Faculty Profile

Viveka Vadyvaloo

Viveka Vadyvaloo

Associate Professor


Affiliated Organizations

  • American Society for Microbiology (member)
  • Center for Health in the Human Ecosytem, University of Idaho (member)

Phone: 509-335-6043



Dr Vadyvaloo was born and raised on the East coast of South Africa where the waters are warm due to the warm Mozambique current in the Indian ocean. She later obtained her PhD in Biochemistry from the University of Stellenbosch on the West coast of South Africa where the cold Benguela current waters are home to many great white sharks. She then moved to the US where she pursued further postdoctoral training.

Personal Statement

As far as a career in science goes I cannot say that there was one defining thing that inspired me to pursue this career path; perhaps during my formative years I just seemed to have an aptitude for science in comparison to my peers and then it just happened! I am not one to pursue hobbies but I do enjoy running to keep fit and de-stress, scratch cooking, and hiking when the opportunity presents itself. What else is in my life other than research? A big fluffy grey doodle-dog, of course!!

Education and Training

  • 2009-2010: Research Assistant Professor, Washington State University, Pullman WA
  • 2004-2008:Postdoctoral fellow, Rocky Mountain Laboratories, NIAID, NIH
  • 2003-2004:Postdoctoral Fellow, Howard Hughes Medical Institute at UCLA
  • 2003: University of Stellenbosch, South Africa
  • 2000: MS, Molecular Microbiology, University of Kwazulu-Natal, Pietermaritzburg
  • 1996: BS (Hons), Microbiology, University of Kwazulu-Natal, Pietermaritzburg
  • 1995: BS (Microbiology, Human Physiology), University of Kwazulu-Natal, Durban-Westville

General Research / Expertise

Dr Vadyvaloo does research on the flea-borne zoonotic disease, bubonic plague. This often fatal disease is well-known due to the devastating and widespread loss of human life, and its profound influence on the development of modern civilization, noted in the wake of three major plague pandemics: The 5-7th century Justinian plague, the 14th century Black Death and the Modern plague (spanning ~1860 – 1950).  Bubonic plague has however re-emerged as a public health problem since the 1990’s, and has been classified by the CDC as a re-emerging threat. Yersinia pestis is the bacterial etiological agent of the plague and it is primarily spread by flea-bite. Because Y. pestis is maintained in nature in plague sylvatic cycles by a plethora of rodent species and the fleas that parasitize them, the disease is difficult to eradicate. Sylvatic cycles are composed of an epizootic phase, which increases the risk of transmission and human disease, and an enzootic/quiescent stage in which, Yersinia pestis, persists and maintains its reservoir.  
The general mechanisms of how Y. pestis quiescently persists in nature are unknown. It is well understood that while the vertebrate host of Y. pestis is usually a dead end host for the pathogen where the bacteria are either eliminated by the immune system, or cause death to the host, some flea species have the ability to maintain a chronic infection of Y. pestis and have potential to serve as reservoir hosts for this pathogen. The overall research focus of the Vadyvaloo lab is to identify how the plague bacterium establishes infection in the flea to be subsequently transmitted and persist with this idea that fleas can serve as a reservoir host for the pathogen. Additionally we are in search of alternate natural long term reservoir hosts for this pathogen.

Research Contributions

1) Identifying the Y. pestis molecular determinants that direct its ability to adapt to, and chronically infect its flea vector has potential to inform targeted intervention of these processes. Towards this final outcome we have been involved in characterizing the whole genome bacterial gene expression profiles in the fleas and subsequently have described regulatory factors that shape adaptation of the bacterium to form a transmissible infection.

2) We have described that Y. pestis has the ability to enter and survive within a ubiquitous soil amoeba implicating amoeba as a reservoir host for the bacterium during the inter-epizootic periods. We envisage that the research work on understanding the Y. pestis-amoeba interaction has the potential to inform improved surveillance methods since current methods are unsuccessful at detecting Y. pestis in the environment during the quiescent period. The information has also the potential to predict outbreaks if any correlation can be drawn with amoeba abundance and epizootics in the environment. This is helpful to inform the public about which areas and seasonal periods present as a risk.

Research Details

Plague epizootics can be supported by a biofilm-mediated gut regurgitative transmission mechanism but the basis of the enzootic/quiescent stage is unknown.  Biofilm-mediated regurgitative transmission and persistence requires that the bacterium once acquired in an infected blood meal by the flea vector must adapt to this environment in order to form a transmissible and/or persistent infection. The Vadyvaloo lab is interested in understanding what the bacterial molecular mechanisms are that direct these processes especially as they relates to the multiple layers of gene regulation that must occur for physiological adaptation to life in the flea gut. To do this, research on identification and functional mechanistic understanding of bacterial gene regulation at both transcriptional (e.g. DNA binding transcriptional regulators) and post-transcriptional (e.g. small non-coding RNAs) levels is being undertaken using molecular biology techniques (e.g. mutant generation, qRT-PCR, RNAseq, Northern analysis, EMSA, transcriptional and post-transcriptional fusions).  A key element of this research is our rare ability and infrastructure to test our mutants in the natural and biologically relevant flea model.  We are currently one of a very few labs in the world that maintains flea vectors and performs research in these understudied aspects of plague - the Y. pestis insect specific life stage.

Newer reasearch in my lab focusses on undertanding how Y. pestis persists during the quiescent inter-epizootic cycle that is aimed at identifying potential alternate reservoir hosts for Y. pestis.  As an initial step in this research direction we have established that Y. pestis enters and is able to survive in association with a ubiquitous soil free-living amoeba. Continued work in this field is to establish the relevance of this model in a natural setting using creative modification to the traditional gentamicin protection assay to determine intracellular survival, and microscopic methods.



Select Publications
  • Benavides-Montaño JA, Vadyvaloo V. (2017) Yersinia pestis resists predation by Acanthamoeba castellanii and exhibits prolonged intracellular survival.  Applied Environmental Microbiology 83(13). pii: e00593-17. doi: 10.1128/AEM.00593-17. Print 2017 Jul 1. PMID: 28455335 PMCID: MC5478993
  • Vadyvaloo V and Hinz AK. (2015) A LysR-Type Transcriptional Regulator, RovM, Senses Nutritional Cues Suggesting that It Is Involved in Metabolic Adaptation of Yersinia pestis to the Flea Gut. PloS One. 10(9):e0137508. Doi: 10.1371/journal.pone.0137508 PMID: 26348850 PMCID: PMC4562620
  • Vadyvaloo V, Viall AK, Jarrett CO, Hinz AK, Sturdevant DE, Hinnebusch BJ. (2015) Role of the PhoP-PhoQ gene regulatory system in adaptation of Yersinia pestis to environmental stress in the flea digestive tract. Microbiology 161(6):1198-1210 PMID: 25804213 PMCID: PMC4635514
  • Rempe KA, Hinz AK, Vadyvaloo V. (2012) Hfq regulates biofilm gut blockage that facilitates flea-borne transmission of Yersinia pestis. J Bacteriol. 194(8):2036-40. PMID: 22328669 PMCID: PMC3318476
  • Vadyvaloo V, Jarrett C, Sturdevant DE, Sebbane F, Hinnebusch BJ. (2010) Transit through the flea vector induces a pretransmission innate immunity resistance phenotype in Yersinia pestis. PLoS Pathog 6(2):e1000783. PMID: 20195507 PMCID: PMC2829055

PubMed List of Publications