The basics of herd health fills books (e.g., Brand et al. 1996, Radostits et al. 2001). Although general statements about herd health programs are common, they are useful only as starting points when developing a herd health program for a specific herd. A major mistake is to focus on a single component, such as a vaccination program, as is often done. A vaccination program alone is not a herd-health program. Successful herd health programs require the careful integration of disease biology, knowledge of which is held by the veterinarian, with production cycle management on the specific premises, knowledge of which is held by the producer. For example, the vaccine recommendations made by experts nation-wide almost universally contain the same list of agents and administration timing guidelines. Yet for what may be good reasons a large portion of cow-calf herds do not follow these recommendations. Vaccines differ widely in their efficacy, even when used properly. Few vaccines are highly efficacious, many are marginally efficacious under the best of circumstances and some of the older ones may even be detrimental. Almost no sound cost-benefit field studies have been done for many vaccines. Depending on the type of vaccine, different errors in their use, both in administration and timing of administration, markedly reduce their efficacy. Due to these errors, some studies have found that up to two-thirds of some vaccines are used ineffectively (JAVMA 209:1618, 1996). General statements about infectious agents are also useful only as starting points. Each infectious agent has specific characteristics, such as transmission route, chronic carrier frequency, environmental survival duration and infection detection ease, that must be taken into account to successfully control or prevent that particular infection in a particular herd in a particular region. Specific herds have different risk factors, such as different housing and density for different groups during the production cycle, different purchasing and quarantine policies, different exposure to non-herd cattle, different nutritional status, and different environments, that must be taken into account when planning a herd health program specifically for that herd. For example, herds that graze commingled with other herds during the breeding season are at significantly higher risk of acquiring trichomoniasis than are herds that do not.

A successful herd health program for a specific herd must be reexamined on a regular basis, both to adjust for changes in herd management and to incorporate new information. Ongoing research continually improves our understanding of specific infectious diseases, such as host-specific leptospirosis. These new findings and the application of new technology leads to new vaccines, such as Brucella abortus strain RB51, that are considerably more useful or more effective than the older ones. New strains of infectious agents are emerging, such as BVD type II and Salmonella typhimurium DT104, that behave differently than the pre-existing ones. By their very nature, infectious agents have built-in mechanisms for evolving very rapidly to evade mammalian defense mechanisms and to take advantage of new opportunities inadvertently presented by man in his changing management of domestic livestock and their environment. These new strains sometimes require different control and preventive practices than the old strains. Completely new diseases, such as digital dermatitis or "hairy foot wart", emerge and spread across the country. We don't yet know how to get this infection out of a herd once it is there but we likely know how to keep it out in the first place. Modern transportation systems enable these agents to march almost unnoticed between herds that are widely separated. Never the less, some fundamental general principles are worth keeping in mind.

What are the big ones currently in your herd? What are the big wrecks that you don't want but that your herd has a high potential for? While some problems are $1 problems, some are $1,000 problems. Although much of herd health has traditionally focused on preventing infectious disease, keep in mind that other causes of production loss are economically more important in most herds most of the time. For example, in many herds the single largest cause of production loss is dystocia in first calf heifers. In some high risk herds, 10% of calves born to heifers are lost within 24 hours of birth due to this problem. In contrast, other profitable herds have very little dystocia in heifers, suggesting that the problem can be reduced by management. Further, numerous studies have shown that many of the calves surviving dystocia are at increased risk of subsequent disease and poor performance. This suggests that if over 10% of the heifers in your herd experience dystocia, it would likely pay to investigate ways of reducing it. Numerous studies have also shown that another large loss in many herds is the failure to settle cattle, particularly heifers that have just had their first calf, and thus to obtain a calf in the first place. Because dead and poor doing calves are easily seen, the even larger loss due to calves that were never there is very easily overlooked. Unfortunately, the $1,000 problems often appear like $1 problems and vica versa. We also tend to remember the unusual and to forget the common.

This is a very important principle to remember when dealing with disease outbreaks. Even in outbreak situations more animals in the affected group have infections and are subclinical or silent cases than there are clinical cases. Clinical cases are those cases that can be detected by simply observing the animal and by performing a simple clinical exam, such as taking their temperature. Clinical cases are the ones most people worry about because the effect on the animal is obvious; they clearly don't feel good, they often loose considerable condition and they are often at risk of dying. On the other hand, subclinical cases are those that require special laboratory testing to detect but the animal appears completely normal. For most diseases, both infectious and non-infectious, the ratio between clinical cases and subclinical cases is typically 1:5 to 1:20. Under some circumstances, a herd can be widely infected with an infectious agent but few if any clinical cases occur at all. For some infections such as Bovine Leukemia Virus (BLV) the ratio may be 1:100, meaning that clinical cases rarely occur.

Many clinical cases are due to infectious agents that are in most herds most of the time but that usually don't cause clinical disease. Thus, the occurrence of clinical cases is an indicator that something is amiss in the management of those animals.

A surprising number of infectious agents are endemic, meaning that they are active in most herds and that most animals in the herd become infected by and must become immune to them at some point in their life. Examples are the scours viruses, rotavirus and coronavirus, and the protozoa associated with scours, cryptosporidiosis and coccida. In areas of "endemic stability", this includes anaplasmosis. In most herds most of the time, young animals acquire silent subclinical infections by such agents and develop protective immunity. This does not mean that the production of these animals is unaffected. For example, a recent study found that 86% of U.S. beef herds not vaccinating for BVD, which was the majority of the herds in the study, had BVD active in them (Paisley, LG et al. Therio 46:1313, 1996). Relative to the number of infections, clinical BVD cases are relatively uncommon if they occur at all. Essentially, clinical cases of most diseases should be regarded as red flags indicating that something in the management of those animals was seriously wrong. The fact that most herds don't experience continual clinical outbreaks of the endemic infectious agents is primary evidence of this. Subclinical infectious disease that results in immunity occurs when the susceptible animal's innate defense mechanisms are sufficient and they are challenged by a low infectious dose. Clinical infectious disease results when the susceptible animal is challenged by an infectious dose of the organism that is too large for their innate resistance to handle. For example, newborn animals are very susceptible to infection because both their innate defenses and immune systems are immature at birth. They are rendered even more susceptible by the failure of passive transfer and inadequate pre- and post-partum nutrition of their dam. Innate resistance of older calves is maximized when their management (e.g., weaning, dehorning, castrating), environment or other disease is not overly stressful and when they are not experiencing a nutritional deficiency. If an animal normally resistant to an infection is stressed severely enough, even a low challenge may cause clinical disease. Thus, the occurrence of clinical cases is usually an indicator of more general problems in animal husbandry, not the sole problem in itself.

It is very important to note that while vaccination can increase the resistance of the susceptible animal, other factors under management control are often considerably more important. For example, if an animal is deficient in critical nutrients such as protein, energy, copper, selenium, vitamin A or vitamin E, it is both more susceptible to infectious disease and cannot respond fully to vaccination because the immune system function is compromised. This is not to suggest that these nutrients should be supplied in excess (some are toxic in excess) or in the more expensive forms available. Instead, if a nutrient deficiency problem is suspected, a veterinarian can sample carefully selected animals for appropriate testing and professional nutritionists consulted with the results. This may include liver biopsies as well as serum samples from healthy appearing animals during critical times of the year. Because of the complex dynamics between forage levels through the forage cycle and animal liver stores through the production cycle, the number and timing of this sampling should be established by consulting experts familiar with the problem in a region. Further, if through management errors the challenge dose is large enough or the stress high enough, it will overwhelm the protection afforded by any vaccination.

Good explanations of the balance between resistance and disease challenge and fitting these into the beef cow production cycle are those authored by Dr. Ed J. Richey, Univ of Florida Beef Extension veterinarian:

• Keep herd health simple and make it fit the beef cattle operation (1991) (pdf)
• Constructing Diagrams to Represent the Management System of a Beef Herd, Bulletin 278 (html, pdf)

Richey, E, R Hendry, S Cornwell (1992). Herd Health for the Beef Cattle Operation. The Bovine Proceedings 24:156-167.

For more information on the above epidemiologic concepts for disease in animal groups, see:

Epidemiology Concepts for Disease in Animal Groups

For examples of on-line information on trace minerals, see the following :

• Trace Mineral Nutrition in Beef Cattle (JA Paterson, Mont State, TE Engle, Colo State, 2005, 22 pg pdf)
• Trace Mineral Contents of Harvested Forages (1992 NAHMS survey, 2 pg pdf)
• Forage Analyses from Cow/Calf Herds in 23 States (Beef '97, 28 pg pdf)
• Trace minerals for Beef Cows (Alberta Dept. of Ag, Saskatchewan Dept. of Ag. html)
• Chapt 5: Minerals in: Nutrient Requirements of Beef Cattle: Seventh Revised Edition: Update 2000 (2000),
• Trace minerals for California Beef Cattle (J Maas, UC Davis
• Vitamins for Beef Cattle (1993, HB Sewell, U Missouri, html)

The management practices required to minimize the exposure of susceptible animals depend on the characteristics of the specific infectious agent and which animals are susceptible. Infectious dose is kept low by such things as minimizing animal density, keeping susceptible animals away from contaminated areas and from sick animals, preventing the buildup of contaminated materials under cover such as in barns, and preventing contamination of feed and water. For example, a few adult cows continually shed low levels of the scours viruses. These viruses then contaminate the hair coat and udders of other cows in the herd, which is the reason that calving should not be done on the winter feed ground. Calving heifers separate from cows, moving cows and heifers off of winter feedgrounds at least two weeks before the start of calving, keeping calving cows and heifers in open pastures and only bringing those experiencing calving difficulty or mothering difficulty into a corral or barn area, and moving pairs out to a low density nursing pasture within 24 hours of calving will do more to prevent calf scours than any vaccine. The most important component is keeping animal density low. For example, if snow is an annual problem either remove it from south-facing hillsides to provide more open space or change the herd to a later calving season. Exposure to direct sunlight kills most infectious agents but they can survive for long periods inside barns or anywhere else that they are protected from direct exposure to sunlight. Most infectious agents survive well in damp conditions, including ponds and water troughs. If the environmental temperatures are warm enough, some pathogenic bacteria such as salmonella can even replicate in contaminated feeds. Drying kills many agents but some, such as scours rotavirus and salmonella, survive drying very well.

Infectious disease problems cannot be controlled by focusing solely on the clinically affected animals.

In the midst of an infectious disease outbreak, a common error is to focus infection control strategies only on the clinically affected animals, not recognizing that subclinically infected animals are also shedding the agent. For example, in the midst of a scours outbreak all the calves in the group in which the outbreak occurred should be regarded as potentially infected and shedding. A common error is to remove the healthy appearing calves from the affected group and then introducing newborn calves to this new group. The subclinically affected calves then transmit the scours agent to the newly introduced susceptible calves and the outbreak continues, contaminating more ground. In the midst of an outbreak appropriate sanitation practices must be applied to all oral treatment equipment, such as balling guns, nose tongs and esophageal feeders. For example, in the midst of salmonellosis outbreaks, normal appearing animals can be shedding salmonella in their oral and nasal secretions and urine as well as feces. As noted above, agents such as salmonella can survive very well in the dried organic films remaining on such equipment. If this equipment is not adequately sanitized between animals then the infection will be transmitted to other susceptible animals that are being treated with it, such as calves being given oral fluids for reasons other than salmonellosis.

For on-line information on considerations in bovine salmonellosis control, see: Bovine Herd Salmonellosis, Including DT104: Eleven Characteristics to Keep in Mind.

Because subclinical (silent) cases of most diseases are more numerous than clinical cases in a herd, the economic cost of subclinical disease exceeds that of clinical disease.

Although the cost of clinical cases is often obvious, particularly if they result in death, the cost of subclinical disease in that herd is usually greater but much less obvious. In fact, the effects of subclinical disease are often overlooked altogether. Several infectious agents that affect reproduction, such as BVD, leptospirosis and vibriosis, likely cause far more early embryonic death than visible late term abortions in infected pregnant cattle. The following example is particularly instructive. In a feedlot study of bovine respiratory disease (pneumonia, Wittum, TE et al. JAVMA 209:814, 1996) 30% of the crossbred steers, all from a single source, were pulled for treatment of clinical respiratory disease. None died but being pulled and treated for clinical disease was associated with a 22 lbs. reduction in gain as well as the labor and drug costs. However, at slaughter a surprising 70% of the calves that had never shown signs of clinical illness had lung scaring indicating that they had had subclinical pneumonia. These subclinically affected calves, which represented 50% of the entire group, gained 43 lbs. less than their herdmates without lesions. Another lesson from this study is that vaccination is not absolutely protective as all of these steers received MLV IBR and BVD three weeks prior to feedlot entry and again at entry.

New infectious agents often enter a herd and are unnoticed for some time before clinical disease occurs and a diagnosis is finally made.

Because of the iceberg phenomenon, infectious agents often enter a herd and become well established long before the first clinical cases are recognized and efforts are finally made to obtain a diagnosis. Often the first clinical cases are passed off as "just one of those things that happen". Only when several cases happen in a row and somebody notices that something different is occurring are veterinarians called, necropsies done and the appropriate samples submitted to diagnostic labs. This means that these agents can establish a solid foothold across the herd before preventive measures blocking transmission to susceptible animals are taken against them. For diseases that primarily infect young animals but are manifested only in mature animals, such as Johnes disease and BLV, this means that a significant percentage of the herd’s replacement youngstock can be infected over several years before the presence of the disease is recognized. Once this occurs many years are required to eliminate such a disease from a herd raising its own replacements.

Evidence from outbreaks suggests that trichomoniasis can be in a herd for several years in the form of late calving cows and decreasing calf crop before it finally causes the huge wreck that gets everyone's attention. The infection starts with a few animals one or more seasons before the epidemic outbreak occurs. The initial signs, such as a few cows in heat late in the breeding season, a few late-calving cows and a few abortions, are overlooked. This suggests doing two things. First, become familiar with the early signs of such diseases coming your way and monitor your herd for them. Second, put safeguards in place now to reduce the chance of the big wreck from those diseases such as salmonellosis, and trichomoniasis that are traveling around among cow-calf herds. The first step is to determine what the nasty wrecks are that you don't want. The second step is to determine what you can do to increase your herd's biosecurity against them. The third step is to implement these changes. Often, these are the changes you would have to make to control the infection were your herd to acquire it. Because this means changing human behavior, it is often hard to accomplish.

Carriers of subclinical infection are the reason for the old but true saying that "Most disease is bought and paid for!" and are what keep it in a herd.

For most infectious diseases, the single largest risk factor for acquiring infection is the purchase of subclinically infected animals that are carrying the infectious agent. Many infectious agents causing problems are host-adapted, meaning that they establish long term carrier states in a few animals and that these are usually subclinical (silent) infections. Examples are bovine paratuberculosis, bovine salmonellosis (particularly S. dublin and perhaps Salmonella DT104), bovine leptospirosis caused by L. borgpetersenii serovar hardjo type hardjobovis (formerly L. hardjo var bovis), BLV, BVD, brucellosis, trichomoniasis, vibriosis and anaplasmosis.

For example, between 0.5% and 2% of the beef cow population are persistently infected (PI) carriers for BVD and, as noted above, BVD is very widespread, occurring in a majority of herds. Surviving PI animals appear normal but are constantly shedding billions of BVD virus, infecting most susceptible animals, including many vaccinates, that they come into direct contact with. Their calves will also be PI carriers as will most of the calves born to any susceptible female that was between 30 and 120 days pregnant when she was exposed to the PI shedder. Note that although BVD vaccines provide good protection against the dam developing clinical disease, they do not provide nearly as good protection for her fetus, the modified live vaccines providing better protection than the killed. This means that if you buy 100 replacement heifers from BVD status unknown sources, you have between an 63% and an 86% chance of buying one or more of these long term carrier animals. If you buy pregnant heifers in late gestation, you have between an 86% and 98% chance because you are in essence purchasing two individuals per heifer. As an aside, more PI animals than the 1 to 2% are caused by this infection but they die young or are culled due to poor performance. The occurrence of these poor doers is one of the indicators of the presence of BVD infection in a herd. For diseases such as Johne’s disease and leptospirosis, the risks are higher. For leptospirosis caused by L. hardjo, in beef cattle the chronic carrier rate is between 4% and 14%. In dairy cattle, the prevalence of Johnes is around 15%. That means if one were to buy only 10 heifers from Johnes status unknown sources, the likelihood of one or more being chronically infected with Johnes disease is 80%. If you were to buy 100, the likelihood of one or more being infected is 99.99%, a virtual certainty.

• For on-line information on BVD, see Bovine Viral Diarrhea Virus (K. Brock, Auburn)
• For on-line information on Johne's Disease, see Johne's Information Center, Dr. MT Collins, Univ. Wisconsin

Once this type of infection is in the herd, careful consideration must be given as to how the continual development of new carriers can be prevented. In the case of leptospirosis, for the vaccine to be of any benefit in preventing infection and thus preventing the development of a new carrier, the susceptible animals have to be fully vaccinated (at least two doses as these are killed bacterins) before the infection is typically being transmitted to them. The other risk factors for this transmission must also be considered. For example, the potential for transmission in stagnant water contaminated by urine from carrier animals, such as in livestock ponds or dugouts, compared to the use of piped and tanked water supplies. For some agents, the risk of transmission from mixing older with susceptible younger animals, particularly the practice of holding back slower growing but otherwise normal appearing animals, must be recognized. Rather than continual mixing and sorting of groups, all-in, all-out group management, such as is used in the swine industry, reduces the potential for disease transmission from carriers to susceptible animals. Continual sorting and mixing also markedly increases stress as animals challenge each other to reestablish social dominance hierarchies.

Quarantine isolation of purchased animals will not protect your herd against these chronic carriers!

A very important point to recognize is that isolation alone of any length will not protect your herd from these chronic carriers among newly purchased animals. The practice of isolation alone will only protect a herd from outside animals acutely infected with short incubation period diseases that were picked up while moving through the marketing process. After an incubation period, such animals may break with clinical disease after arriving on the premises. To be effective the isolation period has to be longer than the typical incubation and recovery period for this type of disease. Purchased animals can be vaccinated during the isolation period so they are protected against those agents circulating in the herd. Depending on the specific infectious agent, a quarantine that includes rigorous testing for chronic infections will help somewhat but is not bulletproof for the reason below. Some, such as BVD PI carriers, can be detected by the appropriate testing. The carriers of some conditions, such as digital dermatitis or leptospirosis, can be eliminated by appropriate antibiotic treatments during the isolation period. On the other hand, relatively few herds isolate newly purchased animals (NAHMS, 1997).

With respect to bringing in animals, clearly the most dangerous time is bringing in new animals around the time of calving that will expose newborn calves. The most dangerous animal to bring in under these circumstances is the young salebarn calf that is brought in to replace dead calves on nursing cows. Such calves are often colostrum deprived as the colostrum was likely used for retained calves and they are very susceptible to many diseases that they may have picked up in the herd of origin or during the marketing process. Some of the biggest scours wrecks that I know of appear to have been precipitated by the purchase of baby salebarn calves. The other potentially dangerous exposure is purchased colostrum or raw milk. Colostrum only fights disease in the calf's body and both may be contaminated with infectious agents such as salmonella and Johne's disease, either because the source cow was shedding these agents in her udder or because her udder skin was contaminated with these agents from the environment.

Even using the best laboratory tests, subclinical (silent) disease is considerably harder to detect and diagnose than is clinical disease and is more error-prone.

Laboratory tests usually do not work nearly as well for diagnosing subclinical disease as they do for diagnosing clinical disease because the disease process and thus the characteristic being tested for is not as advanced. For example, subclinically infected animals usually do not shed nearly as many of the infectious organisms as do clinically infected animals. For infections such as bovine paratuberculosis (Johne’s disease) or salmonellosis, the level of shedding by the subclinically affected animal is often so low that the laboratory tests cannot pick it up from a single sample. This means that subclinically affected animals are usually much more difficult to detect than are clinical cases. This is the reason that multiple tests are often required before clinically normal animals are declared free of an infection.

For example, fecal culture of animals clinically affected with Johne’s disease will typically detect more than 95% of these animals because they are often shedding millions of paratuberculosis organisms per gram of feces. Fecal culture of subclinically infected animals will typically detect 40% of these animals because they are often shedding fewer than 100 paratuberculosis organisms per gram of feces, which is the detection threshold of the culture test. This means that of the 15 infected heifers of the 100 you purchased above, a single fecal culture would detect 6, leaving 9 infected ones in the bunch.

Besides erring in not detecting all the infected animals (the sensitivity side), many of the serological tests also error by indicating that some animals are infected when they are not (the specificity side). This is because some of the antigens in the test also occur in other non-pathogenic organisms that the animals experience. While the sensitivity of the serological ELISAs for Johne's is around 40%, their specificity is at best around 98% and may be as low as 90% depending on the situation. This means that if 100 non-infected animals were tested, there is an 87% chance that one or more will have a positive test with the best specificity and with the lower specificity, on average 10 animals will be falsely identified as infected.

The results of testing a group with infected animals in it are even more paradoxical. In the group of 100 heifers with the 15 infected ones among them, the Johnes ELISA with 40% sensitivity and 90% specificity would typically identify 15 animals as test positive and 85 as test negative. The paradox is that although 15 animals are actually infected of the 15 test positive, 9 would actually be uninfected (false positives) and of the 85 test negative, 9 would actually be infected (false negatives). This testing paradox due to less than perfect tests (very few are perfect) is often not well understood by those using these tests.

For many infectious diseases, the single most important piece of information that a purchaser can have is honest, sound knowledge about the status of the herd of origin with respect to the infections of concern.

When establishing herd health programs against particular problems, understand and exploit the opportunities that that Mother Nature presents. For example, internal parasites are major a problem in grazed cattle under some situations, such as in areas with high water tables or irrigated pastures. Repeated use of wormers to suppress these infections without considering the timing of the worming with respect to the parasite life cycle in pasture and cattle management is fighting Mother Nature, is expensive and is seldom successful in the long run. Further, the frequent use of large amounts of highly efficacious anthelmintics alone, particularly if under-dosed, inevitably leads to parasite resistance. More economical and sustainable control programs are based on the opportunities presented by the parasite life cycle, both in the cow and on the ground, including the timing of worming and of cattle movement onto pastures rested without cattle for a sufficient period, and the immunity of older animals. What is used to design these programs is key information such as what triggers larvae overwintering in the cow to emerge and start producing eggs, how long the eggs take to hatch under different moisture and temperature conditions, how long the free-living larvae will survive on pasture during the summer and over winter, and how long it takes after ingesting larvae for eggs to be produced.

As noted above, the immune system is compromised if cattle are deficient in critical nutrients. Because immunity is also important against internal parasites, if such cattle are expose to these infections they will have higher burdens and will suffer more production loss. Unfortunately, the areas of nutritional deficiencies often overlap the areas conducive to the free-living part of the internal parasite life cycle.

Continued success is far more likely if a disease problem is attacked at multiple points rather than attacking it at a single control point.

Establishing a vaccination program for your herd requires consideration of complex issues. To quote Brand et al. (1996): "A vaccination program must be based on the disease status of the herd, reproductive status of youngstock and cows, potential interference by maternally derived antibodies, potential effects of vaccine-induced titers on suitability for export or introduction into bull studs, whether the herd is open or closed, prevailing farm and area conditions, national or regional vaccination strategies, the possible advantageous/disadvantageous postvaccination sequalae, and the cost benefit ratio of a vaccination program (emphasis mine). Furthermore, the vaccination schedule should be known, as well as the antigenic form of vaccine to be used (inactivated, modified live, live, or deletion vaccine), route of administration (intramuscularly, subcutaneously, or intranasally), and whether a booster vaccination is needed and when." Because the immune system requires time to respond to vaccines, the final dose should be given sufficiently in advance that the animal can be fully protected when the exposure or stress occurs. Vaccines requiring priming doses must be given sufficiently ahead of the second dose for the second dose to stimulate adequate protection. Failure to follow the administration instructions in this regard is a common error that markedly reduces vaccine efficacy.

Many vaccines are likely only marginally beneficial, biological and economically.

Some vaccines, such as the oil adjuvant vibrio (Campylobacter fetus) and the muscle clostridial toxoids (e.g., Clostridium chauvoei (blackleg), Cl. septicum (malignant edema)), are highly efficacious. At the other end of the spectrum are the older Pasteurella whole cell bacterins that don't contain leucotoxoids as some evidence suggests that they actually increase the severity of bovine respiratory disease under some circumstances. Others fall in between. For example, a controlled study of the trichomoniasis vaccine showed that 63% of vaccinated heifers delivered calves while only 32% of the controls did so and the vaccinates were culture positive for 3.8 weeks while controls were for 5.4 weeks (Kvasnicka Am J Vet Res 53:2023(1992)). Although the vaccine improved the situation, it certainly didn't prevent the problem. Other control measures such as rigorous testing of young bulls, culling of older bulls and late calvers may be more beneficial economically. As noted above, some vaccines such as leptospirosis are considerably more effective against non-host adapted strains than host-adapted strains. A general rule of thumb is that if a natural infection after birth results in a chronic carrier animal, which means that that animal's immune system was not able to eliminate the infection, then vaccination of that animal isn't going to stimulate the immune system sufficiently to prevent infection either. Thus, a general conclusion is that many vaccines will reduce the number of animals infected, will reduce the proportion of those that become clinical cases among those that are infected and will reduce the amount and duration of shedding in those that are infected.  But for many diseases vaccination will not completely prevent the problem and other control measures may be equally or more important. Unfortunately, it is human nature to look for the single magic bullet that can be given once and forgotten.

The evidence from sound studies of a positive economic benefit from the use of vaccines across large numbers of herds is severely lacking. The lack of sound evidence doesn't necessarily mean that the cost-benefit isn't positive. Anecdotal evidence suggests that the severe clinical outbreaks of Type II BVD tended to occur in herds that were not properly vaccinated for BVD. For bovine respiratory disease, about half of the studies indicate equivocal benefit while half indicate marginal benefit of use in calves prior to weaning. As noted in the pneumonia example above, their use clearly doesn't completely prevent the problem. To get the needed evidence of benefit, producers need to make the evidence from sound randomized, multi-herd, concurrent controlled, blinded field trials a condition of purchase.

USDA vaccine licensing does not require evidence of efficacy in cattle under normal farm and ranch conditions and only requires evidence of efficacy against specific aspects of the disease.

The USDA monitors vaccines for safety, purity, potency and efficacy, concentrating primarily on safety and purity (freedom from other infectious agents or toxic materials). This is done by monitoring the procedures and sanitation in the plants producing the product. To show efficacy of vaccines the manufacturer performs laboratory challenge of specially selected animals rather than using controlled field studies of vaccine efficacy under actual use conditions. The Espeseth and Greenberg document formerly on the USDA website stated "It is generally more difficult to demonstrate significant efficacy under field conditions. Field efficacy studies are often inconclusive because of uncontrollable outside influences." Further, if other sound, independent evidence shows that a USDA-approved product is not efficacious under most circumstances, the law does not prevent its production or sale. Thus, a USDA-approved and licensed product may not be efficacious under the under field conditions experienced by your animals. Further, the aspect of the disease against which efficacy must be demonstrated is quite specific. For example, for the BVD vaccines evidence of efficacy against the clinical gastointestinal disease syndrome is required but efficacy against fetal infection, which is essential for preventing the persistent carrier state and the most important component for control of BVD in breeding herds, is not. Vaccine labels and label claims must be approved by the USDA prior to use.

For on-line information on USDA vaccine licensing policies, see USDA Center for Veterinary Biologics - Biologics Regulations and Guidance

• Memorandums - VS Memorandum 800.202 General Licensing Considerations: Efficacy Studies, 2002 (pdf)

• Pfizer information sheet "Facts about each level of protection claim" (note - this is a clear description of the meaning of label claims and is not a product endorsement)

Vaccine Program Recommendations

My recommendation is that in concert with their herd veterinarian, producers design a vaccination program for the specific circumstances of their herd. Without knowledge of the herd specifics and of the area I am unwilling to make blanket recommendations. I also suggest that producers put their vaccine requirements out to bid. To attract good bids from suppliers, smaller producers may need to join together. With the above caveats in mind, the following are on-line vaccine recommendations in title alphabetical order from a number of experts:

The Internet contains a wealth of relevant materials, one reason being that a major mission of the agricultural extension service is to communicate information to producers. The Internet provides an excellent mechanism for doing so to the dispersed producer audience. As a result, many very useful extension publications are on the Web. The medical literature can also be searched for free on-line through the National Library of Medicine. Because approximately half of the veterinary literature is cataloged by the NLM, you can locate and read the abstracts for much of the veterinary literature. Cornell Consultant also provides an on-line means of identifying the most recent relevant clinical literature as selected by Dr. Maurice White, a Cornell food animal clinician. As the WorldWideWeb matures, the amount and quality of information will likely increase.

Cattle Learning Center: Practical Solutions for Cattle Producers

Cornell Consultant: A Diagnostic Support System for Veterinary Medicine (Dr. M E White)

This is a unique resource to establish differentials and to identify current papers on a disease. Cornell Consultant has a direct link to PubMed with a search string already entered for specific diseases and links to other on-line resources.

National Library of Medicine PubMed

One of the great features of PubMed is the "related article" function that enables you to find the closely related papers that they have indexed close to a good hit that you have found.

You can order published papers through PubMed, through the Cornell Flowers Library, or by Adobe Acrobat PDF file through e-mail from the University of Washington healthlinks. The later takes credit cards and a couple of days.

• Brand, A, JPTM Noordhuizen, YH Schukken (1996). Herd Health and Production Management in Dairy Practice. Wageningen Pers, Wageningen.
• Chenoweth, PJ, MW Sanderson (2005). Beef Practice: Cow-Calf Production Medicine, Blackwell Publishing.
• NAHMS beef cow-calf studies (National Animal Health Monitoring System, 1997). Beef Cow-Calf Health & Management Practices (Beef '97) pdf.
• Radostits, OM, ed. (2001). Herd Health: Food Animal Production Medicine, 3^rd ed.WB Saunders, Philadelphia.