Sole Ulcer and Rusterholz Ulcer

Sole ulcer (also known as Rusterholz ulcer) is a common, painful, non-infectious claw disease of cattle, primarily affecting the weight-bearing surface of the sole, typically at the typical site (the sole–heel junction, near the apex of the sole). It is characterized by a circumscribed area of sole horn loss, exposing the corium, often leading to hemorrhage, necrosis, and secondary infection. The condition is a major cause of lameness in dairy cattle, particularly in high-producing, intensively managed herds, and is associated with significant economic losses due to reduced milk production, impaired fertility, increased culling, and treatment costs. Sole ulcer is a manifestation of claw horn disruption, often linked to subacute ruminal acidosis (SARA) and laminitis, which weakens the suspensory apparatus of the distal phalanx, leading to sinking of the pedal bone and compression of the corium. The disease is classified as a claw horn lesion, distinct from infectious causes of lameness such as digital dermatitis or foot rot. It occurs predominantly in adult dairy cows, especially during early lactation and in the periparturient period, but can also affect beef cattle and heifers under intensive feeding systems. The economic impact is substantial, with each case estimated to cost between $200 and $500, including treatment, milk loss, and increased culling risk.

The primary etiology of sole ulcer is multifactorial, involving metabolic, nutritional, and management factors. The central underlying cause is subacute ruminal acidosis (SARA), which results from excessive intake of highly fermentable carbohydrates (starch, sugars) and insufficient dietary fiber, leading to a drop in rumen pH below 5.5. This acidic environment triggers the release of endotoxins (lipopolysaccharides) from gram-negative bacteria, histamine, and other vasoactive substances, which cause systemic inflammation and vascular changes in the digital microcirculation. These changes lead to impaired blood flow, edema, and degeneration of the suspensory apparatus of the distal phalanx (the laminae), allowing the pedal bone to sink and rotate within the hoof capsule. The resulting compression of the corium (the soft tissue beneath the sole horn) causes ischemia, hemorrhage, and necrosis, culminating in the formation of an ulcer. Nutritional factors include high concentrate-to-forage ratios, inadequate particle size of forage, and deficiencies in minerals such as zinc, copper, and biotin, which are essential for horn quality. Management factors include poor hoof trimming, excessive standing on hard surfaces, inadequate bedding, and poor hygiene, which exacerbate the mechanical stress on the claws. Additionally, genetic predisposition, high milk yield, and parity (older cows are more susceptible) contribute to the etiology. Infectious agents are not primary causes but can secondarily infect the exposed corium, leading to complications such as abscesses and deep sepsis.

Sole ulcer is one of the most prevalent claw diseases in dairy cattle worldwide, with herd-level prevalence ranging from 5% to 30% in intensive systems. It is more common in Holstein-Friesian cows than in other breeds, likely due to higher milk production and larger body size. The disease is most frequently diagnosed in adult cows, particularly in the first 60 to 120 days of lactation, with a peak incidence in early lactation and during the periparturient period. Heifers are less commonly affected, but can develop sole ulcers if they are overfed concentrates during the rearing period. The condition is more prevalent in tie-stall and free-stall housing systems with concrete floors, compared to pasture-based systems, due to increased standing time and mechanical stress on the claws. Seasonal variation is observed, with higher incidence in winter months when cows are housed indoors. Morbidity can be high, with up to 30% of cows in a herd affected annually, and the disease is a major cause of premature culling, accounting for 10% to 20% of culling decisions. Economic losses are substantial, including reduced milk yield (up to 2-3 kg/day), decreased fertility (increased calving interval), and treatment costs. In beef cattle, sole ulcer is less common but can occur in feedlot operations with high-concentrate diets.

The pathophysiology of sole ulcer is initiated by subacute ruminal acidosis (SARA), which is defined as a rumen pH below 5.5 for more than 3 hours per day. This condition arises from the rapid fermentation of non-structural carbohydrates, leading to an accumulation of volatile fatty acids (VFAs), particularly propionate and butyrate, and a decrease in rumen pH. The acidic environment damages the ruminal epithelium, allowing the absorption of endotoxins (LPS) and histamine into the bloodstream. These vasoactive substances cause systemic inflammation and activation of the complement cascade, leading to endothelial damage and increased vascular permeability in the digital microcirculation. This results in edema, hemorrhage, and thrombosis within the corium, compromising blood flow to the laminae. The suspensory apparatus of the distal phalanx, which is composed of the dermal and epidermal laminae, undergoes degeneration and weakening, allowing the pedal bone to sink and rotate within the hoof capsule. The downward displacement of the distal phalanx compresses the corium of the sole, particularly at the typical site, leading to ischemia, necrosis, and ulceration. The ulcer exposes the corium, which is highly innervated and vascular, causing severe pain and lameness. Secondary bacterial infection (e.g., Fusobacterium necrophorum, Trueperella pyogenes) can lead to abscess formation, deep sepsis, and involvement of the distal interphalangeal joint, resulting in more severe complications. The systemic effects of SARA also include decreased rumen motility, altered VFA ratios (decreased acetate:propionate ratio), and increased risk of other metabolic diseases such as ketosis and displaced abomasum.

Intrinsic predisposing factors include high milk yield, which increases metabolic demands and susceptibility to metabolic stress; parity, with older cows (3rd lactation and beyond) being at higher risk due to cumulative wear and tear on the suspensory apparatus; genetics, as certain bloodlines have weaker horn quality or conformation; and transition period stress, which involves hormonal changes, negative energy balance, and immune suppression. Extrinsic factors include ration formulation errors, such as excessive concentrate feeding, insufficient forage particle length (less than 2-3 cm), and inadequate dietary fiber; poor feeding management, such as sorting of feed and inconsistent feed delivery; housing and environmental factors, including concrete flooring, inadequate bedding, overcrowding, and poor manure management leading to wet and unhygienic conditions; and hoof care practices, such as infrequent or improper trimming, which can exacerbate claw horn overgrowth and abnormal weight distribution. Additionally, lack of exercise and prolonged standing, especially in free-stall barns with uncomfortable stalls, increase the risk. Nutritional deficiencies, particularly of biotin, zinc, copper, and methionine, can impair horn quality and resilience. Other diseases, such as laminitis, digital dermatitis, and foot rot, can predispose to sole ulcer by causing structural changes in the claw.

Clinical signs of sole ulcer include varying degrees of lameness, which can range from mild (locomotion score 2) to severe (locomotion score 4-5, with reluctance to bear weight on the affected limb). Affected cows often show a characteristic 'toe-tip' walking or 'pointing' of the foot, and may spend more time lying down. On close inspection, the affected claw (usually the lateral claw of the hind limb) may be warm to the touch, and there may be swelling of the coronary band. The ulcer itself is visible after trimming the sole, appearing as a circumscribed area of red or black discoloration, often with a defect in the horn exposing the corium. The lesion is typically located at the typical site, which is the axial aspect of the sole, just caudal to the apex, near the heel. In chronic cases, there may be granulation tissue (proud flesh) protruding from the ulcer, and secondary infection can lead to abscess formation, which may cause a tract extending to the coronary band or the heel. Systemic signs are usually absent unless there is severe secondary infection, which can cause fever, decreased appetite, and reduced milk yield. Herd-level signs include increased prevalence of lameness, reduced milk production, and impaired reproductive performance.

Differential diagnoses for sole ulcer include: 1) White line disease (white line abscess), which is characterized by a separation of the white line and a tract of dirt and debris, often leading to abscess formation; 2) Digital dermatitis (Mortellaro disease), an infectious condition affecting the skin of the heel and interdigital space, causing painful erosions and proliferative lesions; 3) Foot rot (interdigital necrobacillosis), an infectious condition causing swelling and necrosis of the interdigital tissues, with a characteristic foul odor; 4) Laminitis (acute or chronic), which causes diffuse hemorrhage and yellow discoloration of the sole, and may lead to sole ulcers as a sequela; 5) Toe ulcer, which is a similar ulcerative lesion but located at the toe, often associated with overgrowth and abnormal weight bearing; 6) Heel horn erosion, which is a non-painful condition characterized by pitting and erosion of the heel horn, often secondary to poor hygiene; 7) Fracture of the distal phalanx, which causes severe lameness and is diagnosed by radiography; 8) Septic arthritis of the distal interphalangeal joint, which is a severe infection of the joint, often secondary to deep penetrating wounds or neglected sole ulcers; 9) Sole abscess, which is a localized infection of the sole, often caused by a foreign body, and may be difficult to distinguish from sole ulcer without trimming; 10) Foreign body penetration (e.g., wire, nail), which causes a puncture wound and subsequent infection. Definitive diagnosis is based on hoof trimming and visual inspection, with radiography used to rule out bone involvement.

The diagnostic algorithm for sole ulcer begins with a thorough herd history, including nutrition, housing, and lameness prevalence. A complete physical examination is performed, with emphasis on locomotion scoring (using a 1-5 scale) to identify affected cows. The affected limb is examined, and the hoof is cleaned and trimmed to allow visualization of the sole. The typical site is inspected for the presence of an ulcer, hemorrhage, or necrosis. If the lesion is not obvious, a hoof tester is used to apply pressure to the sole to elicit a pain response. If an ulcer is found, the depth and extent of the lesion are assessed, and the presence of granulation tissue or purulent discharge is noted. If secondary infection is suspected, a probe may be used to explore the tract, and radiography may be indicated to evaluate for osteomyelitis or joint involvement. In cases where SARA is suspected as the underlying cause, rumen fluid analysis (via rumenocentesis or ororuminal sampling) is performed to measure pH, and blood samples are taken for BHB, NEFA, and calcium levels. The diagnostic algorithm also includes assessment of claw conformation and trimming records, as well as evaluation of the environment and feeding practices. A definitive diagnosis is made based on the characteristic lesion at the typical site, with differential diagnoses ruled out by location and appearance.

Laboratory findings in sole ulcer are primarily related to the underlying metabolic disturbances, particularly SARA. Rumen fluid analysis typically reveals a pH below 5.5, decreased protozoal motility, and a reduced methylene blue reduction time (less than 3 minutes), indicating impaired fermentation. Blood biochemistry may show elevated BHB levels (greater than 1.2 mmol/L) indicating subclinical ketosis, and elevated NEFA levels (greater than 0.5 mmol/L) indicating negative energy balance. Ionized calcium may be low (less than 1.0 mmol/L) in cows with concurrent hypocalcemia. Magnesium and phosphorus levels may be altered. Complete blood count is usually within normal limits unless there is secondary infection, in which case there may be leukocytosis with a left shift and elevated fibrinogen. In cases of secondary infection, serum amyloid A and haptoglobin may be elevated. Milk production records may show a decline, and somatic cell count (SCC) may be elevated if mastitis is concurrent. However, there are no specific laboratory markers for sole ulcer itself; the diagnosis is primarily clinical.

Imaging modalities are not routinely used for sole ulcer but can be helpful in complicated cases. Ultrasonography of the digit can be used to assess soft tissue swelling, abscess formation, and involvement of the distal interphalangeal joint. It can also be used to evaluate the suspensory apparatus and the corium. Radiography is the most useful imaging modality for sole ulcer, particularly to rule out osteomyelitis of the distal phalanx, fractures, or septic arthritis. Radiographs may show a radiolucent area at the site of the ulcer, gas opacities in cases of infection, or periosteal new bone formation in chronic cases. In cases of suspected SARA, ultrasonography of the liver may reveal increased echogenicity due to fatty infiltration, and rumen ultrasound can assess rumen fill and motility. However, imaging is not essential for diagnosis and is reserved for cases with suspected complications.

Cytology and histopathology are rarely needed for sole ulcer diagnosis but can be useful in research or in cases of suspected neoplasia. Histopathology of the affected corium shows necrosis, hemorrhage, and inflammatory cell infiltration, with neutrophils and macrophages. In chronic cases, there may be fibrosis and granulation tissue. If secondary infection is present, bacterial colonies may be visible. Cytology of exudate from the ulcer may show degenerate neutrophils and bacteria. In cases of SARA, rumen epithelial biopsy may show hyperkeratosis and parakeratosis. However, these tests are not routinely performed in clinical practice.

Treatment of sole ulcer involves both local and systemic measures. The primary goal is to relieve pain and pressure on the affected area, promote healing, and prevent complications. The affected claw should be trimmed to remove loose, necrotic horn and to establish drainage. The ulcer should be cleaned and disinfected with an antiseptic solution (e.g., povidone-iodine or chlorhexidine). A hoof block (e.g., a wooden or plastic block) should be applied to the healthy claw to elevate the affected claw and reduce weight-bearing pressure. This is crucial for pain relief and healing. Systemic anti-inflammatory drugs, such as flunixin meglumine (1.1-2.2 mg/kg IV or IM, q24h for up to 3 days) or meloxicam (0.5 mg/kg IV or SC, single dose), are recommended to reduce pain and inflammation. Antibiotics are indicated if there is evidence of secondary infection, such as purulent discharge or cellulitis. Commonly used antibiotics include procaine penicillin G (22,000 IU/kg IM, q24h for 3-5 days), ceftiofur (2.2 mg/kg IM or SC, q24h for 3-5 days), or oxytetracycline (10 mg/kg IV or IM, q24h for 3-5 days). In cases of severe infection, a regional intravenous perfusion of antibiotics (e.g., ceftiofur or penicillin) may be performed. Supportive therapy includes ensuring adequate nutrition and hydration. If SARA is present, dietary adjustments are necessary, including reducing concentrate intake, increasing forage particle length, and adding buffers such as sodium bicarbonate (0.5-1.0% of diet DM) or magnesium oxide. In chronic cases with extensive granulation tissue, surgical debridement may be required. In cases of deep sepsis involving the distal interphalangeal joint, amputation of the digit may be considered as a salvage procedure.

The prognosis for sole ulcer is generally good if treated early and appropriately. With proper trimming, hoof block application, and pain management, most cows recover within 2-4 weeks. However, the prognosis is guarded in cases with deep infection, joint involvement, or chronic laminitis. Cows with sole ulcer are at increased risk of recurrence and other claw diseases. Milk yield may not fully return to pre-lesion levels, and there is an increased risk of culling. Negative prognostic indicators include delayed treatment, severe lameness (locomotion score 4-5), presence of granulation tissue, and involvement of the distal interphalangeal joint. In such cases, the cow may become a chronic lameness case, leading to poor welfare and economic loss. Early detection and treatment, along with herd-level prevention strategies, are key to improving outcomes.

Follow-up care for sole ulcer includes re-examination of the affected claw after 2-4 weeks to assess healing. The hoof block should be removed once the ulcer has healed, typically after 4-6 weeks. The cow should be monitored for lameness and milk production. Herd-level follow-up involves reviewing the nutrition program, particularly the forage-to-concentrate ratio and particle size, to prevent SARA. Rumen fluid pH should be monitored in a sample of cows to assess the effectiveness of dietary changes. Locomotion scoring should be performed regularly (e.g., monthly) to detect new cases. Hoof trimming should be scheduled at least twice a year, and footbaths may be used to control infectious causes of lameness. Transition cow management should be optimized to reduce metabolic stress. Records of lameness incidence and treatment outcomes should be maintained to evaluate the effectiveness of prevention programs.

Clinical pearls: 1) Always examine the sole of the affected claw after trimming, as sole ulcers are often hidden by overgrown horn. 2) Apply a hoof block to the healthy claw to relieve pressure on the ulcer; this is the most important step in treatment. 3) Use systemic NSAIDs to control pain and inflammation, which improves recovery. 4) In cases of SARA, focus on dietary correction, as treating the ulcer without addressing the underlying acidosis will lead to recurrence. 5) Early detection through regular locomotion scoring and hoof trimming is key to preventing severe lesions. Pitfalls: 1) Failing to trim the affected claw adequately, leaving necrotic tissue and preventing drainage. 2) Not applying a hoof block, leading to continued pressure and delayed healing. 3) Overusing antibiotics without evidence of infection, contributing to antimicrobial resistance. 4) Ignoring the herd-level problem and only treating individual cows, leading to high prevalence. 5) Misdiagnosing sole ulcer as digital dermatitis or foot rot, leading to inappropriate treatment.

Current drug protocols for sole ulcer are based on Plumb's Veterinary Drug Handbook and AABP guidelines. For pain management, flunixin meglumine is administered at 1.1-2.2 mg/kg IV or IM, once daily for up to 3 days. Meloxicam is given at 0.5 mg/kg IV or SC as a single dose. For secondary infection, procaine penicillin G is used at 22,000 IU/kg IM, once daily for 3-5 days. Ceftiofur hydrochloride is administered at 2.2 mg/kg IM or SC, once daily for 3-5 days. Oxytetracycline is given at 10 mg/kg IV or IM, once daily for 3-5 days. For regional intravenous perfusion, ceftiofur (500 mg) or penicillin (5 million IU) is diluted in 60 mL of saline and infused into the digital vein after applying a tourniquet for 30 minutes. For SARA management, sodium bicarbonate is added to the diet at 0.5-1.0% of dry matter, and magnesium oxide at 0.2-0.4% of dry matter. Withdrawal times must be observed: flunixin meglumine has a meat withdrawal of 4 days and milk withdrawal of 36 hours; meloxicam has a meat withdrawal of 15 days and milk withdrawal of 5 days; procaine penicillin G has a meat withdrawal of 5 days and milk withdrawal of 72 hours; ceftiofur has a meat withdrawal of 3 days and milk withdrawal of 0 hours; oxytetracycline has a meat withdrawal of 28 days and milk withdrawal of 96 hours. Always consult the label and a veterinarian for specific protocols.

Evidence-based literature on sole ulcer emphasizes the strong association with subacute ruminal acidosis (SARA) and laminitis. A landmark study by Nocek (1997) demonstrated that feeding high-concentrate diets to dairy cows induced laminitis and subsequent sole ulcers. Research by Greenough and Vermunt (1991) described the pathogenesis of claw horn lesions, linking them to metabolic and mechanical factors. A meta-analysis by Charfeddine and Pérez-Cabal (2017) found that sole ulcer is a major cause of lameness in dairy cattle, with a heritability of 0.1-0.2, indicating a genetic component. Studies on hoof trimming have shown that regular trimming reduces the incidence of sole ulcers (e.g., Manske et al., 2002). The use of hoof blocks has been shown to improve recovery rates (e.g., Kofler et al., 2004). Nutritional interventions, such as increasing forage particle length and adding buffers, have been shown to reduce SARA and associated claw lesions (e.g., Krause and Oetzel, 2006). The AABP and ECBHM have published consensus guidelines on lameness management, emphasizing the importance of early detection, treatment, and prevention. Overall, the literature supports a multifactorial approach to managing sole ulcer, focusing on nutrition, housing, and hoof care.