Tuesday, October 11

Food and antibiotic resistance genes

Antibiotic resistance (AR) and horizontal transmission of resistance genes is a major health problem in the modern world. Antibiotic abuse and dysbiosis seem to be the main causes, but an interesting potential source of these genes is just being explored. I came across a paper which analyzed the level of AR genes in common retail foods (1). 

The specific markers examined were ermB, ermC, tetS/M and tetA, which encode ribosomal modification and tetracycline (Tet) efflux mechanisms. Foods analyzed included different kinds of cheese (Cheddar, Swiss, Colby, Mozzarella), yogurt, raw milk, shrimp, pork chop, deli turkey, deli beef, mushroom and spinach. They found AR microbes in nearly all samples, either from raw or ready-to-eat foods. The only foods which showed no detectable AR microbes were processed cheese (heat treated during manufacture) and yogurt. 20 of the 23 cheese samples contained Tetr and/or Emr* (tetracycline and erythromycin resistance genes, respectively), and the number of Tetr microbes was greater than that of Emr in this food. 

The presence of selected AR genes from cheese and milk was analyzed by conventional PCR. It was found that:

- Among Tetr isolates recovered from cheese, about 10% contained the tetS/M gene. 7 out of 11 tetS/M+ were Staphylococcus thermophilus and two isolates were Lactococcus lactis. Two additional isolates had 97% 16S rRNA gene sequence identity to unidentified Lactococcus sp. and 93-94% identity to Lactococcus garvieae and Lactococcus lactis, similar to an isolate from milk. This suggests that Lactococcus might be a common organism from milk. Another tetS/M+ isolate from raw milk was identified as Leuconostoc sp. Two isolates from cheese presented the tetA gene, as well as several isolates from raw pork meat; and were identified as Pseudomonas sp. 

- Among Emr isolates from cheese, more than 50% had the ermB gene. The carrier organisms identified were Staphylococcus sp. (5 out of 28) and S. thermophilus ( 23 out of 28). One isolate, characterized as Pseudomonas sp., from packaged sliced chicken lunchmeat contained the ermC and tetS/M genes, suggesting a multidrug resistance phenotype. 

MIC analysis showed resistance to tetracycline, erythromycin, clarithromycin and clindamycin in several isolates, some of them showing multidrug resistance.

Because of the importance of horizontal gene transfer of AR genes to the human microbiota, the authors tested the potential transfer between some strains identified to resident oral bacteria. They used Staphylococcus mutans as recipient, which is a cariogenic oral pathogen. The plasmid (20-25kb) isolated from bacteria from food samples was succesfully transferred to S. mutans, confirmed by PCR amplification. MIC test showed that the transformed S. mutans had significantly increased resistance to tetracycline compared with the parental strain.  

The presence of AR genes in other foods and the horizontal transfer of resistance genes to the human microbiota has been confirmed in other studies (2, 3, 4, 5). The common food source of most of these studies is cheese/dairy, which shows the higher number of CFU and AR gene heterogeneity because of the presence of lactic acid bacteria. This is also relevant for fermented foods. 

The picture gets worse if we consider that the presence of AR bacteria and multiple resistance genes have been found in microbiota of breast-fed babies without previous exposure to antibiotics, as well as in some breast-milk samples (6, 7). 

In my opinion, antibiotic resistance is the main public health problem nowadays. While it may be smart to avoid certain foods which have potential carriers, the problem dont lies in the presence of AR genes per se, but in the horizontal transfer between AR bacteria and human commensal bacteria, which can then transfer resistance genes to pathogenic bacteria that are present in the human microbiota. These AR genes can also be transferred to pathogenic bacteria that can colonize the human digestive tract. As persistence of AR genes in the absence of antibiotic selective pressure has been observed, it seems that some AR bacteria might have a fitness advantage over wild-type strains. Thus, in evolutionary terms, reducing the exposure to antibiotics would not solve the problem (at least not in the short term) because the AR phenotype and the compensatory mutations associated are part of the evolution (compensatory evolution) of bacteria. 

Having this in mind, the most prudent preventive measure is maintaining a healthy immune system and gut microbiota via nutrition. Competition among bacterial populations is an important aspect of pathogen colonization. In this way, dysbiosis contributes to the establishment of pathogenic colonies in the gut. Avoiding any exposure to environmental pathogens is a double edge sword: you are avoiding the bad ones but also the good ones. 

ResearchBlogging.orgWang HH, Manuzon M, Lehman M, Wan K, Luo H, Wittum TE, Yousef A, & Bakaletz LO (2006). Food commensal microbes as a potentially important avenue in transmitting antibiotic resistance genes. FEMS microbiology letters, 254 (2), 226-31 PMID: 16445749


  1. Hi Lucas,

    Regarding your old post on ketogenic diet and microbiota, why do you think bifidobacterium decreased on low carb? I would generally guess this is a negative...?

  2. Hi john,

    Im writing a post on the subject.