D congolensis is a gram-positive, non-acid-fast, facultative anaerobic actinomycete. It is the only species in the genus, but a variety of strains can be present within a group of animals during an outbreak. It has 2 characteristic morphologic forms—filamentous hyphae and motile zoospores. The hyphae are characterized by branching filaments (1-5 µm in diameter) that ultimately fragment by both transverse and longitudinal septation into packets of coccoid cells. The coccoid cells mature into flagellated ovoid zoospores (0.6-1 µm in diameter).
The natural habitat of D congolensis is unknown. Attempts to isolate it from soil have been unsuccessful, although it is probably a saprophyte in the soil. It has been isolated only from the integument of various animals and is restricted to the living layers of the epidermis. Asymptomatic chronically infected animals are considered the primary reservoir.
Factors such as prolonged wetting by rain, high humidity, high temperature, and various ectoparasites that reduce or permeate the natural barriers of the integument influence the development, prevalence, seasonal incidence, and transmission of dermatophilosis. The organism can exist in a quiescent form within the epidermis until infection is exacerbated by climatic conditions. Epidemics usually occur during the rainy season. Moisture facilitates release of zoospores from preexisting lesions and their subsequent penetration of the epidermis and establishment of new foci of infection. High humidity also contributes indirectly to the spread of lesions by allowing increases in the number of biting insects, particularly flies and ticks, that act as mechanical vectors. Shearing, dipping, or introducing an infected animal into a herd or flock can spread infection.
Dermatophilosis is contagious only in that any reduction in systemic or local skin resistance favors establishment of infection and subsequent disease.
To establish infection, the infective zoospores must reach a skin site where the normal protective barriers are reduced or deficient. The respiratory efflux of low concentrations of carbon dioxide from the skin attracts the motile zoospores to susceptible areas on the skin surface. Zoospores germinate to produce hyphae, which penetrate into the living epidermis and subsequently spread in all directions from the initial focus. Hyphal penetration causes an acute inflammatory reaction. Natural resistance to the acute infection is due to phagocytosis of the infective zoospores, but once infection is established, there is little or no immunity. In most acute infections, the filamentous invasion of the epidermis ceases in 2-3 wk, and the lesions heal spontaneously. In chronic infections, the affected hair follicles and scabs are sites from which intermittent invasions of noninfected hair follicles and epidermis occur. The invaded epithelium cornifies and separates in the form of a scab. In wet scabs, moisture enhances the proliferation and release of zoospores from hyphae. The high carbon dioxide concentration produced by the dense population of zoospores accelerates their escape to the skin surface, thus completing the unique life cycle.
Lesions on horses with long winter hair coats develop 'paint-brush' lesions leading to crust or scab formation with yellow-green pus present under larger scabs. With short summer hair, matting and scab formation is uncommon; loss of hair with a fine paint-brush effect can be extensive. Persistent wetting of pasterns in wet yards, stables, or at pasture leads to lower limb infection; white legs and the white-skinned areas of the lips and nose are more severely affected. Generalized disease is also associated with prolonged wet weather. Outbreaks occur on farms with previously affected horses. Histopathologic examination reveals the characteristic branching hyphae with multidimensional septations, coccoidal cells, and zoospores in the epidermis. The organisms are usually abundant in active lesions but can be sparse or absent in chronic lesions.
Presumptive diagnosis depends largely on the appearance of lesions in clinically diseased animals and demonstration of D congolensis in stained smears or histologic sections from scabs. A definitive diagnosis is made by culture and identification. An indirect fluorescent antibody technique and a single dilution ELISA test have been developed for large serologic and epidemiologic surveys. The most practical diagnostic test is cytologic examination of fresh crusts and/or impression smears of the underside of freshly avulsed lesions. Fresh crusts are minced on a glass microscope slide with a sterile scalpel blade in several drops of sterile saline. The slide is allowed to air dry and is then stained with a fast Giemsa stain or Diff-Quik® . The organisms are seen under oil immersion as 2-6 parallel rows of gram-positive cocci that look like railroad tracks. Differential diagnoses include dermatophytosis and immune-mediated scaling diseases (eg, pemphigus foliaceus).
Treatment is recommended in horses because these lesions interfere with use and are painful. Organisms are susceptible to a wide range of antimicrobialsincluding erythromycin, spiramycin, penicillin G, ampicillin, chloramphenicol, streptomycin, amoxicillin, tetracyclines, and novobiocin.
Usually, chronic infections can be rapidly and effectively cured with a single IM injection of procaine penicillin (22,000 IU/kg) and streptomycin (22 mg/kg). If this fails, the penicillin-streptomycin combination can be administered for 5 days, or a single injection of long-acting oxytetracycline (20 mg/kg) can be substituted.
The lesions should be gently soaked and removed. Topical antibacterial shampoo therapy is effective as adjuvant therapy. Chlorhexidine and benzoyl peroxide are recommended. In food-producing animals, topical applications of lime sulfur are a cost-effective adjuvant to antibacterial therapy. Insecticides applied externally are frequently used to control biting insects.