Pneumocystis jirovecii pneumonia (PCP) is a potentially life-threatening infection, which predominantly occurs in the immuno-compromised host. It has been rarely reported in immunocompetent subjects. In them, the infection presents with fulminant respiratory failure along with fever and dry cough in contrast to an indolent course in the immuno-compromised population. The most significant risk factors for PCP in non-HIV infected hosts are glucocorticoid use and cell mediated immunity defects. We report a rare case of Pneumocystis jirovecii pneumonia in an immunocompetent patient. Keywords: Immunocompetent host, pneumocystis jirovecii, pneumonia
Pneumocystis jirovecii pneumonia (PCP) is a potentially life-threatening infection, which predominantly occurs in the immunocompromised host. However, individuals with normal immune systems may also harbor asymptomatic lung colonization and may serve as a reservoir for the spread of Pneumocystis. [1] We report a case of PCP in an immunocompetent patient.
A 56-year-old male of Indian race from Qatar, while on holiday in North India, presented with cough for 1 month, and dyspnea and hemoptysis for 7 days prior to admission. He was a diagnosed case of systemic hypertension and type 2 diabetes mellitus. He had been diagnosed with tuberculoid leprosy 35 years ago, and was treated with dapsone for 6 years after which he had done well. On examination, he was found to be tachypneic, with a respiratory rate of 26 breaths/min and examination of the respiratory system revealed bilateral crepitations. His saturation, on room air, was 70%. An initial arterial blood gas done on oxygen via a mask revealed type I respiratory failure with oxygen saturation of 90.4% and partial pressure of oxygen (PO 2 ) of 63.4 mmHg. Chest radiography had nonhomogenous opacities in the bilateral middle and lower zones [Figure 1]. Initial investigations were unremarkable except for leucocytosis (11,000/mm 3 ) and glycated hemoglobin (Hba1c) of 7.4%.
He was initiated on treatment for community-acquired bronchopneumonia and atypical pneumonia. Treatment for influenza A virus (H1N1) infection was also initiated as there were reports of similar infections in the community. Noninvasive ventilation was initiated with which he maintained 95% saturation. On the second day, in spite of treatment, he did not maintain saturation off oxygen and further testing of induced sputum was sent for Gram staining, Ziehl-Neelsen staining, modified acid-fast bacilli (AFB) staining, and silver methylamine preparation to look for PCP. Oocysts of Pneumocystis jirovecii were isolated on silver methenamine staining. He was initiated on co-trimoxazole (trimethoprim/sulphamethoxazole two tablets three times a day), along with steroids (prednisolone tablets 40 mg twice a day, which was gradually tapered off). His condition improved and he was switched over to oxygen via a mask by the third day. Large areas of ground-glass appearance in bilateral lung fields with interstitial septal thickening consistent with PCP were seen on a high-resolution computed tomography (HRCT) of the chest, done on the seventh day [Figure 2]. Fourth-generation human immunodeficiency virus (HIV) enzyme-linked immunosorbent assay (ELISA) was done, which was negative. Western blot analysis also was done for confirmation, which was also negative. A cluster of differentiation (CD4) count done at that point was 296 cells/MCL.
The patient gradually improved and started maintaining saturation off oxygen by the 10th day. A repeat chest x-ray [Figure 3] done on the 14th day revealed marked clearing of the lung lesions. He was discharged in a stable condition on the 15th day and co-trimoxazole was continued for a total of 21 days, along with steroids. CD4 done 1 month later was 984 cells/MCL, implicating that the low CD4 count was a transient decrease due to the illness.
PCP has been rarely reported in immunocompetent subjects. [2] It is speculated to result either from an infection de novo or from reactivation of a latent childhood infection. [3] In spite of the absence of HIV infection, the individuals can be predisposed to PCP. In them, the infection presents with fulminant respiratory failure, along with fever and dry cough as was in our case; this is in contrast to an indolent course in the immunocompromised population. [4] Experiments have shown that the Pneumocystis organisms can replicate in the lung alveolus of immunocompetent hosts and remain infectious; hence, this organism is found even in healthy adults in a normal community. [5] Immunocompetent individuals might harbor a short-lived infection and when immunosuppressed and susceptible, may cause the development of clinical PCP infection. [6] The most significant risk factors for PCP in non-HIV-infected hosts are glucocorticoid use and cell-mediated immunity defects, which lead to alterations in the lung surfactant, thereby predisposing to pneumonia. [4],[5] Individuals who have been affected with Hansen’s disease have shown wide-ranging immunity, from strong cellular immunity in paucibacillary type to poor cellular immunity (with potent humoral immunity) in multibacillary type. [7] Historically, this patient had tuberculoid leprosy, implicating a strong cellular immunity. This case was unusual as this patient was neither HIV infected nor on glucocorticoid or immunosuppressants. The only risk factor in him was that he was a diabetic. The restoration of immune status as indicated by normal CD4 counts a month later also implicates that the patient’s baseline immune status was normal.
PCP should always be considered in patients, even in non-HIV settings, who present with dry cough and dyspnea with type 1 respiratory failure. Since these patients have nonproductive cough, it is important to get induced sputum for examination as the oocysts of pneumocystis are attached to the type 2 pneumocytes. High index of suspicion is required to diagnose these cases.
We would like to acknowledge the help of the Department of Microbiology, Christian Medical College & Hospital, Ludhiana, Punjab, India.
Source of Support: None, Conflict of Interest: None
[Figure 1], [Figure 2], [Figure 3] |
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