A 73-year-old man who had been diagnosed with type 2 diabetes mellitus at 35 year of age, who had severe diabetic neuropathy and diabetic-ESRD complained of respiratory distress and sudden chest pain.
On the first day of treatment, he visited the emergency room.
A physical examination revealed that his body temperature was 35.4°C, his heart rate was 90 beats/min with a regular rhythm; and his blood pressure was 130/77 mmHg.
A physical examination revealed coarse crackles on bilateral lung auscultation.
The laboratory data showed a WBC count of 8,800/μL with a shift to the left (neutrophils 82%), Hb 10.2 g/dL, blood urea nitrogen (BUN) 82.2 mg/dL, creatinine (Cre) 6.50 mg/dL, HbA1c 5.9%, creatine kinase (CK) 189 IU/L, C-reactive protein (CRP) 8.51 mg/dL, brain-type natriuretic peptide (BNP) 127.4 pg/mL.
A chest radiograph revealed perihilar consolidations and air bronchograms (Fig.1).
An electrocardiogram revealed ST-segment elevation and poor R-wave progression in leads V1-V3, and echocardiography revealed apical and ventricular asynergy.
The patient was therefore diagnosed with acute myocardial infarction and congestive heart failure.
Coronary angiography was performed, revealing severe angiostenosis in the septal branch.
PCI was therefore performed.
The patient required continuous maintenance dialysis.
On the following day, the patient went into cardiorespiratory arrest and cardiopulmonary resuscitation was performed, followed by mechanical ventilation.
On day 8, ventilator assistance was discontinued.
However, the patient produced an increasing volume of sputum, which began to appear purulent.
Pseudomonas aeruginosa was identified from a sputum culture, and tazobactam/piperacillin (TAZ/PIPC) (4.5g q12h) was administered.
Despite this therapy, the patient's respiratory condition worsened and a chest computed tomography (CT) scan on day 15 revealed bilateral perihilar opacities, pleural effusion, and atelectasis.(Fig.2).
We suspected the development of complications such as microbial substitution, pneumomycosis and thus performed sputum culturing and serum fungal antigen tests.
The administration of TAZ/PIPC was changed to meropenem (0.5 g/day).
On day 16, the patient's serum tested positive for Cryptococcus antigen.
On day 21, cryptococcal bodies were identified in two sets of blood cultures and liposomal amphotericin B (L-AMB) (3 mg/kg/day) was administered.
On day 23, cryptococcal bodies were identified in the sputum, cerebrospinal fluid, and bilateral pleural effusion (Fig.3).
The patient was therefore diagnosed with disseminated cryptococcosis.
On day 25, brain CT revealed the absence of intracranial hypertension and a brain abscess.
The patient was not infected with human immunodeficiency virus (HIV).
The administration of L-AMB (3 mg/kg/day) was continued.
On day 31, chest CT revealed a solitary nodule in the left lingular segment for the first time, which was suspected to be a pulmonary cryptococcus lesion (Fig.4a).
After several days, all of the sputum, blood, bilateral pleural effusion, and cerebrospinal fluid cultures tested negative.
On day 52, chest CT revealed another lung nodule in the right pulmonary apical region.
These nodules gradually decreased in size until day 79 (Fig.4b and c).
Although L-AMB was considered effective, the C-reactive protein level remained elevated and the bilateral pleural effusion continuously increased.
The patient lost consciousness because of decreased vital capacity with increasing bilateral pleural effusion and was diagnosed with CO2 narcosis.
The patient's general condition deteriorated.
On day 87, ventricular fibrillation occurred and the patient died.
Autopsy was not performed.
At a later date, the Cryptococcus isolate was identified and classified as Cryptococcus neoformans var. grubii (serotype A) by a genetic analysis.