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Flea-borne spotted fever is an emerging insect-borne rickettsial infection caused by Rickettsia felis and has been identified worldwide. This study sought to explore the prevalence of rickettsiae associated with fleas on companion dogs and cats from Walker and Montgomery Counties in East Texas. Fleas were collected from animals entering local veterinary clinics for routine checkups. Collected fleas were identified as Ctenocephalides felis or Pulex irritans and analyzed by polymerase chain reaction for the presence of rickettsiae and subsequent sequencing. An estimation of the bcMLE (bias-corrected maximum likelihood estimation) of pooled samples was calculated. Four hundred eighty-eight fleas (comprising C. felis and P. irritans) were collected from 16 cats and 77 dogs. Our results demonstrate R. felis in 21 pools of fleas from dogs (bcMLE 15.28%) and a bcMLE of 7.25% from flea samples collected from cats. Sequence analysis revealed R. felis as the only Rickettsia that could be amplified in our samples using the rickettsial citrate synthase gene and subsequent sequencing. In this study, the presence of R. felis in fleas from companion cats and dogs suggests a potential risk of flea-borne spotted fever in humans who encounter flea-infested animals.

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Older horses and those prone to obesity may be at a higher risk for inflammation than younger and leaner counterparts. Previous research indicated a postprandial elevation in plasma concentrations of interleukin-1ß (IL-1ß), a pro-inflammatory cytokine, after consuming 1.2 g of non-structural carbohydrates/kilogram of body weight. However, these studies utilized horses of mixed age and body condition. The current study evaluated post-prandial IL-1ß concentrations in horses specifically comparing lean to over-conditioned and middle aged to older. Our results suggest that at least two weeks of daily consumption of a high non-structural carbohydrate diet is required to induce a post-prandial increase in IL-1ß concentrations in younger and leaner horses. In opposition to this, older and over-conditioned horses experience plasma increased on the first day of feeding and thereafter. Feeding management practices of older and over-conditioned individuals should emphasize lower non-structural carbohydrate intakes and further research should elucidate mechanisms of IL-1ß activation.

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Colorado tick fever virus (CTFV) belongs to the genus Coltivirus of the Reoviridae family, and it is the causative agent of Colorado tick fever. Symptoms of the infection are characterized by sudden biphasic fever, headache, and petechial rash, while severe forms of the disease can include meningoencephalitis, hemorrhagic fever, and death in children. However, the mechanisms underlying CTFV induced pathology and severe complications remain unknown. As CTFV is spread by tick bites and disseminates systemically via hematogenous routes, we performed in vitro analysis examining the interactions between endothelial cells (ECs) and CTFV. Our findings indicate that dermal microvascular ECs, HMEC-1, are susceptible and permissive to CTFV infection. To investigate the role of CTFV infection on endothelial barrier function, we assessed transendothelial electrical resistance (TEER) by xCELLigence and observed a dose-dependent decrease in cell index, indicating increased vascular permeability starting at approximately hour 18 (MOI=1) and hour 26 (MOI=0.1). Since CTFV induced cytopathic effect and increased vascular permeability in HMEC-1 cells, we hypothesized that CTFV causes apoptotic cell death. Our results showed that HMEC-1 cells infected with CTFV at 48 h caused a significant increase in Annexin V staining with reduced viability compared to uninfected cells suggesting CTFV induces apoptotic cell death in human ECs. Electron microscopy also was consistent with apoptotic features, including chromatin condensation and cell blebbing. Furthermore, CTFV induced caspase-3/7 activation at 24 and 48 h post-infection (hpi). The inhibition of caspase activity using Z-VAD-FMK reduced CTFV induced cell death and significantly reduced viral titer. These results indicated that CTFV can infect ECs, exerting direct adverse effects, leading to vascular permeability and cell death. Overall, our data suggest that caspase-mediated apoptosis is a critical mechanism by which CTFV induces disease in the host and enhances viral replication. Future studies will examine the viral and cellular determinants involved in CTFV induced apoptosis in human ECs.

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