It is vitally important for producers to monitor outcomes of clinical mastitis and for veterinarians to be involved in developing and evaluating treatment protocols for clinical mastitis, but the ability to assess the results of treatment is often limited because of inadequate records.
Control of mastitis caused by Streptococcus agalactiae and Staphylococcus aureus has resulted in reductions in bulk tank somatic cell count (SCC) but many herds continue to struggle with treatment of clinical mastitis caused by environmental pathogens, says Pamela L. Ruegg, DVM, MPVM, Dipl. ABVP, University of Wisconsin, Madison.
Common environmental mastitis pathogens include both Gram negative bacteria (such as E. coli and Klebsiella spp.) and Gram positive bacteria (such as Streptococcus uberis and Streptococcus dysgalactiae). The immune response successfully eliminates some environmental pathogens (such as mostE. coli) after a brief period of mild clinical disease, Ruegg explains. Other environmental pathogens (such as Streptococci spp.) have become more host adapted and may present as mild clinical cases that erroneously appear to resolve when the case has actually returned to a subclinical state. Ruegg says both of these scenarios make it very difficult for the producers and veterinarians to discern success of mastitis treatments.
“Producers usually look simply at clinical cures, but this can be misleading because in most cases of mild or moderate mastitis, milk will return to normal about four to six days after the case begins (with or without treatment),” says Ruegg.
She believes that we also need to evaluate treatments based on economic outcomes such as:
Recurrence of mastitis in the same cow (should be <20% of cows)
Return of somatic cell counts to levels <200,000 cells/ml (within two months)
Retention of the cow within the herd (not culled within 60 days of mastitis event)
Return to normal milk yield with no loss of quarter.
Ruegg says it’s a common misperception that producers and even veterinarians can have that when clinical mastitis signs abate that it means the quarter has been cured (see sidebar). “Many Gram positive mastitis pathogens are host-adapted and cause long periods of subclinical infection which are demonstrated by high somatic cell counts,” Ruegg notes. “These infections often develop into short-term mild clinical symptoms that appear to be cured when the milk returns to a normal state but in many cases the infection has simply returned to a subclinical state.”
Subclinical mastitis infections can be difficult to diagnose and there is no sure way to identify them. “In the short run, it is hard to determine if the cow is cured and I don’t recommend determining when to stop treatment based on tests such as the California Mastitis Test (CMT),” Ruegg says. “The somatic cells are part of the immune response of the cow and the SCC will gradually drop and should be <200,000 cells/ml if bacteriological cure has occurred by about three to six weeks post-treatment.” Ruegg adds that mastitis caused by Gram negative pathogens often stimulates a large and successful immune response that rapidly clears the pathogens and the SCC may fall below 200,000 cells/ml faster than for Gram positive pathogens.
Bacteriological cure rates are generally used in research studies to assess treatment efficacy but very few producers or veterinarians evaluate bacterial clearance of pathogen from an affected gland, Ruegg says. The ability to achieve a bacteriological cure depends on the pathogen type, case severity, variation in immune response among cows, efficacy of the treatment protocol and the promptness of initiating treatment.
Cow age and treatment response
Treatment response is not just a bug-drug interaction.The complexities of the cow’s immune status as well as her age can also have an effect. Older cattle have a greater risk of both subclinical and clinical mastitis, and poorer responses to treatment compared to younger cattle. “The influence of the cow on response to treatment doesn’t seem to be well recognized probably because treatment records on many farms are incomplete,” Ruegg says. “Veterinarians need to teach producers to check the history of cows before they begin treatment and devise treatment protocols that take into account the information that is available.”
For example, she says, bacteriological cure rates have been shown to decline with parity; perhaps longer duration therapy is appropriate for a cow experiencing her second clinical case or for an older cow with a history of two to three months of high SCC. “We also need to make sure that cows are not treated inappropriately. Cows with long histories of repeated clinical cases are not good candidates for treatment,” she says.
Training farmers to review mastitis records before treating is an important role of the herd veterinarian, Ruegg states. “It is very common for me to find cows that have been treated repeatedly and that have a history of chronically increased SCC, even over the course of a couple of lactations. If the SCC of a treated cow remains increased for months and the cow has recurrent mild cases of mastitis, it is very important to determine the pathogen and then make some hard decisions.”
Ruegg explains that these potential decisions include:
Targeting treatment — right drug, right duration
Drying off a quarter that has shown that is will not cure
Culling the cow
Making a no further treatment decision — simply deciding that future cases will be dealt with by milk discard only.
Mastitis is caused by a diverse group of bacteria and the probability of cure is highly influenced by the characteristics of the pathogen. “Ideally, we need to know the pathogen before we initiate treatment or at least soon after treatment is initiated so that we can adjust our therapy accordingly,” Ruegg advises. “The reason that this is so important now, is because mastitis is caused by a much more diverse set of pathogens as compared to 10–15 years ago. When I started as a young veterinarian, most mastitis was often caused by Staph. aureus, some Strep. ag and E. coli.”
Today, she says, clinical mastitis caused by Staph. aureus and Strep. ag are rare on most modern dairy farms. “Herds that use biosolids for bedding often expose teats to a very diverse microflora and a wide variety of pathogens may cause mastitis on many of these farms,” she explains. “Combining pathogen identification with information about the cow such as age or history of previous cases can be used to make important decisions about the need for antibiotic treatment or the appropriate duration of treatment.”
We need to start educating farmers about the differences in mastitis cases, Ruegg adds. “Treatment protocols need to be developed based on the probability of success and we need to help farmers recognize how to evaluate if their protocols are working.”
It’s common to treat first and get a diagnosis later, if one is obtained at all. Even if a diagnosis is not immediately available, Ruegg says producers can submit milk samples to labs for rapid provisional diagnosis and then readjust therapy when the pathogen is diagnosed 24–48 hours after beginning treatment. Ruegg believes this is the direction that we need to move but right now she doesn’t think this is happening enough.
“For example, a first lactation cow that is about 150 days in milk and diagnosed with her first case of mild mastitis caused by E. coli probably doesn’t require any antimicrobial treatment, but if the mastitis was caused by coagulase-negative Staph. (CNS), two days of intramammary therapy would probably be sufficient. While we need more clinical trials, based on the limited evidence that I have seen, five days of therapy may be appropriate for mastitis caused by environmental streptococci.”
Ruegg says if the cow had developed mastitis caused byStaph. aureus, she would recommend eight days of intramammary therapy. “While this scenario seems complicated, targeted intramammary therapy can result in big savings and better treatment outcomes, especially for large dairy farms.”
Giving antibiotics to cows that won’t respond is both a waste of money and an unnecessary potential introduction of the compounds into the dairy food production system, Ruegg says. “On most dairy farms, the vast majority of antimicrobial treatments are administered for treatment of mastitis. We need to ensure that we are using drugs properly. The use of extended duration therapies should be targeted at cows that are likely to benefit, for example, a new Staph. aureus case in a young cow or perhaps a third lactation cow with an environmental strep infection in the first week of calving (during the period of peripartum immune depression).” Ruegg says when extended duration therapy is routinely used for all cases without regard to causative pathogen, considerable milk will be discarded unnecessarily.
One age-old treatment that many veterinarians and producers use but that has no scientific data to support it is frequent milking/oxytocin administration for mastitis. “We were all taught to do this when we were in veterinary school and somehow it just feels like the right thing to do, even though the data doesn’t indicate that the practice improves any outcomes,” Ruegg says. “Based on the research data, I don’t recommend it, but it probably doesn’t hurt and does encourage the farm personnel to observe the cow more frequently.”
Clinical vs. bacteriologic cure
Pam Ruegg, DVM, MPVM, Dipl. ABVP, outlines the difference between clinical and bacteriologic cure of mastitis:
Clinical cure is usually defined by the return of abnormally appearing milk to normal appearance. The defini-
tion would also include the recovery of other clinical symptoms such as decreased swelling of the udder, reduced milk yield or decreased temperature and increased appetite.
Bacteriologic cure is often defined as the absence of bacteria from milk samples obtained at some point after treatment has been completed. Different time periods after treatment are used by different researchers but the milk samples are usually collected around 14–21 days after treatment has ended.