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 Table of Contents  
ONLINE ONLY - CASE REPORT
Year : 2022  |  Volume : 6  |  Issue : 1  |  Page : 53

Atypical mycobacterial cutaneous infection caused by mycobacterium abscessus complex: An unusual presentation masquerading actinomycosis


1 Department of Dermatology, SKNMC, Pune, Maharashtra, India
2 Department of Pulmonary Medicine, SKNMC, Pune, Maharashtra, India

Date of Submission15-Sep-2020
Date of Decision19-Dec-2020
Date of Acceptance02-Jan-2021
Date of Web Publication25-Feb-2022

Correspondence Address:
Gaurav Harishchandra Khandait
Department of Dermatology, SKNMC, Pune, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/cdr.cdr_121_20

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  Abstract 


Atypical mycobacterial infections are caused by mycobacteria other than those from the Mycobacterium tuberculosis complex and Mycobacterium leprae. They are ubiquitous, aerobic, nonmotile, and acid-fast bacilli seen in soil and water. Here, we report the case of a 31-year-old married female who presented with multiple painful pus-filled lesions over both the breast, abdomen, and back associated with yellow-colored discharge for 6 months. Tuberculosis-polymerase chain reaction revealed the presence of atypical mycobacteria which on further investigation with matrix-assisted laser desorption/ionization-time of flight isolated Mycobacterium abscessus species.

Keywords: Atypical mycobacteria, matrix-assisted laser desorption/ionization-time of flight, Mycobacterium abscessus complex, tuberculosis-polymerase chain reaction


How to cite this article:
Khandait GH, Bagane R, Khatu SS, Palaskar N, Patokar AS, Pophale H. Atypical mycobacterial cutaneous infection caused by mycobacterium abscessus complex: An unusual presentation masquerading actinomycosis. Clin Dermatol Rev 2022;6:53

How to cite this URL:
Khandait GH, Bagane R, Khatu SS, Palaskar N, Patokar AS, Pophale H. Atypical mycobacterial cutaneous infection caused by mycobacterium abscessus complex: An unusual presentation masquerading actinomycosis. Clin Dermatol Rev [serial online] 2022 [cited 2022 May 22];6:53. Available from: https://www.cdriadvlkn.org/text.asp?2022/6/1/53/338583




  Introduction Top


Mycobacterium abscessus is an acid-fast bacillus classified as pathogenic rapid-growing nontuberculous mycobacteria (NTM). M. abscessus was first described by Moore and Frerichs in 1953, and these organisms are ubiquitous in the environment.[1] In 1992, after its separation from the Mycobacterium chelonae group, that the M. abscessus group strains acquired recognition as the important human pathogens associated with significantly higher fatality rates than any other rapidly growing mycobacteria. M. abscessus strains are responsible for a wide spectrum of infections in the immunocompetent and immunocompromised hosts.[2] The single most important factor for determining the course and prognosis of a M. abscessus infection is the underlying immune status of the host.


  Case Report Top


A 31-year-old married female presented with multiple painful pus-filled lesions over both the breast, abdomen, and back associated with yellow-colored discharge for 6 months. She was a known case of rheumatoid arthritis on weekly methotrexate 15 mg once a week for 3 months and hydroxychloroquine 200 mg twice a day for 3 months. There was no history of fever, weight loss, abdominal pain, or chronic cough. No history of trauma or discharge with granules was noted.

Clinical examination revealed multiple well-defined erythematous papules and plaques studded with pustules with crusting over few lesions, present over the abdomen, back, and breast. The discharge was devoid of granules. Atrophic scars and sinuses were present over the back [Figure 1].
Figure 1: Multiple well-defined erythematous papules and plaques studded with pustules with crusting over few lesions, present over the abdomen, back, and breast. Atrophic scars and sinuses were present over the back

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No granules were seen on placing a saline-soaked gauze overnight at the site of the lesion. Laboratory examination of pus for bacterial or fungal elements showed negative results. Gram stain showed beaded short to long Gram-positive organism. Acid-fast bacilli (AFB) staining revealed AFB with neutrophils, Langhans giant cells, macrophages, and epithelioid cells. The potassium hydroxide (KOH) mount examination was negative. On cytology with low power (×10) richly cellular smear, ill-formed granuloma and mixed inflammatory infiltrate, whereas on high-power (×40) langhans giant cells, macrophages, mixed inflammatory infiltrate were observed [Figure 2].
Figure 2: Cytology (×40): Shows Langhans giant cells, macrophages, mixed inflammatory infiltrate

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Histopathology, on low power (x10) showed psoriasiform elongation of rete ridges, lymphoplasmacytic infiltrate and on high-power (×40) granulomas containing epithelioid cells, langhans and foreign-body giant cells, mixed inflammatory infiltrate were seen [Figure 3]. On culture using Lowenstein Jensen media, smooth white-colored colonies and on colony smear, abundant AFB were seen [Figure 4]. No growth on Sabouraud's dextrose agar or blood agar was seen.
Figure 3: Histopathology (×40): Shows granulomas containing epithelioid cells, Langhans and foreign-body giant cells, mixed inflammatory infiltrate

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Figure 4: Lowenstein Jensen media: Shows smooth white-colored colonies and on colony smear, abundant acid-fast bacilli

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Tuberculosis-polymerase chain reaction was suggestive of atypical mycobacteria. Further investigation with matrix-assisted laser desorption/ionization-time of flight (MALDI-TOF) mass spectrometry concluded M. abscessus subspecies. MALDI-TOF test mass spectrometry was used for pathogen identification and to accelerate the detection of antimicrobial resistance. The organism showed sensitivity tolinezolid, clarithromycin, amikacin, tobramycin, tigecycline, and cotrimoxazole. The antibiotic resistance and sensitivity were also confirmed with traditional antibiotic-susceptibility test.

Routine investigations, including hemogram, blood sugar, urine routine and microscopy, renal function test, liver function test, and thyroid function test were within the normal limits. Viral markers for hepatitis B were normal. No abnormality was detected on chest X-ray and HRCT-thorax. Mantoux test and cartridge-based nucleic acid amplification test were negative.

She was counseled and reassured about the condition. She was started on oral clarithromycin 500 mg twice a day and linezolid 600 mg twice a day. Topically, she was advised mupirocin ointment twice a day. She did not give consent for injectable Amikacin. She was referred to rheumatologist for further rheumatoid arthritis management and started on leflunomide. She was followed up over a period of 3 months, and it was observed that lesions were resolving during this course of treatment [Figure 5].
Figure 5: Lesions were resolving during the course of treatment

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  Discussion Top


Mycobacteria are divided into two major groups for the purpose of diagnosis and treatment. Mycobacterium tuberculosis complex comprises M. tuberculosis and NTM, which comprise all of the other mycobacteria species that do not cause tuberculosis. NTM can cause pulmonary disease resembling tuberculosis, skin and soft-tissue infections (SSTIs), central nervous system infections, bacteremia, and ocular and other infections.[3] M. abscessus complex is a group of rapidly growing, multidrug-resistant NTM species that are ubiquitous in soil and water. Species comprising Mycobacterium avium complex are the most common pathogenic NTM species. However, infections caused by M. abscessus complex are more difficult to treat because of antimicrobial drug resistance. M. abscessus complex is also resistant to disinfectants, and therefore, can cause postsurgical and postprocedural infections.[4]

M. abscessus was first isolated from a knee abscess in 1952. M. abscessus and M. chelonae were originally considered to belong to the same species, but in 1992, M. abscessus was reclassified as an individual species. M. abscessus complex comprises three entities, M. abscessus subsp. abscessus, M. abscessus subsp. massiliense, and M. abscessus subsp. Bolletii. M. abscessus subsp. Bolletii is recognized as a rare pathogen with a functional inducible erythromycin ribosome methyltransferase (erm) (41) gene. In most M. abscessus subsp. M. abscessus, this gene leads to macrolide resistance. M. abscessus subsp. Massiliense has been proposed to have a nonfunctional erm (41) gene, leading to macrolide susceptibility and a favorable treatment outcome for infections.[5] Another study showed that M. abscessus produces a clavulanate-insensitive broad-spectrum β-lactamase that limits the in vivo efficacy of β-lactams, except cefoxitin and to a lower limit, imipenem.[6]

Definitive diagnosis of M. abscessus complex infection in humans is invariably determined by the isolation of M. abscessus complex from the clinical specimens. Clinical and laboratory differentiation from actinomycosis can be done by using chocolate agar, brain–heart infusion broth, and Brucella blood agar. Identification was classically based on phenotypic tests urease, catalase, and fermentation of sugar. MALDI-TOF allows accurate identification at the genus level, but species identification remains uncertain and depends on mass spectrometry system and the species studied.

SSTIs are also commonly caused by M. abscessus complex, ranging from localized skin infections to deep tissue infections. The two major mechanisms are by direct contact with contaminated material or water through traumatic injury, surgical wound, or environmental exposure and secondary involvement of skin and soft tissue during disseminated disease. SSTIs caused by M. abscessus complex have been reported in patients who recently underwent cosmetic procedures mesotherapy, tattooing, and acupuncture. M. abscessus complex SSTIs can also develop after exposure to environmental sources, such as spas and hot springs.[7] More often, however, these SSTIs develop among hospitalized postsurgical patients, in whom surgical wound infections are most commonly due to M. abscessus subsp. Massiliense. Disseminated M. abscessus complex infections with skin and soft-tissue involvement also commonly occur. M. abscessus complex skin infection has diverse presentations, including cutaneous nodules (usually tender), erythematous papules/pustules, and papular eruptions or abscesses.

M. abscessus complex is notoriously resistant to standard anti-tuberculous agents and most antimicrobial agents. The Clinical and Laboratory Standards Institute recommends testing rapidly growing mycobacteria for susceptibility to macrolides (clarithromycin and amikacin), aminoglycosides, fluoroquinolones, imipenem, doxycycline, tigecycline, cefoxitin, cotrimoxazole, and linezolid. The recommended drug-susceptibility testing method is broth microdilution in cation-adjusted Mueller-Hinton broth supplemented with oleic albumin dextrose catalase. While inherently resistant to antimicrobial therapies, current evidence suggests that M. abscessus demonstrates the greatest sensitivity toamikacin, cefoxitin, and clarithromycin.[2]

The treatment of serious M. abscessus complex disease usually involves initial combination antimicrobial therapy with a macrolide (clarithromycin 1000 mg daily or 500 mg twice daily or azithromycin 250 mg–500 mg daily) plus intravenous agents for at least 2 weeks to several months followed by oral macrolide-based therapy. The drugs of choice for initial intravenous administration include amikacin (25 mg/kg) three times per week plus cefoxitin (up to 12 g/d given in divided doses) or amikacin (25 mg/kg) three times per week plus imipenem (500 mg) two to four times per week.[3]

A study showed that 92% of antibiotic treatment failure which is defined as recurrence or persistence of positive culture after 12-month treatment for M. abscessus pulmonary infections was caused by different M. abscessus genotype coinfections. A negative conversion at 12 months of treatment completion was significantly higher in M. abscessus isolates of the C28 sequevar, smooth colonies, and those susceptible to clarithromycin.[8] Despite the high in vitro susceptibility rates of our M. abscessus complex isolates to amikacin, treatment with this antibiotic was associated with a statistically significant higher failure rate. A plausible explanation is that aminoglycoside-induced renal toxicity was also high in our patients treated with intravenous amikacin (60%). The paucity of bactericidal antibiotics to treat these organisms in addition to the immune state of the hosts affected by these infections could explain, in some cases, the poor therapeutic outcomes of M. abscessus group infections.[9] Recent in vitro research suggests newer agents warranting further investigation include carbapenem/rifampicin combinations, inhaled antibiotics, tigecycline, and clofazimine.


  Conclusion Top


We are reporting this case because of its unusual clinical presentation and to increase the awareness among clinicians that atypical mycobacteria should be put in mind before starting treatment and that all AFB-positive smears should be further processed either by culture or by molecular methods. Multidrug therapy is advised to prevent antibiotic resistance and antibiogram should be performed to confirm susceptibility, even in the setting of early clinical improvement.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient (s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initial s will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Kwon YH, Lee GY, Kim WS, Kim KJ. A case of skin and soft tissue infection caused by Mycobacterium abscessus. Ann Dermatol 2009;21:84-7.  Back to cited text no. 1
    
2.
Kasperbauer SH, De Groote MA. The treatment of rapidly growing mycobacterial infections. Clin Chest Med 2015;36:67-78.  Back to cited text no. 2
    
3.
Griffith DE, Aksamit T, Brown-Elliott BA, Catanzaro A, Daley C, Gordin F, et al. An official ATS/IDSA statement: Diagnosis, treatment, and prevention of nontuberculous mycobacterial diseases. Am J Respir Crit Care Med 2007;175:367-416.  Back to cited text no. 3
    
4.
Nessar R, Cambau E, Reyrat JM, Murray A, Gicquel B. Mycobacterium abscessus: A new antibiotic nightmare. J Antimicrob Chemother 2012;67:810-8.  Back to cited text no. 4
    
5.
Benwill JL, Wallace RJ Jr. Mycobacterium abscessus: Challenges in diagnosis and treatment. Curr Opin Infect Dis 2014;27:506-10.  Back to cited text no. 5
    
6.
Soroka D, Dubee V, Soulier-Escrihuela O, Cuinet G, Hugonnet JE, Gutmann L, et al. Characterization of broad-spectrum Mycobacterium abscessus class A β-lactamase. J Antimicrob Chemother2014;69:691-6.  Back to cited text no. 6
    
7.
Kothavade RJ, Dhurat RS, Mishra SN, Kothavade UR. Clinical and laboratory aspects of the diagnosis and management of cutaneous and subcutaneous infections caused by rapidly growing mycobacteria. Eur J Clin Microbiol Infect Dis 2013;32:161-88.  Back to cited text no. 7
    
8.
Koh WJ, Jeong BH, Kim SY, Jeon K, Park KU, Jhun BW, et al. Mycobacterial characteristics and treatment outcomes in Mycobacterium abscessus lung disease. Clin Infect Dis 2017;64:309-16.  Back to cited text no. 8
    
9.
Maurer FP, Bruderer VL, Ritter C, Castelberg C, Bloemberg GV, Böttger EC. Lack of antimicrobial bactericidal activity in Mycobacterium abscessus. Antimicrob Agents Chemother 2014;58:3828-36.  Back to cited text no. 9
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]



 

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