Articles

Molecular Monitoring of Plasmodium vivax Infection after Radical Treatment in Southeastern Iran

Abstract

Background: The aim was to evaluate the relapse risk of vivax malaria in patients who received radical treatment in Hormozgan Province, a malarious area located on southeast of Iran.
Methods: A total of 95 symptomatic vivax malaria infected patients were enrolled in urban health centers of Bandar- Abbas, Minab, Bandar-Jask and Bashagard districts of Hormozgan Province, southeast of Iran from January 2008 to March 2009 for consideration as a case- series study. DNA was extracted from parasite infected whole blood samples. A polymorphic region of Plasmodium vivax merozoite surface protein 1 (pvMSP1) was selected and a PCR method was employed for all the samples to amplify the specific variable gene fragment. The obtained fragments in primary and secondary samples were sequenced. Both nucleotide and amino acid sequences of the samples were investigated for returned patients.
Results: 3.2% of the patients experienced a second attack between 83-199 days after the initial episode of infection. Alignment of nucleotide and their deduced amino acid sequences between pair sequences of primary and secondary isolates revealed 8 and 6 dissimilarities respectively for the first case, and 9 and 7 dissimilarities for the second case. Although microscopical examination of recurrent thick blood smear of the third patient confirmed new P. vivax  infection, the venous blood sample was accidentally missed. Sequencing results of primary and returned isolates 1P, 1S, 2P, 2S and 3P in this study showed an identity with BP13, T117, BP13, TC28 and Chesson genotypes respectively.
Conclusion: The returned (secondary) isolates may account to be for the sake of reinfection.

Adak T, Sharma VP, Orlov VS (1998) Stud- ies on the Plasmodium vivax relapse pattern in Delhi, India. Am J Trop Med Hyg. 59: 175–179.

CDC of Ministry of Health & Medical Edu- cation (2008) Annual report of malaria cases. I.R.Iran

Chen N, Aullif A, Rieckmann K, Gatton M, Cheng Q (2007) Relapses of Plasmo- dium vivax infection result from clonal hypnozoites activated at predetermined intervals. J Infect Dis 195: 934–941.

Coatney GR, Cooper WC, Young MD (1950) Studies in human malaria.xxx. A sum- mary of 204 sporozoite- induced infec- tion with the Chesson strain of Plasmo- dium vivax. Journal of National Ma- laria Society. 9: 381–396.

Collins WE, Jeffery GM (1996) Primaquine resistance in Plasmodium vivax. Am J Trop Med Hyg. 55: 243–249.

Collins WE, Sullivan JS, Morris, CL, Gal- land GG, Richardson B (1996) Obser- vations on biological nature of Plasmo- dium vivax sporozoites. J Parasitol. 82:216–219.

Craig AA, Kain KC (1996) Molecular analy- sis of strains of Plasmodium vivax from paired primary and relapse infection. J Infect Dis. 174: 373–379.

Gogtay NJ, Desai S, Kadam VS, Kamtekar KD, Dalvi SS, Kshirsagar NA (2000) Relapse pattern of Plasmodium vivax in Mumbai: a study of 283 cases of vivax malaria. J Assoc Phys India. 48: 1085–1086.

Haghdoost A, Mazhari SH, Bahaadini K (2006) Estimating the relapse risk of Plasmodium vivax in Iran under national chemotherapy scheme using a novel method. J Vect Borne Dis. 43: 168–172.

Hay SI, Guerra CA, Tatem AJ, Noor AM, Snow RW (2004) The global distribu- tion and population at risk of malaria: past, present, and future. Lancet Infect Dis. 4: 327–336.

Imwong M, Snounou G, Pukrittayakamee S, Tanomsing N, Kim JR, Nandy A, et al. (2007) Relapse of Plasmodium vivax infection usually result from activation of heterologous hypnozoites. J Infect Dis.195: 927–933.

Kirchgatter K, del Portillo HA (1998) Mole- cular analysis of Plasmodium vivax re- lapses using the MSP1 molecule as a ge- netic marker. J Infect Dis. 177: 511–515.

Koepfli C, Mueller I, Marfurt J, Goroti M, Sie A, Oa O, Genton B, Beck HP Fleger I (2009) Evaluation of Plasmodium vivax Genotyping Markers for Molecular Moni- toring in Clinical Trials. J Infect Dis. 199:1074–1080.

Krotoski WA (1985) Discovery of the hyp- nozoite and a new theory of malarial relapse. Trans R Soc Trop Med Hyg.79: 1–11.

Leslie T, Rab MA, Ahmadzai H, Durrani N, Fayaz M, Kolaczinski J, Rowland M (2004) Compliance with 14-day prima- quine therapy for radical cure of vivax malaria-a randomized placebo-controlled trial comparing unsupervised with su- pervised treatment. Trans R Soc Trop Med Hyg. 98:168–173.

Leslie T, Mayan I, Mohammed N, Erasmus P, Kolackzinski J, Whitty CJM, Rowland M (2008) A andomized Trial of an Eight-Week, Once Weekly Primaquine Regimen to Prevent Relapse of Plasmo- dium vivax in Northern Frontie Province, Pakistan. PLoS ONE www.plosone.org 8.

Manson J (1975) Patterns of Plasmodium vivax recurrence in a high-incidence coastal area of El Salvador, C.A. Am J Trop Med Hyg. 24:581–585.

Mendis K, Sina BJ, Marchesini P, Carter R (2001) The neglected burden of Plas- modium vivax malaria. Am J Trop Med Hyg. 64: 97–106.

Pukrittayakamee S, Imwong M, Looareesu- wan S, White NJ (2004) Therapeutic responses to antimalarial and antibacterial drugs in vivax malaria. Acta Tropica.89: 351–356.

Rowland M, Durrani N (1999) Randomized controlled trials of 5- and 14-days pri- maquine therapy against relapses of vivax malaria in an Afghan refugee settlement in Pakistan. Trans R Soc Trop Med Hyg. 93: 641–643.

Wernsdorfer WH (1988) Principles and prac- tice of malariology. Churchill Livingstone, London.

Zakeri S, Barjesteh H, Djadid N (2006) Mero- zoite surface protein-3Q is a reliable marker for population genetic of Plasmodium vivax. Malaria J. 5: 53–58.

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Keywords
P.vivax relapse re-infection recrudescence pvMSP1 Iran

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How to Cite
1.
Nateghpour M, Ayazian Mavi S, Keshavarz H, Rezaei S, Abedi F, Edrissian G, Raeisi R. Molecular Monitoring of Plasmodium vivax Infection after Radical Treatment in Southeastern Iran. J Arthropod Borne Dis. 1;4(1):24-30.