Pneumocystis (Carinii) Jiroveci Pneumonia


Article Author:
Justina Truong


Article Editor:
John Ashurst


Editors In Chief:
Laurie Graham
Andrew Wilt
Mary Cataletto


Managing Editors:
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Frank Smeeks
Kristina Soman-Faulkner
Benjamin Eovaldi
Radia Jamil
Sobhan Daneshfar
Saad Nazir
William Gossman
Pritesh Sheth
Hassam Zulfiqar
Navid Mahabadi
Steve Bhimji
John Shell
Matthew Varacallo
Ahmad Malik
Mark Pellegrini
James Hughes
Beata Beatty
Hajira Basit
Phillip Hynes


Updated:
2/22/2019 6:49:34 PM

Introduction

Pneumocystis Carinii Pneumonia (PCP), now referred to as Pneumocystis Jirovecii Pneumonia is a fungal infection that most commonly affects the immunocompromised and, in some cases, can be severely life-threatening. Typically, patients at risk are those with any underlying disease states that alter host immunity such as those with cancer, the HIV, transplant recipients, or those taking immunosuppressive therapies and medications. Patients presenting with PCP may show signs of fever, cough, dyspnea, and, in severe cases, respiratory failure. Pneumocystis is thought to be transmitted from person to person through an airborne route. Asymptomatic lung colonization can occur in people with normal immune systems, and they may unknowingly become reservoirs (asymptomatic carriers) for the spread of Pneumocystis to immunocompromised individuals. Although it is still the most common and serious opportunistic respiratory infection in patients with AIDS, thanks to the widespread use of prophylaxis and antiretroviral therapy, the incidence of infection in this population has declined substantially. [1][2]

Etiology

Pneumocystis was originally thought to be a member of the protozoan class but was reclassified as an ascomycetous fungus in 1988. Its life cycle had been said to resemble that of both a protozoan and a fungus, and the debate over its correct classification led to further studies. Through careful phylogenetic analysis of small subunit ribosomal RNAs, researchers have been able to compare plant, animal, fungi, and protozoan lineages. Ultimately, investigators have concluded with distinct certainty that Pneumocystis is, in fact, a member of the fungi family based upon cell wall composition, the structure of key enzymes, and gene sequencing. The Pneumocystis genus includes several species including P. carinii and P. jirovecii which infect rats and humans, respectively.[3][4]

Epidemiology

Pneumocystis first appeared in Europe following World War II as a cause of pneumonia in premature and malnourished infants in orphanages. Not much was known about the organism at the time, and after the HIV epidemic during the 1980s, studies into this illness increased significantly. PCP is now known to affect patients worldwide and is spread from person to person via the airborne route. Although typically seen in immunocompromised individuals, PCP has rarely been seen in those with functional and competent immune systems. Many risk factors for acquiring and developing PCP exist. Groups at a significantly higher risk of developing PCP are patients with cancer (most specifically hematologic malignancies), transplant patients who have undergone hematopoietic cell or solid organ transplants, patients undergoing treatment for certain inflammatory or rheumatologic conditions, or patients with any condition that results in defects in cell-mediated immunity. The most significant risk factor for contracting PCP in HIV-uninfected patients is the use of glucocorticoids combined with immunosuppressive therapy. One study showed that of patients with a first-time PCP, 91% had used glucocorticoids within one month of infection.[5][6]

PCP is most commonly described in HIV-infected individuals as an AIDS-defining illness. At the beginning of the HIV epidemic, rates of infections were documented as high as 20 per 100 persons in patients with CD4+ counts less than 200 cells/microL. The decline in PCP rates began after 1989 with the introduction of primary prophylaxis and antiretroviral therapy at a rate of 3.4% per year between the1992 and 1995 and most dramatically between 1996 and 1998 at a rate of 21.5% per year. A 2016 published prospective cohort study of HIV-infected individuals calculated incidence rates of PCP per 1000 person-years of 29.9 from 1994 through 1997, 7.7 from 1998 through 2002, and 3.9 from 2003 through 2007. Although the rate of infection has declined significantly in the United States and other industrialized countries, this opportunistic infection is proving to be a leading cause of significant infection in immunocompromised individuals.[7]

Pathophysiology

Pneumocystis jirovecii has a predilection to infect the lung in at-risk individuals. Microscopic examination reveals that Pneumocystis attaches to Type I alveolar epithelium, which allows the fungus to transition from its small trophic form to the larger cystic form. Adherence of Pneumocystis to alveoli is not the singular cause of diffuse alveolar damage, but rather it is the host's own inflammatory response that causes significant lung injury and impaired gas exchange, leading to hypoxia and possibly respiratory failure. Pneumocystis is primarily an alveolar pathogen, but in the setting of severely immunocompromised individuals, the rare disseminated form may be seen. Examples of extra-pulmonary manifestations may be seen in those patients who are undergoing non-systemic or second-line prophylaxis and include hepatosplenomegaly and thyroid, ocular, ear, or skin lesions.

Histopathology

Histology is often done on specimens to make a diagnosis of PCP. Stains like giemsa, crystal violet and Diff-Quick can be used to detect both the cyst and trophozoite. The walls can be stained with Toluidine blue or methenamine silver. 

History and Physical

Patients presenting with PCP may have subtle or obvious signs of illness. Literature notes that HIV-infected patients will likely have a more indolent and subtle onset of symptoms such as a non-productive and dry cough, 95%; low-grade fever, greater than 80%, and progressive dyspnea, 95% over the course of several weeks. In contrast, those not infected with HIV patients can present similarly but may have a more abrupt onset of symptoms and accompanying respiratory distress or failure. Both patient populations will typically have some degree of hypoxemia and respiratory distress at the time of presentation.

History must be aimed at evaluating the patient for underlying causes of immunodeficiency and, as such, their risk of contracting an opportunistic infection. As mentioned before, PCP is considered an AIDS-defining illness and therefore a history of HIV infection must be obtained along with whether the patient is undergoing antiretroviral therapy (ART). History may reveal signs and symptoms such as fatigue, weight loss, myalgia/arthralgia, rash, and headache, which may point to an undiagnosed and underlying HIV infection. Also important during the evaluation is to ascertain if a patient has recently been on glucocorticoids or had a change to their dose of immunosuppressive therapies.

Physical exam findings are important in determining a patient's level of distress. No classic exam findings point directly at a Pneumocystis infection, but many findings are indicative of a respiratory illness such as pneumonia. The exam may reveal crackles and rhonchi on auscultation, but 50% of cases will have normal and clear lung sounds. Other common physical exam findings include associated dyspnea, tachypnea, and tachycardia. Patients will likely present with a fever, most times greater than 38.1 C. HIV-infected patients often will present with oral thrush as a co-infection; therefore, it is important to do a thorough head-to-toe examination to evaluate for any other signs that may be indicators of an underlying immunologic disorder.

Evaluation

Diagnosis of PCP is multifactorial and may include clinical suspicion, patient risk factors, laboratory evaluations, chest radiograph, chest CT, sputum studies, evaluation of bronchoalveolar lavage fluid, or lung biopsies. Laboratory findings can be nonspecific for PCP and of most notable mention is an elevated serum lactate dehydrogenase (LDH) in HIV-infected patients. Immunocompromised individuals without HIV may have elevated serum LDH for a variety of reasons; therefore, LDH is not a highly valuable diagnostic tool in this patient population. Most fungi, including Pneumocystis, contain beta-D-glucagon in their cell walls. Elevation of serum beta-D-glucagon in the setting of those with clinical signs and risk factors for pneumonia should raise suspicion for Pneumocystis infection and prompt further diagnostic evaluation. An arterial blood gas analysis should be obtained in patients who are hypoxic with tachycardia and signs of respiratory distress to assess the severity of their illness, and results will likely show an elevated Alveolar-arterial (A-a) oxygen gradient in the setting of PCP.[8][9][10]

A chest radiograph will typically reveal diffuse bilateral peri-hilar interstitial infiltrates. These changes become increasingly homogenous as the disease course progresses. Other radiographic findings seen may include solitary or multiple nodules which may progress to become cavitary lesions, lobar infiltrates such as upper lobe lesions in patients receiving certain antimicrobial medications and pneumothorax in some cases. If there is a clinical concern for infection with Pneumocystis and negative chest radiograph, CT of the chest should be performed and may show ground glass attenuation or cystic lesions with high sensitivity.

Since Pneumocystis cannot be cultured, definitive diagnosis requires detection and identification of the organism by polymerase chain reaction assays of respiratory specimens, dye staining, or fluorescein antibody staining. Testing of this manner requires microscopic examination of a patient's sputum or bronchoalveolar lavage fluid, and these samples only should be obtained when safe and if the patient is stable. Definitive diagnosis of PCP may not always be possible. For example, patients with HIV/AIDS will have fewer neutrophils and a higher number of organisms present in their sputum and bronchoalveolar lavage fluid, making the diagnosis easier or more likely attainable. In contrast, patients with immunosuppression and without HIV infection will likely have a lower organism burden in their sputum or bronchoalveolar lavage fluid samples, making the diagnosis difficult. Regardless, if there is clinical concern or suspicion for PCP in a high-risk patient the practitioner should treat the patient accordingly, regardless of whether a definitive diagnosis has or can be made.

Treatment / Management

Treatment for a presumed PCP should not be withheld while diagnostic measures are pending. Treatment should be initiated in patients who have known risk factors and when clinical suspicion for infections exists. Most studies for PCP treatment have been performed in HIV-infected versus HIV-uninfected patients. Treatment in mild cases can be performed with oral therapies on an outpatient basis unless, of course, the patient cannot tolerate oral therapies, has a moderate or severe case that requires corticosteroids, or the patient requires a drug regimen that may only be given intravenously.[11][12][13]

Due to its efficacy, the first-line treatment choice for both HIV-infected and uninfected patients is 21 days of Trimethoprim-Sulfamethoxazole (TMP-SMX). For mild to moderate treatment, TMP 15 to 20 mg/kg/day and SMX 75 to 100 mg/kg/day, given orally in 3 divided doses or TMP-SMX DS, 2 tablets 3 times per day. For moderate to severe cases, TMP 15 to 20 mg/kg/day and SMX 75-100 mg/kg/day given intravenously (IV) every 6 to 8 hours with a switch to oral when the patient shows clinical improvement. In patients with a mild allergy to TMP-SMX, desensitization should be attempted as this is the most effective drug of choice. In patients with severe allergies to TMP-SMX, desensitization is no longer recommended, and it is more appropriate to choose a different drug regimen.

Alternative drug regimens for the treatment of PCP in those with sulfa allergies and mild to moderate disease include Atavaquone 750 mg, by mouth twice per day, Trimethoprim 15 mg/kg/day by mouth twice per day plus Dapsone 100 mg by mouth every day, or Primaquine 30 mg by mouth every day plus Clindamycin by mouth 450 mg every 6 hours or 600 mg every 8 hours. Alternative treatment for moderate to severe cases includes Pentamidine 4 mg/kg IV once daily over 60 minutes or Primaquine 30 mg by mouth every day plus Clindamycin IV 600 mg every 6 hours or 900 mg every 8 hours. Primaquine can only be orally administered, and patients who cannot tolerate oral medications should be given IV Pentamidine, but caution should be used due to its increased toxicity and side effects when compared to Primaquine. Caution must be used in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency if Dapsone or Primaquine are used as they can cause an increased risk of hemolytic anemia.

In HIV-infected patients with a moderate or severe disease, current recommendations suggest the addition of glucocorticoids to the treatment regimen as their use has been shown to improve clinical outcome and mortality. HIV-infected patients with a room air arterial blood gas partial pressure of oxygen that is less than or equal to 70 mm Hg, an alveolar-arterial (A-a) gradient greater than or equal to 35 mm Hg, or hypoxia on pulse oximetry should receive steroids. Corticosteroids also may be recommended in HIV-uninfected patients with PCP due to the potential for high mortality and fulminant course of illness, but data is limited on whether there are benefits or a decrease in in-hospital mortality. Dosing for prednisone should be started as soon as possible or within 72 hours of starting treatment for PCP and is as follows: 40 mg by mouth twice per day on days 1 through 5, 40 mg by mouth daily days 6 through 10, and 20 mg orally daily on days 11 through 21. IV methylprednisone can be given at 75% of the prednisone dose if oral therapy cannot be tolerated. HIV-infected patients who are not already on them should have antiretroviral therapy (ART) initiated within two weeks of Pneumocystis treatment or as soon as they are stable enough to begin treatment. Patients will usually show slightly worsening clinical signs around days 3 to 4 due to the host's inflammatory response to dying organisms and then improvement afterward.

Prophylaxis treatment guidelines have been established for certain patient populations. Patients who are immunocompromised such as those with malignancy and who are taking glucocorticoid doses greater than 20 mg daily for one month or longer, patients who have received bone marrow suppressive therapies or antineoplastic therapies, and those who have undergone hematopoietic cell or solid organ transplantation should receive primary prophylaxis for Pneumocystis. First-line prophylaxis treatment is Trimethoprim-sulfamethoxazole 1 double-strength tablet by mouth daily or 1 single-strength tablet by mouth daily. For those with sulfa allergies, recommended prophylaxis includes Dapsone 100 mg by mouth daily or 50 mg by mouth twice each day, Dapsone 50 mg by mouth daily plus pyrimethamine 50 mg plus leucovorin 25 mg by mouth weekly, Dapsone 200 mg plus pyrimethamine 75 mg plus leucovorin 25 mg by mouth weekly, Atovaquone 1500 mg by mouth daily, Atovaquone 1500 mg plus pyrimethamine 25 mg plus leucovorin 10 mg by mouth daily, or Aerosolized pentamidine 300 mg monthly via Respigard II nebulizer. HIV-infected individuals should receive prophylaxis with the same medications recommended above when CD4+ count is below 200 cells/microL or CD4+ less than 14 percent, presence of oropharyngeal candidiasis, and a CD4+ of 200-250 cells/microL when ART cannot be started or if monitoring of CD4+ count every 3 months is not possible.

Prognosis of treatment depends on many factors including the degree of hypoxia at presentation, age, prior PCP, elevated serum LDH, low CD4+ count, and presence of other opportunistic infections, such as CMV. The presence of any of the above-mentioned factors carries a higher risk of mortality and poor outcome. Mild to moderate disease has overall mortality rates as high as 65%. Patients with severe disease and respiratory failure who require mechanical ventilation and intensive care unit (ICU) admission have mortality rates as high as 84%.

Patients should be monitored for adverse reactions and signs of treatment failure when started on antimicrobial therapies. Monitoring should include vital signs (most notably oxygen saturation), labs such as complete blood counts, liver function enzymes, renal function, glucose, and electrolytes. Treatment is considered failed if the patient does not show signs of clinical improvement after 4 to 8 days. No definitive studies exist regarding the guidelines for treatment failure management, but most many studies agree that combination treatment with primaquine plus clindamycin may be the most effective regimen for salvage therapy. It is important to also search for concurrent infections that may be causing illness besides Pneumocystis and treat those accordingly.[14]

Differential Diagnosis

  • ARDS
  • Viral or bacterial pneumonia
  • Tuberculosis
  • Legionella pneumonia
  • Mycoplasma infections

Complications

  • Lymphadenopathy
  • Bone marrow involvement leading to pancytopenia
  • Involvement of the GI tract and thyroid gland
  • ARDS
  • Respiratory failure

Pearls and Other Issues

Pneumocystis was once considered an AIDS-defining illness, but due to prophylaxis and antiretroviral therapy, the incidence of disease in HIV-infected individuals has been drastically reduced.

Symptoms include fever, exertional dyspnea, and dry cough, and the diagnosis should be suspected in anyone with compromised immunity such as cancer, transplant patients, or those on immunosuppressive therapies.

Treatment is with trimethoprim-sulfamethoxazole although other lines of therapy exist for those with allergies or severe illness.

Prophylaxis is also with trimethoprim-sulfamethoxazole and recommended in certain populations such as HIV- infected individuals with CD4+ counts less than 200 cells/microL or CD4+ less than 14%, presence of oropharyngeal candidiasis, and a CD4+ of 200-250 cells/microL when ART cannot be started or if monitoring of CD4+ count every 3 months is not possible. 

The illness can be categorized as mild, moderate, or severe and new recommendations suggest the use of glucocorticoids in HIV-infected patients with a room air arterial blood gas partial pressure of oxygen that is less than or equal to 70 mm Hg, an alveolar-arterial (A-a) gradient greater than or equal to 35 mm Hg, or hypoxia on pulse oximetry should receive steroids.

Any patients needing corticosteroids should be admitted to the hospital for monitoring and into the ICU for respiratory failure and continued monitoring.

Enhancing Healthcare Team Outcomes

PCP is best managed by a multidisciplinary team that includes a pulmonologist, infectious disease expert, pharmacist, intensivist, nurse, respiratory therapist and a dietitian. Once the diagnosis of PCP is made, the patient should be urged to discontinue smoking, as nicotine tends to worsen the symptoms and complicates therapy. Since most patients with PCP are frail, a dietary consult should be sought to increase the calorie intake. The pharmacist should educate the patient on the importance of medication compliance. Patients receiving corticosteroids should be followed closely to monitor the side effects. Finally, these patients need lifelong follow up with monitoring of CD 4 counts, viral load, and progression of the disease.[13] (Level V)

Outcomes

In the past, PCP carried a high mortality, but over the past two decades, the mortality rates have dropped because of earlier diagnosis and treatment. Currently, at least 10-20% of patients with PCP will die. PCP carries an even worse prognosis in patients without HIV infection, with mortality rates over 50%. In general, the mortality rates are much higher when there is an underlying lung disorder and in patients who require mechanical ventilation.[11][15] (Level V)


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Pneumocystis (Carinii) Jiroveci Pneumonia - Questions

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A patient with AIDS has contracted Pneumocystis jiroveci pneumonia. What is the first line medication for this infection?



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Which of the following fungus causes pneumonia in AIDS patients?



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A 17-year-old male with AIDS presents with worsening exertional dyspnea, fever, and a nonproductive cough. His temperature is 102 F, heart rate 120 beats/min, and respiratory rate 19. A physical exam reveals mild crackles and rhonchi bilaterally. A chest x-ray shows diffuse bilateral infiltrates. He has no known drug allergies. What is the best initial treatment?



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A patient with AIDS is found to have pneumocystis jiroveci pneumonia but is allergic to sulfonamides. What medication can be used instead?



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Pneumocystis carinii (jiroveci) pneumonia is an infection most commonly seen in individuals with which condition?



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A patient with human immunodeficiency virus (HIV) and severe dyspnea undergoes a bronchial lavage. The lavage is stained with methenamine silver, which reveals numerous small cyst-like organisms. The patient most likely developed which of the following conditions?



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Pneumocystis jiroveci is classified as which of the following?



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What is the most common presenting feature of Pneumocystis jiroveci pneumonia?



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Which of the following laboratory tests would be most helpful for diagnosis for a patient with suspected Pneumocystis jiroveci pneumonia?



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Pneumocystis jiroveci pneumonia on a chest radiograph usually presents with:



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What is the initial drug of choice for Pneumocystis jiroveci pneumonia (PCP)?



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A patient with HIV infection is being treated with trimethoprim-sulfamethoxazole (TMP-SMX) for Pneumocystis jiroveci pneumonia. Which adverse reaction is least likely to occur during TMP-SMX therapy?



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What is the drug of choice to treat Pneumocystis jiroveci pneumonia?



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A patient presents with exertional dyspnea, nonproductive cough, and fever. A chest x-ray shows perihilar infiltrates, and a methenamine silver stain shows cysts. The patient's symptoms worsen with erythromycin therapy. What is the most likely diagnosis?



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What drug is most commonly used for the treatment of Pneumocystis jiroveci?



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Pneumocystis infection often is identified by which of the following tests?



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At what CD4 count is a patient with AIDS at risk for pneumocystitis jiroveci pneumonia (PCP)?



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Which of the following diseases has the highest mortality rate in young infants with HIV?



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Which of the following diseases suggests the diagnosis of HIV?



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Which medication is used for the treatment of Pneumocystis jiroveci pneumonia in a patient with severe HIV?



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Chest radiograph shows diffuse air-space disease in an HIV positive male with a CD 4 count of 196. Treatment for which condition should be initiated?



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Which of the following is an effective treatment for patients with Pneumocystis jiroveci pneumonia?



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Bronchoalveolar lavage from a certain patients reveals cysts resembling crushed ping-pong balls. What is the most likely etiologic diagnosis?



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What drug is commonly used for the treatment of Pneumocystis jiroveci pneumonia?



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An old patient is hospitalized in intensive care and intubated for Pneumocystis jirovecii pneumonia. Which of the following would not be part of appropriate care?



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A 46-year-old male presents to the emergency department with mental status changes. His significant other reports that he has HIV and is on highly active antiretroviral therapy with multiple medications. The patient has been coughing and reports shortness of breath. Vital signs: blood pressure is 115/70 mmHg; heart rate 38 beats per minute, respiratory rate 30, temperature 38.5°C, and oxygen saturation 76 percent on room air. There are bilateral interstitial infiltrates on the chest x-ray. ECG shows sinus bradycardia without acute changes. Oxygen is started. How should the bradycardia be managed?



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Which of the following is the drug of choice to treat Pneumocystis jirovecii pneumonia?



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Which of the following is the most common opportunistic infection in HIV/AIDS patients?



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Which of the following is the most common opportunistic infection associated with HIV/AIDS?



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Which of the following is the preferred initial treatment for Pneumocystis jiroveci pneumonia?



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A patient with AIDS is hypoxic, febrile, and reports a dry cough. Chest x-ray shows bilateral interstitial infiltrates. Sputum studies show cellular debris, mononuclear cells, with positive silver stain. What is the most likely diagnosis?



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Which of the following precautions is unnecessary when caring for a patient with Pneumocystis jiroveci pneumonia secondary to AIDS?



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A patient with HIV has been diagnosed with pneumonia caused by the pathogen Pneumocystis jiroveci. The patient has a sulfa allergy. Which of the following antibiotics would be best indicated to treat this infection?



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A patient has been diagnosed with Pneumocystis pneumonia. Which of the following antibiotics is a first-line treatment for this disease?



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Pneumocystis jiroveci characteristically causes:



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Which of the following risk factors is most common among HIV-negative patients with Pneumocystis jirovecii pneumonia (PJP)?



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A 45-year-old male presents complaining of 3 weeks of cough, fevers, and progressive shortness of breath. The patient has a history of HIV/AIDS and notes he has been somewhat noncompliant with his antiretroviral medications. His last CD4 count 6 months ago was 400 cells/microL. His vitals show heart rate 75 bpm, blood pressure 128/72 mmHg, temperature 100.8F, and oxygen saturation of 90% on room air. The lungs have clear breath sounds on auscultation. Based on the most likely cause of this patient’s symptoms, what findings would be expected to be seen on chest radiograph?



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A 39-year-old male presents to the emergency department complaining of an acute worsening of the cough and shortness of breath he has had the last few weeks. The patient has a known history of HIV and has recently run out of his medications. He does not know what they were. Vitals and exam reveal that the patient is mildly hypoxic on room air with tachypnea and some difficulty speaking full sentences but is otherwise maintaining his airway. The patient’s chest radiograph shows bilateral interstitial infiltrative markings and labs are remarkable for a CD4 count of 160 cells/microL and elevated lactate dehydrogenase (LDH). An arterial blood gas is performed, and calculated A-a gradient is greater than 40 mmHg. The patient has a history of anaphylactic reaction to sulfa medications. Which of the following is the best choice for treatment?



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A 62-year-old female with chronic lymphocytic leukemia currently undergoing treatment with cyclophosphamide presents with worsening cough, fevers, and shortness of breath on exertion. The patient was seen in the clinic for similar symptoms last week and was treated with azithromycin and a short course of prednisone. The patient remarks that she does not feel any better and has been feeling more weak and tired. Chest radiograph taken today shows new bilateral interstitial and alveolar infiltrates in a perihilar distribution in comparison to one taken last week. Vitals show heart rate 95 bpm, blood pressure 110/65 mmHg, temperature 101.0F, and oxygen saturation 89% on room air. Given the patients most likely diagnosis, what would be expected to be seen on microscopy?



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Pneumocystis (Carinii) Jiroveci Pneumonia - References

References

Ricciardi A,Gentilotti E,Coppola L,Maffongelli G,Cerva C,Malagnino V,Mari A,Di Veroli A,Berrilli F,Apice F,Toschi N,Di Cave D,Parisi SG,Andreoni M,Sarmati L, 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. 2017     [PubMed]
Mecoli CA,Saylor D,Gelber AC,Christopher-Stine L, Pneumocystis jiroveci pneumonia in rheumatic disease: a 20-year single-centre experience. Clinical and experimental rheumatology. 2017 Jul-Aug     [PubMed]
Amber KT, Balancing the risks and benefits of prophylaxis: a reply to     [PubMed]
Fillâtre P,Revest M,Belaz S,Robert-Gangneux F,Zahar JR,Roblot F,Tattevin P, [Pneumocystosis in non-HIV-infected immunocompromised patients]. La Revue de medecine interne. 2016 May     [PubMed]
Masur H, HIV-Related Opportunistic Infections Are Still Relevant in 2015. Topics in antiviral medicine. 2015 Aug-Sep     [PubMed]
Rey A,Losada C,Santillán J,Fiorentini F,Schiaffino M,Peroni HJ,Giunta D,Barcán L,Waisman G, [Pneumocystis jiroveci infection in patients with and without HIV: A comparison]. Revista chilena de infectologia : organo oficial de la Sociedad Chilena de Infectologia. 2015 Apr     [PubMed]
Solano L MF,Alvarez Lerma F,Grau S,Segura C,Aguilar A, [Pneumocystis jiroveci pneumonia: Clinical characteristics and mortality risk factors in an Intensive Care Unit]. Medicina intensiva. 2015 Jan-Feb     [PubMed]
Sabbagh W,Darwich NS, Pneumocystis Jiroveci Pneumonia and Newly Diagnosed Human Immunodeficiency Virus (AIDS) in a 63-Year-Old Woman. The American journal of case reports. 2018 Aug 8     [PubMed]
Langevin B,Saleh M, Radiological presentation of Pneumocystis jiroveci pneumonia mimicking bacterial pneumonia. BMJ case reports. 2016 Jun 3     [PubMed]
Waks AG,Tolaney SM,Galar A,Arnaout A,Porter JB,Marty FM,Winer EP,Hammond SP,Baden LR, Pneumocystis jiroveci pneumonia (PCP) in patients receiving neoadjuvant and adjuvant anthracycline-based chemotherapy for breast cancer: incidence and risk factors. Breast cancer research and treatment. 2015 Nov     [PubMed]
Newberry L,O'Hare B,Kennedy N,Selman A,Omar S,Dawson P,Stevenson K,Nishihara Y,Lissauer S,Molyneux E, Early use of corticosteroids in infants with a clinical diagnosis of Pneumocystis jiroveci pneumonia in Malawi: a double-blind, randomised clinical trial. Paediatrics and international child health. 2017 May     [PubMed]
Singh R,Bemelman FJ,Hodiamont CJ,Idu MM,Ten Berge IJ,Geerlings SE, The impact of trimethoprim-sulfamethoxazole as Pneumocystis jiroveci pneumonia prophylaxis on the occurrence of asymptomatic bacteriuria and urinary tract infections among renal allograft recipients: a retrospective before-after study. BMC infectious diseases. 2016 Feb 25     [PubMed]
Liebling M,Rubio E,Ie S, Prophylaxis for Pneumocystis jiroveci pneumonia: is it a necessity in pulmonary patients on high-dose, chronic corticosteroid therapy without AIDS? Expert review of respiratory medicine. 2015 Apr     [PubMed]
Jain SB,Wig N,Nagpal SJ,Mishra N,Vajpayee M,Guleria R,Pandey RM,Sharma SK, Evaluation of the current management protocols for prophylaxis against Pneumocystis jiroveci pneumonia and other opportunistic infections in patients living with HIV/AIDS. AIDS care. 2011 Jul     [PubMed]
Williams KM,Ahn KW,Chen M,Aljurf MD,Agwu AL,Chen AR,Walsh TJ,Szabolcs P,Boeckh MJ,Auletta JJ,Lindemans CA,Zanis-Neto J,Malvezzi M,Lister J,de Toledo Codina JS,Sackey K,Chakrabarty JL,Ljungman P,Wingard JR,Seftel MD,Seo S,Hale GA,Wirk B,Smith MS,Savani BN,Lazarus HM,Marks DI,Ustun C,Abdel-Azim H,Dvorak CC,Szer J,Storek J,Yong A,Riches MR, The incidence, mortality and timing of Pneumocystis jiroveci pneumonia after hematopoietic cell transplantation: a CIBMTR analysis. Bone marrow transplantation. 2016 Apr     [PubMed]

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