Mycobacterium abscessus in a Patient With Recent COVID-19 Pneumonia

Final Diagnosis:

Mycobacterium abscessus pneumonia with COVID-19

History of the Present lllness

A 40-year-old man, with a medical history of obesity, presents to an outside hospital with 2 days of shortness of breath, cough, and fevers. He recently tested positive for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), two days before coming to the hospital. Upon his initial evaluation, he is found to be hypoxic, requiring a nonrebreather mask for oxygenation. Due to increased oxygen requirements and the elevated work of breathing, he was subsequently intubated within 24 hours of admission.

Medical History
Obesity

Key Medications

None

Epidemiological History

The patient is married, and has a monogamous relationship with his wife with whom he has 5 children. Born and raised in Puerto Rico, he has been living in Philadelphia, Pennsylvania, for over 15 years. He works as a commercial truck driver, traveling within Pennsylvania and New Jersey. He has not traveled outside those states in over 6 months.

Physical Examination

On examination, he was intubated, on extracorporeal membrane oxygenation (ECMO), with findings significant for a diffuse morbilliform rash on the arms, legs, and abdomen. He had coarse breath sounds, which were diminished at the bases. His invasive lines and peripheral lines all appeared clean and dry, without bleeding or purulent drainage.

Studies

The patient’s comprehensive metabolic panel was significant for an elevated alanine aminotransferase (ALT) level of 84 U/L (normal range, 4-36 U/L), a complete blood count (CBC) was significant for a hemoglobin level of 8.0 g/dL (normal range, 13.2-16.6 g/dL), and a hematocrit level of 24.5% (normal range, 38.3%-48.6%). His admission chest x-ray showed multifocal airspace opacities and was read as a possible superimposed multifocal pneumonia. A CT chest scan showed diffuse patchy ground glass opacities with central cavitation, small bilateral pleural effusions, and increased supraclavicular lymphadenopathy.

Clinical Course

During his hospitalization the patient received a 10-day course of intravenous remdesivir, as well as convalescent plasma. He was placed in the prone position in the intensive care unit, and received dexamethasone for 5 days, as well as epoprostenol, with no improvement in his oxygenation. Sixteen days after his initial admission, the decision was made to place him on venovenous ECMO. He was canulated for ECMO and then transferred to a tertiary care center for further care. Upon arrival at the tertiary care center, he was afebrile, intubated, and sedated. His updated physical exam was significant for a diffuse morbilliform rash on the arms, chest, and abdomen.

Figure 1

A laboratory evaluation after transfer revealed a comprehensive metabolic panel (CMP) with mild elevation in ALT level to 84 U/L, and a CBC with a hemoglobin level of 8.0 g/dL. Of note, his SARS-CoV-2 nasopharyngeal swab was negative at this time (18 days after his first positive SARS-CoV-2 test). A chest x-ray taken upon transfer showed multifocal airspace opacities and was read as a possible superimposed multifocal pneumonia. The primary team started empiric antibiotics, vancomycin and piperacillin-tazobactam, to cover a nosocomial pneumonia. Next, a CT chest scan showed diffuse patchy ground glass opacities with central cavitation, small bilateral pleural effusions, and increased supraclavicular lymphadenopathy (Figure 1).

After 5 days of empiric antibiotics, the patient’s blood cultures remained negative and a sputum culture showed normal respiratory flora. His antibiotics were discontinued, and he developed a fever of 100.9 F on the same day. Repeat blood, urine, and sputum cultures were checked, and an astute microbiology lab technician noted gram variable rods on his sputum gram stain.

Diagnostic Procedures and Results

A sputum acid-fast bacillus (AFB) stain was performed 3 times, and each was positive for 2+ to 3+ AFB staining. Subsequently, the microbiology lab ran Mycobacterium tuberculosis polymerase chain reaction testing on the patient’s sputum samples, all of which were negative. Five days later there was growth from the AFB media, and samples were sent off to National Jewish Health Hospital for identification and sensitivity testing.

Treatment and Follow Up

Figure 2

The patient was started on empiric antimicrobials to cover rapidly growing mycobacteria. The regimen chosen was eravacycline, azithromycin, moxifloxacin, and imipenem. He eventually was decannulated off ECMO on day 26 of his hospitalization, but failed breathing trials and required a tracheostomy placement. Repeat CT scans of his chest showed marked improvement of his opacifications (Figure 2). On day 17 of his admission, his culture from National Jewish Health Hospital resulted as Mycobacterium abscessus (M abscessus), with susceptibilities to follow. His regimen was then switched to imipenem, amikacin, and clarithromycin. The patient continued to improve, and eventually his tracheostomy was decannulated. Interestingly, his sensitivities resulted many days after his discharge, and showed that the strain of M abscessus with which he was infected was resistant to both imipenem and clarithromycin. Despite this, the patient had returned to his normal baseline, and was able to go back to work just 2 months after his hospitalization.

Discussion

This case highlights the possible complications associated with coronavirus disease 2019 (COVID-19) infection, outside of the immediate effects of the virus itself. It is now known that both CD8+ and CD4+ cells decrease with severe disease.¹ This depression of the immune system leaves patients vulnerable to the complications associated with T-cell lymphopenia. Coincidentally, the degree of lymphopenia is directly correlated with the severity of disease.¹ There are several theories as to the cause of T-cell lymphopenia. One theory is that the massive cytokine release of tumor necrosis factor alpha (TNF-α) and interleukin-6 leads to T-cell apoptosis, whereas another proposes that SARS-CoV-2 infects the T cell itself and causes cell death.² Another still is that the disease causes T-cell exhaustion, which leads to dysfunctional cells.² The unique predicament of having COVID-19 was what left this particular patient so susceptible to the type of secondary infection he developed.

M abscessus typically affects people with cystic fibrosis or elderly people. People with cystic fibrosis have decreased TNF-α and interferon gamma, which has been associated with nontuberculous mycobacterium infections.³ Elderly patients have increased exhaustion markers and dysregulation of their T cells.³ Thus, it is not surprising that patients with no other medical history should become infected with a nontuberculous mycobacteria organism after a significant insult to their lymphocytes. M abscessus itself is an interesting organism. It is part of the rapidly growing mycobacteria groups and classified as such because it produced mature growth on media places within 7 days.⁴ It is also known to contain the erm gene, which conveys resistance to macrolides.⁴ Though the gene is not always active, it must be taken into consideration when choosing empiric therapy.⁴ For this reason, multidrug therapy is used.

High-level resistance was seen in this patient’s case, and what is more surprising is how the patient recovered after being on inadequate antimicrobial therapy. It implies that the patient’s recovered immune system was more responsible for his improvement than the antimicrobials he was taking. This case highlights the gaps in our understanding of the types of opportunistic infections that may occur as a result of COVID-19 infections. As time goes on, these gaps will start to fill, and hopefully allow medical practitioners to be better equipped to treat this complicated disease.

Maliha Ahmed, DO, is an infectious diseases fellow at Thomas Jefferson University Hospital in Philadelphia, Pennsylvania.

References

1. ^{Chen, Z., John Wherry, E. T cell responses in patients with COVID-19. Nat Rev Immunol 20, 529–536 (2020). https://doi.org/10.1038/s41577-020-0402-6}
2. ^{Tavakolpour, S., Rakhshandehroo, T., Wei, E. X., & Rashidian, M. (2020). Lymphopenia during the COVID-19 infection: What it shows and what can be learned. Immunology letters, 225, 31–32. https://doi.org/10.1016/j.imlet.2020.06.013}
3. ^{Lutzky, V. P., Ratnatunga, C. N., Smith, D. J., Kupz, A., Doolan, D. L., Reid, D. W., Thomson, R. M., Bell, S. C., & Miles, J. J. (2018). Anomalies in T Cell Function Are Associated With Individuals at Risk of Mycobacterium abscessus Complex Infection. Frontiers in immunology, 9, 1319. https://doi.org/10.3389/fimmu.2018.01319}
4. ^{Mandel, G. L., Bennette, J. E., & Dolin, R. (2000). Mycobacteria. In Mandell, Douglas, and Bennet's principles and practice of infectious diseases, vol 1-2. New York: Churchill Livingstone.}