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Table of Contents
CASE REPORT
Year : 2020  |  Volume : 8  |  Issue : 3  |  Page : 136-138

A case report of pulmonary mucormycosis


Department of General Medicine, M.R. Medical College, Kalaburagi, Gulbarga, Karnataka, India

Date of Submission09-Jul-2019
Date of Acceptance21-Aug-2019
Date of Web Publication15-Jul-2020

Correspondence Address:
Dr. Surajsingh Ravindra Taur
Department of General Medicine, M.R. Medical College, Kalaburagi, Gulbarga, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/AJIM.AJIM_26_19

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  Abstract 


Pulmonary mucormycosis is a relatively rare pulmonary fungal disease which is difficult to diagnose and lacks effective treatment. The present study reports that the case of a 57-year-old patient who was treated successfully for pulmonary mucormycosis in Basaveshwar Hospital. The patient presented with low-grade fever and a productive cough that persisted for 2 months with no evident cause, and change of voice with weight loss and also suffered from diabetes mellitus. Prior antibiotic treatment with levofloxacin had been ineffective. The culture of mucus obtained by bronchoscopy resulted in a diagnosis of pulmonary mucormycosis. The patient was started on liposomal amphotericin, received a cumulative dose of 1250 mg amphotericin over 2 months, and presented a full recovery.

Keywords: Bronchial mucosal biopsy, pulmonary mucormycosis, sputum for fungal elements


How to cite this article:
Taur SR, Harsoor S, Goudagaon C. A case report of pulmonary mucormycosis. APIK J Int Med 2020;8:136-8

How to cite this URL:
Taur SR, Harsoor S, Goudagaon C. A case report of pulmonary mucormycosis. APIK J Int Med [serial online] 2020 [cited 2020 Oct 31];8:136-8. Available from: https://www.ajim.in/text.asp?2020/8/3/136/289789




  Introduction Top


Mucormycosis is an opportunistic infection that is caused by Mucorales fungi of the Zygomycetes class. The term “zygomycosis,” the previous designation for infections caused by fungi of the order Mucorales, is no longer appropriate due to a recent taxonomic reclassification that abolished Zygomycetes as a class.[1]

Mucorales fungi is ubiquitous, saprophytic, and not fastidious fungi located in soil or decaying organic matter, with three genera that are known to be human pathogens, namely Rhizopus, Absidia, and Mucor. The incidence of pulmonary mucormycosis ranks only second to that of nose and cerebral mucormycosis.[2] The optimal temperature for growth is 28°C–30°C under aerobic conditions, with an incubation period of 2–5 days. Incubation begins with inhalation of the spores or their direct inoculation into abraded skin.[3]

The most common symptoms are persistent high fever (>38°C), cough, hemoptysis, and chest pain.[4] Six distinct clinical presentations of mucormycosis are now recognized: rhinocerebral, cutaneous, pulmonary, gastrointestinal, and central nervous system mucormycosis, and a miscellaneous form involving the bones, breasts, mediastinum, and kidneys. The first case of pulmonary mucormycosis was described in 1876 by Fürbringer.[5] Amphotericin B is a polyene antifungal drug and is the selected drug for the treatment of mucormycosis.[6] Different mucormycosis exhibits different susceptibility to amphotericin B, and the drug concentration of amphotericin B in the lung is lower than other tissues. Therefore, pulmonary mucormycosis infection requires a higher dose of amphotericin B.

The accumulated dose can reach 30 mg/kg, and the total dose can reach 2500–3000 mg for the total treatment course of 1–3 months. Previously, a study has suggested that liposome amphotericin B was safer, with an improved effect and smaller accumulated dose, compared with amphotericin B alone.[7] Due to mucormycosis causing angiemphraxis, the drug may not reach the focus of infection, thus, when the antifungal drug has no good effect, pulmonary lobectomy was suggested.[8]


  Case Report Top


A 57-years-old male presented with 2-month history of fever, cough with expectoration, weight loss, and change in voice. The patient suffered from diabetes mellitus and chronic bronchitis for 3 years and had no history of allergies. The temperature of the patient was 37.5°C on admission, and he was expectorating ~20 ml of yellow or white sputum daily. On admission, a pulse rate of 102 beats/min, normal heart sounds, a respiratory rate of 22 breaths/min, and blood pressure of 100/60 mmHg was reported. The patient was alert, oriented, and in good general condition. Initially, the patient was hypoxic 80%–81% at room air, pulmonary bronchial breath sounds were present, and there were intermittent fine moist rales over the two lower lobes. The abdomen was soft, with no tenderness, or rebound tenderness. The lower limbs were not edematous.

Laboratory investigations

pH of arterial blood, 7.42 (normal reference ranges: 7.35–7.45); partial O2 pressure, 68 mmHg (normal reference ranges: 80–100 mmHg); partial CO2 pressure, 45 mmHg (normal reference ranges: 35–45 mmHg); white blood cell count, 13,300/μl; neutrophils, 64.3% (normal reference ranges: 45%–70%); and hemoglobin (Hb), 9.6 mg/l. In addition, routine urine tests were positive for albumin and urine sugar. Biochemical tests indicated the following results: fasting blood glucose, 113 mg/dl; postprandial 133 mg/dl; erythrocyte sedimentation rate, 58 mm/l; HbA1C 8.9%; and procalcitonin, 0.081 ng/ml (normal reference ranges: <0.5 ng/ml). Microscopic examination of a sputum smear demonstrated moderate numbers of Gram-positive cocci and streptococci, as well as occasional Gram-negative bacilli; however, no fungal spores or pseudohyphae were observed. Sputum culture and acid-fast staining were negative. Bronchial mucosal biopsy revealed features of mucormycosis,

X-ray chest revealed left upper zone non-homogenous opacity [Figure 1]. Ultrasonography of the thorax revealed moderate effusion on the left 700–800 ml and minimal effusion on the right 150–200 ml, with underlying collapse of the lung, diaphragmatic movements were normal.
Figure 1: Chest X-ray (posteroanterior view)

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The patient was started on liposomal amphotericin, and renal function was monitored on regular basis, tolerated the dose of amphotericin and was advised to continue the same till the target dose is achieved.


  Discussion Top


Pulmonary mucormycosis occurs due to the inhalation of fungi spores into the bronchioles and alveoli, which typically results in the rapid progression of pneumonia or endobronchial disease. Rarer results include endobronchial lesions and complications associated with airway occlusion. Hemoptysis commonly occurs with vascular invasion, which can occasionally be fatal. The symptoms of pulmonary mucormycosis are typically nonspecific, even at late stages of infection, and may include fever, dyspnea, coughing, and chest pain. Rare cases can present as progressive subcutaneous emphysema, Pancoast syndrome, Horner's syndrome, or chronic mediastinitis and bronchial perforation.

The radiological manifestations of pulmonary mucormycosis are mostly nonspecific. An abnormal chest roentgenogram result is present in >80% of patients.[9] The reported findings include consolidation, cavitation, the air crescent sign, the halo sign, the reversed halo sign, solitary or multiple pulmonary nodules or masses, bronchopleural fistulae, pulmonary artery pseudoaneurysms, lymphadenopathy, and pleural effusion. Cavitation is observed in as many as 40% of cases, but the air crescent sign is uncommon.

The presence of the air crescent sign often portends a poor prognosis if surgical therapy is delayed. Similar to invasive pulmonary aspergillosis, pulmonary mucormycosis is detected with the highest sensitivity when using high-resolution chest computed tomography to determine the extent of the disease. This technique also usually finds evidence of the infection earlier than standard chest radiographs.[2],[4],[8] The right lung is more commonly involved than the left, and there is a predilection for the involvement of the upper lobes although the reason for this remains unknown. The present case reported a lesion in the right upper lobe, as in the majority of the cases in the literature.[10]

Histopathologically, vascular invasion with tissue necrosis and neutrophilic infiltration of the tissue is common to all types of mucormycosis. Diagnosis is achieved by demonstrating broad (diameter, 6–16 μm), nonseptate (coenocytic), ribbon-like hyphae, with right-angled branching in a tissue biopsy specimen stained with routine hematoxylin and eosin. Special fungal stains are usually not necessary for diagnosis. The less common and less-specific features of pulmonary mucormycosis include bronchial invasion, pneumonia, lung abscesses, and granulomatous pneumonitis.

The differential diagnosis of the disease includes bacterial, viral, and other fungal pulmonary infections. Pulmonary mucormycosis has clinical manifestations for which there is almost no differentiation from those of other more common opportunistic molds such as Aspergillus. The differentiation between mucormycosis and aspergillosis is important as the treatments can differ, and since the patient outcome may be improved by the appropriate early treatment of mucormycosis.[11]


  Conclusion Top


It is important to note that airway cultures can identify a variety of fungi, which may be contaminants, colonizers, or disease producers, particularly in immunocompromised hosts. The determination of their importance requires accurate fungal identification and treated accordingly. Furthermore, one of the key aspects for the successful treatment of pulmonary mucormycosis is the management of any risk factors.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Hibbett DS, Binder M, Bischoff JF, Blackwell M, Cannon PF, Eriksson OE, et al. A higherlevel phylogenetic classification of the fungi. Mycol Res 2007;111:509-47.  Back to cited text no. 1
    
2.
Spellberg B, Kontoyiannis DP, Fredricks D, Morris MI, Perfect JR, ChinHong PV, et al. Risk factors for mortality in patients with mucormycosis. Med Mycol 2012;50:611-8.  Back to cited text no. 2
    
3.
Spellberg B, Edwards J Jr., Ibrahim A. Novel perspectives on mucormycosis: Pathophysiology, presentation, and management. Clin Microbiol Rev 2005;18:556-69.  Back to cited text no. 3
    
4.
Yang YM, Fang BM, Xu XM, Fang F, Pan MM, Zhong XF, et al. Pulmonary mucormycosis: Report of 5 cases and review of 46 cases reported in China. Zhonghua Jie He He Hu Xi Za Zhi 2013;36:572-6.  Back to cited text no. 4
    
5.
Fürbringer P. Observations on pulmonary mucormycosis in humans. Virchows Arch Pathol Anat 1876;66:33065.   Back to cited text no. 5
    
6.
Li WF, He C, Liu XF, Wang SY, Qu JL, Lin ZF. A diagnosis neglected for 6 years: Report of a misdiagnosed case of pulmonary mucormycosis and review of the literature. Chin Med J (Engl) 2010;123:2480-2.  Back to cited text no. 6
    
7.
Wolf O, Gil Z, LeiderTrejo L, Khafif A, Biderman P, Fliss DM. Tracheal mucormycosis presented as an intraluminal soft tissue mass. Head Neck 2004;26:541-3.  Back to cited text no. 7
    
8.
Hamilos G, Samonis G, Kontoyiannis DP. Pulmonary mucormycosis. Semin Respir Crit Care Med 2011;32:693-702.  Back to cited text no. 8
    
9.
Donado Uña JR, Díaz Hellín V, López Encuentra A, Echave Sustaeta JM. Persistent cavitations in pulmonary mucormycosis after apparently successful amphotericin B. Eur J Cardiothorac Surg 2002;21:940-2.  Back to cited text no. 9
    
10.
Butala A, Shah B, Cho YT and Schmidt MF: Isolated pulmonary mucormycosis in an apparently normal host: A case report. J Natl Med Assoc 1995;87:572-4.  Back to cited text no. 10
    
11.
Chung JH, Godwin JD, Chien JW, Pipavath SJ. Case 160: Pulmonary mucormycosis. Radiology 2010;256:667-70.  Back to cited text no. 11
    


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