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Haemodialysis patients have been found to have an increased risk of developing Pneumocystis pneumonia (PcP) compared to the control population. To the best of our knowledge, no data are available on pulmonary colonization with Pneumocystis jirovecii in haemodialysis patients; therefore, the aim of this study was to determine the prevalence of pulmonary colonization with P. jirovecii in haemodialysis patients, and to find the related risk factors. Induced sputa of 62 haemodialysis patients were investigated using quantitative polymerase chain reaction for the presence of P. jirovecii. 20.9% of the patients were colonized with P. jirovecii and 46.2% of whom had CD4 cell counts below 400/μl. There was no significant correlation between colonization and time on dialysis treatment. As haemodialysis patients seem to be at higher risk of PcP than the general population, doctors should be aware of the high rate of P. jirovecii colonization amongst them. Furthermore, colonized patients remain a potential source of transmission of P. jirovecii to other patients or to health care workers.

Background: Pneumocystis pneumonia is a major cause of morbidity and mortality in patients infected with HIV/AIDS. In this study, we evaluated the intestinal microbial communities associated with the development of experimental Pneumocystis pneumonia, as there is growing evidence that the intestinal microbiota is critical for host defense against fungal pathogens., Methods: C57BL/6 mice were infected with live Pneumocystis murina (P. murina) via intratracheal inoculation and sacrificed 7 and 14 days postinfection for microbiota analysis. In addition, we evaluated the intestinal microbiota from CD4+ T cell depleted mice infected with P. murina., Results: We found that the diversity of the intestinal microbial community was significantly altered by respiratory infection with P. murina. Specifically, mice infected with P. murina had altered microbial populations, as judged by changes in diversity metrics and relative taxa abundances. We also found that CD4+ T cell depleted mice infected with P. murina exhibited significantly altered intestinal microbiota that was distinct from immunocompetent mice infected with P. murina, suggesting that loss of CD4+ T cells may also affects the intestinal microbiota in the setting of Pneumocystis pneumonia. Finally, we employed a predictive metagenomics approach to evaluate various microbial features. We found that Pneumocystis pneumonia significantly alters the intestinal microbiota's inferred functional potential for carbohydrate, energy, and xenobiotic metabolism, as well as signal transduction pathways., Conclusions: Our study provides insight into specific-microbial clades and inferred microbial functional pathways associated with Pneumocystis pneumonia. Our data also suggest a role for the gut-lung axis in host defense in the lung., Competing Interests: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.

In order to achieve the programmatic goals established in the National HIV/AIDS Strategy, virologic suppression remains the most important outcome within the HIV care continuum for individuals receiving antiretroviral therapy (ART). Therefore, clinicians have dedicated substantial resources to improve adherence and clinic retention for individuals on ART; however, these efforts should be focused first on those most at risk of morbidity and mortality related to AIDS. Our study aimed to characterize the factors that are associated with AIDS-defining illnesses (ADIs) amongst people living with HIV (PLHIV) who are poorly adherent or retained in care in order to identify those at highest risk of poor clinical outcomes. We recruited 99 adult PLHIV with a history of poor adherence to ART, poor clinic attendance, or unsuppressed viral load (VL) from the Infectious Disease Program (IDP) of the Grady Health System in Atlanta, Georgia between January and May 2011 to participate in a survey investigating the acceptability of a financial incentive for improving adherence. Clinical outcomes including the number of ADI episodes in the last five years, VLs, and CD4 counts were abstracted from medical records. Associations between survey items and number of ADIs were performed using chi-square analysis. In our study, 36.4% of participants had ≥1 ADI in the last five years. The most common ADIs were Pneumocystis jirovecii pneumonia, recurrent bacterial pneumonia, and esophageal candidiasis. Age <42.5 years (OR 2.52, 95% CI = 1.08-5.86), male gender (OR 3.51, 95% CI = 1.08-11.34), CD4 nadir <200 cells/µL (OR 11.92, 95% CI = 1.51-94.15), unemployment (OR 3.54, 95% CI = 1.20-10.40), and travel time to clinic <30 minutes (OR 2.80, 95% CI = 1.20-6.52) were all significantly associated with a history of ≥1 ADI in the last five years. Awareness of factors associated with ADIs may help clinicians identify which poorly adherent PLHIV are at highest risk of HIV-related morbidity.

Background: Data on occurrence and risk factors for pneumocystis pneumonia (PCP) in patients with end-stage renal disease (ESRD) are sparse., Methods: This was a nationwide population-based study assessing occurrence and risk factors for PCP among patients with ESRD and population controls over a 21-year period (1/1 1990 to 31/12 2010). Using Danish registry data, first-time diagnoses of PCP were identified., Results: We identified 13 296 adult patients with ESRD and 244 255 controls, yielding 63 560 and 2 223 660 person-years of follow-up (PYFU), respectively. Fifty-eight first-time diagnoses of PCP were recorded in the ESRD group. Forty-six episodes occurred among renal transplant recipients (RTx) and 12 among haemodialysis patients (HD), yielding incidence rates of 181 (136-242) and 43.1 (24.5-75.9) per 100 000 PYFU. Compared to population controls, we found incidence rate-ratios of 125.9 (78.4-204) among RTx and 29.9 (14.1-59.7) among HD patients. Risk factors for PCP in RTx were age 50-65 years, age > 65 years, diabetes, polycystic kidney disease and hypertensive kidney disease/nephrosclerosis with an IRR of 2.22 (1.14-4.31), 3.12 (1.35-7.21), 3.44 (1.16-10.2), 4.25 (1.55-11.7) and 3.87 (1.49-10.0), respectively, and more than 36 months of dialysis before transplantation with an IRR of 1.99 (1.03-3.84). Among RTx the risk of PCP was highest during the first 6 months post-transplantation and increased from the beginning (IR1990-94 = 111 (46.3-267) per 100 000 PYFU) towards the end of the study period (IR2005-10 = 299 (203-439))., Conclusion: The PCP risk is substantial in RTx within the first 6 months of transplantation, emphasizing the potential benefit of prophylactic treatment in the early post-transplant period. Importantly, we identified subgroups within the RTx group that require more attention.

Introduction: Pneumocystis jirovecii pneumonia (PCP) is one of the most common opportunistic infections in HIV-infected adults. Although the microscopic demonstration of the organisms in respiratory specimens is still the golden standard of its diagnosis, recent advances in the diagnostic tools have been changing the situation., Areas Covered: Colonization of Pneumocystis is highly prevalent among the general population and could be associated with the transmission and development of PCP in immunocompromised individuals. Nested or conventional polymerase chain reaction (PCR) has a high sensitivity, detecting Pneumocystis DNA in induced sputum or oropharyngeal wash, but often produces false positives. Although quantitative real-time PCR is promising for discriminating colonization from PCP, the targeted DNA sequences and the cut-off values remain to be standardized. Serum β-D-glucan is useful as an adjunctive tool for the diagnosis of PCP. High-resolution computed tomography, which typically shows diffuse ground-glass opacities, is informative for evaluation of immunocompromised patients with suspected PCP and normal chest radiography., Expert Opinion: Although these new tools have been making the diagnosis of PCP less invasive and more accurate, any one of them can not make a definitive diagnosis by itself. The diagnostic criteria based on the combination of the testing ought to be established.

Background: The pathogenic effect of concomitant pulmonary cytomegalovirus (CMV) infection on morbidity and mortality of Pneumocystis jirovecii pneumonia (PCP) has been questioned in the case of non-HIV-infected patients., Methods: We conducted a retrospective cross-sectional study of patients who were diagnosed with PCP by bronchoalveolar lavage. We compared demographics, clinical characteristics, morbidity, and mortality in non-HIV-infected PCP patients with (n = 31) and without (n = 75) pulmonary CMV infection. Morbidity was assessed by length of hospital stay, admission to the intensive care unit, and use of mechanical ventilation. Mortality was defined as 30-day and 90-day all-cause mortality., Results: Morbidity and mortality did not differ between PCP patients with and without pulmonary CMV infection. In multivariate analysis using the Cox proportional hazard model, haematological malignancy (relative risk (RR) 0.20, 95% confidence interval (95% CI) 0.06-0.71), PCP treatment duration (RR 0.81, 95% CI 0.75-0.88), changing to a second-line regimen due to treatment failure (RR 4.51, 95% CI 1.61-12.64), and mechanical ventilation (RR 17.99, 95% CI 4.83-67.04) were independently associated with 30-day all-cause mortality. Being a solid organ transplant recipient (RR 0.17, 95% CI 0.05-0.56) and the use of mechanical ventilation (RR 6.49, 95% CI 2.84-14.83) were independently associated with 90-day all-cause mortality. However, concomitant pulmonary CMV infection was not associated with either 30-day or 90-day mortality., Conclusions: Our results suggest that concomitant pulmonary CMV infection does not significantly affect the prognosis of PCP, as indicated by morbidity and mortality in non-HIV-infected patients with PCP. Based on this result, we propose that it is not essential to administer an anti-CMV regimen when CMV is co-isolated from the bronchoalveolar lavage in patients with PCP.

For many years Pneumocystis pneumonia was thought to be caused by the reactivation of a latent infection, but several studies have demonstrated that Pneumocystis jirovecii infection can be acquired de novo. On the basis of our results obtained from a patient with recurrent pneumocystosis, we support the hypothesis that recurrent episodes are caused by reinfection.

Background: Patients with autoimmune inflammatory diseases (AID) account for 13-36% of Pneumocystis pneumonia (PCP) cases in human immunodeficiency virus (HIV)-negative patients. Up to 88% of PCP cases in HIV-negative patients are associated with prior steroid treatment. Pulmonary colonization with Pneumocystis in HIV-negative patients is associated with corticosteroid therapy in up to 75% of cases. The aim of this study was to detect the prevalence and risk factors of pulmonary colonization with Pneumocystis jirovecii in patients with AID receiving corticosteroid therapy in comparison with healthy control persons., Methods: We investigated induced sputa of 102 patients with AID on current corticosteroid treatment and of 117 healthy controls for the presence of P. jirovecii using polymerase chain reaction (PCR)., Results: Twenty-nine patients (28.5%) with AID were colonized with P. jirovecii compared to three healthy controls (2.6%) [p < 0.001, odds ratio (OR) 15.10, 95% confidence interval (CI) 4.43-51.38]. In patients with AID, age over 60 years was significantly associated with colonization (p = 0.015, OR 3.19, 95% CI 1.27-7.94). Multivariate analysis showed age to be independently associated with the colonization of P. jirovecii (95% CI 1.002-1.092). Neither duration nor dose of corticosteroid therapy nor immunosuppressive co-medication had a significant influence on P. jirovecii colonization., Conclusion: Patients with AID, especially those over 60 years of age, display a high prevalence of colonization with P. jirovecii. Clinicians should be aware of this and ensure that they consider the possibility of PCP when pulmonary symptoms arise in these patients.

Pneumocystis jirovecii has emerged as an important pulmonary pathogen. Historically associated with the immunocompromised, it is being increasingly observed in immunocompetent populations. (1→3)-ß-D-glucan (BG) is a major component of the cyst cell wall and plays an important role in the inflammatory response to the organism. Inflammatory synergy by co-stimulation with BG and Toll-like receptor ligands has been demonstrated in vitro and may be a factor in the pathophysiology of Pneumocystis pneumonia. Detection of highly elevated serum concentrations of BG in the serum of patients has been shown to be highly sensitive for the presence of pulmonary P. jirovecii.

We retrospectively investigated 76 patients with cystic fibrosis for the presence of Pneumocystis jirovecii, by performing real-time PCR and nested-PCR assays on 146 archival sputum specimens. P. jirovecii was detected in only 1 patient (1.3%) showing that in our region (Brest, France), the fungus is rarely involved in pulmonary colonization in patients with cystic fibrosis.

Pneumocystis jirovecii dihydropteroate synthase (DHPS) gene mutations are associated with failure of sulfur prophylaxis of Pneumocystis pneumonia. Here the P. jirovecii DHPS gene was amplified from bronchoalveolar fluid of 10 AIDS patients in China. No DHPS gene mutations were observed. The results suggest that the prevalence of DHPS mutations in China may be low.

Chronic obstructive pulmonary disease (COPD) results in significant morbidity and mortality. Smoking has long been recognized as the primary risk factor for development of COPD, but factors determining the severity or pattern of disease in smokers are largely unknown. Recent interest has focused on the potential role of infectious agents and the associated host response in accelerating progression of airway obstruction or in perpetuating its progression following discontinuation of tobacco exposure. Pneumocystis jirovecii is a fungal pathogen that causes pneumonia in immunocompromised individuals. Recent evidence has linked this organism with COPD. Using sensitive molecular techniques, low levels of Pneumocystis have been detected in the respiratory tract of certain individuals and termed colonization. Several findings support the theory that colonization with Pneumocystis is involved in the "vicious circle" hypothesis of COPD in which colonization with organisms perpetuates an inflammatory and lung remodeling response. Pneumocystis colonization is more prevalent in smokers and in those with severe COPD. The presence of Pneumocystis in the lungs, even at low levels, produces inflammatory changes similar to those seen in COPD, with increases in numbers of neutrophils and CD8(+) lymphocytes. HIV-infected subjects who have had PCP develop permanent airway obstruction, and HIV-infected patients have a high prevalence of both emphysema and Pneumocystis colonization. In addition, a non-human primate model of colonization shows development of airway obstruction and radiographic emphysema. Additional studies are needed to confirm the role of Pneumocystis in the pathogenesis of COPD, given that this agent might be a treatable co-factor in disease progression.

We described the characteristics of bronchoalveolar inflammatory cells and their correlation with lung injury in patients with Pneumocystis jiroveci pneumonia. We reviewed all cases of patients with Pneumocystis jiroveci pneumonia in newly diagnosed HIV infected patients admitted to a large metropolitan referral hospital during June 2003 to December 2004. Nine patients (5M, 4F) with Pneumocystis jiroveci pneumonia diagnosed with bronchoscopy and cytological examination of bronchoalveolar lavage (BAL) were identified. There was a positive correlation between peripheral CD8 count and BAL neutrophilia and negative correlation with hypoxemia. Although the number patients in this case series is small, our findings suggest that CD8 cells and alveolar neutrophilic inflammation have a role in lung injury in Pneumocystis jiroveci pneumonia. These findings are consistent with data from animal studies.

We prospectively examined 143 clinical samples from 115 patients including both HIV infected (n=53) and HIV uninfected immunocompromized (n=62) patients, with lung infiltrates and with clinical features suggestive of Pneumocystis carinii pneumonia/ PneumoCystis Pneumonia (PcP), using both microscopic techniques as well as PCR assay. Clinical samples in the present study consisted of bronchoalveolar lavage (BAL), tracheal aspirate (TA), nasopharyngeal aspirate (NPA), sputum and gastric aspirate (GA). Another group of 21 individuals with other respiratory diseases not compatible with PcP served as control during the study period of 15 months. Overall, P. jirovecii positivity rate by PCR was 12.17% (14/115 patients) compared to 3.4% (4/115) by microscopy. None of the specimens in the control group was positive by any of the techniques used. All PCR negative patients including cases and controls showed no evidence of PcP. After resolution of the discrepant results upon review of the clinical data, the sensitivity and specificity were 100% and 99%, respectively, for PCR and 30.7% and 100%, respectively, for microscopy by GMS staining. Thus, our data support the significance of PCR assay for confirming and improving the diagnosis of PcP in high-risk patients.

Invasive fungal infections are an important cause of morbidity and mortality in patients with hematological malignancies, and in particular fungal pneumonia is the main clinical manifestation in this category of patients. The fungal agents responsible for this complication are various, but Aspergillus spp. and other molds such as Zygomycetes or Fusarium spp. represent the most frequently isolated micro-organisms. Less commonly, pneumonia could be due to other 'no-molds' fungal agents such as Candida spp, Cryptococcus spp, or Pneumocystis jirovecii . This review mainly focuses on practical aspects relevant to epidemiology, diagnosis and therapeutic management of the rare cases of pneumonia due to no-molds agents in patients affected by hematological malignancies.

In the present study, in order to improve the detection of Pneumocystis jirovecii dihydropteroate synthase (DHPS) mutations in pulmonary specimens of HIV-infected patients with P. jirovecii pneumonia, we evaluated a microfiltration procedure for the removal of human cell contamination and a nested-PCR method, for amplification in specimens with low parasite load. In the studied population, PCR amplification of the DHPS gene was more successful in unfiltered than in filtered specimens, with both touchdown-PCR and nested-PCR procedures (p<0.05 and p<0.001, respectively), but the amount of host DNA in the samples analysed seems to be inversely related with the successful PCR parasite detection. Amplification of P. jirovecii DHPS gene with nested-PCR was achieved in 77.5% of the specimens studied, demonstrating that this is a useful method for the identification of mutations in pulmonary specimens, including samples with low parasite loads, and will facilitate the evaluation of the relationship between the P. jirovecii DHPS polymorphisms and clinical resistance to sulfa drugs.

Reports of outbreaks of Pneumocystis carinii pneumonia (PCP) among human immunodeficiency virus-negative immunocompromised patients have suggested a person-to-person transmission of P. carinii. In this study, 17 bronchoalveolar lavage isolates from patients in 3 PCP outbreaks were genotyped, 2 in renal transplant recipients and 1 outbreak among patients with haematological disorders. Genotypes in the P. carinii sp. f. hominis (P. carinii f.sp. hominis) mt large subunit ribosomal RNA site 85 were detected by 2 methods: direct sequencing and 3 different allele-specific polymerase chain reaction assays. Although limited data on patient contacts were available, the detected P. c. hominis genotypes do not support person-to-person transmission as the predominant transmission route of P. carinii in humans.

Sulpha agents, which act by inhibiting the enzyme dihydropteroate synthase (DHPS), are used widely for the treatment and prophylaxis of Pneumocystis carinii pneumonia (PCP). Recently, we have shown that mutations in the dihydropteroate synthase (DHPS) gene of Pneumocystis carinii f.sp hominis are associated with failure of sulpha prophylaxis and increased mortality in HIV-1 positive patients with PCP, suggesting that DHPS mutations may cause sulpha resistance. To facilitate detection of DHPS mutations we developed a restriction fragment length polymorphism (RFLP) assay, detecting mutations at codon 55 and 57 of the P. carinii DHPS gene. The RFLP-assay was compared with direct DNA sequencing on 27 PCP isolates from HIV-1 positive patients with a mixture of wildtype and mutant DHPS types. In all samples the RFLP-assay correctly identified wildtype or DHPS mutation at codon 55 or 57. Combined with DNA extraction by a Chelex-based method, this method can be performed within 1 d and allows a fast, cost-efficient and reliable method of detection of DHPS mutations in P. carinii.

In order to determine the pattern of C-reactive protein (CRP) concentrations in HIV-infected patients with various other infections, we conducted a prospective study (for the period 1990-91) of all HIV-seropositive patients hospitalized with fever and a retrospective study (for the period 1990-95) of all patients infected with Mycobacterium avium complex (MAC) and Pneumocystis carinii pneumonia (PCP). Samples from blood, cerebrospinal fluid and sites with clinical signs of infection were obtained for bacteriological culture. Polymerase chain reaction (PCR) determination was performed for cytomegalovirus in blood and CSF. Patients with opportunistic infections had a significantly lower increase in CRP concentration than patients infected with common bacterial pathogens. Patients with PCP and mycobacterial infections had a distinct CRP response after the onset of therapy. Lack of CRP increase at diagnosis of MAC infection was associated with a shorter survival and normalization of CRP after MAC therapy with a significantly longer survival.

A prospective study was undertaken to evaluate the incidence and the course of Pneumocystis carinii colonization in immunocompetent patients with severe pulmonary diseases. A further perspective was to determine the diagnostic values of different detection methods. Bronchoalveolar lavage fluid samples from 77/838 adult HIV-negative patients were examined by Diff-Quik stain, direct immunofluorescence test and polymerase chain reaction. All Diff-Quik stains were negative, but direct immunofluorescence tests and polymerase chain reactions were positive in the samples of 5 patients. The normal number of granulocytes and CD4+T- lymphocytes (median 810 cells/microliters) and normal values of immunoglobulins proved the relative competence of the immune systems of the 77 patients. Although none of these patients received any agent effective against P. carinii, none developed a P. carinii pneumonia within a 120.5-d surveillance period. Nosocomial transmission could be excluded. As the colonization with P. carinii did not result in pneumonia in immunocompetent patients, clinically silent carriers have to be assumed. In non-AIDS patients, sensitive detection methods have to be used to identify colonized persons.

The natural appearance of Pneumocystis carinii in induced sputum samples was studied in 60 HIV-infected patients with severe immunodeficiency and without a history of P. carinii pneumonia (PCP). The patients were prospectively evaluated for occurrence of P. carinii in induced sputum samples, PCP diagnosis and CD4+ cell counts during observation periods of 2 to 31 months. P. carinii was detected in 16 patients all of whom developed clinical PCP. In 5 patients P. carinii was detected 3 weeks to 8 months prior to clinical symptoms. Immunofluorescence using monoclonal antibody 3F6 was more sensitive than toluidine in detecting P. carinii in sputum samples (p < 0.05). In the patients who developed PCP a drop of the mean CD4 count to 40-50 x 10(6)/l was observed 200 days before diagnosis. However, out of 13 patients with CD4 counts of 0-20 x 10(6)/l only 7 developed PCP during 200 days of observation. The results do not support the suggested reactivation of a latent infection present in the vast majority of adults. PCP may instead result from exposure to the organism or presence of an unknown cofactor. We conclude that P. carinii is present in some asymptomatic HIV patients and that the detection of the organism in sputum should be regarded as pathological and prophylaxis or treatment inserted. The risk of transmission of P. carinii to patients with severe immunodeficiency should be seriously considered.

Pneumocystis carinii is an opportunistic pathogen causing life threatening pneumonia (PCP) in immunosuppressed patients and particularly among AIDS patients. Whether the infection results from reactivation or reinfection is debated. Since methods for in vitro cultivation still are not successful, the diagnosis is dependent on direct demonstration of the organism in respiratory specimen. In this thesis laboratory diagnostic methods in terms of staining, sampling, antibody detection and DNA amplification are evaluated. Furthermore, the occurrence of the organism in the Western world versus Africa, and in symptomatic and asymptomatic HIV infected patients is studied and discussed. The use of a monoclonal antibody (MAb), 3F6 in an indirect immunofluorescence assay (IFL) was compared to the two most commonly used chemical stains, silver methenamine and toluidine blue. The IFL method detected both cyst and trophozoite stages of P. carinii and was more sensitive than the chemical stains when applied to sputum samples. Among commercialised MAbs for P. carinii detection by IFL, only the indirect tests were readily applicable to ethanol treated HIV inactivated samples. In contrast to the MAb 3F6, (Dakopatts), the MAb from Northumbria stained only a selection of the cysts and no trophozoites. The relative sensitivity of IFL in detecting the organism in sputum samples compared to bronchoalveolar lavage (BAL) samples was estimated to be at least 70%. The polymerase chain reaction (PCR), which can amplify specific DNA fragments, was used for the demonstration of P. carinii in sputum and BAL specimens. The PCR was shown to be specific and more sensitive than IFL. However, P. carinii DNA was found in a few patients without clinical evidence of present, past or future PCP. Thus the possibility of PCR to detect colonization must be considered. Detection of antibodies to P. carinii by indirect IFL was studied in HIV versus non-HIV patients. A titer rise was seen in 45% of non-HIV patients versus only 3% in HIV patients during a PCP episode. No humoral response was seen in AIDS patients, whereas the serology did support the clinical PCP diagnosis in a proportion of the otherwise immunosuppressed patients. Serology may however not be of help in the acute setting. In the beginning of 1988 PCP had not yet been reported from Central Africa where the AIDS epidemic by then was growing fast. The occurrence of P. carinii in Central Africa was evaluated by a comparative study on induced sputum samples from HIV infected patients with pulmonary infection in Stockholm, Sweden and Lusaka, Zambia.(ABSTRACT TRUNCATED AT 400 WORDS)

We report on a case with an unusual combination of pulmonary pathogens including Pneumocystis carinii, Rhodococcus equi and Toxoplasma gondii in an HIV infected patient. The multiple microbiological procedures required to ascertain the etiological diagnoses of pneumonitis in HIV-seropositive subjects are discussed.

The aim of this study was to evaluate whether the amount of Pneumocystis carinii organisms found at fiberoptic bronchoscopy (FB) performed on HIV-positive patients correlated to the character of the P. carinii pneumonia (PCP). A consecutive series of 105 patients presented with 131 episodes of pulmonary symptoms requiring FB, and in 75 of these episodes a diagnosis of PCP was made. Specimens were stained with Giemsa and methenamine silver nitrate and the number of parasites found was given as: numerous, many, few or none. The following signs and symptoms were registered: cough, dyspnoea, fever, loss of weight, chest radiograph, haemoglobin, WBC, CD4 cell count, PO2 and HIV p24 antigen. The PCP was characterized by the clinical course: mild, moderate, severe, and by the outcome: pulmonary healthy, pulmonary insufficiency and death. No correlations between the number of P. carinii organisms and the clinical course or outcome of the PCP, the symptoms before the FB or the paraclinical examinations were found. In conclusion, the routinely obtained quantitative results of the microbiological examinations of material from the lungs were not correlated to the severity of the PCP.