Mycoplasma

 

Sick kid: The spring of 2005 we lost a lovely buck kid to sepsis and joint arthritis.  He did not respond to Naxel and our vet at the time did not feel that joint fluid could be easily aspirated and cultured.  We were right in the middle of our move back to Oregon and did not focus on it as well as we should have at the time.  A month or two later another kid, a wether 6 weeks old (not related to the buck) and just castrated, showed similar symptoms:  swollen knees, fever, general malaise, loss of appetite, and a desire to not bear weight (hunched up posture and short steps).  By this time we had a local vet with more small ruminant experience.  She was able to draw a sample of joint fluid and send it for culturing specifically for mycoplasma (that takes about 4 weeks and even longer to identify the species and subspecies).  The kid was put on oxytetracycline (in this case Bio-mycin) and responded well with no further symptoms. He went to a loving pet home. ( Unfortunately he was killed about a year later by a stray dog).

The sample initially read as a streptococcus infection, but finally cultured down to Mycoplasma mycoides, mycoides Large Colony (Mycoplasm m.m. LC).  Following is the excerpt from “Goat Medicine” by Smith and Sherman on Mycoplasma m.m. LC.

” M. mycoides subspecies mycoides (large colony type) has a wide geographic distribution.  It is the most frequently reported caprine mycoplasma infection in the United States, particularly from eastern and western coastal states, and is currently known on all continents except South America and Antarctica.  Kids are more frequently and severely affected than adults.  Though variable, mastitis may affect 25% to 33% of does while morbidity {those that get sick}  and mortality rates may exceed 90% in kids on the same premises.  The most common clinical findings in adults are fever, mastitis, pleuropneumonia, and arthritis.  In kids, arthritis, septicemia, and meningitis are more common.  In addition, polyserositis, osteomyelitis, keratoconjuctivitis, abscesses, and abortion are also reported.  Reports from France, California, and Israel suggest that morbidity and mortality are highest in intensive commercial goat dairy operations.  Economic losses caused by decreased production, diagnosis and treatment costs, and death of replacement stock can be devastating in severe outbreaks.Infected, lactating does can be asymptomatic carriers, with high numbers of organisms being shed in the milk.  These does may become clinically ill themselves as a result of management, nutritional, or climatic stresses.  The most explosive disease outbreaks occur among kids after the onset of kidding season.  The principal mode of transmission to kids is the oral route via daily ingestion of infected colostrum and milk.  The mode of transmission among adults is not as clear.  Direct contact is possible but not very efficient.  Transfer of infection during the milking process by introduction into the teat seems to play a larger role, particularly because improvement of sanitary procedures slows infection rates in known-infected herds.  Infection may be introduced into a herd by the introduction of subclinically infected milking does.

Kids should be separated from dams at birth and fed heat treated colostrum prepared as described earlier in this chapter for control of CAE. Kids should then be housed separately from adults and fed pasteurized milk or milk replacer.  When these kids mature and reach their first lactation, the milk should be cultured and the doelings hand milked until a negative culture allows them to enter the milk string.  Herd-wide milk cultures should be repeated on an annual or semiannual basis until all carrier animals are identified and culled.”

Our culprit: As we had fed mixed milk to all of our kids from the spring (when their moms were having their DHIA milk test), we have to assume that all of those does are now possible carriers.  We had the whole herd’s milk tested for mycoplasma with the results being negative.  This means we have an asymptomatic carrier and intermittent shedder.  In other words, a very tough one to isolate.  However, in looking over our DHIA paperwork for the past year, we found one doe whose somatic count (SCC) spiked at the same time that babies got sick.  We are hoped that this was our culprit and sent her on to a non-breeding pet home, but will be treating the entire herd as possible carriers until years of negative testing prove otherwise.

How can anyone be safe?: It is never possible for anyone to truly guarantee that they have a Mycoplasma free herd.  Since the organism can sit undetected for long periods as well as continuing to live without causing symptoms in its host, there is no way to honestly state that a herd is free of it.  Some countries have even declared themselves “Mycoplasma Free” only to have an outbreak occur at a later time.  Small ruminant practitioners seem to agree that mycoplasmas are the next big concern for goat breeders.  Most also agree that it is likely that more herds are carrying the organism than are aware of it.

This being said, after we were over our initial shock, and with the reassurance from other longtime breeders, we realized that it is not as big of a problem as it initially seemed.  We will have some herd management changes and increased costs in milk testing, but our animals should remain healthy and productive.  So far all of our milk cultures both from the spring and this fall, have tested negative for mycoplasma.  We are practicing “manual backflushing” to sanitized the inflations between does when using the milking machine.  We will continue to randomly test the milk and attempt to isolate a carrier.  If one tests positive, but is an exceptional milker and/or show animals, then we will develop a separate string to isolate them in the milking lineup.

As with so many of these diseases, there is always a risk.  Anytime you buy an outside goat, attend a show, visit a farm, or have someone visit your farm, you are taking a risk.  We all have to weigh these concerns along with the benefits that we achieve by participating in events, adding animals, and interacting with the public and other breeders.  We should do our best to maintain the healthiest herds possible while also participating in bettering the goat world in general.

2006 Update: Our herd has had no other problems since the above.  We continue to bottle raise kids.  We are not doing the manual back-flushing of the milking lines as further study led us to conclude that transmission via this manner was unlikely to be an issue in our case.  Especially since we believe the suspect mom was sent on to a pet home.  Also, conversations with other breeders who have had isolated cases further reinforced the opportunistic behavior of this organism.  Please call or email if you have any further questions on our practices.

2007 Update: We are continuing to bottle raise, but are including raw colostrum and milk from only their own mothers.  When we use mixed milk, then it is pasteurized.  We feel that the benefits of raw milk from our CAE neg. herd out way the possibilities of contracting mycoplasma.  If we find ourselves wrong, at least we will be able to isolate a carrier this way. If you wish your reserved kid to be fed heat treated colostrum and pasteurized milk, please let us know, we are happy to comply.

2008 Update:  We have had no other kids ill with mycoplasma, thank goodness.  We did go back to 100% bottle fed babies (instead of the nursery pen method).  It was just getting too complicated for our size of operation.  Something had to become more simplified!

2008 Later Sping Update:  See Kid Management section top for “Spring 2008 Hybrid method # 2” for our latest kid rearing choice.

http://www.goatwisdom.com/ch8diseases/mycoplasma.html  General Information on Mycoplasma

http://www.invivogen.com/family.php?ID=3&ID_cat=1&ID_sscat=1  New Treatment

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