Immunity of fleas (Order Siphonaptera).

The immune response of arthropod vectors plays a key role in the spread and transmission of vector-borne diseases. Although fleas transmit several human pathogens (e.g., Bartonella henselae, Rickettsia felis, R. typhi, and Yersinia pestis), few studies have examined how these vectors respond to infection. In hematophagous arthropods, imbibed pathogens must survive the hostile environment of blood meal digestion, which includes proteolytic digestive enzymes, protease inhibitors and expression of genes associated with protection of epithelial linings. Additionally, insect epithelial cells exhibit local immune defense against ingested pathogens by producing antimicrobial peptides and reactive oxygen species. This review details these and other aspects of insect immunity as it relates to fleas, with an emphasis on the gut immune response to two blood-borne pathogens, R. typhi and Y. pestis.

The Cat Flea (Ctenocephalides felis) Immune Deficiency Signaling Pathway Regulates Rickettsia typhi Infection.

Rickettsia species are obligate intracellular bacteria with both conserved and lineage-specific strategies for invading and surviving within eukaryotic cells. One variable component of Rickettsia biology involves arthropod vectors: for instance, typhus group rickettsiae are principally vectored by insects (i.e., lice and fleas), whereas spotted fever group rickettsiae are exclusively vectored by ticks. For flea-borne Rickettsia typhi, the etiological agent of murine typhus, research on vertebrate host biology is facilitated using cell lines and animal models. However, due to the lack of any stable flea cell line or a published flea genome sequence, little is known regarding R. typhi biology in flea vectors that, importantly, do not suffer lethality due to R. typhi infection. To address if fleas combat rickettsial infection, we characterized the cat flea (Ctenocephalides felis) innate immune response to R. typhi Initially, we determined that R. typhi infects Drosophila cells and increases antimicrobial peptide (AMP) gene expression, indicating immune pathway activation. While bioinformatics analysis of the C. felis transcriptome identified homologs to all of the Drosophila immune deficiency (IMD) and Toll pathway components, an AMP gene expression profile in Drosophila cells indicated IMD pathway activation upon rickettsial infection. Accordingly, we assessed R. typhi-mediated flea IMD pathway activation in vivo using small interfering RNA (siRNA)-mediated knockdown. Knockdown of Relish and Imd increased R. typhi infection levels, implicating the IMD pathway as a critical regulator of R. typhi burden in C. felis These data suggest that targeting the IMD pathway could minimize the spread of R. typhi, and potentially other human pathogens, vectored by fleas.

Th1/Th2 immune responses and oxidative stress in caprine flea allergy dermatitis.

Flea allergy dermatitis (FAD) is the common, often neglected skin disease of goats caused mainly by Ctenocephalides felis. This study aimed to evaluate the immuno-oxidative pathobiology of FAD in goats. Twelve goats from the same herd were divided into two groups of six animals each. The group I (FAD) included animals with natural flea infestation and severe dermatitis lesions. The group II (Healthy control) animals were free from any parasitic infestation. To assess the pathological changes, the markers of oxidative stress (lipid peroxidation, reduced glutathione and total antioxidant capacity), and immune status (Tumour necrosis factor alpha, Interleukin 10, Transforming growth factor beta 1 and Th1/Th2 cytokine ratio) were evaluated from the blood and the serum samples. Remarkable oxidative stress and severe inflammatory response with Th2 cytokine dominance were observed in flea infested animals. Highly antigenic agents of fleas, either secretory or excretory or structural, induced severe inflammatory responses and significant oxidative stress in caprine FAD. Massive release of cytokines may be responsible for severe skin inflammation and lesions in FAD in contrast to other Th2 dominant ectoparasitic skin conditions of goats'.