Co-infection of Pneumocystis jirovecii and Aspergillus in a Patient with Idiopathic Thrombocytopenic Purpura

Co-infection of Pneumocystis jirovecii and Aspergillus in a Patient with Idiopathic Thrombocytopenic Purpura

Pneumocystis jirovecii pneumonia (PCP) is a severe opportunistic infection that primarily affects immunocompromised individuals, particularly those with human immunodeficiency virus (HIV) infection. However, PCP can also occur in non-HIV patients who have undergone organ transplantation, chemotherapy, or high-dose corticosteroid therapy. Invasive aspergillosis (IA) is another opportunistic infection that commonly affects immunocompromised patients, including those undergoing chemotherapy, steroid treatment, transplantation, and individuals with advanced HIV infection. While co-infection with PCP and IA has been reported in HIV patients, it is exceedingly rare in non-HIV patients. This article presents a detailed case study of a 75-year-old woman with idiopathic thrombocytopenic purpura (ITP) who developed a fatal co-infection of PCP and IA while undergoing high-dose corticosteroid therapy.

The patient, a 75-year-old woman, presented to the emergency room with a one-week history of dyspnea. She had been diagnosed with ITP one month prior and was treated with high-dose corticosteroids (prednisolone 60 mg/day, tapered by 10 mg/day). Upon arrival, her vital signs were alarming: blood pressure was 156/122 mmHg, heart rate was 180 beats/min (irregular), respiratory rate was 44 breaths/min, oxygen saturation was 56% on room air, and body temperature was 37.7°C. Laboratory findings indicated severe inflammation, with elevated high-sensitivity C-reactive protein levels (24.29 mg/dL) and an increased white blood cell count (15,340/mL with 89.0% neutrophils). Tests for influenza antigen, respiratory virus, and bacterial polymerase chain reaction (PCR) were negative. However, tests for P. jirovecii and aspergillosis antigen were performed during her emergency room stay.

Initial chest radiography revealed diffuse ground-glass opacities (GGOs) and infiltrations in both lungs. Chest computed tomography (CT) further confirmed these findings, showing diffuse geographic consolidations and GGOs in both lungs, as well as two cavitary lesions in the lower lungs. The patient was admitted to the intensive care unit, where empirical treatment for community-acquired pneumonia was initiated with intravenous (IV) piperacillin/tazobactam (4.5 g every 8 hours) and azithromycin (500 mg/day). Given the suspicion of PCP, IV sulfamethoxazole/trimethoprim (320 mg trimethoprim every 6 hours) and methylprednisolone (60 mg/day) were also administered.

On hospital day 3, the patient required endotracheal intubation and mechanical ventilator support. Antibiotics were switched to meropenem and levofloxacin. By hospital day 7, there was a slight improvement in her condition, with the fraction of inspired oxygen reduced to 45%. Initial serology, PCP PCR, and aspergillus antigen tests were positive, prompting the initiation of itraconazole (200 mg/day) to treat possible chronic cavitary aspergillosis, given the presence of cavitary lesions. Follow-up non-enhanced chest CT showed newly formed GGOs in the left upper lung and cavitary changes in the previous consolidation in the right middle lobe.

On hospital day 9, bedside bronchoscopy and bronchoalveolar lavage (BAL) were performed due to the patient’s unstable condition. PCP PCR and aspergillus antigen tests were conducted using BAL fluid collected from the right middle lobe. By hospital day 11, aspergillosis was confirmed in the BAL fluid cytology. Based on the cytology and CT findings, IA was diagnosed, and the antifungal treatment was changed to voriconazole (200 mg twice daily).

On hospital day 13, percutaneous dilatational tracheostomy and bronchoscopy with BAL were performed in the right upper lobe to obtain further evidence of PCP. However, the second BAL fluid cytology only revealed aspergillosis once again. On hospital day 15, the PCP PCR of the first BAL fluid specimen was positive, but the fungus culture showed no growth after one and two weeks. Unfortunately, the patient’s condition continued to deteriorate, and her family declined further aggressive management, including extracorporeal membrane oxygenation. The patient succumbed to multi-organ failure and septic shock on hospital day 16.

This case highlights the rarity and severity of PCP and IA co-infection in non-HIV patients. To date, only nine such cases have been reported in the literature, making this the tenth documented case. The mortality rate among these cases is alarmingly high, with five out of six patients who required intubation and mechanical ventilation succumbing to acute respiratory failure, resulting in a mortality rate of approximately 83.3%.

The clinical presentation, diagnostic challenges, and management strategies for PCP and IA co-infection are complex. The initial presentation often includes respiratory distress, fever, and radiographic findings of diffuse GGOs and consolidations. Diagnostic confirmation typically involves a combination of serology, PCR, antigen testing, and BAL fluid cytology. Treatment requires a multi-faceted approach, including antimicrobial therapy for PCP and antifungal therapy for IA, along with supportive care. However, despite aggressive treatment, the prognosis remains poor, particularly in patients who require mechanical ventilation.

In conclusion, PCP and IA co-infection is a rare but highly fatal condition in non-HIV patients, particularly those undergoing high-dose corticosteroid therapy. Early recognition, accurate diagnosis, and prompt initiation of appropriate treatment are crucial to improving outcomes. However, the high mortality rate underscores the need for further research and development of more effective treatment strategies for this devastating co-infection.

doi.org/10.1097/CM9.0000000000000343

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