Skip to main content
Veterinární Medicína logoLink to Veterinární Medicína
. 2026 Jan 26;71(1):10–17. doi: 10.17221/83/2025-VETMED

The safety of fermented milk as a feedback method to reduce diarrhoea in newborn piglets

Jan Matiasovic 1,*, Monika Zouharova 1, Petra Strakova 1, Lenka Kavanova 1, Daniela Karasova 1, Jan Gebauer 1, Arpad Csorgo 2, Ivan Rychlik 1
PMCID: PMC12896124  PMID: 41694426

Abstract

Diarrhoea in newborn piglets represents a significant challenge to pig production. Controlled oral exposure, also known as “feedback”, whereby sows are exposed at least two weeks before farrowing to pathogens that cause health problems in piglets, is a traditional method of diarrhoea prevention. One type of feedback involves fermenting cow’s milk with faeces from piglets suffering from diarrhoea and administering it to sows before farrowing. The bacterial composition of the faecal inoculum and fermented milk was compared in this study, and the safety of administering the fermented milk to pregnant sows was evaluated. Using microbiota characterisation by 16S rRNA gene sequencing, the genera Acetobacter, Lactobacillus and Lactococcus formed the core microbiota of the fermented milk. However, Clostridium perfringens accounted for up to 33% of the total microbiota in some fermented milk samples. Interestingly, the drop in pH during the later stages of fermentation inactivated C. perfringens and the samples were thus enriched for inactivated C. perfringens antigen. Our findings contribute to a better understanding of the mode of action of fermented milk when used as a form of feedback.

Keywords: Clostridium perfringens, controlled oral exposure, sow


Diarrhoea in newborn piglets poses a substantial challenge to the global swine industry, resulting in significant economic losses through elevated morbidity and mortality rates, diminished growth performance, and escalating treatment costs (Sjolund et al. 2014; Schulz and Tonsor 2015). Neonatal piglet diarrhoea is a complex, multifactorial disease developing from the interplay of infectious agents, the host’s immunological competence, and various environmental and management factors (Racewicz et al. 2021; Fabiano and da Silva 2023). Key pathogens include a variety of viruses and bacteria, such as rotavirus, porcine epidemic diarrhoea (PED) virus, Escherichia coli and Clostridium perfringens (Vidal et al. 2019; Jacobson 2022). These pathogens can induce severe damage to the intestinal mucosa of piglets, leading to malabsorption, fluid and electrolyte imbalances, dehydration, and, frequently, mortality (Bergeland and Henry 1982).

Piglets are born agammaglobulinaemic, meaning they lack circulating antibodies, and their gastrointestinal tract is initially sterile. The passive immunity they acquire from the sow’s colostrum is therefore indispensable for their protection against early microbial threats (Rooke and Bland 2002; Le Dividich et al. 2005). Consequently, strategies to enhance the sow’s immunity to relevant pathogens are central to preventing neonatal diarrhoea (Krishna et al. 2020; Jacobson 2022). One possible strategy is “controlled oral exposure”, also known as ”feedback”. This protocol has been used in the swine industry for decades (Kohler 1974; Schwartz et al. 2013) and involves the intentional exposure of pregnant sows to farm-specific pathogens to elicit an immune response, thereby enhancing the transfer of specific antibodies to piglets via colostrum and milk. This approach is particularly valuable for diseases for which no effective commercial vaccines are available (Arruda 2010). Historically, feedback protocols involved administering faeces from diarrhoeic piglets or the ground intestines of dead piglets to sows (Arruda 2010; Schwartz et al. 2013). While this method directly exposes sows to the causative agents, including viruses, it also presents the risk of uncontrolled pathogen exposure (Arruda 2010). Another approach to feedback involves the formulation of “cocktails”, in which biological materials from diarrhoeic piglets are inoculated into a medium, such as cow’s milk, before being fed to sows (Neumann et al. 2020). This approach is expected to provide a safer way to expose sows to bacterial pathogens. Although fermented milk cocktails are sometimes used in practice, there is insufficient literature documenting their use. There are no studies examining the bacterial composition of fermented cocktails in relation to the inoculum used – the faeces of piglets with diarrhoea.

The objective of this study, therefore, was to analyse the bacterial composition of fermented milk used for sow feedback, to compare the bacterial composition of the fermentate with the initial faecal inoculum, and to assess the safety of its administration to pregnant sows.

MATERIAL AND METHODS

Faecal samples and milk fermentation

Pairs of faeces–fermented milk were obtained from a pig farm where feedback in the form of fermented milk inoculated with faeces from diarrhoea affected piglets had been utilised for approximately 10 years. Following the routine preparation, the faeces of diarrhoeic piglets were collected from various pens, mixed and used to inoculate five litres of commercially available longlife UHT cow’s milk. The fermentation process was carried out in 5 litre plastic bottles that were hermetically sealed and maintained at a temperature of 37 °C for 24 hours. A total of 16 pairs of faeces–fermented milk samples were collected.

DNA isolation from stool and fermented milk

DNA from faeces and fermented milk was isolated using a QIAamp PowerFaecal Pro DNA Kit (Qiagen, Hilden, Germany) according to the manufacturer’s instructions. For each sample, 250 mg of stool or 250 μl of fermented milk sample was combined with lysis buffer and mechanical disruption beads, then homogenised. The concentration of the extracted DNA was quantified using a DeNovix DS11 FX spectrophotometer (DeNovix Inc., Wilmington, USA).

Bacterial culture of Clostridium perfringens

C. perfringens was grown using Columbia blood agar containing 5% sheep blood (Labmediaservis, Jaroměř, Czech Republic) under anaerobic conditions (AnaeroGen; Oxoid, Basingstoke, UK). Semiquantification of C. perfringens was evaluated using a cross-scale (ranging from one cross for sparse growth to five crosses for abundant growth). The identity of selected colonies was confirmed using the MALDI Biotyper (Bruker Microflex mass spectrometer equipped with MALDI Biotyper Compass 4.1.100.10 software, Database RUO v12.0, updated version; Bruker, Billerica, MA, USA). To determine potential toxin production and to characterise the type of C. perfringens, toxin gene detection (cpa, cpb, cpe, etx, iap, cpb2) was performed using PCR (Baums et al. 2004). To test the impact of pH on C. perfringens growth, 100 μl of overnight cultures of three different C. perfringens strains in Wilkins–Chalgren broth (WCHB) (Thermo Scientific, Waltham, USA) were inoculated into 900 μl of WCHB adjusted to pH 5.0, 4.6, 4.2 or 3.8 using lactic acid. The cultures were then incubated under anaerobic conditions for 1, 3, and 6 h, after which bacterial growth was determined by plating serial dilutions on Columbia blood agar and counting colonies after 24 h of anaerobic culture.

Microbiota composition determined by 16S rRNA gene sequencing

Microbiota composition was analysed by sequencing the V3–V4 variable region of the 16S rRNA gene using an external service (Eurofins, Luxembourg). The obtained raw data were processed with QIIME 2 (Bolyen et al. 2019) using built-in modules DADA2 (Callahan et al. 2016) for trimming and denoising demultiplexed sequences; taxonomic classification was performed using the Greengenes 2 database, v2022.10 (McDonald et al. 2022); sequence diversity was evaluated with diversity core-metrix-phylogenetic and differential abundance was analysed using the composition ANCOMBC module (Lin and Peddada 2020).

The presence of alpha-toxin in fermented milk

The presence of alpha-toxin, a potential product of C. perfringens, in fermented milk was determined by the Monoscreen AgELISA Clostridium perfringens alpha-toxin (BioX Diagnostics S.A., Rochefort, Belgium) according to the manufacturer’s instructions.

Statistical analysis

Significance of differences between samples was evaluated using the Kruskal–Wallis test (richness and evenness), PERMANOVA (beta diversity) and Principal Coordinate Analysis (PCoA) within QIIME 2 plugins. The Chisquared test was used to analyse the correlation between the presence or absence of two different bacterial taxa within samples. P < 0.05 was considered significant.

RESULTS

Diversity of faecal and fermented milk samples

Bacterial richness was significantly higher in faecal samples than in fermented milk (Figure 1A). Similarly, the evenness of bacterial species distribution was significantly higher in faecal than in fermented milk samples (Figure 1B). Analysis of beta diversity using PCoA also significantly separated faecal samples from fermented milk, showing that, despite using faecal samples as inoculum, specific conditions present in milk considerably diverted microbiota development during fermentation from the original inoculum (Figure 1C).

Figure 1. Diversity analysis of faecal and fermented milk samples.

Figure 1

(A) Richness of bacterial composition in faeces and in fermented milk. (B) Evenness of bacterial composition in faeces and in fermented milk. Asterisk indicate significant difference; The data are presented as maximum and minimum, as well as the median. The box represent the 25th and 75th percentiles of values. (C) PCoA analysis of beta diversity of faecal and fermented milk samples; The rings represent faecal samples, and the squares represent fermented milk samples

F = faecal samples; M = fermented milk samples; PCoA = principal coordinate analysis; pd = phylogenetic diversity

Identification of bacterial species in the faeces of piglets with diarrhoea and in fermented milk samples

In total, 1 235 amplicon sequence variants (ASVs) were identified across all analysed samples. A significantly higher abundance of lactic acid bacteria was present in fermented milk samples (Figure 2) than in faecal inoculum, but bacteria metabolising polysaccharides were depleted in milk fermentates. Genera Acetobacter and Lactococcus were identified nearly exclusively in fermented milk samples. Different Lactobacillus species were found in both milk fermentates and faeces.

Figure 2. Bacterial genera and families differentially abundant in fermented milk samples in comparison to faecal inoculum.

Figure 2

The LFC is the estimated mean value of change in the log 2 abundance of a bacterial taxon in fermented milk samples when compared to faecal samples; The error bars represent the standard error of the mean

The correlation of C. perfringens with other bacteria

16S rRNA sequencing indicated that C. perfringens, a significant pathogen of the pig digestive tract, might be present in fermented milk samples. C. perfringens accounted for up to 33% of all bacteria in some fermentates (Figure 3), but not in others, even where the amount of C. perfringens in the faecal inoculum was high. The subsequent phase of the study therefore involved investigating the correlation between the presence of C. perfringens and that of other bacterial species in fermented milk samples. The only, but strong, negative correlation (chi-squared α = 5.02–9) was recorded for the presence of C. perfringens and Lactococcus lactis A346120 (Figure 3). When Lactococcus lactis A346120 reached 5% or more, C. perfringens did not exceed 5%, although in faecal samples that were used as an inoculum for milk fermentation, C. perfringens was present up to 22% (Samples 5F and 6F, Figure 3).

Figure 3. The correlation of C. perfringens and Lactococcus lactis A346120.

Figure 3

The black columns represent the proportion of C. perfringens 16S rRNA out of all bacteria present; The grey pattern columns represent the proportion of Lactococcus lactis A346120; Numbers represent each pair of faecal and fermented milk pair of sample

F = faecal samples; M = fermented milk samples

Presence of C. perfringens in fermented milk samples

Since DNA sequencing can easily detect DNA from non-viable bacterial cells, 16S microbiome profiling can be misleading regarding the presence of viable bacteria in a sample. Therefore, the viability of C. perfringens was assessed by performing a semiquantitative culture detection of C. perfringens in faecal material and fermented milk samples. As the samples were collected in 2023 and 2024, only faecal and fermented milk samples that had been frozen at –20 °C for no longer than six months were evaluated for C. perfringens viability by semiquantitative culture. Viable C. perfringens was detected in all nine tested faecal samples, though in varying abundance, and in eight out of nine tested fermented milk samples (Table 1). C. perfringens was present in low abundance in samples with a pH below 4.88. However, when the pH did not decrease below this value, C. perfringens was highly abundant in three out of four samples (see Table 1).

Table 1. Estimation of C. perfringens viability using semiquantitative culture method and assessment of C. perfringens proportion in samples by 16S rRNA gene sequencing.

Faecal sample Faecal culture* % of C. perfringens DNA in faeces** Fermented milk sample Fermented milk culture* % of C. perfringens DNA in fermented milk** pH of fermented milk
8 F ++++ 34.892 8 M + 17.581 4.23
9 F +++ 19.839 9 M + 14.275 4.32
10 F + 2.255 10 M + 33.373 4.16
11 F + 0.146 11 M 1.930 4.24
12 F ++++ 37.833 12 M + 1.117 3.98
13 F +++++ 1.024 13 M ++++ 32.298 5.62
14 F +++++ 3.909 14 M + 0.150 6.71
15 F ++++ 31.593 15 M ++ 12.259 4.88
16 F +++++ 2.183 16 M ++++ 0 5.92

*Crosses represents the amount of C. perfringens, ranging from one cross for sparse growth to five crosses for the most extensive growth of C. perfringens; **Percentage determined by 16S rRNA gene sequencing

Survival of C. perfringens under different pH conditions

We further tested the hypothesis that C. perfringens growth is inhibited after a specific growth phase by a decrease in pH resulting from the fermentation of sugars by lactic acid bacteria, and that a further reduction in pH leads to partial inactivation. The results (Figure 4) show that pH 4.6 or lower inhibits the growth of C. perfringens. This finding corresponds with the results of semiquantitative cultivation of C. perfringens from fermented milk samples. In fermented milk samples with a pH below 4.8, the number of C. perfringens colonies was low (Table 1).

Figure 4. Survival of C. perfringens under different pH conditions.

Figure 4

The values represent the percentage of C. perfringens relative to the initial dose of inoculum at time points of 1, 3 and 6 h of cultivation. (A–C) Three different C. perfringens strains originating from piglet diarrhoea

5.0 = pH 5.0; 4.6 = pH 4.6; 4.2 = pH 4.2; 3.8 = pH 3.8

Presence of C. perfringens alpha-toxin in fermented milk samples

Given C. perfringens’s ability to grow in milk, we further tested for the presence of C. perfringens alpha-toxin in milk fermentates. The alpha-toxin was not detected in any of the 16 tested fermented milk samples using the ELISA method. However, all C. perfringens isolates were positive for the alpha-toxin gene (cpa) and the beta2-toxin gene (cpb2). Still, it was negative for the beta-toxin gene (cpb), epsilon-toxin gene (etx), iota-toxin gene (iap), and enterotoxin gene (cpe). We thus conclude that the isolates were C. perfringens type A isolates typically present in piglet diarrhoeal faeces.

DISCUSSION

The controlled oral exposure of sows is used with the intention of protecting suckling piglets against pathogens causing neonatal diarrhoea (Kohler 1974). The most commonly used and welldocumented method of controlled oral exposure is feeding sows the faeces of diseased piglets (Schwartz et al. 2013). An alternative protocol involves feeding sows ground intestines from dead piglets. Although these protocols are effective in controlling diarrhoea caused by bacterial and viral pathogens, the primary concern is uncontrolled exposure of pregnant sows to these pathogens (Arruda 2010). Another approach is to provide sow’s milk fermented with faeces from diseased piglets (Neumann et al. 2020). Although uncertainty regarding microbial composition remains, it is reduced to bacteria capable of aerobic or semianaerobic growth in milk. In agreement with such expectations, microbiota richness and evenness were lower in fermented milk samples than in the original faecal samples, documenting the selective conditions during milk fermentation (Lichtenegger et al. 2024). Bacteria underrepresented or completely depleted in fermented milk samples were those metabolising polysaccharides (Flint et al. 2008). On the other hand, the prevailing bacteria, such as Lactobacillus, Acetobacter, and Lactococcus, are taxa previously reported in fermented milk (Zhong et al. 2016). Some of them (Lactococcus) also overlap with the microbiota found in fermented cheese (Korena et al. 2023), which is not too surprising, given that the same milk serves as the environment for microbial multiplication.

Interestingly, in some fermented milk samples, we found a high proportion of C. perfringens 16S rDNA. The high amount of C. perfringens 16S rDNA in fermented milk corresponded with a high amount of C. perfringens 16S rDNA in the faeces used as the inoculum. However, this was not the case in all pairs of faecal inoculum–fermented milk. In some pairs, the amount of C. perfringens 16S rDNA was high in faeces but low or not detected in fermented milk. Interestingly, the depletion of C. perfringens 16S rDNA was correlated with the presence of Lactococcus lactis A346120 in fermented milk. The presence of a high amount of viable C. perfringens in fermented milk may represent a potential health risk. Although production of alpha-toxin by C. perfringens has been associated with diarrhoea in piglets (Czanderlova et al. 2006), this toxin was not detected in any of the fermented milk samples. Milk as a substrate and the culture conditions used, thus, probably do not induce alpha-toxin expression. While this increases the safety of milk fermentates for sows, it also eliminates the chance of developing an antibody response to alpha-toxin (Salvarani et al. 2013). We further evaluated the viability of C. perfringens in fermented milk and found that it was dependent on the pH of the resulting fermented milk. In laboratory cultures, the viability of C. perfringens decreased when the pH was below 4.6. Similarly, the viability of C. perfringens decreased when the pH of fermented milk fell below 4.8. To increase the safety of milk fermentates, it might be advisable to check the pH of milk fermentates on farms and use only batches with pH lower than 4.6. In addition, since there are some species with negative correlation to C. perfringens, e.g. Lactococcus lactis A346120, it might be possible to obtain such strains in pure culture and add them in later phase of milk cultivation or together with faecal inoculum. Such approaches and control measures may improve the preparation of antigenrich but safe fermented milk feedback on farms.

Acknowledgement

We acknowledge the technical assistance of Eva Audová.

Funding Statement

Funded by the Ministry of Agriculture of the Czech Republic (Grant Nos. RO0523 and QK23020036).

Conflict of interest

The authors declare no conflict of interest.

REFERENCES

  1. Arruda PHE. The effects of oral controlled exposure on colostrum characteristics in swine [dissertation]. Ames (IA): Iowa State University; 2010. [Google Scholar]
  2. Baums CG, Schotte U, Amtsberg G, Goethe R. Diagnostic multiplex PCR for toxin genotyping of Clostridium perfringens isolates. Vet Microbiol. 2004 May 20;100(1-2): 11-6. [DOI] [PubMed] [Google Scholar]
  3. Bergeland ME, Henry SC. Infectious diarrheas of young pigs. Vet Clin North Am Large Anim Pract. 1982 Jul;4(2):389-99. [DOI] [PMC free article] [PubMed] [Google Scholar]
  4. Bolyen E, Rideout JR, Dillon MR, Bokulich NA, Abnet CC, Al-Ghalith GA, Alexander H, Alm EJ, Arumugam M, Asnicar F, Bai Y, Bisanz JE, Bittinger K, Brejnrod A, Brislawn CJ, Brown CT, Callahan BJ, Caraballo-Rodriguez AM, Chase J, Cope EK, Da Silva R, Diener C, Dorrestein PC, Douglas GM, Durall DM, Duvallet C, Edwardson CF, Ernst M, Estaki M, Fouquier J, Gauglitz JM, Gibbons SM, Gibson DL, Gonzalez A, Gorlick K, Guo J, Hillmann B, Holmes S, Holste H, Huttenhower C, Huttley GA, Janssen S, Jarmusch AK, Jiang L, Kaehler BD, Kang KB, Keefe CR, Keim P, Kelley ST, Knights D, Koester I, Kosciolek T, Kreps J, Langille MGI, Lee J, Ley R, Liu YX, Loftfield E, Lozupone C, Maher M, Marotz C, Martin BD, McDonald D, McIver LJ, Melnik AV, Metcalf JL, Morgan SC, Morton JT, Naimey AT, Navas-Molina JA, Nothias LF, Orchanian SB, Pearson T, Peoples SL, Petras D, Preuss ML, Pruesse E, Rasmussen LB, Rivers A, Robeson MS 2nd, Rosenthal P, Segata N, Shaffer M, Shiffer A, Sinha R, Song SJ, Spear JR, Swafford AD, Thompson LR, Torres PJ, Trinh P, Tripathi A, Turnbaugh PJ, Ul-Hasan S, van der Hooft JJJ, Vargas F, Vázquez-Baeza Y, Vogtmann E, von Hippel M, Walters W, Wan Y, Wang M, Warren J, Weber KC, Williamson CHD, Willis AD, Xu ZZ, Zaneveld JR, Zhang Y, Zhu Q, Knight R, Caporaso JG. Reproducible, interactive, scalable and extensible microbiome data science using QIIME 2. Nat Biotechnol. 2019 Aug;37(8): 852-7. Erratum in: Nat Biotechnol. 2019 Sep;37(9): 1091. [DOI] [PMC free article] [PubMed] [Google Scholar]
  5. Callahan BJ, McMurdie PJ, Rosen MJ, Han AW, Johnson AJA, Holmes SP. DADA2: High-resolution sample inference from Illumina amplicon data. Nat Methods. 2016 Jul;13(7):581-3. [DOI] [PMC free article] [PubMed] [Google Scholar]
  6. Czanderlova L, Hlozek P, Chmelar D, Lany P. Clostridium perfringens in suckling piglets with diarrhoea and its PCR typing and prevalence in the Czech Republic in 2001–2003. Vet Med-Czech. 2006 Sep;51(9):461-7. [Google Scholar]
  7. Fabiano G, da Silva MKO. Risk management in pig farming: A reality or conjecture? A systematic review. Anim Prod Sci. 2023;63(13):1261-71. [Google Scholar]
  8. Flint HJ, Bayer EA, Rincon MT, Lamed R, White BA. Polysaccharide utilization by gut bacteria: Potential for new insights from genomic analysis. Nat Rev Microbiol. 2008 Feb;6(2):121-31. [DOI] [PubMed] [Google Scholar]
  9. Jacobson M. On the infectious causes of neonatal piglet diarrhoea – A review. Vet Sci. 2022 Aug 10;9(8):422. [DOI] [PMC free article] [PubMed] [Google Scholar]
  10. Kohler EM. Protection of pigs against neonatal enteric colibacillosis with colostrum and milk from orally vaccinated sows. Am J Vet Res. 1974 Mar;35(3):331-8. [PubMed] [Google Scholar]
  11. Korena K, Krzyzankova M, Florianova M, Karasova D, Babak V, Strakova N, Juricova H. Microbial succession in the cheese ripening process-competition of the starter cultures and the microbiota of the cheese plant environment. Microorganisms. 2023 Jul 1;11(7):1735. [DOI] [PMC free article] [PubMed] [Google Scholar]
  12. Krishna VD, Kim Y, Yang M, Vannucci F, Molitor T, Torremorell M, Cheeran MC. Immune responses to porcine epidemic diarrhea virus (PEDV) in swine and protection against subsequent infection. PLoS One. 2020 Apr 28;15(4): e0231723. [DOI] [PMC free article] [PubMed] [Google Scholar]
  13. Le Dividich J, Rooke J, Herpin P. Nutritional and immunological importance of colostrum for the new-born pig. J Agric Sci. 2005 Dec;143(6):469-85. [Google Scholar]
  14. Lichtenegger AS, Posadas-Cantera S, Badr MT, Hacker G. Comparison of the diversity of anaerobic-cultured gut bacterial communities on different culture media using 16S rDNA sequencing. J Microbiol Methods. 2024 Sep; 224:106988. [DOI] [PubMed] [Google Scholar]
  15. Lin H, Peddada SD. Analysis of compositions of microbiomes with bias correction. Nat Commun. 2020 Jul 14; 11(1):3514. [DOI] [PMC free article] [PubMed] [Google Scholar]
  16. McDonald D, Jiang Y, Balaban M, Cantrell K, Zhu Q, Gonzalez A, Morton JT, Nicolaou G, Parks DH, Karst SM, Albertsen M, Hugenholtz P, DeSantis T, Mirarab S, Knight R. Greengenes2 enables a shared data universe for microbiome studies. bioRxiv 2022.12.19.520774 [Preprint]. 2022 Dec 19. [cited 2025 Oct 5]. Available from: 10.1101/2022.12.19.520774 [DOI] [Google Scholar]
  17. Neumann EJ, Ramirez A, Schwartz KJ. Swine disease manual. 5th ed. Perry, Iowa: American Association of Swine Veterinarian; 2020. 198 p. [Google Scholar]
  18. Racewicz P, Ludwiczak A, Skrzypczak E, Skladanowska-Baryza J, Biesiada H, Nowak T, Nowaczewski S, Zaborowicz M, Stanisz M, Slosarz P. Welfare, health and productivity in commercial pig herds. Animals (Basel). 2021 Apr 20;11(4):1176. [DOI] [PMC free article] [PubMed] [Google Scholar]
  19. Rooke JA, Bland IM. The acquisition of passive immunity in the new-born piglet. Livest Prod Sci. 2002 Dec;78(1): 13-23. [Google Scholar]
  20. Salvarani FM, Conceição FR, Cunha CE, Moreira GM, Pires PS, Silva RO, Alves GG, Lobato FC. Vaccination with recombinant Clostridium perfringens toxoids α and β promotes elevated antepartum and passive humoral immunity in swine. Vaccine. 2013 Aug 12;31(38):4152-5. [DOI] [PubMed] [Google Scholar]
  21. Schulz LL, Tonsor GT. Assessment of the economic impacts of porcine epidemic diarrhea virus in the United States. J Anim Sci. 2015 Nov;93(11):5111-8. [DOI] [PMC free article] [PubMed] [Google Scholar]
  22. Schwartz KJ, Henry S, Tokach T, Potter M, Davidson D, Egnor C. Infective material, concepts and procedures for intentional sow herd exposure to porcine epidemic diarrhea virus. Ames (IA): Iowa State University; 2013. 8 p. [Google Scholar]
  23. Sjolund M, Zoric M, Wallgren P. Financial impact of disease on pig production. Part III. Gastrointestinal disorders. In: Proceedings of the 6th European Symposium of Porcine Health Management; 2014 May. 7-9; Sorrento (Italy). p. 1-4. [Google Scholar]
  24. Vidal A, Martin-Valls GE, Tello M, Mateu E, Martin M, Darwich L. Prevalence of enteric pathogens in diarrheic and non-diarrheic samples from pig farms with neonatal diarrhea in the North East of Spain. Vet Microbiol. 2019 Oct;237:108419. [DOI] [PMC free article] [PubMed] [Google Scholar]
  25. Zhong Z, Hou Q, Kwok L, Yu Z, Zheng Y, Sun Z, Menghe B, Zhang H. Bacterial microbiota compositions of naturally fermented milk are shaped by both geographic origin and sample type. J Dairy Sci. 2016 Oct;99(10):7832-41. [DOI] [PubMed] [Google Scholar]

Articles from Veterinární Medicína are provided here courtesy of Czech Academy of Agricultural Sciences

RESOURCES