Journal of Postgraduate Medicine
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Year : 2003  |  Volume : 49  |  Issue : 1  |  Page : 78-80  

Invasive pulmonary aspergillosis complicating chronic obstructive pulmonary disease in an immunocompetent patient.

ZA Ali, AA Ali, ME Tempest, MJ Wiselka 
 Department of Cardiothoracic Surgery, Papworth Hospital, Papworth, UK.

Correspondence Address:
Z A Ali
Department of Cardiothoracic Surgery, Papworth Hospital, Papworth, UK.


Immunocompromised individuals are susceptible to pulmonary aspergillus infection, but invasive aspergillus infection is extremely rare in the presence of normal immunity. We report a case of invasive aspergillosis in an immunocompetent 63-year-old male with chronic obstructive pulmonary disease (COPD). Patients with COPD may be at risk for developing pulmonary aspergillus infection, which should be considered as a diagnostic possibility in patients with unresolving pulmonary infection.

How to cite this article:
Ali Z A, Ali A A, Tempest M E, Wiselka M J. Invasive pulmonary aspergillosis complicating chronic obstructive pulmonary disease in an immunocompetent patient. J Postgrad Med 2003;49:78-80

How to cite this URL:
Ali Z A, Ali A A, Tempest M E, Wiselka M J. Invasive pulmonary aspergillosis complicating chronic obstructive pulmonary disease in an immunocompetent patient. J Postgrad Med [serial online] 2003 [cited 2021 Apr 19 ];49:78-80
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Invasive pulmonary aspergillosis is a well-recognised complication in immunocompromised patients. Immunocompetent individuals rarely develop this infection and do so only in the presence of pulmonary and systemic abnormalities such as fibrotic lung disease,[1] suppurative infection[2] or when they are on corticosteroids.[3] Aspergillosis in patients with chronic obstructive pulmonary disease (COPD) has rarely been reported.[4]

  ::   Case reportTop

A 63-year-old retired steel worker was admitted with a one-week history of pleuritic chest pain, shortness of breath, and haemoptysis. His past medical history included two bouts of bronchopneumonia in 1956 and 1966 and an inferior wall myocardial infarction in 1988. He had been a chronic cigarette smoker [40/day] and had an exercise-tolerance of only 200-300 yards on flat surfaces in keeping with a diagnosis of chronic obstructive pulmonary disease (COPD). There was no past history of tuberculosis or exposure to asbestos.

On examination, the patient was afebrile with a pulse rate of 80 per minute, respiratory rate of 25/min, blood pressure 125/75 mmHg, and a peak expiratory flow rate of 220 l/min. He produced copious amounts of mucoid green-coloured, blood streaked sputum. Auscultation revealed coarse crackles bilaterally. Oxygen saturation was 93% and arterial blood gases demonstrated a pO2 of 7.9 Kpa and a pCO2 of 3.7 Kpa on air. Chest radiograph revealed cardiomegaly but no focal consolidation in the lungs. A ventilation-perfusion (VQ) scan showed matched defects bilaterally suggesting an intermediate probability of pulmonary embolism. On the basis of these findings and a raised white cell count of 12.2 x 109/l a diagnosis of an infective exacerbation of COPD was made. Initial therapy with co-amoxiclav was unsuccessful and treatment with nebulized bronchodilators and ampicillin/erythromycin without steroids was initiated. This regimen evoked a good clinical response and the patient was discharged from hospital after a week.

Seven days after his discharge the patient returned to the hospital with a significant deterioration in his condition. He was short of breath at rest and had a cough productive of purulent copious green/grey sputum with haemoptysis. On examination he had a pulse rate of 90/min, blood pressure of 105/65mms of Hg, respiratory rate of 27/min and was cyanosed. Findings on examination of the chest were consistent with right upper lobe consolidation. Repeat investigations including a chest radiograph confirmed the presence of consolidation. The white cell count had risen to 18.5 x 109/l but both blood and sputum cultures revealed no significant bacterial growth. In view of the evidence of right upper lobe consolidation treatment was initiated with ceftazidime, flucloxacillin, erythromycin and nebulised bronchodilators.

The patient showed no signs of improvement for a week and the chest radiograph revealed persistence of consolidation in the right upper zone with evidence of cavitation. Antibiotics were withdrawn. CT scan of the thorax showed a central right upper lobe cavity distinct from the pleura with non-homogenous patchy consolidation and dilation of the bronchi distal to the lesion. Bronchial washings were obtained at bronchoscopy. Both washings and sputum grew hyphae of Aspergillus fumigatus on Sabourard dextrose agar. Serological tests revealed markedly elevated titres but low precipitans. Bronchial biopsy specimen stained with methenamine silver demonstrated the presence of dichotomously branched septate fungal hyphae invading the lung parenchyma confirming the diagnosis of invasive pulmonary aspergillosis. A chest tube was inserted for pleural effusion and treatment with amikacin, amphotericin B, metronidazole, and meropenem was initiated.

Three days after the initiation of therapy the fever began to subside. At one week, there was a drastic reduction in the volume of sputum and there were no further episodes of haemoptysis. The patient continued to improve while in hospital and was discharged seventeen days after his presentation. At six-week follow-up visit, he showed notable improvement. He was producing only small amounts of white sputum in the mornings, which was only occasionally blood-stained. This was attributed to the development of an area of bronchiectasis distal to cavitation. A variety of tests were performed to exclude underlying immunosuppression. Both neutrophil and lymphocyte counts had returned to normal. Differential counts for CD3, CD4, CD8 CD19, and CD34 lymphocytes were within normal limits. Neutrophil subset analysis failed to identify any abnormality. The patient had tested negative for HIV during his hospital stay with a normal CD4:CD8 ratio. Review of CT chest and abdomen revealed no evidence of lymphadenopathy related to haematological malignancy. Peripheral smear, lactate dehydrogenase and erythrocyte sedimentation rate were normal. By 6 months even these infrequent episodes of haemoptysis subsided completely and the right apical cavity resolved with residual scarring.

  ::   DiscussionTop

Aspergillus infection spreads via airborne route and almost invariably, lung is the site of invasion. Aspergilli have a sporular diameter which allows penetration to the distal pulmonary areas and alveoli. Our case highlights that pulmonary aspergillosis can occur in immunocompetent individuals with COPD even in the absence of risk factors such as corticosteroid or cytotoxic therapy, use of broad- spectrum antimicrobial agents, severe granulocytopenia or qualitative granulocyte defects. This diagnostic possibility should be considered when an aetiological agent is not identifiable in a patient, who fails to respond to antimicrobial agents. Although invasive aspergillosis is often a fatal disease in immunocompromised patients, early diagnosis and institution of appropriate treatment, together with reduction in risk factors, appears to significantly improve the prognosis.[5]

The diagnosis of invasive pulmonary aspergillosis is often difficult. Sputum cultures may be negative. Positive cultures have to be interpreted taking into consideration the fact that the organism colonizes the upper and lower respiratory tract without causing manifestations of the disease. In most cases, the diagnosis is made following tissue isolation of a single species in an appropriate clinical setting. Histological evidence requires invasive methods to obtain diagnostic samples, and both clinicians and patients may be reluctant for undertaking these invasive techniques. Common diagnostic procedures include CT- guided percutaneous needle aspiration, which can be both sensitive and specific for diagnostic evaluation. Bronchoscopy or bronchoalveolar lavage with washings is safe and sensitive and particularly useful in high-risk patients where organisms may be identified quickly with smear. Transbronchial biopsy via fibreoptic bronchoscopy has moderate sensitivity but is highly specific.[6] Lung biopsy with video-assistance or thoracotomy is useful in providing samples large enough to provide tissue diagnosis.

Two antifungal agents are licensed for the treatment of pulmonary aspergillosis - amphotericin B and itraconazole. The comparative response rates of both the agents appear similar.[7] Drug toxicity is the chief concern while using amphotericin B while poor bioavailability due to interactions with several drugs that activate P-450 enzyme systems is a limitation for using itraconazole. Outcome is better if patients have well-controlled underlying disease and a granulocyte count greater than 1000.[8] Surgical resection is a consideration for localized disease that has failed to respond to anti-fungal therapy. Operative removal of residual nodular infiltrates is of proven benefit, especially in neutropenic patients where re-activation is a risk.[9]

This patient had none of the proposed risk factors for aspergillus infection but did suffer from COPD. Other cases of pulmonary aspergillosis in immunocompetent individuals with COPD have been described,[4] and the associated mortality is very high. Our case may have been confounded by the patientís earlier hospitalization and treatment with broad-spectrum antibiotics and nebulized bronchodilators. Nevertheless, in the face of normal immunity, it remains unlikely that these risk factors were causal of the infection. The contribution of these risk factors is difficult to quantify, but in the context of exacerbation of COPD such initial management is expected to be carried out. It is, therefore, valuable to recognize that, in immunocompetent patients with COPD, aspergillus infection should be considered as an important differential diagnosis in respiratory infections that are difficult to treat. [4],[10]


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