Sarah Talarico

National Center for HIV/AIDS Viral Hepatitis STD and TB Prevention

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Trends

Author Order

Document Type

Co-Authors

Nina R. Salama

Fred Hutch Cancer Center

Benjamin J. Silk

Centers for Disease Control and Prevention

Zhenhua Yang

University of Michigan–Ann Arbor

Carl F. Marrs

University of Michigan–Ann Arbor

Lixin Zhang

East China University of Science and Technology

Lauren S. Cowan

National Center for HIV/AIDS Viral Hepatitis STD and TB Prevention

M. Donald Cave

University of Arkansas for Medical Sciences

Kala M. Raz

Centers for Disease Control and Prevention

James E. Posey

National Center for HIV/AIDS Viral Hepatitis STD and TB Prevention

Betsy Foxman

University of Michigan–Ann Arbor

Cooperative Institutions

Centers for Disease Control and Prevention

130

National Center for Immunization and Respiratory Diseases

National Center for HIV/AIDS Viral Hepatitis STD and TB Prevention

Minnesota Department of Health

National Center for Emerging and Zoonotic Infectious Diseases

Epidemic Intelligence Service

University of Washington

Emory University

Computer Emergency Response Team

Government of the United States of America

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Field

Increased H. pylori stool shedding and EPIYA-D cagA alleles are associated with gastric cancer in an East Asian hospital

bioRxiv (Cold Spring Harbor Laboratory) (2018)

Sarah Talarico Christina K. Leverich Bing Wei Jie Ma Xinguang Cao

ABSTRACT Background Helicobacter pylori infection induces chronic inflammation and tissue damage in the stomach, increasing risk for gastric cancer. Paradoxically, these tissue alterations may promote loss of H. pylori infection during cancer progression. H. pylori ’s role in cancer progression beyond initiation is unclear. Geographic variation in gastric cancer risk has been attributed to variation in carriage and type of the H. pylori oncogene cagA. Methods To investigate possible differences in H. pylori load in the stomach and shedding in stool, H. pylori load and cagA genotype were assessed using droplet digital PCR assays on gastric mucosa and stool samples from 49 urea breath test-positive individuals, including 25 gastric cancer and 24 non-cancer subjects at Henan Cancer Hospital, Henan, China. Results Quantitation of H. pylori DNA indicated similar gastric loads among cancer and non-cancer cases, but the gastric cancer group had a median H. pylori load in the stool that was six times higher than that of the non-cancer subjects. While the cagA gene was uniformly present among study subjects, only 70% had the East Asian cagA allele, which was significantly associated with gastric cancer (Fisher’s Exact Test, p = 0.03). Conclusion H. pylori persists in a subset of gastric cancer cases and thus may contribute to cancer progression. In this East Asian population with a high prevalence of the cagA gene, the East Asian allele could still provide a marker for gastric cancer risk. Impact This study contributes to our understanding of H. pylori dynamics in the context of pathological changes.

CagA

Stomach cancer

10.1101/284448

Cite

Citations (1)

Genetic diversity of Mycobacterium tuberculosis PE_PGRS genes and its clinical and epidemiological relevance.

Sarah Talarico

Molecular Epidemiology

Genetic epidemiology

Relevance

Source

Cite

Citations (0)

M1098 Increased Rates of Peptic Ulcer Disease (PUD) and Helicobacter pylori (HP) Related Hospitalizations in U.S. Children: A 15 Year Analysis

Gastroenterology (2008)

Gayle D. Horvitz William S. McRae Sarah Talarico Tejas Mehta Nina R. Salama

Peptic

10.1016/s0016-5085(08)61574-7

Cite

Citations (0)

COVID-19 on the Nile: a cross-sectional investigation of COVID-19 among Nile River cruise travellers returning to the United States, February–March 2020

Journal of Travel Medicine (2022)

Sarah Anne J. Guagliardo Laura A.S. Quilter Anna Uehara Stefanie White Sarah Talarico

Abstract Background Early in the pandemic, cruise travel exacerbated the global spread of SARS-CoV-2. We report epidemiologic and molecular findings from an investigation of a cluster of travellers with confirmed COVID-19 returning to the USA from Nile River cruises in Egypt. Methods State health departments reported data on real-time reverse transcription-polymerase chain reaction-confirmed COVID-19 cases with a history of Nile River cruise travel during February–March 2020 to the Centers for Disease Control and Prevention (CDC). Demographic and epidemiologic data were collected through routine surveillance channels. Sequences were obtained either from state health departments or from the Global Initiative on Sharing Avian Flu Data (GISAID). We conducted descriptive analyses of epidemiologic data and explored phylogenetic relationships between sequences. Results We identified 149 Nile River cruise travellers with confirmed COVID-19 who returned to 67 different US counties in 27 states: among those with complete data, 4.7% (6/128) died and 28.1% (38/135) were hospitalized. These individuals travelled on 20 different Nile River cruise voyages (12 unique vessels). Fifteen community transmission events were identified in four states, with 73.3% (11/15) of these occurring in Wisconsin (as the result of a more detailed contact investigation in that state). Phylogenetic analyses supported the hypothesis that travellers were most likely infected in Egypt, with most sequences in Nextstrain clade 20A 93% (87/94). We observed genetic clustering by Nile River cruise voyage and vessel. Conclusions Nile River cruise travellers with COVID-19 introduced SARS-CoV-2 over a very large geographic range, facilitating transmission across the USA early in the pandemic. Travellers who participate in cruises, even on small river vessels as investigated in this study, are at increased risk of SARS-CoV-2 exposure. Therefore, history of river cruise travel should be considered in contact tracing and outbreak investigations.

Pandemic

10.1093/jtm/taac153

Cite

Citations (1)

O323 Execution of macrophage apoptosis by PE_PGRS33 of Mycobacterium tuberculosis

International Journal of Antimicrobial Agents (2007)

Sudarshana Basu Suschil Pathak A. Banerjee Shresh Pathak Asima Bhattacharyya

10.1016/s0924-8579(07)70213-3

Cite

Citations (0)

Molecular surveillance for large outbreaks of tuberculosis in the United States, 2014–2018

Tuberculosis (2022)

Kala M. Raz Sarah Talarico Sandy Althomsons J. Steve Kammerer Lauren S. Cowan

10.1016/j.tube.2022.102232

Cite

Citations (2)

Mycobacterium tuberculosis PE_PGRS16 and PE_PGRS26 genetic polymorphism among clinical isolates

Tuberculosis (2008)

Sarah Talarico Lixin Zhang Carl F. Marrs Betsy Foxman M. Donald Cave

10.1016/j.tube.2008.01.001

Cite

Citations (42)

Evaluation of Sputum-Culture Results for Tuberculosis Patients in the United States-Affiliated Pacific Islands

Asia Pacific Journal of Public Health (2021)

Smita Ghosh Derrick Felix J. Steve Kammerer Sarah Talarico Richard Brostrom

Sputum-culture confirmation guides tuberculosis (TB) diagnosis and patient management but has previously been reported to be low in the US-Affiliated Pacific Islands (USAPI). We evaluated factors associated with positive sputum-culture results by analyzing TB case surveillance and laboratory data, including sputa quality and quantity for diagnostic specimens from the USAPI. A lower proportion of sputum specimens were reported as culture positive from the USAPI (42%), compared with Hawaii (58%) and the United States (55%). Few (3%) sputa collected from TB patients in the USAPI had both optimal quality and quantity; 40% had optimal quality (mucoid), and 7% had optimal quantity (>5 mL). Suboptimal sputum specimen quality and quantity contributed to fewer sputum-culture positive results in the USAPI. Improving sputum collection and handling might lead to more culture positive results and ultimately improve patient care and TB control in USAPI.

Sputum culture

10.1177/10105395211060119

Cite

Citations (3)

Execution of Macrophage Apoptosis by PE_PGRS33 of Mycobacterium tuberculosis Is Mediated by Toll-like Receptor 2-dependent Release of Tumor Necrosis Factor-α

Journal of Biological Chemistry (2006)

Sanchita Basu Sushil Kumar Pathak Anirban Banerjee Shresh Pathak Asima Bhattacharyya

Combating tuberculosis requires a detailed understanding of how mycobacterial effectors modulate the host immune response. The role of the multigene PE family of proteins unique to mycobacteria in the pathogenesis of tuberculosis is still poorly understood, although certain PE_PGRS genes have been linked to virulence. Tumor necrosis factor-alpha (TNF-alpha) is essential for successfully combating tuberculosis. In this study we provide evidence that PE_PGRS33, a surface exposed protein, elicits TNF-alpha release from macrophages in a TLR2 (Toll-like receptor 2)-dependent manner. ASK1 (apoptosis signal-regulating kinase 1) is activated downstream of TLR2. ASK1 activates the MAPKs p38 and JNK. PE_PGRS33-induced signaling leads to enhanced expression of TNF-alpha and TNF receptor I (TNFRI) genes. Mycobacterium smegmatis expressing PE_ PGRS33 elicits the same effects as purified PE_PGRS33. TNF-alpha release occurs even when internalization of the bacteria is blocked by cytochalasin D, suggesting that interaction of PE_ PGRS33 with TLR2 is sufficient to trigger the effects described. Release of TNF-alpha plays the determining role in triggering apoptosis in macrophages challenged with PE_PGRS33. The death receptor-dependent signals are amplified through classical caspase 8-dependent mitochondrial release of cytochrome c, leading to the activation of caspases 9 and 3. An important aspect of our findings is that deletions within the PGRS domain (simulating those occurring in clinical strains) attenuate the TNF-alpha-inducing ability of PE_PGRS33. These results provide the first evidence that variations in the polymorphic repeats of the PGRS domain modulate the innate immune response.

10.1074/jbc.m604379200

Cite

Citations (201)

Does the lipR gene of tubercle bacilli have a role in tuberculosis transmission and pathogenesis?

Tuberculosis (2008)

Katherine D. Sheline A. M. France Sarah Talarico Betsy Foxman Lixin Zhang

Pathogenesis

10.1016/j.tube.2008.09.004

Cite

Citations (11)