A review of the drought and pathogen/disease paradox

Amazing stuff!

"Of the hundreds of parasites known to infect humans, more than half depend on water. Some, like Giardia and Cyclospora, spread directly through contaminated drinking water or lurk on the surface of poorly washed lettuce. ...

One might assume that drought, which dries up water sources, would help curb the spread of these diseases. This assumption sometimes holds true:

In the early 2000s, for example, a major drought in Kenya reduced schistosomiasis cases in humans by killing off the snails that transmit it. And chytrid fungus, which spells doom for amphibians around the globe, tends to spread poorly under dry conditions.

In other cases, however, drought actually amplifies infectious pathogens that rely on water.

In the 2020s, when drought-induced water shortages forced people in the Horn of Africa to rely on unsafe water sources, major cholera outbreaks followed.

Two years ago, a particularly dry summer in California helped spark one of the largest outbreaks of avian botulism ever recorded.

And now, scientists suggest drought is to blame for Brazil’s first yellow fever outbreak in almost 80 years, even though the disease is spread by mosquitoes. “Species are adapting,” ...

In a review paper published last week in Trends in Ecology and Evolution, scientists set out to investigate this counterintuitive “drought-disease paradox.” By synthesizing nearly 100 previous studies, the authors identified three main mechanisms that determine how a given pathogen will fare when water dries up. “ ...

The researchers found that, as drought dries up rivers and ponds, animals are forced to congregate around a region’s few remaining [and shrinking] watering holes, creating more opportunities for pathogens to spread. ...

Drought, which does more than just reduce available water, can also influence the health of parasites and hosts alike. As water evaporates from freshwater and marine ecosystems, for example, salinity rises. Increased salt concentrations were good news for oyster-infesting Perkinsus parasites but bad news for invasive copepods, which struggled to infect their tilapia hosts during a drought in South Africa. Stress from high temperatures, dehydration, and other drought-induced risk factors, meanwhile, can weaken hosts and make them more susceptible to infection. ..."

From the highlights and abstract:

"Highlights

Drought is becoming a defining ecological force, yet its consequences for infectious diseases remain difficult to predict across systems.

Emerging evidence shows that water limitation can intensify many water-associated diseases, challenging assumptions that drying suppresses transmission.

Rather than acting solely as a climatic stressor, drought restructures transmission by altering host aggregation, parasite persistence, community composition, and contact networks across space and time.

Divergent disease responses to drought can be explained through three recurring mechanisms: the concentration of interactions, the ecological filtering of communities, and spatial heterogeneity in transmission.

Viewing drought as a multiscale ecological restructuring process provides a general framework for predicting disease outcomes in an increasingly water-limited world.

Abstract

Droughts are intensifying worldwide, reorganizing ecosystems and threatening biodiversity and human health. Yet their effects on infectious diseases are poorly understood and sometimes paradoxical, with water limitation often amplifying water-associated infections.

This complexity arises because drought not only reduces water availability but also restructures the host–pathogen interactions that govern transmission. Synthesizing theory and empirical evidence from water-associated diseases, we identify three ecological mechanisms through which drought modifies infection dynamics:

concentrating organisms into shrinking refugia, 

selectively favoring drought-tolerant hosts, vectors, and pathogens, and

amplifying transmission heterogeneity across landscapes.

By linking hydrological change to core epidemiological and ecological processes, this framework highlights parasite traits and strategies likely to be favored during drought while providing a foundation for forecasting infections in a water-limited world."

ScienceAdviser

Drought is reshaping the spread of infectious diseases (original news release)

Plagued by drought: how water scarcity reshapes host–parasite interactions (no public access)

14 distinct foodborne parasites drive ~277 million illnesses worldwide

Bad news! Next time you travel to some of these regions ...

"... finds a new WHO analysis published in The Lancet Global Health; the research highlights “the significant burden” of “these often-overlooked diseases” that disproportionately affect low-resource regions. ..."

From the abstract:

"Background

Over 10 years ago, WHO estimates of hazard-specific foodborne disease burdens showed that parasites exert considerable health burdens globally. We updated these estimates, focusing on 14 invasive parasitic diseases.

Methods

Incidences, deaths, and disability-adjusted life-year (DALY) burdens were estimated for each parasitic disease from 2000 to 2021, using data from systematic reviews and the Global Burden of Diseases, Injuries, and Risk Factors Study.

For some diseases, structured expert judgement was used to estimate proportions of foodborne infection.

Data were pooled via hierarchical meta-regression models with uncertainty propagated through Monte Carlo simulations following disease-specific computational models defined by incidence rates and probability parameters.

Findings

We estimated that 277 million illnesses were caused by potentially foodborne invasive parasites, with approximately 171 million attributable to foodborne transmission.

Considerable heterogeneity by parasite, in magnitude and uncertainty, was observed. Of 4·89 million foodborne DALYs associated with these diseases, highest contributions were from Taenia solium (1·3 million) and Clonorchis sinensis (0·921 million), both also associated with most foodborne deaths.

Burden was greatest in the region of the Americas, predominantly due to Chagas disease, followed by the African region, where neurocysticercosis-associated epilepsy caused most burden.

Burdens decreased globally from 2000 to 2021, except in the Western Pacific region, where the burden, predominantly associated with clonorchiasis, is rising.

Interpretation

Foodborne parasitoses cause considerable suffering, with some populations and regions particularly at risk. These data provide a baseline by which effects of interventions can be assessed and emphasis directed to those parasites exerting the greatest burden."

Global Health NOW: ‘Ebola Is Winning’; and Old Fears Amid a New Uranium Boom

WHO estimates of the global, regional, and national foodborne burdens of 14 invasive parasitic diseases, 2000–21: an updated data synthesis

Hookworms have spent millions of years surviving inside a human host. Really!

Last time I checked, the earliest humans came about only roughly several hundred thousand years ago!

"“The hookworm has spent millions of years perfecting how to assure long-term survival inside a human host and how to get molecules out of its body and into ours,” said co-author of a new study Makedonka Mitreva in a statement. “We asked: What if we could add one more molecule to the roughly 1000 things the worm already secretes, something therapeutically useful to people?” ..."

ScienceAdviser

Genetically modified hookworms produce and deliver therapeutics

Makedonka Mitreva (Source) knows something about hookworms! 😊

New discovery about the parasite behind sleeping sickness

Good news!

"Scientists discovered that the parasite behind sleeping sickness builds an “invisibility cloak” from special proteins, solving a 40-year mystery about how the deadly disease hides in the body for years."

"... Newly discovered ESB2 proteins may be the reason why. These collectively create a barrier structure called a variant surface glycoprotein (VSG). At the same time, the parasite is also precisely editing its genes to hide inside its host. ..."

From the abstract:

"Antigenic variation is an immune evasion strategy used by pathogens, including Trypanosoma brucei. This parasite expresses a single variant surface glycoprotein (VSG) from a large genetic repertoire, which it periodically switches throughout an infection.
VSGs are co-transcribed with expression-site-associated genes (ESAGs) within a specialized nuclear body, but there is substantial differential expression and the regulatory mechanisms remain unclear.

Here we applied TurboID-mediated proximity labelling mass spectrometry to map the subnuclear expression-site body (ESB) post-transcriptional network. We identify and characterize three previously undescribed components: ESB-associated protein 1 (ESAP1) and ESB-specific proteins 2 and 3 (ESB2 and 3). These proteins form discreet subnuclear condensates that are developmentally regulated. ESB2 is an active RNA endonuclease that negatively regulates ESAG transcripts. Its recruitment depends on a hierarchy involving VEX2, ESAP1 and ESB3, a constant flux of active transcription and RNA processing, and its own nuclease activity. Overall, we uncover a molecular mechanism that fine-tunes expression of virulence genes through specialized RNA decay in T. brucei."

Tuesday, March 31, 2026 - Join The Flyover

Parasitic sleeping sickness creates ‘invisibility cloak’ to hide in humans for years "After 40 years, biologists made a breakthrough in understanding the deadly disease."

University of York scientists solve 40-year-old biological mystery behind Sleeping Sickness (original news release) "Scientists at the University of York have cracked a 40-year-old biological cold case by revealing how the parasite that causes Sleeping Sickness stays one step ahead of the human immune system."

Specialized RNA decay fine-tunes monogenic antigen expression in Trypanosoma brucei (open access)

Fig. 1: VEX1 and VEX2 PL–MS identified novel ESB-specific, SLAB and NUFIP body components.

The DNA of the the African trypanosome parasite in magenta and it's protective "cloak" in green

How parasitic ants take over entire ant colonies via matricide

What a horror story about ant colonies! Don't exclusively trust your sense of smell!

"The queen is dead, long live the queen!

After disguising herself and sneaking behind enemy lines, an invader manipulates a group of loyal subjects into attacking and murdering their own queen. She flees the scene of the crime, returning later to institute a new regime—with herself as matriarch. ... a fairly typical life cycle for some parasitic ant species.

Lasius orientalis and L. umbratus, which take over colonies belonging to related ant species rather than founding their own, are what’s known as temporary social parasites. And as scientists report in Current Biology, they follow the same gruesome playbook .

The parasitic queen ant first avoids suspicion by mingling with host workers, cloaking herself with the characteristic scents of the colony. After locating the host queen, the invader douses her with multiple jets of a foul-smelling abdominal fluid. This substance likely contains formic acid, which masks the queen’s natural odor and makes her smell like an enemy—thus transforming her “from mother to menace,” ...

While the intruder beats a hasty retreat, the host queen’s subjects attack and dispose of their unfortunate ruler, who is, biologically speaking, also their mother. The parasitic queen then returns to lay eggs and take control of the workers, who serve their new queen until they die."

From the abstract:

"Matricide — the killing of a mother by her own genetic offspring — is rarely observed in nature, but not unheard-of. Among animal species in which offspring remain with their mothers, the benefits gained from maternal care are so substantial that eliminating the mother almost never pays, making matricide vastly rarer than infanticide.

Here, we report matricidal behavior in two ant species, Lasius flavus and Lasius japonicus, where workers kill resident queens (their mothers) after the latter have been sprayed with abdominal fluid by parasitic ant queens of the ants Lasius orientalis and Lasius umbratus."

ScienceAdviser

This parasitic ant tricks workers into killing their own queen "Scientists capture a unique—and gruesome—example of matricide in the animal kingdom"

Socially parasitic ant queens chemically induce queen-matricide in host workers (open access)

Ants around two similar looking smelling "queens"

After infiltrating a colony and disguising her scent, an invading Lasius orientalis queen (black) sprays a L. flavus host queen (brown) with abdominal fluid—tricking the host workers into attacking and killing their own queen.

Figure 1 Behavioural sequences of two socially parasitic queens causing unwitting matricide by host workers.

Parasite disguises itself with human proteins to evade immune system

Amazing stuff! Very clever!

"Parasites are known to infect human cells through a variety of ingenious mechanisms. Many of them have even evolved sophisticated strategies to evade a host’s immune system by avoiding it entirely.

One type of parasite, Entamoeba histolytica, has developed a very intriguing way to do this. It rips pieces off human cells and steals the proteins to wear them as a disguise. ...

Instead of ingesting cells in such a way that will kill them, this parasite bites chunks off the cells and leaves them wounded. But it doesn’t merely eat these pieces for food; it steals their proteins, namely CD46 and CD55, from the outer membrane of the cell and cloaks them around its own surface. These two proteins are used to shield human cells from being attacked by the immune system.

With the integration of proteins around itself, the immune system’s defenses assume E.  histolytica is a part of the host, allowing amoebae to remain invisible. This process of taking another cell's proteins is called trogocytosis. ..."

From the abstract:

"Entamoeba histolytica is a major cause of diarrheal disease. E. histolytica trophozoites (“amoebae”) can invade the intestine and disseminate via the bloodstream, resisting complement lysis through unknown mechanisms. Amoebae kill human cells by performing trogocytosis. After performing trogocytosis, amoebae display human proteins on their own surface and are resistant to lysis by human serum.

In this study we sought to further evaluate the mechanism by which amoebae resist complement. To test if complement is responsible for lysis of amoebae, C3-depleted serum was compared to replete serum, and C3 was required for lysis. Amoebae were allowed to perform trogocytosis of human cells and exposed to mouse serum. Although they had performed trogocytosis on a different species than the source of the serum, they were protected from lysis. To test if the protection from lysis by mouse serum was due to the functional interchangeability of human and mouse complement pathway proteins, human CD46 or CD55 (negative regulators of complement activation) were exogenously expressed. Amoebae that expressed human CD46 or CD55 were protected from lysis by mouse serum, indicating that display of human proteins was sufficient to inhibit mouse complement activation.

Finally, amoebae were allowed to perform trogocytosis of a cell type in which the complement pathway is not conserved, and they did not become resistant to lysis. Overall, these findings are consistent with the model that trogocytosis enables amoebic acquisition and display of host proteins, including negative regulators of the complement pathway, that provide protection from complement lysis. Since other microbes can perform trogocytosis, this novel mechanism for complement resistance might apply to other infections."

Parasite disguises itself with human proteins to evade immune system

Wily Parasite Kills Human Cells and Wears Their Remains as Disguise

Cross-species protection suggests Entamoeba histolytica trogocytosis enables complement resistance through the transfer of negative regulators of complement activation (open access)

Fig. 2 Trogocytosis of human cells protects amoebae from lysis by mouse serum.

Entamoeba histolytica is a single-cell parasite that causes intestinal disease, but sometimes invades the body, attacking cells and creating liquefying abscesses. ... Image shows E. histolytica (green) attacking human T-cells (white blood cells). 

Katherine Ralston parasitologist

The New World Screwworm spreads in Mexico while the US suspends live animal imports from Mexico

Don't be screwed! Pardon my bad humor!

"The U.S. has suspended live cattle, horse, and bison imports along the Southern border because of the New World Screwworm’s spread in Mexico; screwworm larvae burrow into the flesh of warm-blooded animals (including, rarely, people) and can kill. ..."

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What to know about screwworm as U.S. suspends Mexican cattle imports

Discovery Illuminates How Sleeping Sickness Parasite Outsmarts Immune Response

Good news!

"Researchers have uncovered a key mechanism used by the parasite that causes African sleeping sickness to evade antibodies... Trypanosoma brucei “constantly changes a surface coat made up of millions of copies of a single protein.” ..."

"... Using a mouse model, the researchers showed that Trypanosoma brucei essentially plays a game of hide-and-seek by setting up shop in its hosts’ tissues, allowing it to constantly change its protective surface coat and evade antibodies. ...

The T. brucei parasite constantly changes a surface coat made up of millions of copies of a single protein—the variant surface glycoprotein (VSG). Once one VSG has been recognized by a host’s antibody response, the parasite has already “switched” to a new one, which the immune system hasn’t spotted yet. By changing which of these variant genes is active, the parasite can alter its appearance enough to evade its host’s immune response for long periods. ..."

From the abstract:

"The protozoan parasite Trypanosoma brucei evades clearance by the host immune system through antigenic variation of its dense variant surface glycoprotein (VSG) coat, periodically ‘switching’ expression of the VSG using a large genomic repertoire of VSG-encoding genes. Recent studies of antigenic variation in vivo have focused near exclusively on parasites in the bloodstream, but research has shown that many, if not most, parasites reside in the interstitial spaces of tissues. We sought to explore the dynamics of antigenic variation in extravascular parasite populations using VSG-seq7, a high-throughput sequencing approach for profiling VSGs expressed in populations of T. brucei. Here we show that tissues, not the blood, are the primary reservoir of antigenic diversity during both needle- and tsetse bite-initiated T. brucei infections, with more than 75% of VSGs found exclusively within extravascular spaces. We found that this increased diversity is correlated with slower parasite clearance in tissue spaces. Together, these data support a model in which the slower immune response in extravascular spaces provides more time to generate the antigenic diversity needed to maintain a chronic infection. Our findings reveal the important role that extravascular spaces can have in pathogen diversification."

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Discovery Illuminates How Sleeping Sickness Parasite Outsmarts Immune Response "Parasite spread by tsetse flies persists in hosts by hiding in tissues and evading antibodies"

Tissue spaces are reservoirs of antigenic diversity for Trypanosoma brucei (no public access, but article above contains link to PDF)

Another new wasp species, the 18th new species, all discovered by researchers at Rice University since 2014

Amazing stuff! Will extinction be faster than discovery of all species?

This new species was again discovered on campus of Rice University!

A wasp that parasitizes another wasp!

"A newly identified wasp species, Chrysonotomyia susbelli, has been discovered in Houston, Texas, marking the 18th new species identified by Rice University's Scott Egan and his research team since 2014. The discovery, the fourth wasp species found on the university grounds in seven years, reveals the hidden world of parasitoid wasps and the intricate ecosystems that thrive outside our doors. ..."

From the abstract:

"A new species of the genus Chrysonotomyia Ashmead, Chrysonotomyia susbelli sp. nov., is described from the Rice University campus in Houston, Texas, USA. The species is a parasitoid emerging from Neuroterus nr. bussae galls in leaves of the southern live oak (Quercus virginiana). This represents the 6th species described from North America north of Mexico and the first in the world known to parasitize cynipid gall wasps. This discovery hints at an entire undiscovered niche between Chrysonotomyia parasitoids, cynipid gall wasps, and oaks in the Nearctic, which is a global biodiversity hotspot for oaks and cynipids. This new species description is complemented by mtDNA-COI-barcode data and information on the natural history of this species. We record host association, phenology, and report a leaf-scanning behavior performed by females, presumably to search for host galls. Modifications to the key of New World members of the genus (Hansson 2004) are included to integrate this new species."

Another new wasp species discovered by researchers

Another new wasp species discovered by researchers on Rice campus (original news release)

Description of a new species of Chrysonotomyia Ashmead from Houston, Texas, USA (Hymenoptera, Chalcidoidea, Eulophidae) (open access)

The Chrysonotomyia susbelli. It is "about 1 millimeter long". What a beauty!

Domestic cat parasite linked to speeding up age-related frailty in humans

Pets and pests! Your best friend?

"The single-cell parasite Toxoplasma gondii is well known for triggering risky behavior in hosts, in order to facilitate easier transmission, and can cause serious mental and physical conditions. But now this tiny bug that thrives in cats (via rats and birds) has been implicated in accelerating age-related frailty. ...
But even if it lies dormant and largely asymptomatic, scientists believe it may be partly to blame for accelerating age-related frailty, not through the infection itself but the body’s immune system response to its microscopic invader. ..."

"A common, cat-borne parasite already associated with risk-taking behavior and mental illness in humans may also contribute to exhaustion, loss of muscle mass, and other signs of “frailty” in older adults ...

Approximately 11% to 15% of people in the U.S. have been infected with T. gondii at some point and rates tend to be far higher in older individuals. In some countries, more than 65% have been infected. Once infected, people can unknowingly harbor the parasite for life. ..."

"Abstract

Background

Persistent inflammation related to aging (“inflammaging”) is exacerbated by chronic infections and contributes to frailty in older adults. We hypothesized associations between Toxoplasma gondii (T. gondii), a common parasite causing an oligosymptomatic unremitting infection, and frailty, and secondarily between T. gondii and previously reported markers of immune activation in frailty.

Methods

We analyzed available demographic, social, and clinical data in Spanish and Portuguese older adults [N = 601; age: mean (SD) 77.3 (8.0); 61% women]. Plasma T. gondii immunoglobulin G (IgG) serointensity was measured with an enzyme-linked immunosorbent assay. The Fried criteria were used to define frailty status. Validated translations of Mini-Mental State Examination, Geriatric Depression Scale, and the Charlson Comorbidity Index were used to evaluate confounders. Previously analyzed biomarkers that were significantly associated with frailty in both prior reports and the current study, and also related to T. gondii serointensity, were further accounted for in multivariable logistic models with frailty as outcome.

Results

In T. gondii-seropositives, there was a significant positive association between T. gondii IgG serointensity and frailty, accounting for age (p = .0002), and resisting adjustment for multiple successive confounders. Among biomarkers linked with frailty, kynurenine/tryptophan and soluble tumor necrosis factor receptor II were positively associated with T. gondii serointensity in seropositives (p < .05). Associations with other biomarkers were not significant.

Conclusions

This first reported association between T. gondii and frailty is limited by a cross-sectional design and warrants replication. While certain biomarkers of inflammaging were associated with both T. gondii IgG serointensity and frailty, they did not fully mediate the T. gondii–frailty association."

Hell-no Kitty: Cat parasite linked to speeding up age-related frailty

How a dirty litter box could slow you down as you age

Toxoplasma gondii IgG Serointensity Is Positively Associated With Frailty (open access)

Fig 1 Life cycle. Members of the Felidae family are the only known definitive hosts for Toxoplasma gondii (domestic cats and their relatives). The cat’s waste contains unsporulated oocysts.

The bizarre world of parasitic wasps

Very recommendable! Gruesome! Almost a horror story!

Parasite gives wolves what it takes to be pack leaders

Amazing stuff! So what parasites have which behavioral effects on humans (actually the Wikipedia on Toxoplasmosis mentions a few known prominent cases)? 

Maybe one day we will find out that Putin the Terrible was also infected by Toxoplasmosis! 😊

This study is based on a very unique dataset on the wolf population in the Yellowstone National Park for over 27 years.

"Wolves infected with a common parasite are more likely than uninfected animals to lead a pack, according to an analysis of more than 200 North American wolves. Infected animals are also more likely to leave their home packs and strike out on their own. ...
Warm-blooded mammals can catch the parasite by eating an infected animal or ingesting forms of T. gondii shed in the faeces of infected cats. After a period of acute infection, semi-dormant cysts form in muscle and brain tissue, and persist for the rest of the host’s life. Up to one-third of humans might be chronically infected. ...
a rare opportunity to link infection with behaviour in wild wolves: data on grey wolves (Canis lupus) collected intensively in Yellowstone National Park, Wyoming, over nearly 27 years. ...
The team looked at 256 blood samples from 229 wolves, which had been carefully watched throughout their lives, and had their life histories and social status recorded. ... found that infected wolves were 11 times more likely than uninfected ones to leave their birth family to start a new pack, and 46 times more likely to become pack leaders — often the only wolves in the pack that breed. ..."

From the abstract:

"Toxoplasma gondii is a protozoan parasite capable of infecting any warm-blooded species and can increase risk-taking in intermediate hosts. Despite extensive laboratory research on the effects of T. gondii infection on behaviour, little is understood about the effects of toxoplasmosis on wild intermediate host behavior. Yellowstone National Park, Wyoming, USA, has a diverse carnivore community including gray wolves (Canis lupus) and cougars (Puma concolor), intermediate and definitive hosts of T. gondii, respectively. Here, we used 26 years of wolf behavioural, spatial, and serological data to show that wolf territory overlap with areas of high cougar density was an important predictor of infection. In addition, seropositive wolves were more likely to make high-risk decisions such as dispersing and becoming a pack leader, both factors critical to individual fitness and wolf vital rates. Due to the social hierarchy within a wolf pack, we hypothesize that the behavioural effects of toxoplasmosis may create a feedback loop that increases spatial overlap and disease transmission between wolves and cougars. These findings demonstrate that parasites have important implications for intermediate hosts, beyond acute infections, through behavioural impacts. Particularly in a social species, these impacts can surge beyond individuals to affect groups, populations, and even ecosystem processes."

Parasite gives wolves what it takes to be pack leaders Study is one of the few to show the behavioural effects of Toxoplasma gondii in wild animals.

Parasitic infection increases risk-taking in a social, intermediate host carnivore (open access)

Fig. 1: Map of cougar density and T. gondii seroprevalence in wolves in Yellowstone National Park (YNP).