Antibiotics rely on the ability of the animal to contribute to the resolution of infectious disease. To be effective, the antibiotic must be able to inhibit the growth of the pathogen, or kill it, by interacting with a target.
That might be a cell wall protein that leads to the bacteria essentially exploding. Or the target may be the protein factory within the cell — the ribosome. Some of our antibiotics work on the DNA itself, eliminating the ability of the bacteria to manage its genetic code, leading to cell death.
What all antibiotics have in common is the ability of bacteria to develop resistance. This may be from altering the binding site for activity, developing a way to kick the antibiotic back out of the cell (efflux pumps), or possessing an enzyme that inactivates the antibiotic before it can work. Here is a case from last year where laboratory results suggest that resistance was part of the challenge in some new arrivals.
A producer received calves on Nov. 1, and elected to treat them for control of bovine respiratory disease (BRD) with drug A at initial processing. The calves also received a modified-live, five-way viral vaccine and other typical receiving inclusions.
When they started to break about 10 days later, the sick calves were again treated with drug A, and non-responders were treated again with drug B (of the same class as drug A). On Dec. 1, the producer had treated 25% of the calves for BRD. While certainly not desirable, a 25% morbidity rate by itself doesn’t make this case stand out.
What was concerning was that half the treated calves had died: a case fatality rate of 50%. This is higher than observed in untreated controls in almost all of the approval studies for the antibiotics we have on the market today.
To help determine what was going on, a chronically ill calf was humanely euthanized and samples of its lung submitted. After receiving an antibiotic three times as described above, the Mannheimia haemolytica present in this calf was resistant to the antibiotic class that had been repeatedly used on it, as well as several other key antibiotic groups which we use to treat BRD. We can’t say if this was the dominant pathogen at the beginning of this calf’s illness, but what survived the treatments was a multi-drug-resistant pathogen, which most likely was present at the time of initial treatment.
Brian Lubbers and Gregg Hanzlicek, Kansas State University College of Veterinary Medicine, recently published a summary of susceptibility testing results for Mannheimia haemolytica isolates submitted to the Kansas State Diagnostic Laboratory from 2009 to 2011. The percentage of isolates showing resistance to at least three of our respiratory antibiotics were 42%, 46%, and 63%, respectively. Some of these isolates are resistant to five of our main drugs.
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This doesn’t mean that all BRD pathogens are like this, but it does indicate that some cases for which veterinarians submit samples are displaying this pattern. Many of these samples came from treated animals, some of them treated multiple times, and many are from high-risk, commingled calves. I believe the multi-drug-resistant pathogen was very likely part of the population of Mannheimia haemolytica in the calf at the onset of disease.
I recommend producers work closely with their vet to develop a sound strategy for antibiotic use in their cattle, and that you immediately alert him or her when you encounter very poor BRD treatment response and/or a high case fatality rate. I discourage repeated use of an antibiotic class for both the control of BRD at initial processing and first treatment of BRD cases.
Poor treatment response isn’t always due to antibiotic resistance, and switching antibiotics or getting more exotic with combinations is often not the way out. However, your vet can provide testing to determine if antibiotic resistance is part of the problem, and counsel you on treatment strategies.
Mike Apley, DVM, Ph.D., is a professor in clinical sciences at Kansas State University in Manhattan.
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