Ascaris lumbricoides and Ascaris suum

In brief

What it is

Ascaris is a nematode: a roundworm, meaning an unsegmented worm circular in cross-section, from a vast group that includes both harmless soil organisms and some of the most common parasites of people and livestock. The two members of the genus that concern medicine are the one named from humans by Linnaeus in 1758, Ascaris lumbricoides, and the one named from pigs by Goeze in 1782, Ascaris suum ¹. The adult female in the human small intestine is the largest worm routinely found there, long enough to be recognized without a microscope — the genus is described in the literature as a group of giant parasitic roundworms ⁸ — and the worms are distributed very unevenly between people: a small minority of hosts carry most of the worms, a pattern called overdispersion whose cause remains unknown ^7,38.

The two worms cannot be separated by looking at them. That is not a minor technical problem but the origin of the whole taxonomic argument, which the next section takes up: every claim that they are one species or two rests on molecules rather than on morphology, the two being described as morphologically indistinguishable ^1,8. The molecular resources arrived late. A 273-megabase draft genome of the pig worm — 273 million letters of DNA — was published in 2011, with low repeat content, meaning the share of the genome made up of repeated sequences, at 4.4%, about 18,500 protein-coding genes, and a set of secreted molecules numbering around 750, rich in protein-cutting enzymes that help the larva get through host tissue and in molecules that look built to blunt the host's immune response ³. A reference-quality 296-megabase genome with 17,902 protein-coding genes, assembled from a worm taken from a person in Kenya, followed in 2020 ⁴.

What the worm does for a living is straightforward and the reason it is so successful. It lives in the small intestine, bathed in partly digested food, and sheds enormous numbers of eggs into the feces. It needs no intermediate host, no insect, no snail: the whole cycle is a person or a pig, the ground, and another mouth ¹¹. That simplicity is also the reason the infection is bound so tightly to sanitation, why it has become rare, though not absent, in countries that built sewers — where the cases that remain are often caught from pigs ¹⁵ and where modeled prevalence is lowest ⁶ — and why it persists where open defecation continues ⁹. Sanitation alone is not a quick fix: in a cluster-randomized trial in rural Kenya, with 9,077 children sampled across 622 clusters, a latrine upgrade by itself did not detectably reduce this worm (prevalence ratio 0.89, 95% confidence interval 0.73 to 1.08), whereas household water treatment (0.82, 0.67 to 1.00) and the combination of water treatment, sanitation and handwashing (0.78, 0.63 to 0.96) did ³⁹.

One more feature belongs in the opening description, because it keeps turning up in the clinical sections. The adult worm is a wanderer. It can climb up the small intestine into the stomach and be vomited — 19 of 40 patients in the founding Kashmir series vomited worms during an attack of biliary colic ^14,40 — down into the appendix ⁴¹, or sideways into the ampulla of Vater, the small opening through which the bile duct and pancreatic duct drain into the duodenum ¹⁴. Much of the serious disease this animal causes comes from the larva's journey through the lungs, from an adult worm that has left the place it belongs, or, in the commonest surgical emergency, from a bolus of worms obstructing the small intestine where they normally live ¹³.

One species or two: the question that will not close

Four positions are logically available, and in 2012 Leles and colleagues laid them out explicitly: the two worms are separate species that diverged from a common ancestor before pigs were domesticated; the human worm is derived from the pig worm; the pig worm is derived from the human worm; or the two are one species. They concluded for the fourth, and drew the nomenclatural consequence: if they are one species, the older name wins, so A. lumbricoides Linnaeus 1758 has priority and A. suum Goeze 1782 should be treated as a synonym ¹. That paper is a review and an argument, and fourteen years later the field has not adopted its conclusion as a formal act, which is itself informative.

The evidence arrived in three waves. The first, in the 1990s and 2000s, found host association. Anderson examined nine human cases from North America, a region where the parasite is not endemic, and found that a HaeIII restriction site — a short stretch of DNA cut by the enzyme HaeIII, used here as a marker — in ribosomal DNA, the repeated genes that build the cell's protein factories, was present in more than 96% of pig-derived worms worldwide and in all nine of the North American human worms, but in fewer than 2% of worms from people in endemic countries — those nine people had caught the parasite from pigs ⁴⁹. In China, Peng and colleagues typed 486 human and 329 pig worms from six regions and found five genotypes, with G1 in roughly 63-74% of human worms and G3 in roughly 79-86% of pig worms ⁵⁰. Each host, in other words, carried its own population. Cross-infection had also been tested directly, and early: worms of human and of pig origin were raised in pigs and rabbits in 1968 ⁵¹, and people in Japan were deliberately given worms of both origins in 1951 ⁵². Neither indexed record carries an abstract, so only the existence and the design of those experiments are cited here, not their results. Anderson himself then published a warning that reading species boundaries from a single marker, particularly mitochondrial DNA, could give ambiguous answers ⁵³.

The second wave looked for gene flow, and found it. In 2007, Criscione and colleagues used 23 microsatellite markers and Bayesian clustering — a statistical method that sorts individuals into groups by their genotypes — across worms from several countries. Differentiation was driven first by geography and only second by host within a location, a pattern they read as multiple independent host shifts rather than one; but three concordant statistical methods assigned 4% of Guatemalan worms and 7% of Chinese worms as hybrids ⁴⁷. Five years later the Chinese group reversed its own earlier position. Genotyping 258 worms at 20 microsatellite loci across six provinces, they found cross-infection in every location — and almost all of it in one direction: of 20 cross-infection events, 19 were people carrying pure pig-type worms and only one was a pig carrying a human-type worm. Hybrids were present in both hosts and in every location, and 95% of them came from people ⁴⁸. A later analysis from the same group using simple sequence repeats, another name for microsatellites, put the genetic differentiation index — which runs from 0 for populations interbreeding freely to 1 for populations entirely separate — at 0.0593, a value implying substantial gene flow, and resolved the worms into three clusters interpreted as human-type, pig-type and hybrid ⁵⁴. Peng's own review, published online in 2006 and in print in 2007, had argued the opposite — that cross-infection was limited and pigs were not a significant reservoir in endemic regions — partly on the strength of an experiment showing that eggs of the human-derived genotype established as adults in pigs significantly less well than the pig-derived genotype ³³. Weidong Peng is the first author of that earlier review and the senior author of the 2012 study, so this is one group correcting itself in public.

The third wave is genomic. In 2020 Easton and colleagues assembled a reference-quality genome from a single worm and then sequenced 68 more, collected from 60 people in Kenyan villages where pig husbandry is rare. The result was the hardest to explain away: 63 of the 68 worms had mitochondrial genomes clustering closer to the pig parasite than to the human one, and across the nuclear genomes there were over 11 million single-nucleotide polymorphisms — single-letter differences in DNA between individuals — resolving into just two distinct genetic types that had recombined with one another. Every sample was a genetic mosaic. The authors' phrase is a highly interbred species genetic complex, and their conclusion is that no barrier appears to exist to onward human-to-human transmission of hybrid worms ⁴.

The dissent is in print and should be read. Cavallero and colleagues, who in 2013 analyzed 151 worms and concluded there was homogenizing gene flow making the two variants of a single polytypic species, meaning one species made up of distinguishable regional or host forms ⁵⁵, genotyped 237 worms from Italy, Slovakia and Colombia in 2021 and wrote that, despite the evidence of equilibrium in Italian pig samples, the amount of genetic variation seems to support the existence of two closely related species ¹⁹. The same group, with a larger sample, moved the other way. A field in which two of its most productive laboratories have each reversed direction on the central question is not a field with a settled answer.

Where does 2023 to 2026 leave it? Not resolved, but better described. Multilocus work on worms expelled from children across six districts of Khyber Pakhtunkhwa in Pakistan found divergence under 1% at the mitochondrial cox1 gene (cytochrome c oxidase subunit 1, a mitochondrial gene widely used as a DNA barcode) and sequences of the two named species intermixed in the phylogeny, and concluded for a genetically interconnected species complex rather than clearly separated species. The authors are careful about what intermixing means: they read it as consistent with incomplete lineage sorting, the retention of shared ancestral variants from before the populations split, as well as with historical introgression ³⁴. Indian worms sequenced at two mitochondrial genes, nad1 (NADH dehydrogenase subunit 1) and cox1, gave 27 and 25 haplotypes — a haplotype being one particular version of a DNA sequence — with Indian sequences closely allied to Chinese and Brazilian ones from both hosts, although pig-derived sequences formed a separate clade in the second of the two networks; the authors read the whole as supporting earlier evidence of hybridization ⁵⁶. The indexed abstract has had the gene names stripped out, so which gene gave 27 haplotypes and which gave 25 is a reconstruction from the order in the title. In Thailand, cox1, nad1 and beta-tubulin typing found 13 haplotypes with no clear geographic structuring, all isolates in a single major lineage, and haplotypes shared with the pig parasite ⁵⁷. And in 2026 a scalable method for building mitochondrial genomes out of low-coverage whole-genome data yielded 149 assemblies and named a fourth clade, Clade D, in human samples from Ethiopia, while showing Clade C to consist of pig-derived worms from Europe ⁸. Clade structure is getting finer, not coarser; the clades are maternal lineages, and a maternal lineage is not a species.

The honest statement, and the one this page takes, is the one the modern literature itself now uses: this is one species complex with host-associated populations and ongoing genetic exchange between them. Host association is real and measurable and in some settings strong enough that pigs contribute little to human infection ³³; even where gene flow runs largely along host lines, shared haplotypes show cross-transmission, and the authors of the Cameroon study conclude that control should target both hosts ⁵⁸; and gene flow is also real and measurable and in some settings dominant ^4,48. Which of those is true depends on where you are standing. That is an awkward thing for a taxonomy that demands a single answer, and it is why the two names persist in use while only a minority — including the 2021 three-country analysis ¹⁹ — still argues that these are two closely related species.

Two lines of supporting evidence deserve a mention because they are sometimes cited as though decisive and are not. Comparing microRNA profiles of adult worms from the two hosts found 74 shared candidates out of 171 and 494 detected, which the authors read as additional evidence for a single species; they attribute the large difference in candidate counts to the fast evolution of microRNAs — small RNA molecules that regulate genes — under the different living conditions of humans and pigs, and a technical explanation such as unequal sequencing depth cannot be ruled out from the abstract ⁵⁹. And worms from a chimpanzee and a gibbon in a Chinese zoo were shown by mitochondrial genome comparison to be a single species genetically similar to the human roundworm ⁶⁰, which tells you the genus is not confined to people and pigs but rests on two animals. Finally, the deep history has been probed directly: ancient DNA using a 142-base-pair (142-letter) target in the mitochondrial cytochrome b gene recovered Ascaris sequences from pre-Columbian South American coprolites, preserved ancient feces, that microscopy had called negative, changing the assumed prehistoric distribution of the parasite in the Americas ⁶¹.

The whole history, including what was overturned

The arc runs from two eighteenth-century names to a 2026 mitochondrial clade, and along the way three things were believed and then revised: that the two worms were obviously separate species; that the eggs are practically indestructible, when in fact most die quickly and a minority persist for years ^42,43; and that deworming whole populations of children makes them grow and learn better, which the health trials do not support, although the long-run economic case is still argued ^31,32. A fourth belief, that ivermectin is the weak drug against this worm, is not supported by the pooled randomized trials either ⁶³.

On the lung migration, a caution is owed. Shimesu Koino's 1922 self-experiment, in which he is said to have swallowed counted numbers of eggs and recovered larvae from his own sputum, is usually cited as the demonstration that the larvae pass through human lungs; it appeared in a Japanese journal that PubMed does not index, so it is not cited as a source here and its contents are not carried as fact. What is sourced is the migration route itself, which the current clinical reviews set out plainly ¹¹ and which the animal work follows stage by stage ^36,37, and the lung disease it causes, which carries the name of Wilhelm Loeffler. Loeffler described self-limiting, transient lung infiltrates with blood eosinophilia and mild chest symptoms in 1932 ⁶⁴; the paper of his that PubMed indexes is a later English-language account from 1956, carries no abstract, and is cited here for the eponym alone ¹².

The therapeutic history is a sequence of drugs each better than the last and each, at the time, believed adequate. Santonin, the main constituent of Levant wormseed (Artemisia cina), a relative of wormwood ⁶⁵, and hexylresorcinol were in organized school-based use in Japan into the 1960s ⁶⁶, while oil of chenopodium, steam-distilled from American wormseed and carrying the peroxide ascaridole as its active constituent, was still being used with considerable success in mass treatment campaigns when it was evaluated in 1985 ⁶⁷. What those drugs actually did to a worm had been watched under glass earlier still. In Goodwin's 1958 preparation, oil of chenopodium, hexylresorcinol and tetrachloroethylene — spelled tetrachlorethylene in that paper — all excited the worm before paralyzing it, and santonin merely disordered the movements of its head end, while piperazine produced a clean graded narcosis; Goodwin separately judged piperazine the safest preparation then available for treating this infection, which is a clinical judgment rather than something the bath data could show ⁶⁸. The herbal form of the chenopodium remedy fared worse still when tested properly: in Mayan communities in Chiapas, Mexico, where decoctions were widely used and highly regarded, doses up to 6,000 mg of dried powdered plant per kg of body weight had no significant effect on adult worms of this species, hookworm or whipworm, even though the active compound ascaridole was present in the expected amounts ⁶⁷. Then came the broad-spectrum drugs, and a 1974 Korean mass-treatment study caught the handover in a single table: single-dose pyrantel pamoate, called pyrantel embonate in that paper, cured 91.3% to 98.9% of 301 children depending on dose, against 62.0% and 74.7% for two or three days of piperazine adipate in two separate groups of 71 and 75 patients, and 80.5% for the santonin-kainic acid complex in 77 patients ⁶⁹.

How you get it: the egg, the lung, and the long way round

A person is infected by swallowing an egg. Not a larva, not a worm — an egg that someone else passed in feces and that then sat in soil long enough to mature. The route is hands, unwashed vegetables, water and soil itself, and the predisposing conditions are the ones that put human feces in the ground where people live: poverty, open defecation, absent sanitation and the use of untreated human waste as fertilizer ¹¹. A 2025 Ethiopian case report makes the chain concrete — a family with no sanitation facility, practicing open defecation, drinking untreated surface water, and not participating in the national deworming campaign — and the child in question needed a laparotomy ⁹.

The egg must mature outdoors, and here one of the field's durable textbook claims needs trimming. Eggs are routinely described as extremely resistant and long-lived, able to persist in soil for years. When that was tested directly, by placing pig feces on Danish pasture in spring, summer, autumn and winter and following the eggs for up to 50 weeks, two things emerged. Embryonation — development to the infective stage — occurred only during the summer months. And the majority of eggs, in the authors' own words generally considered to be extremely resistant and long-lived, disappeared rather fast, faster in summer than winter and faster in short grass than when buried 2 cm down ⁴². Set against that, a tracer-pig study found that the infectivity of a contaminated pasture rose during the first two to three years after contamination rather than declining ⁴³. Both are measurements from temperate Denmark. The reconciliation is probably that most eggs die quickly and a minority persist for a long time, which is precisely what makes the soil a reservoir that cannot be cleared by waiting.

Once swallowed, the larva does not stay put. It hatches, penetrates the wall of the small intestine, enters the bloodstream, passes through the liver, reaches the lungs, breaks out of the capillaries into the air spaces, climbs the bronchial tree to the throat, is swallowed a second time, and only then settles in the small intestine to mature ^11,36,37. This detour takes a matter of weeks, during which no eggs are produced and stool tests for eggs cannot find the infection, although in pigs antibody against adult-worm secretions is already detectable 14 days after infection ⁸⁵. It is also when the acute illness happens: the lung phase is Loeffler syndrome ^11,12, which the larval-migration literature describes as acute allergic airway disease driven by an intense type-2 response, the arm of the immune system that fights worms and also drives allergy ^37,86. Cough, wheeze, shifting shadows on the chest film and a high blood eosinophil count are the textbook picture of it rather than a finding of any source opened for this page.

Why the worm takes this route at all is not known. What is known is how much damage the route does. In mice given eggs by mouth, airway hyperresponsiveness — airways that narrow too easily — appeared by day 8, peaked at day 12 and persisted through day 21 even though the infection itself had resolved, with a type-2 cytokine response comparable to a standard experimental allergy model and airway remodeling, meaning lasting structural thickening of the airway wall, that was more marked ⁴⁴. A later study in the same system found that a single episode of larval migration left behind chronic type-2 inflammation, emphysema (destruction of the lung's air sacs), lung bleeding and chronic anemia, long after the parasite had gone ³⁷. In 2026 the same group offered a mechanism: a single worm-derived peptide — a short fragment of a protein — from a protein they identify as Kalirin, retained and presented by lung macrophages, the scavenger immune cells, long after the infection had cleared, and associated with persisting populations of helper T cells, the white cells that direct an immune response ⁸⁶. All of this is in mice, which are not a natural host for this worm and in which the larvae cannot complete their development. The hypothesis that childhood lung migration contributes to adult asthma and chronic obstructive lung disease in endemic regions is explicitly a hypothesis raised by those authors, and it has not been tested in people.

In the definitive host, meanwhile, the worm population regulates itself in a way worth understanding, because it explains why reinfection behaves as it does. When pigs were given 25 eggs per kilogram every single day and examined at 4, 8 and 14 weeks, the number of migrating lung larvae and liver white spots fell sharply over time despite continuous exposure, and the adult worm population appeared to consist of worms acquired early in the exposure period, with later arrivals unable to establish ⁸⁷. The immune system learns to block new larvae while tolerating the residents. The point is made even more starkly by a 30-week trickle-infection experiment followed by a deliberate challenge: the immunized pigs had a 100% reduction in intestinal worms and a 97.2% reduction in liver white spots against non-immune controls ⁴⁶. The human counterpart of that regulation can only be observed, not arranged, and it was observed again in 2026: in a rural Venezuelan community, 128 people were purged and their worms counted, measured and sexed, and higher worm counts tended to go with shorter and lighter worms, a crowding effect that did not reach statistical significance; worm length and weight correlated strongly with egg output; the presence of male worms was what determined whether the eggs were fertile; and worm count tracked the host's age and household rather than the host's sex ². Protective immunity against this parasite is achievable, in pigs, by months of repeated infection — 30 weeks of it in that experiment ⁴⁶ — which is not a treatment plan, but it tells vaccine developers that the target is not impossible.

How many people have it, and by which count

There is no count. Every number in circulation is a model, and the models differ in what they are modeling, which is why the figures quoted in different papers appear to disagree when they do not.

The most widely used estimate for 2010 drew on prevalence data from 6,091 locations in 118 countries, combining model-based geostatistics for sub-Saharan Africa with empirical approaches for all other regions, and fed the Global Burden of Disease 2010 framework. It gave 819.0 million people infected with this worm (95% credible interval 771.7 to 891.6 million), against 464.6 million for whipworm and 438.9 million for hookworm, and attributed 22% of the 4.98 million years lived with disability from soil-transmitted worms to this one, with 65% going to hookworm ⁵. A companion paper from the same group measured a different thing — where transmission is biologically possible — and found 5.3 billion people, including 1.0 billion school-aged children, living in areas of stable transmission for at least one of these worms in 2010, 69% of them in Asia, with another 143 million in areas of unstable transmission ¹⁰. Population at risk is not population infected, and quoting one for the other is a common error.

Reviews in the parasitology literature have long used about 1.2 billion ^3,7,11, a figure that predates the geostatistical work and is passed from paper to paper. A 2025 clinical case report uses just under 900 million, most of them children ⁹, and a 2026 genomics paper over 700 million ⁸. The spread between these figures is not a disagreement about the biology; it is the gap between different modeled syntheses and an older convention.

The Global Burden of Disease series gives a lower and falling number, and it is the one to quote for recent years. In the 2021 round, analyzed in 2024, this worm accounted for 293.80 million of 642.72 million soil-transmitted worm infections and for 647.53 thousand disability-adjusted life years; its age-standardized prevalence fell from 15,930.11 to 3,856.33 per 100,000 between 1990 and 2021 (95% uncertainty interval for 2021, 3,133.93 to 4,760.38; estimated annual percentage change -5.07, 95% confidence interval -5.28 to -4.85), a drop of 75.8%, and most of the 3,472 deaths attributed to these worms in 2021 were attributed to this one ⁶. The gap between 819 million in 2010 and 294 million in 2021 reflects both real decline and different methods, and neither figure is a count.

Scale is easier to grasp from where the disease sits among all other diseases. In the Global Burden of Disease analysis for 2015, ascariasis appeared among exactly eight causes of chronic disease or injury each affecting more than 10% of the world's population, in company with dental caries, tension-type headache, iron-deficiency anemia, hearing loss, migraine, genital herpes and refractive error ³⁵. It is one of the most common conditions that human beings have.

The trend is sharply downward in China, across three decades that included rapid economic development, improved sanitation and mass treatment, although the analysis is a description of the trend and does not attribute it to any particular intervention. Using Global Burden of Disease 2021 data, prevalence of soil-transmitted worms in China fell by 85.08% and disability-adjusted life years by 98.01% between 1990 and 2021, with an estimated annual percentage change in age-standardized prevalence of -6.62% (95% confidence interval -7.40 to -5.83). The burden peaked in the 5 to 9 year age group, and by 2021 whipworm accounted for 78.85% of the age-standardized prevalence of these worms in China. The same analysis projects whipworm rebounding by 2035, a reminder that the species mix shifts as the total falls ⁸⁸. Those are modeled national estimates with a projection attached, not an observation.

The age pattern matters clinically and recurs in every section below. The heaviest burdens are in young children, and the Chinese peak at 5 to 9 years is typical ⁸⁸. In hospital series of bowel obstruction caused by this worm, the mean age of affected patients was five years or under in six of seven studies that reported it ¹³. A 2025 Indonesian survey of 443 children under 7 in West Sumba found 32.5% carrying a soil-transmitted worm, this species accounting for 27.8% of infections, and stunting associated with infection by this worm at an odds ratio of 3.45 (95% confidence interval 1.70 to 7.02), an association the paper locates in the district capital, the Kota Waikabubak sub-district, rather than across all 443 children — a cross-sectional association, in a district that already had a deworming program running, which cannot establish which came first ⁸⁹.

What it does to you

Most people who carry this worm have no symptoms and never know. The reviews are consistent on this and it is the right place to start, because it keeps the rest in proportion: anorexia, nausea, bloating, vague recurrent abdominal pain and intermittent diarrhea are the common complaints when there are complaints at all, and the serious disease is a complication of heavy burdens or of a worm that has gone somewhere it should not ¹¹.

The acute illness that announces a new infection is in the chest, not the abdomen, because the larvae reach the lungs before the worms reach adulthood. This is Loeffler syndrome ^11,12, which the experimental literature describes as acute allergic airway disease driven by an intense type-2 response ^37,86; cough, wheeze, shifting infiltrates on the chest film, a high blood eosinophil count and spontaneous resolution are the textbook picture rather than a finding of any source opened here. It is easy to miss and easy to mistake for asthma or pneumonia, and outside endemic areas it tends to be recognized only through a high eosinophil count and antibody testing, as the Japanese pig-roundworm cases show ^90,91,92.

The classic emergency is small-bowel obstruction in a young child, caused by a bolus of worms. The systematic analysis of published hospital series is unambiguous about its weight: in nine studies of 100 or more patients admitted with this infection, obstruction was the single commonest complication, accounting for between 38% and 87.5% of all complications with a weighted mean of 72%. In twelve studies of 30 or more obstruction cases, case fatality ran from 0 to 8.6%, weighted mean 5.7%, and the mean age of affected patients was five years or under in six of the seven series that reported it ¹³. Those are hospital numbers and over-represent severe disease; they describe who ends up on a surgical ward, not who has the infection.

What that looks like in practice is still being published. An 8-year-old boy in southern Ethiopia presented with vomiting, distension and no passage of stool or gas; ultrasound showed obstruction from a bolus of worms, relieved by laparotomy and enterotomy, and he recovered ⁹. A 7-year-old from the same country presented with peritonitis; at operation the worm mass had twisted the ileum, the last part of the small intestine, through 270 degrees, with 20 cm of gangrenous bowel requiring resection ⁹³. A worm can also lodge in the appendix: in 11 children found at surgery to have one there, eight (72.7%) had the worm sitting quietly with no appendicitis and three (27.2%) had appendicitis associated with it, and no case had been diagnosed before operation ⁴¹.

Hepatobiliary and pancreatic disease, which the next section covers in detail, is the other major complication, and it is not an adults-only disease: the founding Kashmir series was mostly adult women, but its records are indexed as covering children and adolescents too ⁴⁰. Worms also turn up as incidental and sometimes alarming findings: a 73-year-old man being treated for upper gastrointestinal bleeding induced by a non-steroidal anti-inflammatory drug was found at endoscopy to have worms in his duodenum, and a 63-year-old man with cirrhosis that had progressed to liver failure began vomiting and passing large numbers of them while in the hospital. Both cleared on treatment ⁹⁴.

The chronic cost is the hardest thing to pin down, and the literature on it has reversed itself at least once. The intuition that worms steal nutrition and stunt children is supported by cross-sectional association — in a 2025 survey of 443 Indonesian children under 7 in West Sumba, stunting was associated with infection by this worm at an odds ratio of 3.45 (95% confidence interval 1.70 to 7.02), an association the paper locates in the Kota Waikabubak sub-district ⁸⁹ — and by the pig model, where a 1 kg increase in weight gain was associated with a 2.8% lower roundworm egg count, although that association did not survive multivariable adjustment and the pig whipworm looked more damaging than the pig roundworm ⁹⁵. But the randomized evidence, set out in the treatment section below, does not support treating whole populations to make children grow ^30,71. The most defensible statement is that heavy infection in an individual child is bad for that child, and that this does not translate into a measurable average effect across a community.

The Kashmir series: worms in the bile duct

Hepatobiliary and pancreatic ascariasis was described as a clinical disease from Kashmir in 1985, and it exists as a recognized entity largely because one group documented it at scale ⁷². The founding paper was a prospective study of 109 patients with biliary and pancreatic disease in an endemic area: this worm was the cause in 40 of them (36.7%), most of them adult women; 38 (95%) had recurrent biliary colic, 27 (68%) recurrent pyogenic cholangitis, 9 (23%) cholecystitis without stones and 6 (15%) pancreatic disease; 19 (48%) vomited roundworms during an attack of colic, which often led to the diagnosis; and 36 (90%) recovered on symptomatic treatment followed by a worm drug once the acute illness had settled, while 4 needed surgery because the worms were trapped and had become the seed of duct stones ⁴⁰. The mechanism is simple and unpleasant: an adult worm in the duodenum finds the ampulla of Vater and goes in. Once inside the bile duct, the gallbladder, the liver ducts or the pancreatic duct, it obstructs, and when it dies it becomes the nucleus of a stone ⁹⁶.

The defining paper reports 500 patients. 274 had worms in the duodenum, 171 in the biliary tree, 40 in the liver, 8 in the gallbladder and 7 in the pancreatic duct. Five clinical presentations were distinguished: biliary colic in 280, acute cholangitis in 121, acute cholecystitis in 64, acute pancreatitis in 31 and liver abscess in 4. Four patients died — two of pancreatitis, one of pyogenic cholangitis, one of liver abscess. In 211 patients the worms moved back out of the duct system on their own; in 12 they were still there at three weeks and had to be removed surgically or endoscopically. Over a mean follow-up of 48 months (standard deviation 14), 76 patients had worms re-enter the biliary tree after reinfection, and 7 developed duct stones in which a dead worm formed the nidus ¹⁴.

The endoscopic answer came next. Of 156 consecutive patients with the condition, 50 (32%) required endoscopic intervention, either because they did not settle on medical treatment within a few days or because worms had not left the ducts by three weeks. Worm extraction succeeded in all 18 attempts from the ampullary orifice and in 34 of 38 (89.5%) from inside the bile or pancreatic duct, and 41 of 45 patients (91%) had rapid relief. Three patients had endoscopy-related complications ⁹⁷. The treatment logic that emerged, and that the group still recommends, is to treat the clinical syndrome and give an effective anthelmintic drug, and to reserve endoscopy for patients who do not settle, whose worms remain in the duct beyond three weeks, or whose worms die inside it ⁹⁶.

The regional weight of this is easy to underestimate from outside. In Kashmir the group gives this worm as the cause of 36.7% of all biliary disease, 23% of acute pancreatitis, 14.5% of liver abscesses and 12.5% of biliary stone disease ⁹⁶. In a later retrospective account covering 10,100 endoscopic procedures over four decades, the same author adds that recurrent pyogenic cholangitis — repeated episodes of pus in the bile ducts — constituted 12.5% of all biliary disease in that population and was essentially a consequence of this worm ⁷². These are figures from one endemic region with an unusual concentration of the disease and an unusually dedicated endoscopy service; they should not be read as global proportions.

Two things are worth saying about the strength of this evidence. It is observational: a single-center prospective series with no comparison group, which is the appropriate design for describing a disease nobody had described, and the wrong design for estimating the effect of any intervention ⁹⁷. And it is old, with the core data from 1990 and 1993. What has not changed is the anatomy: a worm long enough to enter the ampulla, in a population where many people carry several, will keep producing this disease wherever both conditions hold.

Allergy, asthma and tropomyosin, at their true strength

This worm has a serious claim on allergy, and the claim is routinely overstated in both directions. Stated carefully: the worm makes proteins that human immunoglobulin E binds; one of them is cross-reactive with a major house-dust-mite allergen; infection is associated with increased airway reactivity in children and atopy in adults in meta-analysis; and a randomized trial of deworming did not change the prevalence of allergy. All four of those are true at once.

The molecule at the center is tropomyosin, a structural protein of muscle shared across the invertebrates, which is why one antibody response can recognize a worm, a mite, a cockroach and a shrimp. The worm's version, named Asc l 3, is a chain of 287 amino acids — about 33 kilodaltons by sequence, a kilodalton being a unit of molecular mass, although it runs at about 40 kilodaltons on a gel, as tropomyosins generally do — and it shares between 69% and 98% of its sequence with tropomyosins of other invertebrates ^98,99. It behaves as a real allergen rather than merely as a bound protein: it produced wheal-and-flare, a raised itchy bump with surrounding redness, on skin testing, and released histamine from basophils, the white cells that carry allergic antibody; and antibody against it could account for roughly half of the total immunoglobulin E response to whole worm extract ⁹⁸.

The cross-reactivity is quantified. Using sera from 24 asthmatic patients, extracts of the mites Blomia tropicalis and Dermatophagoides pteronyssinus inhibited 83.3% and 79% of immunoglobulin E binding to worm extract, and mite tropomyosin alone inhibited 85% of it. The worm's own ABA-1, a polyprotein made only by roundworms, had no cross-reactive counterpart in mite extracts, which is why it is proposed as a more specific marker of infection ¹⁰⁰. In 119 children from an endemic area and 112 patients with cockroach allergy, antibody responses to worm and cockroach tropomyosin correlated strongly ⁹⁹. In populations exposed at once to mites, cockroach, this worm and shellfish, more than half of individuals carry antibody to tropomyosin ¹⁰¹. One practical consequence is diagnostic rather than clinical: in the tropics, a positive mite allergy test may partly reflect worm infection ¹⁰².

Does any of this cause asthma? Here the evidence thins. The paper that characterized Asc l 3 found sensitization commoner in asthmatics than non-asthmatics across 175 and 170 subjects, but its own logistic regression suggested the finding was confounded by mite sensitization, and the authors wrote that the role of worm tropomyosin in asthma in the tropics should be further investigated ⁹⁸. A current review names Asc l 3 as having strong allergenic activity associated with asthma and asthma severity in the tropics, while making the general point that most immunoglobulin E-binding worm antigens are not allergens at all — binding and causing symptoms are different things ¹⁰². The co-exposure problem is unresolved: whether year-round mite exposure plus worm infection potentiates type-2 responses and changes the natural history of allergy is simply not known ¹⁰³.

The largest synthesis is a 2022 meta-analysis of 80 studies and 99,967 participants. Overall there was no association between worm infection and allergic disease. But for this worm specifically, infection was associated with increased bronchial hyperreactivity in children (risk ratio — how many times more often the outcome occurred in the infected — 1.41, 95% confidence interval 1.17 to 1.70) and with atopy in infected adults (1.37, 1.18 to 1.61). The reviewers graded the underlying evidence as low to moderate, and noted that no study they found addressed clinical outcomes of allergic disease at all — only markers ¹⁰⁴. Associations of that size, from observational studies, in a field with this much confounding, support further work and do not support a causal claim.

The hygiene hypothesis makes the opposite prediction — that worms protect against allergy and that removing them will unleash it — and that prediction has been tested. In a cluster-randomized trial — one that randomizes whole schools rather than individual children — across 68 rural Ecuadorian schools and 2,373 children, albendazole every two months for a year cut worm prevalence sharply (odds ratio 0.13, 95% CI 0.09 to 0.19) and changed nothing about allergy: atopy odds ratio 0.97 (0.68 to 1.39), wheeze 1.07 (0.54 to 2.11) ¹⁰⁵. That is a properly designed test of a specific fear, and it came back negative. An earlier randomized trial came back the other way and has to be reported alongside it: in 317 Gabonese schoolchildren given praziquantel and mebendazole every three months for 30 months, or placebo, treatment raised the rate of developing skin sensitivity to house dust mite (hazard ratio 2.51, 95% confidence interval 1.85 to 3.41), an effect the authors found to be mediated in part by the reduction in this worm and in whipworm ¹⁰⁶. The fair summary is therefore narrow: removing worms can increase skin-test sensitization, neither trial showed more wheeze or more clinical allergic disease, and the epidemiological association between this worm and airway reactivity, which points the other way again, remains unexplained.

The animal work sits oddly against all of this, and should not be used to settle it. In mice, larval migration through the lungs produced severe allergic airway disease rather than preventing it ⁴⁴, and chronic damage persisting after clearance ³⁷. Mice are not a host in which this worm can complete its life cycle, and the doses used are large. The mouse result is a reason to look harder at human lungs after childhood infection, not evidence about what happens in them.

Pig to person: Denmark, Maine, Japan

In countries with sewers, human ascariasis was long assumed to be imported — caught abroad or carried in on food ⁷³. In Denmark that assumption was tested and found wrong. Worms from Danish patients were compared, by whole-genome fingerprinting (amplified fragment length polymorphism) and by a nuclear ribosomal restriction assay, with worms from Danish pigs and with worms from people in endemic countries. The Danish patients' worms clustered with Danish pigs and separately from worms taken from people elsewhere. The conclusion in the title was flat: ascariasis is a zoonosis in Denmark ¹⁵. The practical corollary, stated in the group's Danish-language secondary publication, is that the main transmission route in developed countries appears to be pigs to people, and that contact with pig manure should be avoided, particularly by young children ⁷³.

The same pattern has turned up elsewhere. In the United Kingdom a report of zoonotic ascariasis was published in 2011; its PubMed record carries no abstract, so it is cited here for the existence and date of the report only ¹⁸. In the United States, surveillance in Maine identified 14 cases of ascariasis between 2010 and 2013 in people who had contact with pigs on small-scale farms, published with a call for health education and improvements in farming and food hygiene ¹⁷. In Japan, nine worms from patients and nine from pigs were typed at the first internal transcribed spacer: six of the patient worms carried the genotype that predominates in humans in endemic countries, and three carried the genotype that predominates in pigs worldwide — so in one country, in one small series, both routes were operating ¹⁶. The global analysis makes the same point with more worms: in 536 barcoded and 410 genotyped parasites from four continents, human infections in Europe were of pig origin, while in Africa there was evidence of cross-transmission between people and pigs ⁷⁶.

Pigs are not the only animals involved. In Copenhagen Zoo, chimpanzees kept expelling worms despite a regular deworming program. Molecular comparison assigned those worms to the pig cluster ⁷⁴, and a follow-up showed that the infection was not being reintroduced from outside but had established a permanent transmission cycle within the troop, with eggs embryonating to the infective stage on site ⁷⁵. Worms from a chimpanzee and a gibbon in a Chinese zoo, meanwhile, proved by mitochondrial genome comparison to be a single species genetically similar to the human roundworm ⁶⁰. The genus moves between primates and pigs with more ease than its two-name taxonomy suggests.

The most distinctive human disease the pig worm causes is not intestinal at all. In people the pig roundworm can mature into egg-laying adults in the gut, as the Danish, Maine and Japanese infections above show ^15,16,17, but its larvae can also wander through the organs without completing development, and what that produces is visceral larva migrans: malaise, cough, liver dysfunction, very high eosinophil counts, and lesions in the liver and lungs ⁹². An outbreak was reported from Kyushu, Japan in 1996 ¹⁰⁷. A 32-year-old man outside Kyushu was later found to have eosinophilic pneumonia with ground-glass opacities — hazy patches on the lung scan — in both lungs and multiple low-attenuation, meaning abnormally dark, liver lesions; liver biopsy showed heavy eosinophil infiltration around the portal veins, the vessels that carry blood from the gut to the liver, and serology, meaning blood antibody testing, was positive for the pig roundworm ⁹⁰. A 62-year-old man in middle Kyushu who liked to eat raw pig liver developed migrating lung shadows with massive eosinophil infiltration on biopsy and recovered on albendazole 600 mg a day for 28 days ⁹¹.

Raw pig liver is the exposure that recurs in the Japanese reports, and the biology is coherent: larvae arrested in pig liver are swallowed whole by a person eating it raw. But two cautions belong here. The attribution in these cases rests on serology rather than on recovering a worm, and the serology is the hard part, because this worm and the dog and cat roundworms Toxocara share extensive antigenic similarity ⁹². A dedicated immunoblot — a test that separates worm proteins by size and shows which of them a patient's antibodies bind — using larval excretory-secretory antigens, the molecules living larvae release, was developed against exactly this problem: 34 sera from patients with high eosinophil counts who were negative for Toxocara tested positive on it, with a calculated specificity of 95% against 30 healthy and 53 other-helminth controls. The same paper notes that serological screening in the Netherlands and Sweden produced remarkably high seroprevalences — proportions of people carrying antibody — for the pig roundworm ⁹². How often this syndrome actually occurs is unknown.

One structural point closes this section. Where people and pigs share ground, treating only the people cannot work, and several of the molecular papers say so explicitly: the Chinese microsatellite study calls for treating infected pigs alongside people in sympatric areas ⁴⁸, and the Cameroon study concludes that effective and sustainable control should target both hosts ⁵⁸. The pig roundworm is also a problem in its own right for farming, and a veterinary review from the Copenhagen group states plainly that it is now evidently zoonotic ⁴³. A companion review of the zoonotic potential of the pig roundworm and the pig whipworm names the two settings where the risk is concentrated: places where pigs and people live in close proximity, and places where pig manure is spread on vegetables grown for human consumption ¹⁰⁸. A 2026 European review puts the same case from the farm side: the pig roundworm is reported on anywhere from 1% to 100% of farms depending on the production system, with higher burdens in outdoor, organic and small-scale systems, control still rests on worm drugs, and the authors name the zoonotic potential of the pig roundworm and the pig whipworm among the reasons that control matters ¹⁰⁹. That is a One Health argument — treating human, animal and environmental health as one problem — reached from the genetics and from the farm rather than from policy.

How it is found, and what each test misses

The standard method is to look for eggs under a microscope, and the standard version of that is the Kato-Katz thick smear: a measured quantity of stool, pressed flat under glycerol-soaked cellophane, with the eggs counted to give a count per gram that stands in for how many worms the person carries. Almost all prevalence mapping and almost all drug trials rest on it ^20,23.

Its sensitivity depends on how heavily infected the population is, which is exactly the wrong dependency. A Bayesian latent class meta-analysis, designed for the situation where no perfect reference test exists, found that double-slide Kato-Katz reached 74% to 95% sensitivity for the three soil-transmitted worms where infection intensity was high, but fell to 53% to 80% where it was low. Across all methods, sensitivity ranged from 42.8% for plain direct microscopy to 92.7% for FLOTAC, a flotation-based egg-counting device, with mini-FLOTAC, its simplified version, comparable to Kato-Katz; for low-intensity infections the sensitivity was lowest for hookworm and for this worm ²⁰. As programs succeed and intensities fall, the test gets worse, so the measured prevalence falls faster than the real one.

Molecular testing closes part of that gap. In 648 participants in the Myanmar delta, any soil-transmitted worm was found in 20.68% by Kato-Katz and 45.06% by quantitative polymerase chain reaction, with the largest discrepancy for hookworm; for this worm specifically the relationship between egg count and DNA copy number was the strongest of the three species ¹¹⁰. In a randomized trial of 320 participants, Kato-Katz sensitivity for this worm at follow-up was 53.8% against the molecular test, while the molecular test was 87.5% sensitive against Kato-Katz, and the choice of test changed the cure rates the trial reported — most dramatically for hookworm ¹¹¹. In 390 Kenyan school children four months after a national treatment round, mini-FLOTAC reached 53.5% and Kato-Katz 63.8% sensitivity against the molecular test ²². The most recent accuracy figures for this worm come from the emodepside trials on Pemba Island, analyzed in 2025: Bayesian latent class modeling gave the molecular test 85.00% sensitivity against 47.70% for Kato-Katz, with slightly lower specificity, 93.40% against 99.40% ¹¹². The earlier trial's own conclusion is worth keeping in view: for this worm a single molecular test was as sensitive as quadruplicate Kato-Katz — four readings of one sample — rather than more sensitive than it, and the gain was in hookworm ¹¹¹.

But the microscope does not only undercall. In 2,799 stool samples from rural Bangladesh, Kato-Katz sensitivity for this worm was 49% against 79% for the molecular test — and 26% of the samples that Kato-Katz called positive for this worm were negative by polymerase chain reaction. Amplicon sequencing — reading the DNA of the amplified test region directly — of ten of them confirmed the worm was genuinely absent. Kato-Katz specificity for this species came out at 68%, against 97% or better for the other species ²¹. The authors' conclusion is worth repeating because it contradicts a widespread assumption: it is widely believed that double-slide Kato-Katz produces few false positives, and in this setting it did not. Something in those stools looked like an egg and was not.

Neither method sees the infection before the worms start laying, which is a gap of weeks covering the entire lung phase. That is the case for antibody tests, and the best current data come from Kenya. Immunoglobulin G against the products adult worms secrete — specifically the IgG1 subclass — discriminated active infection with an area under the receiver operating characteristic curve of 0.83 (95% CI 0.75 to 0.91) against a combined stool and molecular reference, and, crucially for programs, its accuracy did not depend on egg counts the way the other tests do ²². Work in pigs supports extending this backward into the larval phase: antibody against adult worm secretions was detectable at 14 days after infection, well before adults are present ⁸⁵. An earlier pig-derived test built on a 12-kilodalton larval surface antigen, As12, reached 92% sensitivity and 90% specificity for long-term exposure in naturally infected people, which is a different claim from diagnosing a current infection ⁴⁶. The limitation of all antibody tests is the same: they cannot tell current infection from past infection, and in the case of pig-roundworm larva migrans they must contend with heavy cross-reactivity against the dog and cat roundworms ⁹².

For the complications, the test is an image. Ultrasound shows the worm in the bile duct directly, and endoscopy both confirms and treats ^96,97. In the reported non-endemic cases the first finding was a high eosinophil count, which prompted antibody testing ^90,91,92; how often eosinophilia is what triggers the investigation is not something any source opened here measured.

• Kato-Katz thick smearA measured quantity of stool is pressed under cellophane soaked in glycerol and malachite green and the eggs counted under a microscope; it gives both a yes-or-no answer and an egg count per gram, which is the standard proxy for how many worms a person carries ²⁰.The default field test and the basis of nearly all prevalence mapping and drug-efficacy trials ^20,2374-95% sensitive across the three soil-transmitted worms where infection intensity is high, falling to 53-80% where it is low, with this worm and hookworm at the bottom of that range ²⁰.Light infections, prepatent infections before the worms start laying, and single-sex or male-only infections. It also overcalls: in rural Bangladesh 26% of the samples it called positive for this worm were negative by DNA testing, sequencing of ten of those confirmed the worm was absent, and latent class analysis put its specificity for this worm at 68% ²¹.
• Stool quantitative polymerase chain reactionAmplifies and counts worm DNA in stool, reporting a cycle threshold rather than an egg count ¹¹⁰.Confirmation, low-prevalence surveys, and trials where the choice of test changes the measured cure rate ^110,111Sensitivity about 79% against a latent-class reference in Bangladesh, where Kato-Katz reached 49% ²¹; about 87.5% against Kato-Katz in a Tanzanian trial ¹¹¹.Equipment, cold chain and cost place it outside most endemic-country laboratories, and its intensity readings are not yet standardized against worm burden ¹¹⁰.
• Antibody serology against adult worm secretionsMeasures immunoglobulin G, in particular the IgG1 subclass, against the substances adult worms release ²². A related pig test built on a larval surface antigen, As12, reached 92% sensitivity and 90% specificity for long-term exposure in naturally infected people ⁴⁶.Monitoring after mass drug administration ²²; detection during the larval, pre-patent phase has so far been shown only in pigs ⁸⁵Area under the receiver operating characteristic curve — a summary of how well a test separates infected from uninfected people, running from 0.5 for chance to 1 for perfect — 0.83 (95% confidence interval 0.75-0.91) against a combined stool reference in 390 Kenyan children ²².It cannot separate current from past infection, and antibody against the related dog and cat roundworms cross-reacts, which is the central problem in diagnosing pig-roundworm larva migrans ⁹².
• Ultrasound and endoscopic retrograde cholangiopancreatographyUltrasound can show the worm directly in the gut and in the bile ducts; endoscopy both confirms it and removes it ^96,97.Suspected biliary or pancreatic disease in an endemic area ⁹⁶In the Kashmir series, worms were extracted successfully from the ampullary orifice in all 18 attempts and from the bile or pancreatic duct in 34 of 38 (89.5%), with rapid relief in 41 of 45 (91%) ⁹⁷.It is an answer for the complication, not a screen for the infection, and it is not available where most of the disease is.
• Blood eosinophil countA raised count of the white cell that responds to tissue-invading worms. Marked eosinophilia was the finding that prompted serology in the reported cases of pig-roundworm larva migrans ^90,91,92.The prompt for serology in suspected larva migrans ^91,92Non-specific. It points to a migrating worm somewhere, not to this one.Established intestinal infection, in which the eggs may be the only sign. How often the count is normal in that situation is textbook knowledge rather than a finding of any source opened here.

What is done about it, and what used to be done

Against this particular worm, the modern drugs work well, which is not true of its companions. The 2008 benchmark meta-analysis of 20 randomized trials gives single-dose cure rates of 88% for albendazole (95% CI 79-93, 557 patients), 95% for mebendazole (91-97, 309 patients) and 88% for pyrantel pamoate (79-93, 131 patients); albendazole and mebendazole cured only 28% and 36% of whipworm ²⁴. The later and larger network meta-analysis, which pooled 44 trials and 7,273 participants infected with this worm, puts the single-dose cure rates higher: 95.7% for albendazole (95% CI 93.2-97.3; 34 trials, 3,360 participants), 96.2% for mebendazole (92.3-98.1; 13 trials, 1,548), 97.3% for levamisole, the fourth drug on the World Health Organization list (84.2-99.6; only two trials, 149 participants), and 92.6% for pyrantel pamoate (85.6-96.3; 11 trials, 1,374), against 12.7% with placebo, with egg reduction rates of 94.3% to 98.5% and no significant difference between the four. The same analysis finds albendazole the only good option for hookworm (cure rate 79.5%, 95% CI 71.5-85.6) and all four poor against whipworm, mebendazole best at 42.1% (25.9-60.2) ²³.

Current practice follows from that. Albendazole or mebendazole for children and non-pregnant adults; pyrantel pamoate in pregnancy, which is what the clinical reviews advise ^11,28, although six randomized trials of 7,873 pregnant women given albendazole or mebendazole in the second or third trimester found this worm's prevalence cut by about three quarters (risk ratio 0.24, 95% confidence interval 0.19 to 0.29; two trials, 2,488 participants; moderate-certainty evidence), with no detectable effect on low birthweight ²⁹; and treatment of every diagnosed infection, including asymptomatic ones, specifically to forestall the migration complications described above ^11,28.

Ivermectin is often described as the weaker drug against this worm when used alone, and the pooled randomized evidence does not show it. In the 2020 Cochrane review of 30 randomized trials and 6,442 participants in 17 countries, a single dose of albendazole cured 87.8% and a single dose of ivermectin 90.2% (risk ratio 0.99, 95% confidence interval 0.91 to 1.08; three trials, 519 participants; moderate-certainty evidence), and albendazole and mebendazole were indistinguishable (98.0% against 96.9%; six trials, 2,131 participants; high-certainty evidence); egg reduction ran from 96% to 100% for every drug. Twenty of those 30 trials were funded or co-funded by drug manufacturers, which is worth saying out loud ⁶³. Ivermectin is nonetheless being added to albendazole, chiefly because of the whipworm, and the trial evidence on this worm is secondary: in an open-label trial in Ugandan schoolchildren treated for whipworm, co-infecting worms of this species were cured in 100% of the albendazole-plus-ivermectin group against 83.9% with albendazole alone ¹¹³. That is a secondary outcome in a trial powered for a different parasite. In India, a double-blind randomized trial in schoolchildren — 1,067 evaluable at baseline, of whom 416 (38.99%) were egg-positive and 99.52% of those carried this worm, and 304 evaluable after treatment — found essentially no difference: cure at day 7 was 61.64% with albendazole alone and 62.03% with albendazole plus ivermectin (P=0.95), with egg reduction rates of 90.61% and 93.22%. The trial was published in Cureus with three co-authors from the medical affairs department of Mankind Pharma, which makes the fixed-dose combination tested ²⁵.

Those Indian cure rates — both around 62% — are the number in this section that should give pause. The pooled figures for single-dose albendazole against this worm are 88% in the 2008 meta-analysis and 95.7% (95% CI 93.2-97.3; 34 trials, 3,360 participants) in the larger 2017 network meta-analysis ^23,24. A trial in a routinely dewormed Indian school population got 62%. Three features of that trial weaken the comparison: cure was assessed at day 7, earlier than the two to three weeks used in most efficacy trials ¹¹³; the cure rates rest on the 304 children evaluable at follow-up rather than the 416 found positive; and the paper reports egg counts — a median of 3 eggs per gram, with 89.18% of positive samples at 10 eggs per gram or below — that a single Kato-Katz slide read with a multiplier of 24 cannot produce, since the smallest positive count that method can return is 24 eggs per gram, so its parasitology should be treated cautiously ²⁵. The Indian trial is not alone, though. In 12 Rwandan schools in 2017, single-dose albendazole cured 69.9% of infections with this worm by Mini-FLOTAC and reduced egg counts by only 75.4% (95% confidence interval 50.4% to 87.8%), ranging from 0 to 96.8% between schools and falling below the 95% reduction taken to define adequate efficacy, while none of the known resistance-associated changes were found in four beta-tubulin genes ²⁶. In a tribal-majority district of Odisha, India, in 2025, single-dose albendazole cured 66.7% of the 203 treated children carrying this worm but cut their egg counts by 96.2% ²⁷. None of this is evidence of resistance. It is the kind of observation that makes resistance surveillance worth doing, which is the subject of the next section.

Before the benzimidazoles there were three generations of worse options. Santonin, the main constituent of Levant wormseed (Artemisia cina), a relative of wormwood, was in organized school-based use in Japan alongside hexylresorcinol in the 1960s ⁶⁶, and is no longer used in people because of its toxicity ⁶⁵. Oil of chenopodium, steam-distilled from American wormseed and carrying the peroxide terpene ascaridole as its active constituent, was still being used with considerable success in mass treatment campaigns when it was evaluated in 1985 ⁶⁷. Both were dangerous. Three African patients treated with oil of chenopodium for this infection died of liver damage, reported in 1951 ¹¹⁴; and a Mexican child of 2 years and 9 months died in 1996 after a traditional healer gave her 40 mL of the oil, which on analysis contained 39 mg of ascaridole per mL, 1,560 mg in all, against a former recommended pediatric dose of 60 mg and a dose of 1,000 mg reported as lethal in people ¹¹⁵. Santonin is toxic at about 60 mg in children and 200 mg in adults, causing yellow vision that can progress to blindness ¹¹⁶. A 1958 bath preparation showed what these drugs actually did to a worm: oil of chenopodium, hexylresorcinol and tetrachloroethylene all stimulated the worm's movements before immobilizing it, and santonin produced only incoordination of the head end, while piperazine gave a clean dose-dependent narcosis; the author separately judged piperazine the safest preparation then available ⁶⁸. Piperazine itself was a substantial advance and is still an imperfect drug: in the same 1974 Korean study, two or three days of piperazine adipate cured 62.0% in 71 patients and 74.7% in 75 patients, against 91.3% to 98.9% for a single dose of pyrantel pamoate in 301 children ⁶⁹. In 185 Bangladeshi children given piperazine citrate in a double-blind placebo-controlled trial, cure rates were 53%, 31% and 36% for light, moderate and heavy infections, heavier infections both resisted clearance and reinfected faster, and no measure of growth differed from placebo over 11 months ⁷¹.

The herbal version of the chenopodium remedy deserves its own sentence, because the decoction and the distilled oil are not the same preparation and did not perform the same way ⁶⁷. Tested in Mayan communities in Chiapas, Mexico, where decoctions of up to 300 mg of dried plant per kg body weight were widely used and traditionally highly regarded for exactly this infection, doses up to 6,000 mg/kg of dried powdered plant had no significant anthelmintic effect on adults of this species, hookworm or whipworm — and gas chromatography confirmed that ascaridole was present in the expected amounts, so the failure was not a bad batch. The author's proposed explanation for the persistence of the belief is that worms are passed spontaneously after any purgative episode, and the patient credits the remedy ⁶⁷. The distilled oil is a different preparation from the decoction, and in 1985 it was still being used with considerable success in mass treatment campaigns ⁶⁷; the herb as actually taken did not work.

What comes next is emodepside. Its phase 2b trial, in 293 adolescents and adults on Pemba Island, Tanzania, was against hookworm rather than this worm, and it won clearly: 96.6% cure against albendazole's 81.2% (odds ratio 0.14, 95% CI 0.04-0.35, P=0.0001). The cost was tolerability — blurred vision in 39% of recipients at three hours, headache and dizziness in 38% and 30%, though 93% of the adverse events were mild and none serious ⁸¹. Against this worm the human evidence is a secondary analysis of the Pemba dose-finding trials: by both Kato-Katz and molecular testing, emodepside cured more infections with this worm than albendazole did ¹¹². A 2024 review calls the drug highly effective in single doses against ascarids in mammals and in human trials and expects registration for several neglected tropical diseases at once; it is not approved for human use yet ²⁸. Behind it, fundamental work on the worm's own nerve signaling continues: in 2026 the body-cavity fluid of female pig roundworms was found to contain beta-alanine betaine, a previously unrecognized analog of acetylcholine, acting apparently on a receptor subfamily with no counterpart in people or livestock — which is what makes it attractive as a target ¹¹⁷. That is early pharmacology, not a drug.

Finally, the finding that reversed the policy argument. A Cochrane review of 45 trials — 44 of them with 67,672 participants, plus one mortality trial of over a million children — separated two questions that had been run together. Treating children already known to be infected may increase weight gain over the following one to six months: 627 participants, five trials, low-quality evidence, effects ranging from 0.2 kg to 1.3 kg. Treating all children in an endemic area, which is what mass drug administration actually does, probably has little or no effect on average weight gain (mean difference 0.04 kg less, 95% confidence interval 0.11 kg less to 0.04 kg more; 2,719 participants, seven trials, moderate quality), and regular treatment every three to six months showed no effect on average height, hemoglobin, formal tests of cognition, exam performance or mortality ³⁰. A sensitivity analysis restricted to trials with adequate allocation concealment found no effect on any main outcome. The 2019 update — 51 trials, 50 of them with 84,336 participants plus the same mortality trial — was written in part to answer published comments and criticisms, and it did not change those conclusions: regular treatment probably has little or no effect on height (mean difference 0.02 cm more, 95% confidence interval 0.09 cm less to 0.13 cm more; 13 trials), hemoglobin (0.01 g/dL less, 0.05 g/dL less to 0.07 g/dL more; nine trials), formal tests of cognition or school performance, no effect was shown on mortality, and on weight the authors' stated conclusion is that they do not know, because the trials from two settings more than twenty years earlier showed large gains while the trials since 2000 average 0.02 kg (0.04 kg loss to 0.08 kg gain) ³¹. The question is still contested, and the contest runs through one trial. The influential 1998-99 Kenyan school deworming trial was reanalyzed in 2015: once coding errors were corrected, the total gain in school attendance among treated children fell from 7.5% to 3.9% and was no longer statistically significant, and the reported reduction in anemia was not reproduced ⁷⁷; a companion statistical replication found the evidence for an attendance effect to depend on which analysis was used, and to carry a high risk of bias ⁷⁸. The original investigators then tracked the same children for twenty years and reported in 2021, with 84% of them traced, 14% higher consumption and 13% higher hourly earnings among those who had received two to three additional years of childhood deworming ³². So: the health trials have not found the growth, hemoglobin or schooling gains the programs were sold on; whether there are long-run economic effects is a separate argument, made by the group that ran the original trial, and it is open. The case for treating a child who has worms remains either way.

Resistance, the markers, and mass drug administration

Benzimidazole resistance is a well-understood problem in veterinary parasitology: it is documented, mechanistically explained and routinely monitored in sheep and cattle worms, where it is caused by single changes in the beta-tubulin gene at codon 167, 198 or 200 ¹¹⁸. The reason it matters here is that more than 3.3 billion benzimidazole tablets have been distributed in schools since 2010 ⁷⁹, a level of drug pressure that the authors of the gene-family study call unprecedentedly high ⁸⁰.

The genetics in Ascaris turn out to be less tidy than in sheep worms. A 2021 characterization found at least seven beta-tubulin genes in this genus, two of them highly expressed across the whole life cycle. Deep amplicon sequencing of those two genes in more than 200 adult worms — from people in Ethiopia and Tanzania, and from pigs in Belgium — found none of the four single-nucleotide changes associated with resistance in other helminths: F167Y, E198A, E198L and F200Y were simply absent in all three populations ⁸⁰. That is reassuring about the present and unsettling about the method, because a gene family of seven means the codons being watched may not be the codons that matter in this worm.

The genotypic surveillance since then is consistent and, so far, negative; the phenotypic picture is not, because in Rwanda albendazole reduced egg counts by only 75.4% in worms carrying none of the known resistance changes in four beta-tubulin genes ²⁶. In northwestern Thailand in 2026, worms typed at beta-tubulin carried exclusively wild-type alleles at codons 167, 198 and 200 ⁵⁷. On 13 German pig farms, fenbendazole — a veterinary benzimidazole — at 5 mg/kg gave fecal egg count reductions of 99.8% to 100% for the nodular worms (Oesophagostomum, a different pig parasite), and deep sequencing found no resistance-associated changes at codons 134, 167, 198 or 200 in those nodular worms. For the pig roundworm the egg-count results were ambiguous, but a new in-egg larval development assay classified every population tested as susceptible, with half-maximal effect concentrations of 1.50 to 3.36 micromolar — millionths of a mole per liter — of thiabendazole, another benzimidazole, with a mean of 2.24 and a proposed resistance cut-off at 3.90 micromolar ¹¹⁹. That German paper also documents a practical obstacle worth knowing: egg-count reduction testing is unreliable in pigs because pigs eat each other's feces and therefore shed eggs they did not produce. Tools to make genotyping practical in the field exist, including simple isothermal assays — DNA tests run at a single temperature, without a thermal cycler — tested on field samples from Haiti and Panama and shown to tolerate fecal inhibitors, the substances in stool that block DNA tests, although their developers state that they still need validation on large sets of field samples taken before and after treatment ¹¹⁸. A 2026 European review makes the same division plainly: reduced efficacy and resistance among pig worms are reported particularly in the nodular worms, not in the pig roundworm ¹⁰⁹.

Set against this clean genotypic picture are three phenotypic signals, two of which concern this worm. The network meta-analysis found a significant fall in albendazole efficacy between 1995 and 2015, with egg reduction dropping from 72.6% to 43.4% (P=0.049) and cure from 38.6% to 16.4% (P=0.027). The full text places that decline in its whipworm analysis, where albendazole's pooled cure rate was 30.7% and where mebendazole's egg reduction fell over the same comparison from 91.4% to 54.7% (P=0.014), while against this worm every drug stayed above 92% ²³; so it is a warning about the drug class rather than about this parasite. The other two are closer to home: the Rwandan egg reduction of 75.4% in worms with no resistance mutations ²⁶, and the 2025 Indian trial's cure rate of 61.64% for single-dose albendazole against this worm in a routinely dewormed population, against a pooled 88% to 96% ^23,24,25. None of the three is evidence of resistance. All three are reasons to watch.

There is one more study that complicates the drug ranking, and it should be read carefully rather than quoted. In 1,675 Pakistani schoolchildren randomly allocated to pyrantel pamoate, mebendazole or albendazole, with worms recovered from stool one to two days afterward, worms were found far more often after pyrantel pamoate than after albendazole (odds ratio 6.76, 95% CI 4.49-10.18) and somewhat more often after mebendazole (1.50) in the unadjusted analysis; in the study's own multivariable model the two non-albendazole drugs were indistinguishable from each other, with adjusted odds ratios of 7.37 for pyrantel pamoate and 7.73 for mebendazole ¹²⁰. Read naively the unadjusted figures are a drug-efficacy ranking favoring albendazole. Read carefully, the outcome measured is worms expelled and identified in the days after treatment, the study describes itself as both cross-sectional and interventional, and the same odds are used in the same analysis for environmental risk factors. It is a large study with an unusual design, and it is weaker evidence on drug ranking than its size suggests. The same group's multilocus genetic study drew its worms from this cohort, so the two papers are not independent observations ³⁴.

The policy frame around all of this is the World Health Organization target of eliminating these infections as a public health problem, with the 2030 roadmap as the current horizon. That phrase has a technical meaning and is not eradication: it means driving the prevalence of moderate and heavy infections in preschool and school-age children below a set threshold — 1% was the target for 2020 — while the worm itself remains in circulation ^23,79. The agency's own account of progress reports more than 690 country reports over 2008 to 2018, more than a billion people infected, and an explicit warning that caution will be needed in stopping control programs, to avoid a rebound in prevalence and the loss of accrued gains ⁷⁹. That caution is well founded, and it is no longer only modeling. The projection for China has whipworm climbing again by 2035 even as the total burden falls ⁸⁸; and in Timor-Leste, where school-based deworming was interrupted for nearly four years during the COVID-19 pandemic, a national survey of 1,236 children in 2025 found the weighted prevalence of these worms back at 29.3% (95% CI 24.3 to 34.2), against 18% in 2020 and 29% at the 2012 baseline, with this worm accounting for 95.8% of infections and moderate-to-heavy infections in 15.7% of the children ⁸⁴. And a program report written by the agency running the program is a document with an interest in the result, which is worth naming even when the document is careful.

The largest test of whether treatment alone can end transmission reported in 2025. DeWorm3 randomized 120 clusters containing 357,716 people in Benin, India and Malawi to twice-yearly community-wide albendazole or to standard school-based deworming for three years. Twenty-four months after the last dose, the prevalence of the predominant worm at all three sites — the hookworm Necator americanus — was 56% to 60% lower with community-wide treatment (adjusted prevalence ratios 0.44, 95% CI 0.34-0.58 in Benin; 0.41, 0.32-0.52 in India; 0.40, 0.34-0.46 in Malawi), but transmission was interrupted in only 12 of 60 intervention clusters, and the authors conclude that interruption does not appear programmatically feasible within the timeframe they evaluated. The trial was funded by the Gates Foundation ⁸².

Two practical points finish the section. First, treatment does not prevent reinfection: most treated people in endemic areas are reinfected within months ¹¹, and in the only long-run series of its kind, 76 of 500 Kashmir patients had worms re-enter the biliary tree over a mean 48 months ¹⁴. Second, treatment may leave more than the worm behind. A 2026 multi-omics study in pigs — measuring genes, microbes and metabolites together — found that infection shifted the gut bacterial community and dysregulated 182 blood and stool metabolites, the small molecules of metabolism, and that pigs treated with fenbendazole still differed from uninfected controls in gut microbial composition 13 days after the worms were confirmed gone; in oxygen-free culture, bacteria exposed to fenbendazole together with worm proteins produced about 79% more histamine at 48 hours. The authors state their own limitations — no drug-only control group, cross-sectional design — and interpret the treatment effects cautiously ¹²¹. It is a first look, in pigs, at a question nobody had asked.

The pig roundworm as a laboratory animal

One reason so much is known about this parasite is that it comes with a large experimental host that is physiologically close to a person. Pigs are susceptible to their own roundworm, that roundworm is closely related to the human one, and pigs can be infected on schedule, weighed, biopsied and killed. The pig-and-worm system is the standard model for human ascariasis, and the genome paper says so explicitly as part of its rationale ³.

What the model has produced falls into three groups. The first is population biology. Pigs given 25 eggs per kilogram every day showed a sharp fall in migrating lung larvae and liver white spots over 14 weeks despite continuous exposure, with the adult population consisting of worms acquired early — the immune system learning to exclude new arrivals while tolerating residents ⁸⁷. A 30-week trickle infection followed by challenge produced complete protection: no worms in the intestine and a 97.2% reduction in liver white spots ⁴⁶. And genome scanning of 195 experimentally infected pigs found a candidate region on chromosome 4 covering 2.5 megabases associated with worm burden, against a background heritability for infection level of 0.45. No marker reached genome-wide significance in that first scan — that is the strict statistical threshold used when hundreds of thousands of markers are tested at once — although two markers in the region were then confirmed in separate animals ¹²². Why some hosts carry heavy burdens repeatedly remains unanswered; a review on exactly that question concludes that the mechanisms are currently unknown ³⁸.

The second group is immunology. Chronic infection broadly suppressed inflammatory gene expression in the pig intestinal lining — cytokines, the signaling molecules of immunity, and the antigen-processing and costimulatory molecules that immune cells use to display foreign material and switch on T cells, the white cells that direct an immune response — and worm body fluid did the same to human dendritic cells in culture, leaving them unable to drive production of interferon-gamma, a signal of the inflammatory rather than the allergic response, in T cells ⁴⁵. Those are two separate kinds of evidence, one in an animal and one in human cells in a dish, and neither is a clinical observation. Antibody work in pigs has defined which worm products the host actually sees: a phosphorylcholine-containing glycolipid-like larval surface antigen — a fat bearing sugar chains — called As12, actively shed by infective larvae and resistant to enzymatic and chemical treatment, turned out to be a major antibody target in both pigs and people, and although vaccinating with it did not protect, it made a good test for long-term exposure ⁴⁶. A 2025 study extended this backward in time, showing that adult-worm secretions detect specific antibody at 14 days after infection, during the larval phase ⁸⁵. In 2026 the secreted proteome — the full set of proteins a stage releases — was cataloged across three larval stages (larvae from eggs, from lungs and from the trachea), yielding 58 unique proteins of which only 14 were common to all three, the rest being stage-specific ³⁶.

The third group is the growth question, and here the pig model gave a more careful answer than the field studies. 195 pigs were trickle-infected with the pig roundworm and the pig whipworm together, imitating natural co-infection, and weighed over 14 weeks. A 1 kg increase in weight gain was associated with a 4.4% lower whipworm egg count (P=0.00217) and a 2.8% lower roundworm egg count (P=0.02297) or 2.2% lower worm burden (P=0.0488) — but the roundworm association did not survive adjustment for other covariates, and the authors' own conclusion is that the whipworm may be more detrimental to growth than the roundworm ⁹⁵. That is a post-hoc analysis in an animal model, and it points the same way as the human randomized evidence ³⁰: the intuition that this worm in particular stunts children is less securely founded than the intuition feels.

There is a separate and more difficult matter: deliberate infection of people. It has been done, twice at least, and long ago. A 1951 paper from Japan is titled "Experimental infection of man with Ascaris of man and the pig"; its indexed record carries no abstract, so only its existence and its design are cited here, not its results ⁵². In 1972 the New England Journal of Medicine published a report of pulmonary infiltrates, asthma and eosinophilia caused by pig-roundworm infection in adult men; that record also lacks an abstract ⁷⁰. What exists in modern form, for a related soil-transmitted worm, is a formal controlled human infection model: in a 2026 phase 2 trial, 39 hookworm-naive adults were randomized to one of three Na-GST-1 vaccine formulations or to placebo, 10 of them to placebo, and 33 were then deliberately challenged with 50 infective larvae under medical supervision ¹²³. So the design is established and ethically navigable for this family of parasites. For this worm, the modern human evidence remains observational, and the volunteers are pigs.

What is still unknown

Whether this is one species or two is still, formally, unresolved — and more interestingly, it may be the wrong question. The current evidence describes host-associated populations with ongoing gene flow between them, which is a species complex rather than either of the two answers the question offers ^4,34. Two laboratories have reversed their positions in print ^19,33,48,55, the clade structure is still gaining new branches ⁸, and nobody has yet published a population-genomic analysis with enough nuclear data from enough countries to say how much exchange happens where. That study is clearly possible now and has not been done.

Why some people carry hundreds of worms and others, in the same household, carry none is unknown. The pattern is reliable enough to have its own name, predisposition, and a review devoted to it concludes that the generating mechanisms are currently unknown, with immune and genetic candidates still only candidates ³⁸. The pig genome scan found a region on chromosome 4 associated with burden, against a heritability of 0.45; no marker reached genome-wide significance in the original scan, although two markers in the region were then confirmed in separate animals ¹²². In 2026, seven years of data from the Geshiyaro project in southern Ethiopia showed the same people being reinfected round after round in spite of treatment (Kendall's coefficient of concordance 0.43, 95% confidence interval 0.42 to 0.45, a measure of how consistently individuals keep their relative ranking), which is the clearest human evidence yet that predisposition persists under mass treatment; its cause is still unknown ⁸³. The human genetic equivalent of the pig scan has not been done at modern scale.

Whether a childhood lung migration leaves permanent damage in people is unknown, and this is the most consequential open question on the page. In mice a single episode produced chronic type-2 inflammation, emphysema, lung bleeding and anemia persisting after clearance ³⁷, with a proposed mechanism in a retained worm peptide presented by lung macrophages ⁸⁶. Those authors suggest remote episodes may drive asthma and chronic obstructive pulmonary disease in endemic regions. No human cohort has followed children through infection to adult lung function. Until one does, this remains a hypothesis raised in a species the worm cannot complete its life cycle in.

The allergy relationship is unsettled in a specific way. Meta-analysis finds this worm associated with more bronchial hyperreactivity in children and more atopy in adults, on low-to-moderate quality evidence, with no study addressing clinical outcomes ¹⁰⁴; one randomized trial finds that removing the worms does not change allergy prevalence ¹⁰⁵ while an earlier one found that repeated treatment raised the rate of developing skin sensitivity to house dust mite ¹⁰⁶; and the tropomyosin cross-reactivity is real but its clinical weight is unmeasured ^98,102,103. These can all be true if the association is confounded, or if the worm's effect runs through a pathway that deworming for a year does not reverse. Nobody knows which.

The real frequency of pig-roundworm larva migrans in people is unknown. Case reports cluster in Japan and point to raw pig liver ^90,91,107, serological screening in northern Europe produced remarkably high seroprevalences, and the diagnostic test that would settle it has to contend with heavy cross-reactivity against the dog and cat roundworms ⁹². There is no population-based estimate anywhere.

Whether benzimidazole resistance is coming is unknown, and the surveillance may be looking in the wrong place. The resistance-associated changes at the codons monitored in livestock have not been found in this worm in Africa, Europe or Asia ^57,80, and German pig-roundworm populations tested susceptible in an egg-development assay ¹¹⁹, but this genus carries at least seven beta-tubulin genes, and resistance here may not be written in the codons veterinary science taught us to read ⁸⁰. Meanwhile albendazole reduced egg counts by only 75.4% in Rwandan schoolchildren whose worms carried none of those changes ²⁶, and a 2025 Indian trial reported 61.64% cure with single-dose albendazole in a routinely dewormed population against a pooled 88% to 96% ^23,24,25. Neither is evidence of resistance, and both are exactly the kind of signal that ought to trigger genotyping rather than reassurance.

Two older human experiments close this. Koino's 1922 self-experiment, conventionally cited as the demonstration of human lung migration, appeared in a Japanese journal that PubMed does not index, so it is not a source here. A 1951 Japanese study of experimental infection of people with worms of both human and pig origin, and a 1972 American report of pig-roundworm lung disease in adult men, are indexed but carry no abstracts ^52,70. What those experiments found, in the detail a modern reader would want, is not available here; the modern controlled human infection work in this family of parasites has been done with hookworm rather than with this worm ¹²³.

Where it connects

Sources

123 sources, numbered as they are cited. Every one was checked against PubMed or its publisher before it was cited here; the note under each says what it shows and what it does not.

1. 1
   Leles D, Gardner SL, Reinhard K, Iniguez A, Araujo A. Are Ascaris lumbricoides and Ascaris suum a single species?Parasit Vectors · 2012 · 5:42doi:10.1186/1756-3305-5-42 · PMID 22348306

   Review setting out the four possible hypotheses and concluding that the two are one species, with A. lumbricoides Linnaeus 1758 holding taxonomic priority and A. suum Goeze 1782 a synonym. It also supplies the two naming dates used throughout this page. A review and argument, not new primary data; its conclusion is contested by later work.

2. 2
   Escalona N, Mughini-Gras L, Lorenz E, Sequera L, Sequera I, Serrano R, Incani RN. Factors associated with the fertility of the helminth parasite Ascaris lumbricoides: an exploratory study in a rural Venezuelan community.Food Waterborne Parasitol · 2026 · 45:e00363doi:10.1016/j.fawpar.2026.e00363 · PMID 42835706

   Complete fecal evacuations from 128 people, 57% of those consenting, across 45 houses. Higher worm counts tended to go with lower average worm length and weight, a crowding effect that did not reach significance; worm length and weight correlated strongly with egg production, less so in infections containing both sexes; the presence of male worms was the main determinant of egg fertility; and worm count was associated with the host's age and with household, but not with the host's sex. Exploratory and cross-sectional, in one community; the rare modern study that counts and measures the worms themselves in people.

3. 3
   Jex AR, Liu S, Li B, et al. Ascaris suum draft genome.Nature · 2011 · 479(7374):529-33doi:10.1038/nature10553 · PMID 22031327

   The 273-megabase draft genome of the pig roundworm, low repeat content 4.4%, about 18,500 protein-coding genes, a secretome of about 750 molecules rich in peptidases. It also states around 1.2 billion Ascaris infections and about 135,000 deaths annually from geohelminths as a group, figures it cites rather than measures.

4. 4
   Easton A, Gao S, Lawton SP, et al. Molecular evidence of hybridization between pig and human Ascaris indicates an interbred species complex infecting humans.Elife · 2020 · 9:e61562doi:10.7554/eLife.61562 · PMID 33155980

   A 296-megabase reference-quality genome with 17,902 protein-coding genes, plus 68 worms from 60 human hosts in Kenyan villages where pig keeping is rare. 63 of 68 had mitochondrial genomes clustering closer to the pig parasite; over 11 million nuclear single-nucleotide polymorphisms resolved into two genetic types that had recombined. Strong evidence of interbreeding; one country, one sampling frame.

5. 5
   Pullan RL, Smith JL, Jasrasaria R, Brooker SJ. Global numbers of infection and disease burden of soil transmitted helminth infections in 2010.Parasit Vectors · 2014 · 7:37doi:10.1186/1756-3305-7-37 · PMID 24447578

   Prevalence data for 6,091 locations in 118 countries, modeled by model-based geostatistics for sub-Saharan Africa and by empirical approaches for all other regions, then fed into the Global Burden of Disease 2010 framework. 819.0 million people infected with this worm in 2010 (95% credible interval 771.7-891.6 million), against 464.6 million for whipworm and 438.9 million for hookworm. Of 4.98 million years lived with disability from these worms, 22% were attributed to this one and 65% to hookworm. A model built on surveys, not a count.

6. 6
   Chen J, Gong Y, Chen Q, Li S, Zhou Y. Global burden of soil-transmitted helminth infections, 1990-2021.Infect Dis Poverty · 2024 · 13(1):77doi:10.1186/s40249-024-01238-9 · PMID 39444032

   Full text read (PMC11515461). Global Burden of Disease 2021 estimates: 293.80 million cases of ascariasis and 647.53 thousand disability-adjusted life years, out of 642.72 million soil-transmitted worm infections; age-standardized prevalence for this worm 3,856.33 per 100,000 (95% uncertainty interval 3,133.93-4,760.38), down 75.8% from 15,930.11 in 1990, estimated annual percentage change -5.07 (95% CI -5.28 to -4.85); 3,472 deaths from these worms in 2021, mainly from this one. Modeled estimates built on primary data of variable quality, which the authors say should be read with caution.

7. 7
   Dold C, Holland CV. Ascaris and ascariasis.Microbes Infect · 2011 · 13(7):632-7doi:10.1016/j.micinf.2010.09.012 · PMID 20934531

   Short review. Source for approximately 1.2 billion people infected and for the overdispersed distribution of adult worms among hosts. A review; the prevalence figure is quoted from other work, not measured here.

8. 8
   Woolfe L, Kozel K, Adisakwattana P, et al. Scalable assembly of Ascaris mitogenomes from whole-genome data reveals a novel clade.Sci Rep · 2026 · 16(1)doi:10.1038/s41598-026-65562-w · PMID 42728251

   149 high-quality mitochondrial genome assemblies built from low-coverage whole-genome data. It names a fourth clade, Clade D, found in human samples from Ethiopia, and finds Clade C to be pig-derived worms from Europe. The newest word on the clade structure as of this page's review date; a clade defined on mitochondrial DNA alone is a maternal lineage, not a species.

9. 9
   Liyew EF, Tollera G, Mengistu B, et al. Small bowel obstruction due to ascariasis in a child from southern Ethiopia: a case report.J Med Case Rep · 2025 · 19(1):56doi:10.1186/s13256-025-05082-9 · PMID 39953625

   An 8-year-old boy with obstruction relieved by laparotomy and enterotomy. Its introduction gives a current working figure of just under 900 million people infected globally, most of them children, and the discussion sets out the water, sanitation and hygiene failures behind the case. One case; the burden figure is quoted, not measured.

10. 10
    Pullan RL, Brooker SJ. The global limits and population at risk of soil-transmitted helminth infections in 2010.Parasit Vectors · 2012 · 5:81doi:10.1186/1756-3305-5-81 · PMID 22537799

    Maps where transmission is biologically possible rather than counting infections: 5.3 billion people, including 1.0 billion school-aged children, lived in areas of stable transmission for at least one of these worms in 2010, 69% of them in Asia, with a further 143 million in areas of unstable transmission. Prevalence of this worm was statistically higher in peri-urban than in urban or rural areas. Population at risk is not population infected.

11. 11
    Leung AKC, Leung AAM, Wong AHC, Hon KL. Human Ascariasis: An Updated Review.Recent Pat Inflamm Allergy Drug Discov · 2020 · 14(2):133-145doi:10.2174/1872213X14666200705235757 · PMID 32628606

    Clinical review. Gives more than 1.2 billion infected, sets out the complication list from Loeffler syndrome through obstruction, biliary colic, cholangitis, pancreatitis and malnutrition, and states an average cure rate above 95% with treatment while most treated patients in endemic areas are reinfected within months. A review; the prevalence figure is inherited from earlier modeling.

12. 12
    Loeffler W. Transient lung infiltrations with blood eosinophilia.Int Arch Allergy Appl Immunol · 1956 · 8(1-2):54-9PMID 13331628

    A 1956 English-language account by the physician whose name the syndrome carries; his original description was published in German in 1932 (Beitr Klin Tuberk) and is not indexed in PubMed. The PubMed record for this paper has no abstract, so it is cited here only for the eponym, not for any clinical detail or for the date of the first description [107].

13. 13
    de Silva NR, Guyatt HL, Bundy DA. Morbidity and mortality due to Ascaris-induced intestinal obstruction.Trans R Soc Trop Med Hyg · 1997 · 91(1):31-6doi:10.1016/s0035-9203(97)90384-9 · PMID 9093623

    Meta-analysis of published hospital series. In nine studies of 100 or more admitted patients, obstruction was the commonest complication, 38 to 87.5% of all complications (weighted mean 72%). In twelve studies of 30 or more obstruction cases the case fatality rate ran from 0 to 8.6% (weighted mean 5.7%), and mean age was five years or under in six of seven studies that gave it. Hospital series over-represent severe disease; this is not population incidence.

14. 14
    Khuroo MS, Zargar SA, Mahajan R. Hepatobiliary and pancreatic ascariasis in India.Lancet · 1990 · 335(8704):1503-6doi:10.1016/0140-6736(90)93037-p · PMID 1972440

    500 patients from Kashmir: 274 duodenal, 171 biliary, 40 hepatic, 8 gallbladder and 7 pancreatic; presentations were biliary colic (280), acute cholangitis (121), acute cholecystitis (64), acute pancreatitis (31) and liver abscess (4). Four died. 76 had worms re-enter the biliary tree over a mean 48 months of follow-up, and 7 formed duct stones around dead worms. The defining clinical series.

15. 15
    Nejsum P, Parker ED, Frydenberg J, Roepstorff A, Boes J, Haque R, Astrup I, Prag J, Skov Sørensen UB. Ascariasis is a zoonosis in Denmark.J Clin Microbiol · 2005 · 43(3):1142-8doi:10.1128/JCM.43.3.1142-1148.2005 · PMID 15750075

    Whole-genome fingerprinting (amplified fragment length polymorphism) plus a nuclear ribosomal restriction assay. Worms from Danish patients clustered with worms from Danish pigs, and separately from worms taken from people elsewhere in the world. The clearest demonstration that human ascariasis in a developed country is a pig-derived infection.

16. 16
    Arizono N, Yoshimura Y, Tohzaka N, Yamada M, Tegoshi T, Onishi K, Uchikawa R. Ascariasis in Japan: is pig-derived Ascaris infecting humans?Jpn J Infect Dis · 2010 · 63(6):447-8PMID 21099099

    Nine worms from Japanese patients and nine from pigs, typed at the first internal transcribed spacer. Six patient worms carried the genotype that predominates in people in endemic countries and three carried the pig genotype. Nine patients is a small series, but it shows both routes operating in one country.

17. 17
    Miller LA, Colby K, Manning SE, et al. Ascariasis in humans and pigs on small-scale farms, Maine, USA, 2010-2013.Emerg Infect Dis · 2015 · 21(2):332-4doi:10.3201/eid2102.140048 · PMID 25626125

    14 cases of ascariasis in people who had contact with pigs in Maine over four years. A surveillance report, not a genotyped series in its abstract, so it establishes the cluster and the pig exposure rather than proving the worms' origin molecularly.

18. 18
    Bendall RP, Barlow M, Betson M, Stothard JR, Nejsum P. Zoonotic ascariasis, United Kingdom.Emerg Infect Dis · 2011 · 17(10):1964-6doi:10.3201/eid1710.101826 · PMID 22000387

    A letter reporting zoonotic ascariasis in the United Kingdom. The PubMed record carries no abstract, so it is cited here only for the existence and date of the report, not for any number in it.

19. 19
    Cavallero S, Rondón S, Monterrosa IA, et al. Genotyping of Ascaris spp. infecting humans and pigs in Italy, Slovakia and Colombia.Infect Genet Evol · 2021 · 94:104997doi:10.1016/j.meegid.2021.104997 · PMID 34252615

    237 worms from three countries; 110 good cox1 sequences resolving into clades A, B and C. Important as a dissenting voice: the same group that argued for one polytypic species in 2013 writes here that the amount of genetic variation seems to support the existence of two closely related species.

20. 20
    Nikolay B, Brooker SJ, Pullan RL. Sensitivity of diagnostic tests for human soil-transmitted helminth infections: a meta-analysis in the absence of a true gold standard.Int J Parasitol · 2014 · 44(11):765-74doi:10.1016/j.ijpara.2014.05.009 · PMID 24992655

    Bayesian latent class meta-analysis without a perfect reference test. Sensitivities ranged from 42.8% for direct microscopy to 92.7% for FLOTAC. Double-slide Kato-Katz reached 74-95% where infection intensity was high but fell to 53-80% where it was low. The key quantitative statement on why the standard test fails exactly where programs need it.

21. 21
    Benjamin-Chung J, Pilotte N, Ercumen A, et al. Comparison of multi-parallel qPCR and double-slide Kato-Katz for detection of soil-transmitted helminth infection among children in rural Bangladesh.PLoS Negl Trop Dis · 2020 · 14(4):e0008087doi:10.1371/journal.pntd.0008087 · PMID 32330127

    2,799 stool samples. Kato-Katz sensitivity for this worm was 49% against 79% for the molecular test, but the awkward finding is the other direction: 26% of samples called positive for this worm by Kato-Katz were negative by polymerase chain reaction, and sequencing of ten of them confirmed the worm was absent. Kato-Katz specificity for this species was only 68%. It overcalls as well as undercalls.

22. 22
    Mugo RM, Rausch S, Musimbi ZD, et al. Evaluation of copromicroscopy, multiplex-qPCR and antibody serology for monitoring of human ascariasis in endemic settings.PLoS Negl Trop Dis · 2024 · 18(6):e0012279doi:10.1371/journal.pntd.0012279 · PMID 38889190

    390 Kenyan school children four months after national preventive chemotherapy; this worm predominated at 14.9% prevalence. Against the molecular test, mini-FLOTAC reached 53.5% and Kato-Katz 63.8% sensitivity. Antibody of the IgG1 subclass against adult worm excretory-secretory products discriminated infection with an area under the curve of 0.83 (95% CI 0.75-0.91) and, unlike the molecular test, did not track egg counts. Promising, not yet a deployed test.

23. 23
    Moser W, Schindler C, Keiser J. Efficacy of recommended drugs against soil transmitted helminths: systematic review and network meta-analysis.BMJ · 2017 · 358:j4307doi:10.1136/bmj.j4307 · PMID 28947636

    55 trials for cure rates and 46 for egg reduction. All four recommended drugs were highly efficacious against this worm; albendazole was best against hookworm (cure rate 79.5%, 95% CI 71.5-85.6; egg reduction 89.6%, 81.9-97.3); all were poor against whipworm, mebendazole best at 42.1% (25.9-60.2). Between 1995 and 2015 albendazole efficacy fell significantly, egg reduction from 72.6% to 43.4% (P=0.049) and cure from 38.6% to 16.4% (P=0.027) — a decline that the paper's conclusion attaches to the whipworm, not to this worm. Full text read (PMC5611648). Table 1, against this worm: albendazole 95.7% (93.2-97.3; 34 trials, 3,360 participants), mebendazole 96.2% (92.3-98.1), levamisole 97.3% (84.2-99.6; 2 trials), pyrantel pamoate 92.6% (85.6-96.3), placebo 12.7%; egg reduction 94.3-98.5%; 44 trials and 7,273 participants in all. The 1995-2015 declines sit in the whipworm analysis, where mebendazole's egg reduction also fell, from 91.4% to 54.7% (P=0.014). Recommended single doses in the inclusion criteria: albendazole 400 mg, mebendazole 500 mg, levamisole 80 mg or 2.5 mg/kg, pyrantel pamoate 10 mg/kg.

24. 24
    Keiser J, Utzinger J. Efficacy of current drugs against soil-transmitted helminth infections: systematic review and meta-analysis.JAMA · 2008 · 299(16):1937-48doi:10.1001/jama.299.16.1937 · PMID 18430913

    20 randomized controlled trials. Single-dose cure rates against this worm: albendazole 88% (95% CI 79-93, 557 patients), mebendazole 95% (91-97, 309 patients), pyrantel pamoate 88% (79-93, 131 patients). The same drugs cured only 28-36% of whipworm. The benchmark figures for single-dose treatment.

25. 25
    Awasthi S, Nandy M, Datta K, et al. Efficacy and Safety of Albendazole Versus Albendazole and Ivermectin in Reduction of Soil-Transmitted Helminth Infections in School-Age Children (DVERMIN): A Double-Blind, Randomized, Controlled Trial.Cureus · 2025 · 17(2):e79152doi:10.7759/cureus.79152 · PMID 40125167

    1,067 evaluable Indian schoolchildren at baseline, of whom 416 (38.99%) were egg-positive and 99.52% of those carried this worm. Cure at day 7 was 61.64% with albendazole alone and 62.03% with albendazole plus ivermectin (P=0.95); egg reduction 90.61% against 93.22%. Cure rates well below the pooled 88-96% in a routinely dewormed population, which is the finding worth noticing — but read with three caveats. Cure was assessed at day 7, earlier than the 14 to 21 days used in most efficacy trials; the cure rates rest on the 304 children evaluable after treatment, not the 416 found positive; and the reported egg counts (median 3 eggs per gram, 89.18% of positives at 10 eggs per gram or below) cannot be produced by a single Kato-Katz slide read with a multiplier of 24, whose smallest positive value is 24 eggs per gram. Three co-authors are from the medical affairs department of Mankind Pharma, which makes the fixed-dose combination tested.

26. 26
    Krücken J, Fraundorfer K, Mugisha JC, et al. Reduced efficacy of albendazole against Ascaris lumbricoides in Rwandan schoolchildren.Int J Parasitol Drugs Drug Resist · 2017 · 7(3):262-271doi:10.1016/j.ijpddr.2017.06.001 · PMID 28697451

    12 schools in the Huye district of Rwanda. Single-dose albendazole 400 mg: cure 69.9% by Mini-FLOTAC (88.6% by wet-mount microscopy) and fecal egg count reduction 75.4% (95% CI 50.4-87.8% by sample variance), ranging from 0 to 96.8% between schools. No putative benzimidazole-resistance polymorphisms were found in four beta-tubulin isotype genes, so heritable resistance cannot be shown; the authors state that a reduction below 95% nonetheless raises the suspicion of it. The strongest phenotypic signal on this page, and it is uncoupled from the genotype.

27. 27
    Sethi SK, Mandal N, Pattanaik AA, et al. Effectiveness of single-dose albendazole against soil-transmitted helminth infection in children: A longitudinal study in a tribal dominated district of Odisha, India.Indian J Med Res · 2025 · 162(6):873-880doi:10.25259/IJMR_820_2025 · PMID 41648978

    1,246 children across 18 clusters in Nabarangpur, Odisha; the 203 who were positive received albendazole 400 mg, with stool at days 14, 28 and 42 and Kato-Katz egg counts. Egg reduction 96.2% for this worm and 93.8% for hookworm, but cure rates of only 66.7% and 52.94%, which the authors call suboptimal against the World Health Organization thresholds. An effectiveness study without a comparison group; high egg reduction with low cure is the pattern that makes resistance hard to read.

28. 28
    Hon KL, Leung AKC. An update on the current and emerging pharmacotherapy for the treatment of human ascariasis.Expert Opin Pharmacother · 2024 · 25(3)doi:10.1080/14656566.2024.2319686 · PMID 38372051

    Current review of drug treatment. Mebendazole and albendazole for children and non-pregnant adults, pyrantel pamoate in pregnancy, and emodepside named as highly effective in single doses against ascarids in mammals and in human trials. A narrative review; it does not pool new numbers.

29. 29
    Salam RA, Das JK, Bhutta ZA. Effect of mass deworming with antihelminthics for soil-transmitted helminths during pregnancy.Cochrane Database Syst Rev · 2021 · 5(5):CD005547doi:10.1002/14651858.CD005547.pub4 · PMID 33998661

    Six randomized trials, 7,873 pregnant women, albendazole or mebendazole in the second or third trimester. Prevalence of this worm fell markedly (risk ratio 0.24, 95% CI 0.19-0.29; two trials, 2,488 participants; moderate-certainty evidence) and of whipworm less so (0.68, 0.48-0.98); maternal anemia may be reduced by about 15% (0.85, 0.72-1.00; five trials, 5,745 participants; low certainty); probably little or no difference in low birthweight (0.89, 0.69-1.16) or birthweight; the effect on preterm birth and perinatal mortality is uncertain. Evidence that benzimidazoles are used and studied in later pregnancy, set against the clinical reviews' preference for pyrantel pamoate [76].

30. 30
    Taylor-Robinson DC, Maayan N, Soares-Weiser K, Donegan S, Garner P. Deworming drugs for soil-transmitted intestinal worms in children: effects on nutritional indicators, haemoglobin, and school performance.Cochrane Database Syst Rev · 2015 · 2015(7):CD000371doi:10.1002/14651858.CD000371.pub6 · PMID 26202783

    45 trials: 44 with 67,672 participants, plus one mortality trial of over a million children. Treating children known to be infected may add weight (627 participants, five trials, low-quality evidence, 0.2 to 1.3 kg). Treating everyone in an endemic area probably does not: mean difference 0.04 kg less (95% CI 0.11 kg less to 0.04 kg more, 2,719 participants, seven trials, moderate quality), with no detectable effect on height, hemoglobin, cognition, exam performance or mortality. The central reversal in this field. Superseded by the 2019 update [100], whose conclusions are unchanged; the main counter-argument rests on the Kenyan school trial, its reanalyses and its twenty-year economic follow-up [108][109][110].

31. 31
    Taylor-Robinson DC, Maayan N, Donegan S, Chaplin M, Garner P. Public health deworming programmes for soil-transmitted helminths in children living in endemic areas.Cochrane Database Syst Rev · 2019 · 9(9):CD000371doi:10.1002/14651858.CD000371.pub7 · PMID 31508807

    Update of the 2015 edition, written partly to address published comments and criticisms: 51 trials, 50 of them with 84,336 participants plus a mortality trial of over a million children. Regular treatment probably has little or no effect on height (mean difference 0.02 cm, 95% CI 0.09 cm less to 0.13 cm more; 13 trials), hemoglobin (0.01 g/dL less, 0.05 less to 0.07 more; nine trials), formal tests of cognition (eight trials) or school performance (four trials), and no effect was shown on mortality (three trials, low certainty). On weight the authors conclude that they do not know: trials from more than twenty years earlier showed large gains, trials since 2000 average 0.02 kg (0.04 kg loss to 0.08 kg gain). Conclusions unchanged from 2015.

32. 32
    Hamory J, Miguel E, Walker M, Kremer M, Baird S. Twenty-year economic impacts of deworming.Proc Natl Acad Sci U S A · 2021 · 118(14):e2023185118doi:10.1073/pnas.2023185118 · PMID 33790017

    Twenty-year follow-up of the same Kenyan school trial, with an effective tracking rate of 84%: those who received two to three additional years of childhood deworming had 14% higher consumption expenditure and 13% higher hourly earnings, were 9% more likely to live in urban areas, and worked 9% more non-agricultural hours, with most effects concentrated among males and older individuals. Written by the original trial investigators, which is the conflict to name; it is an economic outcome, not a health outcome, and it does not reinstate the growth or hemoglobin findings.

33. 33
    Peng W, Yuan K, Hu M, Gasser RB. Recent insights into the epidemiology and genetics of Ascaris in China using molecular tools.Parasitology · 2007 (online 19 Oct 2006) · 134(Pt 3):325-30doi:10.1017/S0031182006001521 · PMID 17052373

    Review of the Chinese work, reporting experimental infection of pigs with genotype G1 (human-derived) and G3 (pig-derived) eggs and a significant difference in their ability to establish as adults. Concludes cross-infection is limited in endemic regions and pigs are not a significant reservoir there. Directly contradicted by the later Chinese microsatellite work in this list.

34. 34
    Khan AU, Shan T, Khalid M, Firasat S, Afshan K. Multilocus Characterization of Human Ascaris in Pakistan Indicates Ongoing Introgression and Shared Global Haplotypes.Acta Parasitol · 2026 · 71(3)doi:10.1007/s11686-026-01281-6 · PMID 42012546

    1,675 children enrolled across six districts of Khyber Pakhtunkhwa; worms expelled after treatment were sequenced at nuclear ribosomal regions and cox1. Divergence under 1% at cox1, sequences intermixing between the two named species, and a conclusion of a genetically interconnected species complex rather than clearly separated species. The abstract does not say how many worms were sequenced; it describes six nuclear sequence types (Pk_01 to Pk_06). The authors read the intermixing as consistent with incomplete lineage sorting as well as with historical introgression. The worms come from the same cohort of 1,675 children as the drug study [69], so the two papers are not independent.

35. 35
    GBD 2015 Disease and Injury Incidence and Prevalence Collaborators. Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990-2015: a systematic analysis for the Global Burden of Disease Study 2015.Lancet · 2016 · 388(10053):1545-1602doi:10.1016/S0140-6736(16)31678-6 · PMID 27733282

    The whole-disease accounting in which ascariasis appears among exactly eight causes of chronic disease or injury each affecting more than 10% of the world's population in 2015, alongside dental caries, tension-type headache, iron-deficiency anemia, hearing loss, migraine, genital herpes and refractive error. A modeled synthesis, not a survey.

36. 36
    Castañeda S, Adeniyi-Ipadeola G, Wu Y, et al. Characterizing excretory-secretory products proteome across larval development stages in Ascaris suum.Mol Biochem Parasitol · 2026 · 268:111778doi:10.1016/j.molbiopara.2026.111778 · PMID 42632619

    58 unique proteins across larvae from eggs, lungs and trachea, of which 14 were common to all stages and the rest stage-specific. A catalog of candidate targets for blocking the lung migration. Proteomics in culture and in mice; no therapeutic claim is made.

37. 37
    Wu Y, Li E, Knight M, et al. Transient Ascaris suum larval migration induces intractable chronic pulmonary disease and anemia in mice.PLoS Negl Trop Dis · 2021 · 15(12):e0010050doi:10.1371/journal.pntd.0010050 · PMID 34914687

    A single episode of larval migration left mice with chronic type-2 inflammation, emphysema, lung bleeding and chronic anemia after the worms were gone. The authors propose that remote episodes could drive asthma, chronic obstructive pulmonary disease and anemia in endemic regions. That proposal is a hypothesis generated in mice and has not been tested in people.

38. 38
    Dold C, Holland CV. Investigating the underlying mechanism of resistance to Ascaris infection.Microbes Infect · 2011 · 13(7):624-31doi:10.1016/j.micinf.2010.09.013 · PMID 20934532

    Review of why some people carry heavy worm burdens repeatedly and others do not. Its conclusion is the honest one: the mechanisms generating this predisposition are currently unknown, and the immune and genetic candidates remain candidates.

39. 39
    Pickering AJ, Njenga SM, Steinbaum L, et al. Effects of single and integrated water, sanitation, handwashing, and nutrition interventions on child soil-transmitted helminth and Giardia infections: A cluster-randomized controlled trial in rural Kenya.PLoS Med · 2019 · 16(6):e1002841doi:10.1371/journal.pmed.1002841 · PMID 31242190

    622 clusters and 9,077 children in rural western Kenya, two years after the interventions began; 23% of control children carried this worm. Against the control group, prevalence of this worm was lower with water treatment (prevalence ratio 0.82, 95% CI 0.67-1.00), with combined water, sanitation and handwashing (0.78, 0.63-0.96) and with those plus nutrition (0.78, 0.64-0.96), but not detectably with improved sanitation alone (0.89, 0.73-1.08) or handwashing alone (0.89, 0.73-1.09). Uptake of the target behaviors was imperfect and participants could not be blinded; the authors' point is that drinking water deserves more attention as a transmission route.

40. 40
    Khuroo MS, Zargar SA. Biliary ascariasis. A common cause of biliary and pancreatic disease in an endemic area.Gastroenterology · 1985 · 88(2):418-23PMID 3965331

    The founding paper, prospective, in 109 patients with biliary and pancreatic disease in Kashmir: this worm was the cause in 40 (36.7%), mostly adult women; recurrent biliary colic in 38 (95%), recurrent pyogenic cholangitis in 27 (68%), acalculous cholecystitis in 9 (23%), pancreatic disease in 6 (15%); 19 (48%) vomited roundworms during colic, which often led to the diagnosis; 36 (90%) recovered on symptomatic treatment followed by a worm drug, and 4 needed surgery for worms trapped in the ducts with stones formed around the worm fragment. No DOI in the record. A single-center series with no comparison group.

41. 41
    Wani I, Maqbool M, Amin A, Shah F, Keema A, Singh J, Kitagawa M, Nazir M. Appendiceal ascariasis in children.Ann Saudi Med · 2010 · 30(1):63-6doi:10.4103/0256-4947.59380 · PMID 20103960

    11 children found at operation to have worms in the appendix: in 8 (72.7%) the worm sat there without causing appendicitis, in 3 (27.2%) it was associated with appendicitis. No preoperative diagnosis was made in any. Eleven patients, all already undergoing surgery for other worm complications, so the denominator is not the general population.

42. 42
    Larsen MN, Roepstorff A. Seasonal variation in development and survival of Ascaris suum and Trichuris suis eggs on pastures.Parasitology · 1999 · 119(Pt 2):209-20doi:10.1017/s0031182099004503 · PMID 10466129

    Pig feces placed outdoors in four seasons and followed for up to 50 weeks. Eggs embryonated only during the summer months, and the majority of eggs — generally considered extremely resistant and long-lived — in fact disappeared rather fast, faster in summer than winter and faster in short grass than buried in soil. A direct check on the textbook claim that the eggs last for years, in a Danish climate.

43. 43
    Roepstorff A, Mejer H, Nejsum P, Thamsborg SM. Helminth parasites in pigs: new challenges in pig production and current research highlights.Vet Parasitol · 2011 · 180(1-2):72-81doi:10.1016/j.vetpar.2011.05.029 · PMID 21684689

    Review from the Copenhagen group. States that the pig roundworm is now evidently zoonotic, and reports an ongoing tracer-pig study in which soil infectivity rose over the first two to three years after pasture contamination rather than falling. Also notes heritability of host resistance high enough that breeding resistant pigs is conceivable.

44. 44
    Weatherhead JE, Porter P, Coffey A, et al. Ascaris Larval Infection and Lung Invasion Directly Induce Severe Allergic Airway Disease in Mice.Infect Immun · 2018 · 86(12)doi:10.1128/IAI.00533-18 · PMID 30249744

    Mice given worm eggs developed airway hyperresponsiveness from day 8, peaking at day 12 and persisting to day 21 despite the infection resolving, with a type-2 cytokine response comparable to, and airway remodeling more marked than, a standard ovalbumin allergy model. A mouse experiment; mice are not the worm's natural host.

45. 45
    Midttun HLE, Acevedo N, Skallerup P, et al. Ascaris Suum Infection Downregulates Inflammatory Pathways in the Pig Intestine In Vivo and in Human Dendritic Cells In Vitro.J Infect Dis · 2018 · 217(2):310-319doi:10.1093/infdis/jix585 · PMID 29136163

    Chronic infection broadly suppressed cytokine, antigen-processing and costimulatory gene expression in the pig gut lining, and worm body fluid suppressed the same pathways in human dendritic cells in culture, with reduced capacity to induce interferon-gamma in T cells. Separates cleanly into an animal result and an in vitro human-cell result; neither is a clinical finding.

46. 46
    Vlaminck J, Masure D, Wang T, Nejsum P, Hokke CH, Geldhof P. A Phosphorylcholine-Containing Glycolipid-like Antigen Present on the Surface of Infective Stage Larvae of Ascaris spp. Is a Major Antibody Target in Infected Pigs and Humans.PLoS Negl Trop Dis · 2016 · 10(12):e0005166doi:10.1371/journal.pntd.0005166 · PMID 27906979

    Pigs immunized by 30 weeks of trickle infection and then challenged showed a 100% reduction in intestinal worms and a 97.2% reduction in liver white spots against non-immune controls. The 12-kilodalton larval antigen identified, As12, failed as a vaccine but gave a diagnostic test with 98.4% sensitivity in pigs and 92% in naturally infected people (specificity 95.5% and 90.0%). Protection here was induced by repeated infection, not by a vaccine.

47. 47
    Criscione CD, Anderson JD, Sudimack D, Peng W, Jha B, Williams-Blangero S, Anderson TJ. Disentangling hybridization and host colonization in parasitic roundworms of humans and pigs.Proc Biol Sci · 2007 · 274(1626):2669-77doi:10.1098/rspb.2007.0877 · PMID 17725977

    23 microsatellite loci and Bayesian clustering. Differentiation driven first by geography and then by host within a location, consistent with multiple separate host shifts; 4% of worms from Guatemala and 7% from China were assigned as hybrids by three concordant methods. Hybrid assignment is a statistical inference, not a bred cross.

48. 48
    Zhou C, Li M, Yuan K, Deng S, Peng W. Pig Ascaris: an important source of human ascariasis in China.Infect Genet Evol · 2012 · 12(6):1172-7doi:10.1016/j.meegid.2012.04.016 · PMID 22561394

    258 worms, 20 microsatellite loci, six Chinese provinces. Cross-infection in every location: of 20 cross-infection events, 19 were people carrying pure pig-type worms and one a pig carrying a human-type worm. Hybrids were found everywhere, and 95% of them came from human hosts. The same laboratory had argued the opposite in a review published online in 2006 and in print in 2007 [8]; Weidong Peng is the first author of that review and the senior author of this paper.

49. 49
    Anderson TJ. Ascaris infections in humans from North America: molecular evidence for cross-infection.Parasitology · 1995 · 110(Pt 2):215-9doi:10.1017/s0031182000063988 · PMID 7885739

    Nine human cases from North America. A HaeIII restriction site in ribosomal DNA was present in more than 96% of parasites from pigs worldwide and in all nine human worms, but in under 2% of worms from people in endemic areas. Small numbers, but the direction is unambiguous: those human infections came from pigs.

50. 50
    Peng W, Yuan K, Zhou X, Hu M, Abs EL-Osta YG, Gasser RB. Molecular epidemiological investigation of Ascaris genotypes in China based on single-strand conformation polymorphism analysis of ribosomal DNA.Electrophoresis · 2003 · 24(14):2308-15doi:10.1002/elps.200305455 · PMID 12874864

    486 human and 329 pig worms from six endemic regions of China. Five genotypes, G1 to G5; G1 in roughly 63-74% of human worms, G3 in roughly 79-86% of pig worms. The basis of the host-affiliated-genotype picture. Genotypes from one nuclear region, so they describe affiliation, not species boundaries.

51. 51
    Galvin TJ. Development of human and pig ascaris in the pig and rabbit.J Parasitol · 1968 · 54(6):1085-91PMID 5757683

    Title only; no abstract or DOI in the record. Cited for the existence and design of the cross-infection experiments in which worms of human and of pig origin were raised in pigs and in rabbits.

52. 52
    Takata I. Experimental infection of man with Ascaris of man and the pig.Kitasato Arch Exp Med · 1951 · 23(4):151-9; English translation 49-59PMID 14874382

    Title only: the PubMed record carries no abstract and no DOI, and is indexed under experimental ascariasis in humans and swine. Cited for the existence and design of a deliberate human infection experiment with worms of both human and pig origin, not for its results.

53. 53
    Anderson TJ. The dangers of using single locus markers in parasite epidemiology: Ascaris as a case study.Trends Parasitol · 2001 · 17(4):183-8doi:10.1016/s1471-4922(00)01944-9 · PMID 11282508

    Methodological argument that conclusions drawn from mitochondrial DNA alone can be ambiguous, and that multilocus work changed the picture for these two worms. A commentary; no new data.

54. 54
    Zhou C, Jian S, Peng W, Li M. Genetic diversity of Ascaris in China assessed using simple sequence repeat markers.Korean J Parasitol · 2018 · 56(2):175-181doi:10.3347/kjp.2018.56.2.175 · PMID 29742872

    258 worms from humans and pigs in six sympatric regions. A genetic differentiation index of 0.0593 indicating high gene flow, and a population structure falling into three clusters read as human-type, pig-type and hybrid. Microsatellites only; cluster labels are model output.

55. 55
    Cavallero S, Snabel V, Pacella F, Perrone V, D'Amelio S. Phylogeographical studies of Ascaris spp. based on ribosomal and mitochondrial DNA sequences.PLoS Negl Trop Dis · 2013 · 7(4):e2170doi:10.1371/journal.pntd.0002170 · PMID 23593529

    151 worms. No fixed differences between human and pig worms except in the Slovak population. The authors conclude there is homogenizing gene flow and that the two are variants of a single polytypic species.

56. 56
    Thakur M, Mewara A, Lakshmi PVM, Guleria S, Khurana S. Genetic diversity and evolutionary relationships of human-derived Ascaris spp. based on mitochondrial markers.J Helminthol · 2026 · 100:e27doi:10.1017/S0022149X26101242 · PMID 41777021

    Indian worms sequenced at nad1 and cox1 alongside public data: 27 nad1 haplotypes and 25 cox1 haplotypes, with Indian sequences closely related to Chinese and Brazilian human and pig sequences. In the second of the two haplotype networks, pig-derived sequences formed a separate clade, which cuts against the hybridization reading. Supports earlier evidence of hybridization. Mitochondrial markers only, so it cannot by itself demonstrate nuclear gene exchange. The indexed abstract strips the gene names, so which gene gave 27 haplotypes and which gave 25 should be checked against the full text.

57. 57
    Adisakwattana P, Yoonuan T, Watthanakulpanich D, Boonkead P, Phaiphilai K, Phuphisut O. Genetic diversity, population structure, and benzimidazole resistance profiling of Ascaris lumbricoides in northwestern Thailand.Parasitol Res · 2026 · 125(1)doi:10.1007/s00436-026-08727-w · PMID 42474787

    Thai worms typed at cox1, nad1 and the beta-tubulin gene: 13 haplotypes including three new ones, no clear geographic structuring, haplotypes shared with the pig parasite, and exclusively wild-type beta-tubulin at codons 167, 198 and 200. Both a population-genetic and a resistance-surveillance result in one paper.

58. 58
    Nkouayep VR, McManus DP, Mbida M, Gordon CA, Nejsum P. Molecular epidemiology of Ascaris species recovered from humans and pigs in Cameroon.Trans R Soc Trop Med Hyg · 2022 · 116(10):949-958doi:10.1093/trstmh/trac020 · PMID 35385862

    83 worms sequenced at cox1 and nad1. Restricted gene flow correlating with host preference, but shared haplotypes between hosts indicating cross-transmission and hybridization. The authors argue control should target pigs as well as people. A modest sample from one country.

59. 59
    Shao CC, Xu MJ, Alasaad S, Song HQ, Peng L, Tao JP, Zhu XQ. Comparative analysis of microRNA profiles between adult Ascaris lumbricoides and Ascaris suum.BMC Vet Res · 2014 · 10:99doi:10.1186/1746-6148-10-99 · PMID 24766827

    171 microRNA candidates from human-derived worms and 494 from pig-derived worms, 74 shared. The authors read this as additional evidence for a single species. A small-molecule comparison from one pair of worm sources; the large difference in candidate counts is as likely to reflect sequencing depth as biology.

60. 60
    Xie Y, Niu L, Zhao B, et al. Complete mitochondrial genomes of chimpanzee- and gibbon-derived Ascaris isolated from a zoological garden in southwest China.PLoS One · 2013 · 8(12):e82795doi:10.1371/journal.pone.0082795 · PMID 24358225

    Mitochondrial genomes of worms from a chimpanzee and a gibbon in a Chinese zoo, concluding they are a single species genetically similar to the human roundworm. Two animals; it shows the genus is not confined to people and pigs.

61. 61
    Leles D, Araújo A, Ferreira LF, Vicente AC, Iñiguez AM. Molecular paleoparasitological diagnosis of Ascaris sp. from coprolites: new scenery of ascariasis in pre-Colombian South America times.Mem Inst Oswaldo Cruz · 2008 · 103(1):106-8doi:10.1590/s0074-02762008005000004 · PMID 18327505

    Ancient DNA, a 142-base-pair cytochrome b target, recovered from coprolites that were negative on microscopy, including a European sample from which DNA was extracted from 30 eggs. Shows the worm was present in pre-Columbian South America where microscopy had suggested it was rare. Very small numbers, and ancient-DNA work carries a contamination risk the paper addresses but cannot eliminate.

62. 62
    Nejsum P, Hawash MBF, Betson M, Stothard JR, Gasser RB, Andersen LO. Ascaris phylogeny based on multiple whole mtDNA genomes.Infect Genet Evol · 2017 · 48:4-9doi:10.1016/j.meegid.2016.12.003 · PMID 27939588

    Complete mitochondrial genomes for representative haplotypes of clusters A, B and C. Coalescent simulation suggests two divergence events: one early in the Neolithic producing a differentiated pig population (cluster C) and a second about 900 generations ago producing clusters A and B. Dates from coalescent modeling carry wide and unstated uncertainty.

63. 63
    Conterno LO, Turchi MD, Corrêa I, Monteiro de Barros Almeida RA. Anthelmintic drugs for treating ascariasis.Cochrane Database Syst Rev · 2020 · 4(4):CD010599doi:10.1002/14651858.CD010599.pub2 · PMID 32289194

    30 randomized trials, 6,442 participants, 17 countries. Single-dose albendazole cured 87.8% against ivermectin's 90.2% (risk ratio 0.99, 95% CI 0.91 to 1.08; three trials, 519 participants; moderate-certainty evidence), and albendazole 98.0% against mebendazole 96.9% (six trials, 2,131 participants; high-certainty evidence); egg reduction 96% to 100% for all drugs. Twenty of the 30 trials were funded or co-funded by drug manufacturers, which the review states. This is the pooled evidence against the common claim that ivermectin is the weak drug for this worm.

64. 64
    Lee HK, Jin SL, Lee HP, Choi SJ, Yum HK. Löffler's syndrome associated with Clonorchis sinensis infestation.Korean J Intern Med · 2003 · 18(4):255-9doi:10.3904/kjim.2003.18.4.255 · PMID 14717238

    A case report of a different parasite, cited here for one sentence of its introduction only: that in 1932 Löffler described the syndrome of self-limiting, transient pulmonary infiltrates with peripheral blood eosinophilia and mild pulmonary symptoms. It is cited for the date of the original description, which the indexed 1956 paper [36] does not supply.

65. 65
    Sakipova Z, Wong NSH, Bekezhanova T, Sadykova, Shukirbekova A, Boylan F. Quantification of santonin in eight species of Artemisia from Kazakhstan by means of HPLC-UV: Method development and validation.PLoS One · 2017 · 12(3):e0173714doi:10.1371/journal.pone.0173714 · PMID 28301522

    An analytical chemistry paper, cited here for two statements of fact in its own framing: santonin is the main constituent of Artemisia cina, and because of its toxicity to humans it is no longer in use. The study itself is about measuring santonin content in eight Artemisia species for veterinary development.

66. 66
    Matsusaki G, Mihara Y, Mogi K, et al. Studies on anthelmintics for Ascaris lumbricoides.Yokohama Med Bull · 1964 · 15:211-5PMID 14279448

    Japanese school-based anthelmintic work of the santonin and hexylresorcinol era. The PubMed record has no abstract, so it is cited only to establish that santonin and hexylresorcinol were in organized use for this worm at that date.

67. 67
    Kliks MM. Studies on the traditional herbal anthelmintic Chenopodium ambrosioides L.: ethnopharmacological evaluation and clinical field trials.Soc Sci Med · 1985 · 21(8):879-86doi:10.1016/0277-9536(85)90144-3 · PMID 3906906

    Field trials among Mayan farmers in Chiapas, Mexico. Decoctions of up to 300 mg of dried plant per kg body weight were in traditional use and highly regarded; doses up to 6,000 mg/kg of dried powdered plant had no significant effect on adult worms of this species, hookworm or whipworm, although gas chromatography confirmed ascaridole was present in the expected amounts. The author suggests the belief in efficacy comes from worms passed spontaneously after dosing. The cleanest negative trial of the herbal remedy, and separate from the distilled oil: the same abstract records that commercial preparations of oil of chenopodium and its active constituent ascaridole, obtained by steam distillation, had been and continued to be used with considerable success in mass treatment campaigns.

68. 68
    Goodwin LG. A method for recording the effects of anthelmintics on the movements of Ascaris lumbricoides.Br J Pharmacol Chemother · 1958 · 13(2):197-201doi:10.1111/j.1476-5381.1958.tb00217.x · PMID 13536286

    Adult worms from pigs suspended in nylon stockings in warm buffer. Piperazine caused gradual narcosis; tetrachlorethylene, hexylresorcinol and oil of chenopodium all stimulated movement before paralyzing the worm; santonin disordered the movements of the head end only. Concludes piperazine was the safest preparation then available. An in vitro assay on worms from pigs; it says nothing about safety in people directly.

69. 69
    Rim HJ, Ha JH, Lee JS, Hyun I, Uh KB. Pyrantel embonate in mass treatment of ascariasis and comparison with piperazine adipate and santonin-kainic acid complex.Korean J Parasitol · 1974 · 12(2):141-146doi:10.3347/kjp.1974.12.2.141 · PMID 12913476

    301 children given single-dose pyrantel embonate at 2.0, 5.0 or 10.0 mg/kg, with cure rates of 91.3%, 94.4% and 98.9%. Piperazine adipate at 75 mg/kg for two or three days cured 62.0% (71 patients) and 74.7% (75 patients); santonin-kainic acid complex cured 80.5% with 91.0% egg reduction (77 patients). A direct old-against-new comparison that shows how much worse the old drugs were.

70. 70
    Phills JA, Harrold AJ, Whiteman GV, Perelmutter L. Pulmonary infiltrates, asthma and eosinophilia due to Ascaris suum infestation in man.N Engl J Med · 1972 · 286(18):965-70doi:10.1056/NEJM197205042861802 · PMID 5062734

    Title only; the record carries no abstract, though it is indexed under acute disease, adult men, asthma, eosinophilia, immunoglobulins and lung disease. Cited for the existence and date of a human report of pig-roundworm lung disease, not for any number in it.

71. 71
    Greenberg BL, Gilman RH, Shapiro H, et al. Single dose piperazine therapy for Ascaris lumbricoides: an unsuccessful method of promoting growth.Am J Clin Nutr · 1981 · 34(11):2508-16doi:10.1093/ajcn/34.11.2508 · PMID 7304488

    185 Bangladeshi children randomized, double-blind, to piperazine citrate twice over two weeks or placebo. Cure rates were 53%, 31% and 36% for light, moderate and heavy infection; heavier infections were harder to clear and reinfected faster; and no anthropometric measure differed between groups over 11 months. An early, well-designed negative trial of deworming for growth.

72. 72
    Khuroo MS. My 40-Year Encounter with ERCP: A Saga of Service, Syndromes, and Solutions.J Clin Exp Hepatol · 2023 · 13(6):1074-1090doi:10.1016/j.jceh.2023.05.010 · PMID 37975034

    Retrospective account of 10,100 endoscopic retrograde cholangiopancreatography procedures from 1982 onward. Dates the recognition of hepatobiliary and pancreatic ascariasis as a clinical disease to 1985, names the worm as the commonest cause of hepatobiliary and pancreatic disease in Kashmir, and reports recurrent pyogenic cholangitis as 12.5% of all biliary disease there and essentially an aftermath of the worm. A personal review, not a dataset.

73. 73
    Nejsum P, Parker ED, Frydenberg J, Sørensen UBS, Roepstorff A, Prag J. [Ascariasis is a zoonosis in Denmark — secondary publication].Ugeskr Laeger · 2006 · 168(4):384-7PMID 16436241

    Danish-language secondary publication of the above. Its English abstract adds the practical conclusion: the main transmission route in developed countries appears to be pigs to people, so contact with pig manure should be avoided, especially by young children. No new data; cited for the public-health statement.

74. 74
    Nejsum P, Grøndahl C, Murrell KD. Molecular evidence for the infection of zoo chimpanzees by pig Ascaris.Vet Parasitol · 2006 · 139(1-3):203-10doi:10.1016/j.vetpar.2006.02.025 · PMID 16567044

    Chimpanzees in Copenhagen Zoo were found to carry worms that clustered with pig worms by two independent molecular methods. Evidence that the pig parasite crosses into primates other than people.

75. 75
    Nejsum P, Bertelsen MF, Betson M, Stothard JR, Murrell KD. Molecular evidence for sustained transmission of zoonotic Ascaris suum among zoo chimpanzees (Pan troglodytes).Vet Parasitol · 2010 · 171(3-4):273-6doi:10.1016/j.vetpar.2010.03.030 · PMID 20400228

    Follow-up showing the zoo infection was not repeated reintroduction from outside but a self-sustaining cycle within the chimpanzee troop, with eggs embryonating to the infective stage on site. A single zoo, but it shows the pig worm can establish a stable cycle in a non-pig host.

76. 76
    Betson M, Nejsum P, Bendall RP, Deb RM, Stothard JR. Molecular epidemiology of ascariasis: a global perspective on the transmission dynamics of Ascaris in people and pigs.J Infect Dis · 2014 · 210(6):932-41doi:10.1093/infdis/jiu193 · PMID 24688073

    536 worms barcoded at cox1 and 410 genotyped with microsatellites, from Europe, Africa, Asia and Latin America. Marked genetic segregation by host overall, but human infections in Europe were of pig origin and there was evidence of cross-transmission in Africa. The best single global dataset on who infects whom.

77. 77
    Aiken AM, Davey C, Hargreaves JR, Hayes RJ. Re-analysis of health and educational impacts of a school-based deworming programme in western Kenya: a pure replication.Int J Epidemiol · 2015 · 44(5):1572-80doi:10.1093/ije/dyv127 · PMID 26203169

    Re-analysis of the 1998-99 Kenyan trial using the original authors' own methods and data. Most results reproduced, but after correction of coding errors there was little evidence of the reported indirect effect on attendance in neighboring schools, and the combined increase in attendance among treated children fell from 7.5% to 3.9%, no longer statistically significant; the reported reduction in anemia was not reproduced. No effect on examination performance in either analysis.

78. 78
    Davey C, Aiken AM, Hayes RJ, Hargreaves JR. Re-analysis of health and educational impacts of a school-based deworming programme in western Kenya: a statistical replication of a cluster quasi-randomized stepped-wedge trial.Int J Epidemiol · 2015 · 44(5):1581-92doi:10.1093/ije/dyv128 · PMID 26203171

    The companion statistical replication. Year-stratified cluster-summary analysis found no clear evidence of improvement in attendance or examination performance; regression models combining both years gave strong evidence for attendance (adjusted odds ratio 1.82, 95% CI 1.74-1.91) and none for examination performance. The authors conclude that the evidence depends on the analysis method, with substantial missing data and a high risk of bias.

79. 79
    Montresor A, Mupfasoni D, Mikhailov A, et al. The global progress of soil-transmitted helminthiases control in 2020 and World Health Organization targets for 2030.PLoS Negl Trop Dis · 2020 · 14(8):e0008505doi:10.1371/journal.pntd.0008505 · PMID 32776942

    Built from more than 690 country reports covering 2008 to 2018. More than one billion people currently infected; more than 3.3 billion benzimidazole tablets distributed in schools since 2010. Sets the goal of eliminating these infections as a public health problem and warns that stopping programs risks a rebound. A program report from the agency running the programs, which is a conflict worth naming.

80. 80
    Roose S, Avramenko RW, Pollo SMJ, et al. Characterization of the β-tubulin gene family in Ascaris lumbricoides and Ascaris suum and its implication for the molecular detection of benzimidazole resistance.PLoS Negl Trop Dis · 2021 · 15(9):e0009777doi:10.1371/journal.pntd.0009777 · PMID 34570778

    At least seven beta-tubulin genes, two of them highly expressed throughout the life cycle. Deep amplicon sequencing of more than 200 adult worms from people in Ethiopia and Tanzania and from pigs in Belgium found none of the four resistance-associated changes known from veterinary nematodes (F167Y, E198A, E198L, F200Y). Reassuring, and also a warning that resistance in this genus may not be read from the same codons.

81. 81
    Taylor L, Ahmada AA, Ali MS, Ali SM, Hattendorf J, Mohammed IS, Keiser J. Efficacy and safety of emodepside compared with albendazole in adolescents and adults with hookworm infection in Pemba Island, Tanzania: a double-blind, superiority, phase 2b, randomised controlled trial.Lancet · 2024 · 404(10453):683-691doi:10.1016/S0140-6736(24)01403-X · PMID 39153818

    293 participants. Emodepside 30 mg cured 96.6% of hookworm against 81.2% for albendazole (odds ratio 0.14, 95% CI 0.04-0.35, P=0.0001), but 39% had blurred vision at three hours. The trial is about hookworm, not this worm; it is cited here because emodepside is the leading candidate to follow the benzimidazoles and because the side-effect profile is part of the honest picture.

82. 82
    Ajjampur SSR, Aruldas K, Ásbjörnsdóttir KH, et al. Feasibility of interrupting the transmission of soil-transmitted helminths: the DeWorm3 community cluster-randomised controlled trial in Benin, India, and Malawi.Lancet · 2025 · 406(10502):475-488doi:10.1016/S0140-6736(25)00766-4 · PMID 40752908

    120 clusters and 357,716 people randomized to twice-yearly community-wide albendazole or to school-based deworming for three years. Twenty-four months after the last round, prevalence of the predominant species at all three sites — the hookworm Necator americanus — was lower with community-wide treatment (adjusted prevalence ratios 0.44, 95% CI 0.34-0.58 in Benin; 0.41, 0.32-0.52 in India; 0.40, 0.34-0.46 in Malawi), but transmission interruption was achieved in only 12 of 60 intervention clusters against 6 of 60 control clusters, and the authors conclude it does not appear programmatically feasible in this timeframe. Funded by the Gates Foundation. The outcome species is hookworm, not this worm, which limits what it says about ascariasis directly.

83. 83
    Simmonds O, Maddren R, Collyer B, et al. Predisposition to Ascaris lumbricoides reinfection in the Geshiyaro project in southern Ethiopia.Trans R Soc Trop Med Hyg · 2026 · 120(10):1068-1077doi:10.1093/trstmh/trag075 · PMID 42403345

    Seven years of longitudinal parasitological data. Infection status correlated between successive survey rounds (Kendall's tau 0.10-0.30, P < 0.001) and individuals held their relative infection ranking across the whole period (Kendall's coefficient of concordance 0.43, 95% CI 0.42-0.45, P < 0.001). The clearest human demonstration that predisposition persists through repeated mass treatment; it describes the pattern and does not explain it.

84. 84
    Jin H, Magno Neves MAA, Pinto F, Cho M, Mathur A, Yajima A, Martins JS, Choi MH. Soil-transmitted helminthiasis prevalence and infection intensity among school-going children in Timor-Leste after the prolonged interruption of deworming: a cross-sectional survey (2025).Lancet Reg Health Southeast Asia · 2026 · 54:100870doi:10.1016/j.lansea.2026.100870 · PMID 42824852

    School-based deworming in Timor-Leste ran from 2015 to 2019, was interrupted for nearly four years during the COVID-19 pandemic, and resumed in 2022 and 2024. A survey across all 14 municipalities between 26 February and 1 May 2025, with 1,236 analysable samples from 1,960 children aged 6 to 14, found weighted national prevalence of these worms back at 29.3% (95% CI 24.3-34.2), against 18% in 2020 and 29% at the 2012 baseline, ranging from 2.2% to 91.5% between municipalities, with moderate-to-heavy infections in 15.7% of children. This worm accounted for 95.8% of infections; the indexed abstract strips the italicized species name, but the record is indexed under it. The rebound that the program reports warn about, measured. Funded by the Korea International Cooperation Agency and the United Nations Department of Economic and Social Affairs.

85. 85
    Musimbi ZD, Laubschat A, Oser L, et al. Larval ascariasis elicits a prominent IgA and IgG1/2 antibody response to adult Ascaris excretory/secretory antigens in pigs.Front Immunol · 2025 · 16:1606128doi:10.3389/fimmu.2025.1606128 · PMID 40808955

    Pigs sampled at 14 and 35 days after infection. Excretory-secretory products detected parasite-specific antibody not only in the adult phase but during the larval phase, supporting detection of infection before eggs appear. Pig work, aimed at a human diagnostic problem.

86. 86
    Wu Y, Versteeg L, Wu MC, Weatherhead JE. Identification of a persistent Ascaris-derived Kalirin epitope associated with chronic T cell activation in the lung.PLoS Negl Trop Dis · 2026 · 20(6):e0014434doi:10.1371/journal.pntd.0014434 · PMID 42263117

    Immunopeptidomics identifying a single worm-derived peptide retained and presented by lung macrophages long after the parasite has gone, associated with persisting helper T cell populations. A proposed molecular explanation for the chronic mouse lung disease above. Mouse work; no human data.

87. 87
    Nejsum P, Thamsborg SM, Petersen HH, Kringel H, Fredholm M, Roepstorff A. Population dynamics of Ascaris suum in trickle-infected pigs.J Parasitol · 2009 · 95(5):1048-53doi:10.1645/GE-1987.1 · PMID 19673589

    Pigs given 25 eggs per kg every day and killed at 4, 8 and 14 weeks. Despite continuous reinfection, liver white spots and migrating lung larvae fell sharply over time, and the adult population appeared to consist of worms acquired early. The experimental demonstration that the host learns to block new arrivals while tolerating established worms.

88. 88
    Ni B, Zou Y, Tao L, Wang W. Burden of Soil-Transmitted Helminth Infections in China: Historical Trends (1990-2021) and Future Projections (2035).Pathogens · 2025 · 14(11)doi:10.3390/pathogens14111114 · PMID 41305352

    Global Burden of Disease 2021 data for one country. Prevalence of these worms in China fell 85.08% and disability-adjusted life years 98.01% between 1990 and 2021, with an estimated annual percentage change in age-standardized prevalence of -6.62% (95% CI -7.40 to -5.83). Burden peaked in the 5-9 year age group, and the balance between species shifted, with whipworm projected to rebound by 2035. One country, modeled estimates, and a projection rather than an observation.

89. 89
    Kusumasari RA, Adi H, Satoto TBT, Wahab A, Murhandarwati EEH. Malnutrition among children under 7 years of age linked to ascariasis: evidence from West Sumba, Indonesia, despite ongoing deworming program.BMC Public Health · 2025 · 25(1):3920doi:10.1186/s12889-025-25013-z · PMID 41225447

    443 children sampled from integrated health posts; 32.5% carried a soil-transmitted worm, this one accounting for 27.8% of infections. Stunting was associated with infection by this worm at an odds ratio of 3.45 (95% CI 1.70-7.02), an association the abstract locates in the Kota Waikabubak sub-district, the district capital, rather than across all 443 children. A cross-sectional association in one district, with a deworming program already running; it cannot tell which came first.

90. 90
    Sakakibara A, Baba K, Niwa S, et al. Visceral larva migrans due to Ascaris suum which presented with eosinophilic pneumonia and multiple intra-hepatic lesions with severe eosinophil infiltration — outbreak in a Japanese area other than Kyushu.Intern Med · 2002 · 41(7):574-9doi:10.2169/internalmedicine.41.574 · PMID 12132528

    A 32-year-old man with severe cough, marked blood eosinophilia, ground-glass opacities in both lungs and multiple low-attenuation liver lesions; liver biopsy showed heavy eosinophil infiltration around the portal veins and serology was positive for the pig roundworm. One case, diagnosed serologically rather than by finding a worm.

91. 91
    Izumikawa K, Kohno Y, Izumikawa K, Hara K, Hayashi H, Maruyama H, Kohno S. Eosinophilic pneumonia due to visceral larva migrans possibly caused by Ascaris suum: a case report and review of recent literatures.Jpn J Infect Dis · 2011 · 64(5):428-32PMID 21937827

    A 62-year-old man in middle Kyushu who ate raw pig liver, with migrating lung shadows and massive eosinophil infiltration on lung biopsy, treated with albendazole 600 mg a day for 28 days. The clearest published link in this page's sources between eating raw pig liver and the syndrome. One case, and the attribution rests on serology.

92. 92
    Schneider R, Obwaller A, Auer H. Immunoblot for the detection of Ascaris suum-specific antibodies in patients with visceral larva migrans (VLM) syndrome.Parasitol Res · 2015 · 114(1):305-10doi:10.1007/s00436-014-4196-y · PMID 25367210

    34 sera from patients with high eosinophil counts who were negative for Toxocara but positive on a new pig-roundworm immunoblot, against 30 healthy and 53 other-helminth controls, giving a calculated specificity of 95%. It also records that screening studies in the Netherlands and Sweden found remarkably high seroprevalence. A test-development paper; the true frequency of the syndrome remains unknown.

93. 93
    Belay SA, Tadele YG, Mihretie JE, Mulatu NG, Wakjira YN, Wassie MT. Small bowel volvulus secondary to ascariasis in a 7-year-old boy: a case report.Int J Surg Case Rep · 2026 · 138(2):204-207doi:10.1097/RC9.0000000000000055 · PMID 41815473

    A 7-year-old in rural Ethiopia with a 270-degree ileal volvulus around a worm bolus and 20 cm of dead bowel, resected with primary anastomosis. The most severe end of the obstruction spectrum, in one child.

94. 94
    Duruewuru UP, Chukwurah SN, Nnemelu OP, Nduaguba TS, Nwafor EN, Ogbonna KE, Ilika CV. Gastrointestinal Ascariasis: Unusual Presentation in 2 Cases.Niger Med J · 2026 · 66(6):2398-2407PMID 42540124

    Two adults: a 73-year-old being treated for upper gastrointestinal bleeding induced by a non-steroidal anti-inflammatory drug, in whom worms were found incidentally in the duodenum at endoscopy, and a 63-year-old with decompensated cirrhosis who vomited and passed large numbers of worms in the hospital. Both responded to anthelmintic treatment. Two cases; useful as a reminder that this is not only a childhood disease.

95. 95
    Whitehead B, Thamsborg SM, Denwood MJ, Nejsum P. Assessing the impact of Ascariasis and Trichuriasis on weight gain using a porcine model.PLoS Negl Trop Dis · 2022 · 16(8):e0010709doi:10.1371/journal.pntd.0010709 · PMID 35984809

    195 pigs trickle-infected and weighed over 14 weeks. A 1 kg increase in weight gain was associated with a 4.4% lower whipworm egg count (P=0.00217) and a 2.8% lower roundworm egg count (P=0.02297) or 2.2% lower worm burden (P=0.0488), but the roundworm association did not survive multivariable adjustment. The authors' own conclusion is that the pig whipworm may matter more for growth than the pig roundworm. A post-hoc analysis in an animal model.

96. 96
    Khuroo MS, Rather AA, Khuroo NS, Khuroo MS. Hepatobiliary and pancreatic ascariasis.World J Gastroenterol · 2016 · 22(33):7507-17doi:10.3748/wjg.v22.i33.7507 · PMID 27672273

    Review by the group that described the entity. In Kashmir it gives the worm as the cause of 36.7% of all biliary disease, 23% of acute pancreatitis, 14.5% of liver abscesses and 12.5% of biliary stone disease, and sets out when to intervene endoscopically. Regional figures from one endemic area; they do not transfer to other settings.

97. 97
    Khuroo MS, Zargar SA, Yattoo GN, Javid G, Dar MY, Boda MI, Khan BA. Worm extraction and biliary drainage in hepatobiliary and pancreatic ascariasis.Gastrointest Endosc · 1993 · 39(5):680-5doi:10.1016/s0016-5107(93)70222-9 · PMID 8224692

    50 of 156 patients (32%) needed endoscopic intervention. Worms were removed from the ampullary orifice in all 18 attempts and from the bile or pancreatic duct in 34 of 38 (89.5%); 41 of 45 (91%) had rapid relief. Three endoscopic complications. A single-center prospective series with no comparison group.

98. 98
    Acevedo N, Erler A, Briza P, Puccio F, Ferreira F, Caraballo L. Allergenicity of Ascaris lumbricoides tropomyosin and IgE sensitization among asthmatic patients in a tropical environment.Int Arch Allergy Immunol · 2011 · 154(3):195-206doi:10.1159/000321106 · PMID 20861641

    Characterization of Asc l 3, a 287-residue tropomyosin that runs at 40 kilodaltons on a gel; the sequence itself computes to about 33 kilodaltons, so the 40 is the apparent size on electrophoresis, as is usual for tropomyosins. Antibody to it could account for roughly half the total immunoglobulin E response to whole worm extract; it produced skin wheals and released histamine from basophils. Among 175 asthmatics and 170 non-asthmatics, sensitization was commoner in asthmatics, but the authors' own logistic regression suggested this was confounded by mite sensitization. The honest negative inside a positive paper.

99. 99
    Santos ABR, Rocha GM, Oliver C, et al. Cross-reactive IgE antibody responses to tropomyosins from Ascaris lumbricoides and cockroach.J Allergy Clin Immunol · 2008 · 121(4):1040-6.e1doi:10.1016/j.jaci.2007.12.1147 · PMID 18275995

    Worm tropomyosin shares 69% to 98% sequence identity with tropomyosins of other invertebrates, and antibody responses to worm and cockroach tropomyosin correlated strongly in 119 children from an endemic area and 112 cockroach-allergic patients. Establishes the cross-reactivity; it does not show that either causes disease.

100. 100
     Acevedo N, Sánchez J, Erler A, et al. IgE cross-reactivity between Ascaris and domestic mite allergens: the role of tropomyosin and the nematode polyprotein ABA-1.Allergy · 2009 · 64(11):1635-43doi:10.1111/j.1398-9995.2009.02084.x · PMID 19624559

     Sera from 24 asthmatic patients. Mite extracts inhibited 83.3% and 79% of immunoglobulin E binding to the worm extract, and mite tropomyosin alone inhibited 85%. The worm protein ABA-1 had no cross-reactive counterpart in mite extracts. Twenty-four patients, in a laboratory inhibition assay, not a clinical outcome.

101. 101
     Arruda LK, Santos ABR. Immunologic responses to common antigens in helminthic infections and allergic disease.Curr Opin Allergy Clin Immunol · 2005 · 5(5):399-402doi:10.1097/01.all.0000182536.55650.d0 · PMID 16131913

     Early review noting that in populations exposed together to mites, cockroach, this worm and shellfish, more than half of individuals carry antibody to tropomyosin, and that the mechanisms behind the proposed protective effect of worms on allergy remain poorly understood.

102. 102
     Caraballo L, Coronado S. Parasite allergens.Mol Immunol · 2018 · 100:113-119doi:10.1016/j.molimm.2018.03.014 · PMID 29588070

     Review that separates immunoglobulin E binding from allergenic activity: most worm antigens bind the antibody without causing symptoms. It names worm tropomyosin Asc l 3 as having strong allergenic activity associated in the tropics with asthma and asthma severity, and flags that cross-reactivity can distort house-dust-mite allergy testing. A careful review; the asthma link it reports remains associational.

103. 103
     Acevedo N, Caraballo L. IgE cross-reactivity between Ascaris lumbricoides and mite allergens: possible influences on allergic sensitization and asthma.Parasite Immunol · 2011 · 33(6):309-21doi:10.1111/j.1365-3024.2011.01288.x · PMID 21388422

     Review of the co-exposure problem in the tropics, where worm infection and year-round high mite exposure overlap. States plainly that whether co-exposure potentiates type-2 responses and alters the natural history of allergy is unknown, and that the clinical impact of cross-reactivity is supported only indirectly.

104. 104
     Arrais M, Maricoto T, Nwaru BI, Cooper PJ, Gama JMR, Brito M, Taborda-Barata L. Helminth infections and allergic diseases: Systematic review and meta-analysis of the global literature.J Allergy Clin Immunol · 2022 · 149(6):2139-2152doi:10.1016/j.jaci.2021.12.777 · PMID 34968529

     80 studies, 99,967 participants. No overall association between worm infection and allergic disease, but this worm specifically was associated with increased bronchial hyperreactivity in children (risk ratio 1.41, 95% CI 1.17-1.70) and with atopy in infected adults (1.37, 1.18-1.61). The authors grade the underlying evidence as low to moderate and note that no study addressed clinical outcomes of allergic disease.

105. 105
     Cooper PJ, Chico ME, Vaca MG, et al. Effect of albendazole treatments on the prevalence of atopy in children living in communities endemic for geohelminth parasites: a cluster-randomised trial.Lancet · 2006 · 367(9522):1598-603doi:10.1016/S0140-6736(06)68697-2 · PMID 16698413

     68 rural Ecuadorian schools, 2,373 children, albendazole every two months for a year against no treatment. Worm prevalence fell sharply (odds ratio 0.13, 95% CI 0.09-0.19) but atopy did not rise (0.97, 0.68-1.39) and neither did wheeze (1.07, 0.54-2.11). The trial that tested, and did not support, the fear that deworming would unleash allergy.

106. 106
     van den Biggelaar AHJ, Rodrigues LC, van Ree R, et al. Long-term treatment of intestinal helminths increases mite skin-test reactivity in Gabonese schoolchildren.J Infect Dis · 2004 · 189(5):892-900doi:10.1086/381767 · PMID 14976607

     317 Gabonese schoolchildren randomized to praziquantel and mebendazole every three months for 30 months, or to placebo. Treatment significantly increased the rate of developing skin sensitivity to house dust mite (hazard ratio 2.51, 95% CI 1.85-3.41), an effect the authors found to be mediated in part by reductions in this worm and in whipworm. Total immunoglobulin E fell, but that did not mediate the effect. A skin-test endpoint, not clinical allergy; it points the opposite way from the Ecuadorian trial [53] and both belong in the summary.

107. 107
     Maruyama H, Nawa Y, Noda S, Mimori T, Choi WY. An outbreak of visceral larva migrans due to Ascaris suum in Kyushu, Japan.Lancet · 1996 · 347(9017):1766-7doi:10.1016/s0140-6736(96)90844-2 · PMID 8656926

     The report that put pig-roundworm larva migrans on the map in Japan. The PubMed record is a letter with no abstract, so it is cited for the existence, place and date of the outbreak only.

108. 108
     Nejsum P, Betson M, Bendall RP, Thamsborg SM, Stothard JR. Assessing the zoonotic potential of Ascaris suum and Trichuris suis: looking to the future from an analysis of the past.J Helminthol · 2012 · 86(2):148-55doi:10.1017/S0022149X12000193 · PMID 22423595

     Review of the zoonotic question for the pig roundworm and pig whipworm, including the risk where pig manure is used on vegetables. A review; it frames open questions rather than answering them.

109. 109
     Hohensee L, Oser L, Laubschat A, Schlosser-Brandenburg J, Ebner F. Current strategies for controlling gastrointestinal nematodes of pigs in Europe.Parasit Vectors · 2026 · 19(1)doi:10.1186/s13071-026-07715-4 · PMID 42870256

     Review of pig gastrointestinal worms across European production systems. Reported farm-level prevalence ranges from 1% to 100% for the pig roundworm, 2% to 27% for the nodular worms and 0.3% to 75% for the pig whipworm, with higher infection levels in outdoor, organic and small-scale systems and wide methodological heterogeneity behind those ranges. Control still rests on anthelmintics, and the authors note reports of reduced efficacy and resistance particularly in the nodular worms. They name the zoonotic potential of the pig roundworm and the pig whipworm as a reason control matters. A narrative review, not new data.

110. 110
     Dunn JC, Papaiakovou M, Han KT, et al. The increased sensitivity of qPCR in comparison to Kato-Katz is required for the accurate assessment of the prevalence of soil-transmitted helminth infection in settings that have received multiple rounds of mass drug administration.Parasit Vectors · 2020 · 13(1):324doi:10.1186/s13071-020-04197-w · PMID 32580759

     648 participants in the Myanmar delta. Any soil-transmitted worm: 20.68% by Kato-Katz against 45.06% by quantitative polymerase chain reaction, with the biggest gap for hookworm. For this worm specifically the relationship between egg counts and DNA copy number was the strongest of the three species. A single field study in a low-intensity setting.

111. 111
     Barda B, Schindler C, Wampfler R, Ame S, Ali SM, Keiser J. Comparison of real-time PCR and the Kato-Katz method for the diagnosis of soil-transmitted helminthiasis and assessment of cure in a randomized controlled trial.BMC Microbiol · 2020 · 20(1):298doi:10.1186/s12866-020-01963-9 · PMID 33008301

     320 trial participants. Against the molecular test, Kato-Katz sensitivity for this worm at follow-up was 53.8%; against Kato-Katz, the molecular test was 87.5% sensitive. The authors' conclusion: a single real-time polymerase chain reaction is as sensitive as quadruplicate Kato-Katz for this worm and for whipworm, and more sensitive only for hookworm. The point that matters for trials: which test you use changes the cure rate you report.

112. 112
     Lotz CN, Mrimi EC, Schneeberger PHH, Ali SM, Hattendorf J, Keiser J. Performance of real-time polymerase chain reaction and Kato-Katz for diagnosing soil-transmitted helminth infections and evaluating treatment efficacy of emodepside in randomized controlled trials.PLoS Negl Trop Dis · 2025 · 19(2):e0012872doi:10.1371/journal.pntd.0012872 · PMID 39965016

     Secondary analysis of the emodepside dose-finding trials on Pemba Island. By Bayesian latent class modeling, for this worm the molecular test was 85.00% sensitive against 47.70% for Kato-Katz, with slightly lower specificity (93.40% against 99.40%). Measured efficacy was lower by molecular testing for every dose of emodepside and for albendazole, and emodepside cured more infections with this worm and with whipworm than albendazole did. The nearest thing to human efficacy data for emodepside against this worm.

113. 113
     Palmeirim MS, Hürlimann E, Beinamaryo P, et al. Efficacy and safety of albendazole alone versus albendazole in combination with ivermectin for the treatment of Trichuris trichiura infections: An open-label, randomized controlled superiority trial in south-western Uganda.PLoS Negl Trop Dis · 2024 · 18(11):e0012687doi:10.1371/journal.pntd.0012687 · PMID 39591454

     A whipworm trial in Ugandan schoolchildren whose secondary result matters here: against co-infecting worms of this species, cure was 100% with albendazole plus ivermectin against 83.9% with albendazole alone. A secondary outcome in a trial powered for a different parasite, so the comparison is suggestive, not definitive.

114. 114
     Jelliffe DB. Oil of Chenopodium in the treatment of ascariasis; (report of three cases of fatal liver damage in African patients).J Trop Med Hyg · 1951 · 54(7):143-6PMID 24541284

     Title only; no abstract or DOI in the record, which is indexed under ascariasis, Chenopodium, liver and liver diseases. Cited for the existence of three fatal cases of liver damage in patients treated with oil of chenopodium for this infection, not for clinical detail.

115. 115
     Montoya-Cabrera MA, Escalante-Galindo P, Meckes-Fisher M, Sánchez-Vaca G, Flores-Alvarez E, Reynoso-García M. [Fatal poisoning caused by oil of epazote, Chenopodium graveolens].Gac Med Mex · 1996 · 132(4):433-7PMID 8964384

     Spanish-language case report with an English abstract. A girl of 2 years 9 months was given 40 mL of oil of chenopodium by a traditional healer and died of coma, seizures and shock; phytochemical analysis found 39 mg of ascaridole per mL, 1,560 mg in the dose given, against a former recommended pediatric dose of 60 mg and a dose of 1,000 mg reported as lethal in people. One case, and the ascaridole content of such preparations varies.

116. 116
     Sakipova Z, Giorno TBS, Bekezhanova T, et al. Pharmacological evaluation of Artemisia cina crude CO2 subcritical extract after the removal of santonin by means of high speed countercurrent chromatography.Molecules · 2020 · 25(12):2728doi:10.3390/molecules25122728 · PMID 32545512

     Cited for its statement of santonin's toxic dose: about 60 mg in children and 200 mg in adults, causing xanthopsia — yellow vision — which can progress to blindness. The experimental work is on a santonin-free plant extract in mice and is not about this worm.

117. 117
     Williams PDE, Borts DJ, Liu D, Byerley-Duke J, VanVeller B, Martin RJ. A novel anaerobic cholinergic signaling compound, β-alanine betaine, and nAChRs in Ascaris.PLoS Negl Trop Dis · 2026 · 20(9):e0014518doi:10.1371/journal.pntd.0014518 · PMID 42709780

     Body-cavity fluid from female pig roundworms was found to contain beta-alanine betaine, a previously unrecognized analog of the nerve transmitter acetylcholine, which on injection produced a characteristic coiling quite unlike the rigid paralysis produced by levamisole. The receptor subfamily it appears to act on has no counterpart in people or livestock, which is what makes it a drug target. Early-stage pharmacology in worms and in the free-living nematode C. elegans.

118. 118
     Rashwan N, Scott M, Prichard R. Rapid Genotyping of β-tubulin Polymorphisms in Trichuris trichiura and Ascaris lumbricoides.PLoS Negl Trop Dis · 2017 · 11(1):e0005205doi:10.1371/journal.pntd.0005205 · PMID 28081124

     Development of simple isothermal genotyping assays for the resistance codons, tested on field samples from Haiti and Panama and shown to tolerate fecal inhibitors. A tool paper; the authors state it needs validation on large field sample sets before and after treatment.

119. 119
     Fischer HR, Krücken J, Fiedler S, et al. Faecal egg count reduction test, deep amplicon sequencing of isotype-1 β-tubulin gene and in ovo larval development assay reveal susceptibility to benzimidazoles of porcine nematodes Oesophagostomum spp. and Ascaris suum in outdoor-reared pigs in Germany.Int J Parasitol Drugs Drug Resist · 2025 · 29:100612doi:10.1016/j.ijpddr.2025.100612 · PMID 40902421

     13 German farms. Fenbendazole at 5 mg/kg gave fecal egg count reductions of 99.8% to 100% for the nodular worms (Oesophagostomum), and deep amplicon sequencing found no resistance-associated polymorphisms in those worms at codons 134, 167, 198 or 200; for the pig roundworm the egg-count reduction results were ambiguous. A new in-egg larval development assay gave half-maximal effect concentrations of 1.50 to 3.36 micromolar thiabendazole (mean 2.24) and a proposed resistance cut-off of 3.90 micromolar; on that assay all pig roundworm populations tested were susceptible. It also documents why egg-count reduction testing is unreliable in pigs, which eat each other's feces and so shed eggs they did not produce.

120. 120
     Khan AU, Hussain S, Khan M, et al. Effectiveness of Anthelmintic Therapy and Determinants of Ascaris lumbricoides Infection among School-Aged Children: A Community-Based Cross-Sectional Study in Rural Khyber Pakhtunkhwa, Pakistan.Acta Parasitol · 2025 · 70(4):172doi:10.1007/s11686-025-01109-9 · PMID 40779205

     1,675 children randomly allocated to pyrantel pamoate, mebendazole or albendazole, with worms counted in stool one to two days later; overall prevalence 15.1%. Relative to albendazole, worms were far more often recovered after pyrantel pamoate (odds ratio 6.76, 95% CI 4.49-10.18) and more often after mebendazole (1.50); in the multivariable model the two non-albendazole drugs were alike, with adjusted odds ratios of 7.37 for pyrantel pamoate and 7.73 for mebendazole. The same 1,675-child cohort supplied the worms for the group's multilocus genetic study [16]. Read the direction with care: the outcome is worms found after treatment, and the study is described as cross-sectional and interventional at once, which makes it weaker evidence on drug ranking than its size suggests.

121. 121
     Liu F, Streett H, Solano-Aguilar G, Smith AD, Carbaugh D, Urban JF, Li RW. Ascaris-porcine multi-omics integration identifies microbiome-driven histamine elevation and lasting gut perturbations following Ascaris infection and fenbendazole treatment.Virulence · 2026 · 17(1):2728766doi:10.1080/21505594.2026.2728766 · PMID 42725788

     Infection shifted the pig gut bacterial community and dysregulated 182 blood and stool metabolites. What persisted was the difference in gut microbial composition: fenbendazole-treated pigs still differed from time-matched uninfected controls 13 days after worm clearance was confirmed. The indexed title begins in lower case because PubMed strips the italicized genus name from the start of it. In anaerobic culture, bacteria exposed to fenbendazole plus worm proteins produced about 79% more histamine at 48 hours. The authors state their own limitations: no drug-only control group and a cross-sectional design, so the treatment effects are interpreted cautiously.

122. 122
     Skallerup P, Nejsum P, Jørgensen CB, Göring HHH, Karlskov-Mortensen P, Archibald AL, Fredholm M, Thamsborg SM. Detection of a quantitative trait locus associated with resistance to Ascaris suum infection in pigs.Int J Parasitol · 2012 · 42(4):383-91doi:10.1016/j.ijpara.2012.02.010 · PMID 22619754

     Genome scan of 195 experimentally infected pigs. A candidate region on chromosome 4 covering 2.5 megabases, with two single-nucleotide polymorphisms validated in separate animals, against a background heritability for infection level of 0.45. No marker reached genome-wide significance in the original scan, which the authors state plainly.

123. 123
     DiRosato CK, Malkin EM, Lee SM, et al. Na-GST-1 adsorbed on Alhydrogel co-administered with different Toll-like receptor agonists in hookworm-naive adults using a controlled human infection model in the USA: a phase 2, double-blind, randomised controlled trial.Lancet Infect Dis · 2026 · 26(7):692-704doi:10.1016/S1473-3099(26)00018-6 · PMID 41861834

     A hookworm vaccine trial, not an Ascaris study. It is cited here only to establish that controlled human infection models exist for a related soil-transmitted worm — 39 volunteers randomized to one of three vaccine formulations or to placebo, 10 of them to placebo, and 33 then deliberately challenged with 50 infective larvae. Older human infection experiments with this worm and the pig worm do exist, but their records carry no abstracts [103][105].