Some believe stress and weather patterns affect transmission and infection. “From the outbreaks I’ve studied with fingerprinting and with multiple outbreak isolates, the thing that strikes me most is that weather and stress seem to be very critical components of every one of these significant high-mortality outbreaks,” says Rosenbusch.
How the immune system responds to Mycoplasma is only partially understood. Rosenbusch says lung lesions are developed long before antibody responses to Mycoplasma are produced. “But, you can also have an antibody response and still produce lesions. In other words, antibody responses are significant in protection, but you also need a cellular component.”
He adds that it is most likely a combination of innate and acquired immunity in the cellular component. “Dr. Simecka at the University of North Texas Health Science Center has a Mycoplasma model in mice, and they have exquisitely delicate ways of measuring and of answering this question. The innate component of the immune response is probably more important than anything else – more important than T-cells, more important than antibodies. Whatever those cells do probably drives whether the animal is going to have lesions or a high Mycoplasma content in the lung. However, that’s in the mouse and I’m not ready to totally extrapolate for the cow, but that’s the only data we have.”
The enzyme-linked immunosorbent assay (ELISA) test shows that all animals will seroconvert when infected with Mycoplasma. “In fact, it would be difficult to find seronegative animals these days because they see Mycoplasma bovis or other Mycoplasmas that look enough like Mycoplasma bovis that there’s going to be cross-reactivity,” says Rosenbusch. “Seronegatives are very hard to find.”
Rosenbusch adds that there is no question that there is a significant immune response to Mycoplasma, but it’s not protective enough to protect the animal from super infection. “Once an animal is exposed to Mycoplasma bovis and runs its clinical or subclinical course, it probably is immune to further clinical forms of Mycoplasma infection, but it is not protected from super-infection with a different strain.”
It’s unknown if there’s cross-reactivity between strains of Mycoplasma bovis. Two problem species common in cattle are M. bovirhinis and M. bovigenitalium, which are usually considered non-pathogenic. “Yet, cattle will mount seroresponses to those two organisms that will be detected as seroresponses to Mycoplasma bovis,” says Rosenbusch. “I don’t consider those animals protected, but I haven’t tested them.”
What this means for immunologic testing is that you may be confident of a seronegative result. “I would say that animal had not seen either Mycoplasma bovis or some other look-alike,” Rosenbusch explains. “But if I see a seropositive, I don’t know what that means. Many things could cause that seropositive. I’m not encouraging any lab to go into serology at this point because it would be a quagmire.”
Serology could be used to find negative animals, however. Paired serology could indicate increases in titers shortly after arrival to determine if an M. bovis-like agent was producing a seroconversion.
What’s confusing is that in the lab, M. bovis is immunosuppressive and actually kills lymphocytes, B-cells, T-cells and all subsets of T-cells. “And yet the animal in the field does not show significant immunosuppression,” says Rosenbusch. “This has been published. You can give a strain-19 Brucella vaccine and infect with M. bovis and have controls not infected with M. bovis. You’ll see a good response to the strain-19 vaccination in both groups. It doesn’t interfere with concurrent vaccination.”
Environmental contamination of Mycoplasma can be exacerbated by housing conditions such as covered feedlots in some areas of the country.