Over twenty years, Dr. Lehmann has studied the population genetics, ecology, and behavior of the African malaria mosquito, Anopheles gambiae, and its relationship to disease transmission and control. As a postdoc, under Frank Collins at CDC, he studied patterns of gene flow among populations of this species and the degree of isolation between sibling species on the genetic level. This led to studies on the behavioral and ecological mechanisms that promote reproductive isolation (speciation) between diverging populations. In addition, he was tempted again and again to study the factors and processes that determine susceptibility of mosquitoes to pathogen. Over the past ten years, his obsession has been to resolve the “dry season malaria paradox” and uncover how mosquitoes persist through the long dry season without available surface water as larval sites. Studies he has led have produced compelling evidence for aestivation (summer dormancy) and long-distance migration in the persistence of vectors and malaria in dry areas. Before joining NIH, Dr. Lehmann studied the molecular epidemiology of toxoplasmosis, the behavior of the parasitic nematodes in the body of their blackfly host, and the population biology of ectoparasites on rodent hosts.
As part of the Mosquito Ecology research program, we explore broad population biology questions relevant to patterns of malaria transmission and vector control. We are studying the ecology of mosquitoes, addressing questions relevant to patterns of malaria transmission and vector control. Together with colleagues in Mali and elsewhere, we investigate the role of dormancy and long-range migration in the persistence of mosquitoes and malaria in seasonally arid areas, the processes affecting spread of genes within and between populations, and vector-parasite interactions at the population level. The nature of these topics within the One Health paradigm demands novel and creative approaches to answer stubborn old questions and identify new ones. Thus, we combine ecological, behavioral, physiological, genetic, and molecular analyses grounded in field studies to improve understanding of phenotypic diversity in vectors and its epidemiological consequences. The research group is nested in the Malaria Culture and Insectary Unit/Office of the Chief, LMVR, under Dr. Thomas Wellems.
Dr. Adama Dao (MRTC, Mali), Dr. Alpha S. Yaro (MRTC, Mali), Dr. Roy Faiman (LMVR), Dr. Ben Krajacich (LMVR), Mr. Moussa Diallo (MRTC, Mali), Mrs. Margie Sullivan, Mr. Zana L. Sanogo (MRTC, Mali), Dr. Djibril Samake (MRTC, Mali)
Huestis DL, Dao A, Diallo M, Sanogo ZL, Samake D, Yaro AS, Ousman Y, Linton Y-M, Krishna A, Veru L, Krajacich BJ, Faiman R, Florio J, Chapman JW, Reynolds DR, Weetman D, Mitchell R, Donnelly MJ, Talamas E, Chamorro L, Strobach E and Lehmann T. Windborne long-distance migration of malaria mosquitoes in the Sahel. Nature: In Press.
Dharmarajan G, Walker KD, Lehmann T. Variation in tolerance to parasites affects vectorial capacity of natural Asian tiger mosquito populations. Current Biology: In Press.
Faiman R, Dao A, Yaro AS, Diallo M, Djibril S, Sanogo ZL, Ousmane Y, Sullivan M, Veru L, Krajacic BJ, Krishna A, Matthews J, France CAM, Hamer G, Hobson KA, Lehmann T. Marking mosquitoes in their natural larval sites using 2H‐enriched water: A promising approach for tracking over extended temporal and spatial scales. Methods Ecol Evol. 2019 May 17;10(8):1274-85.
Dao A, Yaro AS, Diallo M, Timbiné S, Huestis DL, Kassogué Y, Traoré AI, Sanogo ZL, Samake D, Lehmann T. Signatures of aestivation and migration in Sahelian malaria mosquito populations. Nature. 2014 Dec 18;516(7531):387-90.
Diabate Abdoulaye, Dabire K Roch, Heidenberger Kyle, Crawford Jacob, William Lamp, Culler Lauren, Lehmann Tovi. Evidence for divergent selection between the molecular forms of Anopheles gambiae: role of predation. BMC Evol Biol. 2008 Jan 11;8:5.
Lehmann T, Licht M, Elissa E, Maega BTA, Chimumbwa JM Watsenga FT, Wondji CS, Simard F, Hawley WA. Population Structure of Anopheles gambiae in Africa. J Hered. 2003 Mar-Apr;94(2):133-47.
LMVR Insectaries (including secured area)
As part of the Mosquito Ecology research program, we explore broad population biology questions relevant to patterns of disease transmission and vector control.. Together with colleagues in Mali and elsewhere, we investigate the role of dormancy and long-range windborne migration in the persistence of mosquitoes and malaria in seasonally arid areas, the processes affecting spread of genes within and between populations, and vector-parasite interactions at the population level. The nature of these topics within the One Health paradigm demands novel and creative approaches to answer stubborn old questions and identify new ones. We combine ecological, behavioral, physiological, genetic, and molecular analyses grounded in field studies to improve understanding of phenotypic diversity in vectors and its epidemiological consequences. The research group is nested in the Office of the Chief, LMVR, under Dr. Barillas-Mury.
Faiman F, Yaro AS,Dao A, Sanogo ZL, Diallo M, Samake D, Yossi O, Veru LR, Graber LC, Conte AR, Kouam C, Krajacich BJ, Lehmann T. Isotopic evidence that aestivation allows malaria mosquitoes to persist through the dry season in the Sahel. Nature Ecology & Evolution 2022: In Press.
Dharmarajan G, Walker KD, Lehmann T. Variation in Tolerance to Parasites Affects Vectorial Capacity of Natural Asian Tiger Mosquito Populations v. Curr Biol. 2019 Nov 18;29(22):3946-3952.e5.
Huestis DL, Dao A, Diallo M, Sanogo ZL, Samake D, Yaro AS, Ousman Y, Linton YM, Krishna A, Veru L, Krajacich BJ, Faiman R, Florio J, Chapman JW, Reynolds DR, Weetman D, Mitchell R, Donnelly MJ, Talamas E, Chamorro L, Strobach E, Lehmann T. Windborne long-distance migration of malaria mosquitoes in the Sahel v. Nature. 2019 Oct;574(7778):404-408.
Dao A, Yaro AS, Diallo M, Timbiné S, Huestis DL, Kassogué Y, Traoré AI, Sanogo ZL, Samake D, Lehmann T. Signatures of aestivation and migration in Sahelian malaria mosquito populations. Nature. 2014 Dec 18;516(7531):387-90. *
Diabate Abdoulaye, Dabire K Roch, Heidenberger Kyle, Crawford Jacob, William Lamp, Culler Lauren, Lehmann Tovi. Evidence for divergent selection between the molecular forms of Anopheles gambiae: role of predation. BMC Evol Biol. 2008 Jan 11;8:5.
Lehmann T, Licht M, Elissa E, Maega BTA, Chimumbwa JM Watsenga FT, Wondji CS, Simard F, Hawley WA. Population Structure of Anopheles gambiae in Africa. J Hered. 2003 Mar-Apr;94(2):133-47.
Dr. Adama Dao (MRTC, Mali), Dr. Alpha S. Yaro (MRTC, Mali), Dr. Roy Faiman (LMVR), Dr. Ben Krajacich (LMVR), Mr. Moussa Diallo (MRTC, Mali), Mrs. Margie Sullivan, Mr. Zana L. Sanogo (MRTC, Mali), Dr. Djibril Samake (MRTC, Mali)
LMVR Insectaries (including secured area)
Malaria control: The great mosquito hunt
Mosquitoes may surf winds above Africa more than we realized
Life-Long Mosquito Marking: Are Stable Isotopes the Key?
The Anopheles gambiae 1000 Genomes Consortium
Monitoring Windborne Migration of Disease Vectors, Pathogens, and Pests in Africa to Improve Public Health and Food Security (MWMDVPPiA)
STAT3 dominant-negative disease (STAT3DN)—also known as autosomal dominant hyper-IgE syndrome (AD-HIES) or Job’s Syndrome—results from mutations in the gene that encodes a signaling protein called STAT3. People with this disease tend to have very high levels of an antibody called immunoglobulin E (IgE), recurrent infections of the skin and lungs, recurrent bone fractures, unusually flexible joints, and inflamed skin.
STAT3 dominant-negative disease has widespread deleterious effects on patients’ health, so NIAID scientists aim to develop and enhance treatments to improve patients’ quality of life. In addition, NIAID scientists hope that studying this disease will help them better understand the physiological processes associated with the genetic tendency to develop certain types of infections and allergic diseases.
NIAID investigators identified the role of STAT3 in this disease in 2007. Since then, NIAID-supported researchers have made multiple discoveries about how the loss-of-function mutation in the STAT3 gene leads to patients’ symptoms. NIAID-supported clinical research seeks to determine the effect of STAT3 dominant-negative disease on the immune system, including which immune cells and responses are affected and how these abnormalities translate into patients’ symptoms.
STAT3 dominant-negative disease results from mutations in the gene that encodes a signaling protein called STAT3. This protein is involved in many different activities of the body, explaining why the disease affects not only the immune system but also facial appearance, bones, lungs, skin, and arteries.
People with STAT3 dominant-negative disease (STAT3DN) have very high levels of IgE and may have recurrent infections of the skin and lungs. These infections are often caused by the bacterium Staphylococcus aureus but also may be caused by other bacteria and fungi. Patients also tend to have recurrent bone fractures, unusually flexible joints, and inflamed skin, and may have a rash similar to eczema. Baby teeth in people with this disease often do not fall out on their own. People with STAT3DN also often have distinctive facial characteristics, such as uneven facial features, prominent forehead, deep-set eyes, broad nasal bridge, wide, fleshy nose tip, and protruding lower jaw.
In 2008, NIAID scientists discovered that important immune cells called Th17 cells are missing in people with STAT3DN. NIAID researchers also found in 2011 that an unusually low number of immune memory cells may cause people with the disease to be more susceptible to some viral infections. In 2013 and 2016, NIAID researchers showed that the STAT3 mutation protects people from more severe allergic disease by interfering with the process that causes typical allergic reactions.
A doctor will suspect STAT3DN in a person with eczema, very high IgE, recurrent boils, and pneumonias. Blood tests diagnosing the disease will show normal levels of IgG, IgA, and IgM antibodies but very high levels of IgE antibodies. People with the disease also may show a high number of white blood cells called eosinophils and a poor response to immunizations. Sequencing of the patient’s DNA can confirm the presence of the STAT3 mutation.
The most effective treatments for STAT3 dominant-negative disease are continuous antibiotics and antifungals as needed, as well as careful monitoring for infections, which can be severe even when symptoms do not appear so. Some patients receive antibody replacement therapy. Antiseptic approaches, such as dilute bleach baths, often help prevent skin infections and improve eczema.
Within the Helminth Immunology Section Dr. O’Connell’s research focuses on invasive cestode infections, primarily neurocysticercosis. Patients with basilar subarachnoid neurocysticercosis (racemose disease) often have delayed diagnoses and even after diagnosis are inadequately treated and suffer numerous relapses. This is in part due to the lack of clinical end points for clinicians to follow. We are focusing on the development of biomarkers that inform the clinician when a patient has been successfully cured. The major contributor of morbidity and mortality in subarachnoid neurocysticercosis is the exuberant inflammatory response. By characterizing both this inflammation and what arms of the immune system are effective in controlling parasite growth there may be medical interventions that are selective in tamping down certain aspects of inflammation. Clinically, we provide patients state of the art care while advancing our understanding of neurocysticercosis.
Harrison S, Thumm L, Nash TE, Nutman TB, O’Connell EM. “The local inflammatory profile and predictors of treatment success in subarachnoid neurocysticercosis” Clin Inf Dis. 2020. Dec 3. Online ahead of print. PMID: 33269789
Nash TE, O'Connell EM. “Subarachnoid neurocysticercosis: emerging concepts and treatment.: Curr Opin Infect Dis. 2020 Oct;33(5):339-346. PMID: 32868512
Nash TE, O’Connell EM, Hammoud DA, Wetzler L, Ware JM, Mahanty S. Natural history of treated subarachnoid neurocysticercosis. Am J Trop Med Hyg. 2020. Jan. PMID: 31642423
Polish LB, Pritt B, Barth TFE, Gottstein B, O'Connell EM, Gibson PC. “Echinococcus multilocularis: First European haplotype identified in the United States: An emerging disease?” Clin Infect Dis. 2020 Mar 21 Online ahead of print. PMID: 32198510
O’Connell EM, Harrison S, Dahlstrom E, Nash TE, Nutman TB. A novel, highly sensitive qPCR assay for the diagnosis of subarachnoid and ventricular neurocysticercosis and for assessing response to treatment. Clin Inf Dis. 2020 Apr 15;70(9):1875-1881. PMID: 31232448
O’Connell EM, Mitchell T, Papaiakovou M, Pilotte N, Lee D, Weinberg M, Sakulrak P, Tongsukh D, Oduro-Boateng G, Harrison S, Williams SA, Stauffer WM, Nutman TB. Ancylostoma ceylanicum Hookworm in Myanmar Refugees, Thailand, 2012-2015. Emerg Inf Dis. 2018 Aug;24(8)
16-I-N042, A double-blinded, randomized, placebo-controlled dose escalation study to examine the microfilaricidal kinetics and safety of imatinib for the treatment of Loa loa. Principal investigator.
85-I-0127, Treatment of Cysticercosis including Neurocysticercosis with Praziquantel, Albendazole and other Novel Treatment Modalities. Principal Investigator.
97-I-0096, Evaluation, Treatment and Monitoring of Patients with Known or Suspected Parasitic Infection. Associate investigator.
01-I-0238, Diagnosis and Treatment of Leishmanial Infections. Principal Investigator.
88-I-0083, Host Response to Infection and Treatment in the Filarial Diseases of Humans. Associate investigator.
Dr. O’Connell’s research focuses on invasive cestode infections, primarily neurocysticercosis. Patients with basilar subarachnoid neurocysticercosis (racemose disease) often suffer numerous relapses, in part due to the lack of adequate tests and clinical end points for clinicians to follow. Additionally, the exuberant inflammation in the subarachnoid space during relapses accounts for the significant morbidity and mortality. Our early work focused on the development of biomarkers that facilitate diagnosis and inform the clinician when a patient has been successfully cured. The role of inflammation, host genetics, and anthelmintic therapy in altering the course of disease are active areas of investigation. Clinically, we provide patients state of the art care while advancing our understanding of neurocysticercosis.
Dr. O’Connell is also Principal Investigator on a natural history protocol that seeks to better understand the factors that lead to relapse of cutaneous leishmaniasis, in collaboration with several other researchers.
16-I-N042, A double-blinded, randomized, placebo-controlled dose escalation study to examine the microfilaricidal kinetics and safety of imatinib for the treatment of Loa loa. Principal investigator.
85-I-0127, Treatment of Cysticercosis including Neurocysticercosis with Praziquantel, Albendazole and other Novel Treatment Modalities. Principal Investigator.
97-I-0096, Evaluation, Treatment and Monitoring of Patients with Known or Suspected Parasitic Infection. Associate investigator.
01-I-0238, Diagnosis and Treatment of Leishmanial Infections. Principal Investigator.
88-I-0083, Host Response to Infection and Treatment in the Filarial Diseases of Humans. Associate investigator.
Corda M, Sciurba J, Blaha J, Mahanty S, Paredes A, Garcia HH, Nash TE, Nutman TB, O'Connell EM. A recombinant monoclonal-based Taenia antigen assay that reflects disease activity in extra-parenchymal neurocysticercosis. PLoS Negl Trop Dis. 2022 May 26;16(5):e0010442.
Harrison S, Thumm L, Nash TE, Nutman TB, O'Connell EM. The Local Inflammatory Profile and Predictors of Treatment Success in Subarachnoid Neurocysticercosis. Clin Infect Dis. 2021 May 4;72(9):e326-e333.
Polish LB, Pritt B, Barth TFE, Gottstein B, O'Connell EM, Gibson PC. First European Haplotype of Echinococcus multilocularis Identified in the United States: An Emerging Disease? Clin Infect Dis. 2021 Apr 8;72(7):1117-1123.
Nash TE, O'Connell EM. Subarachnoid neurocysticercosis: emerging concepts and treatment. Curr Opin Infect Dis. 2020 Oct;33(5):339-346.
O'Connell EM, Harrison S, Dahlstrom E, Nash T, Nutman TB. A Novel, Highly Sensitive Quantitative Polymerase Chain Reaction Assay for the Diagnosis of Subarachnoid and Ventricular Neurocysticercosis and for Assessing Responses to Treatment. Clin Infect Dis. 2020 Apr 15;70(9):1875-1881.
Nash TE, O'Connell EM, Hammoud DA, Wetzler L, Ware JM, Mahanty S. Natural History of Treated Subarachnoid Neurocysticercosis. Am J Trop Med Hyg. 2020 Jan;102(1):78-89.
Infectious Diseases Training Program
Clinical testing for Taenia solium DNA by qPCR (Tsol13) and antigen (TsG10) in plasma and cerebrospinal fluid. Please contact Dr. O’Connell directly for requisition form and sample requirements.
U.S. Subarachnoid Neurocysticercosis Network
The LVIS conducts broad and in-depth translational research that focuses on fundamental processes underlying allergic inflammation. Our research program includes studies aimed at mechanistic dissection of fungal associated-asthma and exploration of the pathogenesis of the rare vascular disorder resembling systemic anaphylaxis, a condition known as systemic capillary leak syndrome (SCLS, Clarkson disease). SCLS is a life-threatening disorder of unknown etiology in which patients experience spontaneous and recurrent episodes of hypovolemic shock and edema in the absence of allergic triggers. In the area of fungal asthma, we have identified a fungal protease allergen (Alp1) that is deposited in the airways of patients with severe asthma, and we have elucidated detailed mechanisms by which Alp1 promotes airway smooth muscle contraction and bronchoconstriction. Finally, ongoing studies in the LVIS include G protein-coupled receptor (GPCR)-dependent mechanisms of allergic inflammation, more specifically on the role of Regulators of G protein Signaling (RGS) proteins in lung and inflammatory cells.
Dr. Druey obtained his M.D. from Rush Medical College in Chicago, Illinois. In 1992, following a residency in internal medicine at The New York Hospital/Cornell Medical Center, Dr. Druey became a postdoctoral fellow in the NIAID Laboratory of Immunoregulation. He joined the Laboratory of Allergic Diseases in 1997 to become chief of the Molecular Signal Transduction Section. In 2020, the section was renamed the Lung and Vascular Inflammation Section.
Zhihui (Sherry) Xie, Ph.D., Staff Scientist
Eunice C. Chan, Ph.D., Biologist
Cheung PC, Eisch AR, Maleque N, Polly DM, Auld SC, Druey KM. Fatal Exacerbations of Systemic Capillary Leak Syndrome Complicating Coronavirus Disease. Emerg Infect Dis. 2021 Oct;27(10):2529-2534. doi: 10.3201/eid2710.211155.
Chinn IK, Xie Z, Chan EC, Nagata BM, Koval A, Chen WS, Zhang F, Ganesan S, Hong DN, Suzuki M, Nardone G, Moore IN, Katanaev VL, Balazs AE, Liu C, Lupski JR, Orange JS, Druey KM. Short stature and combined immunodeficiency associated with mutations in RGS10. Sci Signal. 2021 Jul 27;14(693):eabc1940. doi: 10.1126/scisignal.abc1940.
Matheny M, Maleque N, Channell N, Eisch AR, Auld SC, Banerji A, Druey KM. Severe Exacerbations of Systemic Capillary Leak Syndrome After COVID-19 Vaccination: A Case Series. Ann Intern Med. 2021 Jun 15:L21-0250. doi: 10.7326/L21-0250
Wong GS, Redes JL, Balenga N, McCullough M, Fuentes N, Gokhale A, Koziol-White C, Jude JA, Madigan LA, Chan EC, Jester WH, Biardel S, Flamand N, Panettieri RA Jr, Druey KM. RGS4 promotes allergen- and aspirin-associated airway hyperresponsiveness by inhibiting PGE2 biosynthesis. J Allergy Clin Immunol 2020 Mar 19;S0091-6749(20)30372-9.
Raza A, Xie Z, Chan EC, Chen WS, Scott LM, Eisch AR, Krementsov DN, Rosenberg HF, Parikh SM, Blankenhorn EP, Teuscher C, Druey KM. A natural mouse model reveals genetic determinants of Systemic Capillary Leak Syndrome (Clarkson disease). Commun Biol. 2019 Oct 31;2:398.
Redes JL, Basu T, Ram-Mohan S, Ghosh CC, Chan EC, Sek AC, Zhao M, Krishnan R, Rosenberg HF, Druey KM. Aspergillus fumigatus-Secreted Alkaline Protease 1 Mediates Airways Hyperresponsiveness in Severe Asthma. Immunohorizons 2019 Aug 6;3(8):368-377..
The LVIS conducts broad and in-depth translational research that focuses on fundamental processes underlying allergic inflammation. Our research program includes studies aimed at mechanistic dissection of fungal associated-asthma and exploration of the pathogenesis of the rare vascular disorder resembling systemic anaphylaxis, a condition known as systemic capillary leak syndrome (SCLS, Clarkson disease). SCLS is a life-threatening disorder of unknown etiology in which patients experience spontaneous and recurrent episodes of hypovolemic shock and edema in the absence of allergic triggers. In the area of fungal asthma, we have identified a fungal protease allergen (Alp1) that is deposited in the airways of patients with severe asthma, and we have elucidated detailed mechanisms by which Alp1 promotes airway smooth muscle contraction and bronchoconstriction. Finally, ongoing studies in the LVIS include G protein-coupled receptor (GPCR)-dependent mechanisms of allergic inflammation, more specifically on the role of Regulators of G protein Signaling (RGS) proteins in lung and inflammatory cells.
Cheung PC, Eisch AR, Maleque N, Polly DM, Auld SC, Druey KM. Fatal Exacerbations of Systemic Capillary Leak Syndrome Complicating Coronavirus Disease. Emerg Infect Dis. 2021 Oct;27(10):2529-2534. doi: 10.3201/eid2710.211155.
Matheny M, Maleque N, Channell N, Eisch AR, Auld SC, Banerji A, Druey KM. Severe Exacerbations of Systemic Capillary Leak Syndrome After COVID-19 Vaccination: A Case Series. Ann Intern Med. 2021 Jun 15:L21-0250. doi: 10.7326/L21-0250
Chinn IK, Xie Z, Chan EC, Nagata BM, Koval A, Chen WS, Zhang F, Ganesan S, Hong DN, Suzuki M, Nardone G, Moore IN, Katanaev VL, Balazs AE, Liu C, Lupski JR, Orange JS, Druey KM. Short stature and combined immunodeficiency associated with mutations in RGS10. Sci Signal. 2021 Jul 27;14(693):eabc1940. doi: 10.1126/scisignal.abc1940.
Wong GS, Redes JL, Balenga N, McCullough M, Fuentes N, Gokhale A, Koziol-White C, Jude JA, Madigan LA, Chan EC, Jester WH, Biardel S, Flamand N, Panettieri RA Jr, Druey KM. RGS4 promotes allergen- and aspirin-associated airway hyperresponsiveness by inhibiting PGE2 biosynthesis. J Allergy Clin Immunol 2020 Mar 19;S0091-6749(20)30372-9.
Raza A, Xie Z, Chan EC, Chen WS, Scott LM, Eisch AR, Krementsov DN, Rosenberg HF, Parikh SM, Blankenhorn EP, Teuscher C, Druey KM. A natural mouse model reveals genetic determinants of Systemic Capillary Leak Syndrome (Clarkson disease). Commun Biol. 2019 Oct 31;2:398.
Redes JL, Basu T, Ram-Mohan S, Ghosh CC, Chan EC, Sek AC, Zhao M, Krishnan R, Rosenberg HF, Druey KM. Aspergillus fumigatus-Secreted Alkaline Protease 1 Mediates Airways Hyperresponsiveness in Severe Asthma. Immunohorizons 2019 Aug 6;3(8):368-377..
Eunice C. Chan, Ph.D., Biologist
Malaria is a mosquito-borne infectious disease caused by the bite of female Anopheles mosquitoes, which spread infectious Plasmodium parasites into a host. Traditional malaria symptoms include fever, chills, headache, muscle aches and fatigue. Nausea, vomiting and diarrhea also are common. Untreated malaria can lead to severe disease, kidney failure and death. Neurological complications can occur in severe cases, most commonly in young children.
Most malaria cases occur during rainy periods in endemic regions. The World Health Organization estimates that in 2020, globally about 240 million people had malaria and about 627,000 of them died. A disproportionate burden of malarial disease occurs in Sub-Saharan Africa, where children under age 5 account for about 80% of all malaria deaths.
A vaccine to prevent malaria is available; however, its variable efficacy underscores the need for new interventions that offer high-level protection against disease. Malaria is a research priority at NIAID, which is the lead U.S. government agency investigating the disease. Scientists are researching improved vaccines and preventive interventions as well as mosquito control techniques, easy-to-use diagnostics, and improved therapies as parasites continue to develop resistance to currently available antimalarials.
To learn about risk factors for malaria and current prevention and treatment strategies visit the MedlinePlus malaria site.
Escherichia coli (E. coli) bacteria live in the intestines of people and animals, and are key to a healthy intestinal tract. Most E. coli strains are harmless, but some can cause diarrhea through contact with contaminated food or water while other strains can cause urinary tract infections, respiratory illness and pneumonia.
CDC estimates that 265,000 Shiga Toxin-Producing E. coli (STEC) infections occur each year in the United States. Approximately 36 percent of these infections are caused by E. coli O157:H7.
Scientists in NIAID labs and NIAID-supported scientists are using basic, clinical, and applied research to better understand how to detect, treat, and prevent foodborne diseases.
To learn about risk factors for E. coli and current prevention and treatment strategies visit the MedlinePlus E. coli infection site.
Coronaviruses are a large family of viruses that usually cause mild to moderate upper-respiratory tract illnesses in humans. However, three coronaviruses have caused more serious and fatal disease in people: SARS coronavirus (SARS-CoV), which emerged in November 2002 and causes severe acute respiratory syndrome (SARS); MERS coronavirus (MERS-CoV), which emerged in 2012 and causes Middle East respiratory syndrome (MERS); and SARS-CoV-2, which emerged in 2019 and causes coronavirus disease 2019 (COVID-19).
Building on previous research on SARS and MERS, NIAID scientists and NIAID-supported researchers mobilized quickly to develop COVID-19 therapeutics, vaccines and diagnostics. Researchers continue to conduct basic research to understand how coronaviruses infect cells and causes disease, and what interventions can detect, prevent and stop the spread of disease.
NIAID and the Foundation for the National Institutes of Health (FNIH) launched its first in a series of online webinars highlighting recent progress in the new Researching COVID to Enhance Recovery - Treating Long COVID (RECOVER-TLC) program.
A Phase 1 trial testing the safety of an experimental nasal vaccine that may provide enhanced breadth of protection against emerging variants of SARS-CoV-2 is now enrolling healthy adults at three sites in the United States.
Women who receive an mRNA-based COVID-19 vaccination or booster during pregnancy can provide their infants with strong protection against symptomatic COVID-19 infection for at least six months after birth.
Syphilis is a common sexually transmitted infection (STI) caused by Treponema pallidum bacteria. If untreated, syphilis can result in adult neurological and organ damage as well as congenital abnormalities, stillbirth, and neonatal death. After decades of relatively low prevalence, syphilis cases have risen sharply since 2000. NIAID participates in the National Syphilis and Congenital Syphilis Syndemic Federal Task Force and supports a broad syphilis research portfolio with a goal of advancing syphilis diagnosis, prevention and treatment.
Read the Syphilis Fact Sheet the Center for Disease Control and Prevention (CDC).
Syphilis can result in adult neurological and organ damage, as well as congenital abnormalities, stillbirths, and neonatal deaths. NIAID supports research to address these areas including studies featured at the STI & HIV World Congress in Chicago.
Providing optional syphilis tests to most people seeking care at a large emergency department led to a dramatic increase in syphilis screening and diagnosis, according to a National Institutes of Health (NIH)-supported study of nearly 300,000 emergency department encounters in Chicago. Most people diagnosed had no symptoms, which suggests that symptom-based testing strategies alone could miss opportunities to diagnose and treat people with syphilis. The results were published today in the journal Open Forum Infectious Diseases.
