Abstract
Tick-borne infectious diseases can affect many tissues and organs including bone, one of the most multifunctional structures in the human body. There is a scarcity of data regarding the impact of tick-borne pathogens on bone. The aim of this review was to survey existing research literature on this topic. The search was performed using PubMed and Google Scholar search engines. From our search, we were able to find evidence of eight tick-borne diseases (Anaplasmosis, Ehrlichiosis, Babesiosis, Lyme disease, Bourbon virus disease, Colorado tick fever disease, Tick-borne encephalitis, and Crimean–Congo hemorrhagic fever) affecting the bone. Pathological bone effects most commonly associated with tick-borne infections were disruption of bone marrow function and bone loss. Most research to date on the effects of tick-borne pathogen infections on bone has been quite preliminary. Further investigation of this topic is warranted.
Highlights
A wide range of bacterial, viral, and protozoan pathogens can be transmitted by ticks, which act as vectors transporting pathogens to hosts, including humans [1,2]
Bone marrow progenitors belonging to monocytic and granulocytic lineages are prone to infection by A. phagocytophilum [55]
Though an effort has been made to pinpoint the cause of bone marrow suppression during ehrlichiosis, these mechanisms are largely speculative, and further work is needed to determine their exact effects on the bone marrow causing dyshematopoiesis
Summary
A wide range of bacterial, viral, and protozoan pathogens can be transmitted by ticks, which act as vectors transporting pathogens to hosts, including humans [1,2]. Surgery, implanted devices and dissemination hematogenousfrom dissemination from more distant some cases, colonization is accompanied by infectious pathologies including bone marrow infection sites. We surveyed the primary research literature for studies invesgating the changes occurring in the bone structure and function during human tick-borne tigating the changes occurring in the bone structure and function during human tickpathogen infections. Infection in mice and humans often features peripheral cytopenias accompanied by bone marrow abnormalities associated with dyserythropoiesis, dysmegakaryopoiesis impaired red blood cell and platelet regeneration) and hemophagocytic lymphohistiocytosis [41,47,48,49,50,51,52,53]. Bone marrow progenitors belonging to monocytic and granulocytic lineages are prone to infection by A. phagocytophilum [55]. Substantial further research is needed to understand the mechanisms of bone marrow suppression and their consequences in disease progression and outcomes of anaplasmosis
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