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Dive into the research topics where Michael Y. Kosoy is active.

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Featured researches published by Michael Y. Kosoy.


The Journal of Infectious Diseases | 2000

Prevalence of Antibody to Hepatitis E Virus among Rodents in the United States

Michael O. Favorov; Michael Y. Kosoy; Sergei A. Tsarev; James E. Childs; Harold S. Margolis

The recent identification of antibody to hepatitis E virus (HEV) in pigs, sheep, and cattle and characterization of an HEV isolated from domestic pigs suggest animal reservoirs for this virus. To investigate whether rodents might be a natural reservoir of HEV, the prevalence of anti-HEV was determined among a variety of species throughout the United States. Serum samples were obtained from 806 rodents of 26 species in 15 genera. Anti-HEV prevalence was assessed by 2 EIAs (mosaic protein- and 55-kDa protein-based), which gave concordant results. The highest prevalence of antibody was found in the genus Rattus (59.7%; 166/278). Overall, rodents from urban habitats had a significantly higher prevalence of anti-HEV than did animals captured from rural areas. A high prevalence of anti-HEV was found in animals captured on mainland versus barrier islands. The results from this study provide convincing evidence of widespread HEV or HEV-like infection in rodents of the United States.


Journal of Clinical Microbiology | 2003

Bartonella Strains from Ground Squirrels Are Identical to Bartonella washoensis Isolated from a Human Patient

Michael Y. Kosoy; Mike Murray; Robert D. Gilmore; Ying Bai; Kenneth L. Gage

ABSTRACT The most likely animal source of a human case of cardiac disease in Washoe County, Nev., was identified by comparison of DNA sequences of three genes (citrate synthase gltA, 60-kDa heat shock protein gene groEL, and 16S rRNA gene) of Bartonella washoensis cultured from the human patient in question and of Bartonella isolates obtained from the following Nevada rodents: Peromyscus maniculatus (17 isolates), Tamias minimus (11 isolates), Spermophilus lateralis (3 isolates), and Spermophilus beecheyi (7 isolates). Sequence analyses of gltA amplicons obtained from Bartonella from the rodents demonstrated considerable heterogeneity and resulted in the identification of 16 genetic variants that were clustered within three groups in phylogenetic analysis. Each of the three groups was associated with a rodent genus, Peromyscus, Tamias, or Spermophilus. The gltA, 16S rRNA gene, and groEL sequences of a Bartonella isolate obtained from a California ground squirrel (S. beecheyi) were completely identical to homologous sequences of B. washoensis, strongly suggesting that these animals were the source of infection in the human case.


Journal of Clinical Microbiology | 2008

Bartonella tamiae sp. nov., a Newly Recognized Pathogen Isolated from Three Human Patients from Thailand

Michael Y. Kosoy; Christina Morway; Kelly Sheff; Ying Bai; James Colborn; Linda Chalcraft; Scott F. Dowell; Leonard F. Peruski; Susan A. Maloney; Henry C. Baggett; Saithip Sutthirattana; Anussorn Sidhirat; Soichi Maruyama; Hidenori Kabeya; Bruno B. Chomel; Rickie W. Kasten; Vsevolod L. Popov; Jennilee Robinson; Alexander Kruglov; Lyle R. Petersen

ABSTRACT Three strains of a novel Bartonella species (Bartonella tamiae) were isolated from human patients from Thailand. Sequence analysis of six chromosomal regions (16S rRNA, gltA, groEL, ftsZ, rpoB, and the intergenic spacer region) and phenotypical analysis supported the similarity of the three strains and placed them within the genus Bartonella separately from previously described species.


Journal of Mammalogy | 2001

INFLUENCES OF INTRODUCED PLAGUE ON NORTH AMERICAN MAMMALS: IMPLICATIONS FROM ECOLOGY OF PLAGUE IN ASIA

Dean E. Biggins; Michael Y. Kosoy

Abstract Intercontinental movements of invasive species continue to modify the worlds ecosystems. The plague bacterium (Yersinia pestis) has colonized and altered animal communities worldwide but has received much more attention as a human pathogen. We reviewed studies on the ecology of Y. pestis in ancient foci of central Asia and in western North America, where the bacterium apparently has become established much more recently. Although rodent populations on both continents are affected dramatically by epizootics of plague, the epidemiologically important species of Asia demonstrate resistance in portions of their populations, whereas those of North America are highly susceptible. Individual variation in resistance, which is widespread in Asian rodents and allows a microevolutionary response, has been documented in few North American species of rodents. Plague increases costs of sociality and coloniality in susceptible hosts, increases benefits of disease resistance in general, and increases benefits of adaptability to variable environments for species at higher trophic levels. Prairie dogs (Cynomys) epitomize taxa with high risk to plague because prairie dogs have uniformly low resistance to plague and are highly social. Relationships to plague are poorly understood for many North American rodents, but more than one-half of the species of conservation concern occur within the geographic range of plague.


Emerging Infectious Diseases | 2009

Bartonella quintana in body lice and head lice from homeless persons, San Francisco, California, USA.

Denise L. Bonilla; Hidenori Kabeya; Jennifer Henn; Vicki L. Kramer; Michael Y. Kosoy

Persons with lice may be at increased risk for infection with this bacterium.


Journal of Medical Entomology | 2003

Detection of Novel Bartonella Strains and Yersinia pestis in Prairie Dogs and Their Fleas (Siphonaptera: Ceratophyllidae and Pulicidae) Using Multiplex Polymerase Chain Reaction

Heather L. Stevenson; Ying Bai; Michael Y. Kosoy; John A. Montenieri; Jennifer L. Lowell; May C. Chu; Kenneth L. Gage

Abstract We developed a multiplex polymerase chain reaction (PCR) assay that simultaneously detects three types of flea-associated microorganisms. Targets for the assay were sequences encoding portions of the gltA, a 17-kDa antigen, and pla genes of Bartonella spp. Strong et al., Rickettsia spp. da Rocha-Lima, and Yersinia pestis Yersin, respectively. A total of 260 flea samples containing bloodmeal remnants were analyzed from fleas collected from abandoned prairie dog (Cynomys ludovicianus) burrows at the site of an active plague epizootic in Jefferson County, CO. Results indicated that 34 (13.1%) fleas were positive for Bartonella spp., 0 (0%) were positive for Rickettsia spp., and 120 (46.2%) were positive for Y. pestis. Twenty-three (8.8%) of these fleas were coinfected with Bartonella spp. and Y. pestis. A second group of 295 bloodmeal-containing fleas was collected and analyzed from abandoned burrows in Logan County, CO, where a prairie dog die-off had occurred 2–4 mo before the time of sampling. Of these 295 fleas, 7 (2.4%) were positive for Bartonella spp., 0 (0%) were positive for Rickettsia spp., and 46 (15.6%) were positive for Y. pestis. Coinfections were not observed in fleas from the Logan County epizootic site. The multiplex PCR also was used to identify Y. pestis and Bartonella in prairie dog blood and tissues. This report represents the first identification of Bartonella from prairie dogs and their fleas. Prairie dog fleas were tested with PCR, and the Bartonella PCR amplicons produced were sequenced and found to be closely related to similar sequences amplified from Bartonella that had been isolated from prairie dog blood samples. Phylogenetic analyses indicate that the sequences of bartonellae from prairie dogs and prairie dog fleas cluster tightly within a clade that is distinct from those containing other known Bartonella genotypes.


American Journal of Tropical Medicine and Hygiene | 2010

Identification of Bartonella Infections in Febrile Human Patients from Thailand and Their Potential Animal Reservoirs

Michael Y. Kosoy; Ying Bai; Kelly Sheff; Christina Morway; Henry C. Baggett; Susan A. Maloney; Sumalee Boonmar; Saithip Bhengsri; Scott F. Dowell; Anussorn Sitdhirasdr; Kriangkrai Lerdthusnee; Jason H. Richardson; Leonard F. Peruski

To determine the role of Bartonella species as causes of acute febrile illness in humans from Thailand, we used a novel strategy of co-cultivation of blood with eukaryotic cells and subsequent phylogenetic analysis of Bartonella-specific DNA products. Bartonella species were identified in 14 blood clots from febrile patients. Sequence analysis showed that more than one-half of the genotypes identified in human patients were similar or identical to homologous sequences identified in rodents from Asia and were closely related to B. elizabethae, B. rattimassiliensis, and B. tribocorum. The remaining genotypes belonged to B. henselae, B. vinsonii, and B. tamiae. Among the positive febrile patients, animal exposure was common: 36% reported owning either dogs or cats and 71% reported rat exposure during the 2 weeks before illness onset. The findings suggest that rodents are likely reservoirs for a substantial portion of cases of human Bartonella infections in Thailand.


Emerging Infectious Diseases | 2010

Bartonella spp. in Bats, Kenya

Michael Y. Kosoy; Ying Bai; Tarah Lynch; Ivan V. Kuzmin; Michael Niezgoda; Richard Franka; Bernard Agwanda; Robert F. Breiman; Charles E. Rupprecht

We report the presence and diversity of Bartonella spp. in bats of 13 insectivorous and frugivorous species collected from various locations across Kenya. Bartonella isolates were obtained from 23 Eidolon helvum, 22 Rousettus aegyptiacus, 4 Coleura afra, 7 Triaenops persicus, 1 Hipposideros commersoni, and 49 Miniopterus spp. bats. Sequence analysis of the citrate synthase gene from the obtained isolates showed a wide assortment of Bartonella strains. Phylogenetically, isolates clustered in specific host bat species. All isolates from R. aegyptiacus, C. afra, and T. persicus bats clustered in separate monophyletic groups. In contrast, E. helvum and Miniopterus spp. bats harbored strains that clustered in several groups. Further investigation is needed to determine whether these agents are responsible for human illnesses in the region.


Journal of Wildlife Diseases | 1998

ISOLATION OF BARTONELLA SPP. FROM EMBRYOS AND NEONATES OF NATURALLY INFECTED RODENTS

Michael Y. Kosoy; Russell L. Regnery; Olga I. Kosaya; Dana Jones; Eric L. Marston; James E. Childs

Embryos and neonatal offspring of wild-captured cotton rats (Sigmodon hispidus) and white-footed mice (Peromyscus leucopus) were tested for the presence of Bartonella spp. Isolates of Bartonella spp. were obtained from 18 of 31 embryos and 7 of 19 neonates from bacteremic dams of the two species; no isolates were obtained from material from non-bacteremic dams. Sequence analysis demonstrated that the isolates from embryos and neonates matched the phylogenetic group of Bartonella spp. isolates obtained from the mother. No antibodies to homologous Bartonella spp. antigens were detected in maternal and neonatal blood or embryonic tissue. These findings suggest the possibility of vertical transmission of Bartonella spp. among natural rodent hosts.


Proceedings of the National Academy of Sciences of the United States of America | 2014

Declines in large wildlife increase landscape-level prevalence of rodent-borne disease in Africa

Hillary S. Young; Rodolfo Dirzo; Kristofer M. Helgen; Douglas J. McCauley; Sarah A. Billeter; Michael Y. Kosoy; Lynn M. Osikowicz; Daniel J. Salkeld; Truman P. Young; Katharina Dittmar

Significance Understanding the effects of biodiversity loss on zoonotic disease is of pressing importance to both conservation science and public health. This paper provides experimental evidence of increased landscape-level disease risk following declines in large wildlife, using the case study of the rodent-borne zoonosis, bartonellosis, in East Africa. This pattern is driven not by changes in community composition or diversity of hosts, as frequently proposed in other systems, but by increases in abundance of susceptible hosts following large mammal declines. Given that rodent increases following large wildlife declines appear to be a widespread pattern, we suggest this relationship is likely to be general. Populations of large wildlife are declining on local and global scales. The impacts of this pulse of size-selective defaunation include cascading changes to smaller animals, particularly rodents, and alteration of many ecosystem processes and services, potentially involving changes to prevalence and transmission of zoonotic disease. Understanding linkages between biodiversity loss and zoonotic disease is important for both public health and nature conservation programs, and has been a source of much recent scientific debate. In the case of rodent-borne zoonoses, there is strong conceptual support, but limited empirical evidence, for the hypothesis that defaunation, the loss of large wildlife, increases zoonotic disease risk by directly or indirectly releasing controls on rodent density. We tested this hypothesis by experimentally excluding large wildlife from a savanna ecosystem in East Africa, and examining changes in prevalence and abundance of Bartonella spp. infection in rodents and their flea vectors. We found no effect of wildlife removal on per capita prevalence of Bartonella infection in either rodents or fleas. However, because rodent and, consequently, flea abundance doubled following experimental defaunation, the density of infected hosts and infected fleas was roughly twofold higher in sites where large wildlife was absent. Thus, defaunation represents an elevated risk in Bartonella transmission to humans (bartonellosis). Our results (i) provide experimental evidence of large wildlife defaunation increasing landscape-level disease prevalence, (ii) highlight the importance of susceptible host regulation pathways and host/vector density responses in biodiversity–disease relationships, and (iii) suggest that rodent-borne disease responses to large wildlife loss may represent an important context where this relationship is largely negative.

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Ying Bai

Centers for Disease Control and Prevention

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Lynn M. Osikowicz

Centers for Disease Control and Prevention

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Kenneth L. Gage

Centers for Disease Control and Prevention

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Sarah A. Billeter

Centers for Disease Control and Prevention

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Leonard F. Peruski

Centers for Disease Control and Prevention

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Henry C. Baggett

Centers for Disease Control and Prevention

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