Diagnosing and treating bovine foot disorders (Proceedings)

Lameness examination

Examined at a distance, then up close by hands-on.

Footrot (interdigital necrobacillosis, infectious pododermatitis)

This is the most popular owner diagnosis but only really accounts for 15-20% of lameness. The etiology is as follows: maceration of intedigital skin via trauma, followed by invasion by Fusobacterium necrophorium and Bacteroides melanogenicus.

Clinical signs include swelling, redness, pain , skin fissures and necrotic tissue in the interdigital space. If allowed to persist, infection commonly invades deeper structures. (ie: DIP joint)

Treatment options include:systemic and/or topical antimicrobials and removing necrotic material that is unattached. As for vaccination, Fusobacterium necrophorum bacterin administered as 2 doses, 3-4 weeks apart followed by a yearly booster may decrease the severity and incidence of infection.

Interdigital dermatitis

Interdigital dermatitis is nothing more than an acute to chronic inflammation of the interdigital skin. It does not extend into subcutaneous tissues. Chronic inflammation can result in heel horn erosion and undermining of the heel bulbs.

Etiologies:Continuous wet and unhygienic conditions, laminitis, Bacteroides nodosus and a spirochete

Clinical signs include: slight to moderate lameness – paddling?, mild to severe redness of the skin and mild to moderate swelling with pain to the touch.

Papillomatous digital dermatitis (hairy heel warts)

Transmissible dermatitis on the plantar/palmar surface of the pastern and on the heels. There is complete erosion of the epidermis that is replaced by granulation tissue.1

Etiologies: Moisture, Bacteroides, Campylobacter, Spirochete (Treponema)

Clinical signs include: Lameness and weight shifting – one small lesion can be extremely painful to touch, ulceration around the coronary band in the bulb area and papillary hyperplasia of epidermis – fronds (fingerlike projections)

Treatment options include: cleaning, topical oxytetracycline or lincomycin spray, oxytetracycline under a bandage, foot baths (agents in footbaths are frequently inactivated by organic debris, therefore, the baths need to be fresh- can get expensive to properly maintain)

Injectable oxytetracycline – not very effective

Subsolar abscess

Etiologies include, puncture wounds, concrete or grinder burns, white line disease and bruising. Basically anything that compromises the horn. Clinical signs are obviously mild to severe lameness and an alteration of stance to shift weight, however, there is usually no swelling unless there is joint, tendon or soft tissue involvement above the hoof. Treatment and diagnostic modalities include:

Curettage all undermined horn. Protect unaffected sensitive laminae.

Explore all tracts, especially those areas with erupting granulation tissue.

Radiographs to examine deeper structures.

Place a wooden block on good claw

Bandage?

Systemic antibiotics if deep tissue is involved

Tenosynovitis

The etiology of this condition usually includes an extension of digital disease into the deeper structures to involve the flexor tendon sheaths. However, trauma due to lacerations or punctures directly involving these structures also commonly occurs. Owners often consider lacerations that don't immediately make the animal lame as something they can treat themselves, however, when the trauma involves the tendon sheaths, it often progresses to something far more serious.

Clinical signs of tenosynovitis include:

Severe lameness

Swelling and/or draining of synovial fluid from tendon sheath

Distended sheath – usually unilateral (remember, the digital flexor tendon sheaths don't communicate)

Ultrasound works well to differentiate between infection in sheath and surrounding tissue

Treatment

Provide adequate drainage and flush daily, just like an open joint and cover with a sterile bandage. If unilateral, a wooden block is placed on the sound claw. Amputation if infection extends into other side or above fetlock.

In cases of traumatic lesions presented early on, flushing the wound following a thorough daily cleaning and debridement is key. I usually use regional IV analgesia because this needs to be aggressive. I like to cover the wound with a sterile half limb wet to dry bandage. Common sequela of tenosynovitis include: tendon separation, fibrosis/adhesions and chronic lameness.

Septic arthritis/physitis

Septic arthritis/physitis can occur via three basic mechanisms which are outlined as follows:

Primary – penetration into joint, trauma

Secondary – extension into joint from adjacent infection

Tertiary – systemic or hematogenous spread (ie: navel ill, polyarthritis, endocarditis etc.)

The primary etiologic agent we deal with is bacteria such as E. coli. This is especially true in neonates which in turn are commonly deficient in passively acquired maternal antibodies.

The clinical presentation includes severe lameness, heat and swelling (articular and periarticular). In cases of hematogenous origin, signs of systemic involvement may also occur secondary to endocarditis (jugular pulse, murmur, undulating fever), pneumonia (fever, cough), diarrhea and omphalophlebitis.

Diagnosis can generally be made or inferred from physical exam. A leukogram may be beneficial as well. Synovial fluid aspirate findings may include turbidity and elevated volume, cells and protein. Culture can be performed on valuable animals. In cases of hematogenous origin, blood cultures and sensitivity may improve the outcome if results are obtained in time.

Treatment options include joint lavage with antibiotics if early or arthrotomy in cases of duration in valuable animals. Systemic antibiotics and non-steriodal anti-inflammatory drugs can be beneficial as well. The prognosis in these cases is guarded if less than 7 days duration and one joint, poor if longer than one week duration and grave with multiple joint involvements.

Osteomyelitis

The etiology of osteomyelitis can be either hematogenous or a sequele to trauma. Hematogenous agents often encountered include Salmonella, Pasteurella, and Streptococcus. Neonates get physitis, which subsequently spreads to adjacent bone, usually secondary to a failure of passive transfer. In addition, infection from the navel can also establish itself in the vertebral bodies.

Open fractures and deep wounds are obvious sources of bacteria for osteomyelitis.

Clinical signs of osteomyelitis include:

Pain, heat, swelling and potentially exudate

Neurological signs if in the vertebrae

A limb wound that does not heal and periodically drains could be a sequestrum. These animals are usually not lame!

Treatment options for osteomyelitis include: aggressive bone debridement, culture and sensitivity, long term antibiotic treatment – local and systemic, regional IV infusion, bone screw, antibiotic beads and NSAID's

Osteomyelitis of P3 is on of the more common manifestations that we encounter. This is usually secondary to a penetrating wound or advancement of infection from the adjacent soft tissue. If only P3 is involved, I commonly curette the bone (under regional intravenous analgesia) aggressively and pack it with Betadine soaked gauze. After applying more dry gauze and possibly some cotton, this becomes a wet-to-dry bandage.

Fractures

Fractures of P3 and P2 are commonly encountered. Animals are acutely lame. With P3 fractures, swelling is not present. In addition, pain may be difficult to elicit with hoof testers. However, percussion with hoof testers may reveal pain in addition to hyperextension and flexion of the digits. Radiographs provide a definitive diagnosis. Treatment of P3 and P2 fractures is generally very successfully accomplished by applying a wooden block on the sound claw for 6-8 weeks. Fractures of P1 are not as common and carry a more guarded prognosis for complete soundness due to subsequent DJD in the fetlock joint. Treatment of these fractures requires a cast that encases the foot, unless comminution is present, in which case a full limb cast is required to prevent collapse of fragments.

Laminitis "founder"

Laminitis usually occurs in cattle less than 3 years of age that are on a high concentrate diet with minimum long stem roughage. The condition is also associated with parturition due to stress, endocrine changes and changes in diet. Laminitis can also be secondary to mastitis or metritis and the accompanying endotoxemia.

The pathogenesis can be described as follows: hyperemia=>hemorrhage=>thrombosis=>vasculitis=>hypoxia=>edema and necrosis of sensitive laminae=>separation=>rotation=>white line disease (inferior quality horn production)

Clinical signs of acute cases include lameness in all 4 feet, heat in all 4 feet and a characteristic stance to remove pressure from affected feet. Other signs include weight shifting, lateral recumbency, muscle tremors, stiff stilted gait, and an increased heart and respiratory rate. Chronic manifestations are often more commonly noted and are characterized by hoof changes including hemorrhages and bruising beneath the sole, white line separation, heel horn erosion, wide flat hooves, stress rings, dropped sole and yellowish, waxy, soft hoof horn of inferior quality.

Treatment of acute laminitis primarily relies upon finding and correcting the underlying cause. In cases of overwhelming exposure to concentrates, laxatives such as magnesium oxide coupled with activated charcoal may be beneficial. Non-steroidal anti-inflammatory drugs are indicated not only for some anti-inflammatory effect but also to combat endotoxemia. Antihistamines may be beneficial early in the disease. Supportive therapy such as supplying soft bedding is necessary as well. Chronic cases are best managed by regular foot care.

The most common things we deal with are the various conditions that arise from the production of inferior quality horn. Inferior horn results in such conditions as sole ulcer, sand crack, horizontal fissure and white line separation. A widely accepted view of the events that lead to the production of inferior quality horn is that multiple factors are involved. The end result is an adverse effect on the keratinocyte that interferes with its ability to synthesize keratin proteins or membrane-coating material. Interference with nutrient supply may be a result of an inflammatory process in the corium from circulating vasoactive substances or localized trauma. Deficiency of a nutrient may also result in abnormal keratinocyte activity. Vasoactive substances such as endotoxin or histamine disturb blood flow in the microvasculature of the corium. Restriction of blood flow to these capillaries leads to ischemia and necrosis. Abnormalities of hoof horn production tend to be self perpetuating in that damage to the keratinocytes leads to inferior quality horn which gives rise to the production of more faulty horn and so on.

Sole ulcers (rusterholz ulcer)

Sole ulcers are characterized by a very distinct location at the junction of the heel and the sole. Factors that play a role in the etiology include: low heels, long toes, overgrown claws, corkscrew claw, excessive trimming, high concentrate-low roughage diet, standing in slurry and cubicles that are too small in a freestall barn.

Clinical signs include:pain (lameness), swelling depending on extent of involvement, ulcer at junction of heel and sole, granulation tissue erupting like a volcano with or without draining tract

Sand crack – vertical hoof fissure

Eighty five percent of vertical hoof fissures occur in the front limb on the lateral claw. We commonly see these in heavier cows/bulls 1.5 years of age or older. I have seen these in increasing frequency in rodeo stock.

The etiology involves many factors which are believed to include dry weather, previous bouts of laminitis, stress separations and coronary band trauma.

Clinical signs are fissures of the vertical hoof from the weight-bearing surface toward the coronary band. The fissure may or may not involve the coronary band depending upon duration and severity. Degree of lameness depends upon whether there is secondary infection of the deeper tissues and depth.

Treatment involves trimming to shorten and roll the toe to quicken "break over" and put less pressure on the toe. In addition, oils or linaments to soften the hoof are beneficial. Curettage of the fissure either with a hoof knife or with a Dremel tool provides drainage and prevents packing of soil and manure.

Thimble claw – horizontal hoof fissures

The etiology of horizontal fissures most commonly includes systemic illness or laminitis that interferes with normal hoof growth. This leads to hardship or stress lines due to interrupted horn growth at the coronary band. Clinical signs include lesions in all four feet at the same distance from the coronary band and separation from the new hoof growth. (leads to lameness, similar to hang nail in humans) Treatment is centered around the removal of all unattached hoof wall. The prognosis is good if no deeper structures are involved

White line disease

The true definition of white line disease is the separation and subsequent suppuration of the area between the sensitive and insensitive laminae. As you probably recall, the white line is the junction of the horn of the wall and sole. Most commonly affected areas include the abaxial wall of the rear limb lateral claw and the front limb medial claw. Various factors can contribute to the development of white line disease. Often this is recognized as a sequele to laminitis. Thin walled hooves, overgrowth of the hoof and wet conditions contribute to the development of this condition.

Clinical signs of white line disease in uncomplicated cases (separation without infection of the deeper tissues) usually manifest as mild to moderate lameness. However, in cases where suppuration has occurred, severe lameness, swelling at the coronary band, and navicular bursitis with drainage above the coronary band may be noted. The most severe manifestation is the spread of this infection to the distal interphalageal joint.

Corkscrew claw

Corkscrew claw is the rotation of the lateral hoof wall toward the axial plane. This condition is a result of a malalignment of the middle and distal phalanx. The third phalanx is often curved on its abaxial margin. These abnormalities result in a lateral to medial deviation of the abaxial wall causing the wall to curl under the sole. Claws most severely affected and most commonly recognized as the first claws affected are the lateral claws of the hind limb. The condition becomes evident usually by 1 to 3 years of age and is associated with many complications such as lateral collateral ligament strain, localized periostitis, subsolar abscess, sole ulcers and bruising. In addition, a lifetime of corrective trimming goes along with the condition. Corkscrew claw has a low degree of heritability, but greater expression results from feeding for increased performance. I tell my clients not to use these animals unless they are for a terminal cross.

Interdigital fibroma (corns)

Interdigital fibroma is hyperplasia and fibrosis of interdigital skin. The etiology is thought to be due to chronic irritation to the interdigital skin. There also appears to be an inherited predisposition to this condition due to the fact that bilateral or quadrilateral lesions may appear in young animals. As in the case of corkscrew claw, overfeeding or pushing these animals for performance increases the expression of this characteristic. Wet, filthy conditions are also thought to play a role. Clinical signs depend upon the degree of hyperplasia present. Corns don't cause the animal pain until there is trauma to the corn when it reaches the weight bearing surface or when it is being pinched by the claws or becomes ulcerated.

References

1. Greenough PR. (1997) Lameness in Cattle Greenough PR, Weaver AD, eds. Philadelphia, PA, W.B. Saunders Company.

2. Berry SL, Ertze RA, Read DH, et al (2004): Field evaluation of prophylactic and therapeutic effects of a vaccine against (papillomatous) digital dermatitis of dairy cattle in two California dairies. Proceedings of the 13th International Symposium and 5th Conference on Lameness in Ruminants. p 147.

3. Nocek J. (1997) Bovine acidosis: Implications on laminitis. J Dairy Sci 80:1005.

4. Bailey J, Bargai U, Bergsten C, et al (1997) Lameness in Cattle. Philadelphia, WB Saunders, pp 1-336.