Beta Fulltext view is in preview — article structure may vary. Browse all articles
Contents
Open Access Journal of Mycology & Mycological Sciences Research Article 21 min read

Pneumocytosis: An Emerging Opportunistic Mycosis of Public Health Importance

Pal M* and Gutama KP*
* Corresponding author
ISSN: 2689-7822  10.23880/oajmms-16000175  Received: March 15, 2023  Published: April 25, 2023
 — views
 67 references
PDF
Keywords
Diagnosis Immuno compromised Non-HIV Opportunistic Mycosis Pneumocystis Jirovecii Pneumocystis Jirovecii Pneumonia Prophylaxis
Abstract

Opportunistic mycoses have become a significant causee of morbidity and mortality in both sexes and in all age groups throughout the world. Pneumocytosis caused by Pneumocystis jiroveciiis, a potentially fatal fungal disease, is significant for public health. Pneumocytosis is often the AIDS-defining disease in HIV-infected patients, usually occurring when CD4 count drops below 200 cells/μL. However, the disease is a growing concern to immune compromised patients without HIV infection, such as those who are undergoing organ transplantation, receiving novel immunosuppressive therapeutics or those who have connective tissue diseases. Pneumocytosis is recognized to affect patients all over the world, and is transmitted from person to person through the airborne route. Patients with and without HIV infections have substantially distinct clinical presentations of Pneumocytosis. Disease has a bad prognosis in individuals who are HIV-negative, rapidly progresses, is challenging to correctly diagnose, and produces severe respiratory failure. Interstitial pneumonia in immune compromised patient a patient is the most common clinical symptom. Due to non-specific signs and symptoms, diagnosis of disease poses a problem. Since chest radiographs are not pathognomonic for disease and the organism cannot be cultivated routinely, a definitive diagnosis must be made using histopathology or cytopathology evidence of organisms in tissue, bronchoalveolar lavage (BAL) fluid, or artificial sputum samples. Trimethoprim-sulfamethoxazole (TMP-SMX) is the treatment of choice. Intravenous pentamidine, clindamycin-primaquine, daps one, atovaquone, and echinocandins are among the second-line treatment options in Pneumocytosis.

Introduction

Pneumocystis was first described in 1909 as a stage in the evolution in the life cycle of Trypanosome cruzi by Chagas Chagas C [1]. Subsequently, Delanoe and Delanoe in [2] identified it as a distinct organism. Originally categorized as protozoa, P. jirovecii was later placed in the hemiascomycetes class due to similarities in its 16S ribosomal RNA sequence. As opposed to ergo sterol, which is the normal target for antifungal medications, the cytoplasmic membrane of P. jirovecii is primarily composed of cholesterol Suk CW, et al. [3], Amber KP [4]. Pneumocystis jirovecii pneumonia (PCP) is a potentially fatal fungal infection that is seen in immunocompromised individuals Kovacs JA and Masur H [5], Catherinot E, et al. [6]. The disease remains an important cause of morbidity and mortality in all immunosuppressed patients generally and HIV-infected patients in particular Calderon EJ, et al. [7], Kaplan JE, et al. [8]. The disease is an emerging threat to immunocompromised patients but do not have HIV infection, such as those receiving novel immunosuppressive therapeutics for malignancy, organ transplantation, or connective tissue diseases Tasaka S [9]. The development of PCP in individuals who were not immunocompromised has been recorded in several studies. However, the clinical course and prognosis of PCP are not well understood Kim TO, et al. [10].

It is believed that pneumocystosis is transmitted from person to person by airborne route. Patients with Pneumocystosis may present with fever, cough, and shortness of breath and, in severe cases, respiratory failure Ricciardi A, et al. [11]. The disease can be difficult to diagnose because of nonspecific symptoms and signs and because the immunocompromised host may have co-infection with other organisms. Pneumocystis cannot be cultured, and thus the diagnosis of PCP requires microscopic examination of the sputum, bronchoalveolar fluid (BAL), or lung tissue Thomas CF and Limper AH [12]. First-line treatment trimethoprim/ sulfamethoxazole therapy should be initiated as soon as possible after confirmation of the diagnosis, because the disease is fatal Hughes W, et al. [13]. Poor outcomes are expected when treatment or diagnosis of PCP is delayed Kim TO, et al. 2021 [10]. The primary objective of this paper is to describe Pneumocystis jirovecii as a new pathogen of public health importance. Emphasis is given on the etiology, transmission, epidemiology, clinical spectrum, diagnosis, treatment and prophylaxis.

Etiology

Pneumocystis jirovecii pneumonia (PCP) is an opportunistic infection caused by Pneumocystis jirovecii Fillatre P, et al. [14], Salzer HJ, et al. [15]. Chagas first identified Pneumocystis in humans in 1909, but they were mistaken for a new life cycle stage of the protozoan Trypanosoma cruzi Chagas C [1]. Within a very short time it became clear that this organism infects other host species, is not a trypanosome, and was named Pneumocystis carinii after Carini, a colleague of Chagas Delano M and Delano P [2]. The microorganism that causes the human disease is now known as Pneumocystis jirovecii after Czech parasitologist Otto Jirovec, who was one of the first researchers to study Pneumocystis in humans Stringer, et al. JR [16], Stringer JR, et al. [17]. For many years, the organism was still widely regarded as a protozoan. In 1988, DNA sequence analysis revealed that Pneumocystis was a fungus Edman JC, et al. [18]. The genus Pneumocystis includes several species, including P. carinii and P. jirovecii, which infect rats and humans respectively Fillatre P, et al. [19], Amber KP [4].

Hosts

Pneumocystis organisms have been identified in virtually all mammalian species Vargas SL, et al. [20]. Pneumocystis organisms encompass a family of organisms that possess a range of genetic characteristics and are host specific Gigliotti F, et al. [21]. Pneumocystis carinii is only a Pneumocystis that infects rats, while P. jirovecii is a separate species that infects humans Amber KP [4]. Initial infection with P. jirovecii usually occurs in early childhood; two-thirds of healthy children have antibodies to P. jirovecii between the ages of 2 and 4 Pifer, et al. [22]. Hosts with defective cellular and/or humoral immunity are prone to develop PCP. Impaired immunity, such as that caused by human immunodeficiency virus (HIV) infection, hematologic malignancies, solid organ tumors with chemotherapy, rheumatic diseases, and immunosuppressive medications, is associated with the development of PCP Fillatre P, et al. [14], Salzer HJ, et al. [15], Tasaka S [9].

Transmission

Airborne transmission of Pneumocystis has been demonstrated in animal models Dumoulin A, et al. [23]. Transmitted from person to person mainly by inhalation of airborne particles Fink Elman MA [24], Morris, et al. [25]. Human Pneumocystis DNA has been identified in airborne spores in both rural Wakefield A [26] and hospital settings Bartlett MS, et al. [27]. Transmission of Pneumocystis DNA from Immunosuppressed Patients to Immunocompetent health care workers Vargas SL, et al. [28] and transmission of Pneumocystis infection from mother to child is reported by Miller RF, et al. [29].

Epidemiology

Pneumocystis jirovecii occurs worldwide, with humans being the main reservoir Finkelman MA [24], Morris A et al. [25]. Exposure to this pathogen is widespread, especially in developed countries, and more than 80% of children develop antibodies against it by age 4. Innate cellular immunity usually destroys this pathogen. However, immunocompromised patients with low CD4+ lymphocytes are primarly affected Hof H [30], Hughes WT, et al. [31]. In immunocompromised patients without HIV infection, pneumocystis is a major cause of morbidity and mortality Sepkowitz KA, et al. [32].

Until the 1980s, PCP was considered a rare but fatal infection mainly among patients with acute leukemia and other hematologic malignancies. In the 1980s, the global epidemic of human immunodeficiency virus (HIV)

dramatically increased the prevalence of PCP as one of the most common complications Maini R, et al. [33]. However, PCP is an emerging threat to immunocompromised patients without HIV infection, such as those receiving new immunosuppressive therapies for malignancies, organ transplants, or connective tissue diseases Tasaka S [9]. Additionally, patients receiving chronic corticosteroids for conditions including chronic obstructive pulmonary disease and Wegener’s granulomatosis may be at risk PCP Hof H [30].

The incidence of PCP has declined substantially with the widespread use of PCP prophylaxis and ART Buchacz K, et al. [34]. Currently, most cases of PCP occur in patients who are unaware of their HIV infection status or not receiving ongoing HIV treatment, and in patients with advanced immunosuppression (CD4 count <100 cells/mm) Wolff AJ and O ‘Donnell AE [35]. Although infection rates have declined significantly in the United States and other industrialized countries, this opportunistic infection is a major cause of significant infection in immunocompromised individuals Solano LM, et al. [36]. The HIV-uninfected population at risk for opportunistic infections, including PCP, is growing rapidly due to prolonged survival and escalating use of immunosuppressant’s Sepkowitz KA [37], Bateman, et al. [38].

Clinical symptoms

The clinical manifestations of PCP differ significantly in patients with and without HIV infection. In patients without HIV infection, PCP progresses rapidly, is difficult to correctly diagnose, and causes severe respiratory failure with a poor prognosis Tasaka S [9]. In non-HIV patients, it takes about a week from the onset of fever and dry cough to the development of respiratory failure, whereas PCP in HIV- infected patients has a more gradual disease course lasting 2 weeks to 2 months Kovacs JA, et al. [39]. These differences in the clinical features of PCP are thought to be related to differences in the host immune response Tasaka S, et al. [40].

The main clinical manifestation of P. jirovecii is interstitial pneumonia in immunocompromised patients. As a general rule, the onset is usually insidious, with initial nonspecific symptoms, including loss of appetite, diarrhea, possible weight loss, and a dry cough. Tachypnea with a respiratory rate of up to 50 breaths per minute, dyspnea, and fatigue are also common Hof H [30], CDC [41]. Fever may or may not be present. As the infection progresses, respiratory distress and hypoxia worsen, and patients usually report being unable to take deep breaths. Purulent sputum is rare, but when present, it usually indicates an underlying bacterial infection Hof H [30]. If PCP is untreated, the associated mortality is approximately 100%; however, those who receive treatment have a mortality rate of 5% to 40% CDC [41]. Mortality from PCP increases with acute onset of respiratory failure and delay in the diagnosis of PCP Walzer PD and Smulian AG [42], Thomas CF and Limper AH [12].

Diagnosis

The diagnosis of PCP is multifactorial and may include clinical suspicion, patient risk factors, laboratory tests, chest radiograph, chest computed tomography (CT), sputum examination, bronchoalveolar lavage evaluation, or lung biopsy Lange in B and Saleh M [43]. Because Pneumocystis cannot be easily cultured in the laboratory, microscopic demonstration of the organisms in respiratory specimens has been the gold standard for the diagnosis of PCP Catherinot E, et al. [6], Thomas CF and Limper AH [12]. Cysts can be stained with Grocott Gomori methanamine silver, which has good specificity, but its sensitivity is not satisfactory. Because trophic forms predominate over cyst forms, it is assumed that Giemse and Diff-Quick staining of trophic forms has high sensitivity, but it is not stable depending on the skill and experience of the observer. In addition, diagnosis can be difficult in patients using highly active antiretroviral therapy and PJP chemoprophylaxis, which can lead to low P. jirovecii loads, especially in sputum and oropharyngeal wash samples Silva RM, et al. [44], Tasaka S [9].

In recent years, the usefulness of polymerase chain reaction and serum β-D-glucan assay for the rapid and non- invasive diagnosis of PCP has been revealed Tasaka S [9]. PCR method in bronchoalveolar lavage fluid (BAL) shows high sensitivity and good specificity for the diagnosis of PCP Fan LC, et al. [45]. PCR is very sensitive and specific for detecting pneumocystosis; however, however, it cannot reliably distinguish colonization from active disease Larsen HH, et al. [46], Larsen HH, et al. [47]. Semi quantitative real-time PCR improves differentiation between PCP and colonization in HIV-negative immune compromised individuals with acute respiratory syndromes Gronseth S, et al. [48]. On a chest radiograph, PCP usually presents as bilateral or diffuse ground opacities (GGO). A chest X-ray is sometimes normal. High-resolution computed tomography (HRCT) usually shows diffuse GGO with a patchy distribution Kulhman JE, et al. [49], Fujii T, et al. [50]. It is suggested that an early correct diagnosis and prompt therapy especially in the immunocompromised patients is very important to reduce the morbidity and mortality.

Treatment

If clinical symptoms and imaging findings indicate a reasonable likelihood of PCP, then diagnostic evaluation and early treatment should be performed as soon as possible, regardless of immunocompromised status Avino LJ, et al. [51], Kim TO, et al. [10]. Because of its high efficacy, availability of oral and parenteral formulations, and low cost, trimethoprim (TMP)-sulfamethoxazole (SMX) is a first-line agent for the treatment of mild to severe PCP in both HIV- infected and HIV-uninfected patients Catherinot E, et al. [6], Thomas CF and Limper AH [12], Carmona EM and Limper AH [52]. Unfortunately, the side effects are common and patients with known allergy to sulfonamides cannot tolerate this therapy Cooley L, et al. [53].

Second-line PCP therapeutic options include IV pentamidine, clindamycin-primoquine, dapsone, atovaquone, and echinocandins Klein NC, et al. [54], Dohn MN. et al. [55], Toma E, et al. [56], Tu GW, et al. [57], Kim T, et al. [58]. Atovaquone is less effective but better tolerated than TMP-SMX Limper AH, et al. [59]. Alternatively, pentamidine can be administered intravenously Carmona EM and Limper AH [52]. It is recommended that clinicians wait at least 4 to 8 days before switching drug therapy to a second- or third- line agent because of deterioration or lack of improvement in respiratory function Cooley L, et al. [53]. The recommended duration of treatment is 21 days for HIV-infected patients and 14 days for non-HIV immunocompromised patients Hughes WT, et al. [60]. The guidelines recommend the addition of corticosteroids for HIV-infected patients with PCP Kaplan JE, et al. [8]. Careful observation during PCP therapy is important to assess response to treatment and detect toxicity as early as possible. Post-therapy follow-up includes assessment of early relapse, particularly if therapy has been with an agent other than TMP-SMX or has been shortened due to toxicity Hughes W, et al. [13]. It is advised to undertake additional research on the development of safe, potent and low- cost drugs that can be used for treatment as well as for prophylaxis of this opportunistic fungal disease even by the poor resource nations.

Prophylaxis

There are recommendations for the prevention of PCP for patients with hematologic diseases and solid tumors and recipients of hematopoietic stem cell transplants and solid organ transplants. For immunocompromised patients and other underlying diseases, the indications and dosage for prophylaxis should be carefully considered, taking into account hepatotoxicity, bone marrow suppression Kasiske BL [61], Martin SI and Fishman SA [62]. Although prevention guidelines for HIV-infected individuals are widely accepted and used, there is a lack of widely used in non-HIV patients with compromised immune systems Stern A, et al. [63].

TMP-SMX is the agent of first choice for prophylaxis in HIV-infected and non-HIV-infected hosts. One tablet (80 mg TMP and 400 mg SMX) per day or two tablets 3 times per week is usually recommended. Although the 3-times- weekly regimen was as effective in preventing PCP as the daily regimen, compliance may be improved by the daily regimen Limper AH, et al. [59], Utsunomiya M, et al. [64]. Antiretroviral therapy and PCP chemoprophylaxis with trimethoprim/sulfamethoxazole (TMP/SMX) significantly reduced the incidence of PCP CDC [41]. Patients receiving immunosuppressive drugs after transplantation should receive prophylaxis treatment Tomblyn M, et al. [65].

Other medications that have been studied for the prevention of PCP include pentamidine, atovaquone, dapsone, pyrimethamine, and clindamycin. The most statistically significant results in the prevention of PCP were obtained from patients receiving TMP/SMX doses. Patients who have contraindications to PCP prophylaxis with TMP/SMX as a result of hypersensitivity or scheduled chemotherapy with methotrexate should use second-line agents Stern A, et al. [63]. Resistance to TMP/SMX was observed in both PCP prophylaxis and treatment. Mutations can occur in the Fas gene of the fungal pathogen. These mutations are associated with prior exposure to drugs with a sulfonamide moiety and result in reduced susceptibility to TMP/SMX. However, this reduced susceptibility does not always mean that P jirovecii becomes fully resistant to these drugs Kazanjian P, et al. [66], Navin TR and others [67].

Conclusion

Pneumocystis jirovecii is an opportunistic fungus that can cause life threatening infection in HIV/AIDS patients, STD patients, and chemotherapy patients. Disease carries a poor prognosis. Although P. jirovecii is a common opportunistic pathogen, its development of can be prevented by maintaining a CD4+ lymphocyte count >200 cells/μL. Lung damage and respiratory failure during pneumocystis pneumonia are mediated by marked inflammatory responses of the host to the body. Trimethoprim-sulfamethoxazole with adjunctive corticosteroid therapy to suppress pulmonary inflammation in patients with severe infection remains the preferred treatment. Recognizing patients who are at risk or who are actively developing symptoms similar to P. jirovecii infection is important for recommending prophylaxis or active treatment. It is emphasized that further work on the pathogenesis and environmental reservoir of P. jirovecii may be rewarding.

References

  1. Chagas C (1909) Uber eine neue Typanosomiasis des Menschen. Mem Inst Oswaldo Cruz 3: 1-3.
  2. Delanoe P, Delanoe M (1912) Sur les rapports des kystes de Carini du poumon des rats avec le Trypanosoma lewisi. C R Acad Sci 155: 658-660.
  3. Suk CW, Bai KJ, Yu MC, Hu TY (2015) Coinfection of Pneumocystis jirovecii pneumonia and pulmonary tuberculosis in a non HIV-infected patient. J Microbiol Immunol Infect 48(6): 711-712.
  4. Amber KT (2017) Balancing the risks and benefits of prophylaxis: a reply to Pneumocystis jiroveci pneumonia in patients treated with systemic immunosuppressive agents for dermatologic conditions. Int J Dermatol 56(1): e4-e5.
  5. Kovacs JA, Masur H (2009) Evolving health effects of Pneumocystis: one hundred years of progress in diagnosis and treatment. JAMA 301(24): 2578-2585.
  6. Catherinot E, Lanternier F, Bougnoux ME, Lecuit M, Couderc LJ, et al. (2010) Pneumocystis jirovecii Pneumonia. Infect Dis Clin North Am 24:107-138.
  7. Calderon EJ, Gutierrez-Rivero S, Durand Joly I, Dei-Cas E (2010) Pneumocystis infection in humans: diagnosis and treatment. Expert Rev Anti Infect Ther 8(6): 683-701.
  8. Kaplan JE, Benson C, Holmes KK, Brooks JT, Pau A, et al. (2009) Guidelines for prevention and treatment of opportunistic infections in HIV-infected adults and adolescents: recommendations from CDC, the National Institutes of Health, and the HIV Medicine Association of the Infectious Diseases Society of America. MMWR Recomm Rep 58(1): 1-207.
  9. Tasaka S (2020) Recent Advances in the Diagnosis and Management of Pneumocystis Pneumonia. Tuberc Respir Dis 83(3): 132-140.
  10. Kim TO, Lee JK, Kwon YS, Kim YI, Lim SC, et al. (2021) Clinical characteristics and prognosis of patients with Pneumocystis jirovecii pneumonia without a compromised illness. PLoS ONE 16(2): e0246296.
  11. Ricciardi A, Gentilotti E, Coppola L, Maffongelli G, Cerva C, Malagnino V, et al. (2017) Infectious disease ward admission positively influences P. jiroveci pneumonia (PjP) outcome: A retrospective analysis of 116 HIV- positive and HIV-negative immunocompromised patients. PLoS One 12(5): e0176881.
  12. Thomas CF Jr, Limper AH (2004). Pneumocystis pneumonia. N Engl J Med 350: 2487-2498.
  13. Hughes W, Leoung G, Kramer F, Bozette S, Safrin S, et al. (1993) Comparison of atovaquone (566C80) with trimethoprim-sulfamethoxazole to treat Pneumocystis carinii pneumonia in patients with AIDS. N Engl J Med 328(21): 1521-1527.
  14. Fillatre P, Decaux O, Jouneau S, Revest M, Gacouin A, et al. (2014) Incidence of Pneumocystis jiroveci pneumonia among groups at risk in HIV-negative patients. Am J Med 127(12): 1242 e11-7.
  15. Salzer HJF, Schafer G, Hoenigl M, Gunther G, Hoffmann C, et al. (2018) Clinical, Diagnostic, and Treatment Disparities between HIV-Infected and Non-HIV-Infected Immunocompromised Patients with Pneumocystis jirovecii Pneumonia. Respiration 96(1): 52-65.
  16. Stringer JR, Cushion MT, Wakefield AE (2001) new nomenclature for Pneumocystis carinii. Proceedings of the Seventh International Workshops on Opportunistic Protists. J Eukaryot Microbiol 48: 184-9S.
  17. Stringer JR, Beard CB, Miller RF, Wakefield AE (2002) A new name (Pneumocystis jiroveci) for Pneumocystis from humans. Emerg Infect Dis 8(9): 891-896.
  18. Edman JC, Kovacs JA, Masur H, Santi DV, Elwood HJ, et al. (1998) Ribosomal RNA sequence shows Pneumocystis carinii to be a member of the fungi. Nature 334(6182): 519-522.
  19. Fillatre P, Revest M, Belaz S, Robert Gangneux F, Zahar JR, et al. (2016) Pneumocystosis in non-HIV-infected immunocompromised patients. Rev Med Interne 37(5): 327-236.
  20. Vargas SL, Hughes WT, Santolaya ME, Ulloa V, Ponce C, et al. (2001) Search for primary infection by Pneumocystis carinii in a cohort of normal, healthy infants. Clin Infect Dis 32(6): 855-861.
  21. Gigliotti F, Harmsen AG, Haidaris CG, Haidaris PJ (1993) Pneumocystis carinii is not universally transmissible between mammalian species. Infect Immun 61(7): 2886-2890.
  22. Pifer LL, Hughes WT, Stagno S, Woods D (1978) Pneumocystis carinii infection: evidence for high prevalence in normal and immunosuppressed children. Pediatrics 61(1): 35-41.
  23. Dumoulin A, Mazars E, Seguy N, Gargallo Viola D, Vargas S, et al. (2000) Transmission of Pneumocystis carinii disease from immunocompetent contacts of infected hosts to susceptible hosts. Eur J Clin Microbiol Infect Dis 19(6): 671-678.
  24. Finkelman MA (2010) Pneumocystis jirovecii infection: cell wall (1à3)-β-D-glucan biology and diagnostic utilities. Crit Rev Microbiol 36(4): 271-281.
  25. Morris A, Lundgren JD, Masur H, Walzer PD, Hanson DL, et al. (2004) Current epidemiology of Pneumocystis pneumonia. Emerg Infect Dis 10(10): 1713-1720.
  26. Wakefield AE (1996) DNA sequences identical to Pneumocystis carinii f. sp. carinii and Pneumocystis carinii f. sp. hominis in samples of air spora. J Clin Microbiol 34(7): 1754-179.
  27. Bartlett MS, Vermund SH, Jacobs R, Durant PJ, Shaw MM, et al. (1997) Detection of Pneumocystis carinii DNA in air samples: likely environmental risk to susceptible persons. J Clin Microbiol 35(10): 2511-2513.
  28. Vargas SL, Ponce CA, Gigliotti F, Ulloa A, Prieto S, et al. (2000) Transmission of Pneumocystis carinii DNA from a patient with P carinii pneumonia to immunocompetent health care workers. J Clin Microbiol 38(4): 1536-1538.
  29. Miller RF, Ambrose HE, Novelli V, Wakefield AE (2002) Probable mother-to-infant transmission of Pneumocystis carinii f. sp. hominis infection. J Clin Microbiol 40(4): 1555-1557.
  30. Hof H (2012) Pneumocystis jirovecii: a peculiar fungus posing particular problems for therapy and prophylaxis. Mycoses 55(s1): 1-7.
  31. Hughes WT, Kuhn S, Chaudhary S, Feldman S, Verzosa M, et al. (1977) Successful chemoprophylaxis for Pneumocystis carinii pneumonitis. N Engl J Med 297(26): 1419-1426.
  32. Sepkowitz KA, Brown AE, Telzak EE, Gottlieb S, Armstrong D (1992) Pneumocystis carinii pneumonia among patients without AIDS at a cancer hospital. JAMA 267(6): 832-837.
  33. Maini R, Henderson KL, Sheridan EA, Lamagni T, Nichols G, et al. (2013) Increasing Pneumocystis pneumonia, England, UK, 2000-2010. Emerg Infect Dis 19(3): 386- 392.
  34. Buchacz K, Baker RK, Palella FJ, Chmiel JS, Lichtenstein KA (2010) AIDS-defining opportunistic illnesses in US patients, 1994–2007: a cohort study. AIDS 24(10): 1549- 1559.
  35. Wolff AJ, O Donnell AE (2001) Pulmonary manifestations of HIV infection in the era of highly active antiretroviral therapy. Chest 120(6): 1888-1893.
  36. Solano LM, Alvarez Lerma F, Grau S, Segura C, Aguilar A (2015) Pneumocystis jiroveci pneumonia: Clinical characteristics and mortality risk factors in an Intensive Care Unit. Med Intensiva 39(1): 13-19.
  37. Sepkowitz KA (2002) Opportunistic infections in patients with and patients without acquired immunodeficiency syndrome. Clin Infect Dis 34(8): 1098-1107.
  38. Bateman M, Oladele R, Kolls JK (2020) Diagnosing Pneumocystis jirovecii pneumonia: a review of current methods and novel approaches. Med Mycol 58(8): 1015- 1028.
  39. Kovacs JA, Hiemenz JW, Macher AM, Stover D, Murray HW, et al. (1984) Pneumocystis carinii pneumonia: a comparison between patients with the acquired immunodeficiency syndrome and patients with other immunodeficiencies. Ann Intern Med 100(5): 663-671.
  40. Tasaka S, Kobayashi S, Kamata H, Kimizuka Y, Fujiwara H, et al. (2010) Cytokine profiles of bronchoalveolar lavage fluid in patients with pneumocystis pneumonia. Microbiol Immunol 54(7): 425-433.
  41. Centers for Disease Control and Prevention (2016) Pneumocystis pneumonia.
  42. Walzer PD, Smulian AG (2005) Pneumocystis species. In: Mandel GL, et al. (Eds.), Mandel, Douglas and Bennett’s Principles and Practice of Infectious Disease. (6thedn), Philadelphia, PA: Elsevier Churchill Livingstone. pp. 3080-3094.
  43. Langevin B, Saleh M (2016) Radiological presentation of Pneumocystis jiroveci pneumonia mimicking bacterial pneumonia. BMJ Case Rep 1-7.
  44. Silva RM, Bazzo ML, Borges AA (2007) Induced sputum versus bronchoalveolar lavage in the diagnosis of pneumocystis jiroveci pneumonia in human immunodeficiency virus-positive patients. Braz J Infect Dis 11(6): 549-553.
  45. Fan LC, Lu HW, Cheng KB, Li HP, Xu JF (2013) Evaluation of PCR in Bronchoalveolar Lavage Fluid for Diagnosis of Pneumocystis jirovecii Pneumonia: A Bivariate Meta- Analysis and Systematic Review. PLoS ONE 8(9): e73099.
  46. Larsen HH, Masur H, Kovacs JA, Gill VJ, Silcott VA, et al. (2002) Development and evaluation of a quantitative, touch-down, real-time PCR assay for diagnosing Pneumocystis carinii pneumonia. J Clin Microbiol 40(2): 490-494.
  47. Larsen HH, Huang L, Kovacs JA, Crothers K, Silcott V, et al. (2004) A prospective, blinded study of quantitative touch-down polymerase chain reaction using oral-wash samples for diagnosis of Pneumocystis pneumonia in HIV-infected patients. J Infect Dis 189(9): 1679-1683.
  48. Grommet S, Rogne T, Hannula R, Asvold BO, Afset JE, et al. (2021) Semiquantitative real-time PCR to distinguish Pneumocystis pneumonia from colonization in a heterogeneous population of HIV-negative immunocompromised patients. Microbiol Spectr 9(1): e00026-21.
  49. Kuhlman JE, Kavuru M, Fishman EK, Siegelman SS (1990) Pneumocystis carinii pneumonia: spectrum of parenchymal CT findings. Radiology 175(3): 711-714.
  50. Fujii T, Nakamura T, Iwamoto A (2007) Pneumocystis pneumonia in patients with HIV infection: clinical manifestations, laboratory findings, and radiological features. J Infect Chemother 13(1): 1-7.
  51. Avino LJ, Naylor SM, Roecker AM (2016) A Review of Pneumocystis jirovecii Pneumonia in the Non–HIV- Infected Population. Ann Pharmacother 50(8): 673-679.
  52. Carmona EM, Limper AH (2011) Update on the diagnosis and treatment of Pneumocystis pneumonia. Ther Adv Respir Dis 5(1): 41-59.
  53. Cooley L, Dendle C, Wolf J, The BW, Chen SC, et al. (2014) Consensus guidelines for diagnosis, prophylaxis and management of Pneumocystis jirovecii pneumonia in patients with haematological and solid malignancies. Intern Med J 44(12b): 1350-1363.
  54. Klein NC, Duncanson FP, Lenox TH, Sherer CB, Quentzel H, et al. (1992) Trimethoprim sulfamethoxazole versus pentamidine for Pneumocystis carinii pneumonia in AIDS patients: results of a large prospective randomized treatment trial. AIDS 6(3): 301-305.
  55. Dohn M, Weinberg W, Torres R, Follansbee S, Caldwell P, et al. (1994) Oral atovaquone compared with intravenous pentamidine for Pneumocystis carinii pneumonia in patients with AIDS. Ann Intern Med 121(3): 174-180.
  56. Toma E, Thorne A, Singer J, Raboud J, Lemieux C, et al. (1998) Clindamycin with primaquine vs. trimethoprim- sulfamethoxazole therapy for mild and moderately severe Pneumocystis carinii pneumonia in patients with AIDS: a multicenter, double-blind, randomized trial (CTN004). CTN-PCP Study Group. Clin Infect Dis 27(3): 524-530.
  57. Tu GW, Ju MJ, Xu M, Rong RM, He YZ, et al. (2013) Combination of caspofungin and low-dose trimethoprim/sulfamethoxazole for the treatment of severe Pneumocystis jirovecii pneumonia in renal transplant recipients. Nephrology 18(11): 736-742.
  58. Kim T, Hong HL, Lee YM, Sung H, Kim SH, et al. (2013) Is caspofungin really an effective treatment for Pneumocystis jirovecii pneumonia in immunocompromised patients without human immunodeficiency virus infection? Experiences at a single center and a literature review. Scand J Infect Dis 45(6): 484-488.
  59. Limper AH, Knox KS, Sarosi GA, Ampel NM, Bennett JE, et al. (2011) An official American Thoracic Society statement: treatment of fungal infections in adult pulmonary and critical care patients. Am J Respir Crit Care Med 183(1): 96-128.
  60. Hughes WT, Rivera GK, Schell MJ, Thornton D, Lott L (1987) Successful intermittent chemoprophylaxis for Pneumocystis carinii pneumonitis. N Engl J Med 316(26): 1627-1632.
  61. Kasiske BL, Zeier MG, Chapman JR, Craig JC, Ekberg H, et al. (2010) KDIGO clinical practice guideline for the care of kidney transplant recipients: a summary. Kidney Int 77(4): 299-311.
  62. Martin SI, Fishman JA (2009) AST Infectious Diseases Community of Practice. Pneumocystis pneumonia in solid organ transplant recipients. Am J Transplant 9(s4): S227-233.
  63. Stern A, Green H, Paul M, Vidal L, Leibovici L (2015) Prophylaxis for Pneumocystis pneumonia (PCP) in non- HIV immunocompromised patients. Cochrane Database Syst Rev 10: CD005590.
  64. Utsunomiya M, Dobashi H, Odani T, Saito K, Yokogawa N, et al. (2017) Optimal regimens of sulfamethoxazole trimethoprim for chemoprophylaxis of Pneumocystis pneumonia in patients with systemic rheumatic diseases: results from a non-blinded, randomized controlled trial. Arthritis Res Ther 19(1): 7.
  65. Tomblyn M, Chiller T, Einsele H, Gress R, Sepkowitz K, et al. (2009) Guidelines for preventing infectious complications among hematopoietic cell transplant recipients: a global perspective. Biol Blood Marrow Transpl 15(10): 1143-1238.
  66. Kazanjian P, Armstrong W, Hossler PA, Lane BR, Bartlett MS, et al. (2000) Pneumocystis carinii mutations are associated with duration of sulfa or sulfone prophylaxis exposure in AIDS patients. J Infect Dis 182(2): 551-557.
  67. Navin TR, Beard CB, Huang L, del Rio C, Lee S, et al. (2001) Effect of mutations in Pneumocystis carinii dihydropteroate synthase gene on outcome of P. carinii pneumonia in patients with HIV-1: a prospective study. Lancet 358(9281): 545-549.
More from this journal

Cite this article

BibTeX
APA
RIS
@article{pal2023,
  title   = {Pneumocytosis: An Emerging Opportunistic Mycosis of Public
Health Importance},
  author  = {Pal M* and Gutama KP},
  journal = {Open Access Journal of Mycology & Mycological Sciences},
  year    = {2023},
  volume  = {6},
  number  = {1},
  doi     = {10.23880/oajmms-16000175}
}
Pal M* and Gutama KP (2023). Pneumocytosis: An Emerging Opportunistic Mycosis of Public
Health Importance. Open Access Journal of Mycology & Mycological Sciences, 6(1). https://doi.org/10.23880/oajmms-16000175
TY  - JOUR
TI  - Pneumocytosis: An Emerging Opportunistic Mycosis of Public
Health Importance
AU  - Pal M* and Gutama KP
JO  - Open Access Journal of Mycology & Mycological Sciences
PY  - 2023
VL  - 6
IS  - 1
DO  - 10.23880/oajmms-16000175
ER  -