Category: 8. Health

Dr. Osterholm is Regents Professor, McKnight Presidential Endowed Chair in Public Health, the director of the Center for Infectious Disease Research and Policy (CIDRAP), Distinguished Teaching Professor in the Division of Environmental Health Sciences, School of Public Health, a professor in the Technological Leadership Institute, College of Science and Engineering, and an adjunct professor in the Medical School, all at the University of Minnesota.

In November 2020, Dr. Osterholm was appointed to President-elect Joe Biden’s 13-member Transition COVID-19 Advisory Board. From June 2018 through May 2019, he served as a Science Envoy for Health Security on behalf of the US Department of State. He is also on the Board of Regents at Luther College in Decorah, Iowa.

He is the author of the New York Times best-selling 2017 book, Deadliest Enemy: Our War Against Killer Germs, in which he not only details the most pressing infectious disease threats of our day but lays out a nine-point strategy on how to address them, with preventing a global flu pandemic at the top of the list.

In addition, Dr. Osterholm is a member of the National Academy of Medicine (NAM) and the Council of Foreign Relations. In June 2005 Dr. Osterholm was appointed by Michael Leavitt, Secretary of the Department of Health and Human Services (HHS), to the newly established National Science Advisory Board on Biosecurity. In July 2008, he was named to the University of Minnesota Academic Health Center’s Academy of Excellence in Health Research. In October 2008, he was appointed to the World Economic Forum Working Group on Pandemics.

From 2001 through early 2005, Dr. Osterholm, in addition to his role at CIDRAP, served as a Special Advisor to then–HHS Secretary Tommy G. Thompson on issues related to bioterrorism and public health preparedness. He was also appointed to the Secretary’s Advisory Council on Public Health Preparedness. On April 1, 2002, Dr. Osterholm was appointed by Thompson to be his representative on the interim management team to lead the Centers for Disease Control and Prevention (CDC). With the appointment of Dr. Julie Gerberding as director of the CDC on July 3, 2002, Dr. Osterholm was asked by Thompson to assist Dr. Gerberding on his behalf during the transition period. He filled that role through January 2003.

Previously, Dr. Osterholm served for 24 years (1975-1999) in various roles at the Minnesota Department of Health, the last 15 as state epidemiologist. He has led numerous investigations of outbreaks of international importance, including foodborne diseases, the association of tampons and toxic shock syndrome, and hepatitis B and HIV in healthcare settings.

Dr. Osterholm was the principal investigator and director of the NIH-supported Minnesota Center of Excellence for Influenza Research and Surveillance (2007-2014) and chaired the Executive Committee of the Centers of Excellence Influenza Research and Surveillance network.

Dr. Osterholm has been an international leader on the critical concern regarding our preparedness for an influenza pandemic. His invited papers in the journals Foreign Affairs, the New England Journal of Medicine, and Nature detail the threat of an influenza pandemic before the recent pandemic and the steps we must take to better prepare for such events. Dr. Osterholm has also been an international leader on the growing concern regarding the use of biological agents as catastrophic weapons targeting civilian populations. In that role, he served as a personal advisor to the late King Hussein of Jordan. Dr. Osterholm provides a comprehensive and pointed review of America’s current state of preparedness for a bioterrorism attack in his New York Times best-selling book, Living Terrors: What America Needs to Know to Survive the Coming Bioterrorist Catastrophe.

The author of more than 315 papers and abstracts, including 21 book chapters, Dr. Osterholm is a frequently invited guest lecturer on the topic of epidemiology of infectious diseases. He serves on the editorial boards of nine journals, including Infection Control and Hospital Epidemiology and Microbial Drug Resistance: Mechanisms, Epidemiology and Disease, and he is a reviewer for 24 additional journals, including the New England Journal of Medicine, the Journal of the AmericanMedical Association, and Science. He is past president of the Council of State and Territorial Epidemiologists (CSTE) and has served on the CDC’s National Center for Infectious Diseases Board of Scientific Counselors from 1992 to 1997. Dr. Osterholm served on the IOM Forum on Microbial Threats from 1994 through 2011. He has served on the IOM Committee on Emerging Microbial Threats to Health in the 21st Century and the IOM Committee on Food Safety, Production to Consumption, and he was a reviewer for the IOM Report on Chemical and Biological Terrorism. As a member of the American Society for Microbiology (ASM), Dr. Osterholm has served on the Committee on Biomedical Research of the Public and Scientific Affairs Board, the Task Force on Biological Weapons, and the Task Force on Antibiotic Resistance. He is a frequent consultant to the World Health Organization (WHO), the National Institutes of Health (NIH), the Food and Drug Administration (FDA), the Department of Defense, and the CDC. He is a fellow of the American College of Epidemiology and the Infectious Diseases Society of America (IDSA).

Dr. Osterholm has received numerous honors for his work, including an honorary doctorate from Luther College; the Pump Handle Award, CSTE; the Charles C. Shepard Science Award, CDC; the Harvey W. Wiley Medal, FDA; the Squibb Award, IDSA; Distinguished University Teaching Professor, Environmental Health Sciences, School of Public Health, UMN; the Wade Hampton Frost Leadership Award, American Public Health Association, and the American Medical Association for Outstanding Government Service. He also has been the recipient of six major research awards from the NIH and the CDC.

An outbreak of Legionnaires’ disease in New York City has infected at least 58 people and killed two, the NYC Health Department reports.

This might put you on edge if you’re near the epicenter or you aren’t feeling well. While the disease is treatable, older adults are more vulnerable to it, so it’s good to be informed.

Legionnaires’ disease is a serious form of pneumonia caused by Legionella bacterium.

People older than age 50 and those with diabetes, kidney failure, cancer, lung disease or a weakened immune system are at higher risk, according to the Centers for Disease Control. Those in long-term care facilities, including nursing homes, can be especially prone to infection because those spaces likely have the large water systems that can become contaminated.

What is Legionnaires’ disease?

Legionnaires’ disease is the “lung manifestation” or pneumonia that’s caused by Legionella bacterium, says Jin Suh, M.D., chief of infectious disease at St. Joseph’s Health in Paterson, New Jersey.

Pontiac fever, a less serious illness caused by the same bacteria can lead to flu-like symptoms such as fever or muscle ache.

In rare cases, Legionella can infect other parts of your body outside of the lungs, such as in the heart and brain, or by way of skin infections, Suh says.

What causes Legionnaires’ disease?

Legionella bacterium naturally occurs in lakes, streams and soil. It’s an environmental pathogen, Suh says. There’s typically not enough bacteria in natural environment to cause illness.

The bacterium can contaminate drinking water and air systems, which is where the bacteria can multiply and lead to outbreaks. It can also grow in sink faucets, shower heads and hot tubs at home.  You can get also Legionnaires’ disease through aspiration, or when something goes down the wrong pipe, but that’s not as common.

Mohamed Hamdy Yassin, M.D., an infectious disease specialist with University of Pittsburgh Medical Center who sees about 15 to 20 cases of Legionnaires’ disease each year, says the infection doesn’t always come from large buildings. Most cases he has seen come from a problem with a home’s water system. If your home water system has problems, or hasn’t run in a while, the bacterium can build up to harmful levels.

“It’s not uncommon to see people living in areas where their water system is not very well maintained,” Yassin says, and those people are at higher risk for the disease.

Another cause for infections is in people who own a second home where the water doesn’t run for months. (In that case, run your water for about 30 minutes before taking a shower or drinking the water, Yassin advises.)

There are at least 60 different strains of Legionella, though the majority of illnesses are caused by Legionella pneumophila, the CDC reports.

Sulfonylureas were associated with an increased risk of cardiovascular events in patients with type 2 diabetes (T2D) compared to dipeptidyl peptidase 4 (DPP4) inhibitors, according to data published in JAMA Network Open.¹ The study, which found the risk was highest for glipizide, suggests sulfonylureas may not be the best choice of medication for patients with T2D who have moderate cardiovascular disease risk.

Sulfonylureas are affordable and effective glucose-lowering agents used for decades in T2D management. However, concerns remain about their cardiovascular safety, based on older trials and observational studies showing higher risk compared to other medications. Additional drawbacks such as hypoglycemia, weight gain, and reduced durability challenge their use as second-line therapy.²

“Patients with type 2 diabetes are at heightened risk of adverse cardiovascular incidents such as stroke and cardiac arrest,” Alexander Turchin, MD, MS, corresponding author on the study, said in a release.³ “While sulfonylureas are popular and affordable diabetes medications, there is a lack of long-term clinical data on how they affect cardiac health in comparison to more neutral alternatives like dipeptidyl peptidase 4 inhibitors.”

Investigators from Harvard Medical School and Brigham and Women’s Hospital conducted a study to compare the risk of cardiovascular events after starting treatment with individual sulfonylureas or DPP4 inhibitors. The comparative effectiveness study included 48165 patients with T2D and moderate cardiovascular risk who were treated at 1 of 10 health systems in the United States between January 2013 and January 2023.

The patients all received metformin monotherapy and then initiated either glimepiride, glipizide, glyburide, or any DPP4 inhibitor, including alogliptin, linagliptin, saxagliptin, or sitagliptin. The primary study outcome was the 5-year risk of a 4-point composite of major adverse cardiovascular events (MACE-4), which included myocardial infarction, ischemic stroke, heart failure hospitalization, or cardiovascular death.

During the study, 18147 patients started glipizide, 14282 started glimepiride, 1887 started glyburide, and 13849 started a DPP4 inhibitor. The study found that over a median follow-up time of 37 months, 6.6% of patients experienced a MACE-4: 2.2% had myocardial infarction, 2.6% had an ischemic stroke, 3% had a heart failure hospitalization, and 0.4% died from any of the conditions. Compared with DPP4 inhibitors, the 5-year risk ratio of MACE-4 was 1.13 for glipizide, 1.07 for glimepiride, and 1.04 for glyburide.

Study limitations included short median follow-up time which made it difficult to detect further differences between the medications, that gliclazide was not in use during the study and few patients were taking glyburide, and that racial and ethnic diversity was limited.

“The potentially different cardiovascular risk between individual sulfonylureas in our study underscores the importance of evaluating each agent in a particular pharmacological class on its own merits,” the authors concluded. “These findings caution against extrapolating results of studies evaluating a single agent to the entire class, and temper concerns about the use of research and development resources for the development of multiple agents in the same pharmacological class.”

READ MORE: Diabetes Resource Center

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References

1. Turchin A, Petito LC, Hegermiller E, et al. Cardiovascular Events in Individuals Treated With Sulfonylureas or Dipeptidyl Peptidase 4 Inhibitors. JAMA Netw Open. 2025;8(7):e2523067. doi:10.1001/jamanetworkopen.2025.23067

2. Wang H, Cordiner RLM, Huang Y, et al. Cardiovascular Safety in Type 2 Diabetes With Sulfonylureas as Second-line Drugs: A Nationwide Population-Based Comparative Safety Study. Diabetes Care 1 May 2023; 46 (5): 967–977. https://doi.org/10.2337/dc22-1238

3. Study compares common type 2 diabetes drugs, finding higher cardiovascular risk for one medication. News Release. Mass General Brigham. July 24, 2025. Accessed August 5, 2025. https://www.massgeneralbrigham.org/en/about/newsroom/press-releases/cardiovascular-risk-of-diabetes-drugs

U.S. health officials issued a warning to travelers about a mosquito-borne illness being transmitted in parts of southeast China.

The Centers for Disease Control and Prevention said there is an outbreak of chikungunya in Guangdong Province, China. Most cases have been reported in the city of Foshan.

Most people infected with the virus develop symptoms that include fever, joint pain, headache, muscle pain, rash and joint swelling, the CDC said Friday in a travel warning. Symptoms usually begin three to seven days after a person has been bitten by an infected mosquito.

The CDC said most people recover in about a week, and there is no treatment. In some cases, severe joint pain can last for several months to years following acute illness.

Newborns and older adults, as well as people with medical conditions such as heart disease and diabetes, are more prone to severe illness. Death from chikungunya is rare, the CDC said.

China held a national conference in July on ways to prevent and treat the virus. Between July 20 and July 26, there were a total of 2,940 new local cases reported in Guangdong Province, China’s National Health Commission said in a July 31 news release. The cases were mild with no reports of severe illness or deaths.

Insect repellents and wearing clothing that covers the skin can help protect people from mosquito bites. Vaccination is recommended for people who are visiting an area with an outbreak, the CDC said. There are two approved vaccines in the United States.

The virus was first detected in Tanzania in 1952, according to the World Health Organization. Since 2004, outbreaks have become more frequent and widespread.

It has been found in Asia, Africa, Europe and North and South America.

For 20 years, oseltamivir (Tamiflu) has carried a black-box warning suggesting that use in pediatric patients may be linked to neuropsychiatric events, including confusion, delirium, and abnormal behavior. 

But a new study in JAMA Neurology debunks this association and suggests that influenza itself, not Tamiflu use, increases a child’s risk of experiencing neuropsychiatric events when ill. 

The study comes from researchers at Monroe Carell Jr. Children’s Hospital at Vanderbilt University who used data from 692,295 children ages 5 to 17 enrolled in Tennessee Medicaid between July 1, 2016, and June 30, 2020. 

Follow-up began on the first day of the influenza season and continued through the earliest occurrence of an outcome event, loss of enrollment, death, age 18 years, or end of the season or study, the authors said. 

The median age of children included in the study was 11 years, and children enrolled in the study experienced a total of 1,230 serious neuropsychiatric events (898 neurologic and 332 psychiatric). Overall, the most common neuropsychiatric events seen during the study period were mood disorders (36.3%) and suicidal or self-harm behaviors (34.2%).

Among the 151,401 influenza episodes, 66.7% (95% confidence interval [CI], 66.5% to 67.0%) were dispensed oseltamivir. Of those, 60.1% were at high risk for influenza complications.

Tamiflu tied to 50% lower risk of events 

Compared with untreated influenza, event rates were lower during oseltamivir-treated influenza periods (incidence rate ratios [IRR], 0.53; 95% CI, 0.33 to 0.88) and posttreatment periods (IRR, 0.42; 95% CI, 0.24 to 0.74).

“Risk of serious neuropsychiatric events increased during periods of influenza infection,” the authors wrote. “During these periods, treatment with oseltamivir was associated with an approximately 50% reduction in the incidence of serious neuropsychiatric events compared with influenza periods without oseltamivir treatment.”

Moreover, children treated with oseltamivir prophylactically had the same rate of events as the baseline group with no influenza.

The authors said the current black-box warning on Tamiflu originated in case reports, not clinical studies of the antiviral. Randomized trials have not shown an association, but evidence from prophylactic trials has shown neuropsychiatric events among adults only.

Our findings demonstrated what many pediatricians have long suspected, that the flu, not the flu treatment, is associated with neuropsychiatric events.

“Our findings demonstrated what many pediatricians have long suspected, that the flu, not the flu treatment, is associated with neuropsychiatric events,” said principal investigator James Antoon, MD, PhD, MPH, assistant professor of pediatrics at Monroe Carell, in a press release. “In fact, oseltamivir treatment seems to prevent neuropsychiatric events rather than cause them.”

Even the ultra-processed foods that are touted as healthy could foil an attempt to diet, according to new research that finds weight loss is greater when ultra-processed foods are avoided.

Researchers at University College London found that the level of processing made a difference even in nutritionally matched diets. Those who ate minimally processed foods lost twice as much weight as those consuming ultra-processed food.

The study is published in Nature Medicine.

What are ultra-processed foods?

According to Harvard Health, unprocessed or minimally processed foods are “whole foods in which the vitamins and nutrients are still intact.”

The food is pretty much in its natural form, though it might have been pasteurized or cooked. Examples are carrots, apples, raw meat, melon and raw, unsalted nuts. Processed foods typically have added salt, oil, sugar or other substances.

But ultra-processed foods have had a lot going on.

“They most likely have many added ingredients such as sugar, salt, fat and artificial colors or preservatives. Ultra-processed foods are made mostly from substances extracted from foods, such as fats, starches, added sugars and hydrogenated fats. They may also contain additives like artificial colors and flavors or stabilizers. Examples of these foods are frozen meals, soft drinks, hot dogs and cold cuts, fast food, packaged cookies, cakes, and salty snacks,” per Harvard Health.

Matched diets, different results

For the study, 55 adults were randomized into two groups — one assigned an eight-week diet of minimally processed foods such as overnight oats or homemade spaghetti bolognese. Per a news release from the university, “after a four-week ‘washout’ period in which participants went back to their normal diets, they switched to a diet of ultra-processed food, such as breakfast oat bars or lasagna ready meal.”

The other group followed the diets in the opposite order.

The two diets were nutritionally matched and followed the Eatwell Guide, which is the UK’s government advice on a healthy, balanced diet — including how much fat, saturated fat, protein, carbohydrates, salt and fiber each included, as well as recommended amounts of vegetables and fruits.

“Participants had plenty of food — more calories than they needed — delivered to their home and were told to eat as much or as little as they wanted, as they would normally. They were not told to limit their intake,” the researchers reported.

They all lost weight, a fact that researchers attributed to the “improved nutritional profile” of their meals, compared to their normal diet. But those eating the minimally processed food lost more weight.

“The findings suggest that when observing recommended dietary guidelines, choosing minimally processed food may be more effective for losing weight,” per the study.

“Previous research has linked ultra-processed foods with poor health outcomes. But not all ultra-processed foods are inherently unhealthy based on their nutritional profile. The main aim of this trial was to fill crucial gaps in our knowledge about the role of food processing in the context of existing dietary guidance, and how it affects health outcomes such as weight, blood pressure and body composition, as well as experiential factors like food cravings,” said Dr. Samuel Dicken, first author of the study, from the Centre for Obesity Research at the university.

“The primary outcome of the trial was to assess percentage changes in weight and on both diets we saw a significant reduction, but the effect was nearly double on the minimally processed diet. Though a 2% reduction may not seem very big, that is only over eight weeks and without people trying to actively reduce their intake. If we scaled these results up over the course of a year, we’d expect to see a 13% weight reduction in men and a 9% reduction in women on the minimally processed diet, but only a 4% weight reduction in men and 5% in women after the ultra-processed diet. Over time this would start to become a big difference,” he said.

The study found that participants consumed fewer calories and less fat when eating minimally processed foods.

Should ultra-processed foods be avoided?

As The New York Times reported, “Federal officials have been sounding the alarm about ultra-processed foods, which account for about 70% of the food supply in the United States. Robert F. Kennedy Jr., the health secretary, said that ultra-processed foods were ‘poisoning’ Americans, and called them a primary culprit of high rates of obesity and chronic diseases.”

As the article noted, ultra-processed foods are “ubiquitous and tend to be cheaper than minimally processed foods.” The Times reported that ultra-processed foods don’t need to be avoided completely. But home cooking with fresh ingredients is better.

A number of studies have linked ultra-processed foods to obesity and other health concerns.

In March 2024, Deseret News reported on a study in BMJ linking ultra-processed foods to dozens of health problems, including obesity, heart disease, certain cancers, diabetes and even premature death.

The study found that there’s great variation in how much ultra-processed food is consumed from one country to the next.

Another study Deseret News reported on concluded that ultra-processed foods with lots of refined carbohydrates and added fats can be as addictive as cigarettes. The study, by researchers at the University of Michigan and published in a special food-focused issue of BMJ, said the findings include sweets and salty snacks, among other foods. It noted that, like other addictive substances, ultra-processed food can:

• Create compulsive use.
• Alter moods.
• Reinforce behaviors.
• Spark “intense urges and cravings.”

When Deseret News recently explored healthy aging, interviewing experts and poring through studies, ultra-processed foods made the list of things to avoid as much as possible.

BMC Infectious Diseases invites submissions for a Collection on Infectious diseases in pregnancy.

Infectious diseases during pregnancy represent a critical area of concern for maternal and fetal health. Infections such as syphilis, HIV, and Zika virus can have severe implications for both the mother and the developing fetus, leading to complications such as congenital infections, vertical transmission, and adverse pregnancy outcomes. Understanding the mechanisms of maternal infections and their potential impacts on fetal development is vital for optimizing prenatal care and improving health outcomes. This Collection seeks to explore the latest research in this field, focusing on the complexities and challenges associated with infectious disease management in pregnancy. 

Addressing infectious diseases in pregnancy is essential not only for safeguarding maternal health but also for preventing long-term effects on child health and development. Advances in prenatal screening and diagnostic techniques have improved our ability to detect and manage infections, enabling timely interventions that can significantly reduce risks. Furthermore, increased awareness and research into gestational infections have led to better guidelines for healthcare providers, fostering a more proactive approach to managing maternal-fetal health during pregnancy. Continued research in this field could lead to further advancements in treatment and prevention, including vaccines, biomarkers, and screening. 

We invite clinicians and researchers in infectious disease management, obstetrics, public health, immunology, epidemiology, maternal-fetal medicine, and related fields to contribute original research articles on topics including but not limited to: 

• Maternal infections and fetal outcomes 
• Congenital infections and their management 
• Vertical transmission of infectious agents
• Advances in prenatal screening techniques
• Perinatal infections: risks and interventions

This Collection supports and amplifies research related to SDG 3: Good Health and Well-being.

All manuscripts submitted to this journal, including those submitted to collections and special issues, are assessed in line with our editorial policies and the journal’s peer review process. Reviewers and editors are required to declare competing interests and can be excluded from the peer review process if a competing interest exists.

Image credits: ©[M]Ute Grabowsky/GettyImages

Since its development in 1926, MST has served as a critical diagnostic tool for cutaneous leishmaniasis (CL) globally, particularly for evaluating DTH to Leishmania infection [25]. It remains widely used in Latin America, where the principal etiological agents of ACL belong to the L. (Viannia) subgenus, including L. (V.) braziliensis, L. (V.) peruviana, L. (V.) panamensis, and L. (V.) guyanensis, which are well-recognized for their ability to stimulate a CD4⁺/Th1-type immune response and thereby elicit DTH reactions [26,27,28,29]. Recently, MST has been employed not only for its original diagnostic purpose but also for epidemiological studies as a screening tool for DTH responses associated with asymptomatic infections caused by L. (L.) infantum and L. (L.) donovani in regions endemic for visceral leishmaniasis. These applications further support the ability of MST as a reliable method for assessing DTH in human Leishmania infections [30,31,32,33,34,35,36,37,38,39,40,41].

By contrast, early studies into the use of MST in cases of ACL caused by L. (L.) amazonensis or L. (L.) pifanoi, particularly in ADCL form, were conducted several decades ago in Brazil [42, 43], Bolivia [44], and Venezuela [45]. These studies consistently reported negative MST results in patients with ADCL, leading to the prevailing view that this clinical form is linked to a specific immunodeficiency in the host. As a result, the absence of DTH in ADCL has been largely attributed to the host’s inability to generate an effective T-cell-mediated immune response, rather than to any direct immunosuppressive action of the parasite itself [46].

DTH suppression due to L. (L.) amazonensis infection was first detected in Brazil during the 1980s through a pioneering study conducted by our research group in Pará State. This study was the first to demonstrate that 57.7% of patients with LCL caused by L. (L.) amazonensis showed no MST reactivity when using homologous promastigote antigen [13]. Subsequent studies confirmed comparable or even higher rates of DTH suppression, ranging from 48.6% to 100% among patients with LCL, thereby establishing the absence of MST reactivity as a hallmark of L. (L.) amazonensis infection across the clinical–immunopathological spectrum of ACL. This phenomenon was most pronounced in ADCL, where MST reactivity was universally absent (100%), but was also observed to varying degrees in patients with LCL (48.6–100%), despite their generally favorable response to antimony therapy [8, 9, 14,15,16].

These findings of DTH suppression in L. (L.) amazonensis-induced LCL is further supported by histopathological findings. Skin lesions typically exhibit a dermal cellular infiltrate that is predominantly macrophagic, with scarce plasma cells and lymphocytes, and a notably rare presence of epithelioid cells, i.e., macrophages that are activated through T-cell-mediated immune response. The macrophages appear vacuolated and heavily parasitized, providing additional confirmation of impaired DTH expression at the site of infection [47]. This histological profile contrasts sharply with that observed in L. (Viannia) braziliensis-induced LCL, where the dermal infiltrate is characterized by a prominent presence of epithelioid cells, corresponding with a high prevalence (≥ 90%) of MST reactivity [48].

The present results demonstrated a complete absence of MST reactivity in all patients analyzed, including those with LCL and BDCL, irrespective of lesion count, clinical presentation, or disease duration, both before and after successfully antimony therapy. Although the absence of MST reactivity in LCL caused by L. (L.) amazonensis has been previously documented [14], this is the first report of such a finding in BDCL. Notably, in contrast to L. (V.) braziliensis infection, in which MST reactivity persists over time, even following antimony therapy, due to continued antigenic stimulation [49, 50], infection with L. (L.) amazonensis in both LCL and BDCL appears to be completely cleared by therapy. This clearance likely prevents the sustained antigenic stimulation of the T-cell-mediated immune response, including DTH, as assessed by MST. These findings suggest a previously unrecognized immunological profile linked to L. (L.) amazonensis infection and highlight the distinct immune mechanisms involved in ACL pathogenesis.

Of particular note is the first documented case of LCL spontaneous cure due to L. (L.) amazonensis, observed 1 year after diagnosis. Remarkably, the patient exhibited no MST reactivity either before or after the spontaneous resolution of the lesion, an observation that challenges current understanding of DTH in human Leishmania infection [26,27,28,29, 51]. Typically, spontaneous cure is associated with the activation of the T-cell-mediated immune response. However, this case suggests that L. (L.) amazonensis infection may inhibit the activation of genetic pathways essential for DTH expression, most likely linked to the CD4⁺/Th1-type immune response, thereby compromising macrophage-mediated resistance to infection [21, 52].

These findings raise a critical question: why do patients with L. (L.) amazonensis-induced LCL and BDCL, despite achieving clinical cure, whether through antimony therapy or spontaneously, fail to develop DTH, assessed by MST reactivity? This contrasts with patients affected by so-called Old and New World visceral leishmaniasis, who, despite profound suppression of the CD4⁺/Th1-type immune response, often exhibit a significant shift toward DTH, assessed by MST reactivity following treatment [53, 54]. A plausible explanation lies in the persistence of low-level infection. In L. (V.) braziliensis-induced LCL, for instance, antimony therapy does not fully eradicate the parasite from healed lesions, allowing ongoing antigenic stimulation and sustained DTH responses [49, 50]. Similarly, in treated or asymptomatic visceral leishmaniasis, incomplete parasite clearance, particularly in the liver, may promote posttreatment DTH conversion through the gradual reactivation of CD4⁺/Th1-type immune response [53,54,55,56]. By contrast, L. (L.) amazonensis infection appears to be entirely eliminated by treatment, potentially precluding such immunological reactivation.

In this case, DTH suppression in L. (L.) amazonensis infection, both in LCL and BDCL, appears to be influenced by two distinct parasite–host interaction mechanisms. The first involves the potential inhibition of genetic pathways that regulate DTH during the active phase of infection [21, 52]. The second, which may represent a novel observation, is associated with the absence of antigenic stimulation following the complete clearance of the parasite through antimony therapy. These findings underscore the critical role of species-specific host–parasite interactions in modulating the T-cell-mediated immune response, particularly the CD4⁺/Th1 and CD4⁺/Th2 pathways, which in turn govern DTH activation [3, 8, 9].

Supporting this hypothesis, it is noteworthy that, based on more than 40 years of clinical experience monitoring patients infected with L. (L.) amazonensis in Pará, Brazilian Amazon, this research group has not observed any cases of relapse following medium- or long-term cure with antimony therapy, particularly among patients with LCL. This observation stands in contrast to the more frequent relapses seen in LCL and BDCL cases due to L. (V.) braziliensis or L. (V.) guyanensis [Silveira, personal observation].

The progression of L. (L.) amazonensis infection appears to be influenced by the extent of DTH suppression, mainly due to the impairment of the CD4⁺/Th1-type immune response, in conjunction with host-specific factors such as age and genetic background. This may lead to the development of BDCL, an intermediate-severity form that predominantly affects young adults and typically requires twice the standard dosage of antimony therapy used for LCL [8, 9, 17]. In the absence of effective immune control, the infection may progress to ADCL, a severe and incurable form resistant to all types of chemotherapy. ADCL primarily affects children under 10 years of age and adults belonging to ethnic groups with heightened susceptibility to L. (L.) amazonensis infection [2, 10]. This clinical form is most frequently observed among historically enslaved individuals of African descent in the pre-Amazon region of Maranhão State, which reports the highest number of ADCL cases in Brazil [57].

In the majority of infected individuals, particularly those with LCL, accounting for ≥ 98% of cases, the parasite’s suppressive effect on the CD4⁺/Th1-type immune response, reflected by the absence of DTH in negative MST, appears to be less pronounced than in patients with BDCL and patients with ADCL. This relative preservation of immune function may be alternatively attributed to the immunomodulatory activity of CD8⁺ T cells, which exhibit significantly higher densities (P < 0.05) than CD4⁺ T cells across the clinical–immunopathological spectrum of ACL due to L. (L.) amazonensis, even after antimony therapy [12, 58]. These findings highlight the pivotal role of CD8⁺ T cells as a key resistance mechanism in the control of L. (L.) amazonensis infection, contributing to protective immunity by producing IFN-γ and promoting Th1 responses not only in human infection [8, 9, 12] but also in murine models [59, 60].

Leishmania (L.) amazonensis primarily modulates the human immune response by disrupting the balance between cellular and humoral immunity. Specifically, it suppresses the CD4⁺/Th1-type immune response, including DTH, which is essential for macrophage activation and effective parasite clearance, while enhancing the less effective, IgG-mediated humoral response [61, 62]. This immunomodulatory effect is particularly pronounced in BDCL and ADCL, which are characterized by high parasite loads [3, 8, 9, 63]. In the present study, patients with LCL exhibited low to moderate IgG titers (80–320), whereas those with BDCL showed significantly higher titers (640–2,560). These findings support the notion that L. (L.) amazonensis facilitates disease progression by impairing protective cellular immunity, primarily the CD4⁺/Th1-type response, while promoting a nonprotective humoral response.

Supporting these observations, a recent methodological advancement deserves attention: the optimization of MST using an L. (V.) lainsoni axenic amastigote antigen to assess DTH in ACL cases in the Brazilian Amazon. This approach yielded significantly higher mean reactivity (18.8 mm ± 13.3) in LCL caused by L. (Viannia) species, compared with the response elicited by the conventional L. (V.) braziliensis promastigote antigen (11.8 mm ± 8.2). Notably, the only patient in the study diagnosed with LCL due to L. (L.) amazonensis exhibited no reactivity to the MST, in contrast to 52 cases associated with L. (Viannia) species. This finding reinforces the suppression of DTH in L. (L.) amazonensis infections, even when using an antigen demonstrated to be more potent than the standard L. (V.) braziliensis antigen [64].

At the time of concluding this study, two individuals previously diagnosed with L. (L.) amazonensis-associated ACL were reevaluated. The first was a 58-year-old woman with ADCL, and the second was a 54-year-old man with BDCL. Both had undergone multiple treatment regimens, including antimonial compounds, pentamidine, and chemoimmunotherapy (BCG combined with Leishvacin), and they ultimately achieved clinical cure (Fig. 4, supplementary material) [17, 65]. Immunological testing revealed negative IFAT/enzyme-linked immunosorbent assay (ELISA)-IgG results for the woman and a negative MST for the man, confirming parasitological cure. Notably, the man’s prior MST conversion, documented 25 years earlier, was likely attributable to transient immunogenic stimulation induced by immunotherapy. These findings represent the first documented confirmation of parasitological cure in ADCL and BDCL caused by L. (L.) amazonensis, as evidenced by negative serological and DTH-based assays.

Finally, to underscore the complexity of the immune responses to L. (L.) amazonensis infection, it should be highlighted that an ADCL case with more than 30 years of disease evolution achieved clinical cure following a single intranasal dose of meglumine antimoniate, despite the patient remaining negative for the MST after cure [66]. Notably, this therapeutic approach was unsuccessful in four patients under our clinical supervision [67].

There is a virus wreaking havoc on the city of Foshan in southern China, infecting thousands of people in just a matter of weeks.

It’s called Chikungunya, and it’s one of many viruses transmitted by mosquitoes.

To fight the spread, the New York Times reported that health officials in China have turned to methods such as drones to find mosquito breeding sites and introduced natural predators like “elephant mosquitoes” and mosquito-eating fish.

Chikungunya virus is not something new, and it is rarely fatal. But the ongoing outbreak is one of the worst China has seen since 2008, according to the New York Times.

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What is Chikungunya?

The mosquito-borne illness was first discovered in the United Republic of Tanzania in 1952, according to the World Health Organization (WHO). The name chikungunya derives from a word in the Kimakonde language of southern Tanzania, meaning “that which bends up” — a reference to the contorted posture of infected people who suffer from severe joint pain.

There have been sporadic outbreaks in the Americas, Asia and Africa. Occasionally, Europe has seen small outbreaks of the virus.

How does it spread?

Infected female mosquitoes can transmit the virus through biting. These same mosquitoes are also responsible for spreading dengue and Zika viruses.

What are the symptoms?

The virus can take up to a week after an infected mosquito bite before its symptoms start to develop, according to WHO. They typically start with a fever and severe joint pain. The joint pain can be debilitating and can last days, weeks or even years in more extreme cases.

Other symptoms include joint swelling, muscle pain, headache, nausea, fatigue and rash. WHO said since these symptoms overlap with other mosquito-borne infections, like dengue and Zika, cases can sometimes be misdiagnosed. A blood sample can help to determine if the infection is chikungunya virus.

Most patients recover fully from the infection; however, there have been some rare cases that have resulted in eye, heart, and neurological complications.

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Is there a treatment or vaccine?

There is no specific antiviral drug treatment for chikungunya infections. Treatment usually involves medications to manage the fever and joint pain.

According to WHO, there are two chikungunya vaccines that have received regulatory approvals or have been recommended for use in populations at risk in several countries, but the vaccines are not yet widely available.

The best way to prevent the virus is to prevent a mosquito bite through repellent with DEET, clothing that minimizes skin exposure, window and door screens and insecticide-treated mosquito nets.