Foot Rot
Pinkeye
Coccidiosis
Pneumonia
Ringworm
Parasites
Blackleg
Johne's Disease
Leukosis
Infectious Bovine Rhinotracheitis
Bovine Virus Diarrhea
FOOT ROT
Foot rot (necrotic pododermatitis, foul foot) is usually seen in most herds to varying degrees. Foot rot is caused by bacterial infestations of

the hoof area. Fusobacterium necrophorum or Bacteriodes melaninogenicus bacteria when injected together can form the typical symptoms of foot rot, however, other organisms common to the environment such as streptococci, staphylococci, corynebacterium, and various fungi are also isolated from foot rot lesions especially when moisture is present. The bacteria enter tissues and begin the infections when cuts, bruises, punctures, or severe abrasions break the skin. Foot rot is often a seasonal disease, occurring during periods of extreme moisture, sudden freezing of muddy yards, or severe drought. Severe drought causes the hooves to crack , thereby allowing the organisms to enter the tissues of the foot.
The first sign of foot rot is usually varying degrees of lameness. The lameness will vary from scarcely noticeable to severe in one or more feet. Foot rot may affect only one animals or may affect a high percentage of the animals.
Lameness is usually followed by swelling of the foot, spreading of the toes, and reddening of the tissue above the hoof. The swelling may develop into an abscess, which when broken will release a discharge with a characteristic foul odour. The animal will usually have an elevated temperature with a loss of appetite and body weight. If the infection is unchecked, it will invade deeper tissues of the foot and possibly one or more joints causing chronic arthritis.

Management practices that help reduce hoof damage or avoid bruising will decrease the incidence of foot rot.
Hooves should be kept trimmed on heavy cows and bulls to help reduce the stress on the soft tissues of the foot.
Reducing mud around water tanks or in corrals through proper drainage will limit the incidence of foot rot. Frozen ground around water tanks and in corrals should be smoothed or cover with straw to limit bruising of the feet. Walk through foot baths containing copper sulphate (1 kg per 20 litres) or formalin (1 part 40% formalin in 9 parts water)placed in doorways or alleyways in dairy operations are sometimes used to reduce foot rot. Ethylenediamine dihydroiodide (EDDI) provided at 50 mg per head per day can also aid in reducing foot rot (see iodine in minerals module for more information), but this practice may increase iodine content in milk.
Early treatment is necessary to prevent animals from becoming chronics. Penicillin, penicillin dihydrostreptomycin combinations, oxytetracycline (terramycin, liquamycin) or sulfonamides (sulfamethazine) are usually effective at treating foot rot when given at recommended dosages and treatment started early.

PINKEYE
Pinkeye (infectious bovine keratoconjunctivitis) is a highly contagious inflammatory infection of the eye that affects primarily the cornea and sclera. The infection caused by the bacteria "Moraxella bovis" occurs more frequently in early summer when maximum (ultraviolet radiation) and maximum fly population is present. Only cattle are affected by the bacteria and young animals are most susceptible. The disease is more prevalent in breeds which have less pigment around the eyes (eg. Hereford, Holstein, Shorthorn) than those with completely pigmented eyes (eg. Angus). Purebred hump-backed Zebu cattle (Brahma and others) are not affected by the bacteria.
The disease is transmitted by direct contact with ocular or nasal discharge of an infected animal. Flies such as face fly, horn fly, stable fly, and house fly can serve as mechanical vectors as can contaminated equipment and people.
All infected eyes do not develop clinical pinkeye but can be carriers for the disease. Up to 80 percent of the cattle in a herd may become infected with infection in 100 percent of the calves and only 50 percent of the cows which show some immunity. Mortality due to pinkeye is rare.

The incubation period is usually 2 to 3 days but can range up to 21 days. Initial signs are moist eyes and slight constriction of the pupil. Photophobia (sensitivity to light) is demonstrated by the animal turning away from the light, blinking, or keeping the eye closed. In a short time tears begin to flow, there is a distinct constriction of the pupil, and a haze, usually centrally, on cornea appears. Tearing becomes copious and a vesicle forms on the cornea which may later rupture to leave a clear punched out ulcer. Opacity (cloudiness) of the cornea develops from the centre and may make the complete cornea opaque by the fourth or fifth day. Enlarged blood vessels appear at the periphery of the cornea at 7 to 10 days and may completely encircle the cornea as the infection progresses. During the next 10 to 15 days the cornea begins to clear from the periphery toward the centre. At the centre of the cornea the blood vessels become devoid of blood and change to a white scar which decreases in size from 25 to 50 days. In less severe cases the lesions may heal without enlargement of the blood vessels of the cornea. Spontaneous recovery may occur anytime in the course of the disease in mildly infected animals. Tissue damage of the eye may be caused by an endotoxin produced by the eye.

Early in the course of the disease, treatment under both upper and lower eyelids with ophthalmic solution or ointments containing antibiotics may be beneficial. Antibacterial powders sprayed into the eye may cause irritation and is not recommended. In cases where there is extensive corneal inflammation, corticosteroid and antibiotic combinations may be injected directly under the conjunctiva. Some animals recover following one injection, but severe cases may require several daily injections.
Controlling the fly population tends to reduce the incidence of pinkeye. Insecticide ear tags have been proven to be effective. Vaccines against the bacteria are available and can be used to immunize the herd, although vaccines are not effective as a preventative during an outbreak. Pastures containing thorns, thistles or long hard stemmed grasses will increase the incidence of pinkeye because these plants serve as irritants to the eyes and skin.

COCCIDIOSIS
Coccidia are single-celled parasites that belong to the family of organisms known as protozoa. The species of coccidia most detrimental to dairy cattle belong to the genus Eimeria (species E. bovis and E. zeurnii) which have a complex life cycles involving development within the infected animals and in the outside environment.
The life cycle begins when a ruminant animal ingests coccidia eggs, known as sporulated oocysts, from the environment. Inside the gastrointestinal tract, sporozoites within the oocyst are released, enter the epithelial cells lining the intestine or cecum, and form structures

called meronts. Meronts divide by an asexual multiplication process, and produce merozoites. Each meront can release hundreds of merozoites into the lumen of the gut. Merozoites penetrate other epithelial cells lining the gut, and continue their development either into second and third generation meronts which release additional merozoites, or into one of two sexual stages known as microgametes and macrogametes. The union of the microgametes and macrogametes results in the production of oocysts which break out of the epithelial cells and pass out in the feces. Each stage of the development of the coccidia cause damage to the intestine. The whole process, from ingestion of the sporulated oocyst to the passage of the oocyst, requires 21 days. The multiplication process can produce millions of oocysts from one sporulated oocyst, however, the passed oocyst must undergo additional development in the environment to become infective. The environment must include adequate moisture, temperature, and oxygen and the process takes 24 to 48 hours. The sporulated oocyst can remain infective for 2 to 3 months and under certain circumstances for a year or more. Coccidial oocyst survive best in moist, shaded areas, can tolerate freezing temperatures, and are fairly resistant to detergents.
Coccidiosis is mainly a problem of young livestock in confinement housing where heat and moisture can stimulate the sporulation of oocysts. Long-term exposure to low levels of coccidia produces an immunity to the coccidia
(coccidia species specific immunity) in older animals. Stresses which reduce the immune response can result in an outbreak of coccidiosis.
Coccidiosis can be grouped into two categories:

Subclinical coccidiosis characterizes 95 percent of all cases where the animals do not show obvious signs of infection yet suffer from reduced feed consumption, feed conversion and growth performance, and
Clinical coccidiosis where animals exhibit diarrhea, dehydration, weakness, depression, anemia, weight loss, rough hair coats, and death. The diarrhea may be mild or severe, contain blood in severe cases, and be soft to watery.
Occasionally nervous symptoms such as muscle tremors, staggering, convulsions, and sometimes blindness are seen.
Treatment of clinical coccidiosis is limited because the drug treatment can not kill all organisms in the environment, damage to the intestinal lining is extensive by the time coccidiosis is diagnosed, and most drugs are coccidiostats
(deccox, rumensin, bovatec, posistac) which inhibit growth of coccidia not coccidiocides which can kill coccidia.
Currently outbreaks of coccidia are treated on a herd basis with sulfonamide compounds (not approved for lactating

dairy cattle) or amprolium in the drinking water or in the feed. Amprolium provided at 10 mg/kg of body weight for 5 days can effective treat animals with coccidiosis.
Prevention is accomplished by limiting exposure to the oocyst by maintaining dry (less than 25% moisture) and clean environments, and feeding the animals in bunks raised off the ground. Coccidiostats such as the ionophores, deccox, rumensin, bovatec, and posistac can provide effective control against coccidia as well as provide improvements in feed efficiency and rate of gain for growing heifers. These ionophores are not currently approved for use in lactating dairy cows. For effective prevention the following can be include in the daily ration: Amprolium at 5 mg/kg body weight for 21 days, decoquinate (deccox) at 0.5 mg/kg of body weight for 28 days during periods of expected exposure, lasalocid (bovatec) at 1 mg/kg body weight for 6 weeks, and monensin (rumensin) at 1 mg/kg body weight.

PNEUMONIA
Respiratory disease is frequently observed in calves been 8 weeks and 8 months of age. This age range is particularly susceptible to pneumonia causing organisms such as Pasteurella sp. and Haemophilus somnus because immunity protection from colostral antibodies has diminished and the self created antibodies are not fully capable of inhibiting the infection. Pneumonia in dairy calves can be compared to shipping fever in beef calves where virus (parainfluenza, infectious bovine rhinotracheitis, bovine respiratory syncytial) plus bacteria plus stress (shipping, mixing, weather changes, poor ventilation, inadequate nutrition) creates pneumonia.
Treatment can be accomplished by reducing the stresses and by antibiotic administration. Reducing the stresses will reduce the incidence of pneumonia as will vaccination against the viruses and bacteria.
RINGWORM
Ringworm is caused by a fungus that attacks the skin and forms ringlike or circular areas that are scabby or crusty in appearance. These areas may appear on the neck, shoulders or other parts of the body. It is contagious to both man and other animals upon direct contact.

To treat the infection, scrub the area with a stiff brush and soapy water and then apply tincture of iodine or other fungicide. Sunlight, adequate vitamin A and disinfection of the animal facilities may prevent the disease.
INTERNAL AND EXTERNAL PARASITES
Internal parasites such as stomach worms can cause unthriftiness and poor growth. It may be cost effective to treat heifers during their first grazing season which is when the heifers are most likely to ingest the larvae or eggs. Anti-helminthics (de- wormers) such as Ivomec
(ivomectin) are available for treating animals with internal parasites.
Lice, mange, and flies are common external parasites on most dairy farms. Lice and mange cause discomfort, a rough, unthrifty appearance, and poor growth in affected animals. Treatment with Ivomec to control internal parasites has some effect on external parasites such as lice and mange. Powders for control of these parasites are also available. Flies can be annoying to dairy cattle of all ages and can cause reduced gain in young animals. Because

many of the flies are blood sucking, they can transmit other bacterial and viral diseases. Use of insecticide sprays, dusters, or oilers can reduce the fly infestation.
BLACKLEG
Blackleg is an acute infectious disease that primarily affects young animals. The disease results in depression, fever, lameness, and death of non-vaccinated animals. Animals become infected by grazing soils contaminated with the spore-forming Blackleg bacteria. Vaccinations for Blackleg are in expensive and highly effective for prevention of Blackleg.
JOHNE'S DISEASE
Johne's disease (paratuberculosis) is characterized by chronic diarrhea, wasting and death in adult cattle. The disease shows up in older

cattle but usually was contracted during early calfhood. The disease is spread by ingestion of feces of infected animals. The disease is difficult to treat and the best course of action is to cull the animals from the herd.
LEUKOSIS
Enzootic bovine leukosis is caused by a virus carried in the blood of infected cattle. Once infected, the animal remains infected for the rest of it's life. Although tumours may develop later in life the major loss is associated with the loss of export markets and semen sales. A small percentage of animals are infected while still in the uterus, most are infected through the use of blood-contaminated instruments such as gouge dehorners, tattooing needles, and common needles.
Many dairy herds in Alberta are designated as Leukosis free herds and have the advantage of being able to sell breeding stock. These same herds usually exist as closed herds and do not purchase animals for inclusion into their herds.

INFECTIOUS BOVINE RHINOTRACHEITIS
Infectious Bovine Rhinotracheitis (IBR) is a viral disease of cattle which is widespread and which can cause serious economic loss. The IBR virus is readily transferred by contact and contamination and is most often introduced into the herd via the addition of purchased animals.
The disease can be transmitted by cattle showing the obvious symptoms and also those not showing the symptoms but carriers nonetheless.
The disease is associated with six different syndromes:
Rednose:The respiratory form of IBR is an upper respiratory infection characterized by fever, profuse nasal discharge, distressed breathing, decreased appetite, and depression. Outbreaks vary from mild to severe.
Conjunctivitis:The eye form of IBR is characterized by inflamed mucous membranes of the eyes, tearing, pus in the corners of the eyes, and occasionally a white discoloration of the cornea. Conjunctivitis may be seen with or without the respiratory form.
Infectious Pustular Vulvovaginitis (IPV):The pustules and inflammation of the vulva and vagina cause a swollen vulva, vaginal discharge, tail switching, and depressed appetite. Lesions similar to those of the vagina occur on the penis and prepuce of infected bulls. This form of
IBR may be transmitted by natural breeding.
Encephalitis:This is not a common form of IBR, inflammation of the brain is seen in calves up to the age of yearlings and causes depression, circling, progressive incoordination, coma and death.
Neonatal Septicemia:This form of IBR is a systemic infection of the newborn, and calves less than one month of age may develop a fatal, generalized disease characterized by fever, nasal discharge, and lesions of the upper gastrointestinal tract.
Abortion:Abortion may be produced by either natural infections or by some vaccines. Abortions typically occur 3 to 6 weeks following vaccination or the clinical signs of the disease, but may occur during an outbreak or up to 90 days following an outbreak.
Antibiotics will prevent or treat secondary bacterial infections but are ineffective against the virus.

Prevention is accomplished by vaccination:
Modified Live Virus (MLV):This form of vaccine is given intramuscularly and can cause abortion in pregnant cattle. If mature cattle are to be vaccinated with this vaccine, the vaccination should be given after calving and at least 3 weeks prior to breeding. Beef calves may be vaccinated from 2 weeks of age to three weeks prior to weaning, but will need to be revaccinated when they enter the feedlot. Animals vaccinated prior to 6 months will need a booster because early vaccination may not provide satisfactory immunity due to immunoglobulins from the colostrum providing protection for up to 4 to 6 months. Replacement heifers should be vaccinated or revaccinated between six and twelve months of age and not later than 3 weeks prior to breeding. A single vaccination at 6 months or older should confer immunity for a lifetime. Vaccines should not be given during periods of stress. The presence of antibodies against IBR in blood will not appear for at least nine days after vaccination.
Intranasal IBR Vaccine:This form of vaccine is a MLV sprayed into the nose. A local response to the vaccine in the nasal passages results in early immunity. Calves may be vaccinated as early as 2 days of age and the vaccine can be give to pregnant cattle. The duration of the immunity is not known and annual revaccination is recommended.
Inactivated IBR Vaccine:This form of vaccine contains a killed virus and eliminates the possibility of abortion, vaccine-caused illnesses, and shedding of vaccine virus. Two injections are required and annual revaccination is recommended. In a very small percentage of vaccinated cattle, severe, sometimes fatal allergic reactions have occurred.
BOVINE VIRUS DIARRHEA

Bovine Virus Diarrhea (BVD) is an acute or chronic viral disease of cattle characterized by fever, diarrhea, abortions at all stages of pregnancy, and erosions of the mucous membranes of the digestive tract. The hardy virus is readily transferred on contaminated boots, feed sacks and equipment. The exposure to BVD is high, however, most exposed cattle have a mild or unobserved infection which results in immunity. The BVD virus spreads rapidly and all animals in a herd may be exposed by the time the disease is first recognized. The virus is shed from infected animals in saliva, nasal and eye secretions, urine, semen, feces, blood, and aborted tissues. At temperatures below 10 degrees Celsius in the laboratory, BVD virus is quite stable and can survive for long periods of time.
Cattle infected with BVD virus may respond with a variety of clinical signs and lesions with a mild infection common.
While BVD usually occurs as an outbreak affecting the entire herd, only a small percentage will show fever, depression, decreased appetite, nasal discharge, ocular discharge, rapid respiration and cough, excessive salivation, diarrhea, and erosions of the lips, mouth and gastrointestinal tract. Less common clinical signs include lameness, cracking between the toes (interdigital lesions), swelling and erosions at the top of the hoof (coronary band), a corneal opacity occurring several days after the onset of illness, a rough dry scruffy skin (hyperkeratosis), and erosions or scabs on the vulva. BVD is frequently diagnosed as respiratory disease with clinical signs of fever, rapid

respiration, cough, nasal discharge and crusted nose. There may be no oral lesions and diarrhea may be minimal or absent.
A sporadic fatal form of mucosal disease results from the inability of the infected animals to produce antibodies to the
BVD virus. This form of the disease may also rarely occur following vaccination. The fatal form may progress slowly taking weeks to months in it's course through the herd with only a few animals sick at any one time. Early signs include a mucous ocular and nasal discharge, depression, and loss of appetite followed by severe erosions of the muzzle and mouth, a watery diarrhea, and dehydration. Death normally occurs within 10 days, although chronic cases may linger for several months.
The BVD virus has a severe effect on the fetus although the infection may go unnoticed in the pregnant cow.
Abortions may occur 3 to 6 weeks following infection or vaccination. Newborn calves may show weakness, incoordination, lesions of the mouth, eye defects, diarrhea, stunted growth, and high mortality. Defective

development of the cerebellum of the brain and cataracts of the lens of the eye are often seen in calves born from dams infected at mid-gestation.
There is no specific treatment for BVD, however, antibiotics and supportive therapy may be indicated.
Prevention of BVD can be accomplished by vaccination of young calves (between 1 day of age and 3 weeks prior to weaning) and replacement heifers (between 9 and 12 months of age). If calves obtained antibodies from the dam in the colostrum, vaccination will be impaired until after 6 months of age. Pregnant cows should be vaccinated after calving and at least 3 weeks before breeding. A single vaccination after 6 to 9 months of age should confer immunity for a lifetime. Modified-live vaccines may provide longer lasting immunity than killed virus vaccines, however, they will cause abortions in pregnant animals.

Animals exposed to BVD virus for the first time usually develop a mild and transient fever and diarrhea, which often goes unnoticed. These animals overcome the virus in a few days and are usually resistant to subsequent exposure to the virus. If an animal is pregnant when exposed to the BVD virus for the first time, her fetus will become infected.
Abortion is a common result no matter what type of BVD virus is involved. However, the fetus is not always aborted.
In early stages of gestation, the BVD virus may only cause eye, brain, skin, and other congenital abnormalities without killing the fetus. After 125 to 150 days of gestation, the immune system is developing and the fetus may be able to resist damage and eliminate the virus. It will be resistant to subsequent exposure to BVD virus.
Some calves are born permanently infected with BVD virus, because they were exposed to the BVD virus before 90 to 125 days after conception. They often appear normal but are tolerant to the virus and shed it for life, becoming important sources of the virus to contact animals. Some of the persistently infected animals are do poorly and appear to be more susceptible to other diseases. Many of them die before two years of age. If they survive to breeding age,

they will give birth to calves which are persistently infected with BVD virus. When exposed to a second BVD virus, persistently infected animals fail to mount an immune response. This new closely related virus will, therefore, cause damage to many body tissues and causing mucosal disease, diarrhea and death.