As the pathologist for the NHDP, my office receives biopsy referrals from any physicians in the United States and its territories for the histopathological diagnosis of leprosy. We also collaborate with other investigators at the NHDP on the histopathological evaluation of tissues from studies in experimental animals.
One area of current research interest is the study of mechanisms of nerve injury in leprosy. We have demonstrated that the experimentally infected armadillo is a unique model of human lepromatous neuritis, and are working to dissect the pathogenesis of nerve injury using ultrastructural and immuno-histochemical techniques in this model. In collaboration with other NHDP investigators, we are also interested in using molecular techniques to study the expression of cytokine genes and other immunological markers in this model. Early findings in this model have suggested that M. leprae may localize to the surface of nerves very early in the course of the infection, and from this location may gain access to the endoneurial compartment via its blood supply. We have proposed that communication between Schwann cells and endothelial cells is responsible for the selective localization of M. leprae to peripheral nerve. We are therefore also working to model the interaction of M. leprae, and M. leprae–infected macrophages, with endothelial monolayers and Schwann cells in vitro, to better understand the mechanisms involved.
A second area of research concerns the mechanisms of reactional states in leprosy. These are immunologically-based phenomena during which patients are acutely ill and may experience marked exacerbation of injury to nerves and other organs. The mechanisms underlying these reactions are poorly understood, and the factors that precipitate them are unknown. We are coordinating a multi-center, prospective clinical study, with field sites in Brazil, Nepal and the Republic of the Philippines, which seeks to determine whether hormonal changes may be a factor influencing the immunological responses of patients to precipitate either Type 1 or Type 2 leprosy reactions.
Scollard, D.M., McCormick, G. M., and Allen, J. Localization of Mycobacterium leprae to endothelial cells of epineurial and perineurial blood vessels and lymphatics. Amer. J. Path. 154: 1611-1620, 1999.
Scollard, D.M. Association of Mycobacterium leprae with human endothelial cells in vitro. Lab. Invest. 80: 663-669, 2000.
Scollard, D.M. Endotheial cells and the pathogenesis of lepromatous neuritis: Insights from the armadillo model. Microbes and Infect. 2: 1135-43, 2001.
Scollard, David M., and Joyce, M. Patricia. Leprosy (Hansen = s Disease). Conn = s Current Therapy, Rakel & Bope, eds, Elsevier Science (USA), 2003, p101-106.
Williams, D.L., Scollard, D.M., and Gillis, T.P. PCR-based diagnosis of leprosy in the United States . Clin. Microbiol. Newsletter 25: 57-61, 2003.
Scollard, D.M., Adams , L.B., Gillis, T.P., Krahenbuhl, J.L., Truman, R.T., and Williams, D.L. The Continuing Challenges of Leprosy. Clinical Microbiology Reviews, 19: 338-381, 2006.
Scollard, D.M., Joyce, M.P., and Gillis, T. P. Development of Leprosy and Type 1 Leprosy Reactions After Treatment with Infliximab: A report of two cases. Clinical Infectious Diseases 43: e19–22, 2006.
Pardillo, EF, Fajardo, TT, Abalos, RM, Gelber, RH, and Scollard, DM. Methods for the classification of Leprosy for Treatment Purposes. Clin Infect Dis. 2007;44:1096-9.
Hagge DA, Marks VT, Ray NA, Dietrich MA, Kearney MT, Scollard DM, Krahenbuhl, JL, Adams LB. Emergence of an effective adaptive cell mediated immune response to Mycobacterium leprae is not impaired in reactive oxygen intermediate-deficient mice. FEMS Immunol Med Microbiol. 2007;5:92-101.
Scollard, DM. The Biology of Nerve Injury in Leprosy: A review of the literature. Leprosy Review, 2008, 79: 242-253.
King K, Browning JC, Metry DW, Prestigiacomo J, Scollard D, Schutze GE, Stryjewska B, and Schwarzwald H. Leprosy and international adoption: a case report and review of diagnostic and treatment dilemmas. Pediatr Infect Dis J. 2009; 28: 322-5
Stefani, MM, Guerra, JG, Martelli, CT, Sousa, ALM, Costa, MB, Oliveira, MLW, and Scollard, DM. Potential Plasma Markers of Type 1 and Type 2 Leprosy Reactions: A Preliminary Report. BioMed Central Infectious Diseases, 2009; 9: 75.
Martinez AN, Lahiri R, Pittman TL, Scollard D, Truman R, Moraes MO, Williams DL., Molecular determination of Mycobacterium leprae viability by use of real-time PCR. J Clin Microbiol. 2009 Jul;47(7):2124-30.
Singh S, Fefer J, Sordillo EM, Wilentz S, Scollard D, Polsky B. Lepromatous Leprosy in a Previously Healthy Patient with Evidence of Concomitant Tuberculosis by Molecular Amplification Testing. Partners Infectious Diseases Images, http://www.idimages.org/, (Accepted, In process for web publication)
Scollard, DM, Stryjewska, MB, Prestigiacomo, JF, Gillis, TP, and Waguespack-LaBiche, J. Hansen’s Disease (Leprosy) complicated by secondary mycobacterial infection. J. Am Acad Dermatol. 2010 May 20. [Epub ahead of print].
Dacso, M, Jacobson, RR, Stryjewska, BM, Prestigiacomo, J, and Scollard, DM. Evaluation of Multi-Drug Therapy for Leprosy in the USA Using Daily Rifampin. Submitted for publication, 2010.
Greenstein, RJ, Gillis,T, Scollard, DM, and Brown, ST. Mycobacteria: Leprosy, a Battle Turned; Tuberculosis, a Battle Raging; Paratuberculosis, a Battle Ignored in Sequelae and Long-Term Consequences of Infectious Diseases; Edited by Pina M. Fratamico, James L. Smith, and Kim A. Brogden;© 2009 ASM Press, Washington, DC.
Frankel, R.I., and Scollard, D.M. Leprosy, in Philip Brachman and Elias Abrutyn, Eds. Bacterial Infections of Humans, 3rd Ed., Springer, 2009.