To many, Mycoplasma bovis is just one of the bacteria associated with bovine respiratory disease complex (BRDC). Compared with other BRDC bacteria such as Histophilus somni or Mannheimia haemolytica, Mycoplasma bovis has some important differences, however.
A big difference is the physical structure of the bacterial cell. Mycoplasma bacteria are considered to be the smallest known organisms capable of dividing on their own. More important to veterinarians and cattle producers is the fact that Mycoplasma organisms do not possess a cell wall. Why is that important? Many common antibiotics, such as penicillin and anything derived from it (e.g. amoxicillin or ampicillin) and the cephalosporins (which include drugs like Excenel® or Excede®) kill bacteria by inhibiting cell wall formation in the new bacteria as they reproduce. As such, these types of antibiotics have no effect on Mycoplasmas.
Mycoplasma bovis is widely distributed throughout feedlot cattle populations. Most calves first encounter the germ before weaning, but if not, they usually become rapidly colonized upon mingling with other calves on their arrival to the feedyard. It only takes about 100 organisms to colonize (become established in) a calf’s nasal passages.
If a very high percentage of feedlot calves are colonized with Mycoplasma, why do some animals become sick from it while others do not?
For most calves, illness from Mycoplasma starts when the bacteria colonizing the nasal passages multiplies rapidly. The major factor that sets this off is stress. Stress – in the form of weaning, long transportation, co-mingling, and adverse weather conditions – increases cortisol in the calf’s bloodstream. This hormone inhibits the immune cells that normally keep bad bacteria confined to the nose. Under the influence of cortisol, 100 Mycoplasma bacteria in the nasal passage can explode to 100 million in just 5 days.
This number of Mycoplasma organisms is now big enough to cause problems. The bacteria move down into the windpipe and larger airways, where they directly damage the ciliated lining of the airways. Cilia are hairlike projections from the respiratory lining cells that sweep out debris and pathogens from the respiratory tract before the germs can damage the lung tissue below.
Once this defense mechanism is out of the picture, Mycoplasma has an easy path to the lung tissue itself. Inflammation in the lungs leads to necrotic areas (areas of tissue death), and now signs of pneumonia in the animal such as increased respiratory rate, cough, and fever are detectable.
The speed at which all this takes place is variable. With heavy bacterial loads and severe prolonged stress, this process can take weeks or sometimes only days. In most cases, however, this bacterial entry into the lungs proceeds more moderately, taking several weeks to cause enough damage to produce clinical signs in the calf. This pace is much slower than that of most other bacterial BRDC pathogens.
Pneumonia is not the end of the story for some calves. For some, the Mycoplasma bovis infection in the lung can seed other parts of the body – a common destination being the joints. The most commonly affected joints are the stifle (knee), carpus, and fetlock. Most of the time, the infection occurs in the tendon sheaths and surrounding tissue, not in the joint space itself. Regardless, swollen, painful joints are the result, often showing up several weeks after a bout of pneumonia.
A droopy or “tipped” ear is another possible sign of Mycoplasma bovis in calves. While it’s more common in dairy calves following Mycoplasma infection through the milk, it shows up in feedlot calves sometimes too. This sign indicates the infection has settled into the inner ear.
The insidious nature of Mycoplasma infections, and their ability to become well-established by the time they’re observed, create challenges for treatment and prevention. That topic is discussed in the article, Mycoplasma Bovis in Feedlot Cattle: Treating and Controlling Infections.