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NAIP Sub-Project at PD_ADMAS

Project Background & Rationale
Background & Rationale: Positive impacts on Indian Agriculture Science & Technologies

Bovine mastitis is the most complex disease condition mainly because of multip causative agents, poor understanding of the early immune response and complexitie associated with mammary epithelial cell damage by both the agents and the ho factors. Decreased milk production accounts for approximately 70% of the total cost o Advisory Committeemastitis.Though, India is the largest milk producer but per capita production is less tha Implementation half of the world average. Additionally, the poor understanding of the underlyin Committee phenomenon in subclinical state of the infection complicates the therapeut Monitoring Unit interventions.
Summary Duration, Cost, Area

About 95% of intramammary infections are caused by Streptococcus agalactia Staphylococcus aureus, Streptococcus dysgalactiae, Streptococcus uberi andEscherichia coli. The remaining 5% are caused by other organisms. Ver Work done comprehensive knowledge of most predominant causative agents and their molecula Brochure signature defining the genetic diversity is not available. Further, understanding th Protocols disease process emphasizing the contribution of agent and host in the context o Launch Programmemodern developments in biological sciences is of paramount importance and this ha not been attempted in India, so far. The studies elsewhere in the world have starte Events giving specific insights but the overall understanding is still very poor to arrive a FAQ definitive intervention/mitigating strategies. It is in this backdrop, the objectives set out Questions and this research programme will enable us to understand the critical aspects of hos Comments microbe interaction. It will also provide an insight into the intricacies of the progressio TENDERS of the disease so that strategies for rapid diagnosis of subclinical mastitis can b evolved. In addition, interventions for mitigation of subclinical and clinical mastitis can b designed and validated for reducing the enormous economic loss incurred due to th disease worldwide.

Pathogens invading the mammary gland cause a complex signalling network tha activates the early immune defense and leads to inflammation. To examine th

importance of mammary epithelial cells in these regulatory pathways, the focus wou be on MEC to infection by specific pathogen. The innate immune response characterized by the induction of pro-inflammatory cytokines, as well as increases other accessory proteins that facilitate host recognition and elimination of th pathogens. Thus, the objectives formulated will facilitate better understanding of diseas process so that interventions can be designed.

If these objectives are not met, the need of the hour will be overlooked and as consequences, the dairy industry in particular and Indian agriculture as a whole w continue to suffer from huge economic losses. Further, quality of milk has also a grea bearing on Public health and such threat to the society will prevail, which will hinder th progress towards making the Indian agriculture globally competitive and ensuring foo and nutritional security. Scientific Challenges to be addressed:

The following scientific problems are to be solved in order to attain the objectives. Th basic works that need to be done are:

1. Finding out the most predominant bacterial pathogens associated with sub-clinical and clinical mastitis and the clonality/genetic diversity of the isolates within a species Is there any association of specific genetic clone within a species associated with subclinical and/or clinical form of the disease?

2. Development of molecular diagnostic method for subclinical mastitis, especially whe somatic cell count is low. 3. Understanding the inflammatory process progression in time course manner emphasizing the mobilization of somatic cells and proinflammatory/anti-inflammatory mediators (chemokine, cytokine, interleukins etc.) in milk and tissues? 4. How the udder tissue especially mammary epithelial cells react to the invasion by specific pathogen in mastitis? How the initial stimulation through receptor-ligand interaction, regulate the global gene expression? 5. Sequential expression of pathogen specific genes in-vivo. 6. Is there any precise organism specific pathway for the mammary epithelial cell damage in mastitis?

7. Whether factors involved in controlling the differential gene expression are organism specific or common to other causal agents? Can these be a target for intervention? 8. Defining the role of epigenetic modification in regulation of differential gene

expression in intramammary infection.

A comprehensive modern biological approach will be adapted to study different aspects in laboratory experimental model (mouse/ rabbits) and in-vitro cell culture system. At times, validation will be attempted in naturally infected animal. Status of Research: i. The World

Mastitis is a major infectious disease affecting high yielding cows in dairy herd Because of its economic impact and due to the animal welfare policy, the pathogenes of this intra-mammary infection was studied extensively over the past 50 years. Th expenses associated with the use of dairy cows for mastitis research constitute a majo drawback. As an alternative, a mouse model of experimentally induced mastitis wa developed few years ago. This model has been increasingly used as it appears to b very suited for studying ruminant mastitis due to genetic similarities in mammary gland of mice and cows. a. Causative agents and changes in milk in Mastitis:

Latest techniques have been developed in the recent years to establish stra differences in genetic make up between isolates. The classification of S aureus isolates in clusters by virulence genes combinations showed that at least on cluster induced a higher inflammatory response. A rapid, sensitive and specific metho for DNA extraction from major gram-positive bacteria directly from milk has bee standardized recently (Cremonesiet al. 2006). A multiplex Real-time PCR wa developed for simultaneous detection of mastitis pathogen, S. aureus, S. uberis and S agalactiae by Gillespie and Oliver (2005). Moreover, the analysis of the associatio between virulence genes and the presence of a subclinical mastitis showed the role o spa and sej gene as risk factors (Lorenza et al.,2007).

Experimental bacterial mastitis served as a prelude to studying the actual infection dairy cows. Pathology of experimental Escherichia coli infection in mice, a laborato animal model for research in Mastitis complex, revealed that the mastitis produced mice resembled naturally occurring coliform mastitis in the cow (Abhraham et al., 2007 At least 15 proteins were involved in host defense out of 181 identified proteins from 36 2-DE spots demonstrating that the proteome of milk is more complex than ha previously been reported and a significant fraction of minor milk proteins are involved protection against infection (Smolenski et al., 2007). Molecular probes reacting in th PCR with bacterial DNA from bovine milk, providing direct and rapid detection of E. co S.aureus, S. agalactiae, S. dysgalctiae, S. parauberis and S. uberis have bee developed in order to avoid the problem in culture dependent isolation and identificatio approaches (Riffon et al., 2001).

b. Proinflammatory/ Inflammatory Mediators in mastitis:

Differential inflammatory cell count (DICC) of mastitis milk leucocyte populations and viable and non-viable PMN in flow cytometric dotplots (polymorphonuclear neutrophi [PMN], lymphocytes and macrophages) could be effectively used to quickly determin the stage of the inflammation even in quarters with a low SCC in sub-clinical mastit (Koess and Hamann 2008)

The relationship between the initial neutrophil influx and the proinflammatory cytokine may be responsible for determining the course of infection in mastitis (Winter al. 2003).

The primary role for IL-8 in the recruitment of neutrophils into the gland, and further tha IL-1beta and TNF-alpha are not necessary for IL-8 production and release in respons to endotoxin in mastitis was demonstrated by Persson et al. (2003). Lee et al. (2006 proposed that the compromised upregulation of inflammatory cytokines in S aureusinfected glands may at least partially; contribute to the chronic course of infectio caused by this pathogen. Lahouassa et al., (2007) demonstrated that bovine mammar epithelial cells were able to release neutrophil-mobilizing chemokines and pro inflammatory cytokines upon bacterial stimulation, strongly suggesting that bovine ME are active contributors to immune and inflammatory responses of mammary gland. I addition, the clinical characteristics and resolution of mastitis may be partly determine by the responses of bovine MEC according to S. aureus strains and bacteria Gram type

CD14 receptor on phagocytes is very important in controlling G-ve infections. Binding LPS to membrane bound CD14 causes release of TNF- and sepsis. Binding of LPS soluble CD14 shed from CD14-bearing cells results in neutralization of LPS and rap recruitment of PMN to the site of infection (Paape et al., 2003). PMN not only kill th pathogens by releasing reactive oxygen intermmediates and proteolytic enzymes bu also cause injury to the mammary gland resulting in permanent scarring and reduce number of milk secretory cells. To minimize the damage to mammary tissue due t neutrophil-induced oxidative stress, PMN undergoes apoptosis (Zhao and Lacass 2007). Studies on Escherichia coli infections in mouse mammary glands showed hig values of the acute phase protein serum amyloid associated (SAA) in blood, system increase of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6 upregulation of mammary expression of the biologically inactive proform of IL-1bet Further it was shown that IL-1beta maturation seemed to occur independently fro caspase-1.

The infection also triggered activation of the nuclear transcription factor-kappa B (NF kappaB) in the mammary gland providing novel insights on the contribution of majo regulatory proteins to the acute inflammatory host response at the local and system level during E. coli mastitis in mice (Notebeart et al., 2008). The role of mamma epithelial cells in the immune defense of the udder and their contribution to pathogen related different courses of mastitis was confirmed by increased mRNA expressio patterns of proteins involved in pathogen recognition such as Toll-like receptors an

nuclear factor-kappa B in response to S. aureus and Escherichia coli. Furthe expression profile of the proinflammatory cytokines tumor necrosis factor alpha, ILbeta, IL-6, and chemokines such as IL-8 and RANTES (regulated upon activation normal T-cell expressed and secreted) also supported their findings (Griesbeck al., 2008). c. Molecular changes in mastitis:

Wellnitz and Kerr (2004) indicated that mammary epithelial cells play an important ro in inflammatory response, through the production of pro-inflammatory cytokines, a acute phase protein, and lactoferrin in their experiments with cryopreserved bovin mammary cells to mouse epithelial response to infection by Staphylococcus aureus o exposure to LPS from Escherichia coli. Differential gene expression in bovine lactatin mammary tissue, including oncogenes (VAV3, C-myc), mediators of apoptos (Caspace 8) and cell regulators (LASP1) was revealed by microarray analys (Suchyta et al., 2004). However, differential display RT_PCR of mRNA from cow with o without mastitis showed up-regulation in expressions of genes involved in sign transduction (Protein kinasee: stk9, jik, cdk8, prkdc, vrk2, tp53), regulation of gen expression (ahcy, ssr1, hnrpu), genes involved in cell growth and differentiation (ostf rsc1a1, ahnak) (Schwerin et al., 2003). However, how these influence the course o mastitis and whether there is any common pathway of udder cell damage and deat whether the process is unique to different causative agents are not clear. Delineation o the molecular event and in-depth understanding of the process involved would pave th way to devise use of nano-particle in diagnosis and control (Schmitt and Henderso 2005). Oviedo-Boyso et al., 2007 reported that knowledge at the molecular level, of th mammary gland immune response during infection by pathogenic bacteria fundamental to the design of effective therapies to control and eradicate bovine mastitis ii. In India

In India, the estimated loss due to mastitis is around Rs 16,702 millions per annum (Yathiraj, 2006). Subclinical mastitis was found more important in India (varying from 10 50% in cows and 5-20% in buffaloes) than clinical mastitis (1-10%). The incidence wa highest in Purebred Holsteins and Jerseys and lowest in local cattle and buffaloes. A investigation on 250 animals from periurban farms indicated that the monsoon seaso was more prone to subclinical mastitis than summer or winter, prevalence increase with higher lactation number and animals in 4th-5th month of lactation were found mor susceptible (59.49%), hind quarters were found more affected (56.52%) than for quarters (43.47%). The factors like herd size, agro climatic conditions of the region variations in sociocultural practices, milk marketing, literacy level of the animal owne system of feeding, and management were found important affecting the incidence o subclinical mastitis. Comparison of efficacy of different diagnostic techniques fo subclinical mastitis, such as Modified California Mastitis Test (MCMT), bromo thym blue (BTB), modified whiteside test, trypsin inhibition test, milk pH, and electr conductivity indicated MCMT to be most sensitive (95.16%) and specific (98.02%) test.

The antimicrobial susceptibility test revealed that most of the bacterial strains (gram positive, gram negative and mixed) isolated from subclinical mastitis milk samples, wer highly sensitive to enrofloxacin 53.91%, least sensitive to oxytetracycline 17.39% an ampicillin 7.83%, and resistant to streptomycin. The therapy with enrofloxacin an nimesulide was found more efficacious (92.30%) in treating subclinical mastitis cow Identification of a mastitis pathogen is required for infection study. More than 99% of th mastitis pathogens are bacteria. Subclinical mastitis was found more important in Ind (varying from 1050% in cows and 520% in buffaloes) than clinical mastitis (110% (Joshi and Gokhle, 2006). The major causative agents for bovine mastitis in Andama areStreptococci followed by Staphylococcus, gram positive, yeast, Candida sp. an gram negative organisms ( A number reports on isolation and characterization of pathogens with special reference to plethor of bacterial species (Wani and Bhat, 2003) including Mycoplasma (Sanjeev Kumar an Haribabu, 2005) and Fungi (Monga 2001) are available but few reports of involvement o viruses in mastitis are available so far. Staphylococcus aureus, Streptococc species and E. coliconstituted major reported pathogens causing mastitis. Most of th published literature in the country on bovine mastitis pertains to studies o chemotherapeutic efficacy of antimicrobials in bovine mastitis cases in dairy catt based on their in-vitro drug sensitivity/antibiogram patterns. S. aureus followed by E coli were reported to be the most predominant pathogens causing both clinical an subclinical bovine mastitis. Further, the dendrogram based antibiogram profile signifie the relatedness among the isolates from different geographic locations irrespective o their affiliation to clinical or subclinical mastitis (Rajeev et al., 2007a). Most prevalent E coli O9 serotype showed heterogenous banding pattern when analysed by ERIC-PC (Prabhu et al. 2007). A study on clinical and subclinical mastitis was conducted for period of five months in crossbred dairy cows to revealed prevalence of S. aureu in 37.93 per cent of clinical mastitis cases but only 3.85 per cent in subclinical mastit (apparently healthy) cases (Parmar et al., 2006).

The IL-2 and IFN-gamma were expressed in normal healthy cows and diseased cow after Azadirachta indica treatment, whereas both the cytokines could not be expresse in cows treated with antibiotic and in untreated diseased cows. The results of th present study indicated anti inflammatory, antibacterial and immunomodulatory potenti of the herb (De and Mukherjee 2008). Enhancement of antioxidative and cellula defense and reduction of somatic cell count in the mastitic animals treated wit Enrofloxacin and Vitamin E plus Selenium as compared to the Enrofloxacin treatmen alone was demonstrated in experiments in buffaloes with subclinical mastit (Mukherjee, 2008).

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Mastitis Prevention for Dairy Cattle: Environmental Control

Alternative Livestock and Aquaculture

Agdex#: Publication Date: Order#: Last Reviewed: History: Written by:

410/662 05/90 90-104 September 2011 Replaces Factsheet #83-091, "Mastitis Prevention: Environmental Control" J. Rodenburg, Dairy Cattle Specialist/OMAFRA

Beef Dairy Goats Horses Poultry Sheep Swine Veal Animal Health, Care and Handling

Topics Explore Table of Contents Governme 1. Introduction nt 2. Feeding


3. Housing 4. Stalls 5. Bedding 6. Tingle Voltage 7. Ventilation 8. Calf Housing 9. Other Management Practices 10. Related Links


Mastitis is one of the most common and costly diseases of dairy cattle. It can be controlled by applying a management program which includes: (1) a clean, stress-free environment; (2) proper maintenance and operation of milking equipment; (3) good milking procedures including teat dipping; (4) a dry cow treatment program; and (5) a program for monitoring udder health status. This Factsheet outlines the environmental factors of mastitis prevention. Mastitis is an infection of the udder, caused by bacteria entering the quarter through the teat end. When the udder is exposed to greater numbers of bacteria, because of a dirty environment, or when teats are damaged, allowing easier bacterial invasion, infection is more likely to occur. About 97% of all mastitis cases are "subclinical". While these cases do not involve visible changes to the quarter or the milk it produces, they do result in lower milk production and an increased somatic cell count. In subclinical cases, the cows' natural resistance to disease limits the spread of the bacteria in the udder. When stress lowers this resistance to disease, subclinical infections are more likely to flare up and become clinical cases. Some types of stress may also allow easier penetration of the teat, thereby increasing the number of new infections. Since clinical cases are easily identified, dairymen tend to be aware of stress factors which cause flare-ups, but less sensitive to factors which cause new infections. This Factsheet emphasizes those environmental factors which influence new infection rates, since reducing the number of new subclinical cases is the most effective way to control mastitis. Infections caused by coliform bacteria are less common than other types, but can cause very severe cases of clinical mastitis. Coliform bacteria are abundant in wet bedding materials, manure and polluted water. Coliform mastitis occurs more frequently in herds which are relatively free of other types of mastitis infections, are housed in unsanitary conditions or milked while the udders are wet. Coliform infections are more common in cows under stress. Where coliform mastitis is a problem, attention should be given to general cleanliness of the environment, and particularly, the cleanliness of bedding materials in stalls. Klebsielia and Streptococcus non-agalactia are other organisms associated with the environment. When culture results show these organisms predominate, environmental control measures should

be reviewed. Three main goals in environmental control of mastitis are as follows: 1. Decrease the number of bacteria in the cow's environment, particularly in areas which come in contact with the udder. 2. Prevent teat injuries. 3. Reduce or eliminate environmental stress.

Although dairymen have often blamed certain feeds for clinical mastitis flare-ups, high energy or high protein diets do not increase or decrease the number of new infections. Feeding high producing cows for maximum production does increase stress on the udder and may cause infected cows to flare-up, however, restricting production to reduce clinical mastitis is not realistic or economical. Health problems at calving, particularly those which result in downer cows increase the risk of mastitis infections. The incidence of these health problems can be reduced by separating the dry cows from the milking herd and feeding a properly balanced dry cow ration. Research has shown that certain vitamins and minerals are important in fighting infections. Deficiencies of selenium, vitamin E and vitamin A increase both the number of new infections and clinical cases of mastitis. Excessive levels of other elements such as iodine, reduce disease resistance. A balanced ration containing recommended levels of all nutrients improves the cow's resistance to all infections including mastitis. Selenium at 0.3 parts per million, vitamin E at 15 international units per kilogram and vitamin A at 3,200 to 4,000 international units per kilogram of dry matter in the total diet are recommended. The formulation of mineral supplements in many typical diets, especially for dry cows, is often inadequate to meet these levels.

Studies comparing housing systems tend to show slightly lower mastitis incidence in free stalls than in tie stalls or loose housing. Regardless of the system used, general cleanliness of the environment is a major factor in determining overall exposure to mastitis organisms. Dirt lots, stagnant ponds, accumulation of manure, overstocking, and irrigation of pasture with manure increase bacterial exposure and risk of mastitis. Loafing areas should be large enough and properly drained to support normal growth of grass, or they should be paved with concrete and cleaned by regular scraping. Cattle should not have access to ponds where they may stand with their teats in the water, or to pasture areas to which manure has recently been applied. Alleys in solid floor freestall barns require regular scraping, and obstructions which may come in contact with teat ends should be eliminated. Sun-burned or frozen teats are more prone to new infections, therefore, the housing system should provide adequate shade, and protection from winter winds, particularly immediately after milking. If cows must exit directly outside from a milking parlour, radiant

heaters in the parlour combined with a brief delay before cows are released, will ensure teats are dry and prevent freezing. It should be noted that many new mastitis infections occur early in the dry period and shortly before calving. Clean well bedded housing facilities for dry cows are at least as important as proper housing of the milking herd.

When stalls are too small, a higher incidence of teat injuries occurs. In free-stall barns, cows are less likely to lie in dirty alleyways if free stalls are of adequate size, and at least nine stalls per 10 cows are provided. Harder stall surfaces such as concrete or wood reduce cow comfort and may increase teat injuries, however, these stalls require less labour and maintenance than clay or lime based stalls, and are satisfactory if enough bedding is used. Some dairymen report reduced problems with cows digging out clay based free stalls when 13 or 14 inch used car tires with holes drilled in the bottom for drainage are embedded in the stall base. Concrete free stalls and cow stands in tie stalls should have a 2% slope to the back. To retain bedding and improve footing, a 25 mm (1") lip may be provided at the back of the stall or cow stand, but openings must be left for drainage of liquids. A metal pipe supported 25 mm (1") above the back edge of the platform provides an excellent "bedding keeper" with adequate space for drainage. Excessively large stalls promote a build-up of manure which increases exposure to mastitis causing organisms. Stall length, and freedom of movement in the tie-up system are more critical than width of stalls or presence of partitions. Recommended stalls sizes are given in Table 1. For tie-stalls, cow trainers, suspended 60 mm (2.5 in.) above the cow's back 150 mm (6 in.) behind the point of the shoulder are highly recommended. For free stalls, a neck or head rail is essential to keep cows back when standing. Cow comfort may be further improved in traditional stall designs by adding a slightly sloping brisket board 200 to 250 mm (8 to 10 in.) high located 700 to 800 mm (28 to 31 in.) from the front of the stall.

Table 1. Dimensions for Tie Stalls.

Cow Size kg 400 500 600 700 lbs 880 1100 1320 1540

Platform Width mm 1050 1150 1250 1350 (in.) 41 45 49 53

Platform Length mm 1450 1550 1650 1750 (in.) 57 61 65 69







* Length is with use of cow trainers. If no trainers used decrease stall length by 100 mm (4 in.).

Table 2. Dimensions for Free Stalls.

Cow Size kg 400 500 600 700 800 lbs 880 1100 1320 1540 1760 mm 1000 1150 1250 1350 1450

Stall Width (in.) 39 45 49 53 57 mm 2100 2200 2300 2400 2500

Stall Length (in.) 83 87 91 95 98

Locate neck rail 900-1100 mm (35-44 in.) above stall surface and 1500-1700 mm (59-67 in.) from rear curb of stalls. New designs, including "mushroom" and "suspended" free stall partitions, figure 1 and figure 2, offer greater freedom of movement and cow comfort than traditional partitions. Fewer injuries are associated with these designs.

Figure 1. Mushroom Partition.

Figure 2. Suspended Partition

In tie stall barns, single head rail stalls allow cows to move forward with head down for feeding, but keep them back when the head is up. These stalls are lowest in cost and can be designed to release an entire row at the same time. Chain ties restrict sideways movement of the head giving greater control over individual feeding. Cows have more freedom to move backwards or forwards making cow trainers essential with this design. Stanchions are more restrictive and may lead to a greater incidence of teat and leg injuries. Of these systems, illustrated below, single headrail tie ups appear the most practical.

Figure 3, figure 4, and figure 5 show three different tie stall design options.

Figure 3. Single headrail tie stall.

Figure 4. Low arch chain tie stall.

Figure 5. Stanchion tie stall.

Both tie stalls and free stalls require regular attention and at least 7 cm (2 1/2 in.) of bedding material to maintain a clean and dry environment for the udder. Bedding is required to keep stalls dry, preventing a build up of bacteria, and for cow comfort. No perfect bedding material has yet been discovered. Free stalls, bedded with sand have proven very effective in minimizing exposure of the udder to bacteria, because bacteria do not grow as quickly in sand as in "organic" bedding materials. However, sand is seldom practical because it is extremely difficult to handle in most manure systems. Green, hardwood sawdust has been implicated in increased incidence of mastitis caused by a coliform organism called Klebsielia, and should be avoided as bedding material. Sawdust and shavings from kiln dried lumber present less risk, if kept dry in storage, and in the stalls, but incidence of Klebsiella infection is still higher than with straw. Adding lime to sawdust has not proven to be beneficial in reducing mastitis. Straw tends to harbour bacteria when it becomes damp, thus leading to increased incidence of mastitis caused by these organisms, however clean dry straw is an excellent bedding system. With all bedding materials, replacing wet soiled material daily, is the key to controlling growth of bacteria in the bedding and to reducing new mastitis infections. Rubber mats improve cow comfort but still require bedding to keep stalls dry and improve footing. A new mat designed in Europe, made of canvas material backed with resilient fibres has been shown to provide greater cow comfort than rubber mats. Though costly, these mats may prove more satisfactory than rubber when little or no bedding material is available.

Tingle Voltage

Stray or tingle voltage on stabling and milking systems has been blamed for high somatic cell counts and increased incidence of clinical mastitis in dairy herds. However, research studies indicate that low levels of tingle voltage are not a direct cause of high cell counts or mastitis. Stray voltage in milking parlours or tie stall barns can lead to nervousness during milking, reluctance to enter the milking parlour and uneven milkout. When these behavioral symptoms are obviously present, irritation, liner slips and increased stress during milking may lead to both clinical flare-ups and new mastitis infections. Stray voltage should be suspected as a contributor to mastitis only when these behavioral symptoms are present. The level of voltage which affects cows is highly variable depending on the electrical conductivity of cow contact points and the environment. It is believed to be in the 1 to 5 volt range under normal housing conditions. Stray voltage results from currents originating on the neutral network of the electrical system which pass through the cow from the stabling, feeding and drinking devices to the earth. A high impedance voltmeter with a full scale reading 2 to 5 volts AC, and which does not record DC voltage on the AC scale can be used to test for stray voltage. Many rural electricians, and the Ontario Milk Marketing Board udder health specialists, are equipped to check barns for stray voltage. Tingle voltage can be eliminated by the proper installation of a "tingle voltage filter", available from most electrical suppliers. Because proper installation of this equipment is critical, this device should be installed by a qualified electrician who is familiar with the equipment. An indicator light can be included in the installation to indicate failure of the filter. In the construction of milking parlours, an equi-potential plane, consisting of 9 or 10 gauge welded wire mesh of any size up to 150 mm (6") should be installed. The wire mesh is embedded in the parlour and pit floor within 50 mm (2") of the surface and bonded to all metal parlour equipment and to the neutral network. With this system, the cow is subjected to equal electrical potential at all contact points, and not subject to electrical currents even if stray voltage is present in the system. Detailed recommendations for dealing with stray voltage problems can be found in the OMAF Publication Stray Voltage Problems with Dairy Cows.

High temperatures (above 25 degrees Celsius), high humidity (above 80%), and manure odours are recognized stresses on dairy cows. High humidity also increases exposure to airborne organisms and increases the moisture content of bedding materials, thereby increasing the rate of bacterial growth in bedding. Adequate ventilation is important in all dairy cattle housing systems, both for cow comfort and to minimize exposure to mastitis causing bacteria.

Calf Housing
When calves fed mastitic milk are allowed to suck each other, infection can occur in the

developing mammary gland, therefore, milk fed calves should be housed in individual pens. Consumption of mastitic milk in itself will not lead to mastitis infection, although milk from clinically-infected cows may cause other health problems.

Other Management Practices

Keeping cattle on their feet for the first hour after milking will reduce the exposure of the teat end to bacteria during a period when the risk of infection is high. The risk of infection is greater after milking because the sphincter muscle at the end of the teat is relaxed permitting easier bacterial invasion. Providing fresh feed during and after milking is a simple way to keep cows standing. Proper fly control, both on the cows and in the stable, is also important. Flies cause stress and also carry mastitis causing bacteria from teat end to teat end. Teat injuries, nearly always result from damage inflicted by the dew claws and hooves of the injured cow, and not by other animals. The frequency of teat injuries can be reduced by providing adequate sized stalls, and by eliminating pendulous udders through selection and culling. Udder supports and teat protectors over the dew claws, can be used to protect the teats of cows with larger udders during the high risk period at calving time. Removing the inside dew claw of newborn heifer calves significantly reduces the chance of self-inflicted teat injury in adult cows. When teats are injured, teat dilators, or cannulae should be used only when absolutely necessary. Ensure dilators or cannulae are handled aseptically since their use greatly increases the risk of bacterial penetration of the teat. A high incidence of mastitis in heifers at calving may result if one or more heifers have sucked the udders of others in the group. Heifers should be checked regularly for sucking activity or abnormal udder development and offending animals fitted with weaners or removed from the group. Mastitis prevention requires a daily commitment from producers to maintain a high standard of cleanliness in the cows' environment and to prevent teat injuries. When high somatic cell counts, or high incidence of clinical cases indicate a herd problem, making appropriate changes in herd management and housing can significantly improve production and profitability of the dairy herd.

For Further Information

Refer to the following OMAF Factsheets: Dry Cow Therapy, Agdex 410/662 Proper Milking Procedures, Agdex 410/725 Understanding the Basics of Milking Machines, Agdex 410/725 Maintenance of Milking and Milk Handling Equipment, Agdex 410/725 Installation Recommendations for a Milk Pipeline, Agdex 410/725

Related Links
Dry Cow Therapy Maintenance of Milking and Milk Handling Equipment Installation Recommendations for a Milk Pipeline

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Ecological Solutions Roundtable

AGRO-BIO - 370 - 11E



Introduction Types of mastitis Microorganisms causing mastitis Factors contributing to mastitis o Environmental factors o Genetic factors o Nutritional factors o Physical and ethological factors o Human factors Diagnosis o Somatic cell count o Bacterial identification and counting Preventive measures o Milking procedures o Hygiene and safety o Feed o Culling and replacement o Drying off period Curative measures o Clay therapy o Homeopathy o Phytotherapy o Oxygen therapy o Others Conclusion Bibliography Useful addresses

By Jean Duval, Agronomist, MSc July 1995 Copyright Ecological Agriculture Projects 1997



Mastitis is a disease that affects a large number of dairy cattle throughout the world. A survey conducted in the major milk-producing countries indicates that each year clinical mastitis afflicts 15% to 20% of cows35. In Canada and the United States, it is thought that 50% of cows have one or more infected quarters. In Denmark, it is estimated that mastitis is the cause of 30% to 40% of veterinary interventions. Using antibiotics is not an ideal solution. Other than the problems they cause with the milk (withdrawal for x days, contamination from antibiotic residues, problems associated with yogurt and cheese processing), antibiotics have not reduced the incidence of mastitis (footnote A)37. Problems associated with resistance or even ineffectiveness are quite real in the case of mastitis caused by coliforms and Staphylococcus aureus15. In organic agriculture, the use of antibiotics is neither normally authorized, nor desirable. There are however a large number of preventive and curative measures available to producers to deal with the problem. Mastitis control also entails a good understanding of the factors that encourage its incidence and the microorganisms that cause it.

Figure 1. Factors influencing the incidence of mastitis.

A. The incidence of contagious mastitis has diminished through the use of antibiotics, but this has been paralleled by an increase in the level of environmental mastitis. Table 1 shows the difference between these two types of mastitis.

Since mastitis is a disease that has different levels of intensity and may be caused by different organisms, there exists a complete lexicon to describe the disease. Indeed, there are a number of types. It is therefore important to be able to recognize the different types of mastitis in order to decide what preventive measures or treatments to use. To clarify the terms used throughout this article, Table 1 provides the definitions and characteristics of the different types of mastitis. Table 1 - Characteristics of the different types of mastitis
Types of Characteristic Symptoms or Definition

Mastitis Acute clinical Hyperacute clinical Subacute clinical Inflammation of the teat, fever above 39C, weak and dejected animal, lack of appetite. Drastic drop in milk yield. Often follows calving and, less seriously, after cow goes dry. Swollen, red, painful quarter. Milk passes with difficulty. Fever over 41C. Cow has no appetite, shivers and loses weight quickly. Lactation often stops. No apparent change in udder, presence of flaky particles in milk, especially in initial ejection. Subject appears healthy. No symptoms. 15 to 40 cases for every clinical case. Milk appears normal. Only change is detection of pathogenic agent in analysis and increased somatic cell count. Mostly caused by Staphylococcus aureus. Repeated but mild clinical attacks, generally without fever. Lumpy milk, quarters sometimes swollen. Quarter may become hard (fibrous indurations). Antibiotic treatments often do not work. Affected quarter is blue and cold to the touch. Progressive discolouration from the tip to the top. Necrotic parts drop off. Cow often dies. Mastitis caused by bacteria such as Staphylococcus aureus and Streptococcus agalactiae, of which other infected cows are the main source. Mastitis caused by bacteria such as coliforms (e.g. E. coli), of which the main source is a contaminated environment, i.e. manure.







There are a great number of microorganisms on and in cow udders. Watts52 identified 137 species and subspecies of microbes that can be associated with the mammary gland of the cow. Several of them are part of the normal flora and, with few exceptions, do not cause mastitis (footnote B). On the contrary, they may protect udders from infection caused by pathogenic bacteria. Several other microorganisms may, however, cause infection in the mammary glands. The most common, those that cause about 90% of mastitis infections, are given in Table 2. There are contagious microorganisms and environmental microorganisms. Infected cows are the main source of contagious microorganisms, which survive and

proliferate on the skin and on teat wounds. They consist of Streptococcus agalactiae, Staphylococcus aureus and Streptococcus dysgalactiae. Environmental microorganisms (Escherischia coli and other coliforms, Streptococcus uberis) do not remain on the teat. Rather, their presence indicates a high degree of contamination of soil, bedding, and water caused, particularly, by manure. To infect a quarter, a microorganism must first enter the quarter and the cow must be unable to get rid of it before it multiplies (footnote C). The following is a typical scenario that leads to mastitis infection. 1. Contact with the microbe: The number of microorganisms multiplies near the orifice (or sphincter) of one or several teats. This is where hygiene and milking habits play an important role in preventing microbes from entering the quarter. 2. Entry of microbe into the teats: Entry may be forced by the milking machine, particularly at the end of milking. Injured teats (injuries, keratin injured inside teat) or teats whose openings are too large may be easily invaded. This is where adjusting milking machines and preventing injuries is critical. 3. Immune response of the cow: the cow's first line of defense is to send white blood cells (leucocytes) to eliminate the microbes that have penetrated the teat. If the response is insufficient, the microbes multiply and the cow shows other immune responses such as fever. The effectiveness of the cow's immune system depends on many factors. This is also an area where farmers can do a great deal to ensure good immune response. B For example, Staphylococcus hyicus, Staphylococcus epidermis and Corynebacterium bovis. C It is possible that some microorganisms enter the udder from other parts of the body, but this theory is still under debate. It therefore must be assumed that the main entry of microbes is the teat. Table 2 - Main microorganisms involved in mammary infections, their characteristics and prevention
Species Main Source Living Conditions Propagation Factors Symptoms Preventive Treatment Wash udders after milking, reduces

Streptococcus agalactiae

Infected cows

Infected Using same rag Mild fever for about 24 hours quarter and for cleaning

udder only


problem by 50%

Cull infected cows

Often quite acute for a few days after calving. May be fatal. Quarter Wash udders On swells and turns purple. after milking, abnormal Quickly affects entire Transmitted by reduces udder and system. In chronic state, hands or rags, problem by teat, udder hardens, aqueous enters during 50% milkers, secretion, eventual milking vagina, atrophy of the quarter. Cull Intermediate form tonsils infected produces granular cows secretion. Milk hotter than normal. Wash udders after milking, Pronounced swelling of reduces one or more quarters. problem by Milk highly abnormal. 50% High fever in serious cases.

Staphylococcus Infected cows aureus

Streptococcus dysgalactiae

Infected cows

Infected quarter, injuries

Cull infected cows

Streptococcus uberis

Wash teats only, dry well Neglected Pronounced swelling of with udder washing, one or more quarters. On cow's disposable Contaminated insufficient Milk highly abnormal. skin, mouth, paper towels drying, lack of High fever in serious environment ground for each cow bedding, cases. Affects mostly dry muddy yards cows and heifers.

Supply generous bedding

Escherischia cold

Contaminated environment

Ground, bedding (sawdust

Dirty calving stall, lack of bedding,

Often very serious. May Wash teats lead to loss of quarter or only, dry well even death. Thin yellow with

and shavings), manure, water

inadequate secretions, with granular disposable udder washing texture resembling bran. paper towels Often high fever. for each cow

Supply generous bedding

Pronounced systematic reaction due to toxins caused by bacteria. Often more than one quarter affected. They become hard, produce thick smelly secretion like cheese and difficult to eliminate. Followed by abscess that bursts, releasing creamy pus, and tissue loss.

Corynebacterium Certain insects pyrogenes

Humid valleys, wooded areas


Mastitis is a difficult problem to comprehend because it is a disease caused by many factors. Microorganisms are responsible for the infection, but for them to enter the mammary glands and establish themselves to the point that they cause an infection, a multitude of factors may be involved (e.g. hygiene, housing, climate, milking machines, feed, genetics) acting simultaneously. It is even more difficult to generalize about the relative importance of each one, as certain factors affect certain microorganisms. Klastrup and his coworkers21 estimate that 25% of the susceptibility to infection is attributable to environmental factors, 20% to genetic factors, and 50% to herd management.


Climate may have a direct or indirect influence on the onset of mastitis. Older texts7,43 insist a great deal on the fact that exposure to intense cold, draughts, excessive humidity or heat predisposes cattle to mastitis. Just as they foster our colds, rapid changes in temperature can encourage mastitis. Research on how temperature influences the incidence of mastitis indicates that temperature extremes interact with other factors to cause mastitis but rarely will temperature alone cause the disease21. Temperature extremes may also affect somatic cell counts. Therefore the incidence of mastitis increases with extreme temperatures. In Florida, a higher rate of clinical mastitis was observed three years in seven during very hot periods28. A particular type of mastitis, often called summer mastitis, is caused by biting insects that contaminate the udder with the bacteria Corynebacterium pyogenes and other anaerobic bacteria. The frequency of this type of mastitis varies according to the regions, with humid valleys being most susceptible. Climate may also have an indirect influence. For example, muddy conditions outdoors caused by abundant rainfall will increase the number of microorganisms and thus increase risks of infection. Housing Just keeping cows indoors increases the incidence of mastitis. When cows are inside, the risk of udder injury increases. There are also microorganisms indoors whose populations are less concentrated outdoors. In Australia, where cows go indoors only to be milked, mastitis caused by coliforms is rare. Although the question is often debated, it would appear that mastitis is less common with loose housing systems than with tied housing systems. It might be thought that mastitis is more frequent with loose housing because the microbes are easily transmitted from one cow to another. However, cows are usually happier in loose housing. They are also less likely to injure themselves or come into contact with soiled bedding and so are less subject to mastitis. The social adjustment of cows within the herd is also clearer with loose housing. According to a Serbian study 27, there were 27% fewer cases of subclinical mastitis and 42% fewer cases of clinical mastitis in loose-housed herds than in herds kept tied. In tied housing, there is greater likelihood of mastitis with some types of stalls. The longer and wider a stall, the more the cow can move, thereby reducing the number of injuries and the incidence of mastitis19. The greatest disadvantage is that the animal's vertical movements are restricted, particularly when getting up or lying down.

Partitioning between the stalls reduces the incidence of mastitis arising from abrupt movements of neighbouring animals and tramped teat. Quality of indoor air In a barn, draughts, excessive humidity and frequent changes in temperature are factors that lead to increased incidence of mastitis. Indirect effects on an animal's immunity have not been seriously studied. However, effects on the concentration of pathogens in stables have been. For example, the bacteria Klebsiella pneumoniae causes more infection when relative humidity is low48, while the number of infections caused by E. coli does not vary with humidity changes. Bedding Whether with loose or tied housing systems, bedding plays an important role in the incidence of mastitis. This is easy to understand when considering the mastitisinfected milk that ends upon the ground, the humidity that favours the development of microbes on bedding, and that cows often spend 14 hours out of 24 in contact with their bedding. In an experiment where cows were housed with and without bedding, the level of mastitis infections doubled where there was no bedding. Inadequate bedding in loose-housed herds, particularly large herds, may lead to serious situations of contagious mastitis. Different materials used as bedding may affect the growth of different microorganisms. Straw is generally most recommended. There is less rapid development of pathogenic microorganisms with chopped straw and cedar sawdust than with newsprint4. Chopped straw, however, is more favourable to Klebsiella than sawdust16. Sawdust and shavings, particularly if heated, encourage the rapid development of coliforms in general and are often responsible for "epidemics" of coliform mastitis36. Stress The more an animal is stressed in its environment, the less efficient its immune system is, and the less it can resist microbial infestations. Therefore, the more stress there is, the greater the chance of mastitis10. Giesecke10 has even demonstrated that stress affects the integrity of intramammary cells, which is yet another factor contributing to mastitis. The following are some sources of stress: - Excessive density of animals. Proximity of cows encourages microbial exchanges and tense relations between animals;

- Irregular management, unpredictable behaviour on the part of the farmer; - Noise; - Stray voltage.
Genetic factors

Recently there has been a lot of research on how hereditary factors influence susceptibility to mastitis. The different dairy cattle breeds are not equally susceptible. High-producing cows are more likely to be affected. Selective breeding that focuses solely on milk production is undoubtedly an important factor in higher rates of mastitis. According to different sources, hereditary factors account for 12% to 20% of susceptibility to mastitis in a single breed. Cows selected for several traits have a higher somatic cell count (better immune response), requiring almost two times less treatment, and their milk is thrown away half as often as the milk of cows selected for one trait, although the latters produce more milk49. Genetically, there is a correlation between the percentage of milk fat and the incidence of clinical mastitis. The more a line of cows produces fat milk, the more it will be susceptible to mastitis. It is therefore important to not select on this basis only.

Despite several serious studies on the subject, the links between diet and mastitis still raise questions in scientific circles. There is agreement on two practices that increase the risks of mastitis - rapid changes in diet and excess or imbalance in the different components of rations. Nitrogen and proteins Excessive nitrogen or protein in feed is often mentioned as one of the factors causing mastitis. According to a Danish study25, there is no definitive link between protein content in diet and the incidence of mastitis. However, there is more evidence regarding the harmful effect of nitrogen that is not in a protein form (e.g. urea and ammonia) on disease incidence. Nonprotein nitrogen (NPN) is particularly hard on white blood cells, or leucocytes, which protect the udder. Abrupt changes to rations based on NPN-rich high moisture corn or alfalfa silage should be avoided. Increases, however modest, of ammonia in

the blood have repercussions on metabolism. If such rations are used, sufficient fibre should be included to feed microorganisms in the rumen that will convert the nonprotein nitrogen into bacterial protein. According to an experiment realized in Germany8, there is a significant relationship between the level of urea in the blood and bacterial colonization in the udder. In another experiment, the addition of urea to rations increased susceptibility to infection and increased the number of infections by more than 16%45. The effect on the immune system is particularly evident when the urea is given in large quantities (over 18Og/day more than nitrogen requirements)2. Concentrates and energy It is recommended that reduced quantities of concentrates be given to a cow with mastitis. It appears this is also true for preventing mastitis, according to a German study22 conducted on 1038 first lactation cows and 572 cows of successive lactations. When the cow rations contained 25% concentrates rather than 40%, the incidence of mastitis was 7% compared to 36% for first lactation cows and 19% in comparison to 37% for other cows. The same study also compared different energy levels in rations. A high energy content in rations increased the incidence of mastitis in first lactation cows whereas it had the opposite effect on the other cows. Calcium-phosphorus ratio An inadequate calcium to phosphorus ratio in rations results in problems with milk fever at calving40. In large herds, up to 50% of animals lacking calcium in their rations will develop coliform mastitis a few hours after calving. This hypocalcemia generally results from an inadequate calcium to phosphorous ratio in rations during the dry period. See page XX for more information on rations to give during the drying off period. Silage and hay Poor quality silage has a very negative effect on the immune system. The overheated proteins and sugars may kill the white blood cells protecting the udder. Cows fed with hay and grain have greater resistance in every way to several pathogens than cows fed with silage38. In some cases, Pseudomonas and Proteus are the only microorganisms that survive the high temperatures produced in silage. Although rare, silage contaminated this way may then be a source of mastitis caused by these organisms.

Mouldy hay and mycotoxins also harm white blood cells and therefore weaken the immune system. Alfalfa and other legumes Legumes, particularly alfalfa, contain estrogenic substances whose concentration varies depending on plant maturity. Turning legumes into silage does not reduce their estrogenic properties. Through a physiological mechanism, that is still not well understood, these external estrogenic substances (that is, they are not produced by the cow herself) tend to foster mastitis. Several studies indicate that alfalfa added to the rations of cows with chronic mastitis exacerbates the infection. What is important is not to feed silage with a high legume content to heifers. This estrogenic intake encourages premature development of the udder and increases the incidence of environmental mastitis21. Selenium and vitamin E In the last ten years, several researchers have looked into the use of supplements and the role of selenium and vitamin E in the prevention and treatment of mastitis. Maintaining an adequate level of selenium in the cow helps prevent mastitis, reduce the severity of infection and shortens its duration. Selenium serves to reinforce the immune system response by increasing the release of leucocytes and increasing the efficiency of phagocytes9. Selenium and vitamin E work together in the cow. Thus, a vitamin E supplement alone of 1000 lU/day reduces the somatic cell count but not the incidence of mastitis3. With both selenium and vitamin E supplements, infections may be reduced by approximately 40% at calving, by 60% for the entire duration of the infection and by 30% for clinical mastitis. The role of selenium is considered to be most significant in the case of subclinical mastitis30. Selenium supplements may play a particularly significant role in cases of mastitis caused by E. coli. For example, cows that are given a selenium supplement of 0.35 mg/kg dry matter are better able to resist mastitis caused by E. coli24. The duration of this type of mastitis is even shorter when cows receive 2 mg of selenium per day per kilo of ration9. Recommended blood levels are 0.2-1.0 g/ml for selenium and more than 4 g/ml for vitamin E. Rations should provide 3 mg of selenium per day in the case of dry cows and 6 mg per day for producing cows. Rations should provide 1000 IU of vitamin E per day for both categories of cow44. Supplementation with vitamin E has a greater

effect on dry cows than on lactating cows, where a good part of vitamin E supplements is eliminated in the milk. Important: It is not useful and even harmful to give large doses of selenium only (that is, without vitamin E), because the effect can be toxic. A selenium dose of 16 mg/day results in higher levels of mastitis unless vitamin E supplements are administered at the same time53. Silica Finnish researchers34 noted that the level of silica in mastitis-infected milk was only 0.39 mg/litre whereas it was 0.81 mg/litre in normal milk. Also, the level of silica in the blood serum of cows infected with mastitis is 1.02 mg/litre rather than 1.63 mg/litre for uninfected cows. Silica, whose role is similar to selenium, has a marked effect on the formation of free radicals, lipid peroxidation and macrophage activity. The silica content in rations may be increased by giving high silica-content feed like cereal straws. Other nutritional factors Vitamin A deficient rations reduce immunity. An Italian researcher experimented with vitamin A and beta-carotene supplements to control mastitis11. According to Katholm18, iron also plays an important role in the prevention of mastitis. It is linked to the protein lactoferrin.

Needs of the calf The famous animal phytotherapist Juliette De Baracli-Levy6 believes that preventing cows from benefitting from the pleasure and stimulation of nursing their calves is one of the principal causes of mastitis. With suckling calves, Levy makes a distinction between the "psychological" and physical factors. It is often observed that cows separated from their calves shortly after calving look and call for them. The question of course is whether cows experience a difficult "emotion". If this hypothesis is accepted, however, it would suggest that cows who find the separation more difficult develop mastitis more easily. On a physical level, the frequency of calf suckling is greater than cow milking. Microorganisms that invade a quarter have very little time to develop. Should cows

therefore be milked more often at the beginning of lactation? Slavic researchers47 have observed that the duration and frequency of mastitis was lower during the first two months following calving with cows that nursed their calves for six to ten days as opposed to one hour, two days or four days. Herd hierarchy With loose housing or pasturing, a hierarchy is created within the herd, a phenomenon that is even more apparent in goats than in cows. It is possible that the least dominant members of the herd, who are often harassed by the others, have a greater tendency to develop diseases. The advantage of loose housing is that the hierarchical relationships between members is clear. Cows in tied housing can be quite stressed when they find themselves in an exercise yard where relationships between cows are not clear. Uterus-mammary glands It has been demonstrated that cows who retain their placentas have mastitis more often that those who do not14. The risk of developing mastitis is increased threefold42. According to German researchers55, mastitis is clearly associated with placenta retention when caused by Actinomyces pyogenes . This type of mastitis represents 17% of cases in Germany. Mastitis that appears within the two months following calving is often linked to uteruses that are not cleaned properly. Discharges of purulent matter dirties the tail and rear end of the animal, and the ground, which favours environmental and, subsequently, udder contamination. Some veterinarians venture further by saying that the reproductive organs may serve as reservoirs of infection. The pathogens thus travel through the blood to the mammary glands. At any rate, beware of placenta retentions! Rumen-mammary glands The rumen is a very important organ of the cow, and the health of the other organs often depends on it. When acidosis occurs in the rumen (too much grain in rations for instance), it creates conditions that foster bacteria likeStreptococcus bovis and eventually yeasts like Candida albicans. Therefore, although rare, the toxins from these substances can travel throughout the system and favor gram-positive bacteria that attack the udder54.

The approach of most laboratory studies is to consider factors in an isolated manner. In mastitis research, there are numerous studies based on farm practices. These studies rely on questionnaires addressed to farmers, analysis results, etc. One such study that

was particularly original was conducted in eastern Ireland46, and integrated human factors with herd management factors. The results are given in the table below. It should be noted that the farmer's age and teat washing did not emerge as determining factors in the incidence of mastitis during the study.

Table 3 - Human factors and milk production

Characteristic Associated factors

Low somatic cell Geographical position of the farm, treatment of dry cows, replacement cows count produced on the farm, positive attitude towards milking, family enterprise. High somatic cell Small herd, irregular maintenance of milking equipment, lack of bedding on cement count floor, udder washing of dirty cows only, little ambition. Low bacterial count High bacterial count High milk yield Treatment of dry cows. Tied housing, obsolete milking equipment, short withdrawal period after antibiotic treatment, limited inclination to seek out information. Average herd, treatment of dry cows, average inclination to seek out information, elimination of cows that are too susceptible. Lack of hot water at milking, use of one cloth only for all cows, infrequent meetings with other farmers, strong will to continue traditional family farming, no vacation.

Low milk yield


To diagnose mastitis, it is necessary to learn how to distinguish between the symptoms of the various types of mastitis infection (see Tables 1 and 2 on page XX and XX respectively). The key points to remember are as follows: Monitor the milk: routine examination of the milk using a filter cup to extract the first three squirts before washing (before milking) is undoubtedly the best way to diagnose mastitis. The presence of lumps, flakes, blood, etc.

must be watched for. Milk that is hotter than normal may be a good indication of a Staphylococcus aureus infection. Palpate the udder: particularly after milking, when it is easy to detect swelling, and fibrous, hard or injured tissue. Be attentive: to other more evident signs such as fever, redness, etc. Since these symptoms are often absent, particularly in cases of subclinical, subacute or chronic mastitis, only half of all mastitis infections, at best, can be detected through observation. Some tests may therefore also be useful, notably cell counts, bacterial identification and the California Mastitis Test (CMT).

All producers registered in a dairy record of performance are familiar with somatic cell counts. Sometimes wrongly referred to as white cell counts, this type of test includes all somatic cells, including white cells (or leucocytes) and epithelial cells. When swelling occurs, the cow's immune system reacts by sending leucocytes to destroy the foreign bodies. The somatic cell count in the milk may thus indicate if a cow is fighting infection. Cell counting came into use largely to ensure that milk from a given herd was fit for human consumption. It is also a highly useful test for mastitis detection, albeit lacking in certain respects. First, cell counts do not distinguish between leucocytic and epithelial cells. For example, for normal milk with a cell count of 50,000 cells per ml, there may by 20% leucocytes and 80% epithelial cells, whereas mastitis infected milk with a cell count of over 500,000 cells per ml, contains 90 to 95% leucocytic cells. It would be easier to determine if a cow was fighting infection if only the leucocytic cells could be counted. Since the count does not make the distinction, it is difficult to interpret the results of a count, especially with average numbers. With high cell counts, the so-called "millionaire" cows, the diagnosis is clearer and is indicative of mastitis. Second, there is tremendous variation between the number of somatic cells with or without mastitis. The number of somatic cells in milk is generally higher in summer months, higher at the beginning and end of lactation and increases with the age of the cow. It also depends upon the genetic history of the cow and bull13. Moreover, an increase in somatic cells may be linked to a functional disorder of the reproductive organs. Even with a sampling and count that are properly carried out, a difference of

25% from one day to another can be expected without the circumstances of the herd having changed29. Third, cows in one herd react differently to infection than cows from another herd. For example, Natzke29 reports that the average cell count of milk from quarters infected by Staphylococcus aureus was 6,700,000 in one herd and 900,000 in another. In the same study, the non-infected quarters had a cell count of 600,000 in one herd and 150,000 in the other. Finally, when a cell count is high, the animal or the milk generally shows obvious symptoms of mastitis. The test therefore tells us nothing more than our attention to symptoms. Despite these shortcomings, the somatic cell count remains an important and practical tool for measuring the general health of a herd or individuals. Natzke29 believes that cell counting is particularly useful for evaluating the long-term health of a herd. Observing cell count trends from one year to the next serves to evaluate if any progress has been made, or if the situation is stable or deteriorating.

In several states and provinces, bacterial counting in milk is done monthly for all dairy farms. It consists of evaluating the size of populations of different microorganisms in milk samples. The identification of microorganisms present in the milk is sometimes useful on the farm to determine exactly what species of bacteria are responsible for the infection. This is the case for example when several cows have the same symptoms. These tests are done at government pathology laboratories.

Sanitary milking habits are important to avoid the spreading of germs or their proliferation. The purpose of hygiene is to prevent the transmission of germs from one teat to another on one cow or from one cow to another. There is no need to get overly excited about germs... but why provoke them? Pasteur admitted at the end of his life that "the terrain is everything, the microbe is nothing", meaning that pathogenic microorganisms could not cause disease in a healthy animal or plant (well fed, etc.). Although optimum health is always the

ultimate goal, it is not always easy in to attain in herd management. Therefore, in the meantime, a little hygiene can't hurt! Udder washing Washing the udder is hygienic and has a stimulating effect on milk flow. Adequate washing is especially important to prevent environmental mastitis, caused by coliforms and other microbes from contaminated environments. Badly washed udders contribute to the transmission of microbes rather than to their destruction. According to Pankey33, the lowest bacterial count in milk is obtained by washing the udder in the following fashion: - Using individual moist paper towels, wet and wash the teats only. Wetting the udder and the teats results in more bacteria getting into the milk than if only the teats are wet. - Dry with individual paper towels. Note that teat dipping before milking in addition to drying off does not give better results than drying alone, and it increases the risks of contamination of the milk by disinfectants. Udder washing This is a recipe for washing udders used by Daniel Lapointe, an organic dairyman from Quebec. Although the antiseptic value of this formula has never been scientifically tested, he has been using it for many years with good results. It consists of mixing 13 litres of hot water, 1 drop of pine oil, 1 capful of peroxide and 1 ounce of clay. Foremilking Removing a little milk by hand before machine milking serves to stimulate milk letdown and to obtain a milk sample containing a high microbial count. A filter cup is used to detect abnormal looking milk (lumpy, etc.). Milking sequence It is important to milk infected cows last. If possible, milking sequence should be as follows: first lactation cows, normal cows, cows with a high cell count and then infected cows.

Other measures during milking It is important to milk completely. With modern milkers, as long as they are well adjusted, the risks of forcing the entry of microbes at the end of milking greatly diminish. The chances of bacteria entering the udder can be reduced by diminishing the amplitude of the vacuum changes and the vacuum change speed on the teats12. To do so, a good vacuum reserve and appropriate piping are necessary. Furthermore, the milker must not slip on the teats and the milkers must be removed carefully. Risk of infection may be diminished if milking is finished by hand, although not realistic for an entire herd. De Baracli-Levy6 even suggests massaging the udder after milking and hitting it up and down in the same way that calves do. It is important to milk twice a day, even with cows that do not produce a lot. The longer the milk remains in the udder, the greater the risk of infection. The first squirts of milk must not go on the ground as this will contaminate the bedding and floor. Postmilking teat dipping Using a disinfectant teat dip after each milking is a means of diminishing by about 50% the risk of infection by contagious microorganisms like Streptococcus agalactiae and Staphylococcus aureus. Teat dipping prevents populations of these microbes from developing sufficiently between milkings. Teat dipping also discourages flies. It is important that the teat dip contain up to 10% of emollients to increase the suppleness of the teats: oils, glycerine, lanoline. Healthy supple skin is an extra insurance against entry of bacteria to the udder. Staphylococcus aureus does not persist on healthy skin. Teat Dip This is another recipe by organic dairyman Daniel Lapointe. You simply mix four litres of water, 5 ml of lavender oil, 5 ml pine oil, 2 ml eucalyptus oil, 12 ml cottonseed oil (available in drugstores) and 5 ml methylene blue. Cleaning equipment after milking It is obviously important to clean and disinfect equipment after milking. Cider or corn vinegar and peroxide are used by some producers as alternatives to phosphoric acid and chlorine.


MATERIAL: Filter cup, hot water at 55C with disinfectant, paper towels, pails for used towels and container for teat dip. MILKING METHOD: 1. Collect first three squirts of milk in a filter cup.

2. Soak towel in hot water with teat dip disinfectant, and wash each teat, using the other side of the towel to wash the teat sphincters.

3. Using another towel, wipe off the four teats and then with the other side of the towel massage the four teats by rubbing vigorously in a circular motion: 0-3 months of lactation = 10 times; 4 -7 months lactation = 15 times; 8 months lactation and more = 20 times.

4. Install milking unit on each cow, without losing vacuum.

5. Shut off the vacuum when milk flow is insufficient, remove the milker claw and immediately wash the teats. Note: Only 15% to 20% of cows need to be milked dry. In this case, press gently on the milker claw while massaging from bottom to top the quarters that still contain milk.

Indoors Abundant bedding prevents injury to the udder, limits exposure to cold damp floors and limits contact of the udder with manure. A minimum of 3 kg of straw per day per

animal must be used (about one ton per cow per year). It is better to use a little bedding often, rather than a large quantity less often. Straw is preferred. Adding lime to the bedding can help in a stable where environmental mastitis is a problem but can also irritate the udder, the teats and the lungs when airborne. It is important to keep the cows from injuring their udders. The floors should not be slippery when the cows are let outdoors and there should be separators between the cows. Disinfecting the stable twice a year is a good practice. Outdoors There should not be any mudholes around the buildings or any place the cows have access to. Along the same lines, watering areas should not be allowed to become mucky. Ideally they should be located on higher ground or have gravel or cement platforms under the drinking areas. There should be no barbed wire left lying around in areas where the cows could injure themselves. Overpopulation in the stable and fields, particularly with loose housing, should also be avoided, as it increases stress on the animals and the risk of contagious mastitis being transmitted.

Changing feed must be done slowly. Excesses must be avoided, particularly concentrates and nonprotein nitrogen feed (e.g. alfalfa and high moisture grain corn silage). A 1.4 to 1.8 calcium to phosphorous ratio must be maintained, even during the dry period. Selenium and vitamin E supplements may be a good choice if the ration does not provide the necessary minimum. For more details, consult the section on nutritional factors on pages x, x and x.

Replacement: Do not buy infected animals; have them tested before purchasing them and examine the udders. Research in several countries has demonstrated that up to 50% of purchased cows have subclinical infections37. It is better to buy only heifers (heifers generally do not have mastitis) or produce your own replacement animals. In any case, heifers should not be suckled as this breaks the teat seal and thus facilitates entry of microorganisms that can cause mastitis at calving.

Culling: Cull animals that are severely or repeatedly affected by mastitis. Cows with injured teats that do not heal should be put at the top of the list of animals to cull. They are up to 10 times more likely to contract mastitis. Cows that maintain a high cell count during all lactations should also be culled.

It is well known that mastitis often affects cows that have recently gone dry. These animals should not be overfed, particularly during dry periods. First lactation cows in particular must also be supervised since they are twice as likely to develop mastitis during the dry period than the others29. In conventional agriculture, treating dry cows with antibiotics is often considered, along with the postmilking teat dip, one of the most effective methods to reduce incidence of mastitis. For organic agriculture, the dry cow must not be overlooked. A change in feed at drying-off is important. The following are the three steps: Post-lactation (7 to 14 days): give a reduced diet of fibrous and poor hay to provoke rapid drop in milk flow and to stimulate the rumen. Drinking water must be drastically reduced. Some organic farmers give 4 drops of sage or menthol essential oil and charcoal two times a day to cut production at this stage. Dry (30-90 days): diet is made up mostly of roughage with a good energy-protein and mineral balance. Pre-lactation (7 to 14 days before calving): moderate quantities of energy-rich concentrates are added to a balanced roughage ration. Use of the teat dip before and after the dry period (i.e. 15 days before calving and 15 days after the dry period) may be beneficial in herds where clinical mastitis is common32.

The following curative measures are particularly for clinical and chronic mastitis. There is a vast range of curative methods that may be used as an alternative to antibiotics: homeopathy, clay therapy, phytotherapy, etc. The advantage of homeopathy over antibiotics is that milking may be continued. The other alternative products used must not go in the bulk milk because tests for detecting antibiotics in milk may react positively to certain products like some essential oils.

When a treatment is being administered it is important to modify other practices: - Infected cows must be fed prudently. Concentrates must be reduced and extra fibres and laxatives must be included. In cases of clinical mastitis, Eckles7 recommends reducing grain rations by one third as soon as symptoms appear and until they disappear; - A purge must be given (except with homeopathic treatments); - Avoid exposing infected animals to cold and draughts; - Milk gently by hand 3 to 6 times a day. Extreme caution must be used with products that are injected into the teat. It is quite difficult to make a clean" injection in a contaminated environment such as a dairy barn without provoking a new contamination in the quarter. In all cases, it is important to immediately contact a veterinarian if there is no rapid improvement.

Clay has several therapeutic properties. On account of its high absorbency, it has proved efficient as dressing to treat inflammation caused by mastitis. To prepare a clay dressing, the clay is mixed with a liquid. Some producers use room-temperature water, while others use olive oil. A good compromise is to use half water, half oil, with the oil giving a more elastic consistency to the paste. The final result must be fairly liquid while adhering well to the udder. When using water, it can be allowed to penetrate slowly into the clay without mixing. The container should be covered with a cloth and set out in the sun. The oil mixture on the other hand must be mixed. In both cases, a wooden spoon must be used and ideally the container should be a non-reactive material like porcelain or glass. The therapeutic effect of the paste may be increased by adding 2 to 3 drops of pine or thyme oil for every two litres of mixture. The clay dressing must be spread over the infected parts of the udder after milking. The clay may be removed once dry and replaced 2 to 3 times a day by a new application. The dressing may be left on all night after evening milking.

In the case of the mixture containing oil, the mastitis has healed when the udder stays oily after the dry clay has been removed. This treatment should produce results in two to three hours in the case of acute mastitis, 4 to 6 hours with less serious forms and two to three days with chronic mastitis. It the treatment does not appear to be having any effect after this time, other measures must be considered.

The following information is general advice only and should not be considered a replacement for professional advice from a homeopathic veterinarian. Prevention Preventive homeopathic treatments are administered using nosodes on an entire herd rather than on individual animals. Nosodes are fragments of pathogenic cells that increase the immune response. Nosode preparation is established according to the species of bacteria causing the problem in the herd. MacLeod23 recommends a nosode of 30 dilutions in liquid form administered by the mouth or in the herd's drinking water. Complexes An alternative to nosodes that is particularly effective for subclinical mastitis is to use in conjunction homeopathic remedies that have proven effective against mammary gland afflictions. MacLeod23 recommends the following combinations as multiple use remedies: Belladonna, Bryonia and Urtica Urens; Phytolacca, Sulphur, Silicea and Carbo vegetabilis. Most homeopathic laboratories (see list of useful addresses on page XX) offer specific complexes for mastitis. The advantage of these complexes, which heal three out of four cases, is that they are easy to use. Some practitioners do not recommend the use of complexes on animals that are to be kept for several years because these substances tend to "confuse" the immune system. Homeopathic treatments are administered through the mucous membrane. Homeopathy is less effective when the infection is caused by injury to the teat. Specific treatments More specific homeopathic remedies are selected according to the symptoms, such as lumpy milk, edema type, etc. Those used by two famous homeopathic veterinarians, Britain's MacLeod and France's Quiquandon, are given in Tables 4 and 5.

Table 4 - Homeopathic remedies used by MacLeod to treat mastitis

Homeopathic Remedy Symptoms Dose

For acute postpartum mastitis. Udder very hot and Belladonna 1 m red, painful to the touch. Animal is hot, and pulse is quick and strong.

1 dose every hour. 4 doses.

Aconitum 6 x

Routine treatment for all acute cases, particularly those that develop rapidly after exposure to cold dry 1 dose every half-hour. 6 doses. wind. Relieves tension and anxiety. Indicated for first calving, heifers with edema of and around the udder. Mammary vein is swollen. 1 dose every 3 hours. 4 doses.

Apis Mellifica 6c

Acute cases: 1 dose every 4 Indicated for swollen and very hard udders. Pain is Bryonia Alba 30 hours. 4 doses. Chronic cases: 1 less intense when pressed. Animal is often Iying dose 2 times a week for one c down. Especially good for chronic cases with fibrosis. month. Arnica Montana 30 c For mastitis resulting from udder injuries. There may then be blood in the secretions. 3 doses per day for 3 days.

Belia Perennis As with Arnica, but for deeper injuries (e.g.: neglected 6c milkers). Useful for clinical and chronic cases. Clinic cases with Phytolacca 30 c sour, coagulated milk. Chronic cases with small clots at mid-lactation. For clinical cases where edema forms plaques sometimes up to perineum. Mixture of Sulphur, Silica and Carbo Vegetabilis that gives good results with clinical and subclinical cases. Lumps are usually big and yellowish, especially in first squirts of milk. Aids suppuration and cleaning of udder in summer

3 doses per day for 4 days. Clinical: 3x/day for 3 days, followed by 1 dose a day for 4 days. Chronic: 1 dose every 3 hours, 4 doses. 1 dose an hour, 4 doses.

Urtica Ulens 6x

S.S.C. 30 c

3 doses a day for 3 days.


1 dose every 3 hours, 4 doses. 1

Sulphuris 6x

mastitis cases (C. pyogenes).

or 2 doses in greater dilution after udder is okay. 2 doses a week for 4 weeks.

Silicea 200 c

Also useful for summer mastitis cases with purulent abscess. Useful for treating internal bleeding that produces pink or bloody milk.

Ipeca 30 c

3 doses a day for 3 days.

Source: Adapted from MacLeod (1981) Legend: x, c and m refer to dilutions 10, 100 and 1,000

Table 5 - Homeopathic remedies used by Quiquandon to treat mastitis

Remedies Belladonna 5 CH Lachesis 5 CH + Belladonna 5CH Lachesis 5 CH + Carbolicum acidum 5 CH Symptoms Hot red mammary gland that is painful to the touch, high fever. Prostrate animal. Violet mammary gland, infiltration of underlying tissue with lateral preference. Prostrate animal. Gangrenous mastitis. Acute inflammation with edema, swollen veins, gangrenous tendency, extremely painful to the touch, quarter may feel cold. Weak heart, small quick pulse. Marked glandular indurations. Chronic mastitis or end of mastitis. Little or no pain to the touch. Hypertrophy followed by atrophy. Hard quarter or nodes inside. Painful to the touch, retromammary ganglia. Cracking around teats. Acute mastitis with hard gland, hot but pale. Animal immobile. Strong pressure brings relief. To dry the pus.

Vipera Reddi

Conium maculatum + Plumbum iodanum 5 CH Phytolacca alternating with Conium Bryonia Silicea

Source: Quiquandon (1982)

In the case of clinical mastitis, particularly that caused by E. coli, good results were obtained with the following homeopathic treatment26: - initial treatment: Aconitum D4, phytolacca D1, bryonia D4 - subsequent treatment: phytolacca D1, bryonia D4, lachesis D8 and Mercurius solubilis D4.

Juliette De Baracli-Levy method This method requires care and attention for one week or more and, from this perspective, is not really practical today for use in commercial herds. It has however proven itself in England where it is has been highly effective against clinical mastitis. Medicinal herbs to use are garlic and wood sage, Teucrium scorodonia, (see useful addresses on page XX for seed sources). Wood sage acts specifically on mammary gland problems. The method is as follows: - Confine animal indoors in airy quarters; - Begin with a two-day fast. Give only water; - Put the bedding in sacks to ensure that the animal does not eat it and provide enough to completely shield the animal from the cold cement; - Each morning of the fast, administer wood sage tea in a single dose. To prepare the wood sage, finely cut two handfuls of the herb, steep in a litre and one half of water, add two teaspoons of honey; - Each night of the fast, give a senna-based laxative. Soak 20 senna cloves in a half litre of cold water for at least six hours, and add one teaspoon of ground ginger. Administer in a single dose;

- On the morning of the third day, administer a mixture of two litres of milk, half a litre of warm water and ten large tablespoons of molasses. Also provide finely cut wood sage mixed with bran and molasses; - At midday and in the evening administer a preparation made by grating two garlic cloves in a litre of water (6 to 8 garlic capsules morning and night are equivalent); - Every morning and evening administer a preparation made with about two-thirds of a gallon container of sweet hay, softened by heating over hot water. Add 1 kg of bran and 10 tablespoons of molasses; - Give the same ration for three days, gradually increasing the quantity of hay according to the animal's appetite; - If available, two handfuls of the following plants: raspberry leaves, Geranium robertianum, Artemisia abrotanum; - When the cow's temperature has returned to normal, put her out to grass in the sun. Kelp Kelp, a variety of seaweed, is one of the rare plants whose effect against mastitis has been proven scientifically50. Its effect is preventive, however, rather than curative. In a seven-year experiment with twin cows, where one was given kelp in its ration and the other not, the incidence of mastitis was greatly reduced in the cows receiving kelp. Kelp has an effect on different types of bacteria, not to mention the numerous minerals it contains. Biodynamic mastitis ointment This ointment, which is applied on the affected quarters, is made with lard and marigold flowers (Calendula officinalis). Here how it is prepared17: - Melt 2 kg of lard in a double boiler; - Add two handfuls of dried marigold flowers; - Heat over low heat for one half hour in the double boiler;

- For a stronger ointment, add marigold extract obtained in the following fashion: fill a glass jar with 50 to 100 ml of dried flowers; cover with ethylacetate (sold in drugstores); seal the container. The ethylacetate will quickly evaporate; - Filter the hot mixture through cheesecloth; - Pour into one litre containers and let cool. Aloe Aloe is particularly indicated for treating udder injuries, which often leads to staphylococcal mastitis. Application of the aloes will quickly heal the tissue. For treatment of the mastitis, Coats and Holland5 recommend injecting 20 to 60 cc of aloes (in gel or juice form) into the infected quarter at least once a day. The teat end must be sterilized before an injection because the aloes will carry all the filth with it into the teat, thus aggravating the situation. Aloes helps to drain the infection, has antiinflammatory properties and is a coagulant. It has a diuretic property also, which serves to soften the hardened udder. Once again, it is important to remember that the milk from cows treated this way cannot be put into the milk tank. Dressings In his 19th century treatise on dairy production, Sheldon43 recommends several treatments with a medicinal plant base for clinical mastitis: 1. Application of compresses (Caution! Hot water can increase inflammation) followed by hop meal, tea leaves or bran, repeated often. A net in the shape of a T attached to the animal keeps the cataplasm in place. The long part of the T goes between the cow's hind legs and is attached with the short ends of the on either side of the udder. 2. Extract or ointment from Belladonna rubbed daily on the udder reduces pain and aids secretion of mammitic milk. 3. Fever and constipation that accompany clinical mastitis may be treated with oil and molasses.


Oxygen therapy is increasingly talked about as a cure-all for disease, both for plants and animals. True, oxygenation is essential for the health of humans and animals. In oxygen therapy, it is usually hydrogen peroxide that is used. There is a mastitis treatment, called Koch Treatment after its inventor Dr. William Frederick Koch, that has an oxygenating substance similar to peroxide for its base, glyoxilide. Tests of this treatment with British Columbia dairy producers, under the supervision of the BC ministry of agriculture, produced very good results. Also, a large number of Michigan dairy producers attest to its effectiveness. Glyoxilide is sold in 5 cc ampoules, which is the treatment dosage. The dose is injected with a hypodermic needle into the cow's neck or shoulder muscle. A single treatment is administered, sometimes two, and rarely three. Glyoxilide provokes reactions in 21-day cycles, reactions that fade with time. Its action extends over one to two years.

Several other methods and products are used to treat mastitis. Doubts may be raised about the effectiveness of methods that have not been proven scientifically (e.g.:injection of egg whites into the teat) but questions may also be raised about scientifically proven methods that risk making the animal suffer (e.g.: injections of copper sulphate, calcium oxide and neem oil into the udder51). The following are some other methods worth mentioning. Natural method One of the proven methods for rapid treatment of mastitis consists of letting a calf vigorously suckle the infected cow, ensuring that the calf suckles the infected quarters. Unfortunately, the calf may become a vector of the microbe in the herd. Acupuncture According to Kendall20, acupuncture is effective against mastitis but the treatment is very long and therefore less appealing compared to the other therapies. Furthermore, there are few acupuncturists that treat bovines at the moment in North America. Antibodies

Certain commercial products are made with antibodies. Colostrum is one such product, from lowa (USA), available through homeopathic veterinarians. It is administered by intramuscular injection. This product will eliminate the problem in less than 12 hours and does not cause loss of milk.

The following are the highlights on methods for preventing and treating mastitis without antibiotics: - There are several types of mastitis. It is to the dairyperson's advantage to be able to distinguish between the different types of mastitis and to be aware of the conditions that can promote the development of the microorganisms responsible. - Many factors can predispose animals to mastitis: environmental, genetic, nutritional, physical, ethological and human factors. It is rarely possible to attribute the occurrence of mastitis to a single cause. Feed and milking hygiene, even during the dry period, are important factors. - Somatic cell counts are a practical albeit imperfect way to detect mastitis. They have proven especially effective for observing a herd over the long term. On a daily basis, visual and physical examination of the udder remain an essential detection method. - Appropriate hygiene during milking, bedding and sufficient space for the animal, culling of repeatedly affected animals and adequate feed, even during the dry period, are ways to prevent mastitis. - Clay dressings, homeopathic remedies, medicinal plants and oxygen therapy may be used as curative methods against mastitis. Mastitis of all types is a disease that must be taken seriously. Consultation with a veterinarian is recommended.

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