INTRODUCTION: The deposition of calcium oxalate crystals in tissue is known to have a strong association with Aspergillus infections. However, there is some evidence to suggest the detection of calcium oxalate crystals is more specific to the Aspergillus (A.) niger strain. We report a case of pulmonary aspergillosis caused by A. niger infection with the detection of calcium oxalate crystals from necrotic lung tissue.
CASE PRESENTATION: A 52 year old female with a history of diabetes and tobacco use presented with a nonproductive cough and a fifteen pound weight loss over the past three months. On exam, the patient was a cachectic, ill-appearing female who was tachycardic and had coarse rhonchi on auscultation. A complete blood count upon admission revealed a leukocytosis with a bandemia. The chemistry panel was consistent with diabetic ketoacidosis and her arterial blood gas showed hypoxia. A chest roentgenogram (X-ray) showed a large right upper lobe consolidation. She was started on ceftriaxone and azithromycin and multiple sputum smears were negative for acid-fast bacilli. Computed Tomography (CT) revealed a right upper lobe infiltrate with small areas of lucencies, suggestive of cavitation. A sputum culture was negative for bacteria, but yielded A. niger. Empiric treatment with caspofungin was started. Repeat CT scan 3 weeks later showed an enlarging cavity in the right upper lobe (RUL). Bronchoscopy showed a plaque-like lesion in the RUL. The bronchoalveolar culture grew A. niger and the cytology showed calcium oxalate crystals in a background of acute inflammatory cells. The patient had recurring episodes of hemoptysis, which were successfully treated with embolization. The patient was ultimately discharged home on voriconazole.
DISCUSSIONS: The association of calcium oxalate crystals and Aspergillosis was first described in 1973 by Nime and Hutchins.1 In their report, Aspergillus niger was identified more frequently than other Aspergillus species and was always associated with the heaviest deposits of calcium oxalate crystals. Since Nime and Hutchins, there have been more case reports suggesting the detection of calcium oxalate crystals is characteristic for A. niger infection. Clinically, it is often difficult to reliably diagnose Aspergillus infection solely on respiratory tract cultures and biopsies are commonly necessary. The presence of calcium oxalate crystals should be considered a sign of true infection, rather than colonization or contamination. In our patient, both sputum and bronchoalveolar cultures grew A. niger with cytology demonstrating calcium oxalate crystals. Furthermore, while it is well known that these calcium oxalate crystals are formed when oxalic acid reacts with calcium ions in tissue fluids and blood, the factors determining where they are deposited remain unclear. The distribution of how calcium oxalate crystals are deposited may be affected by the host's condition along with the type of Aspergillus strain isolated. In our patient who was originally admitted in diabetic ketoacidosis, the acidophilic character of Aspergillus niger and the low pH necessary for oxalic acid2 made the patient more susceptible to infection with A. niger leading to local depostion of calcium oxalate crystals. Widespread oxalosis may not have been observed since the patient was not considered to be severely immunocompromised.
CONCLUSION: This case demonstrates that in the absence of other oxalosis-related conditions, the detection of calcium oxalate crystals on bronchoscopic cytology specimens should serve as an important diagnostic aid in detecting A. niger infections. In addition, the degree of host immunosuppression and the type of Aspergillus species isolated may play a role in the quantity and distribution of calcium oxalate crystals seen clinically.
DISCLOSURE: Rupesh Vakil, No Financial Disclosure Information; No Product/Research Disclosure Information