Bovine biology series
Part - 37 Mammary gland (3/5)
We continue with this third installment of the subseries of five lessons on the mammary gland.
In our first installment, we learned how the udder is developed from rudimentary tissue into a secreting gland. In the second lesson, we described the fully developed udder, its suspension, blood flow and histological features of individual macro components of the udder and teats.
In this installment we learn about disease of the tissue.
I learned in college that mastitis is a term that refers to inflammation of the udder tissues. But, I learned as a youngster very quickly that when a cow came through the milking parlor with an udder or quarter that was injured, swollen, red, or hard, that the milk inside could not go in the milk tank.
I also learned that treating this particular cow was a wholly useless endeavor in almost all cases. Other than dry treating cows in mass, shoving a lactating tube of antibiotic into the end of a teat did not help much.
Early recollections of these sick cows pointed toward some sort of spontaneous recovery, as if the cow herself decided whether or not to get better. I knew nothing about the immune system and very little about microbiology.
I do recall we sold almost all of these cows, unless they got better quickly, we culled them out of the herd.
What has changed in the subsequent thirty years?
Not much, except that our understanding of mastitis has reached a point where we can scientifically explain it better, control it easier, and deal with its consequences more readily.
The basis of udder disease is the presence of microbes, the type that we may describe as pathogenic and disease causing. They elicit an immune response that is measured as increasing numbers of somatic cells that show up in tissue that has been injured by the pathogen bacteria or the by-products of their cellular metabolism.
That inflammation is a part of the natural response mechanism in udder tissue that has, or is undergoing pathogenic bacterial trauma, which is sometimes overlooked. That is, the cow is healthy. For if she did not elicit this inflammatory response with the concurrent immune response of white blood cells - somatic cells, then she would be overwhelmed quickly by these pathogens. The numbers of pathogenic bacteria would increase exponentially; their by-products, usually toxic to a cell, would infiltrate the bloodstream. Blood sepsis would result, and blood septicemia would rapidly become systemic. Death would come soon, within hours or days depending upon the degree of virulence.
Epidemiology is the science of the factors that determine the frequency and distribution of a particular disease, like mastitis.
The epidemiology of mastitis in the bovine and in all mammals is quite simple. Infection, the onset of tissue trauma, occurs when bacteria gain access to the udder tissue through the teat opening, the teat canal, and the teat end.
These bacteria can be divided into two classes: the environmental organisms found almost everywhere in the environment, such as E. coli, Strep uberis, and Pseudomonus species, and the dreaded contagious pathogens, Streptococcus agalactiae and Staphylococcus aureus.
In further defining the epidemiological characteristics of an individual case of mastitis, two factors are involved:
1. The bacterial characteristics, which include the pathogen's ability to survive in the cows' environment, ability to live on the teat end, the ability to gain access and colonize udder tissue, and once there, its ability to set up a mastitic reaction. Also, the ability to survive antibiotic therapy is critical so that we may design a strategy for its control.
2. The transmission characteristics include the sheer numbers measured in the millions or billions per unit space, including the udder tissue itself, efficiency of the humanly controlled part of management, such as milking protocol, free stall management and overall herd environmental hygiene.
Most important is the cows' susceptibility when confronted with the pathogen, such as her age, stage of lactation, level of inherited resistance (related to the size of the udder, the shape of the teat and the size of the physical opening of the teat end). Finally, let us keep in mind that it is important that the cow herself is healthy so that, as I learned at a young age, a healthy cow seems to overcome the disease and recover if the virulence of the pathogen (bacterial characteristics) is not overwhelming and is able to rise up against this pathogen with inflammation and immune system originated somatic cells that quickly and efficiently negate and remove this pathogen. In other words, she is able to recover on her own.
The pathogenesis, or the mechanism by which mammary disease is produced, is namely in three parts: infection of the mammary gland always begins via the teat end, what may be called the invasion of pathogenic bacteria.
The invasion phase is most influenced by the sheer numbers of bacteria presented to the teat end of which its health and physical size are determinants in whether or not these pathogens will gain access. This description, then, is the first line of defense. We know that we help the cause in dipping the cows teat in a substance like iodine so that in spite of the numbers, we can kill some of them.
Just as influential is the overall health of the teat end in the invasion phase. The ability of the teat end sphincter to close quickly after milking, and the presence of keratin immediately inside the teat opening dictate invasion resistance.
We cannot forget the influence of the milking machine, of liner slips, vacuum fluctuations, pulsator efficiency and reverse gradients propelling contaminated milk (from wet udders) into the udder itself during milking.
What follows is the infection period, in which prior to any of the cows' internal response mechanisms,
i. e. the immune system, the bacteria multiply in numbers, spreading their cells and toxins throughout the infected tissue since there is nothing to stop them (depending upon individual bacterial characteristics, of course).
Within some cows, there are already circulating in the bloodstream some natural protective cells as born out of the immune system from a previously dealt with pathogen. This protection, similar or adjacent to vaccination, can ward off the onset of infection because the fighting machinery is already in place.
Finally, once the invasion phase has been won and an infection is established, the cow responds with inflammation. Swelling, redness, hardness, and obviously a secretion that is not milk is produced.
Inflammation, or the degree of it, runs the gamut from extreme overt signs, to minimal and subclinical trauma.
The secretions from an inflamed quarter, once identified, can be cultured so that the causative pathogen can be identified. The lab culture is the standard by which progress is made in controlling the onset of further invasions, as well as hoping to find an answer to the riddle: what caused this infection and what may I use to reduce or eliminate it in this particular cow? Such is the definition of clinical pathology, the diagnosis and control of mastitis.
At the farm level is the valuable California Mastitis Test. This subjective cowside test prompts the herd owner or manager to examine suspect quarters more objectively, via an aseptically taken sample for clinical laboratory analysis. We know that a bulk tank culture is obligatory in monitoring contagious pathogens, and helps point us in the right direction in improving the housing, milking and teat dip aspects of herd and cow management.
If we have learned anything over the decades since milking machines have been used to milk cows, it is that in the case of mastitis, prevention is far superior to treatment. So when we examine the three phases of mastitis: invasion, infection, and inflammation; we should endeavor all efforts towards the first one, hope to avoid the second one, and use the final one as a report card so that we can change something by culling or correcting management in order to reduce or prevent the first one from taking place.
Said another way, keep the clean cows clean by preventing mastitis in them, while removing from the herd those who cannot, or will not, respond to total eradication of the disease on their own accord or via human involvement.
A bulk tank culture done routinely is paramount to identifying and tracking pathogens in the milking system, or the flare-ups of contagious pathogens in infected cows. Individual cow monitoring at the time of calving using a strip cup and CMT paddle test serves as a screen for further culturing via laboratory or clearing the cow for the pipeline.
Free stall management has been discussed so many times already so I'll skip that here, as well as milking management. We have moved away from milking wet cows, for the most part, and we have much better vacuum controllers now that stabilize milking negative pressure. Liner slips are overtly noticed and the bulk of them are not.....I suspect they continue to cause problems in all systems. We have not designed a milking machine yet that eliminates them. Cow teat shape and the changes of it during the milking out period cannot be stabilized, so liner slips are with us for awhile.
I cannot get into a discussion of milking parlor procedure here without getting into some difficulty. Every herd manager has his or her own idea of what works, especially with regard to stripping, pre-dipping and washing. The order of these, or their role or lack of it in the parlor is individual, so we will leave that alone.
Common sense tells us that milking a clean dry cow is obviously the best way to avoid bacterial contamination of the milking machine and the possible invasion of bacteria into the udder at the time of milking. How we choose to get the cow clean, be it in the free stall barn, in the pasture, or in the milking stall, is less important than the fact that she is clean. Dryness is equally important, avoiding the translocation of bacteria of any kind into the milking liner.
Paper towels or cloth towels serve as an adjunct tool in drying. Cloth towels must be laundered with care, and should be discouraged in herds with contagious mastitic pathogens.
Whereas, in most parlors now, the milking efficiency is measured in terms of cows milked per hour, or pounds accumulated over time. The balance of proper milking procedure must be factored in.
Udder disease, mastitis, inflammation of the mammary gland is the end of the story. Once this point has been reached, the battle is lost. Concentrating on treating out of the lost battle is admitting further losses, usually culminating in hospital strings full of cows.
Paying milkers strictly a bonus for quality milk can drive increases in hospital numbers too. I do not know how to get around this problem.
Prevention is well-grounded in study after study, clearly indicating the obligation of the herd manager to address the invasion phase of udder disease.....working hard to prevent large numbers of potential bacterial invaders from reaching the point of entry....the teat end. Thus, keeping clean cows.....clean.
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