Antibiotics Resistance & Animal Husbandry

I read with interest the poll and associated article in the latest edition of the British Medical Journal, Does adding routine antibiotics to animal feed pose a serious risk to human health (BMJ 2013; 347: f4214). The debate is
very topical given the recent publication of the Chief Medical Officers report on antimicrobial resistance as well as a
Department of Health five year strategy for combating antimicrobial resistance.

The article discusses whether the use of antibiotics in animal husbandry leads to humans acquiring antibiotic resistant bacteria. The argument within the article put forward to support the continuing use of antibiotics in animal husbandry suggests that it is not a problem for humans as animals do not share the same pathogenic bacteria. Although this in itself is debateable, I think it misses a
significant point; humans don’t have to develop an infection with these resistant animal bacteria, for there to be a problem. The organism may not matter, but its resistance mechanism does.

Many of the resistant bacteria we see now in patients have acquired the resistance mechanism from other bacteria; bacteria which do not cause human disease. For example the resistance mechanism of Extended Spectrum Beta-Lactamase (ESBL) positive E. coli originated in a non-pathogenic bacteria Kluyvera (found in soil, water and even
slugs and snails!). It is not the organism that causes the problem but rather the transfer of the resistance genes on a mobile genetic element (in this case a  plasmid – see image) from a non-pathogenic bacteria (Kluyvera) to a pathogenic one (E. coli).

Click for larger image

Another example is the VanA gene transferring Vancomycin resistance to Enterococci. The exact origin of the VanA gene is unclear but it has been proposed that Vancomycin resistance has arisen due to the uncontrolled use of the related drug Avoparcin in the swine industry. The VanA gene is on a different type of mobile genetic element called a transposon (see image above) and has been shown to transfer from Enterococci to Staphylococcus aureus to create a Glycopeptide Resistant  Staphylococcus aureus (GRSA).

So, as a microbiologist am I worried by antibiotic use in animals?

Yes, but for different reasons than in the BMJ article. The media-hype surrounding such a controversial subject detracts from the microbiology behind the real issue. Bacteria can swap antibiotic resistance between themselves and when this appears in a bacteria which can cause human infections “superbugs” are created which are resistant to our current antibiotics.

Bacteria are evolving resistance faster than we can produce new antibiotics. There have been extensive bacteria resistant to the antibiotics within the last 20 years e.g.

• Escherichia coli (Cephalosporin, Gentamicin &
Ciprofloxacin resistance)
• Staphylococcus aureus (Flucloxacillin resistance)
• Enterococcus faecium (Vancomycin resistance)
• Neisseria gonorrhoea (Ciprofloxacin resistance)
• Acinetobacter iwofii (Meropenem resistance)
• Pseudomonas aeruginosa (Meropenem, Ciprofloxacin &
    Gentamicin resistance)
• Streptococcus pneumoniae (Penicillin & Ceftriaxone      resistance)

This list isn’t exhaustive but these bacteria are resistant to 6 of the 16 types of antibiotics available; in contrast there has been only one completely new antibiotic class in the same time period. If we don’t take better care of our antibiotics, we will be back in a pre-antibiotic era where 10% of patients with skin infections and 60% of patients with pneumonia died as no treatment will be available.