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Article

Shiga Toxin Genes Detected in Fecal Samples of Illinois Finisher Pigs

by
Kathryn L. Lauder
1,†,
Shafiullah M. Parvej
1,†,
Yiyang Shen
1,
Chongyang Zhang
1,
Jehadi Osei-Bonsu
1,
James F. Lowe
1,2 and
Weiping Zhang
1,*
1
Department of Pathobiology, University of Illinois at Urbana-Champaign, 2001 South Lincoln Ave., Urbana, IL 61802, USA
2
Department of Clinical Veterinary Medicine, University of Illinois at Urbana-Champaign, 2001 South Lincoln Ave., Urbana, IL 61802, USA
*
Author to whom correspondence should be addressed.
†
These authors contributed equally to this work.
Bacteria 2025, 4(4), 52; https://doi.org/10.3390/bacteria4040052
Submission received: 13 June 2025 / Revised: 12 July 2025 / Accepted: 16 September 2025 / Published: 2 October 2025
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Abstract

(1) Background: Pigs can be another host of Shiga toxin-producing E. coli (STEC), suggesting that pork products could be a potential risk to public health. A USDA National Animal Health Monitoring System (NAHMS) study revealed that Shiga toxin genes were detected in more than half of samples nationwide but only about a quarter of samples from the state of Illinois. To characterize the presence of STEC in Illinois pigs better and to explore the discrepancy between Illinois and other swine-producing states, we increased the sampling size and collected samples in different regions of the state and in different months to detect Shiga toxin genes in Illinois finisher pigs and subtyped the Shiga toxin genes further to assess any potential risk of STEC originating from Illinois pigs to human health. (2) Methods: Fecal samples were collected from 471 Illinois finisher pigs at different locations from October 2021 to September 2022. DNA samples were extracted from individual fecal samples and PCR-tested for Shiga toxin genes (stx1, stx2) and then toxin subtypes (stx2a, stx2c, stx2d, and stx2e). (3) Results: The data showed that the stx2 gene was detected in 61% of the fecal samples (285/471), whereas stx1 was detected only in 0.4% of the samples (2/471). The data also indicated a lower prevalence of stx genes in the samples collected in certain cold months (36% in October and 19% in March) compared to that in those from warm months (56% to 100% from April to September). Stx2d, a subtype associated with severe human illness, was detected in 2% of the samples (10/471); in contrast, stx2e, which is expressed by E. coli strains causing diarrhea and edema disease in pigs, was the most detected (49%; 229/471). (4) Conclusions: The high prevalence of Shiga toxin genes in the fecal samples from Illinois finisher pigs suggests that Stx-positive E. coli strains circulate in Illinois pig farms. However, the highly detected stx2e-positive STEC (or enterotoxigenic E. coli, ETEC) strains are associated with diarrhea and edema disease in pigs, indicating the need for disease prevention or control for pigs but unlikely a safety concern for Illinois pork products or a major risk of human illnesses.

1. Introduction

Characterized by the presence of Shiga toxin 1 gene (stx1) and/or Shiga toxin 2 gene (stx2) and the production of Shiga toxin(s), Shiga toxin-producing E. coli (STEC) is a highly virulent pathotype of diarrheagenic E. coli (DEC). STEC infection results in abdominal distress and diarrhea with or without blood but can progress to hemorrhagic colitis (HC), severe hemolytic uremic syndrome (HUS), and renal failure, becoming a serious threat to human health. Globally, STEC is estimated to be responsible for approximately 2.8 million severe infections and about 3890 HUS cases, including 230 deaths annually [1]. In the United States, STEC causes 170,000 to 265,000 clinical cases, 30 deaths, and an estimated loss of >USD 200 million due to hospitalization and absence from work each year [2,3]. STEC strains associated with severe human clinical illness typically produce Shiga toxin type 2 (stx2) rather than type 1 (stx1) [4,5,6,7]. Stx2 and stx1 have various subtypes, including stx1a, 1c, 1d, and stx2a, 2b, 2c, 2d, 2e, 2f, and 2g [8]. Among the stx2 subtypes, stx2a, stx2c, and sxt2d are associated with human clinical cases, particularly HUS. Additional subtypes of stx2 have been identified recently, including stx2h, stx2i, stx2j, stx2k, stx2l, and stx2m, but the association of these newly identified subtypes with clinical illness in humans or animals is yet to be defined. In contrast, STEC is typically not a concern in terms of animal health, rather using animals as a reservoir and contaminating foods to cause human infections. It has been reported, nevertheless, that STEC is linked to skin infections in chickens [9], a reduction in fertility, as well as edema disease (ED) and post-weaning diarrhea (PWD) in pigs though these E. coli strains also produce enterotoxins and are often classified as enterotoxigenic E. coli (ETEC) [10,11].
Pigs and pork products were not considered a major source of STEC infection in humans in the past. Bovids are the primary reservoirs of STEC [6,7], and the consumption of undercooked contaminated beef products is the primary cause of human STEC infections. Recently, however, it was reported that 17% of wild animals carry STEC strains that exhibit close evolutionary relationships with the STEC strains that cause illness in humans [12]. STEC outbreaks in Europe can be traced back to wild boars; in Brazil, 81% of wild capybaras are reported to be STEC carriers. Their frequent contact with domestic ruminants is believed to be attributed to the increasing detection of STEC in wild animals. Though STEC transmission through non-ruminant animals remains controversial, STEC bacteria have been detected in pigs and pork products. A Shiga toxin gene, namely stx2e, along with enterotoxigenic toxins, is commonly present in the ETEC strains that cause neonatal diarrhea, post-weaning diarrhea, and edema disease (ED) in pigs [13]. However, a recent study revealed that other Shiga toxin genes, including stx2a, stx2b, and stx2c, were detected in E. coli strains isolated from finisher pigs in Italy [14]. Moreover, the highly pathogenic STEC strain O157 was found in uncooked ground pork in Canada [15]. Indeed, two STEC outbreaks were reported to be linked to the consumption of pork products: one outbreak in 2014 resulted in 23 confirmed cases of hospitalization and 6 cases of HUS [16], and the other in 2018 accounted for 13 hospitalizations and 1 death [17]. Recent studies suggest that STEC strains are commonly present in pigs, pork products, and samples collected from pig farms [15,18,19,20,21,22,23].
In the United States, one study showed that 5% of retail pork products from the mid-Atlantic region tested positive for an stx gene on RT-PCR [24]. Another study detected a similar frequency of STEC, including the subtype stx2d and serogroup O91, in retail pork and beef products in Washington, D.C. [25]. Concern about STEC, including the highly pathogenic STEC serogroups O26, O91, and O121, in U.S. pork retail products and the link to outbreaks of swine-origin STEC led to a systematic investigation into STEC in U.S. pig farms and facilities. The National Animal Health Monitoring System (NAHMS) of the United States Department of Agriculture (USDA) conducted a nationwide study on the STEC prevalence in U.S. swine farms in 2000 and showed 53.9% and 63.5% of samples were positive for stx1 and stx2, respectively [26]. However, the detection rates for stx1 and stx2 in samples collected from Illinois, the fourth leading state in the production of nursery pigs in the nation, were only 28.3% and 20%. Since there were no noticeable differences in pig genetics and swine farm management practices between Illinois and the other swine-producing states at that time, such significant differences prompted us to systematically reexamine the presence of STEC in the state of Illinois. In this study, we collected fecal samples from individual finisher pigs from different regions of the state in different months and PCR-tested these samples for the presence of stx1 and stx2 genes to examine STEC presence in Illinois swine farms and to explore variations in different months. We further subtyped the stx1- and stx2-positive samples with an emphasis on Shiga toxins which are associated with human illness or post-weaning diarrhea and edema disease in pigs.

2. Materials and Methods

2.1. Animal Care and Use

All samples used in this study were collected post mortem from an abattoir.

2.2. Study Design and Sample Collection

All samples were collected from a large commercial plant located in the midwest of the state harvesting over 15,000 pigs per day in two shifts. This plant receives pigs from all of the swine-dense areas across the state, with a higher percentage originating from areas that are closer to the plant than areas that are more distant (this plant also receives pigs from other nearby states). The pigs that we sampled were transported from swine farms to the plant in the morning and processed in the afternoon of the same day.
Fecal samples were collected individually from pigs, with 50–100 samples per month and one sample per pig, from October 2021 to September 2022. These pigs were from different regions of the state except for those sampled in October, at which time the location was not specified, and for April and June, when the pigs were from the same region (the herd or swine farm information was not provided). Pigs were marked and followed through the plant until the time of visceral inspection. From the visceral tray, feces were collected, stored in sterile 50 mL tubes on ice, and transported back to the laboratory within hours. Additionally, monthly average temperature data for the regions of the swine farms were collected from the weather stations closest to the pig farms, as well as the weather station closest to the packing plant, through the National Weather Service NOAA Online Database. The average monthly temperature data were used to examine variations in stx detection.

2.3. Bacterial Enrichment Culture and DNA Extraction

One gram of fecal material was suspended in 10 mL E. coli enrichment broth BD Difco EC medium (Becton, Dickinson and Company; Sparks, MD, USA), and incubated at 40 °C for 6 h in a shaker incubator at 150 rpm. One milliliter of culture was collected and subjected to DNA extraction, and another ml was stored at −80 °C with 20% glycerol for future use. DNA was extracted using the GeneClean Turbo kit (MP Biomedicals, LLC; Solon, OH, USA) by following the manufacturer’s protocol. Briefly, 1 mL enrichment culture material was boiled and centrifuged (9400× g for 5 min). The supernatant was then mixed with GeneClean Turbo salt solution, centrifuged in a 2 mL cartridge tube, and washed two times with washing buffer. The DNA was eluted with 30 µL of autoclaved distilled water.

2.4. PCR Detection of STEC Stx Genes

Two pairs of PCR primers specific to the stx1 or stx2 genes were used initially to screen the DNA samples (Table 1). A sample in which the stx1 and/or stx2 gene was detected was considered stx-positive. All stx-positive DNA samples were then screened further with PCR primers specific to stx2a, stx2c, stx2d, and stx2e for subtype genes important to human or pig health (Table 1). Additionally, primers specific to fimbria F18 were included to detect E. coli strains associated with pig diarrhea or edema disease.
A duplex PCR was carried out to detect the stx1 and stx2 genes, as described previously [27], whereas a standard single PCR was used for the detection of each subtype gene. PCR was prepared in a 25 μL reaction that consisted of 2.5 μL of 10X PCR buffer, 0.5 μL 10 mM dNTP Mix, 0.125 μL of Taq DNA polymerase (New England Biolab; Ipswich, MA, USA), 1 μL (10 mM) each of the forward and reverse primers, and 2 μL of the DNA sample and brought up to 25 μL with nuclease-free water. The thermal program for duplex PCR was denaturation at 94 °C for 5 min, 35 cycles of denaturation at 94 °C for 1 min, 65 °C for 20 s, 68 °C for 1 min, and a final extension for 7 min at 68 °C. The program for the Stx subtyping PCR was denaturation at 95 °C for 15 min, 35 cycles of denaturation at 94 °C for 50 s, 64 °C for 40 s, 72 °C for 1 min, and a final extension at 72 °C for 3 min. The PCR condition for F18 included denaturation at 95 °C for 30 s, 30 cycles of denaturation at 95 °C for 30 s, 59 °C for 30 s, 68 °C for 1 min, and a final elongation at 68 °C for 5 min. All PCR tests were performed in duplicate.

3. Results

3.1. Stx Was Commonly Detected in the Fecal Samples from the Illinois Finisher Pigs

A total of 471 fecal samples were collected from Illinois finisher pigs from October 2021 to September 2022. Due to COVID-related restrictions, we were unable to access the facility for sample collection in November and December of 2021, as well as January, February, July, and August of 2022. Duplex PCR targeting of the stx1 and stx2 genes detected 285 samples that were positive (61%). The vast majority of the positive samples were positive for stx2, with 285 samples (61%) positive for the stx2 gene and only 2 samples positive for stx1 (together with the stx2 gene; 0.4%) (Table 2).

3.2. Stx Detection Shows Monthly Variations in Illinois Finisher Pigs

The PCR results showed that a high prevalence of the stx genes appeared in the samples collected in certain warm months (Figure 1). The average stx detection in the samples collected in the cold months (October and March) was 36% and 19%, whereas the stx prevalence in the samples collected in warm months (June and September) was 84% and 100%, respectively. The detection levels in April and May were 65% and 56%, when the monthly temperature was moderate.

3.3. Stx2e Is the Predominant Subtype Detected in the Fecal Samples of the Illinois Finisher Pigs

PCR with primers specific to the stx subtype genes detected the predominance of the stx2e gene in the stx2-positive samples (Figure 2). Fecal samples from 229 (out of 471) pigs were stx2e-positive (49%). In contrast, the stx2a and stx2c genes were not detected in any of the samples tested, and the stx2d subtype gene was detected in 10 samples (2%).
Since the stx2e gene is associated with diarrheal disease in weaned pigs and particularly edema disease in growing pigs caused by the ETEC strains that express F18 fimbria, the stx2e-positive samples were tested for the F18 fimbrial gene. The PCR test detected 116 samples positive by using the primers specific to the F18 adhesin gene fedF. A PCR test to detect the K88 fimbrial gene, which is commonly expressed by ETEC strains that cause diarrhea in neonatal and weaned pigs (and typically do not carry Stx genes), was not included in the current study.

4. Discussion

Different from the results of the USA National Animal Health Monitoring System (NAHMS) study, in which about 20% to 28% of Illinois pig samples were stx1- or stx2-gene-positive [26], the data from this study, however, showed that 61% of the fecal samples collected from finisher pigs from different regions of this state were positive for the stx2 gene. The stx gene detection level in the current Illinois finisher pigs is similar to the 70% rate of STEC positivity in the pigs from eight US swine production states studied in [28] and the results for pigs from 13 of the 17 top pig-producing US states reported by NAHMS [26].
The low rate of stx detection in the pigs in Illinois in the NAHMS study was likely caused by a small sample size and a skewed sampling schedule. In the NAHMS study, only 60 samples were collected from Illinois swine farms, substantially underrepresenting the fourth leading state of pig production in the U.S. More significantly, the Illinois samples analyzed by NAHMS were collected during the cold months, from September to March. It is recognized that collecting pig fecal samples during the cold season often leads to lower detection of STEC [29]. Since the current study collected fecal samples from 471 pigs from different regions of the state and these samples were collected in both cold and warm months, the results generated by this study are likely to reflect the prevalence of STEC for Illinois pigs better. Additionally, the sample collection methods, on farms in the NAHMS study versus at a processing plant in this study, may not be a major cause of variations in the detection of the stx gene, particularly since the pigs in the plant were transported in from farms in the morning and processed in the afternoon of the same day.
The data from this study affirmed a possible monthly or temperature-related variation in STEC detection in pigs. The overall trend in stx detection in this study is reflected by the regional average monthly temperature curve (Figure 1), with low stx detection in the months that had an average monthly temperature below 60 °F; on the other hand, there was a high level of stx detection in the months when the temperature increased. After the monthly temperature reached its peak and started to decline, stx detection also peaked and then declined afterward. It was noticed that the stx detection levels were higher in 2022 than those in 2021. However, this variation is because we started the project in October 2021, with the samples included in this study for the year 2021 only collected during cold months; in contrast, the samples collected in the year 2022 were largely from warm months, thus leading to a skewed higher stx detection in the year 2022. It needs to be pointed out that because of COVID-19 restrictions, we were unable to access the facility to collect samples in certain months, including the warm months of July and August. Therefore, a statistical analysis of significant differences in seasonal variation was not conducted. Examining samples from every month should have provided us with a better assessment of the correlation between monthly temperature and the stx detection level. We would also like to point out that Fahrenheit, instead of Celsius, was used in this manuscript because all of the temperature data we acquired were recorded in Fahrenheit.
The current study detected the stx1 gene in only two samples. Moreover, these two stx1-positive samples were also positive for stx2, though we were unable to confirm whether both stx1 and stx2 were from the same isolate since we were unable to culture STEC from these two samples. Since stx2 is the main cause of STEC-related human clinical illness and the foremost causal agent of HUS in children, therefore, we subsequently focused on subtyping stx2 subtype genes. Indeed, STEC strains possessing the stx2 gene without the stx1 gene are reported to possibly be more virulent than strains carrying stx1 or both the stx1 and stx2 genes [30,31]. The low presence of stx1 in the STEC strains from the pigs was not unusual. As reported previously by other research groups, STEC strains from pigs in Poland and Slovakia carried only the stx2 gene [32,33], and pig STEC samples from Korea showed a 4% detection rate for stx1 [34]. In contrast, a high prevalence of stx2 has often been detected in STEC strains isolated from pigs [28,35].
A high prevalence of stx2 in swine farms potentially could be a pork-product-associated public health risk. However, subtyping the stx2 genes from this study revealed that the vast majority of the stx2-positive samples were positive for stx2e but not the subtypes associated with severe human infections. Though stx2e-positive strains were reported in some studies to be the sole STEC pathogen isolated from HUS patients [36,37,38], the subtype stx2e is mainly expressed by the swine-adapted E. coli strains that cause diarrhea or edema disease in pigs but that are not pathogenic or less pathogenic to humans. The other stx2 subtypes, especially 2a, 2c, and 2d, on the other hand, are associated with human infections, particularly HUS. In the current study, we did not detect stx2a or stx2c in any of the samples we collected; however, we detected stx2d in ten samples (10/471; 2%). This may not seem an imminent safety risk for pork products from Illinois, but even a low level of stx2d-STEC presence in pig farms can potentially be a concern for food safety or public health. Swine practitioners and policymakers may need to develop strategies to reduce or eliminate stx2d STEC from swine farms or pork products.
In this study, we did not carry out PCR testing to detect the STEC intimin gene (eae), an important feature of human STEC. The eae gene is known as a key virulence factor that plays a role in the close adherence of STEC bacteria to host cells and produces attaching and effacing lesions [7]. However, stx2e-positive STEC and ETEC strains isolated from pigs rarely carry the eae or enterohemolysin gene [39,40,41].
This study detected a high presence of the pig-specific F18 fimbrial gene, signifying a health and well-being risk to pigs in Illinois. E. coli strains that produce F18 fimbria and the stx2e toxin (together with heat-labile and/or heat-stable enterotoxins; these F18 fimbrial, as well as K88-fimbrial strains, are often classified as ETEC rather than STEC) are the predominant cause of diarrhea in weaned pigs and edema disease (due to F18 ETEC). Though stx2e-positive STEC strains harboring heat-labile and/or heat-stable enterotoxins were isolated from humans, we believe that stx2e-positive F18 fimbrial E. coli strains are mainly ETEC strains and are associated with diarrhea and edema disease in pigs. The lower detection of the F18 fedF gene compared to that for the stx2e gene could be an indication of the presence of K88 ETEC strains since K88 fimbrial ETEC strains circulate more frequently in U.S. pig farms [41]. Future studies, however, are needed to characterize the stx-positive E. coli strains in swine farms and to define their potential risk to pig health or human health, thus developing better strategies to improve disease prevention further for pigs and humans.

5. Conclusions

Based on the data from this study,
  • Shiga toxin genes are highly prevalent in Illinois finisher pigs (61%) but are mostly represented by the stx2e gene, which is associated with diarrhea and edema disease in pigs;
  • The Shiga toxin genes that are associated with human severe diseases are detected at a very low level in Illinois finisher pigs, suggesting a low risk of Illinois pork products to public health or food safety.
  • Attention may be needed to develop better strategies against pig diarrhea and edema to reduce the presence of E. coli strains harboring Shiga toxin genes in finisher pigs.

Author Contributions

Conceptualization: W.Z. and J.F.L.; methodology: K.L.L., Y.S., C.Z., and J.O.-B.; validation: K.L.L., C.Z., and S.M.P.; formal analysis: K.L.L. and S.M.P.; investigation: K.L.L.; data curation: K.L.L. and S.M.P.; writing—original draft preparation: S.M.P.; writing—review and editing: W.Z.; visualization: K.L.L.; supervision: W.Z.; project administration: W.Z.; funding acquisition: W.Z. All authors have read and agreed to the published version of the manuscript.

Funding

This project is supported by the Agricultural Experimental Station at the University of Illinois at Urbana-Champaign (grant no. IL-888-909) and USDA-NIFA Agriculture and Food Research Initiative Competitive (grant no. 2017-67015-31471).

Institutional Review Board Statement

Not applicable.

Informed Consent Statement

Not applicable.

Data Availability Statement

The data are included in this manuscript, and the original raw data are available upon request.

Acknowledgments

We thank the local pig processing facility for its support and assistance with the sample collection.

Conflicts of Interest

All authors declare no conflicts of interest for this study; the funding agency had no involvement in the study design or data interpretation.

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Bacteria 04 00052 g001
Figure 1. The average monthly temperature (°F) in central Illinois and the prevalence of the stx genes (%) detected in Illinois finisher pigs. Note: The dotted line indicates that data from some months were missing.
Figure 1. The average monthly temperature (°F) in central Illinois and the prevalence of the stx genes (%) detected in Illinois finisher pigs. Note: The dotted line indicates that data from some months were missing.
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Bacteria 04 00052 g002
Figure 2. The relative dominance of the stx subtype genes and the F18 fedF gene detected using PCR in Illinois finisher pigs. Note: The dotted line indicates that data from some months were missing.
Figure 2. The relative dominance of the stx subtype genes and the F18 fedF gene detected using PCR in Illinois finisher pigs. Note: The dotted line indicates that data from some months were missing.
Bacteria 04 00052 g002
Table 1. PCR primers used to detect stx1, stx2, and stx subtype and F18 fimbrial fedF genes. Note: F, forward primer; R, reverse primer. The length of each amplicon is in nucleotide base pairs (bp).
Table 1. PCR primers used to detect stx1, stx2, and stx subtype and F18 fimbrial fedF genes. Note: F, forward primer; R, reverse primer. The length of each amplicon is in nucleotide base pairs (bp).
PrimersSequenceLengthReferences
Stx 1-F5′ CTA GCT AGC ATG AAT AAT TTA TAT GTG ′3642 bpThis study
Stx 1-R5′ TCA CGG CCG TTA TTA ATC CCA CAA TAT ′3
Stx 2-F5′ CCA TGA CAA CGG ACA GCA GTT ′3477 bp[27]
Stx 2-R5′ TGT CGC CAG TTA TCT GAC ATT C ′3
Stx 2a-F5′ GCG ATA CTG AGC ACT GTG GCC ′3347 bp[8]
Stx 2a-R5′ GCC ACC TTC ACT GTG AAT GTG ′3
Stx 2c-F5′ GAA AGT CAC AGT TTT TAT ATA CAA CGG GTA ′3177 bp
Stx 2c-R5′ CCG GCC ACC TTT ACT GTG AAT GTA ′3
Stx 2d-F5′ AAA GTC ACA GTC TTT ATA TAC AAC GGG TG ′3280 bp
Stx 2d-R5′ GCC TGA TGC ACA GGT ACT GGA C ′3
Stx 2e-F5′ CGG AGT ATC GGG GAG AGG C ′3411 bp
Stx 2e-R5′ CTT CCT GAC ACC TTC ACA GTA AAG GT ′3
Fed-F5′ATG CGT TTA AAA TAT ATC TTG ATC′3900 bpThis study
Fed-R5′CTG TAT CTC GAA AAC AAT GGG C′3
Table 2. Prevalence of stx1, stx2, and stx subtype and F18 fimbrial FedF genes detected using PCR from the fecal samples of Illinois finisher pigs from different months.
Table 2. Prevalence of stx1, stx2, and stx subtype and F18 fimbrial FedF genes detected using PCR from the fecal samples of Illinois finisher pigs from different months.
Month# of Samplesstx1stx2stx2astx2cstx2dstx2eF18
October-2150-18 (36%)--6 (12%)17 (34%)11 (22%)
March-22100-19 (19%)---19 (19%)8 (8%)
April-22992 (2%)64 (65%)--1 (1%)55 (56%)14 (14%)
May-2250-28 (56%)---21 (42%)3 (6%)
June-22102-86 (84%)--2 (2%)52 (51%)35 (34%)
September-2270-70 (100%)--1 (1%)65 (93%)42 (60%)
Total (%)4712 (0.4%)285 (61%)0010 (2%)229 (49%)113 (24%)
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Lauder, K.L.; Parvej, S.M.; Shen, Y.; Zhang, C.; Osei-Bonsu, J.; Lowe, J.F.; Zhang, W. Shiga Toxin Genes Detected in Fecal Samples of Illinois Finisher Pigs. Bacteria 2025, 4, 52. https://doi.org/10.3390/bacteria4040052

AMA Style

Lauder KL, Parvej SM, Shen Y, Zhang C, Osei-Bonsu J, Lowe JF, Zhang W. Shiga Toxin Genes Detected in Fecal Samples of Illinois Finisher Pigs. Bacteria. 2025; 4(4):52. https://doi.org/10.3390/bacteria4040052

Chicago/Turabian Style

Lauder, Kathryn L., Shafiullah M. Parvej, Yiyang Shen, Chongyang Zhang, Jehadi Osei-Bonsu, James F. Lowe, and Weiping Zhang. 2025. "Shiga Toxin Genes Detected in Fecal Samples of Illinois Finisher Pigs" Bacteria 4, no. 4: 52. https://doi.org/10.3390/bacteria4040052

APA Style

Lauder, K. L., Parvej, S. M., Shen, Y., Zhang, C., Osei-Bonsu, J., Lowe, J. F., & Zhang, W. (2025). Shiga Toxin Genes Detected in Fecal Samples of Illinois Finisher Pigs. Bacteria, 4(4), 52. https://doi.org/10.3390/bacteria4040052

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