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A Case of Pneumonia Caused by Pneumocystis jirovecii Resistant to Trimethoprim-Sulfamethoxazole.

Lee SM, Cho YK, Sung YM, Chung DH, Jeong SH, Park JW, Lee SP - Korean J. Parasitol. (2015)

Bottom Line: Molecular studies demonstrated mutations at codons 55 and 57 of the dihydropteroate synthase (DHPS) gene, which is associated with the resistance to TMP-SMX.A positive result of HIV immunoassay and elevated titer of HCV RNA indicated HIV infection as an underlying condition.To the best of our knowledge, this is the first case of TMP-SMX-resistant PCP described in Korea.

View Article: PubMed Central - PubMed

Affiliation: Division of Pulmonology and Allergy, Gachon University Gil Medical Center, Incheon 405-760, Korea.

ABSTRACT
A 50-year-old male visited the outpatient clinic and complained of fever, poor oral intake, and weight loss. A chest X-ray demonstrated streaky and fibrotic lesions in both lungs, and chest CT revealed multifocal peribronchial patchy ground-glass opacities with septated cystic lesions in both lungs. Cell counts in the bronchoalveolar lavage fluid revealed lymphocyte-dominant leukocytosis, and further analysis of lymphocyte subsets showed a predominance of cytotoxic T cells and few T helper cells. Video-assisted wedge resection of the left upper lobe was performed, and the histologic examination was indicative of a Pneumocystis jirovecii infection. Trimethoprim-sulfamethoxazole (TMP-SMX) was orally administered for 3 weeks; however, the patient complained of cough, and the pneumonia was aggravated in the follow-up chest X-ray and chest CT. Molecular studies demonstrated mutations at codons 55 and 57 of the dihydropteroate synthase (DHPS) gene, which is associated with the resistance to TMP-SMX. Clindamycin-primaquine was subsequently administered for 3 weeks replacing the TMP-SMX. A follow-up chest X-ray showed that the pneumonia was resolving, and the cough was also alleviated. A positive result of HIV immunoassay and elevated titer of HCV RNA indicated HIV infection as an underlying condition. This case highlights the importance of careful monitoring of patients with P. jirovecii pneumonia (PCP) during the course of treatment, and the molecular study of DHPS mutations. Additionally, altering the anti-PCP drug utilized as treatment must be considered when infection with drug-resistant P. jirovecii is suspected. To the best of our knowledge, this is the first case of TMP-SMX-resistant PCP described in Korea.

No MeSH data available.


Related in: MedlinePlus

Photomicrography of Pneumocystis jirovecii pneumonia. (A) Hematoxylin and eosin staining shows eosinophilic frothy exudates in alveolar spaces accompanied by mild interstitial inflammation (H&E, ×200). (B) Grocott-Gomori’s methenamine silver (GMS) stain visualized many cystic- and trophic-form organisms (arrows) in alveolar exudate, consistent with Pneumocystis jirovecii infection (GMS, ×400).
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f3-kjp-53-3-321: Photomicrography of Pneumocystis jirovecii pneumonia. (A) Hematoxylin and eosin staining shows eosinophilic frothy exudates in alveolar spaces accompanied by mild interstitial inflammation (H&E, ×200). (B) Grocott-Gomori’s methenamine silver (GMS) stain visualized many cystic- and trophic-form organisms (arrows) in alveolar exudate, consistent with Pneumocystis jirovecii infection (GMS, ×400).

Mentions: Bronchoscopy was performed, but no endobronchial lesions were observed. Bronchoalveolar lavage (BAL) was performed in the right middle lobe. Cell counts in BAL revealed a lymphocyte-dominant leukocytosis (white cells 342/μl, neutrophils 9%, lymphocytes 37%, eosinophils 5%, and macrophages 49%). Further analysis of lymphocyte subsets showed a predominance of cytotoxic T cells (cytotoxic T cells 98.3%, T helper cells 1.7%, natural killer cells 3%, and B cells 0.1%). Cytologic studies, acid-fast bacillus stain, and PCR for tuberculosis and non-tuberculotic mycobacteria in the BAL fluid exhibited negative results. A tuberculin skin test and interferon-γ release assay (Quantiferon®; Carnegie, Victoria, Australia) were also negative. A video-assisted wedge resection of the left upper lobe was performed. Upon histological examination, hematoxylin and eosin (H&E) staining revealed eosinophilic frothy exudates in alveolar spaces accompanied by mild interstitial inflammation, and Grocott-Gomori’s methenamine silver (GMS) stains, performed during the histological examination, revealed many cystic- and trophic-form organisms (arrows) in the alveolar exudate, consistent with P. jirovecii infection (Fig. 3). Trimethoprim-sulfamethoxazole (TMP-SMX) was administered orally (2 double strength TMP-SMX tablets every 8 hr) [11]. The patient’s fever subsided within 3 days (from 38.5˚C to 37.0˚C), and the streaky and fibrotic lesions observed in both lungs on the chest X-ray were also markedly improved (Fig. 1B) after 12 days of TMP-SMX administration, which enabled the patient to be discharged.


A Case of Pneumonia Caused by Pneumocystis jirovecii Resistant to Trimethoprim-Sulfamethoxazole.

Lee SM, Cho YK, Sung YM, Chung DH, Jeong SH, Park JW, Lee SP - Korean J. Parasitol. (2015)

Photomicrography of Pneumocystis jirovecii pneumonia. (A) Hematoxylin and eosin staining shows eosinophilic frothy exudates in alveolar spaces accompanied by mild interstitial inflammation (H&E, ×200). (B) Grocott-Gomori’s methenamine silver (GMS) stain visualized many cystic- and trophic-form organisms (arrows) in alveolar exudate, consistent with Pneumocystis jirovecii infection (GMS, ×400).
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4510680&req=5

f3-kjp-53-3-321: Photomicrography of Pneumocystis jirovecii pneumonia. (A) Hematoxylin and eosin staining shows eosinophilic frothy exudates in alveolar spaces accompanied by mild interstitial inflammation (H&E, ×200). (B) Grocott-Gomori’s methenamine silver (GMS) stain visualized many cystic- and trophic-form organisms (arrows) in alveolar exudate, consistent with Pneumocystis jirovecii infection (GMS, ×400).
Mentions: Bronchoscopy was performed, but no endobronchial lesions were observed. Bronchoalveolar lavage (BAL) was performed in the right middle lobe. Cell counts in BAL revealed a lymphocyte-dominant leukocytosis (white cells 342/μl, neutrophils 9%, lymphocytes 37%, eosinophils 5%, and macrophages 49%). Further analysis of lymphocyte subsets showed a predominance of cytotoxic T cells (cytotoxic T cells 98.3%, T helper cells 1.7%, natural killer cells 3%, and B cells 0.1%). Cytologic studies, acid-fast bacillus stain, and PCR for tuberculosis and non-tuberculotic mycobacteria in the BAL fluid exhibited negative results. A tuberculin skin test and interferon-γ release assay (Quantiferon®; Carnegie, Victoria, Australia) were also negative. A video-assisted wedge resection of the left upper lobe was performed. Upon histological examination, hematoxylin and eosin (H&E) staining revealed eosinophilic frothy exudates in alveolar spaces accompanied by mild interstitial inflammation, and Grocott-Gomori’s methenamine silver (GMS) stains, performed during the histological examination, revealed many cystic- and trophic-form organisms (arrows) in the alveolar exudate, consistent with P. jirovecii infection (Fig. 3). Trimethoprim-sulfamethoxazole (TMP-SMX) was administered orally (2 double strength TMP-SMX tablets every 8 hr) [11]. The patient’s fever subsided within 3 days (from 38.5˚C to 37.0˚C), and the streaky and fibrotic lesions observed in both lungs on the chest X-ray were also markedly improved (Fig. 1B) after 12 days of TMP-SMX administration, which enabled the patient to be discharged.

Bottom Line: Molecular studies demonstrated mutations at codons 55 and 57 of the dihydropteroate synthase (DHPS) gene, which is associated with the resistance to TMP-SMX.A positive result of HIV immunoassay and elevated titer of HCV RNA indicated HIV infection as an underlying condition.To the best of our knowledge, this is the first case of TMP-SMX-resistant PCP described in Korea.

View Article: PubMed Central - PubMed

Affiliation: Division of Pulmonology and Allergy, Gachon University Gil Medical Center, Incheon 405-760, Korea.

ABSTRACT
A 50-year-old male visited the outpatient clinic and complained of fever, poor oral intake, and weight loss. A chest X-ray demonstrated streaky and fibrotic lesions in both lungs, and chest CT revealed multifocal peribronchial patchy ground-glass opacities with septated cystic lesions in both lungs. Cell counts in the bronchoalveolar lavage fluid revealed lymphocyte-dominant leukocytosis, and further analysis of lymphocyte subsets showed a predominance of cytotoxic T cells and few T helper cells. Video-assisted wedge resection of the left upper lobe was performed, and the histologic examination was indicative of a Pneumocystis jirovecii infection. Trimethoprim-sulfamethoxazole (TMP-SMX) was orally administered for 3 weeks; however, the patient complained of cough, and the pneumonia was aggravated in the follow-up chest X-ray and chest CT. Molecular studies demonstrated mutations at codons 55 and 57 of the dihydropteroate synthase (DHPS) gene, which is associated with the resistance to TMP-SMX. Clindamycin-primaquine was subsequently administered for 3 weeks replacing the TMP-SMX. A follow-up chest X-ray showed that the pneumonia was resolving, and the cough was also alleviated. A positive result of HIV immunoassay and elevated titer of HCV RNA indicated HIV infection as an underlying condition. This case highlights the importance of careful monitoring of patients with P. jirovecii pneumonia (PCP) during the course of treatment, and the molecular study of DHPS mutations. Additionally, altering the anti-PCP drug utilized as treatment must be considered when infection with drug-resistant P. jirovecii is suspected. To the best of our knowledge, this is the first case of TMP-SMX-resistant PCP described in Korea.

No MeSH data available.


Related in: MedlinePlus