Advice from Robin Densem - Agnew Equine Veterinary Practice

Robin is a director at Agnew Equine, a 100% equine practice covering Cheshire, Staffordshire and Derbyshire. Robin is particularly interested in medicine and was awarded a certificate in Equine Internal Medicine in 2011, the only vet in the area to have achieved this qualification.

Figure 1. Sun burn on horses muzzle with a crusty secondary Dermatophilus congolensis infection.

Figure 2. A cobs pastern showing the characteristic skin fold above the heel hub.
All about mud fever
The normal skin of a healthy horse is an effective barrier to infection
Mud fever is a very common syndrome seen in equine practice. True mud fever is caused by a specific bacteria Dermatophilus congolensis, the same organism that causes rain scald. The term mud fever is generally used as a colloquial term to describe skin infections of the lower limb of horses, the cause of the infection is often complex.
The skin of a normal horse is a very effective barrier to infection and can easily resist the bacteria it is constantly bombarded with. If the skin becomes damaged in any way its barrier function is diminished, which may allow infections to become established. For mud fever to occur, two scenarios are required; the skin surface must be compromised and the compromised skin must be exposed to bacteria capable of establishing infection.
The skin surface may be compromised in a number of ways. Persistent wetting of the skin macerates the skin surface (think what your fingers look like when you have been in the bath for too long). Macerated skin is an easy target for bacteria which can colonise it and cause infection. Anything that damages the integrity of the skin surface will also facilitate infections. Skin damage may be associated with wounds, abrasions or sunburn.
The bacteria that result in infection may come from the environment or be normal inhabitants of the skin surface, so called commensal bacteria. Dermatophilus congolensis is a commensal organism; it is always present on the horse’s skin but can only cause infection when the barrier function of the skin is compromised in some way. Figure 1 shows a pony with sunburn on its muzzle. The extensive crusting reaction is caused by a secondary Dermatophilus congolensis infection. As soon as the skin surface is damaged by the sunburn, the ‘waiting’ Dermatophilus bacteria can establish infection. This is an important concept to consider when treating mud fever. Simply treating the infection will not resolve the problem without addressing the factors that have compromised the skin in the first place. Antibiotics may improve the mud fever in the short term, but if the skin remains compromised infection will quickly become re-established.
When treating mud fever it is therefore important to consider ‘predisposing factors’ that affect the barrier function of the skin. Persistent skin wetting is the commonest ‘predisposing factor’ in the development of mud fever, which explains why it is mostly a condition of the wetter winter months. Other factors that may result in skin damage are also important. Sun burn has already been mentioned and generally affects non pigmented white haired areas. This may explain at least in part why white legs are more susceptible to mud fever. Chorioptic mange is a parasitic condition which is very itchy. Affected horses may rub or bite their lower limbs causing abrasions that may then be secondarily infected by bacteria. There is also evidence that some horses are predisposed to developing mud fever because of the conformation of their feet/ pastern. Cobs particularly may have a deep skin fold above the bulbs of their heels (figure 2), a common site for mud fever lesions.
Mud fever clinical signs. So what does mud fever look like? Early lesions are skin reddening, mild scaling and hair loss often on the back of the pastern (figure 3). Lesions may progress and become more extensive with marked exudation and patches of firmly adherent scabs (figure 4). Areas may be painful on palpation and lameness may occur particularly if cellulitis develops.
Mud fever diagnosis is usually based on clinical signs. A thorough history and full clinical examination are important in an attempt to identify any predisposing factors e.g. history of persistent wetting. In some cases samples may be collected from the skin to isolate the bacteria involved in the infection (as this may direct antibiotic selection for treatment) and to identify any underlying predisposing factors e.g. Chorioptic mange.
Mud fever treatment re quires a two pronged attack- treat the infection and identify and remove predisposing factors.
Treating the infection. A variety of bacteria may be implicated in mud fever infections including various Dermatophilus, Streptococcus and Staphylococcal species. In mild to moderate cases topical antibiotic creams are very effective as high concentrations of antibiotic are applied at the site of the infection- the skin surface. Preparation of the skin is important especially if lots of discharge and crusts are present. The bacteria are at the skin surface below the crusts and so for treatment to be effective the crusts must be removed before the antibiotic creams are applied. Removal of the crusts is best achieved by shampooing the affected area with a medicated shampoo using warm water. Leave the skin lathered for 5-10 minutes and the crusts should be softened nicely and easily removed. Drying the skin following shampooing is important (remember persistent wetting is an important predisposing factor in the development of mud fever) and this best done by ‘patting’ the skin dry or even using a hair dryer (on a low setting) as this minimizes skin trauma. Clipping the hair from affected areas may facilitate treatment as legs are easier to dry and creams can be applied more easily. In cases that are very painful this may require sedation. In severe cases, particularly those associated with cellulitis systemic, antibiotics may be required.
Removing predisposing factors is a really important part of treating mud fever and is aimed at identifying and treating the factors that compromise the barrier function of the skin. Persistent wetting can be avoided by stabling the horse when conditions are wet. In mild mud fever cases simply stabling the horse (and therefore avoiding the predisposing factor) may be all that is required to control infection. If Chorioptic mange is implicated the parasite infection must be treated. If predisposing factors are identified and addressed reinfection will hopefully be avoided.
Prevention of mud fever is optimal but in real terms it is difficult. Avoiding exposure to recurrent wetting is difficult in normal management systems as even exposure to early morning dew and wet grass may macerate the skin surface. Whilst all attempts should be made to avoid predisposing factors, the difficulty in doing so means that some horses that are particularly susceptible to infection, mud fever should be considered as a disease that is manaes rather than cured.
Avoid over treatment. As a final word of caution, try to aboid prelonged applicaion of medicated agents. There is increasing evidence that this resuls in chemical injury to the skin, comprimising its barrier funtions and perpetuating infection. If in doubt speak to your vet.


Persistent skin wetting compromises its barrier function and facilitates infection.

Figure 3. Mild mud fever lesion with skin reddening and crusting.

Figure 4. Severe mud fever with extensive exudation.