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Department of Microbiology, Biochemistry and Molecular Genetics

Nikhat Parveen, Ph.D., M.S., B.Sc


International Center for Public Health (ICPH)
225 Warren Street Room E350T

Phone: (973) 972-5218



Ph.D., 1995, University of Hawaii, Manoa, Honolulu
M.S., 1981, Punjab Agricultural University
B.Sc, 1978, University of Delhi






Relevant Publications:

Chan, K., Alter, L., Barthold, S. W., and N. Parveen. 2015. Disruption of bbe02 by insertion of a luciferase gene increases transformation efficiency of Borrelia burgdorferi and allows live imaging in Lyme disease susceptible C3H mice. PLoS ONE 10(6): e0129532. doi:10.1371/journal.pone.0129532.
Chan, K., Marras, S. A. E., and N. Parveen. 2013. Sensitive multiplex PCR assay to differentiate Lyme spirochetes and emerging pathogens Anaplasma phagocytophilum and Babesia microti. BioMed Central Microbiology. 13(1):295. (Highly Accessed)
Chan, K., Awan, M., Barthold, S. W., and N. Parveen. 2012. Comparative molecular analyses of Borrelia burgdorferi sensu stricto strains B31 and N40D10/E9 and determination of their pathogenicity. BioMed Central Microbiology. 12:157.
Chan K, Casjens S, and N. Parveen. 2012. Detection of established virulence genes and plasmids to differentiate Borrelia burgdorferi strains. Infection and Immunity. 80(4): 1519-29.
Parveen N. and Cornell K.A. 2011. Methylthioadenosine/S-adenosylhomocysteine nucleosidase, a critical enzyme for bacterial metabolism. Molecular Microbiology. 79(1):7-20.
Cornell KA, Primus S, Martinez JA, and N. Parveen. 2009. Assessment of methylthioadenosine/S-adenosylhomocysteine nucleosidases of Borrelia burgdorferi as targets for novel antimicrobials using a novel high-throughput method. J. Antimicrobial Chemotherapy. 63(6):1163-1172.
Saidac, D. S., Marras, S. A. E., and N. Parveen. 2009. Detection and quantification of Lyme spirochetes using sensitive and specific molecular beacon probes. BioMed Central Microbiology. 9:43-52.
Parveen, N., M. Caimano, J. D. Radolf, and J. M. Leong. 2003. Growth of the Lyme disease spirochete in the mammalian host results in enhanced glycosaminoglycan binding and increased surface expression of DbpA and DbpB. Molecular Microbiology 47(5): 1433-44.
Fischer, J.R. Parveen, N., Magoun, L., and J. M. Leong. 2003. Decorin-binding proteins A and B confer distinct mammalian cell type-specific attachment by Borrelia burgdorferi, the Lyme disease spirochete. Proc. Natl. Acad. Sci. U S A. 100(12): 7307-12.
Parveen, N., and J. M. Leong. 2000. Identification of a candidate glycosaminoglycan-binding adhesin of Lyme disease spirochete, Borrelia burgdorferi. Molecular Microbiology 35(5): 1220-34.


Courses Taught


TIII5021Q MolecPathogen of Bacteria

TIII5155Q Critical Readings in III:A

TIII5620Q Classic/21st Cent Pathogens

Current Research

Virulence Factors Of Pseudomonas Aeruginosa And Lyme Disease Spirochete, Borrelia Burgdorferi

My laboratory is studying the molecular basis of pathogenesis of bacterial species, Borrelia burgdorferi, Treponema pallidum and Pseudomonas aeruginosa. These clinically important bacterial pathogens are transmitted to humans using different mechanisms and also show different disease manifestations. B. burgdorferi is transmitted by Ixodes tick vector, T. pallidum by sexual contact and P. aeruginosa, a ubiquitously present organism, is transmitted through ventilation or by direct contact of the patient with the contaminated source.

B. burgdorferi, a spirochete, is causative agent of Lyme disease, a multisystemic illness that affects various organs including joints, heart, nervous system and skin. If untreated, parveen_figure2_2010.jpgit may result in chronic disease with the symptoms including arthritis, acrodermatitis or neuroborreliosis. It is an extracellular pathogen often found adhering to the host cells in the biopsy specimens of the patients. We have been studying the molecular mechanisms involved in the attachment of Lyme disease spirochetes to a variety of host cells. The specific interaction between the spirochete and host cells may be responsible for the tissue tropism exhibited by B. burgdorferi. Our objective is to understand whether different B.burgdorferi adhesins show affinity for different host receptors on various host cells. We use genetics, biochemical techniques and tissue culture system to identify and characterize the bacterial and host molecules involved in this interaction in vitro. We have already identified two types of glycosaminoglycan receptors on mammalian cells that are recognized by several B. burgdorferi proteins and we are further characterizing this interaction. Mouse is a natural host of B. burgdorferi and C3H mice show several manifestations of Lyme disease observed in humans. We have recently adapted firefly luciferase-based detection system for B. burgdorferi. Using a combination of bioluminescent B. burgdorferi and mouse model of infection, we will further analyze the contribution of each bacterial ligand-host receptor interaction in Lyme pathogenesis. Tissue colonization by the spirochetes will be monitored non-invasively by employing in vivo imaging system. Recently, we have initiated studies to understand molecular basis of T. pallidum pathogenesis using this as a surrogate system.

P. aeruginosa is an opportunistic pathogen and produces a wide variety of virulence factors. parveen_figure2010.jpgIt results in a variety of illnesses and is responsible for high morbidity and mortality in immunocompromised and elderly patients. Due to a highly adaptable nature of P. aeruginosa and its ability to survive even in detergents, it is a major contributor to infections in the hospital environment. We have been studying the quorum-sensing mediated induction of several virulence factors in this organism both as free-living organism and in association with its different hosts. We will assess the role of selected virulence factors in biofilm formation while P. aeruginosa is present in communities along with the other organisms. Our current focus is to investigate genetics of production and regulation of PrpL protease and pyocyanin pigment of P. aeruginosa and examine the roles of these virulence factors in tissue destruction. The roles of these two virulence factors in corneal damage, in burn wounds and in the cystic fibrosis patients will then be examined.



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