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CASE REPORT
Year : 2023 | Volume
: 12
| Issue : 1 | Page : 92-95
Healthcare-Associated nontuberculous mycobacterial endocarditis following coronary artery angiography
Kalpak Bhatt1, Harsh Toshniwal1, Vipul Shah2, Dhruv Patel1
1 IDTM Clinic, Ahmedabad, Gujarat, India
2 Healthcare Infectious Disease Clinic, Ahmedabad, Gujarat, India
Correspondence Address:
Kalpak Bhatt
IDTM Clinic, Office No. 402, 4th Floor, Gala Business Centre-2 Rajhans Society, SV Desai Marg, Ahmedabad - 380 006, Gujarat
India
Source of Support: None, Conflict of Interest: None
CheckDOI: 10.4103/ijmy.ijmy_147_22
Infective endocarditis in a patient with structural heart disease following coronary artery angiography is a rare complication. We report a rare case of Mycobacterium chelonae infective endocarditis following coronary artery angiography in a young male with congenital heart disease. This case illustrates the diagnostic as well as therapeutic challenges we faced when managing this rare infectious entity.
Keywords: Infective endocarditis, Mycobacterium chelonae, nontuberculous mycobacteria
Infective endocarditis in a patient with structural heart disease following coronary artery angiography is a rare complication. In these clinical settings, bacterial pathogens are much more common as compare to mycobacterial and fungal agents. Among the mycobacterial causes of infective endocarditis, nontuberculous mycobacteria (NTM) have historically shown preference over Mycobacterium tuberculosis (MTB). NTM infective endocarditis is considered very difficult to treat with antimicrobial therapy alone as it has intrinsic as well as acquired resistant to many antimicrobials. Successful treatment of NTM infective endocarditis requires a combination of surgical intervention and prolonged course of effective antimicrobial therapy. We report a rare case of Mycobacterium chelonae infective endocarditis following coronary artery angiography in a young male with congenital heart disease (CHD). This case illustrates the diagnostic as well as therapeutic challenges we faced when managing this rare infectious entity.
Case ReportA 23-year-old male presented with high-grade fever and dry cough for the last 2 months. Before 1 ½ months to this presentation, he underwent coronary angiography for evaluation of his CHD. He is a known case of the double-chambered right ventricle and perimembranous ventricular septal defect (VSD). The patient's preangiographic laboratory investigations were within normal limits and he does not have any other contributing personal or family history.
On examination, the patient had fever (103°F), tachycardia (Pulse 120/min), and normal blood pressure (110/70 mmHg) with mild hypoxia (oxygen saturation: 93% on room air). The general examination was unremarkable except pallor.
His cardiovascular system examination revealed tachycardia, a Grade 4 pan systolic murmur over the precordial region. The rest of the systemic examination findings were normal. He was hospitalized with suspected infective endocarditis.
Laboratory investigations
Hemoglobin 11.3 g%, leucocyte count 4070/mm[3], normal differential count, platelet count 99,500/mm[3], creatinine 0.75 mg/dl, alkaline aminotransferase 40, C-reactive protein 67 (0–5), and erythrocyte sedimentation rate 120 mm/1st h. Urine microscopy was normal; three sets of blood cultures (each set containing 1 bottle of Aerobic and 1 bottle of Myco F) (specimens were processed on Bactec 9050 USA system) were sent. After 7 days, all blood cultures showed growth. On smear organism found to be acid-fast bacilli (AFB) [Figure 1], further processing conformed it to be NTM. NTM speciation was done by line probe assay (LPA) and identified as M. chelonae [Figure 2]. His two-dimensional (2D)-echo revealed the same CHD finding without any vegetation. The patient refused transesophageal echocardiography (TEE). The patient was started on amikacin, clarithromycin, and doxycycline.
Figure 1: Smear of ZN stain from positive blood culture bottle showing short solid-stained AFB morphologically resembling to NTM/MOTT. NTM/MOTT: Nontuberculous mycobacteria/Mycobacteria other than tuberculosis, AFB: Acid-fast bacilli
Figure 2: Hain LPA genotype Mycobacterium CM strip showing presence of band number 5 and 10 suggestive of Mycobacterium chelonae 
along with presence of well-developed control bands. LPA: Line probe assayDrug susceptibility test of NTM with Minimum Inhibitory Concentration (MIC) in bracket is as follows. Sensitive drugs are Linezolid (2), amikacin (1), tigecycline (0.06), tobramycin (2), clarithromycin (0.06) and resistance drugs are sulfamethoxazole (76) and trimethoprim (4), ciprofloxacin (4), cefepime (32), amoxicillin (64) clavulanic acid (32), doxycycline (16), and minocycline (8). Later treatment was modified according to the sensitivity report (doxycycline stopped).
The patient was discharged after 8 days of admission in afebrile condition. He came for regular follow-ups, and drug toxicities were monitored. He was asymptomatic until after 1 ½ months of treatment. He came to us on an unscheduled visit with swelling of left palm, which was painless, nontender, fluctuant, and 3 cm × 4 cm size of 10 days duration. Aspiration of the abscess was done and sent for microbiological workup. Smear shown AFB detected 3+. His mycobacterial culture grew the same NTM (M. chelonae). At this time, the conventional 2D-Echo did not show any vegetation. However, the patient refused TEE at this time also. After 2 months of therapy, his repeat blood culture remained persistently positive for M. chelonae.
After 1 month of abscess on the left palm, the patient underwent TEE which did not show any vegetation and same chemo-therapy was continued as he was asymptomatic, and the left palm abscess improved. At the end of 3 ½ months of therapy, the patient became febrile again and started having vomiting and weakness. He underwent computed tomography angiography thoracic inlet, which was negative for endocarditis of coronary arteries. His blood culture was still persistently positive for M. chelonae. After 3 weeks, repeat TEE was done, which showed 4 mm × 5 mm hyperechoic tissue attached to septal tricuspid leaflets [Figure 3].
Figure 3: TEE showing vegitation (4mm x 5 mm) attached to septal tricuspid leafletsHe underwent intracardiac repair surgery
INFUNDIBULAR RESECTION + VSD CLOSURE + REMOVAL OF VEGETATION AND TRICUSPID VALVE REPAIR. Mycobacterial culture of vegetation grew the same organism. He was put on intravenous (IV) imipenem cilastatin, linezolid, amikacin, moxifloxacin, and oral clarithromycin.
De-escalation of therapy was done after 3 weeks. Linezolid, amikacin, and clarithromycin were continued for 6 months. He became afebrile remained symptom-free till the completion of treatment. His treatment was stopped in January 2016 and remained asymptotic during further follow-up consultation till December 2018.
DiscussionThe term infective endocarditis denotes infection of the endocardial surface of the heart and implies the physical presence of microorganisms in the lesion, and in most cases, cardiac valves are affected; however, the disease may occur within septal defects or on the mural endocardium. The term Infective endocarditis is preferred over bacterial endocarditis because chlamydia, rickettsia, mycoplasma, fungi, mycobacteria, and perhaps even viruses may be responsible for the syndrome.[1] A new form of the disease, healthcare-associated infective endocarditis, has emerged secondary to introducing new therapeutic modalities (IV catheters, hyperalimentation lines, pacemakers, dialysis shunts, etc).[2],[3] Continuous changes in epidemiology and management strategies of infective endocarditis have been elucidated. Staphylococcus aureus has become the most common microorganism of the bacterial infective endocarditis, particularly associated with increasing foreign material implant, while Streptococcus viridans infections reduced. However, there is no updated elaboration on recent changes in mycobacterial endocarditis. Mycobacterial endocarditis is rare. It showed a significant predilection of nontuberculous over tuberculous mycobacteria in terms of infective endocarditis.[4] The improvement in mycobacterial culture techniques and the increasing utility of modern molecular methods for the identification of previously unidentified organisms has produced a significant resurgence of interest in disease caused by the NTM[1] NTM have been categorized into different groups based on characteristic colony morphology, growth rate, and pigmentation (the Runyon system of classification). This system has become less valuable due to the availability of more rapid molecular methods of diagnostics. Based on growth rate (growth within or after 7 days), NTM can be divided into two groups: Rapidly growing mycobacteria (RGM) and slowly growing mycobacteria. There are currently six groups or complexes of RGM based on pigmentation and genetic relatedness.[1] In General, RGM Rapid-growth NTM, including M. chelonae, Mycobacterium abscessus, and Mycobacterium fortuitum, accounted for 68% of the isolates[5] and thus were the predominant mycobacteria for the different infections in the body. There have been systemic reviews on infective endocarditis caused by M. fortuitum[6],[7] in 2002 and by M. abscessus[8] and M. chelonae[9] in recent years. M. chelonae is an opportunistic pathogen that is a normal inhabitant of the environment. Humans are believed to be infected through exposure to environmental sources. Water is thought to be the most common source of infection. It has been found in surface salt water and fresh water sources worldwide. M. chelonae can produce 5 of the 6 major clinical syndromes, including chronic respiratory disease, skin and soft tissue, skeletal, disseminated infections, and catheter-related infections. Lymphadenitis is rarely seen.[10] In our case, it led to infective endocarditis involving tricuspid valve. Traditionally, biochemical testing to identify the M. chelonae was the “gold standard” before the advent of the newer identification methods. Biochemical testing for the M. chelonae has been considered more unreliable and costly than 16S rRNA sequencing and may potentially compromise patient care because of its long turnaround time.[10] Molecular methods are currently the gold standard for the identification of Mycobacteria. 16S rRNA gene sequencing identifies most Mycobacterium species but cannot further characterize individual species in the RGM Group.[11] Numerous studies have been published to identify mycobacteria by matrix-assisted laser desorption ionization time-of-flight mass spectrometry. These studies have shown almost a 100% accurate identification for members of the M. chelonae and M. abscessus groups.[12],[13] LPA s for the identification of both MTB and NTMs are used predominately used outside of the United States. In our case, M. chelonae was identified by LPA (The Hain Lifescience GmbH AFB identification system Treatment of infections due to NTM remains difficult as they are resistant to many of the first-line antituberculosis medications and because of so few other agents available for therapy. The correlation between in vitro sensitivity and clinical treatment outcomes for some drugs and NTM species has been poor; the role of antibiotic susceptibility testing in guiding treatment remains under debate.[4],[14]
M. chelonae is one of the more antibiotic-resistant RGM species, and only a few antibiotics are available for treatment. Clarithromycin is the drug of choice.[10]
Untreated M. chelonae isolates generally have low or intermediate MICs compared with achievable drug levels to clarithromycin (100%), amikacin (90%), and cefoxitin (70%).[15]
In treating serious skin, soft tissue, and bone infections, clarithromycin should be combined with parenteral antibiotics (cefoxitin, amikacin, or imipenem). The macrolides are the most reliable oral agents that show in vitro activity to M. chelonae. The most active parenteral agent is amikacin; a combination of amikacin and high-dose cefoxitin is recommended as an initial therapy until clinical improvement is noted. As cefoxitin is not available in India, we treated this patient with a combination of imipenem cilastatin, linezolid, amikacin, moxifloxacin, and clarithromycin. Length of therapy should be from 4 up to 6 months for more severe skin and bone infections.[16] However, there is no definitive duration defined for Infective endocarditis caused by M. chelonae.[17],[18]
Surgery is generally indicated with extensive disease, abscess, breast implants, and catheters when drug therapy may be complex.[10] In our case, patient had to undergo INFUNDIBULAR RESECTION + VSD CLOSURE + REMOVAL OF VEGETATION AND TRICUSPID VALVE REPAIR for source control.
ConclusionEndocarditis due to NTM is difficult to manage clinical entity. Intrinsic resistant to many antimicrobials and requirement of prolonged injectable antibiotics leading to various adverse drug reactions adds to the difficulty in curing this condition. Our case illustrates the importance of surgical intervention in successful treatment of NTM endocarditis in addition to prolonged antimicrobials. Inability to clear bacteremia with adequate antibiotics should be considered as a strong indication for surgical intervention even though the size of vegetation is small.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that his name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
References
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