IN FOCUS Treating canine juvenile onset generalised demodicosis

A guide to the well-known demodicosis which can present in several forms and seems to be on the rise in the UK

DAVID GRANT

David Grant, MBE, BVetMed, CertSAD, FRCVS, graduated from the RVC in 1968 and received his 1 2 FRCVS in 1978. David was hospital director at RSPCA Harmsworth for 25 years and now writes and lectures FIGURE (1) Generalised demodicosis in a young Staffordshire internationally, mainly in dermatology. female. This dog was found abandoned in the street and was systemically ill. Marked lichenification indicating a anine demodicosis is a common cutaneous disease chronic nature can be seen and the erythema of the legs and face is strongly suggestive of the diagnosis (2) The flank of this two- caused by two species – canis and Demodex year-old West Highland White female dog illustrates an extreme injai. There is a third short-bodied species previously example of “redde” . The dog had not been diagnosed C initially, allowing the disease to become generalised. There are described but currently considered to be a variant of D. mini-pustules, some exudation and marked yellow crusts, all canis, and not differing in its clinical presentation. D. canis indicating secondary pyoderma is the focus of this article. Demodicosis may be localised, generalised (juvenile onset or adult onset) or demodectic pododermatitis. Some cases of pododermatitis may have originated as generalised cases but not resolved, while others present just with pododermati- sis but are still considered under the generalised heading. Generalised demodicosis due to D. canis is one of the oldest dermatoses to be described in veterinary literature. In the Middle Ages, it was known as “redde mange” due to the erythematous lesions of some cases (Figures 1 and 2). Juvenile onset demodicosis is the most common type of generalised case and is described here. Until recently, juvenile onset demodicosis was considered a difficult condition to cure and earlier texts warned that euthanasia needed consideration in the most advanced cases. Recent advances in treatment have altered this 3 guarded prognosis into a favourable outcome for the major- FIGURE (3) The dog in Figure 1 following treatment with a ity of affected dogs. weekly spot on of moxidectin combined with imidacloprid. The spot on was administered by a vet weekly for 12 weeks until It is known that a genetic predisposition to develop gen- clinical resolution to ensure compliance. Systemic eralised juvenile demodicosis exists. The primary defect were administered for eight weeks leading to the disease is unknown, however. With advanced proliferation, dogs develop T-cell exhaustion favour- incidence in some breeds and why not all pups in a litter ing increasing mite proliferation and secondary pyoderma. suffer from demodicosis. Indiscriminate breeding of dogs Treatment with effective acaricidal products reverses T-cell such as Staffordshire Bull Terriers by back street breeders exhaustion and leads to a clinical cure. It is unclear why has led to a marked increased incidence of the disease in some dogs develop generalised demodicosis at a young age recent years in the UK. and why these dogs after treatment usually remain cured. There are four stages to the life cycle: eggs (lemon If there were an underlying primary genetic cause, it would pip shaped), six-legged larvae, eight-legged nymphs and be logical to expect relapse to be common, but that is not eight-legged adults. The are transferred from the the case. mother to the pups in the first two to three days of life, It has been suggested that dogs with demodicosis have which explains why lesions tend initially to involve facial an inherited Demodex specific T-cell deficit of varying and pedal regions. After initial transfer of mites has severity (Miller et al., 2013). This would explain the higher occurred, the disease is non-contagious.

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