Editor’s note: First of a two-part series on Mycoplasma mastitis. Click here to read the first part: Mycoplasma mastitis: Prevention and control.

It once was considered strictly a “California” disease that only affected very large herds. Now it’s on the rise throughout the country, and may soon be knocking on your own door, if it hasn’t already. What is this “new” disease challenge that actually has been around for decades?  Mycoplasma mastitis.

Veterinarians who have dealt with Mycoplasma first-hand can attest to the dread that accompanies its clinical emergence. One of them who has more than three decades of experience with it is Paul Blackmer, DVM, owner of Veterinarian’s Outlet, Chino, Calif.

Mycoplasma mastitis is a doubly insulting disease,” says Blackmer. “Not only can it be remarkably contagious when it is present, but it absolutely does not respond to antibiotic therapy. In fact, treatment can actually cause epidemics, because it frequently is spread by unsound intramammary therapy practices. It’s a problem that dairy producers must manage their way out of, because they can’t treat their way out.”

Client education required
Blackmer believes that helping clients understand the serious nature of Mycoplasma mastitis is a fundamental obligation of all practicing dairy veterinarians. “Preventing Mycoplasma outbreaks requires consistent adherence to specific management steps, on the part of both the owner and the individuals who manage the cows hands-on,” he states. “Everyone must understand the negative consequences that a breakdown in the system could cause.”

Those consequences can include nonresponsive, clinical mastitis; a dramatic drop in individual-cow milk production; loss of single quarters that can advance to complete cessation of lactation; and – worst of all – rampant spread of clinical mastitis from cow to cow. 

What’s more, the mammary system isn’t the only area that can be affected by Mycoplasma, according to Mark Wustenberg, DVM, Technical Services Specialist, Monsanto Dairy, Bay City, Ore. A former practicing veterinarian who focused heavily on milk quality, Wustenberg says respiratory disease and/or arthritis also can plague Mycoplasma-infected animals – usually heifers. 

The outlook becomes even grimmer when the effect of the disease on calves is weighed. “Calves that are fed Mycoplasma-infected milk can contract inner ear and respiratory infections, swollen joints and generalized septicemia that may become active as clinical mastitis upon freshening in first-calf heifers,” says Wustenberg.  (See Case Study 3 on page 46 of this issue).

Just how bad can it get? Within the past year, Blackmer has seen more than one dairy lose over 100 cows to clinical Mycoplasma mastitis in less than a month’s time. “Make no mistake,” says Blackmer, “this disease is a very real threat to the economic and biological stability of a dairy.”

Changing landscape fuels spread
When Mycoplasma mastitis was first identified and diagnosed in the 1960s, clinical cases were confined mostly to the then large-herd dairy states like California and Florida. Blackmer attributes this to the owner-milks-cows versus labor-milks-cows phenomenon. “When herds in most of the country were small enough that the owner did most of the milking, Mycoplasma was kept well in check, because owners tended to identify and deal with problem cows quickly,” he explains. “In larger herds, where employees do the milking and parlor through-put is a major priority, clinical cases can go undetected longer, and breakdowns in standard milking procedures are more likely to happen.”

Allan Britten, DVM, MS, owner of Udder Health Systems, Inc., Bellingham, Wash., says recent consolidation and expansion of herds across the country have created conditions that are ripe for Mycoplasmaa outbreaks. He and the other experts offer these explanations why:

  • Animal stress.  Mycoplasma bacteria – particularly  M. bovis – are endemic to the bovine respiratory and reproductive tract of many outwardly healthy cows and calves. Clinical experience has shown that Mycoplasma outbreaks occur most frequently during times of stress, such as calving, extreme weather shifts and periods of commingling with new animals. It is believed that the opportunistic organism takes hold when cows’ immune systems are compromised. Plus, overcrowding increases the likelihood that Mycoplasma bacteria could travel from the respiratory or reproductive tract of one animal to the mammary system of another.
  • Animal movement.  Mycoplasma often is introduced when replacement animals – particularly heifers – are commingled into a herd. Heifers are frequent carriers because they often are raised away from the dairy in “high-
    traffic” facilities and commingled with other animals, then shipped to the dairy for freshening. If heifers were fed Mycoplasma-infected milk, there also is the chance that they will harbor systemic Mycoplasma infections that break at calving. “Today there’s almost no such thing as a ‘closed herd,’” says Britten, adding that breeding bulls are another potential source of herd contamination.
  • Milking practices. The principles of good milking hygiene are fundamental to preventing the spread of Mycoplasma from cow-to-cow once a clinical mastitis infection is established. Expansion herds tend to have more problems with milking machine function, teat-end condition, hygienic udder preparation and thorough teat dipping, simply because it takes time for employees to gain experience and for the routines of the larger dairy to start clicking.
  • Hospital management. Start-up and expansion dairies often relegate the hospital to one of the last structures to be completed. This leaves substandard or no facilities for segregating clinical mastitis cows, allowing Mycoplasma-infected animals to spread the infection to their herdmates.

These factors explain why more Mycoplasma cases are creeping into other parts of the country. In Wisconsin alone, the incidence of clinical Mycoplasma mastitis outbreaks has climbed from just two herds in 1992 to 83 herds in 2000, with a total of approximately 319 herd outbreaks during that time span (see Figure 1).  Similarly, herds in the Pacific Northwest (mostly in Washington) have been experiencing a noticeble increase in the presence of Mycoplasma from just 18 positive herds in 1993 to 126 in 2000 (see Figure 2). “It’s not that we just started screeening for Mycoplasma and began to find it,” says Britten. “We’ve been looking for it consistently, and we’re truly seeing more of it.”

“Usually, when a Mycoplasma outbreak occurs, it’s because something has broken in the regular routine,” says Wustenberg. “It takes a while for start-up and expansion dairies to establish routines, which is how Mycoplasma flares up.”

Eliminating one unsound management practice, however, can protect dairies from taking unnecessary risks with the disease. “Infusing anything into the udder from a bottle is almost a guaranteed method of spreading Mycoplasma,” says Wustenberg. “Once a bottle is contaminated, it becomes the perfect reservoir for the organism to proliferate.  Injecting home brews, saline or anything else from a bottle into the udder is a recipe for disaster.”

Blackmer adds that a misguided treatment practice is infusing dexamethasone along with intramammary antibiotic therapy to reduce udder-tissue swelling.  “One complaint we hear frequently about undiagnosed, clinical Mycoplasma cases is that the udder seems full but the milk won’t come out,” he explains. “That’s because it is the blood vessels and supporting structures in the parenchyma – not the milk-storing alveoli – that become inflamed in Mycoplasma infections. The short-term result of this treatment is that the swelling goes down, but accompanying antibiotic therapy is completely ineffective, and the course of the disease remains unchanged. In the meantime, the bottle of dexamethasone often is contaminated with Mycoplasma.  It is an ill-advised and completely irresponsible practice.”

Next issue: Mycoplasma diagnosis, prevention and control.

Mycoplasma outbreak examples

The circumstances that lead to a Mycoplasma mastitis outbreak vary greatly. Following are recent examples of cases observed by Mark Wustenberg, DVM:

  • A herd that switched from teat dipping to teat spraying, resulting in poor coverage of the teats with disinfectant.
  • An expansion herd that was having difficulty getting new animals to use the parlor. The milkers shifted their efforts from good udder hygiene to moving cows – which already were affected by commingling and stress – through the parlor.
  • A herd that started using a new teat dip that was difficult to see on the teats, at about the same time that a new batch of heifers was brought in. Teat dipping was sometimes skipped because of the problem with dip color.
  • A herd that was diluting medi-cation with hypertonic saline and then infusing it intramammarily. 


The story of the organisms that cause Mycoplasma mastitis continues to unfold, via research and clinical impressions. Following is a summary of what is currently known about the bugs and the infections they cause.

  • Mycoplasma mastitis was first reported in the United States in New York in 1962. Much of the early research on the disease was performed by D.E. Jasper at Cornell University.
  • There are at least nine strains of Mycoplasma that have been isolated from milk. Not all are pathogenic for mastitis:
    • Mycoplasma alkalescens
    • Mycoplasma agrinini
    • Mycoplasma bovigenitalium
    • Mycoplasma bovirhinis
    • Mycoplasma bovis (responsible for 50% or more of Mycoplasma mastitis infections)
    • Mycoplasma californicum
    • Mycoplasma canadense
    • Mycoplasma capricolum
    • Untypeable Mycoplasma
  • Mycoplasma organisms have no protective cell walls and minimal genetic material. They are resistant to antibiotics in clinically infected cows. It appears that the organisms are capable of rapidly changing their surface proteins. An animal’s immune system targets disease-causing bacteria for destruction by locking onto the shape and size of the bacteria’s surface structures. In the case of Mycoplasma, these structures keep changing, the immune system is confused and the organisms escape.
  • Infected animals are the single most important reservoir of Mycoplasma species that cause mastitis.
  • Herds with and without clinical Mycoplasma mastitis may include both young and mature asymptomatic carriers. The organism may be shed in nasal discharges of calves and vaginal discharges of heifers at calving.
  • Mycoplasma bacteria are capable of surviving (but not growing) in milk (60 days), air, manure (236 days), urine, feed, straw, water, etc.
  • It has been shown that the vaginal discharges and urine of cows after calving are greatly contaminated with several Mycoplasma species.  Milking teats contaminated with vaginal discharges and urine could likely lead to clinical mastitis.
  • Once established in the milking herd, infections are most often spread during milking or mastitis cannula infusion. 
  • Intermittent shedding by asymptomatic carriers may interfere with the accuracy of screening milk from incoming animals.
  • Cows of all ages and at any stage of lactation are susceptible to Mycoplasma mastitis infections. However, cows in early lactation seem to suffer more frequently and severely because the infection may be enhanced by existing inflammatory processes in fresh-cow udders. Clinical signs include:
    • Sudden onset of edematous swelling of the udder.
    • Severe clinical mastitis that resists treatment, but produces little other effect on the cow. Affected animals continue to eat and drink normally, although the udder tissue may be painful.
    • Involvement of more than one quarter and up to all four.
    • A marked drop in milk production and increase in individual SCC.
    • Abnormal udder secretions that may vary from watery milk with a few clots to a thick, purulent material in advanced cases. Acutely infected cows may show a tannish secretion with sandy or flaky sediments that resemble cooked cereal in a whey-like fluid. Udder secretions may become purulent and last for several weeks.
    • Swollen, meaty udders that do not involute properly during milking.
  • In most cases, infections become established via invasion of the mammary system through the teat orifice. The exception to this may be systemically infected heifers that were infected as calves.
  • From 10 to 50% of cows may return to a high level of milk production after surviving clinical Mycoplasmaa mastitis during a previous lactation but may continue to be intermittent shedders of Mycoplasma organisms in their milk for the rest of their productive lives.
  • Lameness due to an arthritis caused by the presence of Mycoplasma in the hocks and fetlocks of mastitic and non-mastitic cows is frequently seen in infected herds. Arthritic involvement indicates probable long-term presence of the bacteria in the animal.
  • The organism is very sensitive to the pH changes in milk. Best recovery rates are achieved when fresh milk samples are delivered to the lab and plated soon after collection. However, samples also can be refrigerated for up to three days, and freezing milk samples does not interfere appreciably with the ability to culture Mycoplasma.
  • It appears that any germicide that effectively controls Staph. aureus will control Mycoplasma. Because iodine disinfectants and sanitizers appear to be the most effective against both Staph. aureus and Mycoplasma organisms, it is recommended that iodine be the sanitizer of choice in a Mycoplasma outbreak.


    Bushnell, R.B. (July 1984). Mycoplasma Mastitis. Symposium on Bovine Mastitis, Veterinary Clinics of North America: Large Animal Practice 6:2.
    Gonzalez, R.N. (1996). Mycoplasma Mastitis in Dairy Cattle: If Ignored, It Can Be a Costly Drain on the Milk Producer. National Mastitis Council Regional Meeting Proceedings 37-44.
    Kirk, J.N., & Lauerman, L.H. (April 1994) Mycoplasma Mastitis in Dairy Cows. Compendium of Clinical Education in Veterinary Medicine 16:4.
    Kirk, J.N. Mycoplasma Mastitis: Overview. University of California-Davis, Veterinary Medicine Extension Service, Veterinary Medicine Teaching and Research Center publication, Tulare, Calif.
    Rosenbusch, R.F. U.S.-Israeli Scientists Target Cattle and Sheep Diseases. Iowa State University Office of Biotechnology publication, Ames, Iowa.