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An Overview of Parasite Diversity
Published in Eric S. Loker, Bruce V. Hofkin, Parasitology, 2023
Eric S. Loker, Bruce V. Hofkin
An advantage of having a solid understanding of the phylogenetic relationships for both host and associated parasite lineages is that we gain insights into when and how hosts acquired their parasites. This is certainly also true for human parasites, as indicated in the following two examples. The first pertains to the sucking lice (Anoplura) that we harbor. All sucking lice are blood-feeding ectoparasites of mammals. Humans are unusual as compared to our nearest relatives for harboring lice representing two different species, each of a different genus, Pediculus humanus and Pthirus pubis. The former species is of particular note for serving as a vector of the bacterium causing epidemic typhus (Rickettsia prowazekii) and other pathogens. In contrast, chimpanzees and gorillas each harbor one sucking louse species (Pediculus schaeffi and Pthirus gorillae, respectively). A number of phylogenetic studies have ascertained both the pattern of relationships among primates, including apes, and among their sucking lice (Figure 2.23A). Such studies have estimated the time of divergence based on the amount of sequence change occurring for both lice and primates, an application of the molecular clock hypothesis.
The Black Death and Other Pandemics
Published in Scott M. Jackson, Skin Disease and the History of Dermatology, 2023
Epidemic typhus is an infection with a bacterium called Rickettsia prowazekii that is transmitted from person to person by the human body louse; the bacterium resides in the feces of the louse. This louse is slightly different from the lice that infest the hair of schoolchildren. Instead, it infests the body and garments of persons of poor health and hygiene living in unclean conditions. Scratching the louse bites causes the person to rub the louse feces into the wound, thus inoculating the body with the bacterium. The signs and symptoms of typhus include fever, chills, headache, rapid breathing, body aches, cough, nausea, vomiting, confusion, and a rash. The red, petechial rash starts on the torso and spreads outward to the arms and legs. The mortality rate of untreated epidemic typhus is anywhere from 10 to 60 percent; with antibiotics, the condition is uniformly survivable. Epidemic typhus should be distinguished from endemic (murine) typhus, which occurs worldwide and is spread by the rat flea, and typhoid, a febrile condition with red spots on the skin caused by S. typhi, made famous in the twentieth century by the life and career of “Typhoid Mary.”
Mitochondria and Embryo Viability
Published in Carlos Simón, Carmen Rubio, Handbook of Genetic Diagnostic Technologies in Reproductive Medicine, 2022
Irene Corachan Garcia, Laura Iñiguez Quiles, Antonio Diez-Juan
The oldest eukaryotic microfossils date back 1.45 billion years (Figure 15.2). At that time, the oceans were mostly anoxic due to marine H2S-producing bacteria. Eukaryotes arose and diversified in this anoxic environment. The mitochondrial genome appears to have a monophyletic origin from a-Proteobacteria with Rickettsiales and several Rickettsia-like endosymbionts identified as the a-Proteobacterial order most closely related to mitochondria (3,7,8). New lines of research suggest that the host that acquired the mitochondrion was a prokaryote. Under this view, the ancestral mitochondrion was a facultative anaerobe, perhaps similar in physiology and lifestyle to modern Rhodobacteriales (4). However, phylogenetic analyses of both protein-coding genes and rRNA genes specified by mitochondrial DNA (mtDNA) demonstrate that the mitochondrial genome originated from the eubacterial, not the archaeal, domain of life (9,10). The mitochondrial genome appears to have a monophyletic origin from α-proteobacteria, with the order Rickettsiales and several Rickettsia-like endosymbionts identified as the α-proteobacteria most closely related to mitochondria (3,7,8). In particular, Rickettsia prowazekii, the pathogen that causes epidemic typhus and is transmitted in the feces of lice, stands out as the most genetically similar (9). While these views of mitochondrial evolution continue to shape our understanding of its functions, the evidence is clear that these organelles have a diverse repertoire of roles in the cell.
Emerging and threatening vector-borne zoonoses in the world and in Europe: a brief update
Published in Pathogens and Global Health, 2019
Bacterial order Rickettsiales causes wide range of related diseases spread by ticks, fleas, chiggers and lice. Spreading abilities, morbidity and mortality rates of Rickettsiales are high. Typhus fever caused by Rickettsia prowazekii was classified as the category B on the list of bioterrorism agents [81]. The most common rickettsiosis in Europe is Mediterranean spotted fever caused by Rickettsia conorii. Even though the disease had been endemic to Southern Italy for many years [82], it has been spreading recently [83]. This infection may represent a severe threat, as its mortality rate is about 32% [84]. Anaplasmosis caused by Anaplasma phagophytophila has also a strongly increasing and widespread occurrence in Europe [85,86]. Recently, new human rickettsial infections have been recognized in Europe [82,87]. In general, rickettsioses occurrence increases in northern countries, which had been traditionally Rickettsia free [88]. It is supposed that this increasing occurrence is associated with the rise of temperature and decreasing number of frosty days [83,89,90]. Several rickettsial vaccines were developed; however, they were difficult, expensive and very hazardous to produce [91]. There is still no approved vaccine available yet [92].
How relevant are in vitro culture models for study of tick-pathogen interactions?
Published in Pathogens and Global Health, 2021
Cristiano Salata, Sara Moutailler, Houssam Attoui, Erich Zweygarth, Lygia Decker, Lesley Bell-Sakyi
Most pathogenic Rickettsia spp. must be handled at BSL3, posing particular problems for studies on tick-bacterial interactions. Thus, as with highly pathogenic viruses, such as CCHFV, tick cell cultures are a useful substitute for live, intact ticks enabling a range of studies at the cellular and molecular level. Growth of Rickettsia rickettsii, causative agent of Rocky Mountain spotted fever in humans, was compared in tick (DALBE3 and IDE2) and mammalian cell lines at temperatures between 28°C and 34°C; raising the incubation temperature induced expression of rickettsial proteins in infected tick cells possibly associated with pathogenicity for mammalian cells [152]. In the absence of a louse cell line, tick (ISE6) and insect (Sf9) cell lines were used as models to analyze the effect on the proteome of Rickettsia prowazekii, causative agent of louse-borne human epidemic typhus, of growth in arthropod and mammalian environments [153]. In this study, rickettsial stress response proteins were upregulated in both arthropod cell lines and in a murine cell line, compared to levels in bacteria grown in hen egg yolk sacs, indicating possible limitations of cell cultures to model the in vivo situation. Nevertheless, comparison of siRNA expression profiles and coding transcriptomes of R. prowazekii grown in tick (AAE2) and human cell lines revealed novel siRNAs unique to arthropod cells and evidence for alternative transcription start sites used by rickettsial genes depending on the host cell environment [154]. A review of tropism in a range of pathogenic Rickettsia spp. found that the arthropod host range in vivo was reflected in the susceptibility of tick and insect cell lines in vitro, with tick-borne spotted fever group Rickettsia generally growing better in tick cells and insect-borne typhus group Rickettsia growing better in insect cells [155]. A recent study using both tick cell lines and experimentally infected vector ticks found that while two Rickettsia parkeri proteins, RickA and Sca2, played a role in actin polymerization in tick cells in vitro and in vivo, their absence did not affect patterns of R. parkeri dissemination in live, intact ticks [156].