Infectious footrot in sheep is caused by Dichelobacter nodosus and Fusobacterium necrophorum. It presents as either benign footrot, which is confined to the interdigital skin, or virulent footrot, which involves underrunning of the hoof matrix. Clinical signs include lameness and lesions between the toes. Diagnosis involves detecting the organisms via smears, PCR or ELISA. Treatment involves topical antibiotics, footbathing in zinc sulfate or copper sulfate solutions, and parenteral antibiotics. Control relies on quarantining new animals, cleaning facilities, and footbathing infected flocks every 10 days.
Infectious footrot in sheep is caused by Dichelobacter nodosus and Fusobacterium necrophorum. It presents as either benign footrot, which is confined to the interdigital skin, or virulent footrot, which involves underrunning of the hoof matrix. Clinical signs include lameness and lesions between the toes. Diagnosis involves detecting the organisms via smears, PCR or ELISA. Treatment involves topical antibiotics, footbathing in zinc sulfate or copper sulfate solutions, and parenteral antibiotics. Control relies on quarantining new animals, cleaning facilities, and footbathing infected flocks every 10 days.
Infectious footrot in sheep is caused by Dichelobacter nodosus and Fusobacterium necrophorum. It presents as either benign footrot, which is confined to the interdigital skin, or virulent footrot, which involves underrunning of the hoof matrix. Clinical signs include lameness and lesions between the toes. Diagnosis involves detecting the organisms via smears, PCR or ELISA. Treatment involves topical antibiotics, footbathing in zinc sulfate or copper sulfate solutions, and parenteral antibiotics. Control relies on quarantining new animals, cleaning facilities, and footbathing infected flocks every 10 days.
Infectious footrot in sheep is caused by Dichelobacter nodosus and Fusobacterium necrophorum. It presents as either benign footrot, which is confined to the interdigital skin, or virulent footrot, which involves underrunning of the hoof matrix. Clinical signs include lameness and lesions between the toes. Diagnosis involves detecting the organisms via smears, PCR or ELISA. Treatment involves topical antibiotics, footbathing in zinc sulfate or copper sulfate solutions, and parenteral antibiotics. Control relies on quarantining new animals, cleaning facilities, and footbathing infected flocks every 10 days.
Veterinary Preventive Medicine I (MEDI-302), 3(3-0)
Dr. Zeeshan Ahmad Bhutta Department of Clinical Sciences, Faculty of Veterinary Sciences, Bahauddin Zakariya University, Multan, Pakistan ETIOLOGY • Dichelobacter (Bacteroides) nodosus is the essential causal pathogen. • F. necrophorum aids D. nodosus in the invasion of the foot and contributes in the inflammatory reaction. • The type IV fimbriae of D. nodosus are recognized as a major virulence factor, are highly immunogenic, and provide the basis for the classification of D. nodosus strains into two major classes based on the genetic organization of the fimbrial gene region, • class I containing strains of serogroups A, B, C, E, F, G, I, and M • class II consisting of serogroups D and H. 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. • 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. Epidemiology • Geographic Occurrence • Footrot of sheep is common in all countries where there are large numbers of sheep, except that it does not occur in arid and semiarid areas unless the sheep have access to wet areas such as subirrigated swales. • Host Occurrence • Sheep are the species principally affected, but goats are also susceptible. • Infection has been identified in farmed red deer and in cattle and is considered the cause of overgrown and deformed claws in wild mouflon in Europe. • With environmental conditions of moisture and warmth, the disease in sheep has a high attack rate, and a large proportion of a group of sheep can be affected within 1 to 2 weeks. • Both claws of a foot and more than one foot (usually all) on the sheep will be affected. • The disease is common, and in high-risk areas the prevalence of infected flocks is high. • Source of Infection • The source of infection of D. nodosus is discharge from the active or chronic infection in the feet of affected animals. Epidemiology • Methods of Transmission • Infection is usually introduced into a flock by the introduction of carrier sheep, although sheep can become infected from the environment when footrot-free sheep use yards, roads, or trucks that have been used by footrot-infected sheep in the immediate past. • Spread within a flock is facilitated by the flocking nature of sheep and heavy environmental contamination around communal drinking and feeding areas. • Spread from ewe to lamb in intensive systems can be rapid, within 5 to 13 hours. Pathogenesis • Maceration of the interdigital skin from prolonged wet conditions underfoot allow for infection with F. necrophorum. • This initial local dermatitis associated with infection with F. necrophorum at the skin and the skin– horn junction may progress no further, but the hyperkeratosis induced by this infection facilitates infection by D. nodosus if it is present. • The preliminary dermatitis has been named “ovine interdigital dermatitis” and is also called “foot scald.” Clinical Findings • Sheep • Virulent Footrot • In a flock, a sudden onset of lameness of several sheep is the usual presenting sign of footrot because the disease is not detected before this occurs. • The pain associated with infection is severe, and affected sheep will limp or carry the affected leg. • Usually more than one foot is affected, and affected sheep may graze on their knees. • On close examination the earliest sign of virulent footrot is swelling and moistness of the skin of the interdigital cleft and a parboiled and pitted appearance at the skin– horn junction in the cleft. • This inflammation is accompanied by slight lameness, which increases as necrosis underruns the horn in the cleft. Clinical Findings • The underrunning starts as a separation of the skin–horn junction at the axial surface just anterior to the bulb of the heel and proceeds down the axial surface and forward and backward. • There is destruction of the epidermal matrix beneath the hard horn, which is subsequently separated from the underlying tissues. • In severe cases both the axial and the abaxial wall and the sole are underrun, and deep necrosis of tissue may lead to the shedding of the horn case. • The separation may not be obvious on superficial visual examination but can be detected by trimming the feet with a knife or secateurs. • There is a small amount of distinctive, gray, foul-smelling exudate, but abscessation does not occur. Clinical Findings • Both claws of the one foot will be involved, and commonly more than one foot is involved. • When extensive underrunning has occurred, lameness is severe. • A systemic reaction, manifest by anorexia and fever, may occur in severe cases. • Recumbent animals become emaciated and may die of starvation. • Secondary bacterial invasion and/or fly strike may result in the spread of inflammation up the legs. Clinical Findings • Benign Footrot • Benign footrot is manifest with interdigital lesions, a break at the skin–horn junction, and separation of the soft horn, but the disease does not progress beyond this stage to severe underrunning of the hard horn of the foot. • The interdigital skin becomes inflamed and covered by a thin film of moist necrotic material; the horn is pitted and blanched. • It is difficult to distinguish between an established infection with benign footrot and the early stages of virulent footrot. • With virulent footrot, it is common to find all stages and severity levels of the disease in the same flock. Clinical Findings • Goats • Footrot is associated with D. nodosus and is manifested by severe interdigital dermatitis. • There may be some separation of the skin– horn junction at the axial surface, but the disease is less invasive, and there is much less underrunning of the horn of the sole or the abaxial surface of the foot compared with sheep. • Cattle • Infection with D. nodosus is also associated primarily with a severe interdigital dermatitis, and there may be lameness. • There is fissuring and hyperkeratosis of the interdigital skin, with pitting and erosion at the skin–horn junction in the cleft. • There is also fissuring, pitting, and erosion on the horny bulbs of the heel. • There may be underrunning at the heel, but it is usually minimal. Clinical Pathology • Detection of Organism • Smears • PCR • ELISA DDX Treatment • Topical Treatment • Local applications include • chloramphenicol (10% tincture in methylated spirits or propylene glycol) • Oxytetracycline (5% tincture in methylated spirits) • cetyltrimethyl ammonium bromide or cetrimide (20% alcoholic tincture) • Zinc sulfate (10% solution) • copper sulfate (10% solution) • Dichlorophen as a 10% solution in either diacetone alcohol or ethyl alcohol. Treatment • Footbathing for Treatment and Control • Zinc Sulfate Solution (10% to 20%) • Sheep are stood for 1 hour in a footbath containing a 10% to 20% zinc sulfate solution with 2% sodium lauryl sulfate with sufficient depth to cover the coronet. • The treatment is repeated in 5 days, then after a further 21 days • Copper Sulfate Solution (5%) Treatment • Antibiotic Treatment • Penicillin/streptomycin (single IM dose of 70,000 U/kg procaine penicillin and 70 mg/ kg dihydrostreptomycin) • Erythromycin (single IM dose of 10 mg/kg) • Long-acting oxytetracycline (single IM dose of 20 mg/kg) • Lincomycin/spectinomycin (single SC dose of 5 mg/kg lincomycin and 10 mg/kg spectinomycin) • Gamithromycin (single SC dose of 6 mg/kg) • Long-acting amoxicillin (single IM dose of 15 mg/kg) 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. Control • 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. • Alum-precipitated vaccines require two doses 4–6 wk apart to establish effective immunity, which persists for 2–3 mo. • 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. Any Question?