Word Count: Text: 3329; Abstract: 250 words 31 1. Abstract 32 Spotted Fever Group Rickettsiae (SFGR) can cause mild to fatal illness. The early 33 interaction between the host and rickettsia in skin is largely unknown and the 34 pathogenesis of severe rickettsiosis remains an important topic. A surveillance of 35 SFGR infection by PCR of blood and skin biopsies followed by sequencing and 36 immunohistochemical detection was performed on patients with a recent tick bite 37 between 2013 and 2016. Humoral and cutaneous immunoprofiles were evaluated in 38 different SFGR cases by serum cytokine and chemokine detection, skin 39 immunohistochemical (IHC) staining and transcriptome sequencing (RNA-seq). A 40 total of 111 SFGR cases were identified, including 79 Candidatus Rickettsia 41 tarasevichiae (CRT), 22 R. raoultii, 8 R. sibirica, and 2 R. heilongjiangensis. The 42 sensitivity to detect SFGR in skin biopsies (9/24, 37.5 %) was significantly higher 43 than in blood samples (105/2671, 3.9 %) (p<0.05). As early as one day after the tick 44 bite, rickettsia could be detected in the skin. R. sibirica infection was more severe 45 than CRT and R. raoultii. Increased levels of serum IL18, IP10, MIG and decreased 46 IL2 were observed in R. sibirica febrile patients compared to CRT febrile patients. 47 RNA-seq and IHC staining could not discriminate between SFGR-infected and 48 uninfected tick-bite skin lesions. However, the type I interferon (IFN) response was 49 differently expressed between R. sibirica and R. raoultii infection at the cutaneous 50 interface. It is concluded that skin biopsies were more reliable for the detection of 51 SFGR Rickettsiae in human patients, although the immunoprofile may be complicated52 by immunomodulators induced by the tick bite.53 on July 10, 2020 by guest http://iai.asm.org/ Downloaded from 3 BACKGROUND 54 Pathogenic members of the Rickettsia genus are Gram-negative, obligate intracellular 55 bacteria that have a life cycle which involves both an arthropod vector and a host [1]. 56 Spotted Fever Group Rickettsiae (SFGR) belongs to one pathogenic clade of 57 Rickettsia and is mainly transmitted by ticks. The spectrum of rickettsial diseases 58 ranges from mild influenza-like illness to life-threatening disease [2]. The pathogenic 59 events that occur in rickettsial infection begin with the entry of bacteria transmitted by 60 the feeding tick. The initial target cells are CD68 + cells including macrophages and 61 dendritic cells [3]. Then, the organism spreads throughout the body and infects mainly 62 endothelial cells lining small and medium-sized blood vessels [4]. Most of the clinical 63 characteristics of rickettsial diseases are attributed to the disseminated infection of 64 endothelial cells [1]. Skin has long been recognized as a physical barrier providing 65 protection from injury. As a first line of defense, skin possesses an abundant 66 population of cells and molecular mediators of innate and adaptive immunity, 67 resulting in what is recognized as the skin immune system [5]. Af...
IntroductionTicks are the most important obligate blood-feeding vectors of human pathogens. With the advance of high-throughput sequencing, more and more bacterial community and virome in tick has been reported, which seems to pose a great threat to people.MethodsA total of 14 skin specimens collected from tick-bite patients with mild to severe symptoms were analyzed through meta-transcriptomic sequencings.ResultsFour bacteria genera were both detected in the skins and ticks, including Pseudomonas, Acinetobacter, Corynebacterium and Propionibacterium, and three tick-associated viruses, Jingmen tick virus (JMTV), Bole tick virus 4 (BLTV4) and Deer tick mononegavirales-like virus (DTMV) were identified in the skin samples. Except of known pathogens such as pathogenic rickettsia, Coxiella burnetii and JMTV, we suggest Roseomonas cervicalis and BLTV4 as potential new agents amplified in the skins and then disseminated into the blood. As early as 1 day after a tick-bite, these pathogens can transmit to skins and at most four ones can co-infect in skins.DiscussionAdvances in sequencing technologies have revealed that the diversity of tick microbiome and virome goes far beyond our previous understanding. This report not only identifies three new potential pathogens in humans but also shows that the skin barrier is vital in preventing horizontal transmissions of tick-associated bacteria or virus communities to the host. It is the first research on patients’ skin infectome after a tick bite and demonstrates that more attention should be paid to the cutaneous response to prevent tick-borne illness.
Background Human babesiosis is a common zoonosis caused by Babesia and is attracting an increasing concern worldwide. The natural course of babesiosis infection and how the human immune system changes during the course of babesiosis infection are not clear. Methods We followed up 1 case infected with Babesia venatorum for 5 years. The patient was immune-intact and received no standard treatment. Clinical data were obtained from medical records. Microbiological tests, ribonucleic acid (RNA) sequence, and serum cytokines and chemokines were detected at different time points. Results The patient was confirmed as B venatorum infection based on his tick-bite history, clinical manifestations, and positive results of microbiological tests. The parasitemia of the patient persisted for approximately 2 months. With flu-like symptoms aggravating, most cytokines and chemokines in RNA and protein levels increased progressively and reached the peak when fever occurred; and their concentrations decreased to baseline during the same time as clearance of babesia parasites. Conclusions Babesia venatorum infection could take a mild self-limited course in immune-intact individuals. The natural changes of most cytokines and chemokines demonstrated very similar trends, which correlated with blood parasitemia and clinical manifestations. Cytokine profiles involving multiple inflammatory cytokines might be a good indicator of babesia infection.
Species of the Aspergillus section Nigri are taxonomically very complex. The taxonomic assignment of Aspergillus awamori is unclear.
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