Severe alopecia due to demodicosis in roe deer (Capreolus capreolus) in Belgium

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The Veterinary Journal The Veterinary Journal 174 (2007) 665–668 www.elsevier.com/locate/tvjl

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Severe alopecia due to demodicosis in roe deer (Capreolus capreolus) in Belgium H. De Bosschere a, J. Casaer b, A. Neukermans b, K. Baert c, T. Ceulemans d, P. Tavernier e, S. Roels a,* a

Veterinary and Agrochemical Research Centre (VAR), Groeselenberg 99, 1180 Brussels (Ukkel), Belgium b Research Institute for Nature and Forest (INBO), Gaverstraat 4, 9500 Geraardsbergen, Belgium c CLO-DVL Burgemeester Van Gansberghelaan 115, 9820 Merelbeke, Belgium d Hubertus Vereniging Vlaanderen v.z.w., Lambertmontlaan 410, 1030 Brussel, Belgium e Faculty of Veterinary Medicine, University of Ghent, Salisburylaan 133, 9820 Merelbeke, Belgium Accepted 17 October 2006

Abstract Demodex mites are part of the normal fauna of hair follicles of many, if not all, healthy mammal species. Normally these parasites live in harmony with their host, however in states of putative immunosuppression the acarids undergo excessive proliferation and cause clinical disease, which may be localised or generalised. This paper describes four cases of demodicosis in roe deer (Capreolus capreolus) with localised to generalised alopecia. Ó 2006 Elsevier Ltd. All rights reserved. Keywords: Roe deer; Demodex; Demodicosis; Alopecia; Capreolus capreolus

Demodex mites are normal inhabitants of the hair follicles or sebaceous glands of all species of domestic animals and humans, and perhaps all mammals (Nutting, 1976; Yager and Scott, 1993; Jones et al., 1997; Baker, 1999). The mites found in the different hosts are regarded as separate species, although they are similar morphologically. Demodex spp. are obligate parasites, completing their life cycle in the hair follicle or its adnexae (Nutting, 1976; Yager and Scott, 1993). The mites are rapidly killed by desiccation on the surface of the skin, but move from follicle to follicle, and it is probably during this migration that transmission to another host takes place. Transmission usually occurs by direct contact from dam to offspring during nursing in the neonatal period (Yager and Scott, 1993). Demodex mites mostly exist in harmony with the host. The lack of pathological changes at the site of mite residence in healthy individuals might be due to local immuno*

Corresponding author. Tel.: +32 2 3790 547; fax: +32 2 3790 479. E-mail address: [email protected] (S. Roels).

1090-0233/$ - see front matter Ó 2006 Elsevier Ltd. All rights reserved. doi:10.1016/j.tvjl.2006.10.015

suppression stimulated by the mites, which allows them to survive in the host skin (Akilov and Mumcuoglu, 2004). In dogs, it appears that puppies genetically predisposed to develop demodectic mange have a selective defect of cutaneous T-cell mediated immunity that permits massive proliferation of the mite population (Jubb et al., 1985) and an autosomal recessive mode of inheritance has been suggested (Scott et al., 2001). The severity of this T-cell defect varies, which explains the differences in the clinical expression of affected dogs. Since affected dogs are rarely lymphopenic and have no hypocellularity of the T-cell areas in the lymph nodes and spleen, the deficiency appears to be one of function rather than numbers (Scott et al., 2001). See Figs. 1–3. The pathogenesis of demodicosis in humans is not fully understood. However, it is quite apparent that immunological mechanisms mediate its development. Certain individuals appear predisposed to demodicosis and both human leukocyte antigens (HLA) and other immune factors may play a role (Akilov et al., 2005). The incidence

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Fig. 1. Roe deer (R05-002) showing extreme generalised alopecia on the flanks, legs and neck.

Fig. 2. Roe deer (R06-002) with patchy alopecic areas on the flanks and legs.

Fig. 3. Microphotograph of the skin with Demodex mites sections (1) present in the dilated follicle next to the sebum gland (2) Also notice the dermal inflammation (3) and the follicular atrophy (4).

increases in old age and is more frequently seen in people with a fair complexion. Genetic factors also play a role in increased susceptibility of certain individuals (Mumcuoglu

and Akilov, 2005) such as inmunosuppressed patients on chemotherapy or those with acquired immunodeficiency syndrome (AIDS). When the equilibrium between the host and the parasite is altered in favour of the mites excessive proliferation occurs and localised or generalised lesions of demodectic mange are produced (Yager and Scott, 1993; Jones et al., 1997). The mites are thought first to occupy hair follicles with intact hairs and then move into the sebaceous glands to feed and reproduce. Increasing numbers of mites cause distension of glands and follicles eventually causing hair loss. The exact cause of the hair loss is not known, and a mite-induced retardation of hair growth has been proposed. Clinical demodicosis is likely to be a secondary disorder (Frost, 1999) caused by host-specific mites and is uncommon to rare in most animal species except the dog (Yager and Scott, 1993). Reports of demodicosis in wild deer are very scarce and only a few reports have been described (Desch and Nutting, 1974; Bukva, 1987; Bukva et al., 1988; Bukva and Preisler, 1988; Kadulski, 1996; Bildfell et al., 2004; Szczurek and Kadulski, 2004). The present report describes four clinical demodicosis cases in roe deer, all characterised by severe alopecia. The deer were collected via the Research Institute for Nature and Forest (INBO) network and examined at INBO. Brain, skin and lung samples were examined at the Veterinary and Agrochemical Research Centre (VAR). Brain samples were tested for chronic wasting disease (CWD) with a commercial antigen test kit (IDEXX chronic wasting disease (CWD) Antigen Test Kit, EIA, IDEXX Laboratories). The skin and lung samples were fixed in a 4% formalin solution and processed routinely for histopathological evaluation. Macroscopic signs of skin problems (e.g. alopecia) characterised all four animals and microscopic examination confirmed demodicosis as the most likely aetiology of the lesions. More data and the results of the tests we performed can be found in Table 1. Demodex mites are generally considered normal inhabitants of the hair follicle and sebaceous glands (Hargis, 1995) and most animals are parasitised by a Demodex species. Histopathological lesions of demodicosis show acanthosis, hyperkeratosis, superficial seropurulent crust and variable degree of ulceration. Follicular changes vary from areas of no inflammatory infiltrates to follicles exhibiting extensive purulent folliculitis and furunculosis. Secondary bacterial infection of affected follicles is common. The surrounding dermis often contains plasma cells, macrophages, lymphocytes and neutrophils. Variable numbers of cigar-shaped mites are often found to be present in affected follicles. In some instances, inflamed follicles rupture, spilling the mites and associated inflammatory cells into the surrounding dermis where they provoke discrete pyogranulomas in the surrounding dermis (Jones et al., 1997). The observed lesions in the four roe deer reported here corresponded

H. De Bosschere et al. / The Veterinary Journal 174 (2007) 665–668

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Table 1 Data and results of the four roe deer with alopecia due to demodicosis

Origin

Condition CWD test Skin – macroscopic

Skin – microscopic

Lungs – macroscopic

Lung – microscopic

R06-002 Buck

R06-003 Doe

R04-005 Doe

R05-002 Doe

Shot (30th January 2006)

Shot (30th January 2006)

Meeuwen-Guitrode Thin Negative – Multiple focal to generalised alopecia (especially flanks, legs, head, neck) – Broken hairs (pruritus?) – Presence of Lipotena spp. – Orthokeratotic hyperkeratosis, normal thickness to light acanthosis of the epidermis, dilatation of the hair follicles with presence of –Demodex mites, presence of Demodex mites in the sebum glands, sebum gland hypertrophy and hyperplasia, atrophic hair follicles, perifollicular fibrosis, dermal fibrosis and oedema, perifollicular and perivascular infiltration of lymphocytes and macrophages, congestion – PAS staining negative for dermatophytosis – Multiple pale and soft nodules (diameter 40 mm) – Presence of Varestrongylus / Caprocaulus capreoli eggs, different developmental stages Diffuse presence of parasite larvae and eggs, severe congestion, severe inflammatory reaction characterised by lymphocytes, plasma cells, macrophages and giant cells, pulmonary fibrosis and degeneration of lung parenchyma.

Meeuwen-Guitrode Thin Negative Multiple focal to generalised alopecia

Found dead (13th March 2004) Mazenzele Thin Negative Severe generalised alopecia – severe generalised alopecia

Found dead (22nd February 2005) Meeuwen-Guitrode Thin Negative Severe generalised alopecia – severe generalised alopecia

– Orthokeratotic hyperkeratosis, normal thickness of the epidermis, atrophic hair follicles, pigment incontinence, mild to moderate perivascular infiltration of round cells, perifollicular fibrosis, dermal fibrosis, presence of Demodex mites in dilated hair follicles – PAS staining negative for dermatophytosis

– Orthokeratotic hyperkeratosis, normal thickness of the epidermis, presence of very few atrophic hair follicles, pigment incontinence, mild to moderate perivascular infiltration of round cells, perifollicular fibrosis, dermal fibrosis – PAS staining negative for dermatophytosis

– Orthokeratotic hyperkeratosis, normal thickness to light acanthosis of the epidermis, dilatation of the hair follicles with presence of Demodex mites, presence of Demodex mites in the sebum glands, sebum gland hypertrophy and hyperplasia, atrophic hair follicles, perifollicular fibrosis, dermal fibrosis and oedema, perifollicular and perivascular infiltration of lymphocytes and macrophages, congestion – PAS staining negative for dermatophytosis – Multiple pale and soft nodules – Presence of Varestrongylus / Caprocaulus capreoli eggs, different developmental stages Diffuse presence of parasite larvae and eggs, severe congestion, severe inflammatory reaction characterised by lymphocytes, plasma cells, macrophages and giant cells, pulmonary fibrosis and degeneration of lung parenchyma.

with those described in the literature, although in our cases bacterial infections, pyogranulomas and ulcerations were absent. Generally, clinical demodicosis is considered to be associated with immunosuppressive disorders (Jones et al., 1997) but the predisposing factors for the development of generalised demodicosis are not fully understood. Some of the more significant factors are however known to include immune status, breed and breeding line, age, length of hair coat, nutritional status, stage of oestrus cycle, parturition, stress, endoparasitism and debilitating disease. Of these, immunity is thought to be the most significant. Both immunodeficiency and immune-mediated injury to the skin may play a role (Frost, 1999).

The following features may explain the clinical manifestation of demodicosis in the four deer in the present study: (1) Fieldworkers from Hubertus Vereniging Vlaanderen determined that in the years 2004 and 2005 many young roe deer died due to parasitic worm infestation. Two out of the four deer we examined were severely infected with small lungworms (Varestrongylus/Caprocaulus capreoli) and possibly also with intestinal worms (not analyzed). Data on the lung and intestinal parasitism of the other two animals were lacking but there may have been high parasitic infection pressure.

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(2) In the Flemish region, the roe deer population is currently estimated at >20,000 individuals. This figure has doubled in the past 10 years and is and more than three times greater than 20 years ago (Casaer, 2003a,b). Similar changes in roe deer populations have been noted all over Europe (Andersen et al., 1988). In the area under consideration, local densities of >25 roe deer per 100 ha of forest can be found, reflecting the highly fragmented and patchy structure of the Flemish forests surrounded by agricultural land and urban settlements, in combination with the increasing recreational use of the forests and surrounding areas, all of which impose high stress levels on the roe deer population. (3) The four animals studied were diagnosed during the winter when food was scarce and the weather wet and cold. This may have resulted in poor body condition and the severe alopecia as a consequence of the demodicosis may, at least in part, have resulted from inadequate thermal regulation. (4) Three of the four roe deer originated from the same area (Meeuwen–Guitrode) and a further roe deer with patchy alopecia similar to that of R06-002 and R06-003 has been subsequently recorded in this area. We conclude that high parasitic burden, stress due to overpopulation and scarcity of food may have all contributed to immunosuppression in the deer leading eventually to overt demodicosis. This is turn would have reduced the likelihood of survival, especially of R04-005 and R05002; these animals were almost completely bald, which would have compromised thermoregulation and may have partly accounted for the emaciation. However, this can only be speculative as due to limited pathological examination other underlying diseases beyond CWD could not be excluded. Acknowledgement The staff of the department of Biocontrol (VAR) is thanked for its technical assistance in preparing the slides and performing the laboratory tests. References Akilov, O.E., Mumcuoglu, K.Y., 2004. Immune response in demodicosis. Journal of the European Academy of Dermatology and Venereology 18, 440–444.

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