Calf enteritis is also known as scours (Fig. 13-4). Calf scours is a major cause of death in the first few weeks of life. Calves infected in the first few days of life are often infected with bacteria (e.g., Escherichia coli and Clostridium perfringens). Cattle infected between 10 to 14 days of life are often infected with viruses (e.g., rotavirus and corona virus). Another type of infection that occurs in this age bracket is Cryptosporidium (Fig. 13-5). Salmonella may present at any age.

FIGURE 13-4 White scours occurs when partially digested white milk is passed in the feces. (From Blowey RW, Weaver AD: *Color atlas of diseases and disorders of cattle,* 2nd ed. London, Mosby, 2003.)

Technician Note

Calf scours is a major cause of death in the first few weeks of life.

The major clinical sign is diarrhea leading to dehydration. Management of calf scours should include good hygiene, proper passive transfer through colostrum, vaccinations, and good feeding practices.

Technician Note

Dehydration is a major side effect of diarrhea associated with scours.

Foot Rot

Infectious foot rot is a contagious and common disease of cattle. Animals of all ages are susceptible, but the very young are rarely afflicted. The condition is painful, and animals in pain do not thrive. Major economic losses result from weight loss, low production, and costs of treatment.

Technician Note

Foot rot can cause economic losses due to weight loss, low production, and costs of treatment.

Foot rot is often caused by a mixed infection involving two primary bacterial organisms. Dichelobacter (formerly Bacteroides) nodosus is an anaerobic bacterium that has the ability to destroy keratin. Fusobacterium necrophorum is an anaerobic bacterium thought to be necessary for D. nodosus to invade, by causing dermatitis between the claws, which D. nodosus then can use as an entry point. Corynebacterium (Actinomyces) pyogenes may be involved, especially in the formation of deep abscesses.

Technician Note

The two primary agents of foot rot are Dichelobacter nodosus and Fusobacterium necrophorum.

The development of foot rot is largely influenced by management and environmental factors. The organisms favor moist or wet ground conditions. Trauma to the interdigital area from lacerations, abrasions, punctures, or softening from continual moisture allows the organisms to gain a foothold and cause disease. Foot rot is uncommon in dry environments and in animals with healthy, intact skin in the interdigital cleft. Infected animals shed the organism directly from wounds into the soil, where other animals can pick it up by foot contact with the soil. Untreated animals can be a source of herd infections for months to years.

One or more feet may be affected. Cattle may be mild or moderately lame, but severe lameness affecting multiple individuals in a herd is the common presentation. Inflammation and necrotic tissue are present in the affected interdigital clefts and often produce an exudate and characteristic bad odor. Local swelling is common and may cause the claws to spread apart. A skin fissure often develops, with swollen, necrotic skin edges and purulent exudate (Fig. 13-6). The infection may extend to undermine the hoof walls in the areas adjacent to the interdigital infection (Fig. 13-7). The pain causes lameness, with the animal limping or holding the leg up in an attempt to avoid bearing weight. Fever may develop, especially with deep tissue infection. Deep abscesses and infection of the coffin and pastern joints and associated tendons may develop.

FIGURE 13-6 Sloughing of skin in the interdigital space. The necrotic tissue was cleaned off before this photograph was taken. (From Blowey RW, Weaver AD: *Color atlas of diseases and disorders of cattle,* 2nd ed. London, Mosby, 2003.)

Foot rot is most commonly diagnosed from clinical signs. Gram stain of exudates may demonstrate the organisms, but this test usually is not necessary. Culture of the primary organisms is difficult.

The most important treatment is debridement of affected skin and hoof trimming to remove as much infected tissue as possible and “open up” infected areas to contact with air. Topical antibacterial agents, either antibiotics or antiseptics/astringents (copper sulfate, zinc sulfate, or 4%–5% formalin), are commonly applied to all affected areas after trimming and debriding. Temporary bandages may be necessary after extensive debridement is performed. Foot baths can be strategically placed so that animals must travel through them; these may help provide long-term treatment of a herd. Zinc sulfate is preferred for foot baths because it does not stain like copper sulfate and does not irritate and burn tissue like formalin. Systemic antibiotics are sometimes used and are always indicated in cases of deep-seated infection. Drug residues must be considered.

Management practices must be assessed, especially with the goal of eliminating constant moisture conditions. Affected animals should be separated from the herd as soon as they are noticed to prevent further contamination of the environment.

Regular hoof trimming, regular use of foot baths, and management to eliminate moist ground conditions are the most important preventative measures. Vaccinations against foot rot have been developed; however, the short duration of protection and the incidence of local injection site reactions have led to limited use of the vaccines. Still, in herds where foot rot is a continual problem, vaccination may reduce the number and severity of infections. Chronically infected animals should be culled.

Johne Disease

Johne disease is also known as paratuberculosis. Johne disease is caused by Mycobacterium avium subspecies paratuberculosis. Although the incidence of clinical disease in herds is only about 1% annually, there is no treatment. The disease is contracted through contact with infected animals via the fecal–oral route. Infection of most animals occurs around 30 days of age. Clinical signs usually do not occur until 3 to 5 years of age but have been seen in cattle as young as 12 to 18 months.

The four stages of Johne disease infection are silent infection, subclinical, clinical, and advanced clinical. Johne infection begins with a silent infection usually between 30 days and 2 years of age. Animals with silent infection shed the disease but do not show clinical signs. Cattle in the subclinical stage of the disease are also known as carrier animals. These animals are spreading the disease but are still not showing clinical signs. Only about 15% to 25% of these animals will test positive for paratuberculosis on fecal culture. If the animal is identified, it can be culled at this time, but most of these animals move onto the clinical stage of the disease while they remain in the herd. Because these animals are still shedding the disease but cannot be identified, Johne disease is difficult to completely remove from herds. The clinical stage of the disease is the first time that infected animals may show signs of the disease. The problem with Johne disease is the tip of the iceberg concept (Iceberg concept). The Iceberg concept states that for every animal with clinical signs born in the herd, another 15 to 20 animals are infected, fewer than half of which will be detected by a sensitive fecal culture. When the disease worsens, the animal is considered to have moved to the advanced clinical stage of the disease.

Technician Note

Johne disease is difficult to remove from herds.

Clinical signs include continuous or intermittent profuse watery diarrhea and sometimes weight loss (Fig. 13-8). The most important aspect of Johne disease is the economic loss associated with decreased production. Decreases in production can be associated with reduced feed efficiency, decreased milk production, reduced slaughter weights, increased incidence of mastitis, and premature culling.

FIGURE 13-8 Eight-year-old Santa Gertrudis cow infected with Johne disease has a profuse watery diarrhea. (From Blowey RW, Weaver AD: *Color atlas of diseases and disorders of cattle,* 2nd ed. London, Mosby, 2003.)

Upon necropsy, pale, enlarged intestinal lymph nodes are often found. Another common clinical finding is thickened rugal folds within the intestine. Differential diagnosis includes salmonellosis, parasites, and bovine virus diarrhea (BVD). Care should be taken when handling infected livestock because of potential zoonosis. Johne disease can cause Crohn disease in humans.

Technician Note

Johne disease can cause Crohn disease in humans.

Johne disease has no effective treatment. Diagnosis is made from biopsy and histopathology of the intestinal lymph nodes. Cattle should be tested, and animals found to be positive should be culled. Prevention includes culling of all heifers from infected cows, good hygiene, and pasteurization of pooled colostrums. Producers should purchase cattle only from herds certified as free from Mycobacterium subspecies paratuberculosis; these are essential sources of noninfected cattle. Segregation of calves from cows until they are older than 1 year may also help control Johne disease.

Leptospirosis

Leptospirosis is caused by the bacterium Leptospira. Leptospira is a spirochete. Common serovars are Leptospira pomona, Leptospira hardjo, and Leptospira grippotyphosa. The disease is contracted through urine or the urine-contaminated environment (e.g., contaminated wildlife and water). Leptospirosis can be found worldwide but is most commonly found in wet, warm climates. Leptospira can persist in water-saturated soil for 183 days.

The disease often presents as an abortion storm (Fig. 13-9). Stillbirths, loss of milk production, septicemia, hemoglobinuria (red water disease), weak neonates, and reduced fertility can be seen within infected herds. Periodic ophthalmia (recurrent uveitis) may be seen in an infected horse. Even after resolution of clinical signs, animals can spread leptospirosis in the urine for 10 to 118 days.

FIGURE 13-9 Aborted fetus possibly due to leptospirosis. (From Blowey RW, Weaver AD: *Color atlas of diseases and disorders of cattle,* 2nd ed. London, Mosby, 2003.)

Technician Note

Leptospirosis often presents as an abortion storm.

Upon necropsy, animals infected with L. pomona have swollen, dark kidneys (Fig. 13-10). Diagnosis of the disease is often accomplished by paired serum samples or histopathology.

FIGURE 13-10 Dark swollen kidneys are often seen upon necropsy of an infected cow with leptospirosis. (From Blowey RW, Weaver AD: *Color atlas of diseases and disorders of cattle,* 2nd ed. London, Mosby, 2003.)

Prevention of the disease should include vaccination and purchase of leptospirosis-free livestock. Prompt vaccination and antibiotic therapy, if performed early, may be beneficial. Leptospirosis is zoonotic, and care should be taken to prevent contraction of the disease.

Technician Note

Leptospirosis is zoonotic.

Listeriosis

Listeriosis is caused by the bacterium Listeria monocytogenes. Listeria monocytogenes is a small, motile, gram-positive, non–spore-forming, extremely resistant, coccobacillus. Listeria monocytogenes can survive in a wide range of temperatures. The organism is most commonly contracted from the consumption of contaminated silage. Moldy silage or silage with a high pH is more likely to be contaminated with the bacteria.

Technician Note

Listeriosis is often contracted through contaminated silage.

Clinical signs of the disease include fever, facial nerve paralysis, tongue hanging from the mouth (Fig. 13-11), circling (Fig. 13-12), drooping ears, blindness, and abortion. The uterus can also become infected with L. monocytogenes, causing metritis, abortion, stillbirth, neonatal death, and possibly carrier animals.

FIGURE 13-11 Prolapse of the tongue in a cow infected with listeriosis. (From Blowey RW, Weaver AD: *Color atlas of diseases and disorders of cattle,* 2nd ed. London, Mosby, 2003.)

Differential diagnosis includes rabies, poisoning, botulism, and bacterial meningitis. Treatment should include penicillin and nonsteroidal antiinflammatory drugs. Prevention should include proper management of silage feeds.

Lumpy Jaw

Lumpy jaw is also known as actinomycosis. Lumpy jaw is caused by the bacterium Actinomyces bovis, a gram-positive rod. The bacteria often gain access to the body through the oral cavity when the animal consumes coarse hay or sticks that penetrate the mucosa and allow entrance of the bacteria. Another common entrance point for the bacteria is from skin punctures that occur around the head. The bacteria then travel through the soft tissue to the adjacent bone and develop into granulomatous masses (Fig. 13-13).

FIGURE 13-13 Guernsey cow with right maxillary swelling and several granulomatous masses that have broken through the skin. (From Blowey RW, Weaver AD: *Color atlas of diseases and disorders of cattle,* 2nd ed. London, Mosby, 2003.)

Clinical signs include mass formation on the mandible or maxillary jaw (Figs. 13-14 and 13-15). The animal is often unaffected until the mass interferes with mastication. Once mastication is affected, the animal often loses weight quickly and is culled.

FIGURE 13-14 Crossbred Hereford with “lumpy jaw.” A large fist-sized mass is laying over the angle of the mandible. (From Blowey RW, Weaver AD: *Color atlas of diseases and disorders of cattle,* 2nd ed. London, Mosby, 2003.)

Treatment is often ineffective, although attempts can be made with antibiotics and debridement.

Malignant Edema

Malignant edema is caused by the bacterium Clostridium septicum, which is a large, spore-forming rod. The bacteria are found in soil and in the gastrointestinal (GI) tracts of some animals. The disease is contracted most commonly through superficial contaminated wounds. The head and neck are most commonly infected, although infection can occur anywhere on the body.

Clinical signs include the formation of an edematous lesion; gas lesions are less common. The animal loses weight and develops a fever, then toxemia develops.

Treatment includes penicillin and nonsteroidal antiinflammatory drugs. Vaccinations are available, but the disease is often sporadic and vaccination may be needed only in endemic areas.

Mastitis

Mastitis (inflammation of the mammary gland) causes an estimated loss of more than $1 billion to the dairy industry in the United States each year (Fig. 13-16). Diagnosis and treatment of mastitis is critical for the health of dairy animals and for the successful production of milk that is safe for human consumption. Nondairy animals may also develop mastitis and suffer from the related pain and inflammation (Fig. 13-17). Mastitis is almost always caused by bacterial infection (septic mastitis), but inflammation without infection may occur if a teat or udder is traumatically injured (e.g., laceration, getting kicked or stepped on).

Approximately 95% of mastitis cases are caused by two organisms: Streptococcus agalactiae and Staphylococcus aureus. These bacteria tend to cause local infections of the mammary glands and seldom cause systemic illness. Both of these bacteria can be spread from cow to cow (contagious mastitis). Streptococcus agalactiae is relatively easy to treat with antibiotics and good sanitation practices. Staphylococcus aureus tends to form microabscesses that resist penetration by antibiotics, making infection difficult to treat.

Technician Note

The two most common agents of mastitis are Streptococcus agalactiae and Staphylococcus aureus.

Other causes of mastitis include coliforms (especially E. coli, Klebsiella spp., Enterobacter aerogenes). They release endotoxins, which enter the bloodstream and can cause endotoxemia and even death. Acute septic mastitis is characterized by fever, anorexia, rumen atony, dehydration, and diarrhea. The affected milk is watery and looks like Gatorade. Treatment involves systemic antibiotics, nonsteroidal antiinflammatory drugs, possible fluid therapy, and stripping of all milk every 2 to 4 hours (Fig. 13-18).

FIGURE 13-18 Udder infected with gangrenous mastitis. The overlying skin of the infected quarter has sloughed off over a 1- to 2-month period. (From Blowey RW, Weaver AD: *Color atlas of diseases and disorders of cattle,* 2nd ed. London, Mosby, 2003.)

Corynebacteria can also cause mastitis. The milk is thick and creamy, sometimes called “mayonnaise mastitis.” Mastitis from corynebacteria is difficult to impossible to treat successfully. Mastitis caused by leptospirosis results in milk that is thick but contains no clots or blood, and affected quarters are not hard and hot. The condition is sometimes called “cold mastitis.” Leptospirosis is a fastidious bacterium that is difficult to culture. Mycoplasma rarely causes mastitis, but if it does, there is no cure and most animals are culled. Environmental streptococci (e.g., S. uberis, S. bovis, and S. dysgalactiae) and Enterococcus spp. all can cause mastitis.

Mastitis is divided into two major categories based on clinical signs. Clinical mastitis has clinical signs that need no special equipment for detection, for example, palpation of a hard, hot mammary gland or visualization of abnormal milk (clumps of exudates or foul odor). Subclinical mastitis has no obviously visible clinical signs in the udder or in the milk and must be detected by special diagnostic testing. Definitive diagnosis of mastitis is made through sampling and testing milk (Box 13-1).

BOX 13-1 Types of Mastitis

Contagious mastitis: Can be spread directly from cow to cow, usually at milking time (milking machines or contaminated hands or towels).

Environmental mastitis: Spread to individual cows through environmental contamination of bedding, soil, standing water, or feces.

Gangrenous mastitis: Severe infection that results in destruction of the affected quarter, with necrosis and sloughing. Severe Staphylococcus infections and wounds that allow Clostridium spp. to become established may result in gangrenous mastitis.

Clinical mastitis: Visible signs of disease in the milk and/or the affected quarter.

Subclinical mastitis: No visible signs of disease. Causes the greatest economic loss to dairy farmers because of lowered production. Requires special diagnostic testing of the milk for diagnosis.

Mastitis Tests

Strip Cup (Plate) Examination

The strip cup is a special milk collection cup with a black lid (Fig. 13-19). The first milk that is expressed from the teat, called the foremilk, should be squirted onto the black lid and observed for abnormalities and odor. Normal milk should be watery, chalky colored, and free of solid clumps; it should not have a sour or fetid odor. Clumps (Fig. 13-20), clots, flakes, abnormal color (Fig. 13-21), blood (Fig. 13-22), and bad odor all are indicators of possible mastitis. Strip cup examination is an important screening test but detects only “clinical mastitis” (obvious clinical signs); it does not detect subclinical mastitis (without visible clinical signs). Further testing is necessary to confirm the disease. Some studies indicate that in any given herd, 90% to 95% of the cows/heifers will test positive for subclinical mastitis.

Technician Note

Strip cup examinations are the cheapest screening test available for mastitis.

Somatic Cell Counts

Leukocytes and epithelial cells enter the mammary gland as a result of damage due to inflammation caused by mastitis. The amount of mammary inflammation can be indirectly measured through a somatic cell count (SCC). A milk cell counter stains the cells with a fluorescent dye then rapidly counts the number of cells. Measurements are taken from each quarter, each cow, or the bulk tank. SCC is not a direct test for mastitis because several other factors (e.g., such as stress and antibiotics) can affect SCC.

California Mastitis Test

The California mastitis test (CMT) is one of the most commonly used field tests to identify individual cows affected with mastitis. The test specifically identifies which quarters (or halves) are affected, which is important because mastitis seldom involves an entire udder; more commonly only one or two quarters are diseased. The test is sensitive enough to detect subclinical mastitis and roughly quantifies the severity of inflammation. Inflammation in the udder stimulates migration of white blood cells (WBCs) into the affected gland and causes the death of some of the epithelial (milk-producing) cells of the affected gland. These sloughed epithelial cells and WBCs, referred to as “somatic cells,” enter the milk, where they may be detected. The CMT basically uses detergent chemicals to lyse somatic cells in the milk, which releases their DNA. The test then detects the released DNA by changes in the consistency of the tested milk. The consistency reflects the SCC of the milk; the higher the count, the more severe the inflammation.

The test uses a white plastic test “paddle” with four cups labeled A to D (Fig. 13-23). The test should not be performed on the foremilk, which typically contains higher SCCs, even in normal milk. The udder is cleaned, and the foremilk is discarded. Then, each quarter is milked into a separate paddle cup. Only enough milk to cover the bottom of the cup is necessary (2–3 ml). One way to ensure the proper volume of milk is to fill all of the cups with several squirts of milk, then briefly tilt the paddle vertically so that excess milk spills from the cup. The test reagent is then added, using an equal volume of reagent as milk in each cup (Fig. 13-24). The paddle is kept horizontal and gently moved in a circular path to produce swirling of the cup contents. The test is read after about 10 seconds of mixing, while continuing to swirl the paddle. Interpretation must be prompt because mild positive reactions tend to disappear after 20 to 30 seconds.

FIGURE 13-23 California mastitis paddle.

Accurately recording of the results is important for identifying which quarters are affected and require treatment. The paddle has a handle, which should be consistently pointed in the same direction (relative to the cow) so that the technician can always be sure which teats correspond to which sample cup. For instance, if the handle is always pointed toward the cow’s head, then the results can be accurately recorded no matter which side of the cow the technician stood on to take the samples.

Interpretation of the CMT involves two variables: changes in consistency and changes in color. Consistency changes correspond to the SCC and are placed into one of five possible categories (Tables 13-1 and 13-2 and Fig. 13-25). Color changes correspond to the pH of the mixture. The test reagent contains bromcresol purple, a pH indicator that remains purple in alkaline conditions and turns yellow in acidic conditions (pH 5.2). A grade of “+” is given for alkaline milk and “Y” for acidic milk. Acidic milk is unusual. Normal milk has a pH from 6.4 to 6.8.

TABLE 13-1

California Mastitis Test: Grading Test Reactions

Symbol	Suggested Meaning	Description of Visible Reaction	“Quickie” Description
N	Negative	Mixture remains liquid with no evidence of formation of a precipitate.	Water
T	Trace	Slight precipitate forms and is best seen by tipping the paddle back and forth and observing the mixture as it flows over the bottom of the cup. Trace reactions tend to disappear with continued movement of the fluid.	Slime
+1	Weak positive	Distinct precipitate forms, but there is no tendency for gel formation. The precipitate may disappear with continued movement of the paddle.	Thick slime
+2	Distinct positive	Mixture thickens immediately with some suggestion of gel formation. As the mixture is swirled, it tends to move and twirl the center of the cup, leaving the bottom of the outer edge of the cup exposed. When the motion is stopped, the mixture levels out again and covers the bottom of the cup.	Gel
+3	Strong positive	Gel is formed, causing the surface of the mixture to become convex. Usually a central peak projects above the main mass after motion of the paddle has stopped. Viscosity is greatly increased so that the mass tends to adhere to the bottom of the cup.	Jelly

TABLE 13-2

California Mastitis Test: Interpretation of Results

Test Score	Interpretation in Cattle
N	Normal (0–200,000 cells/ml)
T	Normal (150,000–500,000 cells/ml)
1	Suspicious (500,000–1,500,000 cells/ml)
2	Mastitis (1,500,000–5,000,000 cells/ml)
3	Mastitis (>5,000,000 cells/ml)

Technician Note

To interpret results of the California mastitis test, technicians observe the consistency and color changes that occur within the sample.

False-positive results may occur in late lactation, during estrus, and when the foremilk is tested; the SCC tends to be naturally high in all of these situations. Also, trauma to the udder or teat elevates SCC, indicating inflammation but not necessarily infection.

Positive quarters usually are treated with oxytocin and a thorough milk-out or intramammary infusion.

Wisconsin Mastitis Test

The Wisconsin mastitis test (WMT) is commonly used by milk receiving plants to measure the quality of the farm bulk tank milk sample picked up by the milk hauler. The principle of the WMT is the same as that of the CMT. Instead of a subjective rating, the amount of gel that forms is measured in millimeters that remain in a calibrated tube. The WMT is conducted under more precise procedures and standard temperature conditions.

Milk Culture and Sensitivity

Milk culture is seldom necessary to confirm the diagnosis of mastitis, but it may be helpful for screening a herd for subclinical cases or identifying the bacteria in cases that are severe or refractory to routine antibiotic therapy. Samples may be collected individually from each quarter, or all four quarters may be pooled together for a screening sample for each animal.

Samples should be collected into sterile tubes; glass tubes with screw caps are preferred. Tubes should be labeled and paperwork finished before the procedure. Box 13-2 details the sample collection process.

BOX 13-2 Collecting Milk Culture and Sensitivity Samples

1. Wash hands thoroughly and put on examination gloves to reduce the chances of environmental contamination.

2. Wash teats in a sanitizing solution and dry teats with individual paper towels.

3. Strip and discard one to two squirts of milk from each teat.

4. Dip teats in germicidal teat dip and allow 30 seconds of contact time. Dry each teat with an individual paper towel.

5. Thoroughly clean the teat orifice with a cotton swab soaked in alcohol. Begin with the far teats, then the near teats (prevents contaminating the near teats when reaching across to swab the far side).

6. Open the sterile tube and hold it at a 45-degree angle so that debris cannot fall into the tube. Do not allow anything to touch the opening of the tube. Collect one to two squirts from each quarter. Begin with the near teats, then collect the far teats.

7. Cap the tube immediately.

8. Tubes should be refrigerated (4°C [39°F]), not frozen, until they can be processed in the laboratory. Processing should occur within 24 hours by swabbing on a blood agar plate and should be followed by routine microbial culture methods. In rare cases when processing cannot be done within 24 hours, the samples should be frozen as soon as possible.

Metritis

Uterine infections are common in cattle after calving because of the high incidence of retained placentas and dystocia. The most common type of uterine infection is endometritis, an infection of the lining of the uterus. It is characterized by a whitish to yellowish mucopurulent vaginal discharge in a cow that has recently given birth (Figs. 13-26 and 13-27). Because the infection is superficial, cows generally show no signs of systemic disease. Occasionally, bacterial infections extend into the deeper layers of the myometrium (metritis), where there is access to blood vessels. Bacteria and bacterial toxins may be absorbed into the bloodstream, resulting in septicemia, endotoxemia, and associated severe systemic illness and shock. Cows with metritis require intensive medical therapy in order to survive. Chronically, bacterial endometritis may develop into pyometra, with accumulation of purulent exudates in the uterus.