The material that follows is taken from an interview with John Mayer, DVM, Midlands Consulting, Omaha, NE.
Mayer: Our primary method is postmortem examination, with virus isolation and bacterial culture. We also collect swabs of nasal secretions from groups of live cattle – both normal animals and those that are visibly sick, so we have a basis for comparison. Unfortunately, results from both of these methods are obtained after the disease process is well underway.
The real value of the results is that they provide data on the organisms present in animals from various origins, of various ages, arriving in the feedlot at various times of the year, and in various conditions. With that data we can identify trends, which are subsequently helpful in controlling disease.
The poultry industry has a great advantage over the cattle industry in diagnosing causative agents. When poultry producers are faced with an outbreak, they can immediately sacrifice and necropsy a sample of the flock without incurring financial setback or alarming customers. The cattle industry, particularly custom feeders, obviously can’t do that. So, we gather as much data as possible and apply it to future circumstances.
Mayer: We place all incoming cattle into two categories, low risk and high risk, based on the factors above and others. For example, we also consider whether an animal is direct from the ranch or has been through a sale barn, whether or not a calf was weaned before shipping, whether or not the animal was vaccinated before weaning and/or shipping, the length of the haul, the degree of shrink, the degree of commingling, and so on. Actually, the list can become quite lengthy, which means it’s never a black-and-white determination; animals can arrive with a combination of low and high risk factors.
Risk Factors in Incoming Cattle
|Low Risk||High Risk||High Risk|
|Direct from ranch||From sale barn/order buyer||From sale barn/order buyer|
|Vaccinated before weaning||Not vaccinated before weaning||Not vaccinated before weaning|
|Weaned before shipping||Not weaned before shipping||Not weaned before shipping|
|Low commingling||High commingling||High commingling|
|Short haul||Long haul||Long haul|
We use these categories to adjust our arrival processing routine. For example, we place low-risk cattle in their home pens as quickly as possible, while we spend more time observing and evaluating high-risk cattle. In some circumstances we may selectively mass medicate.
Mayer: Probably the greatest variable in susceptibility is the immune status of the individual animal. Under what are apparently identical circumstances, some will get sick while some won’t. And some sick ones will recover while some will die.
There’s no question that the healthiest, most resistant calves come from cows in good health, with a solid vaccination record, and which have been provided ample colostral antibodies. Also, cattle that have had the opportunity to develop their own active immunity – either through exposure or vaccination – before shipment are much less susceptible to respiratory disease in the feedlot
Mayer: The most prevalent cause is neither viruses nor bacteria. It’s management; it’s the facts of life in cattle feeding.
Many bacteria and some viruses are normal inhabitants of the bovine respiratory tract. They exist there without causing any problems until they have an opportunity to grow. Those opportunities come in the form of stress – weaning, shipping, commingling, handling, weather, change in feedstuffs, change in weather, or exposure to a new environment, which suppresses the immune system. Some of those stressors we can control, and some are simply inherent in the logistics of cattle feeding.
As regards organisms, infectious bovine rhinotracheitis (IBR) virus and bovine viral diarrhea virus (BVDV) are the most prevalent viral invaders, and Mannheimia haemolytica is the most prevalent bacteria found in live animals.
Most diagnoses, however, are made on dead animals. These generally are cattle that have been treated a number of times without response, and identifying the causative agent is difficult at best, particularly if the disease process is well advanced.
At necropsy we may see lesions that look like typical Pasteurella, but we know that something – probably a virus – preceded that infection; numerous experiments, for example, have shown that severe M. haemolytica challenge doesn’t produce disease without prior viral challenge. So, we see what looks like Pasteurella lesions, and we are able to culture Pasteurella from the lesions, but we may not be able to isolate any virus because the animal’s fever response has limited the virus’ replication. In addition, the further we are into the disease process, the more types of bacteria are likely to be present. Then, the fact that the animal has been treated with antibiotics skews the findings of the diagnostic laboratory’s sensitivity testing.
What this all adds up to is that we are quite unlikely to identify the original cause of the disease. All we are likely to identify is the opportunistic organisms that invaded after the initial infection was established. Actinobacillus pyogenes, for example, is virtually always found in lung abscesses and fluids, but it’s rarely if ever considered a primary cause of BRD.
Mayer: Yes, definitely. I’d say 100 percent of BRD outbreaks are multi-organism infections, established by viral invasion and complicated by bacteria, with more bacteria invading as the disease advances.
Viruses damage the upper airways and compromise the action of the cilia, which are responsible for sweeping particles of all kinds – bacteria, dust, mold, pollen, and so on – up and away from the lungs. This lack of ciliary clearance creates sort of an open house situation for growth of the respiratory tracts’ normal bacteria as well as bacteria transmitted from other animals. Different serotypes of a single organism, such as M. haemolytica type 1A versus 2A, also can become involved.
Mayer: It depends on how you define pathogenicity.
In my mind, BVD virus may be the most pathogenic because of its immunosuppressive nature. An animal infected with BVD virus is particularly vulnerable to other viruses as well as bacterial infection. And to make matters worse, that animal may not be helped by antibiotics. Antibiotics alone can’t cure bacterial disease, especially if it’s well established. The antibiotic must work in conjunction with a healthy immune system to clear the infection.
The same is true of vaccination. We tend to equate vaccination with immunity, but a compromised immune system can’t respond to vaccination. Even a healthy immune system is merely primed by vaccination. In the event of disease challenge, it still has to go to work.
IBR virus is a major problem because of its pervasiveness. As I mentioned earlier, the vast majority of BRD is initiated by a viral infection. And since IBR virus is so prevalent, we can be fairly confident that it plays a primary role in the BRD complex.
M. haemolytica is probably the most pathogenic organism from a strictly histopathological standpoint. It causes severe, explosive lesions which can spread through the lungs overnight. I consider it the primary bacterial agent in the true shipping fever BRD we see early in the feeding period.
M. multocida also is quite pathogenic in that it appears later in the course of infection and may be the straw that breaks the camel’s back, so to speak. P. multocida also occurs – often without P. haemolytica – late in the feeding period and in yearling-type cattle. This ability to infect what are generally considered lower-risk cattle suggests P. multocida may be more pathogenic in these older animals.
So, it’s not easy to say that any one organism is worse, or more pathogenic, than another, because they all are intertwined in the incidence of BRD.
Mayer: Yes. Control stress. Vaccinate early. And when treatment is needed, start early and use a broad-spectrum antibiotic.
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