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Featured researches published by James A. Comer.


Clinical Infectious Diseases | 2004

Rickettsia parkeri: A Newly Recognized Cause of Spotted Fever Rickettsiosis in the United States

Christopher D. Paddock; John W. Sumner; James A. Comer; Sherif R. Zaki; Cynthia S. Goldsmith; Jerome Goddard; Susan L. F. McLellan; Cynthia L. Tamminga; Christopher A. Ohl

Ticks, including many that bite humans, are hosts to several obligate intracellular bacteria in the spotted fever group (SFG) of the genus Rickettsia. Only Rickettsia rickettsii, the agent of Rocky Mountain spotted fever, has been definitively associated with disease in humans in the United States. Herein we describe disease in a human caused by Rickettsia parkeri, an SFG rickettsia first identified >60 years ago in Gulf Coast ticks (Amblyomma maculatum) collected from the southern United States. Confirmation of the infection was accomplished using serological testing, immunohistochemical staining, cell culture isolation, and molecular methods. Application of specific laboratory assays to clinical specimens obtained from patients with febrile, eschar-associated illnesses following a tick bite may identify additional cases of R. parkeri rickettsiosis and possibly other novel SFG rickettsioses in the United States.


PLOS Pathogens | 2009

Isolation of Genetically Diverse Marburg Viruses from Egyptian Fruit Bats

Jonathan S. Towner; Brian R. Amman; Tara K. Sealy; Serena A. Carroll; James A. Comer; Alan Kemp; Robert Swanepoel; Christopher D. Paddock; Stephen Balinandi; Marina L. Khristova; Pierre Formenty; César G. Albariño; David Miller; Zachary Reed; John Kayiwa; James N. Mills; Deborah Cannon; Patricia W. Greer; Emmanuel Byaruhanga; Eileen C. Farnon; Patrick Atimnedi; Samuel Okware; Edward Katongole-Mbidde; Robert Downing; Jordan W. Tappero; Sherif R. Zaki; Thomas G. Ksiazek; Stuart T. Nichol; Pierre E. Rollin

In July and September 2007, miners working in Kitaka Cave, Uganda, were diagnosed with Marburg hemorrhagic fever. The likely source of infection in the cave was Egyptian fruit bats (Rousettus aegyptiacus) based on detection of Marburg virus RNA in 31/611 (5.1%) bats, virus-specific antibody in bat sera, and isolation of genetically diverse virus from bat tissues. The virus isolates were collected nine months apart, demonstrating long-term virus circulation. The bat colony was estimated to be over 100,000 animals using mark and re-capture methods, predicting the presence of over 5,000 virus-infected bats. The genetically diverse virus genome sequences from bats and miners closely matched. These data indicate common Egyptian fruit bats can represent a major natural reservoir and source of Marburg virus with potential for spillover into humans.


Emerging Infectious Diseases | 2006

Nipah Virus-associated Encephalitis Outbreak, Siliguri, India

Mandeep S. Chadha; James A. Comer; Luis Lowe; Paul A. Rota; Pierre E. Rollin; William J. Bellini; Thomas G. Ksiazek; Akhilesh C. Mishra

Nipah virus, not previously detected in India, caused an outbreak of febrile encephalitis in West Bengal.


Emerging Infectious Diseases | 2007

Person-to-person transmission of Nipah virus in a Bangladeshi community.

Joel M. Montgomery; M. Jahangir Hossain; Michael Bell; Abul K. Azad; Mohammed Rafiqul Islam; Mohammed Abdur Rahim Molla; Darin S. Carroll; Thomas G. Ksiazek; Paul A. Rota; Luis Lowe; James A. Comer; Pierre E. Rollin; Markus Czub; Allen Grolla; Heinz Feldmann; Stephen P. Luby; Jennifer L. Woodward; Robert F. Breiman

Transmission of this virus highlights the need for infection control strategies for resource-poor settings.


Emerging Infectious Diseases | 2006

Foodborne Transmission of Nipah Virus, Bangladesh

Stephen P. Luby; Mahmudur Rahman; M. Jahangir Hossain; Lauren S. Blum; M. Mushtaq Husain; Rasheda Khan; Be-Nazir Ahmed; Shafiqur Rahman; Nazmun Nahar; Eben Kenah; James A. Comer; Thomas G. Ksiazek

TOC summary line: Nipah virus was likely transmitted from fruit bats to humans by drinking fresh date palm sap.


Emerging Infectious Diseases | 2004

Crimean-Congo hemorrhagic fever in Turkey.

S. Sami Karti; Zekaver Odabasi; Volkan Korten; Mustafa Yilmaz; Mehmet Sonmez; Rahmet Caylan; Elif Akdogan; Necmi Eren; Iftihar Koksal; Ercument Ovali; Bobbie R. Erickson; Martin J. Vincent; Stuart T. Nichol; James A. Comer; Pierre E. Rollin; Thomas G. Ksiazek

Nineteen cases of suspected Crimean-Congo hemorrhagic fever reported from Turkey.


Emerging Infectious Diseases | 2009

Recurrent Zoonotic Transmission of Nipah Virus into Humans, Bangladesh, 2001-2007

Stephen P. Luby; M. Jahangir Hossain; Be-Nazir Ahmed; Shakila Banu; Salah Uddin Khan; Nusrat Homaira; Paul A. Rota; Pierre E. Rollin; James A. Comer; Eben Kenah; Thomas G. Ksiazek; Mahmudur Rahman

More than half of identified cases result from person-to-person transmission.


Journal of Virology | 2006

Marburgvirus Genomics and Association with a Large Hemorrhagic Fever Outbreak in Angola

Jonathan S. Towner; Marina L. Khristova; Tara K. Sealy; Martin J. Vincent; Bobbie R. Erickson; Darcy A. Bawiec; Amy L. Hartman; James A. Comer; Sherif R. Zaki; Ute Ströher; Filomena Gomes da Silva; Fernando del Castillo; Pierre E. Rollin; Thomas G. Ksiazek; Stuart T. Nichol

ABSTRACT In March 2005, the Centers for Disease Control and Prevention (CDC) investigated a large hemorrhagic fever (HF) outbreak in Uige Province in northern Angola, West Africa. In total, 15 initial specimens were sent to CDC, Atlanta, Ga., for testing for viruses associated with viral HFs known to be present in West Africa, including ebolavirus. Marburgvirus was also included despite the fact that the origins of all earlier outbreaks were linked directly to East Africa. Surprisingly, marburgvirus was confirmed (12 of 15 specimens) as the cause of the outbreak. The outbreak likely began in October 2004 and ended in July 2005, and it included 252 cases and 227 (90%) fatalities (report from the Ministry of Health, Republic of Angola, 2005), making it the largest Marburg HF outbreak on record. A real-time quantitative reverse transcription-PCR assay utilized and adapted during the outbreak proved to be highly sensitive and sufficiently robust for field use. Partial marburgvirus RNA sequence analysis revealed up to 21% nucleotide divergence among the previously characterized East African strains, with the most distinct being Ravn from Kenya (1987). The Angolan strain was less different (∼7%) from the main group of East African marburgviruses than one might expect given the large geographic separation. To more precisely analyze the virus genetic differences between outbreaks and among viruses within the Angola outbreak itself, a total of 16 complete virus genomes were determined, including those of the virus isolates Ravn (Kenya, 1987) and 05DRC, 07DRC, and 09DRC (Democratic Republic of Congo, 1998) and the reference Angolan virus isolate (Ang1379v). In addition, complete genome sequences were obtained from RNAs extracted from 10 clinical specimens reflecting various stages of the disease and locations within the Angolan outbreak. While the marburgviruses exhibit high overall genetic diversity (up to 22%), only 6.8% nucleotide difference was found between the West African Angolan viruses and the majority of East African viruses, suggesting that the virus reservoir species in these regions are not substantially distinct. Remarkably few nucleotide differences were found among the Angolan clinical specimens (0 to 0.07%), consistent with an outbreak scenario in which a single (or rare) introduction of virus from the reservoir species into the human population was followed by person-to-person transmission with little accumulation of mutations. This is in contrast to the 1998 to 2000 marburgvirus outbreak, where evidence of several virus genetic lineages (with up to 21% divergence) and multiple virus introductions into the human population was found.


PLOS Pathogens | 2008

Chapare virus, a newly discovered arenavirus isolated from a fatal hemorrhagic fever case in Bolivia.

Simon Delgado; Bobbie R. Erickson; Roberto Agudo; Patrick J. Blair; Efrain Vallejo; César G. Albariño; Jorge Vargas; James A. Comer; Pierre E. Rollin; Thomas G. Ksiazek; James G. Olson; Stuart T. Nichol

A small focus of hemorrhagic fever (HF) cases occurred near Cochabamba, Bolivia, in December 2003 and January 2004. Specimens were available from only one fatal case, which had a clinical course that included fever, headache, arthralgia, myalgia, and vomiting with subsequent deterioration and multiple hemorrhagic signs. A non-cytopathic virus was isolated from two of the patient serum samples, and identified as an arenavirus by IFA staining with a rabbit polyvalent antiserum raised against South American arenaviruses known to be associated with HF (Guanarito, Machupo, and Sabiá). RT-PCR analysis and subsequent analysis of the complete virus S and L RNA segment sequences identified the virus as a member of the New World Clade B arenaviruses, which includes all the pathogenic South American arenaviruses. The virus was shown to be most closely related to Sabiá virus, but with 26% and 30% nucleotide difference in the S and L segments, and 26%, 28%, 15% and 22% amino acid differences for the L, Z, N, and GP proteins, respectively, indicating the virus represents a newly discovered arenavirus, for which we propose the name Chapare virus. In conclusion, two different arenaviruses, Machupo and Chapare, can be associated with severe HF cases in Bolivia.


Emerging Infectious Diseases | 2005

Genetic Characterization of Nipah Virus, Bangladesh, 2004

Brian H. Harcourt; Luis Lowe; Azaibi Tamin; Xin Liu; Bettina Bankamp; Nadine Bowden; Pierre E. Rollin; James A. Comer; Thomas G. Ksiazek; Mohammed Jahangir Hossain; Robert F. Breiman; William J. Bellini; Paul A. Rota

Until 2004, identification of Nipah virus (NV)-like outbreaks in Bangladesh was based on serology. We describe the genetic characterization of a new strain of NV isolated during outbreaks in Bangladesh (NV-B) in 2004, which confirms that NV was the etiologic agent responsible for these outbreaks.

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Pierre E. Rollin

Centers for Disease Control and Prevention

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Thomas G. Ksiazek

National Institutes of Health

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Stuart T. Nichol

Centers for Disease Control and Prevention

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Christopher D. Paddock

Centers for Disease Control and Prevention

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Paul A. Rota

Centers for Disease Control and Prevention

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Sherif R. Zaki

Centers for Disease Control and Prevention

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Bobbie R. Erickson

Centers for Disease Control and Prevention

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Cynthia S. Goldsmith

Centers for Disease Control and Prevention

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