In western Canada, TTN is generally used to describe a clinical syndrome of cattle, typically beef feedlot cattle, characterized by lameness localized to the distal aspect of a hind limb (distal hind limb) in the absence of any obvious signs of swelling. Inspection of the feet of affected limbs usually reveals white line separation along the apex of the toe.1–4 Debridement of affected claws to the level of the corium with hoof nippers frequently reveals either a dark purulent exudate or a dry black area of necrosis.4 Aggressive debridement often confirms that the disease has progressed to involve P3. Accordingly, Gyan et al3 suggested that TTN be defned as infammation or necrosis of the corium, which may or may not extend to inflammation, necrosis, or lysis of P3. It could be argued that this is too broad of a definition because an animal, particularly a live animal, might be assumed to have TTN solely on the basis of lameness and the presence of apical white line separation in the affected claw or claws. However, postmortem examination of affected feet frequently reveals extensive necrosis of P3 and inflammation of the associated soft tissues. Although the antemortem and postmortem findings associated with TTN may vary, from a practical management standpoint, the severity of disease is somewhat irrelevant because feedlot veterinarians are primarily concerned about ensuring that feedlot personnel correctly identify the cause of lameness rather than the severity of pathological lesions so that affected cattle can be appropriately treated and managed. The standard treatment for cattle with TTN includes parenteral antimicrobial administration with or without removal of the affected portion of the apex of the toe to confirm the diagnosis and facilitate drainage.
Although assigning a diagnosis of TTN to lame cattle might represent a pragmatic approach for consolidating the many different manifestations of the disease, the rather simplistic definition for TTN has its detractors. Specifically, some argue that proper examination of the foot of a lame animal should provide sufficient information for a proper diagnosis, which in many instances may lead to the lesion being defined as toe necrosis. The International Committee for Animal Recording describes toe necrosis as necrosis of the tip of the toe with involvement of bone tissue.5 In western Canada, veterinarians frequently refer to confirmed toe necrosis as P3 necrosis, TTN, or, more recently, TTN syndrome.3,4,6–9 Complicating matters is the fact that there is another moniker used to describe what appears to be the same disease. In the early 1980s, Sick et al1 documented the first outbreak of TTN in North American feeder cattle, which was followed by a report by Miskimins2 in the early 1990s. In both instances, the authors described the presence of purulent discharge at the tips of the toes of affected cattle and ascribed the term toe abscesses to the disease. The epidemiology, clinical findings, and postmortem findings detailed in both of those reports1,2 are remarkably similar to what veterinarians currently refer to as TTN or TTN syndrome. Of particular interest are descriptions of the postmortem findings, which include rounding of the apex of the toe, white line separation, P3 necrosis, arthritis, cellulitis, tendonitis, tenosynovitis, myositis, and systemic pathological changes consistent with bacteremia.1,2,4,8,9 Consequently, TTN syndrome has entered the lexicon because that term denotes that, although the condition my initially begin with TTN, affected animals that die or are euthanized because of the disease invariably have P3 necrosis in conjunction with various other sequelae.
Perhaps 1 point that all researchers and feedlot veterinarians can agree on is that apical white line separation is associated with lameness. Specifically, lame cattle do not develop P3 necrosis in the absence of white line separation.3 Given the anatomic structure and importance of the white line to the bovine foot,10,11 the presence of white line separation as a prerequisite for TTN seems logical. The white line is an inherently weak junction of the hoof wall and sole and is composed primarily of laminar horn produced by the laminar corium. Laminar horn undergoes suboptimal keratinization, resulting in immature nontubular horn that is soft and flexible and predisposed to mechanical failure and foreign body penetration. Consequently, bacteria associated with TTN likely gain access to the deep tissues of the hoof through a breach in the white line.
The pathogenesis of TTN has not been fully elucidated; however, the epidemiology and clinical findings support an abrasion theory. That theory posits that during transport and handling at auctions and processing shortly after feedlot arrival, cattle abrade the soles and apical region of the white line of their hooves on hard coarse surfaces, such as metal trailer and concrete flooring. This abrasion compromises the integrity of the white line, leading to its separation and the subsequent colonization of the foot tissues with bacteria that cause P3 necrosis and the myriad of associated sequelae. This theory seems plausible because the incidence of TTN is greatest for cattle within days to weeks after feedlot arrival,1,2,6 which coincides with exposure of the cattle to abrasive flooring surfaces. Moreover, the apical white line region of claws with TTN is significantly thinner than that of healthy claws,7 which strongly suggests an abrasive mechanism. There is also anecdotal evidence that a hyperexcitable temperament is a risk factor for TNN.1,4 Presumably, overcrowding or overly aggressive handling results in cattle forcing themselves against the animals ahead of them in alleyways and chute systems. As the force exerted by those cattle increases, they lose traction, especially in the hind limbs that are being used for propulsion, and this loss of traction results in rasping of the solar horn and white line on the handling system flooring. Paradoxically, to improve cattle footing and traction, the flooring of feedlot handling systems frequently consists of stamped or etched concrete or has metal cleats installed in it, which may be risk factors for white line abrasion. Once the white line is compromised, repetitive loading and unloading of the claws during ambulation presumably lead to apical white line separation. This last supposition is supported by the finding of macroscopic feed and bedding particles within the hoof capsule of affected claws, which suggests that white line separation can be sufficient to allow foreign material to become entrapped within the claw. This is important because white line separation is often difficult to appreciate in a non-weight-bearing foot,4,7 a fact that further suggests the separation must occur under physiologic loading.
The veterinary literature contains little information regarding the effects of physiologic loading on the hind feet of cattle, with only a few studies12–15 conducted related to materials testing and finite element analysis. Studies describing the extent of white line separation in diseased claws with and without loading are lacking. The purpose of the study reported here was to compare the extent of white line separation created during physiologic loading in bovine claws with and without evidence of TTN. The overall aim was to gather information about the possible role of mechanical loading on the pathogenesis of TTN in cattle.
Supported by the Government of Saskatchewan Agriculture Development Fund.
The authors declare that there were no conflicts of interest.
The authors thank Dr. Mike Jelinski, Dr. Elizabeth Homerosky, Dr. Fritz Shumann, and Merle Friesen for donation of the diseased and control specimens used in this study and Rob Peace for assistance with the experimental setup.
Fastray, Bosworth, Chicago, Ill.
Denstone, Modern Materials Inc, South Bend, Ind.
MTS Bionix, Model 370.02 Axial/Torsional, MTS Systems Corp, Eden Prairie, Minn.
Point Grey Chameleon3 5MP monochrome camera with 16-mm focal length, FLIR, Richmond, BC, Canada.
Analyze 10, Analyze Direct Inc, Overland Park, Kan.
WACOM Cintiq 21UX, Portland, Ore.
SPSS, version 22 for Windows, SPSS Inc, Chicago, Ill.
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