Resistance is Futile (antibiotic resistance)

Very simply put, antibiotics either kill or stop the growth of susceptible bacteria. Antibiotic resistance is the ability of bacteria to escape or neutralize the effects of an antibiotic which is designed to cure (or prevent) infection. When bacteria are able to outwit an antibiotic which previously could control its harmful effects, it is considered resistant.

Bacteria have the ability to adapt rapidly to changes in their environment. They are single-cell organisms with few genes, so even one small, random mutation may prove extremely important. Bacteria can acquire pieces of DNA that code for resistance from other bacteria, meaning that bacteria can become resistant to many antibiotics because of the transfer of just one piece of DNA. Every time an antibiotic is used, sensitive bacteria are killed, but a few resistant cells may be left to grow and multiply. And because bacteria can reproduce rapidly, they can evolve rapidly. Any mutation that helps them outwit an antibiotic can quickly become the dominant strain in the bacterial population. Not only the target bacteria is exposed to antibiotics when a sick animal is treated. Most of the normal flora which are either helpful or harmless to the host animal will be exposed to any antibiotic drugs used. So these “innocent bystanders” also have the opportunity to develop resistance. Thus, exposure to antibiotics provides selective pressure, making any surviving bacteria more likely to be resistant.

At the same time that more kinds of bacteria are becoming resistant, multiple-drug resistance is also increasing. Approximately 30% of infections caused by streptococcus pneumoniae (including pneumonia, meningitis, etc.) are resistant to penicillin. In the 1970s, virtually all were susceptible to penicillin. Diseases we once believed we could eradicate, such as tuberculosis and gonorrhea, are alive, well, and increasingly resistant to antibiotics. Many other infections which are not as well-documented (because they are not considered public health risks), like inner-ear infections and urinary tract infections, are now routinely caused by resistant bacteria.

Because all antibiotic use—whether for humans or animals— clearly contributes to increasingly widespread resistance, the WHO, CDC, FDA, and USDA have programs to monitor the spread of antibiotic resistance and to decrease the overuse of antibiotics. About half of all antibiotics produced in the United States are used to treat animals, and the majority of these are used in poultry and livestock production. The AMA, American Society for Microbiology, and American Public Health Association have all called for a ban on nontherapeutic use of antibiotics in food animals. Lobbies for the food and pharmaceutical producers are so adept at challenging any attempt at restriction, though, that when the FDA proposed to eliminate all fluoroquinolone use in poultry production, it took five years before they were able to put the ban in place.

Scrutiny of the relationship between antibiotic use in companion animals and the spread of resistance is fairly recent. It has becomes apparent that companion animals can serve as a potential reservoir for antibiotic-resistant zoonoses (diseases that can be transmitted from man to animals). There are well-documented cases in which companion animals have become infected with resistant strains of bacteria acquired from humans, and vice versa. These cases include a resistant strain of e. coli spread from a dog to its owner, and cases of MRSA, a resistant staph infection, spread from owners to dogs, horses, and cats.

In the last few years, the AVMA, ACVIM, AAHA, CVMA (Canada), BSAVA (Britain), and FVE (Europe) have all developed formal statements concerning the ‘prudent use’ of antibiotics. These documents provide advice on minimizing the development and spread of resistant bacteria in veterinary medicine. Suggestions include parameters for duration of use, optimal dosing, selecting the narrowest-spectrum antibiotic, culture/susceptibility testing recommendation, and ethical use of “extra-label” antibiotics.

Many of the largest veterinary hospitals have initiated their own guidelines for using antibiotics. Drugs are classified as fi rst choice (amoxicillin, first generation cephalosporins, etc.), which can be used empirically; second choice (fluoroquinolones, second and third generation cephalosporins, etc.), drugs which must be justifi ed by culture and susceptibility testing; and last choice antibiotics (vancomycin, etc.) which require culture/susceptibility testing and consultation with an infectious disease specialist.

Why is this so important for us to understand, and is there anything we can do to help stop the rise of bacterial resistance? First of all, make sure you always complete the course of antibiotics prescribed for your wolfhound and for yourself, too. Ask for culture/susceptibility testing whenever practical. Be aware that although still very rare, resistant strains of staph, like MRSA, can be transferred between humans and companion animals. Both humans and domestic animals can be carriers without showing overt signs of disease. There is doubtless more transfer of bacteria (both resistant and non-resistant) between us and the animals we share our homes wtith—it just hasn’t been documented. Lastly, don’t be surprised if your veterinarian is reluctant to prescribe anything but first-choice antibiotics for your IW without insisting on tests.

In our quick-fix society, it’s so easy to reach for a pill without thinking about the consequences. Antibiotics were arguably the biggest medical breakthrough of the twentieth century. What if the marvel of the twentieth century no longer works for us in the twenty-first? What a tragedy that would be.