Contagious Footrot in Sheep
- Lameness in Sheep
- Overview of Lameness in Sheep
- Interdigital Dermatitis in Sheep
- Contagious Footrot in Sheep
- Foot Abscess in Sheep
- Impacted or Infected Oil Gland in Sheep
- Interdigital Fibroma in Sheep
- Septic Laminitis in Sheep
When there is concurrent invasion by Dichelobacter nodosus of foot scald, contagious footrot results. The Australians separate footrot into two categories, benign or virulent, depending on the strain of D nodosus present. In the USA, however, benign and virulent footrot are considered to be the same (due to the difficulty of differentiating the two) and are treated accordingly.
Benign Footrot
The infection is confined largely to the interdigital skin, with only minimal underrunning of the adjacent horn. Clinically, benign footrot appears similar to ovine interdigital dermatitis, but D nodosus is involved—a situation that is hard to assess because culture of D nodosus is difficult and rarely done. The odor, however, is characteristic. Lameness is common but less severe than in virulent footrot. The etiology and pathogenesis are the same, but the strains of D nodosus are less virulent and lack the hoof-invasive properties of the strains that cause virulent footrot. D nodosus may also be isolated from cattle, but strains affecting cattle usually cause only the benign form of footrot in sheep. The economic effect of benign footrot is much less than that of virulent footrot. Running the sheep through foot baths containing 10% w/v zinc sulfate once every 14 days during the wet season is usually adequate for control. Since the advent of long-acting antibiotics such as tetracycline, their use has been adopted with good results.
Virulent Footrot
Virulent footrot is a specific, chronic, necrotizing disease of the epidermis of the interdigital skin and hoof matrix that begins as an interdigital dermatitis and extends to involve large areas of the hoof matrix. Because the sensitive lamina and its network of capillaries are destroyed by the infection, the hoof wall (corium) loses its blood supply and anchorage to the underlying tissue and becomes detached. Footrot is extremely contagious and, under suitable conditions and susceptible genetics, morbidity may approach 100%. The infection is also rarely found in goats, deer, and cattle. The potential for genetic selection for increased resistance to footrot has been established.
Etiology:
Fusobacterium necrophorum, a gram-negative anaerobic bacteria, is a normal resident of manure-contaminated environments. Under favorable environmental conditions, it colonizes the moist, macerated interdigital skin and provides ideal conditions for invasion by D nodosus at the skin/hoof interface. By action of proteases, D nodosus, also a gram-negative anaerobe and obligate pathogen, liquefies the cells of the stratum granulosum and stratum spinosum, causing the separation of the hoof wall from the basal epithelium. It works its way down the interdigital horn to the heel, then to the sole, and finally to the lateral side of the hoof. D nodosus has been found to survive <3 wk outside the host, but it can remain sequestered in cavities, cracks, or deformities of the affected foot for the life of the sheep. There are at least 20 different strains of D nodosus, with varying pathogenicity. Transmission occurs most rapidly when conditions are warm and moist; however, cold, moist conditions are also conducive to transmission.
Clinical Findings:
The most obvious sign is lameness, but the foot is seldom carried or packed. In chronically infected sheep, the hoof becomes gnarled and distorted. When more than one foot is infected, some sheep become recumbent or walk on their knees. Brisket and knees tend to become hairless and ulcerated. Affected sheep do not compete well for food, lose body condition, and produce less wool. Rams with infected hindfeet may be unwilling to breed, and ewes with hindfeet lesions may be unable to bear the weight of a ram at service.
In early cases, examination of the feet generally reveals nothing more than interdigital dermatitis. In slightly more advanced cases, in which the infection has begun to extend into the hoof matrix, there is slight detachment of the hoof wall at the interface of the interdigital skin and hoof. As the disease progresses, the separation of the horn spreads further under the heel and sole. Running one’s thumb between the wall and the underlying tissue in the interdigital space often detaches the wall from the heel and sole, revealing a white, slightly moist (but not purulent), odorous substance. Finally, the outer wall is affected. The horny hoof may eventually be attached only at the toe and the coronet on the lateral side of the foot. The odor of the necrotic tissue is characteristic and helps to diagnose the disease. Myiasis is a common sequela during fly season; it may extend to the area of the sheep where the infected feet come into contact with the body when the sheep is recumbent. The clinical disease persists until the environment dries or the sheep are treated. After apparent healing, D nodosus remains hidden in small pockets within the foot, where it is detectable only by extensive trimming, and becomes active again when moist conditions recur. These sheep are carriers and generally remain infected for life. Immunity to footrot after infection does not seem to occur, because relapses are the norm.
Diagnosis:
In flocks with virulent footrot, underrunning and separation of the hard horn of the hoof of one or more feet, complete with the characteristic odor, is diagnostic. If the problem is discovered early when interdigital dermatitis is the only sign, it should be assumed that the condition is an early stage of contagious footrot, and treatment should be initiated immediately.
Treatment:
Treatment efforts may be directed toward temporary control of the disease or total eradication. At certain times, eg, during a wet season, temporary control may be the only realistic goal.
Traditionally, treatment consisted of foot bathing using antibacterial solutions after careful hoof trimming to remove all dead horn and expose infected tissue and bacteria to air. However, foot soaking for 30–60 min has been shown to be more effective even when trimming is not done. In fact, Australian research has shown that trimming may do more damage than good. The most effective solution is 10% w/v zinc sulfate with 0.2% v/v of laundry detergent containing nonionic surfactants such as sodium lauryl sulfate. Aerosol sprays have been used in lieu of foot bathing and include zinc sulfate, tincture of iodine, tetracycline, copper sulfate, formalin, chlorine bleach, and other disinfectants. However, sprays are not as effective as foot bathing or soaking in zinc sulfate.
The advent of long-acting antibiotics used in combination with topical foot treatments has improved recovery and reduced carrier animals. Parenteral treatment using a long-acting oxytetracycline at 13.6 mg/lb gives a duration of effect in cattle of 7–8 days and probably a similar duration of effect in sheep. However, sheep must be placed in a “clean” area (ie, one in which no sheep have been kept for at least 3 wk) or in a completely dry lot after they are run through a foot bath and given the antibiotic. Sheep will become reinfected as soon as the antibiotic is cleared if returned to a contaminated environment. The feet of treated sheep should be examined once a week to identify those not responding to treatment. Sheep that do not respond should be isolated and preferably culled. D nodosus is extremely difficult to eradicate from animals that have relapsed numerous times. Furthermore, subclinical or relapsing cases take valuable time to handle, identify, and isolate, and they remain a source of infection for other animals.
Prevention and Control:
Animals from unknown premises or auction houses should not be purchased. Any sheep to be added to the flock should be quarantined for several weeks to prevent the spread of footrot and other chronic diseases. During the quarantine period, the animal’s feet should be lightly trimmed and examined closely for pockets and other malformations that suggest a previous D nodosus infection. Vehicles (eg, trucks, trailers) or facilities in which unknown or infected sheep have been held should be thoroughly cleaned and disinfected before placing uninfected sheep in them. If it is not possible to thoroughly disinfect transport vehicles, zinc sulfate can be liberally scattered over the floor to reduce viable bacteria.
Because the incubation period of footrot is ~14 days, foot bathing at 10-day intervals will control spread of the organism in affected flocks during periods of the year when the sheep are in wet conditions. Footrot has been controlled by placing foot baths with 10% w/v zinc sulfate solution around water troughs, forcing sheep to walk through them and stand in order to drink. Lame sheep should be separated for treatment and not returned to the flock until all evidence of footrot is gone.
D nodosus vaccines accelerate healing in affected sheep and aid in protecting unaffected sheep. They are recommended as an additional tool to control or eradicate the disease. However, their effectiveness depends on the strain(s) causing the infection and those present in the vaccine. No vaccine contains all the various strains of D nodosus, and use of vaccination without other means of control will most likely select for strains not contained in the vaccine. Alum-precipitated vaccines require two doses 4–6 wk apart to establish effective immunity, which persists for 2–3 mo. Lesions heal within 4–6 wk if immunity is established. Oil-emulsion vaccines induce immunity within 3 wk of the initial dose and may persist for 3–4 mo. In endemic areas, revaccination is recommended at intervals of 3–6 mo. Reaction to the vaccine is common, resulting in large granulomas and occasional abscesses. Vaccines for F necrophorum have not generally shown much benefit in either treatment or prevention. Lately, the vaccine appears to be unavailable in the USA.
Addition of zinc to trace mineral salt, reportedly effective in reducing hoof rot in cattle, has not been shown to be particularly helpful for sheep footrot. However, zinc is important for immunity and skin/hoof health. Providing it in a well-balanced trace mineral mix may be helpful in locations deficient in zinc.
Eradication:
A successful eradication program requires planning, commitment, and an investment of time and money. Eradication can be achieved only by eliminating all cases of D nodosus infection in a flock and preventing its reintroduction. This may be done by replacing affected stock with footrot-free sheep or by rigorously treating all new infections and culling affected sheep that do not respond readily to treatment. Eradication is easiest when the environment is dry; at other times, treatments should be directed more toward control of transmission. Affected sheep have to be identified by close examination of all four feet; no other diagnostic tests are available (although some exciting European research using PCR and interdigital swab samples is showing great promise as a diagnostic tool). Subclinical cases constitute a major problem. They will relapse as soon as they are placed in wet conditions and the infection spreads rapidly. Other ruminants (goats, deer, cattle) are potential sources of D nodosus. If they are in contact with the sheep, they should be considered in the eradication program.
To begin, the feet of all sheep should be trimmed and carefully examined. The flock should then be divided into affected and unaffected groups. Sheep with no visible lesions are foot bathed, isolated, and placed on “clean,” dry ground. (This group may have some degree of genetic resistance, and identifying them in some way is recommended. Retaining offspring from this group could further help control the disease.) This group should receive an injection of long-acting tetracycline at 13.6 mg/lb, and any lame sheep should be removed immediately. The group of sheep with footrot lesions are culled or, after careful hoof trimming, the feet are soaked for at least 30 min, and the animals are treated with antibiotic and kept separated from the lesion-free group. This second group should undergo foot soaking once a week for a total of three times and/or be medicated with long-acting oxytetracycline at the time of soaking. At the end of this period, their feet should again be examined and trimmed. Any sheep with an active case of footrot should be culled. This group must be monitored closely during the next wet period to detect any carriers, which are usually the first animals to show lameness. When no relapses have occurred for 1 mo or longer, this group may be placed with the clean flock. However, placing a single active or subclinical case in the clean flock can negate all of the previous hard work.
Australia has implemented an effective eradication program involving many flocks. The program has three phases. The control phase is used during periods of active spread or to reduce the number infected. During this phase, vaccination, foot bathing, and parenteral antibiotics can all be used. The eradication phase must take place during the dry season and cannot begin until several weeks after the use of all medications has been stopped and 10–12 wk after vaccination. Foot bathing and vaccination tend to mask the presence of infection. During this phase, all four feet of every sheep are inspected every 3–4 wk. Infected sheep can be treated with parenteral antibiotics at the first inspection only. After this, infected sheep are culled at each inspection. This continues until there are two completely negative, consecutive flock examinations. In the surveillance phase, all lame sheep in the flock are examined immediately. If footrot is present, the flock goes back to phase 1 or 2 again.
Resources In This Article
- Lameness in Sheep
- Overview of Lameness in Sheep
- Interdigital Dermatitis in Sheep
- Contagious Footrot in Sheep
- Foot Abscess in Sheep
- Impacted or Infected Oil Gland in Sheep
- Interdigital Fibroma in Sheep
- Septic Laminitis in Sheep