Mercury is a pollutant with a particularly insidious chemistry. Released into the atmosphere by coal combustion, industry and artisanal gold mining, elemental and inorganic mercury eventually settles into wetlands, lake sediments and flooded soils, where anaerobic microbes — sulphate-reducing bacteria chief among them — bolt a carbon atom onto the metal to produce methylmercury. That organic form is lipophilic, crosses biological membranes with ease, binds strongly to sulphur-containing proteins and, crucially, biomagnifies: each step up the food web concentrates it further. For amphibians the exposure routes are unusually numerous. Tadpoles graze contaminated periphyton in ponds; adults hunt invertebrates on land; and the highly permeable skin that makes frogs and toads such elegant physiological instruments also makes them poor barriers against dissolved contaminants. Because amphibians straddle aquatic and terrestrial food webs, and because their populations have been declining worldwide for decades, understanding how much mercury they carry — and where it goes inside their bodies — matters both for conservation and for reading the health of entire landscapes. Recent surveys in North America and Europe have detected methylmercury in adult amphibians across broad geographic ranges, including in urban toads living close to major cities, underscoring how little this exposure has been mapped at the level of individual organs, let alone the organs of their parasites.

The new work, led by Tímea Brázová of the Institute of Parasitology at the Slovak Academy of Sciences in Košice, together with colleagues from the Academy’s Institute of Geotechnics and the I. I. Schmalhausen Institute of Zoology in Kyiv, took advantage of a grim but ethically unimpeachable resource: toads killed on roads during their breeding migrations. Road traffic is among the best-documented causes of amphibian mortality in Europe, and using already-dead carcasses allowed the team to sample wild adults without killing a single animal for research. The researchers collected common toads (Bufo bufo) from two sites in eastern Slovakia chosen for their contrasting levels of environmental contamination, assisted in the field by Košice’s municipal forestry service and the staff of the Vihorlat Protected Landscape Area. From each specimen they dissected five host tissues — skeletal muscle, liver, kidneys, lungs and skin — and recovered the parasitic nematodes harboured by their hosts, creating paired host-and-parasite datasets that could be compared across the two habitats.

The analytical design was deliberately modern. Total mercury concentrations were quantified separately in every tissue and worm sample, and the resulting values were fed into Bayesian multilevel regression models built with the brms framework, which interfaces with the Stan probabilistic programming language. Rather than forcing the data into rigid classical tests, Bayesian hierarchical modelling estimates full probability distributions for each candidate effect — habitat, sex and the body condition factor — and quantifies uncertainty even at the modest sample sizes typical of wildlife toxicology. Model adequacy was screened with posterior predictive checks and dedicated residual diagnostics, and effect estimates were derived with contemporary marginal-effects tooling. In parallel, the team ran a standard parasitological work-up, computing prevalence, abundance and intensity of infection according to the conventional ecological definitions, and carried out a morphometric assessment based on fourteen external body traits, testing whether chronic mercury exposure had sculpted visible anatomical differences between toads from contaminated versus comparatively clean ground.

The first result was, in one sense, textbook toxicology. In both populations, mercury followed a strictly tissue-specific pattern, piling up highest in the body’s detoxification machinery — above all the kidneys, closely followed by the liver. The biology behind this ordering is well understood. The kidney receives a substantial share of cardiac output and actively filters circulating metal complexes; renal tubule cells produce metallothioneins, small cysteine-rich proteins whose thiol groups bind divalent metals such as inorganic mercury and lock them into inert intracellular complexes. The liver, meanwhile, is the metabolic hub where contaminants are transformed, conjugated and either stored or shunted into bile. Muscle — the tissue humans typically consume from fish — ranked far lower, while lung and skin, two exchange surfaces in constant contact with water and air, occupied intermediate ground. What made the pattern scientifically valuable was its consistency: the same internal hierarchy appeared in toads from both the polluted and the cleaner site, suggesting that tissue-level routing of mercury within the body is governed by organ physiology even as overall burden is set by the environment.

The Bayesian models then delivered their sharpest single verdict: habitat, not biology, was the primary driver of mercury burden. Neither sex nor body condition had a statistically meaningful effect on host tissue mercury concentrations. In other words, a lean male from the contaminated site carried a heavier internal load than a robust female from the clean one, regardless of individual characteristics. The parasitological data, however, told a more complicated story. At the contaminated site, infection levels were markedly higher, with nematode prevalence reaching one hundred percent — every single toad examined was infected. And across the dataset, female toads harboured significantly higher parasite abundances than males, a pattern that could reflect sex differences in foraging ecology, hormonal modulation of immune defences, or pollutant-driven immunosuppression. The observation dovetails with a recent meta-analysis reporting that environmental contaminant exposure generally heightens amphibians’ susceptibility to parasitism, and it hints that pollution may be reshaping not just contaminant loads but entire host-parasite relationships.

Perhaps the most quietly unsettling result was what the team did not find. Fourteen measured morphological traits, compared between the two populations, revealed no statistically discernible differences. Chronic mercury exposure, at the levels these toads experienced, had left no visible signature on their bodies. Toads from the contaminated site looked, to the calipers, exactly like their unpolluted counterparts — even as their kidneys and livers carried heavier metal burdens and their infection rates ran far higher. For biomonitoring, that is a caution: external morphology can appear entirely normal while internal physiology is anything but. It also means the classic “canary in the coal mine” image needs refining for amphibians. The warning signs of mercury in these animals are written in biochemistry and organ burdens, not in body shape — at least across the trait set measured here — and researchers relying on visual or morphological screening alone could easily conclude that a population is healthy when its tissues tell a different story.

The heart of the paper lies in its bioconcentration factors — ratios comparing mercury concentrations in parasites with those in host tissues — and in the counterintuitive way those ratios flip with exposure. Under high environmental contamination, the toads’ own detoxification organs accumulated more mercury than their nematodes did. Under lower contamination, the relationship reversed: the worms sequestered mercury more efficiently than any host tissue. The interaction is therefore concentration-dependent, and it reframes what parasites are actually doing inside polluted animals. At modest exposure, an intestinal worm can function as a biological sink, intercepting metal from the host’s gut contents and locking it away — arguably a service, since that metal is not circulating toward the host’s own organs. Under heavy exposure, the worms appear to saturate, and the host’s kidneys and liver shoulder the accumulating load. Notably, parasite abundance alone was not a strong predictor of host mercury levels; it is the ambient exposure concentration, not the number of worms, that governs where the metal ultimately resides. For a field that has long debated whether parasites protect their hosts from toxicants or aggravate their plight, this study offers a cleaner answer: both, depending on dose.

The implications reach in several directions at once. For decades, parasitologists and toxicologists worked largely in parallel — one group counting worms, the other weighing metals — even as scattered studies on fish, seals and lizards hinted that helminths can concentrate heavy metals to levels exceeding those of their hosts. The present work extends that logic to an amphibian host-parasite pair under natural, contrasting field conditions and demonstrates that ecotoxicological risk assessments ignoring a host’s parasite community may misjudge where contaminant mass actually sits within the body, and therefore misestimate toxicological risk to the animal itself and to whatever preys upon it. Conservation programmes for declining amphibian populations may need to read mercury exposure and infection status together rather than separately, since the two interact. And the ethical sampling model — converting roadkill into high-resolution contaminant data — offers wildlife agencies a low-cost, zero-lethal template for surveillance that could be replicated along any migration route in Europe. Funded by the Slovak VEGA grant agency and the European Next Generation EU recovery and resilience programme, the Košice-based team argues that host-parasite dynamics must now be built into ecotoxicological frameworks outright rather than treated as biological noise. In the chemistry of a polluted landscape, it turns out, even the worms have a role — and whether they act as allies or accomplices of the toad depends entirely on how much mercury is in the mud.