Factors Controlling the Microflora of the Healthy Mouth
Michael J. Hill, Philip D. Marsh in Human Microbial Ecology, 2020
If all teeth are extracted in a person, the oral microflora loses the habitats associated with the teeth and only the flora of the oral mucosa remains. If an artificial denture is worn, however, microbial deposits similar to dental plaque colonize the denture, including the fitting surface resting against the palatal mucosa and alveolar crest (Figure 24). The substrates for microbial growth are derived from saliva, host diet, mucosal cell debris, and microbial interactions. The microflora of this unique habitat is dominated by Gram-positive bacteria, mainly Streptococcus, Actinomyces, and Lactobacillus species. Gram-negative cocci (Veillonella spp), make up 10% and Gram-negative rods only 1%, while spirochaetes are absent (Figure 15).23 Small numbers of the yeast Candida albicans are commonly present, constituting 0 to 1% of the flora (Figure 7).
Oral Biofilms and Their Implication in Oral Diseases
Chaminda Jayampath Seneviratne in Microbial Biofilms, 2017
The microbial composition of endodontic infections is largely characterised by Gram-negative anaerobic species belonging to the Bacteroidetes phylum [14,15], or Gram-positive facultative anaerobic enterococci, particularly Enterococcus faecalis. E. faecalis has been implicated in about 24–77% of endodontic lesions. E. faecalis possesses various survival and virulence factors such as its ability to compete with other microorganisms, invade dentinal tubules and resist nutritional deprivation [16]. However, high-throughput molecular studies have revealed an even greater diversity of the microbiota in the infected root canals. This mosaic includes uncultivable members of the phyla Spirochaetes, Deferribacteres, Synergistetes, Firmicutes, Bacteroidetes, Actinobacteria and Proteobacteria [17–20]. There are interindividual variations in the microbial spectrum of infected root canals, that is, the microbial communities in infected root canals of different individuals are not exactly the same [17,19,21–24], and may also differ according to the location of the affected tooth [25,26]. Even within a single infected root canal, the microbial composition in the apical and coronal regions differs: the former typically has a higher level of microbial diversity than the latter, and the dominant microbes are different (the apical area mainly contains obligate anaerobes) [17,27]. Shifts in the microbial composition occur at different phases of endodontic infections (i.e. chronic versus acute), which also indicates underlying differences in the immunological responses at the affected regions [28].
Biology and Distribution of Ticks of Medical Importance
Jürg Meier, Julian White in Handbook of: Clinical Toxicology of Animal Venoms and Poisons, 2017
Unicellular parasites, including microorganisms, are transmitted by and large via the salivary glands. Spirochaetes transmitted by Argasidae may also use the route of the coxal glands. Borrelia burgdorferi may possibly be regurgitated. Coxiella burnetti, a rikettsia-like bacterium, is excreted with the tick’s faeces and later inhaled into the lungs; this is an example of what is known as the stercoral route. As for filariae, their stage 3 larvae leave the tick actively, breaking through the integument and invading the final host by penetrating through the skin at the site of the lesion made by the tick rostrum.
In vivo imaging of Lyme arthritis in mice by [18F]fluorodeoxyglucose positron emission tomography/computed tomography
Published in Scandinavian Journal of Rheumatology, 2018
A Pietikäinen, R Siitonen, H Liljenbäck, O Eskola, M Söderström, A Roivainen, J Hytönen
Lyme borreliosis (LB) is an infectious disease caused by Borrelia burgdorferi sensu lato spirochaetes (later referred to as B. burgdorferi). Dissemination of the spirochaetes from the initial infection focus to the target organs is thought to occur via the blood or lymphatic vasculature. In the late disseminated stage of the disease, symptoms can occur in various organs including the heart, and in the joints and the nervous system (1, 2). Standard antibiotic treatment eradicates the bacteria and cures the infection in most cases, but a subgroup of patients have persisting symptoms after treatment (3). These symptoms are probably caused by infection-induced autoimmunity or sterile inflammatory responses to persisting B. burgdorferi antigens, but not persisting live bacteria. However, there are no proper in vivo imaging techniques to visualize the different manifestations of B. burgdorferi infection in humans.
Lyme Neuroborreliosis Presenting as Multiple Cranial Neuropathies
Published in Neuro-Ophthalmology, 2022
Aishwarya Sriram, Samantha Lessen, Kevin Hsu, Cheng Zhang
In addition to the clinical presentation and imaging, the diagnosis of Lyme disease was made based on serological and CSF studies. For serological testing, a two-tiered approach is recommended: immunofluorescence assay or ELISA, followed by reflexive immunoblotting. This screening test (and confirmatory blot testing) can be falsely negative in early stages of Lyme disease. When positive, however, patients must undergo confirmatory testing. For the two-tiered approach, the sensitivity is 30–40% in early infection and 70–100% in disseminated disease, and the specificity is >95% in all stages.12 Our patient initially had elevated Lyme antibodies by ELISA. Western blot was then performed, which detected two out of three IgM bands, indicating acute infection. The blot also detected 2 out of 10 positive IgG bands. At least 5 of the 10 IgG bands must be detected to be considered positive, but detection of fewer IgG bands can occur in acute infection as the IgG response usually appears after 30 days.12 IgM positivity and IgG negativity a month after symptom onset may be false positive; however, in our case, the testing was performed 1 week after symptom onset. Notably, but rarely, a positive immunoblot can represent exposure to other spirochaetes.
Reversible Choriocapillaris Flow Voids in Acute Syphilitic Posterior Placoid Chorioretinitis
Published in Ocular Immunology and Inflammation, 2022
Mia Mikowski, Teodoro Evans, Lihteh Wu
Although reported to occur at any stage of the disease, syphilitic ocular involvement most commonly occurs during the secondary and tertiary stages of the disease. The mechanism by which T. pallidum causes ASPPC remains poorly understood. According to one theory, during secondary syphilis, circulating soluble immune complexes are carried by the choroidal circulation and deposited at the RPE, choriocapillaris and retinal vessels. Complement fixation supposedly ensues and an inflammatory process leads to ASPPC.6 An alternative hypothesis implicates direct infection. Gass and colleagues7 have reasoned that based on their similar sizes, macular placoid lesions are analogous to syphilitic mucocutaneous lesions. And since syphilitic mucocutaneous lesions are known to harbor spirochetes, it is likely that treponemal organisms are also present in the macular placoid lesions.7 Accordingly, the treponemes gain access to the general circulation from the original site of inoculation. From there, the spirochetes are carried to the eye via the bloodstream. It should come as no surprise that the macular area is affected during ocular involvement, given its ample vascular supply. Once in the macular area, the spirochetes elicit an active inflammatory reaction which results in ASPPC.7
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