Search

A 47-year-old, non-smoking woman was admitted to the National Tuberculosis and Lung Diseases Research Institute for diagnosis of progressive exertional dyspnoea and numerous small thin-walled, air-filled cysts equally distributed throughout both lungs revealed in HRCT (high resolution computed tomography) examination. Histological assessment of specimens obtained by open lung biopsy revealed proliferation of immature smooth muscle, showing the expression of the antigen HMB45. On this basis, diagnosis of lymphangioleiomyomatosis was established. The disease caused essential ventilation damage of the lungs (FEV1 1.34 L; 39.71% pred, VC 4.02 L; 94.96% pred, FEV1/ /VC 0.33-4 1.81% pred, DLCO 3.65 mmol/min/Kpa 38.35% pred).During the observation, despite the lack of immunological disorders, the patient developed Pneumocystis jiroveci pneumonia (PCP) that was treated with trimethoprimsulfamethoxazole. Lymphangioleiomyomatosis is a rare disease which results from a defect of TSC genes. The disease is not related to immunological defects or disorders. However, the considerable cystic destruction of the lungs can predispose the patient to opportunistic infections such as the one in the presented case.

Background: Pneumocystis jiroveci (old name Pneumocystis carini) can cause severe pneumonia in immune-compromised patients, most commonly those who are HIV infected., Case Report: A 68-yr-old man, who eight years earlier had undergone trauma related splenectomy, was admitted to ITU after a cardiac arrest due to septic shock caused by unknown pathogen. He had been treated for three weeks with various antibiotics without improvement. On the second day after resuscitation, high concentration of lgM anti-Pneumocystis jivecii antibodies was found, and high-dose trimetoprim therapy was started and continued for two weeks, Further treatment was complicated by ventilator-associated pneumonia (Acinetobacter baumannii); the patient eventually recovered without any neurological sequelae, and was transferred to a low-dependency area after 4 weeks in ITU., Conclusion: We conclude that Pneumocystis jiroveci infection should be suspected as a cause of severe pneumonia in splenectomised patients.

In spite of a considerable progress which was made in the laboratory diagnosis of pneumocytosis, a method delivering unequivocal diagnostic information is still missing. The purpose of the study was to compare diagnostic effectiveness of the fluorescent antibody method using monoclonal antibody in the examination of bronchoalveolar lavage fluid with routine serologic examination of immunocompromised patients affected by interstitial pneumonia. It was demonstrated that the method with monoclonal antibody was more useful for examining bronchoalveolar lavage samples confirming the suspicion of Pneumocystis pneumonia in 1 person among every 5 examines.

In the years 1998-2008 there were examined for pneumocystosis serum samples collected from 5223 children with respiratory tract infections, aged up to 10 years. The examinations were carried out for the presence of specific IgG and IgM antibodies with an indirect immunofluorescent antibody test. Specific anti-Pneumocystis antibodies were detected in 68,7% of the examined children, including 68,49% with IgG and 2.85% with IgM antibodies. The highest percentages of IgM and IgG positive samples were encountered, respectively, in children aged up to 6 months (4,17%) and in those in the second half of the first year of life (73%). The results of the examinations indicated that in Poland the prevalence of pneumocystosis in children with symptoms of respiratory tract infection is similar to that described by foreign authors for healthy, immunocompetent children.

Pneumocystis jiroveci (P. jiroveci) is the etiological agent of pneumocystis pneumonia (PCP) in immunodeficient patients. The increased interest of clinicians in this particular pathogen during the past decade was prompted by rising numbers of patients with immunosuppression caused by AIDS, chemotherapy, or organ transplantation. Premature, seriously ill infants at intensive care units constitute a potential risk group for infection with P. jiroveci. Recent advances in medical sciences, owing mainly to developments in molecular biology, permitted the verification of the taxonomic position of pathogens and contributed to a better understanding of new aspects of pathophysiology and pathogenesis of PCP. It has been demonstrated that the genus Pneumocystis represents a heterogeneous group of opportunistic fungi exhibiting narrow host specificity. Pneumocystis jiroveci is the species which is specific for humans. The present paper outlines the clinical symptoms of PCP in infants, currently used diagnostic methods, and treatment procedures in PCP.

The polymerase chain reaction (PCR) and indirect immunofluorescent test (IF) were used for examination of serum samples obtained from infants with respiratory tract infections. Sixty (11.9%) out of the 503 examined infant samples were positive for anti-P. carinii IgM and 354 (70.4%) contained anti-Pneumocystis IgG. P. carinii DNA was found in 6 (6.7%) sera from 90 of infected infants. Five out these 6 samples were for anti-Pneumocystis antibodies positive; 4 contained both IgG and IgM classes and one had only IgG. The sixth sample had neither IgG nor IgM, despite of P. carinii DNA presence. The results of the studies indicated that for diagnosis Pneumocystis carinii pneumonia (PCP) in infants on serum specimens detection of antibodies by IF test is of greater value than Pneumocystis DNA amplification by PCR method.

The frequency of Pneumocystis carinii occurrence in BAL of 38 HIV-infected patients was determined with three different method. BAL sediments were stained with Giemsa method, silvered according to Gomori-Grocott method and studied with indirect immunofluorescence assay. Using Giemsa method staining Pneumocystis carinii was diagnosed in 81.6% of patients, in Gomori-Grocott method--in 31.6% of patients, but results of indirect immunofluorescence assay were positive only in 23.,7%. In our study staining BAL sediments with Giemsa method allowed to detect Pneumocystis carinii in the highest percentage of examined patients.

The studies were undertaken to evaluate the usefulness of a nested PCR assay in the diagnosis of Pneumocystis carinii pneumonia (PCP) in AIDS patients. To achieve the end, 51 excretions samples from the respiratory tract were collected from HIV-infected patients with respiratory symptoms, and examined for the presence of specific DNA. A portion of the mitochondrial large-subunit rRNA gene of Pneumocystis carinii was amplified with outer primers pair pAZ 102E, pAZ 102H and internal primers pAZ 102X, pAZ 102Y. Positive nested PCR results were obtained with 36 out of 51 examined samples. Some 52.8% of the positive results were obtained with samples collected from patients without clinical diagnosis of PCP. It was concluded, that the nested PCR method, being too sensitive, is not suitable for the routine diagnosis of PCP in AIDS patients.

Since serological methods used in the diagnosis of pneumocystosis may be helpful to a various extent, depending on the stage of a diagnosed infection, it was decided to evaluate the usefulness of some the methods in the course of infection. Wistar rats were used in the experiments. The animals were administered hydrocortisone injections for 12 weeks to induce immunosuppression and activate naturally occurring asymptomatic infections with Pneumocystis carinii. Blood samples and specimes of lung tissues were collected, then they were examined for the presence of specific IgG and IgM antibodies, circulating antigen of Pneumocystsis carinii and circulating immune complexes using immunoenzymatic assays. The results of the above experiments indicated, that in an early stage of infection, the examinations of serum samples for circulating immune complexes were helpful, particularly for these with IgM antibodies

In 116 out of 845 patients treated for small cell lung cancer (SCLC) in the Institute of Tuberculosis and Chest Disease in Warsaw in the years 1980-1994 infection was the main or coexistent cause of death. In 4.1% infection was proved of bacterial origin and in further 6.5% of probable bacterial origin (in the later group cultures were negative or not done but fungal infection, pneumocystosis pneumonia and tuberculosis were excluded on autopsy). In 1.54% infection was of fungal origin, 1.2% patients died of Pneumocystis carinii pneumonia and 0.35% of tuberculosis. The majority of patients who died with and/or from infection had treatment-related leukopenia and 99 of them were treated with corticosteroids. Fungal infection, pneumocytosis and tuberculosis were found more frequently than bacterial infection in patients treated with cumulative dose of prednisone above 2000 mg. 33.62% patients had no symptoms or signs of infection. No connection was found between the absence of symptoms and treatment with steroids or the grade of leukopenia. In all cases infection was recognised very late, in 58 only at autopsy.

A new data from investigations on Pneumocystis carinii were presented as well as an application of molecular techniques to the diagnosis of P. carinii pneumonia.

During a period of 10 months, 87 children with Pneumocystis carinii pneumonia accompanied transient cellular immunity disorders and with normal humoral immunity were observed. It is suggested that change the invasiveness of the parasite has changed. The necessity of taking into consideration a pneumocystis etiology in diagnosis of respiratory tract diseases among children is pointed out.

An infection with Pneumocystis carinii with clinical symptoms of pneumonia is particularly frequent in patients with AIDS. The authors discuss current knowledge on Pneumocystis carinii pneumonia, including clinical course, possibility of diagnosis, and chemotherapy in patients with AIDS.