xianglin Wu

  2. Center for Medical Experiments (CME), Guangming District People’s Hospital, Shenzhen, 518106, China

    Mingzhu Zhai, Aohong Xu & Yi Zheng

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Contributions

XW and YZ: conception and writing the original draft; MZ and AX: investigation, data curation, writing—review and editing. All authors read and approved the final manuscript.

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Correspondence to Yi Zheng.

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The study was reviewed and approved by the Medical Ethics Committee of Guangming District People’s Hospital.

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Wu, X., Zhai, M., Xu, A. et al. Disseminated Mycobacterium abscessus infection with idiopathic CD4+ T-lymphocytopenia: a case report and review of the literature. J Med Case Reports 18, 645 (2024). https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s13256-024-05009-w

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Journal of Medical Case Reports

ISSN: 1752-1947