Bacteria pyruvate metabolism modulates AFB1 toxicity in Caenorhabditis elegans.

Aflatoxin B1 (AFB1), the most potent mycotoxin and Group 1 human carcinogen, continues to pose a significant public health burden, particularly in developing countries. Increasing evidence has shown the gut microbiota as a key mediator of AFB1 toxicity through multiple interactive host-microbiota activities. In our previous study we observed that disturbances in bacterial pyruvate metabolism might have a significant impact on AFB1 in the host. To further investigate the impact of the pyruvate pathway on AFB1 toxicity in C. elegans, we engineered two bacterial strains (triple-overexpressed and triple-knockout strains with aceB, lpd, and pflB). Additionally, we employed two mutant worm strains (pyk-1 and pdha-1 mutants) known to affect pyruvate metabolism. Our results revealed that the co-metabolism of pyruvate by the host and bacterial strains synergistically influences AFB1 toxicity. Remarkable, we found that bacterial pyruvate metabolism, rather than that of the host, plays a pivotal role in modulating AFB1 toxicity in C. elegans. Our study sheds light on the role of gut microbiota involved in pyruvate metabolism in influencing AFB1 toxicity in C. elegans.

Host-microbiota affects the toxicity of Aflatoxin B1 in Caenorhabditis elegans.

Aflatoxins are a group of potent fungal metabolites produced by Aspergillus and commonly contaminate groundnuts and cereal grains. Aflatoxin B1 (AFB1), the most potent mycotoxin, has been classified as Group 1 human carcinogen because it can be metabolically activated by the cytochrome P450 (CYP450) in the liver to form AFB1-DNA adducts and induce gene mutations. Increasing evidence has shown the gut microbiota as a key mediator of AFB1 toxicity through multiple interactive host-microbiota activities. To identify specific bacterial activity that modulates AFB1 toxicity in Caenorhabditis (C.) elegans, we established a 3-way (microbe-worm-chemical) high-throughput screening system using C. elegans fed E. coli Keio collection on an integrated robotic platform, COPAS Biosort. We performed 2-step screenings using 3985 Keio mutants and identified 73 E. coli mutants that modulated C. elegans growth phenotype. Four genes (aceA, aceB, lpd, and pflB) involved in the pyruvate pathway were identified from the screening and confirmed to increase the sensitivity of all animals to AFB1. Taking together, our results indicated that disturbances in bacterial pyruvate metabolism might have a significant impact on AFB1 toxicity in the host.

Detoxification mechanisms of nickel sulfate in nematode Caenorhabditis elegans.

Nickel is the most prevailing metal allergen with the highest sensitization rate among the "TOP 25" contact allergens and can affect about 15% of the human population. It is an essential trace metal in plants, animals, and humans. However, the environmental levels of nickel are considerably higher than what is needed for human life. Exposure to high levels of nickel can lead to skin allergies, lung fibrosis, and carcinogenesis. Few existing studies have closely examined the toxicity of nickel, let alone investigated the effective detoxification pathways. Here, we developed a high-throughput screening platform to comprehensively evaluate the nickel toxicity in wild-type C. elegans and explore the underlying detoxification mechanisms in transgenic nematodes. We demonstrated that nickel exerted multiple toxic effects on growth, brood size, feeding, and locomotion in C. elegans. Of which, brood size is the most sensitive endpoint. Nickel was found to first bind to phytochelatin (PC) after entering the worms' body and this PC-Ni complex was further transported by the ABC transporter, CeHMT-1, into the coelomocytes for further detoxification. Our study also demonstrated that the high-throughput screening platform is a promising system for evaluation and investigation of the ecological risks of heavy metals.

High-throughput assessment of toxic effects of metal mixtures of cadmium(Cd), lead(Pb), and manganese(Mn) in nematode Caenorhabditis elegans.

Heavy metals, a class of persistent environmental toxicants, are harmful to human health. Cd and Pb are two of the most common toxic heavy metals that have been linked with cancers and malfunction of the nervous system. Notably, contamination of Mn usually coexisted with Cd and Pb in environmental and occupational settings. Studies regularly examined the toxic effects on individual metals; however, potential health and toxic effects of mixtures containing two or more heavy metals are unknown. Here, we investigated toxic effects of Cd, Pb, Mn, and their binary and ternary mixtures in the nematode Caenorhabdities elegans. The toxic outcomes, including effects on growth, reproduction, and feeding, were measured via high-throughput platform analysis. The transgenic strain BY250 with GFP in dopaminergic neurons was used to explore the neurodegenerative effects induced by single metals or their mixtures. The combination index(CI) for mixtures effect was calculated using isobolograms methods. Following the exposure, we found significant toxic effects in C. elegans. For single metals, the toxicity order for growth, reproduction, and feeding were Pb > Cd > Mn. For mixtures, the mixture of Cd + Mn induced a less than addictive effect in C. elegans, whereas the mixtures of Cd + Pb, Pb + Mn, and Cd + Pb + Mn induced greater-than-additive effects. Both single metals and their mixtures induced abnormality in dopaminergic neurons. These results showed combinative toxic and neurodegenerative effects of heavy metal mixtures, and future studies will focus on characterization of concentration-response patterns and identification of potential molecular mechanisms in C. elegans model.

Toxicogenomic responses to zearalenone in Caenorhabditis elegans reveal possible molecular mechanisms of reproductive toxicity.

In this study, the possible molecular mechanisms of zearalenone (ZEA)-induced reproductive and developmental toxic effects in Caenorhabditis elegans (C. elegans) were investigated. Differential gene expression profiles were identified, and 171, 245, and 3149 genes were down- or up-regulated (>2.0 fold) in 10, 20, and 40 µg/ml ZEA treated groups, respectively, as compared to untreated controls. Pathway specific mapping showed that the major differentially expressed genes were collagen synthetic pathways regulating genes, col-121 and dpy-17. Real-time PCR reconfirmation of key genes, related to cuticle collagen synthetic pathway, found dramatic changes in the expression of the genes dpy-31, sqt-3, col-121, and dpy-17 following exposure to ZEA (40 µg/ml), which indicated the significance of these genes in ZEA-induced toxicity. Cuticle collagen plays many key roles in the development and reproduction of C. elegans. The hypersensitive responses in transgenic and mutant worms also confirmed the roles of these genes in lethality and reproductive response to ZEA exposure, which indicates that ZEA blocked the normal collagen processing and cuticle formation. Taken together, our results demonstrate that disruption of the collagen biosynthetic pathway might be a key mechanism in ZEA-induced reproductive and developmental toxic effects in C. elegans.

Trans-/multi-generational effects of deoxynivalenol on Caenorhabditis elegans.

Deoxynivalenol (DON, vomitoxin) is one of the most widely distributed trichothecene mycotoxins commonly found in cereal food and feeds. Significant acute and potential chronic toxic effects of DON have been observed in animals and human populations. However, potential adverse effects associated with DON exposure across multiple generations have not been extensively investigated. In this study, Caenorhabditis elegans (C. elegans) were used to evaluate the trans-/multi-generational toxicities of DON via 3 physiological endpoints: growth, brood size, and feeding ability. DON concentration at higher than 100 µg/mL significantly inhibited growth, decreased brood size, and reduced food intake in a concentration-dependent manner. Gradual decline in DON-induced impairments was observed in the filial generations when only the parental generation was exposed. However, greater damages in filial generations were found as compared to the parental generation (p < 0.01) with all generations continuously exposed to DON. Overall, the endpoints of brood size and food intake were more sensitive for both trans- and multi-generational toxic effects of DON. Additionally, the interactions between concentrations and generations significantly influence the response of C. elegans to DON exposure, based on a mixed-effect model with multi-level analysis. Taken together, our results demonstrated that DON exposure produced significant trans-/multi-generational toxic effects on C. elegans, which may serve as a model organism to explore molecular mechanisms of long-term adverse health effects of DON.

Aflatoxin B1-Induced Developmental and DNA Damage in Caenorhabditis elegans.

Aflatoxin B1 (AFB1) is a ubiquitous mycotoxin produced by toxicogenic Aspergillus species. AFB1 has been reported to cause serious adverse health effects, such as cancers and abnormal development and reproduction, in animals and humans. AFB1 is also a potent genotoxic mutagen that causes DNA damage in vitro and in vivo. However, the link between DNA damage and abnormal development and reproduction is unclear. To address this issue, we examined the DNA damage, germline apoptosis, growth, and reproductive toxicity following exposure to AFB1, using Caenorhabditis elegans as a study model. Results found that AFB1 induced DNA damage and germline apoptosis, and significantly inhibited growth and reproduction of the nematodes in a concentration-dependent manner. Exposure to AFB1 inhibited growth or reproduction more potently in the DNA repair-deficient xpa-1 nematodes than the wild-type N2 strain. According to the relative expression level of pathway-related genes measured by real-time PCR, the DNA damage response (DDR) pathway was found to be associated with AFB1-induced germline apoptosis, which further played an essential role in the dysfunction of growth and reproduction in C. elegans.

Differential Toxicities of Nickel Salts to the Nematode Caenorhabditis elegans.

This study focused on assessing whether nickel (Ni) toxicity to the nematode Caenorhabditis elegans was affected by the molecular structure of the Ni salt used. Nematodes were exposed to seven Ni salts [Ni sulfate hexahydrate (NiSO4·6H2O), Ni chloride hexahydrate (NiCl2·6H2O), Ni acetate tetrahydrate (Ni(OCOCH3)2·4H2O), Ni nitrate hexahydrate (N2NiO6·6H2O), anhydrous Ni iodide (NiI2), Ni sulfamate hydrate (Ni(SO3NH2)2·H2O), and Ni fluoride tetrahydrate (NiF2·4H2O)] in an aquatic medium for 24 h, and lethality curves were generated and analyzed. Ni fluoride, Ni iodide, and Ni chloride were most toxic to C. elegans, followed by Ni nitrate, Ni sulfamate, Ni acetate, and Ni sulfate. The LC50 values of the halogen-containing salts were statistically different from the corresponding value of the least toxic salt, Ni sulfate. This finding is consistent with the expected high bioavailability of free Ni ions in halide solutions. We recommend that the halide salts be used in future Ni testing involving aquatic invertebrates.

Toxicity testing of neurotoxic pesticides in Caenorhabditis elegans.

The use of pesticides is ubiquitous worldwide, and these chemicals exert adverse effects on both target and nontarget species. Understanding the modes of action of pesticides, as well as quantifying exposure concentration and duration, is an important goal of clinicians and environmental health scientists. Some chemical exposures result in adverse effects on the nervous system. The nematode Caenorhabditis elegans (C. elegans) is a model lab organism well established for studying neurotoxicity, since the components of its nervous system are mapped and known, and most of its neurotransmitters correspond to human homologs. This review encompasses published studies in which C. elegans nematodes were exposed to pesticides with known neurotoxic actions. Endpoints measured include changes in locomotion, feeding behavior, brood size, growth, life span, and cell death. From data presented, evidence indicates that C. elegans can serve a role in assessing the effects of neurotoxic pesticides at the sublethal cellular level, thereby advancing our understanding of the mechanisms underlying toxicity induced by these chemicals. A proposed toxicity testing scheme for water-soluble chemicals is also included.

Ecotoxicity of manufactured ZnO nanoparticles--a review.

This report presents an exhaustive literature review on the toxicity of manufactured ZnO nanoparticles (NPs) to ecological receptors across different taxa: bacteria, algae and plants, aquatic and terrestrial invertebrates and vertebrates. Ecotoxicity studies on ZnO NPs are most abundant in bacteria, and are relatively lacking in other species. These studies suggest relative high acute toxicity of ZnO NPs (in the low mg/l levels) to environmental species, although this toxicity is highly dependent on test species, physico-chemical properties of the material, and test methods. Particle dissolution to ionic zinc and particle-induced generation of reactive oxygen species (ROS) represent the primary modes of action for ZnO NP toxicity across all species tested, and photo-induced toxicity associated with its photocatalytic property may be another important mechanism of toxicity under environmentally relevant UV radiation. Finally, current knowledge gaps within this area are briefly discussed and recommendations for future research are made.

Toxicity of manufactured zinc oxide nanoparticles in the nematode Caenorhabditis elegans.

Information describing the possible impacts of manufactured nanoparticles on human health and ecological receptors is limited. The objective of the present study was to evaluate the potential toxicological effects of manufactured zinc oxide nanoparticles (ZnO-NPs; 1.5 nm) compared to aqueous zinc chloride (ZnCl2) in the free-living nematode Caenorhabditis elegans. Toxicity of both types of Zn was investigated using the ecologically relevant endpoints of lethality, behavior, reproduction, and transgene expression in a mtl-2::GFP (gene encoding green fluorescence protein fused onto the metallothionein-2 gene promoter) transgenic strain of C. elegans. Zinc oxide nanoparticles showed no significant difference from ZnCl2 regarding either lethality or reproduction in C. elegans, as indicated by their median lethal concentrations (LC50s; p = 0.29, n=3) and median effective concentrations (EC50s; Z = 0.835, p = 0.797). Also, no significant difference was found in EC50s for behavioral change between ZnO-NPs (635 mg Zn/L; 95% confidence interval [CI], 477-844 mg Zn/L) and ZnCl2 (546 mg Zn/L; 95% CI, 447-666 mg Zn/L) (Z = 0.907, p = 0.834). Zinc oxide nanoparticles induced transgene expression in the mtl-2::GFP transgenic C. elegans in a manner similar to that of ZnCl2, suggesting that intracellular biotransformation of the nanoparticles might have occurred or the nanoparticles have dissolved to Zn2+ to enact toxicity. These findings demonstrate that manufactured ZnO-NPs have toxicity to the nematode C. elegans similar to that of aqueous ZnCl2.

A transgenic strain of the nematode Caenorhabditis elegans as a biomonitor for heavy metal contamination.

Metallothionein (MT), a protein involved in metal regulation and detoxification, has been used widely as a biomarker of metal exposure. In the present study, a transgenic strain of the free-living soil nematode Caenorhabditis elegans was developed using the C. elegans MT-2 (mtl-2) promoter to control the transcription of green fluorescence protein (GFP) reporter. Response of this transgenic system to Cd, Hg, Cu, Zn, Ni, Pb, and As exposure in aquatic media was tested by quantifying GFP expression after 24 h of exposure. Response in Cd-spiked soil was tested in a similar manner. The mtl-2 transcription also was measured using real-time reverse transcription-polymerase chain reaction to gain a mechanistic understanding of the transgene expression. Green fluorescence protein is induced by Cd, Hg, Cu, and Zn in a time- and concentration-dependent manner; mtl-2 transcription is consistent with the GFP response. The minimum concentrations of Cd, Hg, Cu, and Zn that induce GFP response are 2- to 1000-fold lower than concentrations affecting traditional endpoints, such as lethality or behavioral change. The system responds to Cd in soil in a similar manner. Neither Ni nor Pb induces GFP, and neither induces mtl-2 transcription. Arsenic does not induce GFP, yet an increase in mtl-2 transcription was found, suggesting that As may interfere with GFP signaling. This mtl-2::GFP transgenic bioassay represents an alternative approach to quantify, both easily and quickly, a surrogate of MT in response to metal exposure (e.g., Cd, Hg, Cu, and Zn) in a variety of environments and potentially may be used for quantitative or semiquantitativebiomonitoring of metal contamination in soils and aquatic systems.

Caenorhabditis elegans: an emerging model in biomedical and environmental toxicology.

The nematode Caenorhabditis elegans has emerged as an important animal model in various fields including neurobiology, developmental biology, and genetics. Characteristics of this animal model that have contributed to its success include its genetic manipulability, invariant and fully described developmental program, well-characterized genome, ease of maintenance, short and prolific life cycle, and small body size. These same features have led to an increasing use of C. elegans in toxicology, both for mechanistic studies and high-throughput screening approaches. We describe some of the research that has been carried out in the areas of neurotoxicology, genetic toxicology, and environmental toxicology, as well as high-throughput experiments with C. elegans including genome-wide screening for molecular targets of toxicity and rapid toxicity assessment for new chemicals. We argue for an increased role for C. elegans in complementing other model systems in toxicological research.

A comparative study on the relationship between various toxicological endpoints in Caenorhabditis elegans exposed to organophosphorus insecticides.

The toxicity of 10 organophophorus (OP) insecticides-acephate, dimethoate, dichlorvos, dicrotophos, monocrotophos, methamidophos, phosphamidon, omethoate, phosdrin, and trichlorfon-was evaluated in Caenorhabditis elegans using lethality, movement, and acetylcholinesterase (AChE) activity as the endpoints after a 4-hr- exposure period. The OP insecticides tested showed LC50 values ranging from 0.039 mM (for dichlorovs) to 472.8 mM (for methamidophos). The order of toxicity for lethality and movement was not significantly different when tested using the rank order correlation coefficient. AChE activity was markedly affected by all the OP insecticide exposures that caused significant inhibition in movement, indicating that the mechanism of toxicity of OP insecticides in C. elegans is the same as in higher animals. All OP insecticides induced greater than 50% inhibition of AChE at the lowest tested OP insecticide concentration resulting in inhibition in movement. While a significant correlation was evident between LC50 values in C. elegans and the LD50 values in rats for the 10 OP insecticides studied, a correlation was not evident between EC50 values in C. elegans and LD50 values in rats. Overall, the two endpoints, LC50 and movement, were more reliable and easier to perform than measurement of AChE activity in C. elegans for determining the toxicity of OP insecticides. Further, ranking of these endpoints with respect to the OP insecticides studied indicates that these parameters in C. elegans are predictive of OP insecticides mammalian neurotoxicity.

Reversible AChE inhibitors in C. elegans vs. rats, mice.

We are investigating whether Caenorhabditis elegans could be used as a screen for vertebrates by comparing the responses of components of its cholinergic system to well-characterized toxicants. We assessed whether C. elegans displays similar toxicity as rats and mice to reversible acetylcholinesterase (AChE) inhibitors, and sought to corroborate that the toxicity mechanism is the same. To determine relative potencies, movement-concentration curves were generated, 50th percentiles for movement were located, ranked and compared statistically to rat and mouse oral acute LD50s. The ranking was significantly correlated to rat and mouse rankings (alpha=0.05). We measured a concentration-dependent decrease in AChE activity correlating to a decrease in movement for each carbamate, suggesting that the mechanism of toxicity is the same. Finally, as seen in mammals, inhibition of AChE activity occurred before a movement decrease. The response of C. elegans to carbamate exposure shows significant correlation to rat and mouse data.

Measuring Movement to Determine Physiological Roles of Acetylcholinesterase Classes in Caenorhabditis elegans.

A difference in movement has been hypothesized to exist between Caenorhabditis elegans strains lacking one of two main genes for acetylcholinesterase (AChE), ace-1(+) and ace-2(+). We explored the precision of movement as an endpoint by measuring and comparing the movements of these strains (VC505 and GG202, respectively) and of N2 (wild-type). The order of movement of the strains is: N2 > VC505 > GG202; therefore, loss of the ace-2(+) gene is more detrimental to movement. We then compared the sensitivities of the three strains to an AChE inhibitor (propoxur) by generating movement-concentration curves, identifying effective concentrations that decreased movement by 50% (EC(50)), and comparing them. EC(50) show an order of: N2 approximately GG202 < VC505. Therefore, the enzymes encoded by ace-1(+) were more susceptible to propoxur than those of ace-2(+), suggesting that the innate difference in the AChE classes' contributions to movement will not always determine the strain sensitivity. Measuring movement was sufficiently precise to record differences following genetic manipulation and further chemical exposure.

Shedding of foodborne pathogens by Caenorhabditis elegans in compost-amended and unamended soil.

A study was done to characterize the shedding of foodborne pathogenic bacteria by Caenorhabditis elegans, evaluate the persistence of worm populations cocultured with foodborne pathogens, and determine if C. elegans disperses ingested pathogens in soil as a result of shedding. Escherichia. coli O157:H7, Salmonella enterica serotype Poona, and Listeria monocytogenes, as well as E. coli OP50, a non-pathogenic strain, were studied. Synchronous populations of C. elegans were fed for 24 h on confluent lawns of nalidixic acid-adapted bacteria. C. elegans shed viable cells of ingested bacteria on tryptic soy agar supplemented with nalidixic acid (50 microg ml(-1)) (TSAN) throughout a 5-h post-feeding period. C. elegans persisted for up to 10 days by feeding on bacteria that had been shed and grew on TSAN. Eggs harvested from C. elegans cultured on shed foodborne pathogens had the same level of viability as those collected from C. elegans grown on shed E. coli OP50. After 6-7 days, 78%, 64%, 64%, and 76% of eggs laid by C. elegans that had fed on E. coli O157:H7, S. Poona, L. monocytogenes, and E. coli OP50, respectively, were viable. Worms fed on E. coli O157:H7 were inoculated into soil and soil amended with turkey manure compost. Populations of C. elegans persisted in compost-amended soil for at least 7 days but declined in unamended soil. E. coli O157:H7 was detected at 4 and 6 days post inoculation in compost-amended and unamended soil, and in unamended soil inoculated with E. coli OP50. Populations of E. coli O157:H7 in soil amended with turkey manure compost were significantly(alpha = 0.05) higher than those in unamended soil. Results indicate that C. elegans can act as a vector to disperse foodborne pathogens in soil, potentially resulting in increased risk of contaminating the surface of pre-harvest fruits and vegetables.

Migration of Caenorhabditis elegans to manure and manure compost and potential for transport of Salmonella newport to fruits and vegetables.

A study was done to determine if a free-living, bacterivorous nematode, Caenorhabditis elegans, migrates to bovine manure, turkey manure, composted bovine manure, composted turkey manure, and manure-amended soil inoculated with Salmonella Newport. Movement of the worm to lettuce, strawberries, and carrots was also studied. C. elegans moved most rapidly to turkey manure and strawberries, with 35% and 60% of worms, respectively, associating with samples within 30 min. Survival and reproduction of C. elegans in test materials were not affected by the presence of S. newport. Bovine manure and bovine manure compost inoculated with S. newport (8.6 log10 CFU/g) were separately placed in the bottom of a glass jar and covered with a layer of soil (5 cm) inoculated (50 worms/g) or not inoculated with C. elegans. A piece of lettuce, strawberry, or carrot was placed on top of the soil before jars were sealed and held at 20 degrees C for up to 10 days. In the system using soil inoculated with C. elegans, S. newport initially in bovine manure was detected on the surface of lettuce, strawberry, and carrot samples within 3, 1, and 1 days, respectively. The pathogen was detected on lettuce, strawberry, and carrot within 1, 7, and 1 days, respectively, when initially present in bovine manure compost. With one exception, the pathogen was not detected on the produce over the 10-day incubation period when C. elegans was not present in the soil. Results indicate that C. elegans has the potential for transporting S. newport in soil to the surface of preharvest fruits and vegetables in contact with soil.

Using transgenic Caenorhabditis elegans in soil toxicity testing.

Soil bioassays are important tools for evaluating toxicological effects within the terrestrial environment. The American Society for Testing and Materials E2172-01 Standard Guide outlines a method for conducting laboratory soil toxicity tests using the nematode Caenorhabditis elegans. This method is an efficient tool for extracting C. elegans from soil samples and can be carried out after a 24-h exposure period using relatively small amounts of soil. Drawbacks of this method include problems with (1) recovery of nematodes from soils containing a high percentage of organic matter, and (2) distinguishing indigenous nematode species from nematodes added for the laboratory test. Due in part to these issues, C. elegans has not been extensively accepted for use in soil testing. To address these concerns and improve upon the American Society for Testing and Materials method, this project focused on using transgenic strains of C. elegans carrying a GFP-expressing element. Lethality and behavior tests revealed that the transgenic nematodes respond similarly to the wild-type N2 strain, indicating that they can be used in the same manner in soil testing. The GFP marker is easily identifiable not only within soils containing a large amount of organic matter, but also in field-collected soils containing indigenous nematodes. These results support the use of transgenic GFP C. elegans in soil bioassays as a tool to further the reliability of laboratory toxicity tests.

Potential role of Diploscapter sp. strain LKC25, a bacterivorous nematode from soil, as a vector of food-borne pathogenic bacteria to preharvest fruits and vegetables.

Diploscapter, a thermotolerant, free-living soil bacterial-feeding nematode commonly found in compost, sewage, and agricultural soil in the United States, was studied to determine its potential role as a vehicle of Salmonella enterica serotype Poona, enterohemorrhagic Escherichia coli O157:H7, and Listeria monocytogenes in contaminating preharvest fruits and vegetables. The ability of Diploscapter sp. strain LKC25 to survive on agar media, in cow manure, and in composted turkey manure and to be attracted to, ingest, and disperse food-borne pathogens inoculated into soil or a mixture of soil and composted turkey manure was investigated. Diploscapter sp. strain LKC25 survived and reproduced in lawns of S. enterica serotype Poona, E. coli O157:H7, and L. monocytogenes on agar media and in cow manure and composted turkey manure. Attraction of Diploscapter sp. strain LKC25 to colonies of pathogenic bacteria on tryptic soy agar within 10, 20, 30, and 60 min and 24 h was determined. At least 85% of the worms initially placed 0.5 to 1 cm away from bacterial colonies migrated to the colonies within 1 h. Within 24 h, > or =90% of the worms were embedded in colonies. The potential of Diploscapter sp. strain LKC25 to shed pathogenic bacteria after exposure to bacteria inoculated into soil or a mixture of soil and composted turkey manure was investigated. Results indicate that Diploscapter sp. strain LKC25 can shed pathogenic bacteria after exposure to pathogens in these milieus. They also demonstrate its potential to serve as a vector of food-borne pathogenic bacteria in soil, with or without amendment with compost, to the surface of preharvest fruits and vegetables in contact with soil.