Nontuberculous mycobacterial hypersensitivity pneumonitis related to a home shower: treatment and secondary prevention

Abstract

A 57-year-old physician with increasing dyspnoea and hypoxaemia had a high-resolution CT scan of the chest, which disclosed diffuse pulmonary ground glass opacities, more pronounced in the upper lobes with minimal mediastinal lymphadenopathy. Transbronchial biopsy of the right middle and lower lobes was performed, demonstrating varying degrees of well circumscribed organising granulomatous pneumonitis thought to be most consistent with hypersensitivity to nontuberculous mycobacteria. Cultures of water obtained from the patient’s home shower were positive for Mycobacterium avium complex. The patient began substituting baths for showers, experiencing some gradual improvement of his symptoms. Subsequently, he installed point-of-use 0.2 micron membrane filters on his shower, and resumed regular showering after installation with continued symptomatic improvement. CT scans at 3 and 18 months revealed improvement and resolution, respectively. Four years later, he continues to shower in filtered home shower water and remains clinically well.

Background

Causative exposures to inciting agents of hypersensitivity pneumonitis are increasingly being reported in the home environment.¹ In particular, Mycobacterium avium complex (MAC) has been recovered from hot and cold water in showers and from showerheads,² with infection and hypersensitivity pneumonitis reported previously in association with routine use of household shower and bath water.^{3 4} The distinctive features of the currently reported case are its resolution without antimycobacterial therapy, and the remarkable lack of recurrence with continued showering in source water over a 4 year follow-up period with point-of-use 0.2 micron water filtration. These observations are particularly noteworthy as there is no standard approach to the treatment of this disorder.

Case presentation

A 57-year-old physician was admitted with increasing dyspnoea and chest discomfort.

He had been well until 4 months prior to admission, when as director of a ventilatory care unit, he used a pulse oximeter that he had been calibrating to check his oxygen saturation. He noted that it was 89% at rest and declined into the 70s% upon ambulation. Shortly thereafter, he noted progressive exertional dyspnoea becoming profound over the 9 days prior to admission. He denied fever, chills, cough, orthopnea, paroxysmal nocturnal dyspnoea, or any other specific complaints. Despite a previous history of paroxysmal atrial fibrillation and hypertension, he had been well-controlled and in sinus rhythm on flecainide and atenolol.

Upon arrival in the emergency department, he was noted to be in atrial fibrillation with a rate of 184/min. After treatment with intravenous labetolol 5 mg and diltiazem 20 mg, his heart rate was reduced to 80–90/min with atrial flutter. Upon examination, his temperature was 98^o F, pulse was 82/min, respirations were 20/min, blood pressure was 133/65; and, room air arterial blood gas: pH=7.46, pCO₂=35, pO₂=56, HCO₃=24, Sat.=90%. Remarkable findings included soft rales audible diffusely in both lungs, without wheezing. There was no digital clubbing, cyanosis, or edema.

Investigations

Laboratory findings included: white blood cell=10.4 K/µl, erythrocyte sedimentation rate=4 mm/h, creatine kinase=185 U/l, troponin=0 ng/ml. A chest radiograph revealed mildly hypoventilated, but clear lung fields. ECG disclosed atrial flutter with variable A-V block and a ventricular rate of 71/min. Intravenous dofetilide was begun with return to sinus rhythm. A high-resolution CT scan of the chest was performed, which disclosed diffuse pulmonary ground glass opacities, more pronounced in the upper lobes (figure 1), with minimal mediastinal lymphadenopathy. A contrast angiographic study showed no evidence of pulmonary embolism. Pulmonary function testing suggested mild restriction with no significant response to bronchodilator.

Figure 1.

High resolution CT scan of the chest, which disclosed diffuse pulmonary ground glass opacities, more pronounced in the upper lobes. There was also minimal mediastinal lymphadenopathy.

Differential diagnosis

Differential diagnostic possibilities considered were hypersensitivity pneumonitis, idiopathic interstitial pneumonitis, or a diffuse infiltrative reaction to flecainide. As flecainide had been discontinued, the patient and his physicians elected to maintain a period of watchful waiting following hospital discharge. One month later, since his dyspnoea had not improved, transbronchial biopsy of the right middle and lower lobes was performed, demonstrating well circumscribed organising granulomatous pneumonitis (figure 2) most consistent with hypersensitivity to nontuberculous mycobacteria (NTM). Grocott’s methenamine silver and auramine-rhodamine stains, and all cultures were negative.

Figure 2.

Histopathology of transbronchial biopsy of the right middle and lower lobes, which demonstrated varying degrees of well circumscribed organising granulomatous pneumonitis most consistent with hypersensitivity to nontuberculous mycobacteria, NTM (‘hot tub lung’).

Outcome and follow-up

Cultures of water obtained from the patient’s home shower were positive for NTM. The patient began substituting baths for showers, experiencing some gradual improvement of symptoms. Subsequently, he installed point-of-use 0.2 micron pore size membrane filters on his shower (Pall Medical, Port Washington, New York, USA). Following filter installation, he resumed regular showering with continued symptomatic improvement. CT scans at 3 and 18 months revealed improvement and resolution, respectively. Four years later, he continues to shower in filtered home water and remains clinically well.

Discussion

It has long been recognised that aerosolised water contaminants can cause febrile respiratory illness and hypersensitivity pneumonitis,⁵ MAC infections and illness characterised by features such as fever, cough, dyspnoea and hypoxia in immunocompetent children and adults have been reported, most often in association with hot tub exposure.^6–9 Radiographic features of ‘hot tub lung’ on high-resolution CT include the appearance of centrilobular nodules of ground glass attenuation, resembling subacute hypersensitivity pneumonitis.^{10 11} Thus, it has been debated whether this entity should be treated as an infection or a hypersensitivity reaction.¹² Indeed, whereas, granulomata are seen on tissue biopsies, acid fast organisms are infrequently demonstrated;⁸ and, while continuing exposure to hot tub water results in ongoing, progressive respiratory difficulty, discontinuation of exposure without antimicrobial therapy leads to prompt improvement in symptoms, pulmonary function and radiographic abnormalities, suggesting a hypersensitivity pneumonitis.^{7 13–16}

Causative exposures to inciting agents of hypersensitivity pneumonitis are increasingly being reported in the home environment.¹ In particular, MAC has been recovered from hot and cold water in showers and from showerheads,² with infection and hypersensitivity pneumonitis reported previously in association with routine use of household shower and bath water.^{3 4} The distinctive features of the currently reported case are its resolution without antimycobacterial therapy, and the remarkable lack of recurrence with continued showering in source water over a 4 year follow-up period with point-of-use 0.2 micron filtration. These observations are particularly noteworthy as there is no standard approach to the treatment of this disorder; and, although the literature describes clinical improvement with mere avoidance of source water exposure, continued exposure after source decontamination and cleansing has been deemed inappropriate, as MAC may persist in plumbing even after repeated decontamination and cleansing.¹⁷

Learning points.

• ▶Aerosolised water contaminants, including NTM can cause febrile respiratory illness and hypersensitivity pneumonitis;
• ▶MAC infections and illness, characterised by features such as fever, cough, dyspnoea and hypoxia in immunocompetent children and adults have been reported, most often in association with hot tub exposure;
• ▶Radiographic features of ‘hot tub lung’ on high-resolution CT include the appearance of centrilobular nodules of ground glass attenuation, resembling subacute hypersensitivity pneumonitis; and whereas, granulomata are seen on tissue biopsies, acid fast organisms are infrequently demonstrated;
• ▶While continuing exposure to hot tub water results in ongoing, progressive respiratory difficulty, discontinuation of exposure without antimicrobial therapy leads to prompt improvement in symptoms, pulmonary function and radiographic abnormalities;
• ▶MAC has been recovered from hot and cold water in showers and from showerheads, with infection and hypersensitivity pneumonitis reported in association with routine use of household shower and bath water, a risk which may be effectively mitigated with point-of-use 0.2 micron water filtration.