Can Somatic Cell Counts Get Too Low?


Leo L. Timms

Iowa State University, 4 Kildee Hall, Dairy Science Extension,
Ames, IA 50011-3150 USA
E-mail: ltimms@iastate.edu

Take Home Messages

Somatic cells are white blood cells which function to fight infection and repair tissue damage. Somatic cell levels or numbers in the mammary gland do not reflect the pool of cells which can be recruited from the blood to fight infections. Therefore, a low somatic cell count does not mean that cow's are more susceptible to mastitis. The key to mastitis prevention is healthy cows with healthy cells that can be recruited quickly to fight mastitis battles in the udder when needed.

Introduction

Research and field experience during the last decade has proved that high somatic cell counts (SCC) have a negative effect on milk production/cow, milk processing characteristics, and overall quality and profitability of the dairy industry (1,6,12). Therefore, many producers have successfully strived to lower herd SCC, spurred on by quality premiums from processors. A major question that has arisen from this excellent shift in herd cell counts is "Can SCC be too low?" Better stated, the real question is "Are cows or herds with low cell counts at greater risk to mastitis infections due to lower immunity in the mammary gland?"

What are Somatic Cells?

Somatic cells are white blood cells or body defense cells whose primary functions are to eliminate infections and repair tissue damage. These cells are constantly circulating in the blood stream. When infection, irritation, or damage occurs, the body then sends large quantities of somatic cells to the injured site. There are a few different types of cells. Phagocytes (PMN's and macrophages) are the primary somatic cells in the mammary gland (PMN's especially during infection). Their purpose is to phagocytize or engulf and destroy bacteria, flooding the infected site until most of the organisms are destroyed. Lymphocytes are another important somatic cell type. Although they are a small percentage of the total mammary cells, they may play a major role. T lymphocytes orchestrate or conduct the immune response through secretion of lymphokines (soluble immune factors). B lymphocytes (controlled by T lymp.) produce antibodies which are essential for presentation of bacteria for phagocytosis.

Somatic cells and the immune response are very specific. Somatic cells are sent in high number only when and where they are needed (i.e., infected or damaged sites). Therefore, high SCC indicate mammary infection.

Low Somatic Cell Counts and Infection Risk

Are low SCC cows at greater risk to mastitis infections? This is a common question in the field. Research at Virginia Polytechnic Institute (2) indirectly addressed this. One objective of the trial was to determine if low SCC cows on initial test in first lactation were at higher risk to mastitis infections as compared to cows with moderate or high SCC on initial test.

Data was comprised from 30 herds and 3432 first lactation animals. Milk, fat, and SCC measures were obtained from monthly DHI samples, and bacteriology was performed quarterly. Cows were grouped into three SCC classes based on initial first lactation test: <100,000 cells/ml, 100,000 - 400,000 cells/ml, and >400,000 cells/ml. Results for first lactation SCC are shown in Figure 1.

Figure 1. Mean logarithms, base 2, somatic cell counts in first lactations by classes of cell counts at initial DHIA test.

Although differences were small, the initial ranking based on cell counts were maintained through first and subsequent lactations. Differences among initial classes for infection percentages consistently favored low cell count animals. Results gave no indication that cows initially low in cell count are at greater risk to subsequent mastitis infections.

Cell Number or Cell Competency?

Cell Function and Staphylococcus aureus infection

Research has centered on the issue of what's most important for infection protection - strict cell numbers or competency of cells. Research examining cell function in cows chronically infected wtih S. aureus provides some answers.

Cows used for this research had experimentally-induced chronic S. aureus infections with cell counts consistently exceeding 1 million cells/ml. Lymphocytes from infected animals were unresponsive to stimulation as compared to uninfected animals (9). Phagocytic ability of milk leukocytes was also reduced and high numbers of phagocytic cells (as seen during mammary infection) had a detrimental effect on lymphocyte function (10). These results show that it is not strictly cell number. If it were only cell number, then how can a cow with a million cell count harbor an infection like S. aureus? The answer is that the competency of the cells is compromised and depressed.

Cell Function in the Early and Late Dry Period

Research has shown that the incidence and highest risk of mammary infection occurs during the dry period (Figure 2). The risk is not linear across the dry period, but is very high during the first and last two weeks of the dry period, and very low throughout the rest. During the early and late dry period, the gland is in a metabolic transitional state. A large amount of milk accumulates in the udder (no flushing or milk out effect) serving as a rich food source for bacteria as well as increasing intramammary pressure which may irritate the udder and serve to distend teat ends, making them leaky or more open to bacterial penetration. During these times, the highest amounts of somatic cells exist compared to any other natural mammary occurrence during the cow's lifetime. Somatic cell counts of >1 million cells/ml or more is normal. Yet in the face of a high level of cells, the gland is highly susceptible to infection. During these periods, the phagocytic cells are preoccupied engulfing or eating milk components (fat, protein) thus decreasing their bactericidal capabilities, or ability to kill mastitis-causing organisms.

Figure 2. Incidence of new infections during the dry and lactation periods.

Intramammary Devices (IMD)

Research has been conducted to artificially elevate SCC using IMD and potentially afford protection via the SCC increase (3, 5, 7, 11, 16). Intramammary devices have either been polyethylene loops or glass beads strung on a nylon string. They are placed in the gland or teat cistern, respectively, using a special cannula. Their purpose is to stimulate a continual low influx of somatic cells to enhance mammary gland immunity.

Data from controlled studies shows the following:

This research did show that the loop may be useful for severe coliform infections, potentially decreasing severity of toxic signs and symptoms. This may be due to the constant influx or enhanced speed at which cells enter the gland, rather than strict cell number.

Nutrition (Vitamin E - Selenium) and Environmental

Mastitis

Research at Ohio State (OSU) and Penn State have evaluated Vitamin E (Vit E) and selenium (Se) and its role in prevention of environmental intramammary infection (4, 13, 14, 15). Results from an OSU study are shown in Figure 3. Animals supplemented with Vit E - Se during the dry and early postpartum periods had: 1) 42% reduction in calving infections; 2) 32% reduction in clinical mastitis (57% during first four days of lactation); 3) 45% shorter infection duration; 4) 57% reduction in quarter days infected; and 5) 68% reduction in high cell count cows. Low plasma Se was associated with increased mastitis in the Penn State Study. Research at OSU shows that animals supplemented with adequate Vit E - Se have an increased speed of recruitment of cells to the mammary gland as compared to deficient animals. Penn State research shows increased blood cell competency in supplemented, adequate Vit E - Se cows and herds.

Figure 3. Reduction in mastitis parameters following dietary supplementation with vitamin E and injectable selenium.

Vitamin E and selenium supplementation probably works on circulating blood cells. Vitamin E and selenium are integral to immune function and may enhance circulating cell function and competency. This may enhance the cell's ability to respond to infection faster. Similar results have been seen with Vit E - Se supplementation and metritis, thus further evidence for its effects at the level of blood cells.

Many other studies evaluating both macro and micronutrients, (energy, protein, minerals, vitamins) have shown decreased cell function and immunity when nutrients are deficient. This emphasizes the importance of a well balanced ration presented in a manner to maximize dry matter intake, especially in high producing, early lactation cows.

Cell Number or Cell Competency

There's no question that a finite number of cells is needed once an infection invades the udder. However, the previously described research elucidates the importance of cell competency and speed of cell recruitment to the mammary gland as major factors in infection prevention.

Low SCC vs. High SCC Herds

Why do low SCC cows get clinical mastitis, which is sometimes toxic or lethal? Is it decreased immunity or because those are the only potential pathogens facing the herd?

Characteristics of infections in high and low SCC herds are shown in Table 1. High SCC herds (>400,000) mainly deal with high levels of contagious, invasive organisms (e.g., S. aureus, Streptococcus agalactiae). These infections are usually subclinical, but harbor many cows and quarters and cause substantial udder damage and milk loss. If clinical, they are usually mild with a few flakes, clots, and some swelling. Environmental infections are rarely seen because they are opportunists and can't compete with the highly invasive organisms.

Table 1. Infection characteristics of high and low SCC herds.
Herds with high SCC (>400,000) Herds with low SCC (<200,000)
contagious mastitis (invasive) environmental mastitis (opportunistic)
mainly subclinical clinical (high temp, systemic signs)
clinical (flakes, clots) few cows or quarters
many cows and quarters little secretory damage
major milk losses massive gland damage
few or no environmentals (opportunists) milk loss/cow loss

Low SCC herds usually have low levels of contagious invasive pathogens and are containing the spread through proper milking procedures. Thus, when they do get infections, they are usually environmental. Environmental infections when clinical are usually characterized by swelling, clotty milk, and sometimes high temperature, systemic signs, toxic effects, and death. These organisms are opportunistic, not invasive, thus most animals who get these are usually suppressed or heavily stressed (dry cows, early lactation animals). Because of this, environmental infection prevalence is usually confined to a few cows or quarters. There is little secretory damage with these infections, but great potential for lower gland damage which can usually be repaired in a few weeks.

Low SCC cows or herds are not more susceptible to environmental organisms, but rather it's the only infection they can get. Unfortunately, the clinical signs are very vivid and thus get the attention of many producers.

Somatic Cells - What are Really Needed?

Somatic cells and the immune response are very specific. There is always a circulating army of cells waiting to be dispatched to areas of infection or irritation in the udder. There is no need for high cell levels. These cells can potentially harm the gland (epithelial damage upon gland entry, tissue damage as a result of lytic enzyme release from dying cells, leading to lost milk production). However, when infection or irritation occurs and cells are needed, the key is to mobilize competent cells to the udder as fast as possible. The key to this is healthy animals. If an animal is healthy, it will respond to mammary infection with adequate cells despite having a low SCC.

The key to success is healthy animals. This starts with balanced nutrition, including vitamins and micronutrients. Coupled to this should be excellent milking management and herd health. The final major key is EXCELLENT HERD SANITATION. Limit what gets on those teat ends! If an infection doesn't get to the teat end, then animals won't need to utilize or tax their somatic cell army.

Overall Goal - Lowest SCC

The overall goal for producers and our industry is to produce and process milk with the lowest cell counts. For the producer, the lowest cell count means increased income from more milk/cow, a higher milk price, and decreased mastitis costs. Residue risks and treatment woes are also reduced. Lowest cell count milk means increased profits for processors due to higher quality and quantity of product. The ultimate benefactor is the consumer who gets a consistent supply of highest quality dairy products at the most economical price.

So can the SCC be too low? The research and field data say NO. If this isn't convincing enough, then just ask the producer with a herd cell count <100,000 cells/ml. Their testimonial will provide the icing for the cake.

References

  1. Barbano, D.M. 1987. Mastitis and its impact on product yield and quality. Proc. 26thAnnual Meeting of the National Mastitis Council.
  2. Coffey, E.M., W.E. Vinson, and R.E. Pearson. 1986. Somatic cell counts and infection rates for cows of varying somatic cell count in initial test of first lactation. J. Dairy Sci. 69:552.
  3. Craven, N. And A.W. Hill. 1986. Local cellular reaction release of neutrophil chemotaxin from abraded polyethylene devices implanted in bovine udders. Br. Vet.J. 142.170.
  4. Erskine, R.J., R.J. Eberhart, L.J. Hutchinson, R.W. Scholz, and S.B. Spencer. 1987. Blood selenium concentrations and glutathione peroxidase activities in dairy herds with high and low somatic cell counts. JAVMA. 190:1417.
  5. Jaster, E.H., A.R. Smith, T.A. McPherron, and D.K. Pedersen. 1982. Effect of an intramammary polyethylene device in primiparous dairy cows. Am. J. Vet. Res.43:1587.
  6. Jones, G.M., R.E. Pearson, G.A. Clabaugh and C.W. Heald. 1984. Relationships between somatic cell counts and milk production, J. Dairy Sci. 67:1823.
  7. Nickerson, S.C., W.J. Thompson, S.P. Oliver, and R.M. Akers. 1988. Effects of intracisternal bead devices on lacteal secretion components, plaque formation, and bacterial infection during the nonlactating period. Am. J.Vet. Res. 49:1205.
  8. Niemialtowski, M., B.J. Nonnecke, and S.P. Targowski. 1988. Phagocytic activity of milk leukocytes during chronic staphylococcal mastitis. J. Dairy Sci. 71:780.
  9. Nonnecke, B.J. and J.A. Harp. 1985. Effect of chronic staphylococcal mastitis on mitogenic responses of bovine lymphocytes. J. Dairy Sci. 68:3323.
  10. Nonnecke, B.J. and J.A. Harp. 1988. Effects of Staphylococcus aureus on bovine mononuclear leukocyte proliferation and viability: Modulation by phagocytic leukocytes. J. Dairy Sci. 71:835.
  11. Paape, M.J. G.Ziv., R.H. Miller, and W.D. Schultze. 1986. Update on the use of intramammary devices in the control of mastitis. Proc. 25th Annual Meeting of the National Mastitis Council. P. 87-103.
  12. Raubertas, R.A. and G.E. Shook. 1982. Relationship between lactation measures of somatic cell concentration and milk yield. J. Dairy Sci. 65:419.
  13. Smith, K.L. and H.R. Conrad. 1987. Vitamin E and selenium supplementation for dairy cows. Proc. Roche Technical Symposium, Daytona Beach, Florida. P. 47-66.
  14. Smith, K.L., H.R. Conrad, B.A. Amiet, P.S. Schoenberger, and D.A. Todhunter. 1985. Effect of vitamin E and selenium dietary supplementation on mastitis in first lactation dairy cows. J. Dairy Sci. 68 (Suppl. 1):190.
  15. Smith, K.L., J.H. Harrison, D.D. Hancock, D.A. Todhunter, and H.R. Conrad. 1984. Effect of vitamin E and selenium supplementation on incidence of clinical mastitis and duration of clinical symptoms. J. Dairy Sci. 67:1293.
  16. Stephens, L.R. and J.W. Browning. 1984. The effect of polyethylene intramammary devices on the somatic cell count and milk production of dairy cows. Aust. Vet J. 61:229.