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 Table of Contents  
Year : 2019  |  Volume : 21  |  Issue : 2  |  Page : 89-93

Post-operative infective endocarditis with aortic root abscess due to Mycobacterium abscessus

Department of Microbiology, Sree Chitra Tirunal Institute of Medical Sciences and Technology, Thiruvananthapuram, Kerala, India

Date of Submission21-Oct-2019
Date of Decision19-Nov-2019
Date of Acceptance27-Nov-2019
Date of Web Publication17-Jan-2020

Correspondence Address:
Dr. Heera Hassan
Ad-hoc Assistant Professor, Department of Microbiology, Sree Chitra Tirunal Institute of Medical Sciences and Technology, Thiruvananthapuram, Kerala
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jacm.jacm_28_19

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Aortic root abscess is a complication of native and prosthetic valve infective endocarditis with a higher risk for prosthetic valves. The patients with aortic root abscess may present with symptoms ranging from pyrexia of unknown origin to arrhythmia. The usual aetiological agents are Staphylococcus aureus, alpha-lytic Streptococci and other skin flora. Here, we present a case report of aortic root abscess in a patient with a history of aortic valve repair. The aetiological agent was identified as Mycobacterium abscessus. This is probably the first case report of aortic root abscess with M. abscessus. The patients responded to empiric antibiotics without surgery.

Keywords: Aortic root abscess, BacT Alert, GeneXpert, Mycobacterium chelonae, Mycobacterium abscessus, Vitek MS

How to cite this article:
Hassan H, Ponnambath DK, Raja K. Post-operative infective endocarditis with aortic root abscess due to Mycobacterium abscessus. J Acad Clin Microbiol 2019;21:89-93

How to cite this URL:
Hassan H, Ponnambath DK, Raja K. Post-operative infective endocarditis with aortic root abscess due to Mycobacterium abscessus. J Acad Clin Microbiol [serial online] 2019 [cited 2022 Jan 20];21:89-93. Available from: https://www.jacmjournal.org/text.asp?2019/21/2/89/276121

  Introduction Top

Mycobacterium abscessus complex comprises a group of rapidly growing, multidrug-resistant, non-tuberculous mycobacteria (NTM) that are responsible for a wide spectrum of skin and soft-tissue diseases, central nervous system infections, bacteraemia, ocular infections and pulmonary disease in vulnerable hosts with the underlying structural lung disease. Bacteraemia is often associated with intravenous catheter use.  M.abscessus Scientific Name Search  contributes to about 13.6% of culture-positive cases of mycobacterial endocarditis.[1] To the best our knowledge, this is the first reported case of M. abscessus causing aortic root abscess (a complication of mycobacterial endocarditis). Aortic root abscess is a complication of infective endocarditis affecting the aortic valve. It is more common in prosthetic valve than native valve endocarditis. Cardiac defects such as bicuspid aortic valve, aortic valve regurgitation and degenerative aortic stenosis are risk factors for its development. The aetiological agents depend on whether the affected valve is native or prosthetic. The most common microorganism causing post-operative prosthetic valve endocarditis is Staphylococcus epidermidis followed by Staphylococcus aureus and Candida.

  Case Report Top

A 27-year-old male with a history of aortic valve repair in December 2017 for the bicuspid aortic valve was admitted twice in January and February 2018 with sternal wire infection of the surgical wound site. There were no other risk factors such as diabetes, alcoholism and intra-venous drug abuse. Sternal wire removal was done, but the patient developed high-grade fever and there was persistence of wound discharge. The pus culture from the wound was sterile after 48 h of incubation. Clinically, there were symptoms and signs suggestive of infective endocarditis. Along with this, trans-oesophageal echocardiography (ECHO) suggested the possibility of aortic root abscess. The routine ordinary blood cultures were sent but were sterile, and a diagnosis of culture-negative endocarditis was made. Hence, a repeat surgery for aortic valve repair was planned and the patient received Vancomycin Gentamicin and Rifampicin for a total of six weeks, following which the patient improved and refused further treatment.

By the end of July 2018, the patient was readmitted to the cardiology intensive care unit with a low-grade fever, cough and vomiting of three days duration. There was accompanied haemoptysis too. Physical examination revealed pus discharge from the previous surgical wound site. Clinically, the patient was in acute cardiac failure and was diagnosed to have prosthetic valve dysfunction with aortic root abscess. Erythrocyte sedimentation rate (ESR) was 37 mm/h (normal reference range for men <50 years of age is 0–15 mm/h), total leucocyte count was 3400 cells/mm 3, procalcitonin (PCT) was 0.3 ng/ml (normal value – <0.09 ng/ml) and C-reactive protein (CRP) was 30.5 mg/L (normal value – <6 mg/L) at the time of admission. Two days later, ESR increased to 50 mm/h, PCT became 0.4 ng/ml and CRP increased to 49 mg/L. Cardiac computed tomography (CT) was done which showed persistent soft-tissue thickening around the aortic root and focal area of conglomerated tree in bud nodules noted in the upper lobe of the right lung, which was suggestive of the possibility of active endobronchial infection. Pus from the wound site and three sets of blood cultures (in BacT/Alert bottles for BacT/Alert (bioMerieux Inc., Durham, NC) were sent to the microbiology laboratory for culture. The pus culture was sterile after 48 h of incubation. All the BacT/Alert bottles came positive within 24 h. Gram staining was done and it revealed long Gram-positive bacilli in scattered arrangement. Considering the morphological similarity to acid-fast bacilli (AFB) in microscopy, acid-fast staining too was done using 20% sulphuric acid as the decoloriser. The smear revealed AFB [Figure 1]. The blood in BacT/Alert was subcultured to blood agar, MacConkey agar and Lowenstein–Jensen (LJ) medium. The results were promptly informed to the clinicians. The presence of AFB in blood together with the possibility of endobronchial infection in CT made us probe into the past history.
Figure 1: Acid-fast bacilli from blood in BacT/Alert bottles

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The past history revealed sputum tests for persistent cough a year back and the results of which were told to be normal. Family history of persistent cough was positive in a sibling. Parents had an untimely death and the cause of which is not known. It was advised to shift the patient to a negative pressure isolation room till a definitive diagnosis is made. Meanwhile, the sputum was subjected to AFB staining, AFB culture and GeneXpert. No AFB were seen in sputum AFB staining. Chest X-ray was not done.

On the next day, the subcultures of blood onto blood agar and MacConkey agar were examined for growth. The colonies in blood agar were 0.5 mm-sized dry, white, rough, non-lytic and were acid fast [Figure 2]. The colonies in MacConkey agar were lactose fermenting. There were cream-coloured rough colonies in LJ medium too [Figure 3]. Sputum GeneXpert (Cepheid Inc., California, USA) was sent to another laboratory and was reported to be negative. Considering the rapid growth of the colonies (within two days), a preliminary report of NTM was given.
Figure 2: Growth on blood agar

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Figure 3: Growth on Lowenstein–Jensen medium

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The patient was being administered Ceftriaxone, Gentamicin and Rifampicin since admission. Clarithromycin was started after the preliminary report. After a week of treatment, the aortic root abscess decreased in size. The frequency of fever episodes also became less. Mycobacterium was identified as M. abscessus by Vitek MS (bioMerieux, Marcy I'Etoile, France, version 3.2 MALDI-TOF) from the Christian Medical College (CMC), Vellore, Tamil Nadu, India. The patient was transferred to the Infectious Diseases Department of Medical College Hospital, Thiruvananthapuram, and was given Linezolid, Amikacin, Clarithromycin and Moxifloxacin for two weeks following which he became symptomatically better. The patient absconded from the treatment while awaiting the results of Mycobacterial sensitivity by MIC broth dilution from the Department of Microbiology in CMC, Vellore, Tamil Nadu, India. The organism was susceptible to Amikacin (16 μg/ml), but resistant to Linezolid (64 μg/ml), Moxifloxacin (>16 μg/ml), Imipenem (64 μg/ml), Clarithromycin (>64 μg/ml intrinsic resistance without exposure to Clarithromycin), Tetracycline (>32 μg/ml), Minocycline (>32 μg/ml) and Cotrimoxazole (>32 μg/ml). The patient probably responded to Amikacin, which was given for two weeks. There was no documented side effects to the antibacterial therapy that was given. Follow-up was not possible as the patient had absconded.

Infection control: The patient was located in the negative pressure isolation room and full infection control precautions were taken because of the active focus of endobronchial infection revealed by cardiac CT, though recommendations of adequate infection control to minimise risks of person-to-person transmission of M. abscessus exist only in individuals with cystic fibrosis.[2]

  Discussion Top

Aortic root abscess results when uncontrolled infective endocarditis causes mycotic aneurysm of one of the sinuses of Valsalva, which is in free communication with the aortic root above the valve cusps. The risk factors for aortic root abscess in endocarditis are bicuspid aortic valve, aortic valve regurgitation, degenerative aortic stenosis and patients with multivalvular disease.

Some of the organisms which were isolated with relation to aortic root abscess to date are S. aureus, Streptococcus pneumoniae, Enterococcus faecalis and Candida sake. Virulent organisms that infect the native aortic valve almost always cause root abscess, less virulent bacteria such as Viridians Group Streptococci may do so if there is a diagnostic delay.

M. abscessus complex comprises a group of rapidly growing, multidrug-resistant, NTM that are responsible for a wide spectrum of skin and soft-tissue diseases, central nervous system infections, bacteraemia, ocular infections and pulmonary disease in vulnerable hosts with the underlying structural lung disease. Bactaeremia is often associated with intravenous catheter use.[3] Mycobacterial endocarditis is rare. It showed a significant predilection of non-tuberculous over tuberculous mycobacteria in terms of infective endocarditis. Due to the increased resistanance to antimicrobial therapies than other pathogens, mycobacteria are often refractory to antimicrobial treatments and are associated with a very high mortality. Rapid-growth NTM including Mycobacterium chelonae, M. abscessus and Mycobacterium fortuitum accounted for 68% of the isolates, thus being the predominant mycobacteria for the infections.[1]

The most common predisposing risk factors for mycobacterial infections include medical procedures (central venous access, haemodialysis catheter indwelling, various surgical operations including mammoplasty, arthroplasty and cardiothoracic operations), immunocompromised (HIV/AIDS), haematological malignancies or those treated with immunosuppressive drugs after solid-organ transplantation. More recently, the use of tumour necrosis factor-α blockers has become an additional risk factor.[4] Of these cardiac surgery, foreign material implant and intravenous drug use are the major underlying aetiologies for the development of mycobacterium endocarditis.[1] Nosocomial infections were once evidenced from sources such as cardioplegic solutions, water supplies, antiseptic solutions and valve prosthesis preservation solutions.

The decontamination process of bioprosthetic valves after explantation from animals used chemicals such as glutaraldehyde.[5] However, mycobacteria, which are highly prevalent in the environment, are known to be resistant to those disinfectants (including 8% aqueous formaldehyde, 2% alkaline glutaraldehyde and free chlorine), and the inappropriate disinfection has been suspected in NTM infections eventually causing (Infective Endocarditis) IE. Oxidizing disinfectants (peracetic acid and hydrogen peroxide based) may provide a safe alternative to aldehyde-based products, particularly in glutaraldehyde-resistant NTM outbreaks.[6]

M. abscessus is widespread in the environment and has been documented as a source of nosocomial infection in immunocompromised patients. The organism is capable of colonising the respiratory tract and causes pulmonary disease in certain high-risk groups such as patients with cystic fibrosis or prior pulmonary mycobacterial infection, particularly tuberculosis.,[7] Although M. abscessus infections can occur in both immunocompetent and immunocompromised hosts, immune status and underlying comorbidities contribute to the disease severity, and disseminated infections are typically seen in patients with impaired immunity.[7] M. abscessus has the ability to form biofilms and to grow even in distilled water. Due to its occurrence in municipal water supply systems as a result of its resistance to common disinfectants, M. abscessus may also cause cutaneous infections that usually resolve themselves but may occasionally also require medical or surgical treatment.[7]

Rapid diagnosis and prolonged combination therapy are mandatory for proper treatment and to minimize mortality as M. abscessus is inherently resistant to multiple antibiotics.[7] Species-specific identification of M. abscessus by conventional methods is time-consuming and may not be reliable, and recently developed molecular methods have provided more accurate identification. Our study is limited by not being able to confirm the species identification of mycobacterium with the current recommendations such as a nucleic acid probe or 16SrRNA sequencing (Center for Disease Control and Prevention CDC recommendation).

M. abscessus-specific treatment is required for complete resolution of the infection. Clinically, aortic root abscess is suspected in any patient with aortic valve endocarditis who fails to improve within 72 h on appropriate antibiotics, particularly with prosthetic valve infection. The persistence or recrudescence of fever, raised white blood cell counts and raised CRP or development of cutaneous manifestations or embolic phenomenon while on treatment all indicate uncontrolled infection. Aortic root abscess is well demonstrated with the help of trans-oesophageal ECHO than transthoracic ECHO. Urgent surgery is said to be the treatment of choice along with an appropriate antibiotic cover. Infective endocarditis caused by rapidly growing mycobacteria is always refractory to treatment due to drug resistance and delayed diagnosis leading to inappropriate treatment.[8] Typically, antibiotics with a maximum in vitro activity against M. abscessus isolates include Amikacin, Clarithromycin, Tigecycline and Cefoxitin. To a lesser extent, Linezolid and Imipenem are also effective against nearly 50% of clinical M. abscessus isolates. Endocarditis caused by M. abscessus generally has very poor prognosis and can be a result of various factors that may lead to drug resistance, including the presence of biofilms, type of antimicrobial agent used and the presence of inducible erm (41) gene. A combined antimicrobial therapy with prolonged treatment duration is often the regimen of choice. Susceptibility testing for M. abscessus should include at least Clarithromycin, Cefoxitin and Amikacin (and preferably also Tigecycline, Imipenem, Minocycline, Doxycycline, Moxifloxacin, Linezolid, Cotrimoxazole and Clofazimine if a validated method is available) to guide, but not dictate, treatment regimens. M. abscessus pulmonary disease treatment should comprise an initial phase antibiotic regimen (including intravenous and oral antibiotics) followed by a continuation phase antibiotic regimen (including inhaled and/ororal antibiotics).[2] In our case, this treatment protocol was not followed.

For individuals with M. abscessus complex isolates from pulmonary diseases that demonstrate constitutive macrolide resistance, the initial phase antibiotic regimen should include a minimum four-week course of intravenous Amikacin, intravenous Tigecycline and (where tolerated) intravenous Imipenem.[2] In our case, extrapolating the interpretation of extended Clarithromycin susceptibility results for M. abscessus, at day 3–5, the Clarithromycin resistance implies a 23S ribososmal RNA point mutation at a genetic level enabling the micro-organism to express a high-level constitutive macrolide resistance phenotypically.[2] This intrinsic resistance shows that the pathogen could belong to any of the subspecies of M. abscessus.[2] Aortic root abscess is a life-threatening complication of both native and prosthetic valve infections which requires close co-ordination between cardiologist, microbiologist and surgeon for successful management. The overall mortality of endocarditis with atypical mycobacteria such as M. fortuitum complex after valve replacement is 88%. Due to the rarity of studies, mortality rate of endocarditis due to M. abscessus is unavailable.[1]

The emergence of globally circulating virulent clones of M. abscessus complex species [9] along with the reports of aldehyde resistance in rapid growers of mycobacteria during the largest outbreak ever reported of M. abscessus complex infections in Brazil in 2009–2010[10],[11] is a cause of concern for the medical fraternity.

In our case, the combination of aortic root abscess and atypical mycobacterium makes the situation very grave. The patient required prolonged treatment for complete recovery. The possibility of contamination of prosthetic valve leading to aortic root abscess cannot be ruled out.

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 initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Yuan SM. Mycobacterial endocarditis: A comprehensive review. Rev Bras Cir Cardiovasc 2015;30:93-103.  Back to cited text no. 1
Haworth CS, Banks J, Capstick T, Fisher AJ, Gorsuch T, Laurenson IF, et al. British Thoracic Society Guideline for the management of non-tuberculous mycobacterial pulmonary disease (NTM-PD). BMJ Open Respir Res 2017;4:e000242.  Back to cited text no. 2
Lee MR, Sheng WH, Hung CC, Yu CJ, Lee LN, Hsueh PR. Mycobacterium abscessus complex infections in humans. Emerg Infect Dis 2015;21:1638-46.  Back to cited text no. 3
Winthrop KL, Chang E, Yamashita S, Iademarco MF, LoBue PA. Nontuberculous mycobacteria infections and anti-tumor necrosis factor-alpha therapy. Emerg Infect Dis 2009;15:1556-61.  Back to cited text no. 4
Centers for Disease Control and Prevention. Isolation of mycobacteria species from porcine heart valve prostheses MMWR Morb Mortal Wkly Rep 1977;26:42-3.  Back to cited text no. 5
Burgess W, Margolis A, Gibbs S, Duarte RS, Jackson M. Disinfectant susceptibility profiling of glutaraldehyde-resistant nontuberculous mycobacteria. Infect Control Hosp Epidemiol 2017;38:784-91.  Back to cited text no. 6
Colombo RE, Olivier KN. Diagnosis and treatment of infections caused by rapidly growing mycobacteria. Semin Respir Crit Care Med 2008;29:577-88.  Back to cited text no. 7
Williamson JC, Miano TA, Morgan MR, Palavecino EL. Fatal Mycobacterium abscessus endocarditis misidentified as Corynebacterium spp. Scand J Infect Dis 2010;42:222-4.  Back to cited text no. 8
Bryant JM, Grogono DM, Rodriguez-Rincon D, Everall I, Brown KP, Moreno P, et al. Emergence and spread of a human-transmissible multidrug-resistant nontuberculous Mycobacteriu m. Science 2016;354:751-7.  Back to cited text no. 9
Duarte RS, Lourenço MC, Fonseca Lde S, Leão SC, Amorim Ede L, Rocha IL, et al. Epidemic of postsurgical infections caused by Mycobacterium massiliens e. J Clin Microbiol 2009;47:2149-55.  Back to cited text no. 10
Leão SC, Viana-Niero C, Matsumoto CK, Lima KV, Lopes ML, Palaci M, et al. Epidemic of surgical-site infections by a single clone of rapidly growing mycobacteria in Brazil. Future Microbiol 2010;5:971-80.  Back to cited text no. 11


  [Figure 1], [Figure 2], [Figure 3]


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