Introduction

Demodex spp. is a mite from the Demodicidea family of the Prostigmata order of Arachnida class; and it is the mandatory commensals of the pilosebaceous units. Despite there are lots of Demodex species, only two species can live as parasites in the human body [1]. D. folliculorum, which has long opistosome, lives in pilosebaceous units as single or groups whereas D. brevis, which has short opistosome, lives mostly in sebaceous and meibomian glands as single [2,3]. It has been found that D. folliculorum is always located posterioinferior of the hair follicle and feeds with the contents of the follicular epithelial cells by puncturing the cell wall with knife-like chelicera. D. brevis feeds with the epithelia of the sebaceous glands in the same way [2,3]. In humans, forehead, cheeks, nose, chin and nasolabial region are the most common sites of infestation and it can rarely be located in different parts of the body such as neck, scalp, ear, chest, back, breast, hip and genital organs [3]. As the age increases, the incidence of Demodex spp. infestation also increases; the prevalence is 100% in middle-aged and elderly adults [4-6]. The density of Demodex spp. is lower than 5 Demodex spp./cm2 in the general population [4,7]. Demodex spp. is passed to infants through close contact or breastfeeding immediately after birth, but due to low sebum production, Demodex spp. density is low in children [4,5,8]. How the Demodex spp. becomes pathogenic is still controversial, but it is thought that increased number of Demodex spp. or transition to the dermis could cause this infestation [7].

Demodex spp. could play a role in the etiopathogenesis of diseases such as acne rosacea, acne vulgaris, blepharitis, perioral dermatitis, pustular folliculitis, papillary pustular lesions of the scalp, pityriasis folliculorum, chronic renal failure, and basal cell carcinoma, pustular lesions in acquired immunodeficiency syndrome, keratoconjunctivitis, recurrent chalazions and meibomian gland dysfunctions [9-18]. For the diagnosis of the disease, cellophane tape method, preparation of skin scrapings in potassium hydroxide, punch biopsy and standardized skin surface biopsy can be used [2,4,7].

Malignant hematologic diseases are generally divided into lymphoid and myeloid neoplasms. The myeloid malignancies are myelodysplastic syndromes, myeloproliferative neoplasms (chronic myeloid leukemia, primary myelofibrosis, polycythaemia vera, essential thrombocytosis), acute myeloid leukemia, myeloid sarcoma and myeloid neoplasms with eosinophilia. The most important lymphoid malignancies are chronic lymphocytic leukemia/small lymphocytic lymphoma, hairy cell leukemia, plasma cell myeloma, solitary plasmacytoma, non-Hodgkin's lymphoma, Hodgkin's lymphoma, lymphoplasmacytic lymphoma and acute lymphoblastic leukemia [10,11]. Bone marrow infiltration, dysfunctions of T and B cells and hypogammaglobulinemia are the main causes of immunosuppression in hematologic malignities. In addition, neutropenia and lymphopenia, which leads to mucosal injury, are the side effects of various chemotherapeutic agents [12]. There are studies reporting that the incidence of Demodex spp. may increase due to immunosuppression for such reasons as immunosuppressive drug usage, advanced age, etc. However, the patogenity of this increased Demodex spp. is controversial [9-18].

We have an original study published in 2007 regarding the occurrence of Demodex spp. in patients with rheumatoid arthritis [13]. To the best of our knowledge, our current study is the first study investigating the presence and density of D. folliculorum and D. brevis in hematologic cancer patients.

Besides, it is also the first study investigating D. folliculorum and D. brevis in chemotherapy patients. The present study aimed to investigate the prevalence and infestation of D. folliculorum and D. brevis in patients with haematological cancers and to define if chemotherapy influences the presence of Demodex mites or not.