In many species, the female needs to obtain nutrients from a blood meal before it can produce eggs, whereas in many other species, obtaining nutrients from a blood meal enables the mosquito to lay more eggs. A mosquito has a variety of ways of finding nectar or its prey, including chemical, visual, and heat sensors. Both plant materials and blood are useful sources of energy in the form of sugars, and blood also supplies more concentrated nutrients, such as lipids, but the most important function of blood meals is to obtain proteins as materials for egg production.When a female reproduces without such parasitic meals, it is said to practice autogenous reproduction, as in Toxorhynchites; otherwise, the reproduction may be termed anautogenous, as occurs in mosquito species that serve as disease vectors, particularly Anopheles and some of the most important disease vectors in the genus Aedes. In contrast, some mosquitoes, for example, many Culex, are partially anautogenous: they do not need a blood meal for their first cycle of egg production, which they produce autogenously; subsequent clutches of eggs are produced anautogenously, at which point their disease vectoring activity becomes operative.Among humans, the feeding preferences of mosquitoes typically include: those with type O blood, heavy breathers, an abundance of skin bacteria, high body heat, and pregnant women. Individuals attractiveness to mosquitoes also has a heritable, genetically-controlled component.Female mosquitoes hunt their blood host by detecting organic substances such as carbon dioxide (CO2) and 1-octen-3-ol (mushroom alcohol, found in exhaled breath) produced from the host, and through visual recognition.
Presumably, these genetic abnormalities lead to the activation of the NF-κB pathway and/or other cellular activation pathways which promote the survival, proliferation, and/or other malignant phenotypic traits in pDC and thereby cause BPDCN. Diagnosis
BPDCN is suggested by a biopsy of skin lesions which reveals the infiltration by medium-sized blast (i.e. immature) cells into the dermis while sparing the epidermis. These cells exhibit irregular nuclei, fine chromatin, and at least one small nucleolus. Such blast cells may also be observed in the circulation, bone marrow, or other tissues and  suggest BPDCN. However, the diagnosis of this disease requires determination that these cells are pDC blast cells rather than AML, T-cell lymphoblastic lymphoma (TCLL), or aggressive NK-cell leukemia (NKL) blast cells. Various studies have offered similar but not identical criteria to make this determination. All studies agree that pDC should have a typical plasmacytoid morphology and express a particular profile of marker proteins as detected by immunoassay and/or flow cytometry. However, the studies disagree on which marker proteins to profile. One studys profile assayed 1) CD4, CD56, CD123 (i.e. Interleukin-3 receptor, and TLC1, which are expressed on 80–100% of pDC but uncommon on AML, TCLL, or NKL blasts); 2) CD2AP and CLEC4C which are unique to pDC; and 3) myeloperoxidase, lysozyme, CD34, CD14, CD11c, and CD163 which are unique to AML, TCLL, or NKL blasts. Two other studies recommended assaying somewhat different sets of marker proteins. Treatment
There have been no controlled studies to define the optimal treatment for BPDCN.