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

Introduction

In the realm of infectious diseases, co-infections can pose significant challenges. One such rare and potentially fatal combination is the co-infection of Pneumocystis jirovecii and Aspergillus. This article delves into a case of this co-infection in a patient with idiopathic thrombocytopenic purpura (ITP).

Background on Infections

Pneumocystis jirovecii pneumonia (PCP) is a well-known life-threatening opportunistic infection. While it commonly occurs in patients with human immunodeficiency virus (HIV) infection, it can also afflict those without HIV. This includes individuals who have undergone organ transplantation, chemotherapy, or high-dose corticosteroid therapy. Invasive aspergillosis (IA) is another opportunistic infection that targets immunocompromised patients. Such patients may be undergoing chemotherapy, steroid treatment, transplantation, or be individuals with advanced HIV infection.

PCP and IA co-infection in HIV patients has been reported. However, in non-HIV patients, the number of reported cases is extremely limited. Only nine cases of co-infection with PCP and IA in non-HIV patients have been documented in the literature.

Case Presentation

A 75-year-old woman presented to the emergency room (ER) with a week-long history of dyspnea. One month prior, she was diagnosed with ITP and was on corticosteroid therapy (prednisolone 60 mg/day, tapered 10 mg/day). On arrival, her vital signs were alarming: blood pressure 156/122 mmHg, heart rate 180 beats/min (irregular), respiratory rate 44 breaths/min, oxygen (O₂) saturation 56% (on room air), and body temperature 37.7°C. Laboratory results indicated severe inflammation, with a high level of high-sensitivity C-reactive protein (24.29 mg/dL) and a white blood cell count of 15,340/mL (89.0% neutrophils). Tests for influenza antigen, respiratory virus, and bacterial polymerase chain reaction (PCR) (16 and 5 types, respectively) were negative. Tests for P. jirovecii (SEE AMP; Seegene, Seoul, Republic of Korea) and aspergillosis antigen (V Max Molecular devices, San Jose, CA, USA) were conducted during her ER stay.

Initial chest radiography revealed diffuse ground-glass opacities (GGOs) and infiltration in both lungs. Chest computed tomography (CT) showed diffuse geographic consolidations and GGOs in both lungs, along with two cavitary lesions in both lower lungs.

Treatment and Course

She was admitted to the intensive care unit. Empirical treatment for community-acquired pneumonia was initiated with intravenous (IV) piperacillin/tazobactam 4.5 g every 8 h and azithromycin 500 mg/day. Given the possibility of PCP infection, IV sulfamethoxazole/trimethoprim (320 mg trimethoprim every 6 h) and methylprednisolone 60 mg/day were also administered.

On hospital day 3, endotracheal intubation and mechanical ventilator support were started. Antibiotics were switched to meropenem and levofloxacin. By hospital day 7, the fraction of inspiration O₂ was reduced to 45%, and the patient showed some clinical improvement. Initial serology, PCP PCR, and aspergillus antigen tests were positive. Considering the two cavitary lesions, itraconazole (200 mg/day) was initiated to treat possible chronic cavitary aspergillosis. Follow-up non-enhanced chest CT revealed 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 aspergillosis antigen tests were done using BAL fluid from the right middle lobe. On hospital day 11, aspergillosis was reported in BAL fluid cytology. Based on cytology and CT results, IA was diagnosed, and the antifungal agent was changed to voriconazole (200 mg twice/day).

On hospital day 13, percutaneous dilatational tracheostomy and bronchoscopy with BAL were carried out in the right upper lobe to look for evidence of PCP. However, the results of BAL fluid cytology (second) only showed aspergillosis again.

After a few days, her condition deteriorated. Her family declined aggressive management, including extracorporeal membrane oxygenation. On hospital day 15, the results of PCP PCR of the BAL (first) fluid specimen were positive, but the fungus culture showed no growth after 1 and 2 weeks. On hospital day 16, the patient succumbed to multi-organ failure and septic shock.

Discussion

PCP and IA co-infection is rare but can be fatal. To the best of our knowledge, this patient is the tenth reported case of PCP and IA co-infection in a non-HIV patient. Among the six cases (including this one) of co-infection who underwent intubation and mechanical ventilation, five died from progression to acute respiratory failure. This translates to a mortality rate of approximately 83.3%.

Conclusion

This case highlights the rarity and severity of PCP and IA co-infection in non-HIV patients, especially those on high-dose corticosteroid therapy like in ITP. It emphasizes the need for early diagnosis and appropriate management strategies in such complex cases. Further research is required to better understand the pathogenesis, improve diagnostic methods, and develop more effective treatment regimens for this challenging co-infection.

doi: 10.1097/CM9.0000000000000343

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