Chronic Pneumonia in Feeder Calves? Thank Mycoplasma Bovis

 

In this era of advanced vaccine technology and long-acting, expensive, powerful antibiotics, why do chronic pneumonia cases (“chronics”, “lungers”, “railers”) continue to occur? Mycoplasma bovis is considered the bacterial pathogen most often responsible for the development of chronic pneumonia in feeder operations. While Mannheimia haemolytica causes the dramatic pneumonia signs of fever, depression, appetite loss and rapid death, Mycoplasma bovis (M. bovis) is the underlying problem that continues to send calves back to the treatment pen. The organism has several unique survival mechanisms allowing it to dodge the immune system and suppress the calf’s normal response to disease. Once it establishes infection in the lungs, it can travel in the bloodstream to joints, organs, and nerves. These calves generally stay relatively alert with a fair appetite and are seldom pulled quickly for treatment. It may take 7-14 days after the lungs are severely affected before a calf shows dramatic clinical signs and, by that time, permanent damage has already occurred. In the absence of consistently effective vaccines, management practices and prompt treatment are crucial to controlling Mycoplasma pneumonia. Because the disease is spread by close and repeated contact, improving ventilation, sanitation and reducing stocking density will disrupt the spread of Mycoplasma. The two most important factors in the treatment of Mycoplasma pneumonia are early recognition and prolonged therapy. Metaphylaxis, where treatment is applied to the whole group (either on arrival or once 10-20 % of the calves are showing clinical signs of bovine respiratory disease or “BRD”), is one way to get an early start on Mycoplasma. Continuous therapeutic levels of effective antibiotics for 10 to 14 days are necessary because, without this, 30 to 70% of the calves will relapse, causing more lung damage, and requiring further treatment.

 

Traditionally, Mycoplasma bovis was considered normal bacteria in the nasal passages of healthy calves but with stress such as transportation and commingling, it descended into the lungs and spread throughout the body causing disease. However, recent studies found the M. bovis observed during BRD outbreaks are often due to calf-to-calf transmission of one strain among the cattle. Infection is widespread once cattle reach a feedlot situation; after 2 weeks on feed studies found 40-100% of calves will carry the organism. The disease is spread by close and repeated contact with nasal secretions of infected calves, especially in areas with poor ventilation and overcrowded facilities. The source of the M. bovis clones that spread among pen mates is either newly purchased calves or chronic calves housed in neighboring pens. There is evidence that transportation and other stressors (such as weaning, commingling, or extreme weather) increases shedding and therefore spread of the organism. Historically, the environment (watering troughs, feed bunks, bedding, old round bales of hay) has not been considered a major risk factor for spread of disease but new evidence has shown that M. bovis can persist longer under cool, damp, shaded conditions than previously thought and can be an important source of the organism.

 

There are no early clinical signs that indicate Mycoplasma is a problem at first treatment. Cattle are typically pulled for evaluation and treatment based on one or more of the following signs: depression, separation from the group, lack of rumen fill or “gutted” appearance, cough, excessive nasal discharge and difficult or rapid breathing. Respiratory signs with fever of 104°F or above confirms the diagnosis of BRD. However, certain later clinical signs strongly suggest M. bovis involvement:

1. Late Pneumonia-Usually 3-4 weeks after arrival to the backgrounder/ stocker operation/feedlot or 1-2 weeks after an initial treated case of pneumonia

2. Initially treated as routine case of respiratory disease (BRD) but calf does not respond to antibiotic treatment or suffers repeated relapses of pneumonia after antibiotic therapy.

3. Moderate fever/ Occasional cough

4. Development of lameness with swelling and pain in one or more joints, commonly the stifle, carpus (“knee”), hock and elbow may occur in 15-50% of cases. Some cases of pneumonia appear to respond to therapy but develop lameness without reappearance of the respiratory component.

5. Extreme weight loss (Wasting or “cachectic”)

6. A small percentage develop ear infections with drooped ear that occasionally drain pus.

 

 

Diagnosis of Mycoplasma pneumonia in a live calf is challenging and is based on the history of repeated antibiotic therapy and clinical signs of chronic pneumonia and sometimes arthritis. Only lung fluid removed from the lung via bronchoalveolar lavage can be used for culture or PCR to identify the organism. The diagnosis can be made most reliably at necropsy if Mycoplasma bovis is cultured in an animal with lung lesions as seen in Figure 1. Arthritis is present in 15%-50% of cases with the stifle joint most commonly affected. Mixed lung infections with other disease-causing bacteria such as Mannheimia haemolytica, Pasteurella multocida, and Histophilus somni are common but antibiotic therapy may eliminate these other bacteria that initiated and/or contributed to disease.Response to antibiotic treatment is variable and frequently unrewarding. Mycoplasma organisms have no cell wall and are unaffected by penicillin and other “beta lactams” (Polyflex, Excenel, Excede, Naxcel) that kill bacteria by destroying the cell wall. Currently Draxxin, Baytril and NuflorGold (available by prescription only) are FDA approved to treat Mycoplasma pneumonia. Use of other antibiotics is considered “Extra label” and requires a valid veterinary/client/patient relationship. These antimicrobials provide an opportunity for the host’s immune response to develop and counteract infection, but M. bovis has defense mechanisms that include an ability to vary its surface proteins and to form protective biofilms, making it difficult for antibodies to do their work.