Common Bovine Diseases

Common Bovine Diseases

Bacterial Diseases


Anthrax is also known as splenic fever. Anthrax is caused by Bacillus anthracis. Bacillus anthracis is a gram-positive, nonmotile, spore-forming bacterium. Cattle are often infected through contaminated pastures or by eating contaminated feedstuffs. Anthrax is commonly found in soils that have neutral or alkaline pH. In these types of soils the bacteria often multiply. As the bacteria multiply, they rise to infectious levels, which explains the several years between outbreaks. Outbreaks often occur after flooding in endemic areas. During an outbreak, insects can spread the disease from animal to animal.

Anthrax can affect all warm-blooded animals, including humans. The disease is acute, febrile, and characterized by septicemia. Cattle with anthrax are often found dead. The death often is sudden and occurs in an otherwise seemingly healthy animal. If animals do not present as deceased, clinical signs include ataxia and bleeding from the orifices (nose, mouth, vulva, and anus). The blood often is dark and fails to clot. The incubation period of anthrax is 1 to 14 days (average 3–7 days). Other clinical signs include localized swelling of subcutaneous tissue, especially in areas of the neck, shoulders, and thorax. Another major clinical sign is the absence of rigor mortis. Death often results within a few days of infection.

If the veterinarian suspects anthrax in a deceased animal, a necropsy should not be performed. When the bacteria are exposed to oxygen from an open carcass, they form spores that are resistant to extreme temperatures and chemical disinfectants. Diagnosis should be based initially on a blood smear. The disease can be confirmed by laboratory tests and growth of B. anthracis on an agar plate. Differential diagnosis includes bloat, clostridial disease, lightning strike, anaplasmosis, and bacillary hemoglobinuria. When necropsy is performed, the characteristic finding is an enlarged, dark, and soft-textured spleen (Fig. 13-1).

If anthrax is identified in the early stages, aggressive systemic penicillin or oxytetracycline therapy may be useful. Vaccination should be practiced in endemic areas. Efforts should be made to control the disease as quickly as possible. Anthrax is a reportable disease, and the state veterinarian should be contacted immediately. The cattle in question should be quarantined. Any materials that were contacted by the dead animal and the dead animal itself should be cremated and buried deeply within the earth. Producers should disinfect all livestock areas, use insect repellents, control rodents and wild animals, and practice good sanitary conditions for themselves.


Brucellosis is also known as Bang disease and contagious abortion. Brucellosis is caused by Brucella abortus, but it also can be caused by Brucella melitensis or Brucella suis. Brucella spp. are gram-negative rods that grow best in a carbon dioxide–enriched aerobic environment. The infection occurs when cattle ingest infected placenta, feedstuffs, fetuses, tissue, milk, or uterine discharge. Congenital infection may occur. Much of the United States is free of B. abortus, but some wild animals still carry the infection and could infect cattle. Infection results in abortion between 7 and 8 months of gestation. Most cows abort only once and then become carriers. Carriers shed the organism in the milk, fetus, placenta, and uterine discharge.

The major clinical sign of brucellosis infection within a herd is abortion storms. Infected cows may be more prone to retained placentas, endometritis, and infertility. Bulls may develop orchitis and epididymitis. Synovitis (hygromas) may occur, and fistulous withers may be seen in horses.

Differential diagnosis includes trichomoniasis, leptospirosis, neosporosis, and infectious bovine rhinotracheitis (IBR). A diagnosis can be confirmed through blood agglutination tests, milk ring tests, and complement fixation (CF) tests. The Rose Bengal test can be used as a rapid screening test.

Screening for the disease is possible and is carried out especially in endemic areas. When a positive animal is identified, the entire herd should be tested and positive animals slaughtered. Calves can be vaccinated against the disease. The vaccine is often called Bang vaccine. Some states require vaccination of heifer calves 4 to 8 months of age. Bull calves and steer calves should not be vaccinated for fear of causing a chronic infection in reproductive organs. The disease is zoonotic and is called “undulant fever” in humans. Pasteurization of milk kills the bacteria, although consumption of unpasteurized milk products is dangerous for the human population because of the increased risk of infection.


Blackleg is caused by Clostridium chauvoei, which is a large, anaerobic, spore-forming, rod-shaped organism. The development of blackleg is often sporadic. Infected animals harbor the bacteria in their muscles. When the infected animal gets an open wound or undergoes bruising, the area provides an anaerobic environment for the bacteria to thrive in.

The disease often presents in feedlot cattle. Although most animals are found dead in the absence of clinical signs, cases caught early can present acutely with depression and lameness (Fig. 13-2). Upon necropsy, necrotic muscle can be isolated. The necrotic muscle has a distinct rancid smell. Often the affected muscle lies adjacent to normal tissue. The diagnosis is often made based on these characteristic necrotic lesions (Fig. 13-3) and confirmed by fluorescent antibody staining.

Differential diagnosis includes malignant edema, anthrax, and lightning strike. Prevention of blackleg includes vaccination on enzootic farms. Cattle caught in the early stages of the disease should be treated with penicillin and nonsteroidal antiinflammatory drugs.

Calf Enteritis

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.

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.

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.

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.

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.

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.

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.

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.

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 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.

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.

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.


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.

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.

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).

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.

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


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.

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).

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).

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.

FIGURE 13-19 Strip cup test.

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.

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.

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.

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.


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.

Common organisms causing uterine infections are Actinomyces (Corynebacterium) pyogenes, streptococci, staphylococci, coliforms, and gram-negative anaerobes; mixed infections are common. Uterine culture is seldom performed in cases of endometritis. Aerobic cultures often grow a “mixed bag” of organisms that may or may not be actual pathogens, and anaerobic culture is difficult to perform. Uterine biopsy is also rarely used. However, both procedures can be done in cattle, using the same instruments and methods as those used in the horse.


Pinkeye is also known as infectious bovine keratoconjunctivitis and infectious ophthalmia. Pinkeye is caused by Moraxella bovis, a gram-negative bacterium. Bright sunlight, irritants, stress, and dry dusty environments often exacerbate the disease.

Clinical signs include blepharospasm, lacrimation, photophobia, keratitis, conjunctivitis, and corneal opacity and ulceration (Figs. 13-28 and 13-29).

Diagnosis is often made based on clinical signs. Prevention of pinkeye should include low stocking rates, fly prevention, and attempts to control dust and bright sunlight, which all are factors predisposing to pinkeye. Treatment often consists of antibiotic therapy and isolation of infected animals. Vaccinations for pinkeye are available but controversial.

Shipping Fever

Shipping fever is also known as pasteurellosis. Pasteurellosis is caused by Mannheimia (Pasteurella) haemolytica and sometimes Pasteurella multocida. Pasturella spp. are gram-negative bacteria. Haemophilus somnus is also another causative agent of shipping fever. These bacteria are normal flora of the upper respiratory system and often become overabundant after stress or viral infection.

Clinical signs often include depression, low head carriage, wet cough, open-mouth breathing, weight loss, fever, and wheezing or cracking noises upon auscultation of the lungs (Fig. 13-30).

Upon necropsy, the lungs often are dark red and swollen (Fig. 13-31). Abscesses may be present (Fig. 13-32). Diagnosis depends on bacterial culture from necropsied lung tissue.

Treatment should include antimicrobial therapy and nonsteroidal antiinflammatory drugs in advanced cases. Prevention is possible with Pasteurella toxoid vaccines.


Vibriosis is caused by the gram-negative curved or spiral polar flagellated bacterium Campylobacter fetus subspecies venerealis or Campylobacter fetus subspecies fetus. The disease is transmitted venereally. Other forms of contraction include contaminated instruments, infected semen, and contaminated bedding. The bacteria cause early embryonic death, an extended calving season, infertility, and occasionally abortion.

Clinical signs of the disease in cows are often absent. The only indication of vibriosis may be an extended calving season due to early embryonic losses and irregular estrous cycles. Most cases of infertility are limited to replacement heifers.

Diagnosis of the disease requires culture of the organism from vaginal mucus, reproductive discharges, aborted fetuses (lung and stomach contents), or sheath aspirates from bulls. Vaccinations are available, and antibiotic-treated semen should be used.

Wooden Tongue

Wooden tongue is also known as actinobacillosis. Wooden tongue is caused by the bacterium Actinobacillus lignieresii. Actinobacillus lignieresii is a gram-negative coccobacillus. When the bacteria gain access to the oral cavity, they cause a hard, tumorous abscess of the tongue (hence the name wooden tongue).

Clinical signs include abscessation of the tongue and possible swelling of the ventral jaw (Figs. 13-33 and 13-34). The bacteria, a normal flora of the upper GI tract, can also cause cutaneous actinobacillosis if other areas of the body are infected (Fig. 13-35).

Stay updated, free articles. Join our Telegram channel

Aug 11, 2016 | Posted by in INTERNAL MEDICINE | Comments Off on Common Bovine Diseases

Full access? Get Clinical Tree

Get Clinical Tree app for offline access