Epidemiology: Open Access
Open Access

The rickettsiae are true endosymbionts or endobionts; any organism that lives within the body or cells of another organism in a mutualistic –formerly called symbiotic- relationship with the host body or cell, often but not always to mutual benefit, providing cellular machinery missing from their host's genome, according to the reductive nature of arthropod genomes. The benefit to arthropods can be seen in studies that show an increase in arthropod fecundity and survival. Rickettsias are intracellular endosymbionts found in a range of arthropod tissues; those that cause disease are transmitted to humans by bites or contact with infected arthropod secretions. It's impossible to think about rickettsiae without thinking about their arthropod vectors and vertebrate reservoirs. To have a better understanding of the effect the study of rickettsial diseases in humans necessitates a deeper understanding than just the recognised rickettsial organisms and their traditional vectors. The Rickettsia genus is divided into two ancestral clades, one carried by arthropods and the other by other eukaryotes. Indeed, there is a growing amount of research on the identification of rickettsial carriage in arthropods that aren't hematophagus ectoparasites. Rickettsial endosymbionts are found in up to 24% of terrestrial arthropods. Rickettsia felis, a spotted-fever group rickettsia species commonly found in fleas, is carried by the parthenogenically reproducing booklouse Liposcelis bostrychophila. There are two ways for rickettsia to be acquired by arthropods [1].

Description

Rikettsia can be transstadially transmitted from one stage of the arthropod life cycle to the next, beginning with the intake of a blood meal from an infected host species. Transovarial transmission or transovarian transmission occurs in certain arthropod vectors as they transmit disease-causing pathogens from parent arthropod to offspring arthropod from infected arthropod mother to her progeny from infected arthropod mother to her progeny from infected arthropod mother to her progeny from infected arthropod mother to her progeny from infected arthropod mother to her progeny from infected arthropod mother to her pro Carriage and propagation of rickettsia within arthropod hosts clearly gives a selection benefit, and endosymbionts are often either obligatory or facultative. As a result of the advancement of newer genome sequence technology, we have observed a proliferation of the rickettsia genus as a result of the survey of many new possible hosts and the identification of novel, yet uncultured, rickettsia. In a similar vein, the intricate interactions between rickettsias and their respective arthropod and mammalian hosts' microbiomes are only now beginning to be revealed. The tick gut microbiome modulation of disease carriage is dynamic and changes in response to a variety of parameters including as life cycle stage, eating state, and host animal interactions, according to a recent review [2].

While the Rickettsia genus is adapted to a wide range of host or- ganisms, the vector host or hosts of individual species might be broad or limiting appropriate. A multitude of causes have influenced the prevalence and distribution of rickettsial diseases during the Anthropocene epoch, resulting in more opportunities for human-vector interactions. 9 The growth of tick habitat range and distribution for Dermacentor reticulatus has been well established as a result of warmer,wetter climates. 10 In the same geographic area, Rickettsia roultii, one of the agents of scalp eschar and neck lymphadenopathy, also known as Dermacentor borne necrosis erythema lymphadenopathy/ tick-borne lymphadenopathy, has emerged. Rickettsias are tiny gram-negative bacteria that live exclusively inside cells due to the loss of metabolic and synthesis pathways required for extracellular existence. Rickettsias require biosafety level 3 (BSL-3) for appropriate containment due to their extreme pathogenicity in humans [3]. Because of the organism's meticulous nature, rickettsia culture is tough and necessitates highly specialised laboratory settings that are familiar with the cell line culture methods required to reproduce them in vitro. Laboratory animals show little to no pathology when infected with rickettsias, and minimal data can be gained using in-vitro methods, therefore the specific processes by which rickettsias exert their pathogenic effects on humans remain mysterious. Genomic analysis of rickettsial infections in humans In contrast to closely similar non-pathogens, there is no evidence of novel virulence genes being acquired [4].

Conclusion

Virulence could be fueled by faulty or ineffective replication systems. Smaller rickettsial genomes are found in more pathogenic rickettsia, resulting in a paradoxical negative connection between rickettsial genome size and human pathogenicity. When rickettsia infects humans, it spreads to endothelial cells, causing them to become dysfunctional and lose their integrity. In rickettsial infection, microvascular thrombosis and increased permeability of the microvasculature with resulting edoema are frequent histologic findings [5]. Human umbilical vein endothelial cells (HUVECs) and human dermal microvascular cells were used to study the processes of rickettsia-mediated human pathology in vitro. Internalization of spotted fever group rickettsia into the endothelium has recently been demonstrated to be mediated by fibroblast growth factor receptor-1.19 when infected with rickettsia, HUVECs express tissue factor20 and release high molecular weight multimers of von Willebrand factor21, both of which are essential components of normal coagulation and may account for thrombosis in the microvasculature.

1. Kingston HW, Hossain M, Leopold S, Anantatat T, et al (2018) Rickettsial Illnesses as Important Causes of Febrile Illness in Chittagong, Bangladesh. Emerg Infect Dis 24(4):638- 645.

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2. Rathi N, Rathi A (2010) Rickettsial infections: Indian perspective. Indian Pediatr 47(2):157-164.

Indexed at, Google Scholar, Crossref

3. Nelder MP, Russell CB, Johnson S, Li Y, et al (2020) Assessing human exposure to spotted fever and typhus group rickettsiae in Ontario, Canada (2013-2018): a retrospective, cross-sectional study. BMC Infect Dis 20(1):5-23.

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4. Wang XR, Burkhardt NY, Kurtti TJ, Oliver JD, et al (2021) Mitochondrion-Dependent Apoptosis Is Essential for Rickettsia parkeri Infection and Replication in Vector Cells. mSystems 6(2):e01209-1220.

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5. Aung AK, Spelman DW, Murray RJ, Graves S (2014) Rickettsial infections in Southeast Asia: implications for local populace and febrile returned travelers. Am J Trop Med Hyg 91(3):451-460.

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