• Pediatric Infection and Vaccine
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• v.4 no.1
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• pp.174-182
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• 1997

Pneumocystis carinii pneumonia mainly occurs in immunocompromised patients and it is also known of major cause of death in children with acute lymphoblastic leukemia. After consolidation chemotherapy, acute lymphoblastic leukemia children is developed Pneumocystis carinii pneumonia frequently no an opportunistic infection but there were no controlled studies which have been performed to evaluate the usefulness of corticosteroid in Pneumocystis carinii pneumonia with acute lymphoblastic leukemia. We experienced a case of Pneumocystis carinii pneumonia in acute lymphoblastic leukemia with febrile neutropenic 6 years old girl. She was treated with trimethoprim-sulfamethoxazole and prednisone. We report this case with brief review of related literature.

• Korean Journal of Veterinary Research
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• v.47 no.3
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• pp.321-324
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• 2007

Pneumocystis (P.) carinii is an opportunistic fungal pathogen of many animal species and human, which can cause fatal pneumonia in immunocompromised individuals. Three 100-day-old pigs with progressive atrophy, anorexia and respiratory distress were submitted to the Cheju National University for diagnosis. Grossly, the lungs were enlarged with rubbery consistency. Histopathologically, the lungs were characterized by diffuse interstitial pneumonia with thickening of alveolar septa due to infiltration of macrophages and lymphocytes. Alveolar lumens were filled with a foamy eosinophilic proteinaceous material in which numerous punctiform organisms. The organisms were demonstrated as P. carinii by Grocott-methenamine-silver staining and immunohistochemistry in lungs of two pigs. In our best knowledge, this is believed to be the first report of P. carinii pneumonia in pigs in Korea.

• Parasites, Hosts and Diseases
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• v.37 no.4
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• pp.271-275
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• 1999

Pneumocystis carinii is the most important opportunistic pathogen of humans in the world. Pneumocystis carinii is experimentally detected in the lungs of rats, mice, rabbits, and monkeys, however, the organisms from different mammals are identical in microscopic morphology. The present study tried to find out more mammalian hosts of P. carinii and also to differentiate the organisms from different mammals by karyotyping. Rats, mice, hamsters, rabbits, cats, and dogs were successfully infected by P. carinii, but guinea pigs and pigs were not. Karyotype of P. carinii from rabbits showed similar size range of chromosomes with that of the prototype, but in different pattern. The patterns from cats and dogs were also different from that of rats. The present study confirms that cats and dogs are infected by P. carinii and at least total three karyotype strains of P. carinii are proven in Korea.

• Pediatric Infection and Vaccine
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• v.12 no.1
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• pp.95-99
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• 2005

Pneumocystis carinii pneumonia is an infectious disease which is highly prevalent in the group of immunosuppressed patients, particularly with hematologic tumors as lymphomas and acquired immune deficiency syndrome(AIDS), severe malnutrition, organ transplantations, high dose corticosteroid therapy. Some cases of Pneumocystis carinii pneumonia in infants with primary immune deficiency were already reported. The authors present a case of Pneumocystis carinii pneumonia developed in an infant who suffered from 10 days of poor feeding and failure to thrive and not included in the risk groups listed above. He had bilateral interstitial infiltrations on the chest radiography, diagnosed as Pneumocystis carinii pneumonia after Gomori-methenamine silver staining of his sputum that was taken through tracheal intubation. He improved after administering Trimethoprim-sulfamethoxazole for 14 days.

• The Korean Journal of Cytopathology
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• v.5 no.1
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• pp.1-9
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• 1994

The cytological and ultrastructural findings of Pneumocystis carinii(PC) obtained from rats by bronchoalveolar lavage (BAL) are described. All developmental forms of the PC organisms were obtained in the lavage fluid. Papanicolaou stain revealed conglomeration of PC as a foamy cast. The cystic walls of PC were well identified on Gomori's methenamine silver stain. Trophozoites and intracystic bodies were stained by Giemsa and Diff-Quik techniques. Some PC organisms were seen within the alveolar macrophages. Ultrastructurally, the cysts were almost circular in shape, and were nearly devoid of surface tubular extensions. The wall of the cyst was composed of an unit membrane, an intermediate electron lucent layer and an external electron dense layer The cysts frequently contained intracystic bodies, so called sporozoites. Occasionally empty or collapsed cysts with no intracystic bodies, and precysts were found. Trophozoites were variable in size and shape with abundant tubular extensions along the single electron dense pellicle. BAL is a useful method for concentrating the various morphologic forms of PC organisms, and is a rapid diagnostic method for PC pneumonia.

• The Korean Journal of Cytopathology
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• v.8 no.1
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• pp.27-34
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• 1997

Pneumocystis carinli is an established cause of pulmonary infections in immuno-compromised hosts. Several cytoiogical stains, such as Papanicolaou, Gomori methenamine sliver(GMS) and Diff-Quik have been used for detection of the organism, but occasionally can be laborious and, due to a degree of nonspecificity, may be misleading. We evaluated the diagnostic utility of immunocytochenmical stains that recognize P. carinii in bornchoalveolar lavage from experimentally Induced P. carinii pneumonia rats(n=15). In audition to routine stains for diagnosis by morphologic recognition of P. carinii on Papanicolaou, GMS and Diff-Quik stains, bronchoalveolar lavage samples were reacted with immunocytochemical stains using monoclonal antibodies(MAB) 092 and 902. In bronchoalveolar lavage P. carinii organisms were detected In 9 of 10 cases(90%) using each MAB 092 and 902, whereas GMS and Diff-Quik stains demonstrated P. carinii in 13(86%) and 11(73%) of 15 cases respectively. In lung tissue specimens(n=15) P. carinii organisms were well identified on GMS stain and immunohistochemical stains using MAB 092 and 902 in ail cases. We believe that the immunocytochemical staining using MAB 092 and/or 902 is a very useful and diagnostic tool In addition to GMS and Diff-Qulk stain to detect P. carinii organisms in bronchoalveolar lavage.

• Parasites, Hosts and Diseases
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• v.38 no.3
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• pp.151-158
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• 2000

Pneumocystis carinii is a major opportunistic pathogen which has been found in the lungs of a wide variety of mammalian host species, and the fact suggests the possibility of intraspecific variation. Until now, P. carinii from different mammalian species are differentiated as subspecies, and the rats are known to be infected by two subspecies. The present study investigated genetic heterogeneity of P. carinii isolates from two strains of rats in Korea and China by molecular karyotyping, RFLP and sequencing analysis. Karyotypes of P. carinii were grouped into three, two from two strains of rats In Korea and one from rats in China. However RFLP of PCR product of ribosomal and MSG gene of the P. carinii isolates showed same pattern. The sequence homology rates of ${\alpha}-tubulin$ DNA of the P. carinii isolates were 96% in Seoul Wistar rats, 93% in Seoul Sprague-Dawley rats, and 85% in Chinese Sprague-Dawley rats. The present finding confirmed that P. carinii from rats in Korea are grouped into two karyotype strains which are different from that of P. carinii from rats in China. The Chinese isolate shows a little different sequences of ${\alpha}-tubulin$ DNA.

• Parasites, Hosts and Diseases
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• v.27 no.2
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• pp.101-108
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• 1989

This study was performed to observe the role of Pneumocystis carinii as an etiologic agent of interstitial pneumonia in immunocompromised hosts. Total 90 male Sprague-Dawley rats, approxi. mately 150-180 g, were used. Fifteen of them were used as control group and remaining 75 (5 groups) were as immunosuppression groups; group 1 received prednisolone (25 mg/kg twice weekly) only; group 2 Prednisolone and tetracycline (75 mk/kg/day) ; group 3 Prednisolone, tetracycline and trimethoprim-sulfamethoxasole (50~250 mg/kg/day) : group 4 prednisolone and trimethoprim-sulfamethoxasole; and group 5 prednisolone and griseofulvin (300 mg/kg/day) until death. The survival days of each group rat were calculated, and upon death their lungs were removed immediately and then stamp smears were prepared and stained by Giemsa or toluidine blue O. For histopathologic observation, lungs were fixed in 10% formalin, cut into sections and stained with Gomori's methenamine silvei, hematoxylin-rosin, and Brovkn & Brenn stain. The results obtained were as follows: 1. The mean survival time of each group rat was 19.3$\pm$5.2 days (group 1), 41.1$\pm$14.0 days (group 2), 50.5$\pm$18.4 days (group 3), 43.0$\pm$22.9 days (group 4) or 21.8$\pm$5.1 days (group 5). Significant differences were noted between group 1 and group 2(p<0.01), group 1 and group 3 (p<0.01), and group 1 and group 4 (p<0.01), which represented bacterial infections were most fatal in immunocompromised rats. Group 5 revealed no difference in the survival day from group 1, while significant differences were noted between group 2 and group 5(P<0.01), group 3 and group 5(p<0.01), and group 4 and group 5(p<0, 01), which represented little importance of fungal infection as the cause of death of the rats. 2. The first fatality due to p. carinii pneumonia occurred 17 days after the beginning of the immunosuppression. The occurrence rate of P. carinii pneumonia in the decreasing order was 92.9% (group 3), 80.0% (group 2 and group 5), 78.6% (group 4) and 33.3% (group 1). With regard to the pathological stage of P. carinii pneumonia, the stage 1 was 11.3%, the stage 2, 28.3%, and the stage 3, 60.4%. 3. Viewing from the duration of immunosuppression, bacterial pneumonia chieay appeared in 1 month, mixed infections (P. carinii and bacteria, or p. carinii and fungi) in 1~2 months, and pure P. carinii pneumonia after 2 months. The present study revealed that P. carinii pneumonia was the most important cause of death of immunocompromised rats later than 1 month after the start of immunosuppression.

• Parasites, Hosts and Diseases
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• v.30 no.3
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• pp.219-226
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• 1992

This study was performed to observe the therapeutic effects of interferon-gamma ($IFN-{\gamma}$) and gamma-globulin (${\gamma}-globulin$) in experimental Pneumocystis carinii pneumonia of immune suppressed mice. After 9 weeks, trimethoprim-sulfamethoxaBole(TMP-SMZ; 10~50 mg/mouse/day), mouse $IFN-{\gamma}(5{\times}10^4$ units/mouse/day) and mouse ${\gamma}-globulin$(20 mg/mouse/day) were administered to the mice for 3 weeks by the experimental group. The therapeutic efficacy was evaluated by body weights, histopatholo단ic and electron microscopic findings of the lungs, and number of p. carinii cysts by Gomori's methenamine silver stain. Body weights of the mice were significantly increased in the group of combination therapy of TMP-SMZ with $IFN-{\gamma}{\;}or{\;}{\gamma}-globulin$, and in the group of TMP- SMZ treatment(p<0.05), however, little effect was found in the group of T-globulin alone. Histopathologic 6ndings of p. carinii pneumonia were much improved in the group of combination therapy of TMP-SMZ with $IFN-{\gamma}$. Treatment with either TMP-SMZ or $IFN-{\gamma}$ significantly reduced the number of cysts in the p. carinii pneumonia, but {\gamma}-globulin alone was ineffective. In electron microscopic findings of p. carinii pneumonia, the number of trophozoites and cysts were reduced by treatment with either TMP-SMZ or $IFN-{\gamma}$, and most of the cysts were empty or containing one or two intracystic bodies. The present results suggested, that combination therapy of TMP-SMZ with $IFN-{\gamma}$ had synergistic effects in treatment of P carinii pneumonia in experi- mental mice.

• Parasites, Hosts and Diseases
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• v.37 no.3
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• pp.149-156
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• 1999

Pneumocystis carinii is pulmonary pathogen of immunocompromised humans or other mammals. Its infection results from activation of organism involves in latent infection or form new infection through the air. Almost all children are known to be infected within 2 to 4 years of birth, though prenatal transplacental transmission has not yet been demonstrated. In this study we observed experimental P.carinii infection in neonatal rats, thus investigating the possibility of transplacental vertical transmission by Diff-Quik staining of the lung impression smears and in-sity hybridization for lung sections. The postive rate of P.carinii infection in immunosuppressed maternal rats was 100%, but that in normal maternal rats was 0%. Cystic forms of P.carinii were observed in three of six 1-week old neonatal rats born of heavily infected mothers, but none of them was positive by in-situ hybridization. Five weeks after birth, cystic forms were detected in four neonatal rats. In the lobes of the lungs, no predilection site of P.carinii was recognized. Counts of cystic forms on smears and the reactivity of in-situ hbridization in the lungs of neonatal rats 0 were signficantly lower than in maternal rats. The present findings suggest that P.carinii is rarely transmitted through the placenta and proliferates less successfully in the lungs of neonatal rats than in mothers.