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Avian Influenza
A study of the H5N1 virus

--general info and chapters
--introduction
--full document (pdf)

Superficial Dermatitis
Ringworm
Dermatophytosis

--general info
--research
--treatment
--references

Malassezia
Malassezia pachydermatis
--general info
--research
--treatment
--references

Mud Fever
D. congolensis

--general info
--barrier-cream
--research
--references
--treatment

MRSA in Pets
Methicillin Resistant
Staphylococcus aureus

--MRSA Research
--Pet-bedding
--Barrier-cream
--Newspaper clip

--Press Release
--Treatment
--Link
--Pricelist


Anti-microbial research applications
--gallery
--health benefits
--background info
--Press Release
--research
--link

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PIC

Parasite Image Collection


Equine cutaneous microflora
Normal resident bacteria
--general info
--research
--references

Equine gut microflora
probiotics
--general info
--research
--references

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Veterinary Microbiology

Dermatophilosis (Dermatophilus congolensis)

Dermatophilus congolensis is the bacterium that can cause the disease mud fever and rain scald in equines. In temperate climates, sheep are also susceptible to the disease, as are cattle in the tropics (Lloyd, 1993). D. congolensis is a Gram-positive, opportunistic actinomycete that produces superficial crusting of the epidermis (Rosser, 1995; Scott et al, 1995).
Taking advantage of warm, dark, moist skin regions, infection is usually present along side trauma to the area and commonly affects the heels and lumbar-sacral region (Hayes, 2002).
The bacteria can be transmitted by arthropods, common in the tropics, however equine exposure to the disease is usually limited to soil transmission (Rosser, 1995; Lloyd, 1993).
During its infective stage, D. congolensis, as a motile coccus, swims in films of water on the skin surface. It is chemotactically attracted towards carbon dioxide diffusing through the skin, which is believed to lead it to areas where the stratum corneum is thin or damaged, increasing susceptibility to infection. It germinates to produce a branching filament, which invades the living epidermis (Lloyd, 1993).
The immune system responds with early mast cell degranulation, vasodilation and an influx of dendritic cells, which accumulate and differentiate beneath the infected epidermis. A concomitant dermal invasion by neutrophils and T and B-lymphocytes lead to epithelial infiltration and scab formation. Hypertrophy of the epidermis also indicates keratinocyte involvement in the host response (Sasiak et al, 1996).
Scab formation lifts the organism away from its nutrient source, stimulating maturation of the filaments, which become transversely and longitudinally septete. Within each septum a coccus is formed and remains dormant until the scab is wet, stimulating motility and its escape from the scab (Lloyd, 1993).
An immune response to D. congolensis may involve immune responses mediated by CD1 antigen presentation and gamma delta T cells. These form part of the antigen receptor complex, in association with lymphocytes (Tizard, 2000).
Sera from animals that are disease-free but in contact with those infected with dermatophilosis have been found to contain antigens (Ag) recognised by sera from naturally exposed and experimentally infected animals. These may be involved in immunity against D. congolensis (Makinde & Gyles, 1999).
Predisposition to the infection is predominantly due to environmental conditions, with animals incurring prolonged exposure to the wet, at a higher risk (Hayes, 2002). Therefore, the disease is more commonly found in animals that live out through the winter months, usually native or heavy breeds. Also, Rosser (1995) found that animals with white haired and white skinned areas, such as white socks, are more susceptible to the infection.

For more information on D.congolensis and Mudfever goto research