Dermatophilus congolensis infection in a horse: Don’t forget the crust!!
Kristiina Ruotsalo, Rebecca Egan
Animal Health Laboratory, University of Guelph, ON
AHL Newsletter 2020;24(1):19-20.
A 20-year-old horse presented to the referring veterinarian with multiple, coalescing, raised, crusty, lesions along the topline, extending from the withers to the tail. Removal of scabs revealed areas of depigmentation and serous discharge. Dermatophilus congolensis infection was clinically suspected and multiple punch biopsies were submitted for histopathology, along with impression smears, and intact crusts for cytological evaluation. A crust with hair was also submitted for culture.
Histology revealed evidence of chronic eosinophilic dermatitis, and secondary pyoderma with epidermal hyperplasia and limited serocellular crusting (Fig. 1A). Thick laminated crusts typical of D. congolensis (Fig. 1B) were not captured in histologic sections of this case, and organisms were not identified. Cytology revealed evidence of marked suppurative inflammation along with limited numbers of eosinophils. Intracellular small coccoid bacteria (suspected to represent secondary bacterial infection) were identified, along with several filamentous strands comprised of parallel rows of cocci (“railroad tracks”), consistent with D. congolensis (Fig. C). Dermatophilosis was also confirmed by bacterial culture.
D. congolensis is a Gram-positive, non-acid-fast, facultative anaerobic actinomycete with a wide host range and worldwide distribution. The natural habitat for Dermatophilus is unknown, although organic matter is thought to have a protective effect on the organisms, and soil may act as a temporary reservoir. Dermatophilus can also survive in the skin of clinically normal animals, possibly acting as a source of infection once favourable conditions are present and they become activated to become motile zoospores. D. congolensis has a distinctive life cycle in which coccoid bodies germinate to produce branching filaments. Establishment of infection depends upon a number of factors, including the virulence of the strain, the general health of the animal, skin trauma and moisture. Moisture may act to dissolve the surface lipid film on skin and to soften the stratum corneum. Trauma from ectoparasites, skin scratches, or other injuries may serve as portals of entry. External parasites may also act as mechanical vectors. Resistance in some animals may have a genetic component.
Once the skin surface has been disrupted, and activated zoospores gain access to the epidermis, infection can develop. The zoospores germinate to form mycelia which invade the viable epidermis and outer root sheaths of hair follicles. Bacterial invasion may be related to the production of exoenzymes. As the filaments invade the epidermis, keratinocytes at these sites begin to cornify and large numbers of neutrophils migrate into the area, causing separation of the epidermis from the underlying dermis. Repeated sequences of bacterial invasion, inflammation, and epidermal regeneration produce the thick crusts characteristic of dermatophilosis. It is unknown why some animals develop mild, localized disease which resolves rapidly and spontaneously whereas others develop chronic, widespread, debilitating disease. Commensal skin bacteria, primarily Bacillus spp., have been shown to produce substances which inhibit the growth of D. congolensis in culture. A similar effect by bacteria normally present on the skin may occur in vivo.
The clinical presentation of D. congolensis is fairly characteristic. The earliest lesions consist of patches of slight erythema which are most visible in unpigmented areas. Papules form next and mature into pustules. Lesions become exudative and matted with hair, forming thick crusts. Removal of crusts reveals areas of eroded, painful and exudative skin when active lesions are present and dry crusts with diffuse scaling and alopecia when chronic lesions are present. Lesion distribution varies by species. In horses, the dorsal thorax, rump and face are usually affected. Occasionally, lesions may be noted primarily on the distal limbs.
Differential diagnoses for the lesions induced by D.congolensis include dermatophytosis, staphylococcal dermatitis, mite infestation, various viral infections, zinc-responsive dermatosis and pemphigus foliaceus. Diagnosis of D. congolensis is based on clinical history, physical examination findings, with demonstration of the organism by cytology, histology, or culture. D. congolensis grows readily on blood agar. In this particular case, the diagnosis would have been missed if crusts had not been submitted along with biopsy samples. Thus, it is important to remember that crusted lesions should be selected for biopsies and care must be taken to ensure that crusts are included for histologic evaluation, as this increased the chances of capturing the organism. In addition, impression smears of a crust for cytological evaluation can be helpful in demonstrating the organisms. As crusts may be dry in more chronic infections, mixing a crust with a few drops of sterile saline and spreading the material onto a glass slide may be necessary. Heat fixation is not necessary and is contraindicated. All that is required for submission to the laboratory are air dried, well-spread unstained slides for cytological evaluation. AHL
Figure 1. Dermatophilus congolensis infection in a horse. A. Skin biopsy from this case capturing epidermal hyperplasia with limited serocellular crusting lining the surface (*). B. Biopsy from a different case, capturing similar epidermal hyperplasia overlain by a thick crust comprised of laminated keratin (**) enmeshed with suppurative exudate. C. Cytologic smear containing filamentous strands of paired cocci consistent with D. congolensis (arrow) in a background of inflammatory cells.
References
1. Marcella, R. Dermatophilosis. In: Equine Infectious Diseases, 2nd ed. Sellon D and Long MT, eds. Elsevier, 2014:283-286.
2. Ginn, PE, Mansell, Rakich JEKL, PM. Skin and Appendages. In: Jubb, Kennedy, and Palmer's Pathology of Domestic Animals, 5th ed. Maxie MG, ed. Elsevier, 2007; vol 1:681-683.