Foot rot is a highly contagious and debilitating disease that primarily affects cloven-hoofed livestock, such as sheep and cattle. It causes severe lameness, resulting in significant pain and difficulty bearing weight. The disease develops from a complex interaction involving specific anaerobic bacteria and particular environmental conditions. For the infection to progress, the host’s natural defenses in the foot must first be compromised, allowing the infectious agents to invade the underlying tissue.
Specific Microbes Responsible
Foot rot is caused by a synergistic infection involving two main bacterial species that colonize the foot in succession. The initial invader is Fusobacterium necrophorum, which causes interdigital dermatitis (foot scald), a mild inflammation of the skin between the toes. F. necrophorum produces leukotoxin, causing tissue necrosis and damaging the protective skin layer to create an entry point. This lesion allows the second, more specialized bacterium, Dichelobacter nodosus, to establish itself. D. nodosus is an obligate anaerobe and the essential causative agent of the characteristic separation of the hoof, driving the severe pathology of the disease.
Environmental Conditions That Enable Infection
The presence of the causative bacteria is not sufficient to trigger an outbreak; specific external factors must align to create a susceptible environment. High environmental moisture is perhaps the most significant factor, as prolonged exposure to wet conditions softens the skin of the interdigital space. This moisture, combined with warm temperatures, creates a perfect breeding ground for the anaerobic bacteria to multiply rapidly.
Warm conditions, generally above 50°F (10°C), accelerate bacterial growth and increase the likelihood of disease transmission and expression. Waterlogged pastures, muddy feedlots, and areas around watering troughs and gates are common sites where the ground remains wet and contaminated. These conditions cause the skin to become macerated, compromising its integrity and making it vulnerable to injury.
Mechanical trauma provides the final necessary condition, as abrasions from rough walking surfaces, such as gravel, frozen ground, or coarse stubble, physically break the softened skin barrier. This minor injury, often unnoticed, provides the bacteria with a pathway to the deeper tissues of the foot. The combination of skin damage, high moisture, and warmth facilitates the transfer and colonization by the infectious agents.
How the Infection Progresses
The infection begins with the establishment of F. necrophorum in the damaged interdigital skin, leading to the initial inflammation and necrosis. This damage creates a lowered oxygen environment, allowing the strictly anaerobic D. nodosus to invade the compromised tissue.
Once established, D. nodosus produces highly potent extracellular serine proteases, which are the main virulence factors of the disease. These enzymes, such as AprV2 and AprV5, are specifically designed to digest keratin, the structural protein that is the primary component of the hoof horn. This enzymatic action effectively dissolves the connections that hold the hard horn to the sensitive underlying tissue.
This digestion process results in the characteristic underrunning of the hoof, causing the sole and wall to separate from the foot. The progressive destruction of these supportive structures leads to the severe lameness and foul odor associated with virulent foot rot.