ORIGINAL_ARTICLE
Extensive ERG11 mutations associated with fluconazole-resistant Candida albicans isolated from HIV-infected patients
Background and Purpose: Azoles are preferred antifungal agents given their inexpensiveness, limited toxicity, and potentiality of oral administration. However, the extensive use of prophylactic azole therapy for chronic infections, especially in immunocompromised patients, has led to an increase in azole resistance, thereby rising health care costs. Fluconazole resistance is associated with poor clinical outcomes and the emergence of new infections. The present study aimed to investigate the mutations of ERG11 gene in fluconazole-resistant Candida albicans isolates. Materials and Methods: This study was conducted on 80 clinical samples collected from HIV-infected patients with suspected candidiasis in Tagore Medical College Hospital and Government Hospital of Thoracic Medicine, Chennai, India, for a period of 18 months (May 2016-December 2017). The antifungal susceptibility pattern was determined by agar diffusion and broth dilution techniques as per the Clinical and Laboratory Standards Institute guidelines. The ERG11 gene of the known fluconazole-resistant strains of C. albicans was amplified by polymerase chain reaction (PCR). In addition, the samples were subjected to sequencing and mutation analysis. Results: A total of 60 Candida species were isolated from HIV patients and were speciated using standard, conventional, and molecular methods. Candida albicans comprised 28.3% (n=17) of the Candida isolates, 59% (n=10) of which were resistant to fluconazole. Sequencing of the amplified product of ERG11 C. albicans gene isolates showed that they were highly mutated and included many nonsense mutations which were not reported earlier. Conclusion: The molecular characterization of ERG11 gene showed many missense and nonsense mutations. Such mutations, which were unique to the geographical area under investigation, could be concluded to account for the development of resistance to fluconazole.
https://cmm.mazums.ac.ir/article_96078_637632c475b0377ebdbc945287cc0334.pdf
2019-09-01
1
6
10.18502/cmm.5.3.1739
AIDS
Antifungal Resistance
Candida species
Candidiasis
ERG11
Fluconazole
Mutation
Sony
Paul
sonymarypaul@tagoremch.com
1
Department of Microbiology, Tagore Medical College and Hospital, Rathinamangalam, Chennai, India
LEAD_AUTHOR
Iyanar
Kannan
kannan_iyan@hotmail.com
2
Department of Microbiology, Tagore Medical College and Hospital, Rathinamangalam, Chennai, India
AUTHOR
Kalyani
Mohanram
kalyanimohanram@gmail.com
3
Department of Microbiology, Saveetha Medical College and Hospital, Chennai, India
AUTHOR
1. Centres for Disease Control and Prevention (US). Antibiotic resistance threats in the United States, 2013. New York: Centres for Disease Control and Prevention, US Department of Health and Human Services; 2013.
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2. Edmond MB, Wallace SE, McClish DK, Pfaller MA, Jones RN, Wenzel RP. Nosocomial bloodstream infections in United States hospitals: a three-year analysis. Clin Infect Dis. 1999; 29(2):239-44.
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4. Hidron AI, Edwards JR, Patel J, Horan TC, Sievert DM, Pollock DA. NHSN annual update: antimicrobial-resistant pathogens associated with healthcare-associated infections: annual summary of data reported to the National Healthcare Safety Network at the centres for Disease Control and Prevention, 2006-2007. Infect Control Hosp Epidemiol. 2008; 29(11):996-1011.
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6. Davoudi AR, Najafi N, Hoseini Shirazi M, Ahangarkani F. Frequency of bacterial agents isolated from patients with nosocomial infection in teaching hospitals of Mazandaran University of Medical Sciences in 2012. Caspian J Intern Med. 2014; 5(4):227-31.
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7. Eggimann P, Bille J, Marchetti O. Diagnosis of invasive candidiasis in the ICU. Ann Intensive Care. 2011; 1:37.
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8. Ji H, Zhang W, Zhou Y, Zhang M, Zhu J, Song Y, et al. A three dimensional model of lanosterol 14alpha-demethylase of Candida albicans and its interaction with azole antifungals. J Med Chem. 2000; 43(13):2493-505.
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9. Marichal P, Koymans L, Willemsens S, Bellens D, Verhasselt P, Luyten W, et al. Contribution of mutations in the cytochrome P450 14α-demethylase (Erg11p, Cyp51p) to azole resistance in Candida albicans. Microbiology. 1999; 145(Pt 10):2701-13.
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10. Podust LM, Poulos TL, Waterman MR. Crystal structure of cytochrome P450 14a -sterol demethylase (CYP51) from Mycobacterium tuberculosis in complex with azole inhibitors. Proc Natl Acad Sci U S A. 2001; 98:3068-73.
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11. Sanglard D, Ischer F, Koymans L, Bille J. Amino acid substitutions in the cytochrome P-450 lanosterol 14 a-demethylase (CYP51A1) from azole-resistant Candida albicans clinical isolates contribute to resistance to azole antifungal agents. Antimicrob Agents Chemother. 1998; 42(2):241-53.
11
12. Nabili M, Abdollahi Gohar A, Badali H, Mohammadi R, Moazeni M. Amino acid substitutions in Erg11p of azole-resistant Candida glabrata: possible effective substitutions and homology modelling. J Glob Antimicrob Resist. 2016; 5:42-6.
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13. Xu Y, Chen L, Li C. Suceptibility of clinical isolates of Candida species to fluconazole and detection of Candida albicans ERG11 mutations. J Antimicrob Chemother. 2008; 61(4):798-804.
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14. Kathuria S, Singh PK, Sharma C, Prakash A, Masih A, Kumar A, et al. Multidrug-resistant Candida auris misidentified as Candida haemulonii: characterization by matrix-assisted laser desorption ionization–time of flight mass spectrometry and DNA sequencing and its antifungal susceptibility profile variability by Vitek 2, CLSI broth microdilution, and E test method. J Clin Microbiol. 2015; 53(6):1823-30.
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15. CLSI. Method for Antifungal disc diffusion Susceptibility testing of yeasts. 3rd ed. Wayne: Clinical and Laboratory Standards Institute; 2009.
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16. CLSI. Reference method for broth dilution antifungal susceptibility testing of yeasts; approved standard. 3rd ed. CLSI document M27-A3. Wayne: Clinical and Laboratory Standards Institute; 2008.
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17. Perea S, Lopez-Ribot JL, Kirkpatrick WR, McAtee RK, Santillán RA, Martínez M, et al. Prevalence of molecular mechanisms of resistance to azole antifungal agents in Candida albicans strains displaying high level fluconazole resistance isolated from human immunodeficiency virus infected patients. Antimicrob Agents Chemother. 2001; 45(10):2676-84.
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18. Wadhwa A, Kaur R, Agarwal SK, Jain S, Bhalla P. AIDS-related opportunistic mycoses seen in a tertiary care hospital in North India. J Med Microbiol. 2007; 56(Pt 8):1101-6.
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19. Nagalingeswaran K, Solomon S, Madhivanan P, Yepthomi T, Venkatesan C, Amalraj E, et al. Correlation between plasma viral load and CD4+T cell count to opportunistic infections in persons with HIV in South India. Int Conf AIDS. 2000; 13:9-14.
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20. Pruthvi BC, Vikram S, Suman SK, Jayaprakash B, Rau NR. Spectrum of clinical presentation and opportunistic infections in HIV: an Indian scenario. Int J Infect Dis. 2008; 12:e484.
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21. Pandey S, Sundar S, Hasan H, Shankar R, Singh RP. Clinical profile and opportunistic infection in HIV/AIDS patients attending SS Hospital, Varanasi. Indian J Prev Soc Med. 2008; 39(1):I2.
21
22. Singh A, Bairy I, Shivananda PG. Spectrum of opportunistic infections in AIDS cases. Indian J Med Sci. 2003; 57(1):16-21.
22
23. Deorukhkar S, Saini S, Stephen M. Non-albicans Candida infections: an emerging threat. Interdiscip Perspect Infect Dis. 2014; 2014:615958.
23
24. Nguyen MH, Peacock JE Jr, Morris AJ, Tanner DC, Nguyen ML, Snydman DR, et al. The changing face of candidemia: emergence of non-Candida albicans species and antifungal resistance. Am J Med. 1996; 100(6):617-23.
24
25. Goldman GH, da Silva Ferreira ME, dos Reis Marques E, Savoldi M, Perlin D, Park S, et al. Evaluation of fluconazole resistance mechanisms in Candida albicans clinical isolates from HIV-infected patients in Brazil. Diagn Microbiol Infect Dis. 2004; 50(1):25-32.
25
26. Lamb DC, Kelly DE, Schunck WH, Shyadehi AZ, Akhtar M, Lowe DJ, et al. The mutation T315A in Candida albicans sterol 14alpha-demethylase causes reduced enzyme activity and fluconazole resistance through reduced affinity. J Biol Chem. 1997; 272(9):5682-8.
26
ORIGINAL_ARTICLE
Application of platelet-rich plasma and platelet lysate in the treatment of experimental lymphocutaneous sporotrichosi
Background and Purpose: Sporotrichosis is a subcutaneous and chronic fungal infection that is caused by a dimorphic fungus, namely Sporothrix schenckii sensu lato. Lymphocutaneous sporotrichosis is the most clinical form, which accounts for nearly 80% of the cases of cutaneous sporotrichosis. Platelets contain several substances with antimicrobial properties. Regarding this, the present study was performed to investigate the effect of blood-based biomaterials, especially platelets in the treatment of lymphocutaneous sporotrichosis. Materials and Methods: This study was performed on 12 golden hamsters, divided into three groups of control, platelet-rich plasma, and platelet lysate. For the purpose of the study, Sporothrix conidia suspension was injected subcutaneously on the back of the animals. After the induction of subcutaneous lesions, the Gomori methenamine silver method was applied to verify lymphocutaneous sporotrichosis. Subsequently, plasma-rich platelet and platelet lysate were injected into the created lesions in the animals in 3-day intervals (due to the short lifetime of platelets). In the final sage, skin tissue samples were examined to check for the presence of yeast cells and their quantification. Results: The data were indicative of the presence of yeast cells with/without bud in the tissue of lymphocutaneous sporotrichosis lesions in the infected animals. Histological investigation revealed that each of the two biomaterials under study (i.e., plasma-rich platelet and platelet lysate) played a positive role in the removal of the yeast cells of sporotrichosis. Conclusion: The results of this study showed that both plasma-rich platelet and platelet lysate were able to effectively prevent from the progression of cutaneous sporotrichosis. Accordingly, much attention has been given to new therapies, including treatment with blood-derived biomaterials.
https://cmm.mazums.ac.ir/article_96121_bf5de2e37e8d26febcf6f5baac8370b6.pdf
2019-09-01
7
12
10.18502/cmm.5.3.1740
animal model
Lymphocutaneous sporotrichosis
Platelet lysate
Platelet-Rich Plasma
treatment
Elahe
Najafi
elahe.najafi863@gmail.com
1
Department of Microbiology, Islamic Azad University, Arak Branch, Arak, Iran
AUTHOR
Ali Arash
Anoushiravani
anoush_aa@yahoo.com
2
Department of Internal Medicine, Arak University of Medical Sciences, Arak, Iran
AUTHOR
Nooshin
Kalafi
3
Department of Microbiology, Islamic Azad University, Arak Branch, Arak, Iran
AUTHOR
Hamid Reza
Mohajerani
mohajeranihr@gmail.com
4
Department of Microbiology, Islamic Azad University, Arak Branch, Arak, Iran
AUTHOR
Ali Reza
Moradabadi
alirezamoradabadi@yahoo.co.uk
5
Department of Medical Laboratory Sciences, Arak University of Medical Sciences, Arak, Iran
AUTHOR
Saman
Mortezaeei
kianm313@gmail.com
6
Department of Medical Laboratory Sciences, Arak University of Medical Sciences, Arak, Iran
AUTHOR
Mojtaba
Didehdar
didehdar_m@yahoo.com
7
Infectious Diseases Research Center (IDRC), Department of Medical Parasitology and Mycology, Arak University of Medical Sciences, Arak, Iran
LEAD_AUTHOR
1. Orofino-Costa R, Macedo PM, Rodrigues AM, Bernardes-Engemann AR. Sporotrichosis: an update on epidemiology, etiopathogenesis, laboratory and clinical therapeutics. An Bras Dermatol. 2017; 92(5):606-20.
1
2. Chakrabarti A, Bonifaz A, Gutierrez-Galhardo MC, Mochizuki T, Li S. Global epidemiology of sporotrichosis. Med Mycol. 2015; 53(1):3-14.
2
3. Mahajan VK. Sporotrichosis: an overview and therapeutic options. Dermatol Res Pract. 2014; 2014:272376.
3
4. van Gils JM, Zwaginga JJ, Hordijk PL. Molecular and functional interactions among monocytes, platelets, and endothelial cells and their relevance for cardiovascular diseases. J Leukoc Biol. 2009; 85(2):195-204.
4
5. von Hundelshausen P, Weber C. Platelets as immune cells: bridging inflammation and cardiovascular disease. Circ Res. 2007; 100(1):27-40.
5
6. Yeaman MR. Platelets in defense against bacterial pathogens. Cell Mol Life Sci. 2010; 67(4):525-44.
6
7. Varshney S, Dwivedi A, Pandey V. Antimicrobial effects of various platelet rich concentrates-vibes from in-vitro studies-a systematic review. J Oral Biol Craniofac Res. 2019; 9(4):299-305.
7
8. Alberta JA, Auger KR, Batt D, Iannarelli P, Hwang G, Elliott HL, et al. Platelet-derived growth factor stimulation of monocyte chemoattractant protein-1 gene expression is mediated by transient activation of the phosphoinositide 3-kinase signal transduction pathway. J Biol Chem. 1999; 274(43):31062-7.
8
9. Kim DH, Je YJ, Kim CD, Lee YH, Seo YJ, Lee JH, et al. Can platelet-rich plasma be used for skin rejuvenation? Evaluation of effects of platelet-rich plasma on human dermal fibroblast. Ann Dermatol. 2011; 23(4):424-31.
9
10. Marx RE. Platelet-rich plasma: evidence to support its use. J Oral Maxillofac Surg. 2004; 62(4):489-96.
10
11. Ahmed M, Reffat SA, Hassan A, Eskander F. Platelet-rich plasma for the treatment of clean diabetic foot ulcers. Ann Vasc Surg. 2017; 38:206-11.
11
12. Mazzucco L, Medici D, Serra M, Panizza R, Rivara G, Orecchia S, et al. The use of autologous platelet gel to treat difficult‐to‐heal wounds: a pilot study. Transfusion. 2004; 44(7):1013-8.
12
13. Knighton DR, Hunt TK, Thakral K, Goodson W 3rd. Role of platelets and fibrin in the healing sequence: an in vivo study of angiogenesis and collagen synthesis. Ann Surg. 1982; 196(4):379-88.
13
14. Yol S, Tekin A, Yilmaz H, Küçükkartallar T, Esen H, Çaǧlayan O, et al. Effects of platelet rich plasma on colonic anastomosis. J Surg Res. 2008; 146(2):190-4.
14
15. Eppley BL, Pietrzak WS, Blanton M. Platelet-rich plasma: a review of biology and applications in plastic surgery. Plast Reconstr Surg. 2006; 118(6):147e-59e.
15
16. Fréchette JP, Martineau I, Gagnon G. Platelet-rich plasmas: growth factor content and roles in wound healing. J Dent Res. 2005; 84(5):434-9.
16
17. Cieslik-Bielecka A, Bold T, Ziolkowski G, Pierchala M, Krolikowska A, Reichert P. Antibacterial activity of leukocyte- and platelet-rich plasma: an in vitro study. Biomed Res Int. 2018; 2018:9471723.
17
18. Yang LC, Hu SW, Yan M, Yang JJ, Tsou SH, Lin YY. Antimicrobial activity of platelet-rich plasma and other plasma preparations against periodontal pathogens. J Periodontol. 2015; 86(2):310-8.
18
19. Lindeboom JA, Mathura KR, Aartman IH, Kroon FH, Milstein DM, Ince C. Influence of the application of platelet‐enriched plasma in oral mucosal wound healing. Clin Oral Implants Res. 2007; 18(1):133-9.
19
20. de Lima Barros MB, de Almeida Paes R, Schubach AO. Sporothrix schenckii and sporotrichosis. Clin Microbiol Rev. 2011; 24(4):633-54.
20
21. Aggour RL, Gamil L. Antimicrobial effects of platelet-rich plasma against selected oral and periodontal pathogens. Pol J Microbiol. 2017; 66(1):31-7.
21
22. Goncalves R, Zhang X, Cohen H, Debrabant A, Mosser DM. Platelet activation attracts a subpopulation of effector monocytes to sites of Leishmania major infection. J Exp Med. 2011; 208(6):1253-65.
22
23. Anitua E, Andia I, Ardanza B, Nurden P, Nurden AT. Autologous platelets as a source of proteins for healing and tissue regeneration. Thromb Haemost. 2004; 91(1):4-15.
23
ORIGINAL_ARTICLE
Molecular diagnosis and genotyping of Pneumocystis jirovecii in bronchoalveolar lavage samples obtained from patients with pulmonary disorder
Background and Purpose: Pneumocystis pneumonia (PCP) is one of the most common and life-threatening fungal diseases in patients with human immunodeficiency, treated with immunosuppressive medications. Immunocompetent people can also be a spreading agent for PCP. Regarding this, the aim of the present study was to diagnose and identify Pneumocystis jirovecii in bronchoalveolar lavage (BAL) samples obtained from patients with pulmonary disorder using a molecular method. Materials and Methods: For the purpose of the study, BAL samples (n=138) were collected from patients, undergoing bronchoscopy at the different departments of university hospitals affiliated to Mashhad University of Medical Sciences, Mashhad, Iran, during a period of one year (i.e., April 2014 until May 2015). Giemsa staining and molecular identification were carried out for each sample. The samples were also subjected to nested polymerase chain reaction (PCR), sequencing, and genotyping based on mitochondrial ribosomal large subunit (mtLSU rRNA) of P. jirovecii. The phylogenic tree was constructed by MEGA6 software. Results: The results of direct microscopic examination revealed the presence of P. jirovecii in 3 (2.2%) out of 138 samples; in addition, nested PCR and sequencing led to the detection of species in 17 (12.3%) samples. Out of patients with positive results, 10 (25%) and 7 (7.1%) cases were immunosuppressed and immunocompetent, respectively. The most common clinical symptoms among patients with pneumocystis were fever, dyspnea, and dry cough. In addition, genotypes III and II were the dominant genotypes in our dataset. Conclusion: Nested PCR and sequencing methods showed higher sensitivity and specificity as compared with a direct staining technique. Genotype III was identified as the most dominant type in patients with pulmonary disorder in Mashhad.
https://cmm.mazums.ac.ir/article_96075_a5658adf773b4646ba0df9546a704d54.pdf
2019-09-01
13
18
10.18502/cmm.5.3.1741
Bronchoalveolar Lavage (BAL)
Iran
Nested-PCR
Pneumocystis jirovecii
Pneumocystis pneumonia (PCP)
Abdolmajid
Fata
fataa@mums.ac.ir
1
Department of Parasitology and Mycology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Bahareh
Abdollahi
abdullahib2@mums.ac.ir
2
Department of Parasitology and Mycology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Fariba
Rezaeitalab
rezaeitalabf@mums.ac
3
Department of Internal Medicine, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Davood
Attaran
attarand@mums.ac.ir
4
Department of Internal Medicine, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Mohsen
Najjari
najjarimh@mums.ac.ir
5
Department of Parasitology and Mycology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Mohammad Javad
Najafzadeh
najafzadehmj@mums.ac.ir
6
Department of Parasitology and Mycology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
LEAD_AUTHOR
1. Chazan R. Contemporary clinical diagnostics of respiratory tract infections. Pol merkur lekarski. 2011;30(179):316-9.
1
2. Cushion MT, Harmsen A, Matsumoto Y, Stringer JR, Wakefield AE, Yamada M. Recent advances in the biology of Pneumocystis carinii. J Med Vet Myc. 1994;32(suppl1):217-28.
2
3. Wakefield AE. DNA sequences identical to Pneumocystis carinii f. sp. carinii and Pneumocystis carinii f. sp. hominis in samples of air spora. J Clin Microbiol. 1996; 34(7):1754-9.
3
4. Respaldiza N, Medrano F, Medrano A, Varela J, De La Horra C, Montes‐Cano M, et al. High seroprevalence of Pneumocystis infection in Spanish children. Clin Microbiol Infect. 2004; 10(11):1029-31.
4
5. Lowe DM, Rangaka MX, Gordon F, James CD, Miller RF. Pneumocystis jirovecii pneumonia in tropical and low and middle income countries: a systematic review and meta-regression. PloS One. 2013; 8(8):e69969.
5
6. Wilson JW, Limper AH, Grys TE, Karre T, Wengenack NL, Binnicker MJ. Pneumocystis jirovecii testing by real-time polymerase chain reaction and direct examination among immunocompetent and immunosuppressed patient groups and correlation to disease specificity. Diagn Microbiol Infect Dis. 2011; 69(2):145-52.
6
7. Thomas Jr CF, Limper AH. Pneumocystis pneumonia. New Engl J Med. 2004; 350(24):2487-98.
7
8. Sowden E, Carmichael AJ. Autoimmune inflammatory disorders, systemic corticosteroids and pneumocystis pneumonia: a strategy for prevention. BMC Infect Dis. 2004; 4(1):42.
8
9. Kovacs JA, Gill VJ, Meshnick S, Masur H. New insights into transmission, diagnosis, and drug treatment of Pneumocystis carinii pneumonia. JAMA. 2001; 286(19):2450-60.
9
10. Özkoç S, Bayram SD. Investigation of Pneumocystis jirovecii pneumonia and colonization in iatrogenically immunosuppressed and immunocompetent patients. Mikrobiyol Bul. 2015; 49(2):221-30.
10
11. Khodadadi H, Mirhendi H, Mohebali M, Kordbacheh P, Zarrinfar H, Makimura K. Pneumocystis jirovecii colonization in non-HIV-infected patients based on nested-PCR detection in bronchoalveolar lavage samples. Iran J Public Health. 2013; 42(3):298-305.
11
12. Morris A, Norris KA. Colonization by Pneumocystis jirovecii and its role in disease. Clinical microbiology reviews. 2012;25(2):297-317.
12
13. Morris A, Wei K, Afshar K, Huang L. Epidemiology and clinical significance of Pneumocystis colonization. J Infect Dis. 2008; 197(1):10-7.
13
14. Shelhamer JH, Gill VJ, Quinn TC, Crawford SW, Kovacs JA, Masur H, et al. The laboratory evaluation of opportunistic pulmonary infections. Annals of internal medicine. 1996; 124(6):585-99.
14
15. Aboualigalehdari E, Mahmoudabadi AZ, Fatahinia M, Idani E. The prevalence of Pneumocystis jirovecii among patients with different chronic pulmonary disorders in Ahvaz, Iran. Iran J Microbiol. 2015; 7(6):333-7.
15
16. Parian M, Fata A, Najafzadeh MJ, Rezaeitalab F. Molecular detection of Pneumocystis jirovecii using polymerase chain reaction in immunocompromised patients with pulmonary disorders in northeast of Iran. Curr Med Mycol. 2015; 1(2):13-8.
16
17. Badiee P. Evaluation of pneumocystis jirovecii in normal population. Jundishapur J Microb. 2013; 42(3):298-305.
17
18. Badiee P, Rezapour A, Abbasian A, Foroutan HR, Jafarian H.
18
Prevalence of colonization and mitochondrial large subunit rRNA mutation of Pneumocystis jiroveci among Iranian children. Iran J Microbiol. 2016; 8(5):326-30.
19
19. Tamura K, Stecher G, Peterson D, Filipski A, Kumar S. MEGA6: molecular evolutionary genetics analysis version 6.0. Mol Biol Evol. 2013; 30(12):2725-9.
20
20. Maskell N, Waine D, Lindley A, Pepperell J, Wakefield A, Miller R, et al. Asymptomatic carriage of Pneumocystis jiroveci in subjects undergoing bronchoscopy: a prospective study. Thorax. 2003; 58(7):594-7.
21
21. Tia T, Putaporntip C, Kosuwin R, Kongpolprom N, Kawkitinarong K, Jongwutiwes S. A highly sensitive novel PCR assay for detection of Pneumocystis jirovecii DNA in bronchoalveloar lavage specimens from immunocompromised patients. Clin Microbiol Infect. 2012; 18(6):598-603.
22
22. Jarboui M, Sellami A, Sellami H, Cheikhrouhou F, Makni F, Ben Arab N, et al. Molecular diagnosis of Pneumocystis jiroveci pneumonia in immunocompromised patients. Mycoses. 2010; 53(4):329-33.
23
23. Peters SE, Wakefield AF, Sinclair K, Millard PR, Hopkin JM. A search for Pneumocystis carinii in post‐mortem lungs by DNA amplification. J Pathol. 1992; 166(2):195-8.
24
24. Beard CB, Carter JL, Keely SP, Huang L, Pieniazek NJ, Moura I, et al. Genetic variation in Pneumocystis carinii isolates from different geographic regions: implications for transmission. Emerg Infect Dis. 2000; 6(3):265-72.
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25. Jarboui MA, Mseddi F, Sellami H, Sellami A, Makni F, Ayadi A. Genetic diversity of Pneumocystis jirovecii strains based on sequence variation of different DNA region. Med Mycol. 2013; 51(6):561-7.
26
26. Gupta R, Mirdha BR, Guleria R, Agarwal SK, Samantaray JC, Kumar L, et al. Genotypic variation of Pneumocystis jirovecii isolates in India based on sequence diversity at mitochondrial large subunit rRNA. Int J Med Microbiol. 2011; 301(3):267-72.
27
27. Volpe G, Sbaiz L, Avanzini C, Caramello P, Savoia D. Genetic diversity of Pneumocystis carinii isolated from human immunodeficiency virus-positive patients in Turin, Italy. J Clin Microbiol. 2001; 39(8):2995-8.
28
28. Dimonte S, Berrilli F, D’Orazi C, D’Alfonso R, Placco F, Bordi E, et al. Molecular analysis based on mtLSU-rRNA and DHPS sequences of Pneumocystis jirovecii from immunocompromised and immunocompetent patients in Italy. Infect Genet Evol. 2013; 14:68-72.
29
29. Khalife S, Aliouat EM, Aliouat-Denis CM, Gantois N, Devos P, Mallat H, et al. First data on Pneumocystis jirovecii colonization in patients with respiratory diseases in North Lebanon. New Microbes New Infect. 2015; 6:11-4.
30
30. Medrano FJ, Montes-Cano M, Conde M, De La Horra C, Respaldiza N, Gasch A, et al. Pneumocystis jirovecii in general population. Emerg Infect Dis. 2005; 11(2):245-50.
31
31. Monroy-Vaca EX, de Armas Y, Illnait-Zaragozi MT, Torano G, Diaz R, Vega D, et al. Prevalence and genotype distribution of Pneumocystis jirovecii in Cuban infants and toddlers with whooping cough. J Clin Microbiol. 2014; 52(1):45-51.
32
32. Nevez G, Jounieaux V, Linas MD, Guyot K, Leophonte P, Massip P, et al. High frequency of pneumocystis carinii sp. f. hominis colonization in HIV‐negative patients. J Eukaryotic Microbiol. 1997; 44:36S.
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33. Visconti E, Marinaci S, Zolfo M, Mencarini P, Tamburrini E, Pagliari G, et al. Very low frequence of Pneumocystis carinii DNA detection by PCR in specimens from patients with lung damage. J Clin Microbiol. 2000; 38(3):1307-8.
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34. Helweg-Larsen J, Jensen JS, Dohn B, Benfield TL, Lundgren B. Detection of Pneumocystis DNA in samples from patients suspected of bacterial pneumonia-a case-control study. BMC Infect Dis. 2002; 2(1):28.
35
ORIGINAL_ARTICLE
A multi-centered study of Pneumocystis jirovecii colonization in patients with respiratory disorders: Is there a colonization trend in the elderly?
Background and Purpose: Pneumocystis jirovecii colonization plays a key role in the progression of pulmonary infection. However, there are limited data regarding the colonization of these fungi in the patients residing in different regions of Iran. Regarding this, the present study was conducted to evaluate the prevalence of P. jirovecii colonization in non-HIV-infected patients with respiratory failure introduced by physicians using nested polymerase chain reaction (PCR). Materials and Methods: This study was conducted on 136 samples obtained from 136 patients with respiratory disorders referring to different hospitals in the capital and north of Iran during 2013-2015. The samples were collected using bronchoalveolar lavage (BAL; n=121) and sputum induction (n=15). Nested PCR method targeting mtLSU rRNA gene was used for the detection of P. jirovecii DNA in the specimens. Results: The nested PCR analysis resulted in the detection of P. jirovecii DNA in 32 (23.5%) patients. The mean age of the participants was 49.04±11.94 years (age range: 14-90 years). The results revealed no correlation between Pneumocystis colonization and gender. The studied patients were divided into two groups of immunocompromised and immunocompetent patients. In the regard, 25.4% of the patients with detectable P. jirovecii DNA were immunocompromised and had cancer, organ transplantation, asthma, sarcoidosis, dermatomyositis, chronic obstructive pulmonary disease, bronchiectasis, and pulmonary vasculitis. On the other hand, Pneumocystis DNA was detected in 21.8% of the immunocompetent patients. Frequencies of P. jirovecii DNA detection in the patients with tuberculosis, hydatid cyst, and unknown underlying diseases were obtained as 20.8%, 25%, and 22%, respectively. The prevalence of Pneumocystis colonization varied based on age. In this regard, P. jirovecii colonization was more prevalent in patients aged above 70 years. Conclusion: As the findings indicated, non-HIV-infected patients, especially the elderly, had a high prevalence of P. jirovecii colonization. Therefore, these patients are probably a potential source of infection for others. Regarding this, it is of paramount importance to adopt monitoring and prophylactic measures to reduce this infection.
https://cmm.mazums.ac.ir/article_96126_c2ac009cb04360280342c641529354ad.pdf
2019-09-01
19
25
10.18502/cmm.5.3.1742
colonization
immunocompetent
Immunosuppressed
Mitochondrial large subunit
(mtLSU)
Pneumocystis jirovecii
Respiratory failures
Mahdi
Abastabar
mabastabar@gmail.com
1
Invasive Fungi Research Center, Mazandaran University of Medical Sciences, Sari, Iran
AUTHOR
Elham
Mosayebi
elham.m19@gmail.com
2
Student Research Committee, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran
AUTHOR
Tahereh
Shokohi
shokohi.tahereh@gmail.com
3
Department of Medical Mycology, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran
LEAD_AUTHOR
Mohammad Taghi
Hedayati
hedayatimt@gmail.com
4
Department of Medical Mycology, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran
AUTHOR
Mohammad Reza
Jabari Amiri
mjpezeshk2@gmail.com
5
Student Research Committee, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran
AUTHOR
Zahra
Seifi
zhrseifi@gmail.com
6
Student Research Committee, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran
AUTHOR
Iman
Haghani
imaan.haghani@gmail.com
7
Department of Medical Mycology, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran
AUTHOR
Masoud
Aliyali
masoud_aliyali@yahoo.com
8
Department of Internal Medicine, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran
AUTHOR
Sasan
Saber
saber@sina.tums.ac.ir
9
Department of Internal Medicine, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Maryam-Fatemeh
Sheikholeslami
m.sheikholslami@gmail.com
10
Department of Molecular Pathology, National Research Institute of Tuberculosis and Lung Disease, Shahid Beheshti University of Medical Sciences, Tehran, Iran
AUTHOR
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45
ORIGINAL_ARTICLE
Indifferent effect of nonsteroidal anti-inflammatory drugs (NSAIDs) combined with fluconazole against multidrug-resistant Candida auris
Background and Purpose: Emergence and development of antifungal drug resistance in Candida species constitute a serious concern. Candida auris as an emerging multidrug-resistant fungus is the most important public health threat with high levels of mortality and morbidity. Almost all C. auris isolates are resistant to fluconazole, and there have been reports of elevated minimum inhibitory concentrations (MICs) to amphotericin B and echinocandins. To overcome the growing challenge of antifungal resistance, a valuable alternative option would be the use of drug combination. Materials and Methods: The present study evaluated the in vitro combination of nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen, diclofenac and aspirin with fluconazole against fluconazole-resistant C. auris in comparison to other fluconazole-resistant Candida species, including C. albicans, C. glabrata, C. parapsilosis, C. tropicalis, and C. krusei originating from patients with candidiasis. Results: The MIC ranges of fluconazole-ibuprofen and fluconazole-diclofenac decreased from 32-256 to 32-128 and 16-256 μg/ml, respectively and remained the same for fluconazole-aspirin against C. auris. However, the combination of fluconazole with ibuprofen resulted in a synergistic effect for 5 strains, including C. albicans (n=2), C. tropicalis (n=1), C. glabrata (n=1), and C. krusei (n=1), by decreasing the MIC of fluconazole by 2-3 log2 dilutions. Conclusion: Although the interaction of NSAIDs with fluconazole was not synergistic against fluconazole-resistant C. auris isolates, no antagonism was observed for any combinations. Therefore, combination with newer azole agents needs to be conducted.
https://cmm.mazums.ac.ir/article_96295_e82131b0da7d1e2708c2c39d6ee5bc90.pdf
2019-09-01
26
30
10.18502/cmm.5.3.1743
antifungal drugs
Candida auris
Multidrug-resistant
NSAIDs
Fatemeh
Ahangarkani
fkani63@gmail.com
1
Student Research Committee, Mazandaran University of Medical Sciences, Sari, Iran
AUTHOR
Sadegh
Khodavaisy
2
Department of Medical Parasitology and Mycology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Shahram
Mahmoudi
sh.mahmoudi93@gmail.com
3
Students Scientific Research Center, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Tahereh
Shokohi
shokohi.tahereh@gmail.com
4
Invasive Fungi Research Center, Mazandaran University of Medical Sciences, Sari, Iran
AUTHOR
Mohammad Sadegh
Rezai
drmsrezaii@yahoo.com
5
Pediatric Infectious Diseases Research Center, Mazandaran University of Medical Sciences, Sari, Iran
AUTHOR
Hamed
Fakhim
fakhiim.hamed@gmail.com
6
Department of Medical Parasitology and Mycology, Faculty of Medicine, Urmia University of Medical Sciences, Urmia, Iran
AUTHOR
Eric
Dannaoui
eric.dannaoui@egp.aphp.fr
7
Université Paris-Descartes, Faculté de Médecine, APHP, Hôpital Européen Georges Pompidou, Unité de Parasitologie-Mycologie, Service de Microbiologie, Paris, France
AUTHOR
Saharnaz
Faraji
8
Student Research Committee, Mazandaran University of Medical Sciences, Sari, Iran
AUTHOR
Anuradha
Chowdhary
dranuradha@hotmail.com
9
Department of Medical Mycology, Vallabhbhai Patel Chest Institute, University of Delhi, Delhi, India
AUTHOR
Jacques F.
Meis
10
Department of Medical Microbiology and Infectious Diseases, Canisius-Wilhelmina Hospital (CWZ), Nijmegen, The Netherlands
AUTHOR
Hamid
Badali
badalii@yahoo.com
11
Pharmaceutical Sciences Research Center, Mazandaran University of Medical Sciences, Sari, Iran
LEAD_AUTHOR
1. Lamoth F, Lockhart SR, Berkow EL, Calandra T. Changes in the epidemiological landscape of invasive candidiasis. J Antimicrob Chemother. 2018; 73:i4-13.
1
2. Cortegiani A, Misseri G, Chowdhary A. What’s new on emerging resistant Candida species. Intensive Care Med. 2019; 45(4):512-5.
2
3. Meis JF, Chowdhary A. Candida auris: a global fungal public health threat. Lancet Infect Dis. 2018; 18(12):1298-9.
3
4. Satoh K, Makimura K, Hasumi Y, Nishiyama Y, Uchida K, Yamaguchi H. Candida auris sp. nov., a novel ascomycetous yeast isolated from the external ear canal of an inpatient in a Japanese hospital. Microbiol Immunol. 2009; 53(1):41-4.
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5. Calvo B, Melo AS, Perozo-Mena A, Hernandez M, Francisco EC, Hagen F, et al. First report of Candida auris in America: Clinical and microbiological aspects of 18 episodes of candidemia. J Infect. 2016; 73(4):369-74.
5
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6
7. Chow NA, Gade L, Tsay SV, Forsberg K, Greenko JA, Southwick KL, et al. Multiple introductions and subsequent transmission of multidrug-resistant Candida auris in the USA: a molecular epidemiological survey. Lancet Infect Dis. 2018; 18(12):1377-84.
7
8. Araúz AB, Caceres DH, Santiago E, Armstrong P, Arosemena S, Ramos C, et al. Isolation of Candida auris from 9 patients in Central America: importance of accurate diagnosis and susceptibility testing. Mycoses. 2018; 61:44-7.
8
9. Schelenz S, Hagen F, Rhodes JL, Abdolrasouli A, Chowdhary A, Hall A, et al. First hospital outbreak of the globally emerging Candida auris in a European hospital. Antimicrob Resist Infect Control. 2016; 5:35.
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10. Eyre DW, Sheppard AE, Madder H, Moir I, Moroney R, Quan TP, et al. A Candida auris outbreak and its control in an intensive care setting. N Engl J Med. 2018; 379(14):1322-31.
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11. Saris K, Meis JF, Voss A. Candida auris. Curr Opin Infect Dis. 2018; 31(4):334-40.
11
12. Abastabar M, Haghani I, Ahangarkani F, Rezai MS, Taghizadeh Armaki M, Roodgari S, et al. Candida auris otomycosis in Iran and review of recent literature. Mycoses. 2019; 62(2):101‐5.
12
13. Forsberg K, Woodworth K, Walters M, Berkow EL, Jackson B, Chiller T, et al. Candida auris: the recent emergence of a multidrug-resistant fungal pathogen. Med Mycol. 2019; 57(1):1-12.
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14. Biswal M, Rudramurthy SM, Jain N, Shamanth AS, Sharma D, Jain K, et al. Controlling a possible outbreak of Candida auris infection: lessons learnt from multiple interventions. J Hosp Infect 2017; 97(4):363-70.
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16. Chowdhary A, Prakash A, Sharma C, Kordalewska M, Kumar A, Sarma S, et al. A multicenter study of antifungal susceptibility patterns among 350 Candida auris isolates (2009-
16
17) in India: role of the ERG11 and FKS1 genes in azole and echinocandin resistance. J Antimicrob Chemother. 2018; 73(4):891-9.
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17. Escandón P, Chow NA, Caceres DH, Gade L, Berkow EL, Armstrong P, et al. Molecular epidemiology of Candida auris in Colombia reveals a highly related, countrywide colonization with regional patterns in Amphotericin B resistance. Clin Infect Dis. 2019; 68(1):15-21.
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18. Mathur P, Hasan F, Singh PK, Malhotra R, Walia K, Chowdhary A. Five-year profile of candidaemia at an Indian trauma centre: high rates of Candida auris blood stream infections. Mycoses. 2018; 61(9):674-80.
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21. Pina-Vaz C, Sansonetty F, Rodrigues AG, Martinez-De-Oliveira J, Fonseca AF, Mårdh PA. Antifungal activity of ibuprofen alone and in combination with fluconazole against Candida species. J Med Microbiol. 2000; 49(9):831-40.
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38. Mahmoudi S, Rezaie S, Ghazvini RD, Hashemi SJ, Badali H, Foroumadi A, et al. In Vitro interaction of geldanamycin with triazoles and echinocandins against common and emerging Candida species. Mycopathologia. 2019; 184(5):607-613.
39
ORIGINAL_ARTICLE
Antifungal effect of the effect of Securigera securidaca L. vaginal gel on Candida species
Background and Purpose: Candida species are opportunistic fungi, capable of causing acute and chronic infections in the gastrointestinal tract, vagina, and oral mucosa, among which Candida albicans is the most important species. The Securigera securidaca L. is used as an antiseptic to treat some diseases in traditional Iranian medicine. The aim of this study was to evaluate the antimicrobial activity of S. securidaca extracts and vaginal gel against different Candida species. Materials and Methods: Antifungal effects of different extracts and vaginal gel of S. securidaca were investigated against Candida species. By using well diffusion test, different concentrations of the collected S. securidaca extracts and vaginal gel were examined to test their antifungal activity against C. albicans, C. parapsilosis, and C. krusei. Results: The ethanol extract and vaginal gel with the ethanol extract of S. securidaca showed the most anti-fungal activity against all three strains. Conclusion: The S. securidaca extract had a significant inhibitory effect on the different species of Candida; however, the highest inhibitory effect was found against C. albicans. In order to treat candidiasis, more research is required to check the efficacy of this plant in this domain.
https://cmm.mazums.ac.ir/article_92558_9cc4300eae93ffcd3308b68a9f66ce21.pdf
2019-09-01
31
35
10.18502/cmm.5.3.1744
Antifungal Effect
candida albicans
Candidiasis
Vaginal gel
Atefeh
Raesi Vanani
atefehraisi1393@gmail.com
1
Student Research Committee, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
AUTHOR
Masoud
Mahdavinia
mahdavimasoud@yahoo.com
2
Toxicology Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
AUTHOR
Heibatullah
Kalantari
kalantarih@yahoo.com
3
Toxicology Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
AUTHOR
Saeed
Khoshnood
saeed.khoshnood22@gmail.com
4
Student Research Committee, School of Medicine, Bam University of Medical Sciences, Bam, Iran
AUTHOR
Maryam
Shirani
mshirani86@yahoo.com
5
Student Research Committee, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
LEAD_AUTHOR
1. Ramesh P, Okigbo R. Effects of plants and medicinal plant combinations as anti-infectives. Afr J Pharm Pharmacol. 2008; 2(7):130-5.
1
2. Hashemi S, Asgarpanah J, Alaee Z, Sadeghian S, Hasani H, Azimi A. In vitro antifungal activity of four medicinal plants used in Iranian Traditional Medicine. Res J Pharmacogn. 2014; 1(1):39-43.
2
3. Anaissie EJ, McGinnis MR, Pfaller MA. Clinical mycology. Ann Internal Med. 2003; 138(9):776.
3
4. Rios JL, Recio MC. Medicinal plants and antimicrobial activity. J Ethnopharmacol. 2005; 100(1-2):80-4.
4
5. Arif T, Bhosale J, Kumar N, Mandal T, Bendre R, Lavekar G, et al. Natural products–antifungal agents derived from plants. J Asian Natural Prod Res. 2009; 11(7):621-38.
5
6. Jamshidzadeh A, Pasdaran A, Heidari R, Hamedi A. Pharmacognostic and anti-inflammatory properties of Securigera securidaca seeds and seed oil. Res J Pharmacogn. 2018; 5(3): 31-9.
6
7. Tofighi Z, Sabzevari O, Rezaei Taleqani Z, Yassa N. Investigation of securigera securidaca seeds extract and different fractions on serum glucose, blood factors and liver morphology in diabetic animals. Iran J Endocrinol Metab. 2016; 18(1):37-45.
7
8. Mard S, Bahari Z, Eshaghi N, Farbood Y. Antiulcerogenic effect of Securigera securidaca L. seed extract on various experimental gastric ulcer models in rats. Pak J Biol Sci. 2008; 11(23):2619.
8
9. Hajzadeh M, Rajaei Z, Ghamami G, Tamiz A. The effect of Salvia officinalis leaf extract on blood glucose in streptozotocin-diabetic rats. Pharmacologyonline. 2011; 1:213-20.
9
10. Lan YB, Huang YZ, Qu F, Li JQ, Ma LJ, Yan J, et al. Time course of global gene expression alterations in Candida albicans during infection of HeLa cells. Bosn J Basic Med Sci. 2017; 17(2):120-31.
10
11. Shirani M, Samimi A, Kalantari H, Madani M, Zanganeh AK. Chemical composition and antifungal effect of hydroalcoholic extract of Allium tripedale (Tvautv.) against Candida species. Curr Med Mycol. 2017; 3(1):6-12.
11
12. Price MF, LaRocco MT, Gentry LO. Fluconazole susceptibilities of Candida species and distribution of species recovered from blood cultures over a 5-year period. Antimicrob Agents Chemother. 1994; 38(6):1422-4.
12
13. Nasrollahi Z, Yadegari MH, Roudber Mohammadi S, Roudbary M, Poor MH, Nikoomanesh F, et al. Fluconazole resistance Candida albicans in females with recurrent Vaginitis and Pir1 overexpression. Jundishapur J Microbiol. 2015; 8(9):e21468.
13
14. Richter SS, Galask RP, Messer SA, Hollis RJ, Diekema DJ, Pfaller MA. Antifungal susceptibilities of Candida species causing vulvovaginitis and epidemiology of recurrent cases. J Clin Microbiol. 2005; 43(5):2155-62.
14
15. Wasser SP. Medicinal mushroom science: history, current status, future trends, and unsolved problems. Int J Med Mushrooms. 2010; 12(1):281-3.
15
16. Das K, Tiwari R, Shrivastava D. Techniques for evaluation of medicinal plant products as antimicrobial agent: current methods and future trends. J Med Plants Res. 2010; 4(2):104-11.
16
17. Balouiri M, Sadiki M, Ibnsouda SK. Methods for in vitro evaluating antimicrobial activity: a review. J Pharm Anal. 2016; 6(2):71-9.
17
18. Kim HJ, Suh HJ, Lee CH, Kim JH, Kang SC, Park S, et al. Antifungal activity of glyceollins isolated from soybean elicited with Aspergillus sojae. J Agricd Food Chemi. 2010; 58(17):9483-7.
18
19. Subcommittee on Antifungal Susceptibility Testing of the ESCMID European Committee for Antimicrobial Susceptibility Testing. EUCAST Technical Note on the method for the determination of broth dilution minimum inhibitory concentrations of antifungal agents for conidia-forming moulds. Clin Microbiol Infect. 2008; 14(10):982-4.
19
20. Cavalcanti Filho JR, Silva TF, Nobre WQ, Oliveira de Souza LI, Silva e Silva Figueiredo CS, Figueiredo RC, et al. Antimicrobial activity of Buchenavia tetraphylla against Candida albicans strains isolated from vaginal secretions. Pharm Biol. 2017; 55(1):1521-7.
20
21. Rehman A, Rehman A, Ahmad I. Antibacterial, antifungal, and insecticidal potentials of Oxalis corniculata and its isolated compounds. Int J Anal Chem. 2015; 2015:842468.
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22. Pfaller M, Diekema D. Epidemiology of invasive candidiasis: a persistent public health problem. Clin Microbiol Rev. 2007; 20(1):133-63.
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23. Calderone RA, Clancy CJ. Candida and candidiasis. Washington, D.C: American Society for Microbiology Press; 2011.
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24. Pfaller MA, Houston A, Coffmann S. Application of CHROMagar Candida for rapid screening of clinical specimens for Candida albicans, Candida tropicalis, Candida krusei, and Candida (Torulopsis) glabrata. J Clin Microbiol. 1996; 34(1):58-61.
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25. Beighton D, Ludford R, Clark DT, Brailsford SR, Pankhurst CL, Tinsley GF, et al. Use of CHROMagar Candida medium for isolation of yeasts from dental samples. J Clin Microbiol. 1995; 33(11):3025-7.
25
26. Kirkpatrick WR, Turner TM, Fothergill AW, McCarthy DI, Redding SW, Rinaldi MG, et al. Fluconazole disk diffusion susceptibility testing of Candida species. J Clin Microbiol. 1998; 36(11):3429-32.
26
27. Behbahani M, Shanehsazzadeh M, Shokoohinia Y, Soltani M.
27
Evaluation of anti-herpetic activity of methanol seed extract and fractions of securigera securidaca in vitro. J Antivir Antiretrovir. 2013; 5(4):72-6.
28
28. Sadat-Ebrahimi S, Hassanpoor Mir M, Amin G, Hajimehdipoor H. Identification of amino acids in Securigera securidaca, a popular medicinal herb in Iranian folk medicine. Res J Pharmacog. 2014; 1(1):23-6.
29
29. Ibrahim RM, El-Halawany AM, Saleh DO, El Naggar EM, El-Shabrawy AE, El-Hawary SS. HPLC-DAD-MS/MS profiling of phenolics from Securigera securidaca flowers and its anti-hyperglycemic and anti-hyperlipidemic activities. Rev Bras Farmacog. 2015; 25(2):134-41.
30
30. Yarmolinsky L, Huleihel M, Zaccai M, Ben-Shabat S. Potent antiviral flavone glycosides from Ficus benjamina leaves. Fitoterapia. 2012; 83(2):362-7.
31
31. Kim TH, Ku SK, Lee IC, Bae JS. Anti-inflammatory effects of kaempferol-3-O-sophoroside in human endothelial cells. Inflamm Res. 2012; 61(3):217-24.
32
32. Tofighi Z, Asgharian P, Goodarzi S, Hadjiakhoondi A, Ostad SN, Yassa N. Potent cytotoxic flavonoids from Iranian Securigera securidaca. Med Chem Res. 2014; 23(4):1718-24.
33
33. Cushnie TT, Lamb AJ. Recent advances in understanding the antibacterial properties of flavonoids. Int J Antimicrob Agents. 2011; 38(2):99-107.
34
34. Lim YH, Kim IH, Seo JJ. In vitro activity of kaempferol isolated from the Impatiens balsamina alone and in combination with erythromycin or clindamycin against Propionibacterium acnes. J Microbiol. 2007; 45(5):473-7.
35
35. Basile A, Giordano S, López-Sáez JA, Cobianchi RC. Antibacterial activity of pure flavonoids isolated from mosses. Phytochemistry. 1999; 52(8):1479-82.
36
36. Sato Y, Suzaki S, Nishikawa T, Kihara M, Shibata H, Higuti T. Phytochemical flavones isolated from Scutellaria barbata and antibacterial activity against methicillin-resistant Staphylococcus aureus. J Ethnopharmacol. 2000; 72(3):483-8.
37
37. Cushnie TT, Hamilton VE, Lamb AJ. Assessment of the antibacterial activity of selected flavonoids and consideration of discrepancies between previous reports. Microbiol Res. 2003; 158(4):281-9.
38
38. Abbassy MA, Kadous EA, Abd-Allah E-SA, Marei GI. Isolation and identification of cardenolide compounds of gomphocarpus sinaicus and their fungicidal activity against soil borne and post harvest fungi. J Life Sci. 2012; 6(9):985.
39
ORIGINAL_ARTICLE
Investigation of cgrA and cyp51A gene alternations in Aspergillus fumigatus strains exposed to kombucha fermented tea
Background and Purpose: Aspergillus fumigatus is one of the most common opportunistic fungus, which causes infection in immunocompromised and neutropenic patients. The current guidelines recommend voriconazole as the initial therapeutic and prophylactic agent for almost all cases, especially in patients with organ transplants, which leads to increased medication resistance in A. fumigatus. The aim of the present study was to evaluate the antifungal activity and effect of kombucha as a natural compound on A. fumigatus growth, as well as on the expression of cgrA and cyp51A genes. Materials and Methods: A panel of 15 A. fumigatus strains with two quality controls of CM237 and CM2627 as susceptible and resistant strains were obtained from Tehran Medical Mycology Laboratory, Tehran,Iran(TMML).Antifungal susceptibility testing assay was performed according to the Clinical and Laboratory Standards Institute (CLSI) M38-A2 document. Moreover, the mycelial dry weight of the fungus was calculated before and after being treated with kombucha. In addition, the quantitative changes in the expression of cgrA and cyp51A genes were analyzed by real-time polymerase chain reaction (real-time PCR) technique. Results: In the present study, the minimum inhibitory concentration ranges of kombucha were measured at 6,170 and 12,300 μg/mL for ten A. fumigatus azole-susceptible strains and 24,700 μg/mL for five A. fumigatus resistant strains. Moreover, changes in mycelial dry weight under kombucha treatment conditions underwent a significant reduction (P≤0.05). A coordinate down-regulation of expression in cgrA and cyp51A genes was observed in all azole-susceptible and -resistant A. fumigatus strains, after treating the fungus with different concentrations of kombucha (P≤0.05). Conclusion: According to the obtained results, kombucha as a natural antioxidant , can exert inhibitory effects against the growth and expression of some genes in A. fumigatusstrains.
https://cmm.mazums.ac.ir/article_96347_61603a44c2766e1e4987a5f45f1ada55.pdf
2019-09-01
36
42
10.18502/cmm.5.3.1745
Aspergillus fumigatus
CgrA gene
Cyp51A gene
Kombucha
Ladan
Nazemi
ladan_nazemi@yahoo.com
1
Division of Molecular Biology, Department of Medical Mycology and Parasitology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Seyed Jamal
Hashemi
sjhashemi@sina.tums.ir
2
Division of Molecular Biology, Department of Medical Mycology and Parasitology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Roshanak
Daie Ghazvini
rdaie@tums.ac.ir
3
Division of Molecular Biology, Department of Medical Mycology and Parasitology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Mina
Saeedi
m-saeedi@tums.ac.ir
4
Medicinal Plants Research Center, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Sadegh
Khodavaisy
5
Division of Molecular Biology, Department of Medical Mycology and Parasitology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Aleksandra
Barac
aleksandrabarac85@gmail.com
6
Clinic for Infectious and Tropical Diseases, Clinical Center of Serbia, Faculty of Medicine, University of Belgrade, Belgrade, Serbia
AUTHOR
Mona
Modiri
7
Division of Molecular Biology, Department of Medical Mycology and Parasitology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Maryam
Akbari Dana
maryam_dana58@yahoo.com
8
Division of Molecular Biology, Department of Medical Mycology and Parasitology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Zahra Zare shahrabadi
Zare shahrabadi
9
Division of Molecular Biology, Department of Medical Mycology and Parasitology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Sassan
Rezaie
srezaie@tums.ac.ir
10
Division of Molecular Biology, Department of Medical Mycology and Parasitology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
LEAD_AUTHOR
1. Van de Veerdonk FL, Gresnigt MS, Romani L, Netea MG, Latgé JP. Aspergillus fumigatus morphology and dynamic host interactions. Nature Rev Microbiol. 2017; 15(11):661-74.
1
2. Soubani AO, Chandrasekar PH. The clinical spectrum of pulmonary aspergillosis. Chest. 2002; 121(6):1988-99.
2
3. Lamoth F. Aspergillus fumigatus-related species in clinical practice. Front Microbiol. 2016; 7:683.
3
4. Latge JP. Aspergillus fumigatus and Aspergillosis. Clin Microbial Rev. 1999; 12(2):310-50.
4
5. Rementeria A, Lopez-Molina N, Ludwig A, Vivanco AB, Bikandi J, Ponton J, et al. Genes and molecules involved in
5
Aspergillus fumigatus virulence. Rev Iberoam Micol. 2005; 22(1):1-23.
6
6. Patterson TF, Thompson GR 3rd, Denning DW, Fishman JA, Hadley S, Herbrecht R, et al. Practice guidelines for the diagnosis and management of aspergillosis: 2016 update by the Infectious Diseases Society of America. Clin Infect Dis. 2016; 63(4):e1-60.
7
7. Meis JF, Chowdhary A, Rhodes JL, Fisher MC, Verweij PE. Clinical implications of globally emerging azole resistance in Aspergillus fumigatus. Philos Trans R Soc B Biol Sci. 2016; 371(1709):20150460.
8
8. Chowdhary A, Sharma C, Hagen F, Meis JF. Exploring azole antifungal drug resistance in Aspergillus fumigatus with special reference to resistance mechanisms. Future Microbiol. 2014; 9(5):697-711.
9
9. Snelders E, Camps SM, Karawajczyk A, Schaftenaar G, Kema GH, Van der Lee HA, et al. Triazole fungicides can induce cross-resistance to medical triazoles in Aspergillus fumigatus. PLoS One. 2012; 7(3):e31801.
10
10. Battikh H, Bakhrouf A, Ammar E. Antimicrobial effect of Kombucha analogues. LWT Food Sci Technol. 2012; 47(1):71-7.
11
11. Sreeramulu G, Zhu Y, Knol W. Kombucha fermentation and its antimicrobial activity. J Agric Food Chem. 2000; 48(6):2589-94.
12
12. Battikh H, Chaieb K, Bakhrouf A, Ammar E. Antibacterial and antifungal activities of black and green Kombucha teas. J Food Biochem. 2013; 37(2):231-6.
13
13. Mahmoudi E, Saeidi M, Marashi MA, Moafi A, Mahmoodi V, Zamani MZ. In vitro activity of Kombucha tea ethyl acetate fraction against Malassezia species isolated from seborrhoeic dermatitis. Curr Med Mycol. 2016; 2(4):30-6.
14
14. Bhattacharya D, Bhattacharya S, Patra MM, Chakravorty S, Sarkar S, Chakraborty W, et al. Antibacterial activity of polyphenolic fraction of Kombucha against enteric bacterial pathogens. Curr Microbiol. 2016; 73(6):885-96.
15
15. Jayabalan R, Malbasa RV, Loncar ES, Vitas JS, Sathishkumar M. A review on kombucha tea-microbiology, composition, fermentation, beneficial effects, toxicity and tea fungu. Compr Rev Food Sci Food Saf. 2014; 13(4):538-50.
16
16. Villarreal-Soto SA, Beaufort S, Bouajila J, Souchard JP, Taillandier P. Understanding kombucha tea fermentation: a review. J Food Sci. 2018; 83(3):580-8.
17
17. Buil JB, Hagen F, Chowdhary A, Verweij PE, Meis JF. Itraconazole, voriconazole, and posaconazole CLSI MIC distributions for wild-type and azole-resistant Aspergillus fumigatus isolates. J Fungi. 2018; 4(3):E103.
18
18. Institute Cals. Reference method for broth dilution antifungal susceptibility testing of filamentous fungi; approved standard. Pennsylvania: Document M38-A2, CLSI; 2008. P. 1-24.
19
19. Krishnan S, Manavathu EK, Chandrasekar PH. Aspergillus flavus: an emerging non-fumigatus Aspergillus species of significance. Mycoses. 2008; 52(3):206-22.
20
20. Bromley MJ, van Muijlwijk G, Fraczek MG, Robson G, Verweij PE, Denning DW, et al. Occurrence of azole-resistant species of Aspergillus in the UK environment. J Glob Antimicrob Resist. 2014; 2(4):276-9.
21
21. Rudramurthy SM, Chakrabarti A, Geertsen E, Mouton JW, Meis JF. In vitro activity of isavuconazole against 208 Aspergillus flavus isolates in comparison with 7 other antifungal agents: assessment according to the methodology of the European
22
Committee on Antimicrobial Susceptibility Testing. Diagn Microbiol Infect Dis. 2011; 71(4):370-7.
23
22. Misch EA, Safdar N. Updated guidelines for the diagnosis and management of aspergillosis. J Thorac Dis. 2016; 8(12): E1771-6.
24
23. Lestrade PP, Bentvelsen RG, Schauwvlieghe AF, Schalekamp S, van der Velden WJ, Kuiper EJ, et al. Voriconazole resistance and mortality in invasive aspergillosis: a multicenter retrospective cohort study. Clin Infect Dis. 2018; 68(9):1463-71.
25
24. Nabili M, Shokohi T, Moazeni M, Khodavaisy S, Aliyali M, Badiee P, et al. High prevalence of clinical and environmental triazole-resistant Aspergillus fumigatus in Iran: is it a challenging issue? J Med Microbiol. 2016; 65(6):468-75.
26
25. Abastabar M, Rahimi N, Meis JF, Aslani N, Khodavaisy S, Nabili M, et al. Potent activities of novel imidazoles lanoconazole and luliconazole against a collection of azole-resistant and-susceptible Aspergillus fumigatus strains. Antimicrob Agents Chemother. 2016; 60(11):6916-9.
27
26. Deghrigue M, Chriaa J, Battikh H, Abid K, Bakhrouf A. Antiproliferative and antimicrobial activities of Kombucha tea. Afr J Microbiol Res. 2013; 7(27):3466-70.
28
27. AL-Kalifawi EJ. Study the antimicrobial effect of kombucha tea on bacteria isolated from diabetic foot ulcer. Int J Sci Technol. 2014; 8(4):27-33.
29
28. Battikh H, Chaieb K, Bakhrouf A, Ammar E. Antibacterial and antifungal activities of black and green Kombucha teas. J Food Biochem. 2013; 37(2):231-6.
30
29. Kumar V, Joshi VK. Kombucha: technology, microbiology, production, composition and therapeutic value. Intl J Food Ferment Technol. 2016; 6(1):13-24.
31
30. Bauer‐Petrovska B, Petrushevska‐Tozi L. Mineral and water soluble vitamin content in the Kombucha drink. Int J Food Sci Technol. 2000; 35(2):201-5.
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31. Pure AE, Ebrahimipure M. Antioxidant and antibacterial activity of kombucha beverages prepared using banana peel, common nettles and black tea infusion. Appl Food Biotechnol. 2016; 3(2):125-30.
33
32. Chakravorty S, Bhattacharya S, Chatzinotas A, Chakraborty W, Bhattacharya D. Kombucha tea fermentation: microbial and biochemical dynamics. Int J Food Microbiol. 2016; 220:63-72.
34
33. Yuniarto A, Anggadiredja K, Aqidah RA. Antifungal activity of Kombucha tea against human pathogenic fungi. Asian J Pharm Clin Res. 2016; 9(5):253-5.
35
34. Santos Jr RJ, Batista RA, Rodrigues Filho SA, Lima AS. Antimicrobial activity of broth fermented with kombucha colonies. J Microb Biochem Technol. 2009; 1(1):72-8.
36
35. Bhabhra R, Miley MD, Mylonakis E, Boettner D, Fortwende J, Panepinto JC, et al. Disruption of the Aspergillus fumigatus gene encoding nucleolar protein CgrA impairs thermotolerant growth and reduces virulence. Infect Immun. 2004; 27(8):4731-40.
37
36. Bhabhra R, Zhao W, Rhodes JC, Askew DS. Nucleolar localization of Aspergillus fumigatus CgrA is temperature-dependent. Fungal Genet Biol. 2006; 43(1):1-7.
38
37. Perlin DS, Shor E, Zhao Y. Update on antifungal drug resistance. Curr Clin Microbiol Rep. 2015; 2(2):84-95.
39
38. Mousavi B, Hedayati MT, Teimoori‐Toolabi L, Guillot J, Alizadeh A, Badali H. cyp51A gene silencing using RNA interference in azole‐resistant Aspergillus fumigatus. Mycoses. 2015; 58(12):699-706.
40
39. Brillowska-Dąbrowska A, Mroczyńska M, Nawrot U, Włodarczyk K, Kurzyk E. Examination of cyp51A and cyp51B expression level of the first Polish azole resistant clinical Aspergillus fumigatus strain. Acta Biochim Pol. 2015; 62(4):837-9.
41
ORIGINAL_ARTICLE
High prevalence of itraconazole resistance among Candida parapsilosis isolated from Iran
Background and Purpose: Candida parapsilosis isolates usually have a low minimum inhibitory concentration (MIC) against azoles. Although Candida parapsilosis isolates usually have low MICs against azoles, recent studies candida invasive infections due to azole resistant-C. parapsilosis isolates . Regarding this, the main aim of this study was to determine the susceptibility pattern of Iranian clinical C. parapsilosis against available azole antifungal drugs. Materials and Methods: This study was conducted on 105 previously-identified isolates of C. parapsilosis sensu stricto. For the purpose of the study, the isolates were subjected to antifungal susceptibility testing against fluconazole (FLZ), itraconazole (ITZ), voriconazole (VRZ), and two new azole drugs, namely luliconazole (LUZU) and lanoconazole (LZN). The broth microdilution reference method adopted in this study was according to the Clinical & Laboratory Standards Institute M27-A3 and M27-S4 documents. Results: According to the results, 89% (n=94) of C. parapsilosis isolates showed a MIC of ≥ 1 μg/ml, indicating resistance against ITZ. Multi-azole resistance was observed in 3.8% of the isolates. In addition, LUZU and LZN demonstrated the highest efficacy with the MIC50 values of 0.5 and 1 μg/ml, respectively. Conclusion: The majority of the isolates showed high MIC values against ITZ. This may have been associated with the long-term ITZ prophylaxis/therapy in patients infected with candidiasis. Hence, the adoption of an appropriate antifungal agent is a crucial step for starting the treatment. Background and Purpose: Although Candida parapsilosis isolates have usually low MICs against azoles but recent study confirmed Candida –related invasive infections due to azoles resistance C. parapsilosis isolates. The main aim of this study was to determine the susceptibility pattern of Iranian clinical C. parapsilosis against available azolesantifungal drugs. .Material and Methods: One hundred and five previously-identified isolates of C. parapsilosis sensu stricto were subjected to antifungal susceptibility testing against fluconazole, itraconazole, voriconazole and two new azole drugs, loliconazole and lanoconazole using the broth microdilution reference method according to CLSI M27-A3 and M27-S4 document.Results: Eighty nine percent (n=94) of C. parapsilosis isolates showed MIC ≥ 1µg/ml which indicated resistance against itraconazole. Multi-azoles resistances were observed in 3.8% of the isolates. Loliconazole and lanoconazole demonstrated the highest efficacy with MIC50 values of 0.5 and 1µg/ml, respectively.Conclusion: The majority of the isolates showed high MIC values against Itraconazole. It may associated with the long term Itraconazole prophylaxis/therapy in patients Infected with candidasis. Hence, choosing the appropriate antifungal is the crucial step for starting treatment.
https://cmm.mazums.ac.ir/article_95985_9d9682d392a00b57d782bad6217af905.pdf
2019-09-01
43
46
10.18502/cmm.5.3.1746
Azoles
Candida parapsilosis
Iranian isolates
Resistant
Fozieh
Hassanmoghadam
fhassanmoghadam@gmail.com
1
Student Research Committee, Mazandaran University of Medical Sciences, Sari, Iran
AUTHOR
Tahere
Shokohi
shokohi.tahereh@gmail.com
2
Invasive Fungi Research Center, Mazandaran University of Medical Sciences, Sari, Iran
AUTHOR
Mohammad Taghi
Hedayati
hedayatimt@gmail.com
3
Invasive Fungi Research Center, Mazandaran University of Medical Sciences, Sari, Iran
AUTHOR
Narges
Aslani
narges.aslani987@gmail.com
4
Infectious and Tropical Diseases Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Iman
Haghani
imaan.haghani@gmail.com
5
Department of Medical Mycology, School of Medicine, Mazandaran University of Medical Sciences, Sari, Iran
AUTHOR
Mojtaba
Nabili
m.nabili2010@gmail.com
6
Faculty of Medicine, Sari Branch, Islamic Azad University, Sari, Iran
AUTHOR
Ensieh
Lotfali
ensiehlotfali@yaho.com
7
Department of Medical Parasitology and Mycology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
AUTHOR
Amirhossein
Davari
amirdavari3317@gmail.com
8
Student Research Committee, Mazandaran University of Medical Sciences, Sari, Iran
AUTHOR
Maryam
Moazeni
moazeni.maryam@gmail.com
9
Invasive Fungi Research Center, Mazandaran University of Medical Sciences, Sari, Iran
LEAD_AUTHOR
1. Messer SA, Jones RN, Fritsche TR. International surveillance of Candida spp. and Aspergillus spp.: report from the SENTRY Antimicrobial Surveillance Program (2003). J Clin Microbiol. 2006; 44(5):1782-7.
1
2. Oberoi JK. Invasive candidasis. JIMSA. 2010; 23(1):25-8.
2
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