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1.  Intestinal Parasitic Infections in HIV-Infected Patients, Lao People’s Democratic Republic 
PLoS ONE  2014;9(3):e91452.
HIV infection is an emerging problem in Laos. We conducted the first prospective study on intestinal parasites, including opportunistic protozoa, in newly diagnosed HIV infected patients, with or without diarrhea. The aims were to describe the spectrum of infections, to determine their prevalence and to assess their associations with diarrhea, CD4 cell count, place of residence and living conditions.
One to three stool samples over consecutive days were obtained from 137 patients. The Kato thick smear method, formalin-ethyl concentration and specific stains for coccidia and microsporidia diagnosis were performed on 260 stool samples. Baseline characteristics regarding relevant demographics, place of residence and living conditions, clinical features including diarrhea, were collected using a standardized questionnaire.
Principal Findings
The 137 patients were young (median age: 36 years) and severely immunocompromised (83.9% at WHO stage 3 or 4, median CD4 cell count: 41/mm3). Diarrhea was present in 43.0% of patients. Parasite infection was found in 78.8% of patients, infection with at least two species in 49.6%. Prevalence rates of protozoan and helminth infections were similar (54.7% and 58.4% respectively). Blastocystis sp. was the most frequent protozoa (26.3%). Cryptosporidium sp., Cytoisospora belli and microsporidia, found at low prevalence rates (6.6%, 4.4%, 2.9%, respectively), were described for the first time in Laos. Cryptosporidium sp. was associated with persistent diarrhea. Strongyloides stercoralis was the most prevalent helminth following Opisthorchis viverrini (20.4% and 47.5% respectively). The most immunocompromised patients, as assessed by a CD4 count ≤ 50 cells/mm3, were more likely to be infected with intestinal parasites.
HIV infection was mainly diagnosed at an advanced stage of immunosuppression in Lao patients. Intestinal parasite infections were highly prevalent regardless of their diarrheal status. Opportunistic infections were reported. Improving the laboratory diagnosis of intestinal parasite infections and the knowledge on their local risk factors is warranted.
PMCID: PMC3963853  PMID: 24662743
2.  Pneumocystis jirovecii Genotype Associated with Increased Death Rate of HIV-infected Patients with Pneumonia 
Emerging Infectious Diseases  2013;19(1):21-28.
Comorbidities might predict presence of specific fungal genotypes.
PMCID: PMC3557975  PMID: 23260763
Pneumocystis jirovecii pneumonia; Pneumocystis jirovecii dihydropteroate synthase; DHPS; HIV; homosexuality; intravenous drug use; dihydropteroate synthase mutations; opportunistic infection; immunocompromised; virus; fungus; fungi; fungal; sulfa resistance; sulfamethoxazole/trimethoprim; SMX/TMP; dapsone; pentamidine; atovaquone; antimicrobial drugs; antibiotic; antifungal drugs
3.  Hypothetical Pneumocystis jirovecii Transmission from Immunocompetent Carriers to Infant 
Emerging Infectious Diseases  2009;14(3):1116-8.
PMCID: PMC2681130  PMID: 19239783
Pneumocystis jirovecii; transmission; pneumonia; molecular typing; genotypes; letter
4.  Mutations of Pneumocystis jirovecii Dihydrofolate Reductase Associated with Failure of Prophylaxis 
Antimicrobial Agents and Chemotherapy  2004;48(11):4301-4305.
Most drugs used for prevention and treatment of Pneumocystis jirovecii pneumonia target enzymes involved in the biosynthesis of folic acid, i.e., dihydropteroate synthase (DHPS) and dihydrofolate reductase (DHFR). Emergence of P. jirovecii drug resistance has been suggested by the association between failure of prophylaxis with sulfa drugs and mutations in DHPS. However, data on the occurrence of mutations in DHFR, the target of trimethoprim and pyrimethamine, are scarce. We examined polymorphisms in P. jirovecii DHFR from 33 patients diagnosed with P. jirovecii pneumonia who were receiving prophylaxis with a DHFR inhibitor (n = 15), prophylaxis without a DHFR inhibitor (n = 11), or no prophylaxis (n = 7). Compared to the wild-type sequence present in GenBank, 19 DHFR nucleotide substitution sites were found in 18 patients with 3 synonymous and 16 nonsynonymous mutations. Of 16 amino acid changes, 6 were located in positions conserved among distant organisms, and five of these six positions are probably involved in the putative active sites of the enzyme. Patients with failure of prophylaxis, including a DHFR inhibitor, were more likely to harbor nonsynonymous DHFR mutations than those who did not receive such prophylaxis (9 of 15 patients versus 2 of 18; P = 0.008). Analysis of the rate of nonsynonymous versus synonymous mutations was consistent with selection of amino acid substitutions in patients with failure of prophylaxis including a DHFR inhibitor. The results suggest that P. jirovecii populations may evolve under selective pressure from DHFR inhibitors, in particular pyrimethamine, and that DHFR mutations may contribute to P. jirovecii drug resistance.
PMCID: PMC525445  PMID: 15504856
5.  Molecular Evidence of Interhuman Transmission of Pneumocystis Pneumonia among Renal Transplant Recipients Hospitalized with HIV-Infected Patients 
Emerging Infectious Diseases  2004;10(10):1766-1773.
Molecular evidence indicates that P. jirovecii may be nosocomially transmitted to severely immunosuppressed patients.
Ten Pneumocystis jirovecii pneumonia (PCP) cases were diagnosed in renal transplant recipients (RTRs) during a 3-year period. Nosocomial transmission from HIV-positive patients with PCP was suspected because these patients shared the same hospital building, were not isolated, and were receiving suboptimal anti-PCP prophylaxis or none. P. jirovecii organisms were typed with the multitarget polymerase chain reaction–single-strand conformation polymorphism method. Among the 45 patients with PCP hospitalized during the 3-year period, 8 RTRs and 6 HIV-infected patients may have encountered at least 1 patient with active PCP within the 3 months before the diagnosis of their own PCP episode. In six instances (five RTRs, one HIV-infected patient), the patients harbored the same P. jirovecii molecular type as that found in the encountered PCP patients. The data suggest that part of the PCP cases observed in this building, particularly those observed in RTRs, were related to nosocomial interhuman transmission.
PMCID: PMC3323259  PMID: 15504262
Epidemiology; Pneumocystis carinii; Pneumocystis jirovecii; interhuman transmission; cluster analysis; sulfa drug resistance; dihydropteroate synthase; single-strand conformation polymorphism; PCP; research
6.  Dihydropteroate Synthase Gene Mutations in Pneumocystis and Sulfa Resistance 
Emerging Infectious Diseases  2004;10(10):1721-1728.
We review studies of dihydropteroate synthase gene mutations in Pneumocystis jirovecii and summarize the evidence for resistance to sulfamethoxazole and dapsone.
Pneumocystis pneumonia (PCP) remains a major cause of illness and death in HIV-infected persons. Sulfa drugs, trimethoprim-sulfamethoxazole (TMP-SMX) and dapsone are mainstays of PCP treatment and prophylaxis. While prophylaxis has reduced the incidence of PCP, its use has raised concerns about development of resistant organisms. The inability to culture human Pneumocystis, Pneumocystis jirovecii, in a standardized culture system prevents routine susceptibility testing and detection of drug resistance. In other microorganisms, sulfa drug resistance has resulted from specific point mutations in the dihydropteroate synthase (DHPS) gene. Similar mutations have been observed in P. jirovecii. Studies have consistently demonstrated a significant association between the use of sulfa drugs for PCP prophylaxis and DHPS gene mutations. Whether these mutations confer resistance to TMP-SMX or dapsone plus trimethoprim for PCP treatment remains unclear. We review studies of DHPS mutations in P. jirovecii and summarize the evidence for resistance to sulfamethoxazole and dapsone.
PMCID: PMC3323267  PMID: 15504256
perspective, Pneumocystis, Pneumocystis jirovecii, pneumonia, Pneumocystis, dihydropteroate synthase, dihydrofolate reductase, mutation, trimethoprim-sulfamethoxazole, dapsone; drug resistance, microbial
7.  Sulfa Resistance and Dihydropteroate Synthase Mutants in Recurrent Pneumocystis carinii Pneumonia 
Emerging Infectious Diseases  2003;9(7):864-867.
Failure of sulfa or sulfone prophylaxis is associated with mutations in Pneumocystis carinii gene coding for dihydropteroate synthase (DHPS). The DHPS genotype was analyzed in AIDS patients who had two separate episodes of P. carinii pneumonia. The results suggest that DHPS mutations can be selected de novo within patients by the pressure of a sulfa or sulfone drug.
PMCID: PMC3023424  PMID: 12890330
Pneumocystis carinii; pneumonia; fungal typing; drug resistance; drug pressure; mutation; dihydropteroate synthase; AIDS; dispatch
8.  Detection of Pneumocystis carinii DNA in Blood Specimens from Human Immunodeficiency Virus-Infected Patients by Nested PCR 
Journal of Clinical Microbiology  1999;37(1):127-131.
The detection of Pneumocystis carinii DNA in blood by PCR could be useful for studying the natural history of pneumocystosis and could also be a noninvasive diagnostic method. The results of previous studies are nevertheless conflicting. In our study, we compared three commercially available DNA extraction kits (GeneReleaser, QIAamp Tissue Kit, and ReadyAmp Genomic DNA Purification System) and proteinase K and proteinase K-phenol-chloroform treatments for the extraction of P. carinii DNA from dilutions of a P. carinii f. sp. hominis cyst suspension mixed with human whole blood. A rapid and simple nested PCR protocol which amplifies a portion of the mitochondrial large-subunit rRNA gene was applied to all the extraction products. The QIAmp Tissue Kit was the most effective kit for the isolation of amplification-ready P. carinii DNA and was used with nested PCR for the testing of whole-blood specimens from 35 immunocompetent control patients and 84 human immunodeficiency virus (HIV)-infected patients investigated for pulmonary disease and/or fever. In HIV-infected patients, P. carinii DNA was detected by nested PCR in blood samples from 3 of 14 patients with microscopically proven P. carinii pneumonia, 7 of 22 patients who were considered to be colonized with P. carinii, and 9 of 48 patients who were neither infected nor colonized with P. carinii. P. carinii DNA was not detected in blood specimens from the 35 immunocompetent patients. P. carinii DNA in blood might represent viable P. carinii organisms or DNA complexes released from pulmonary phagocytes. In conclusion, P. carinii DNA may be detected in whole blood from HIV-infected patients, but the nature and the meaning of the circulating form of P. carinii remain to be established.
PMCID: PMC84186  PMID: 9854076
9.  Identification of Encephalitozoon intestinalis in Travelers with Chronic Diarrhea by Specific PCR Amplification 
With the use of Weber’s modified trichrome and Uvitex 2B techniques, spores of microsporidia were detected in the stools of four travelers presenting clinically with chronic diarrhea. The general health of these patients was not impaired, and human immunodeficiency virus screening was negative. Immune evaluation, including the study of lymphocytic subpopulations, assay of serum immunoglobulins, and an intradermal multitest, showed normal results. Molecular identification of microsporidian species was based on the PCR amplification of a small-subunit rRNA sequence followed by HinfI endonuclease restriction. Encephalitozoon intestinalis microsporidiosis was thus shown in two of the four patients examined. In two patients, therapy based on albendazole made stools devoid of microsporidian spores without influence on the intestinal disorders. The pathogenic role of E. intestinalis in immunocompetent individuals remains to be demonstrated.
PMCID: PMC124803  PMID: 9431916

Results 1-9 (9)