Dermatophilosis in animals is commonly called mycotic dermatitis in sheep and cutaneous streptotrichosis in cattle, although other local names exist, including Senkobo skin disease in central Africa, Kirchi in Nigeria, and Saria in Malawi.
Other names:
- MYCOTIC DERMATITIS
- CUTANEOUS STREPTOTRICHOSIS
- SENKOBO DISEASE OF CATTLE
- LUMPY WOOL OF SHEEP
Etiology:
Dermatophilosis is caused by Dermatophilus congolensis, a dimorphic, Gram-positive bacterium. It requires prior skin damage—often from trauma, ticks, or wet conditions—to establish infection. The organism exists as branching filamentous mycelia and dormant zoospores, which, when activated by moisture, transform into motile cocci that invade the epidermis. Notably, D. congolensis displays significant genetic variability, and isolates from the same region may differ genetically, reflecting wide strain diversity.
Epidemiology of Dermatophilosis:
Geographic Occurrence:
Dermatophilosis is found worldwide but is particularly problematic in tropical and subtropical regions, where high humidity and rainfall lead to outbreaks and significant economic losses. Prevalence can reach 100% in some African herds during peak seasons. In temperate climates, the disease is generally sporadic but still causes economic concerns, especially under certain management practices like shower cooling in dairy cattle.
Host Range:
The disease affects a wide range of animals, including cattle, sheep, goats, horses, donkeys, and occasionally wildlife such as deer, camels, and pigs. Animals of all ages can be infected, including young sucklings.
Source of Infection:
The infection commonly originates from minor skin lesions, especially on the face and feet, in carrier animals. These lesions may seem clinically insignificant, but they serve as a reservoir for infecting others. Healed scabs in wool or hair also harbor viable organisms.
Transmission:
Dermatophilosis spreads through direct contact, particularly from face-to-face or during mounting. Mechanical vectors such as ticks and flies, and contaminated dipping solutions, also play roles in transmission.
Risk Factors by Species:
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Sheep:
The primary risk is prolonged wetting of the fleece, which breaks down protective barriers like the wax layer and stratum corneum. Rain, dipping, or tight yarding post-shearing all contribute to outbreaks. Wet wool promotes zoospore activity and fly transmission. -
Cattle (Temperate Regions):
Disease is less common but can be triggered by wet conditions, fly bites, ear tag wounds, and misting systems. Mounting injuries, especially on the back and flanks, also facilitate infection. -
Cattle (Tropical Regions):
High humidity and rainfall drive repeated seasonal outbreaks. Tick infestation, especially with Amblyomma variegatum, dramatically increases disease risk, up to 7 times higher. Ticks may contribute to immune suppression, making animals more susceptible. -
Horses:
Mechanical transmission via biting flies (Stomoxys calcitrans, Musca domestica) is common. Skin trauma from insects or frequent washing predisposes horses to infection.
Host-Related Risk Factors:
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Breed-dependent resistance:
Indigenous African breeds like N’dama and Muturu cattle, along with native sheep, show strong natural resistance. In contrast, breeds such as Zebu, White Fulani, Renitelo, and various European cattle are notably more vulnerable. -
Variation within breeds:
Even among the same breed, animals can show different levels of susceptibility, indicating the influence of individual genetics. -
Genetic selection reduces disease:
Breeding cattle based on specific immune gene markers (like BoLA class II) has proven effective. For example, dermatophilosis cases in Brahman cattle were dramatically lowered from 76% to just 2% in five years through targeted selection. -
Wool and fleece characteristics in sheep:
Sheep with strong or medium wool, open fleece, low protective wax, and high suint content are more prone to infection due to weaker natural skin defenses.
Pathogen-Related Risk Factors:
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Persistence in controlled environments:
While unstable in nature, the organism can survive up to 4 years in sterile broth cultures and more than 13 years in dried scab material at room temperature. -
Old scabs as hidden infection sources:
Dried scabs can quietly retain infective organisms, serving as long-term sources of infection if not managed properly.
Clinical Signs:
Clinical Signs in Sheep
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Lesions are usually hidden under the fleece but can be felt as hard crusts, commonly called “lumpy wool disease.”
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Crusts typically follow the midline of the back, spreading out like ribs down the sides.
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Lesions are circular, pyramid-shaped, and up to 3 cm in diameter with a concave base and pigmented surface.
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The skin underneath is red and moist.
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Muzzle, face, ears, and scrotum may also be affected.
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Most adult sheep show no illness unless lesions are widespread.
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Lambs can suffer heavy losses if infection is extensive, often complicated by fly strike (myiasis) or secondary pneumonia.
Clinical Signs in Cattle
- Paintbrush-like lesions.
- Lesions evolve into greasy, crusty scabs that are hard to remove, especially at skin folds.
- Scabs harden over time, becoming horny, cream to brown, and may merge to form mosaic-like patches.
- Pain is felt if crusts are forcibly removed in the early stages.
- Beneath scabs, pus and granulation tissue may be seen.
- Healing occurs as scabs lift off on their own, held loosely by hair.
- In calves, lesions often begin on the muzzle, possibly spreading from contact with infected udders or milk scalding.
Clinical Signs in Horses
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Lesions resemble those seen in cattle, with hair clumping over exudative areas.
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Matted hair and debris form firm patches just above the skin.
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When hair is plucked, a distinct, moist, ovoid lesion is revealed.
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Sores are tender, but itching is absent.
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Lesions may begin at the muzzle, moving up the face, and can lead to eye discharge and nasal secretion.
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In some horses, infection is limited to the lower limbs and belly.
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Severe cases may involve the entire back and sides.
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On the legs, lesions commonly affect the pastern, coronet, and cannon bones; lameness may result if the skin cracks.
Clinical Signs in Goats
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Initial signs appear on the lips and muzzle.
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Infection can spread through biting to the feet, scrotum, and inner thighs.
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Lesions may also form on the outer ear.
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Severe crusting can block the ear canals and nostrils.
Differential diagnosis by
- Ringworm
- Scabies
- Pediculosis Fleece rot—sheep
- Staphylococcal dermatitis/folliculitis
Treatment:
Sheep Treatment
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Dips with germ-killing solutions don’t work well because they can’t reach beneath thick scabs—more useful for preventing spread than curing.
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Injections of antibiotics are more effective, especially at high doses:
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Procaine penicillin + streptomycin: 70,000 units/kg + 70 mg/kg
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Erythromycin: 10 mg/kg
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Long-acting tetracycline: 20 mg/kg
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Lincomycin + spectinomycin: 5 mg/kg + 10 mg/kg
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Wet weather helps antibiotics work better.
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Best timing: treat 8 weeks before shearing to allow full healing.
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After shearing, sheep can be dipped in bactericidal solutions to reduce the spread.
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In severe cases, culling infected sheep may be necessary.
Cattle Treatment
In cooler regions:
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Tetracycline: 5 mg/kg weekly
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Long-acting tetracycline: 20 mg/kg one-time shot
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Procaine penicillin G: 22,000 IU/kg for 3 days
In hot, tropical areas:
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Treatment doesn’t work well in large outbreaks or if animals are constantly reinfected.
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Dry weather helps animals recover faster.
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Pair antibiotics with tick control (acaricides) for better success.
Horse Treatment (Simplified & Unique)
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Main approach: Treat the skin with medicated solutions and keep the horse dry.
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Apply daily:
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Povidone–iodine
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Chlorhexidine
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Benzoyl peroxide 2.5% (cleans pores and kills bacteria)
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Scabs can be gently removed under sedation before applying treatment.
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In more serious cases:
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Procaine penicillin G: 20,000 units/kg IM
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Streptomycin: 10 mg/kg IM for 3 days (optional)
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Control Measures:
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Prevent skin damage, wetness, and close contact among animals.
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Isolate infected animals and avoid shared grooming tools.
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In sheep:
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Shear-infected sheep last to reduce the spread.
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Avoid tight yarding post-shearing or dipping.
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Delay dipping (e.g., wait 10 days after shearing) to reduce risk.
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Use bactericidal dips or zinc sulfate (0.5–1%) immediately post-shearing.
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Alum solution (1%) can protect against infection for up to 70 days.
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In cattle (especially in tropical areas):
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Tick control is essential (use acaricides).
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Antibiotic use should be paired with vector management.
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Vaccines have not been successful due to strain-specific immunity.
Conclusion:
Dermatophilosis is a significant skin disease affecting sheep, cattle, and horses, often worsened by wet conditions, skin trauma, or tick infestations. While topical treatments and dips may offer limited success, systemic antibiotic therapy remains the most effective strategy, especially when administered early and in the right dose. Environmental management, such as keeping animals dry, controlling ticks, and timing treatments properly (like before shearing in sheep), plays a crucial role in both recovery and prevention. In some cases, culling severely affected animals is necessary to control outbreaks and reduce long-term impacts.
Frequently Asked Questions (FAQs)
Q1: Is dermatophilosis contagious between animals?
Yes, it spreads through direct contact, contaminated tools, or environments, especially during wet weather.
Q2: Can dermatophilosis be cured completely?
Yes, with timely antibiotic treatment and proper management, most animals recover. However, reinfection is possible without environmental control.
Q3: When should sheep be treated for best results?
Treat about 8 weeks before shearing to allow the skin to heal and avoid complications during wool harvesting.
Q4: Is there a vaccine for dermatophilosis?
No effective vaccine is currently available. Control mainly relies on good hygiene, treatment, and management.
Q5: Can humans get dermatophilosis from animals?
Rarely. It’s a zoonotic disease, but human cases are uncommon and usually mild, mostly affecting those in close contact with infected animals.
