Determination of Aa serotypes to avoid additional antibiotics.

The iai PadoTest Plus is a test for the additional determination of the Aa serotypes. With the iai PadoTest Plus an additional antibiotic dose can be avoided despite detection of Aa.

The iai PadoTest Plus is a test for additionally determining Aa serotypes. As Aggregatibacter actinomycetemcomitans (Aa) is divided into different subtypes with different virulence, the iai PadoTest Plus can be used to avoid additional antibiotics, despite evidence of Aa.

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Nomenclature

Filifactor alocis (Fa)

Characteristics

Gram-positive, extremely difficult to cultivate anaerobes

Pathogenicity

Highly pathogenic

Virulence factors

15 different proteases, Microbial Surface Components Recognizing Adhesive Matrix (MSCRAMMs), F. alocis Complement Inhibitor (FACIN)

Occurrence

Occurs in subgingival specimens in chronic periodontitis (CP) and generalised aggressive periodontitis (GAP) and is associated with supportive tissue loss. Fa is the cause of chronic inflammation and induces the production of proinflammatory cytokines that lead to the apoptosis of gingival epithelial cells. Compared with Pg, Td, Tf, described in the literature as "red complex" and which are most commonly associated with periodontal disease in the literature, Fa was the third largest in a group of GAP patients and the second largest in CP patients. Fa is found predominantly in the biofilm region, originating from the middle or the apical part of the pocket (Schlafer, 2014).

Fa is always closely intertwined with other periodontal germs, and has a symbiotic relationship with Pg, for example, which may result in a structural increase in biofilm.

Treatment

Antibiotic of choice: Metronidazol

Literature

Aruni, A.W., Roy, F. and Fletcher, H.M., 2011. Filifactor alocis Has Virulence Attributes That can Enhance Ist Persistence under Oxidative Stress Conditions and Mediate Invasion of Epithelial Cells by Porphyromonas gingivalis. Infection and Immunity, 79 (10), 3872-3886.

Aruni, W., Chioma, O. and Fletcher, H.M., 2014. Filifactor alocis: The Newly Discovered Kid on the Block with Special Talents. Journal of Dental Research, 93 (8), 725-732.

Aruni, W., Mishra, A., Dou, Y., Chioma, O., Hamilton, B.N. and Fletcher, H.M., 2015. Filifactor alocis- a new emerging periodontal pathogen. Microbes and Infection, 17 (7), 517-530.

Jusko, M., Miedzak, B., Ermert,D., Magda, M., King, B.C., Bielecka, E., Riesbeck, K., Eick, S., Potempa, J. and Blom, A.M., 2016. FACIN, a Double-Edged Sword oft he Emerging Periodontal Pathogen Filifactor alocis: A Metabolic Enzyme Moonlighting as a Complement Inhibitor. Journal of Immunology, 197, 3245-3259.

Schlafer, S., 2014. Filifactor alocis-der noch unterschätze Parodontitis-Keim in der Zahnfleisch-tasche. Zahnmedizin Report, 9:3.

Nomenclature

Prevotella intermedia (Pi)

Characteristics

Gram-negative obligate anaerobes

Pathogenicity

Strongly pathogenic

Virulence factors

Exopolysaccharides (EPS)
Cystein Protease (Interpain A)

Occurrence

It has been documented as a (co-) pathogen of mostly mixed-infection dentoalveolar infections. It is also referred to as an early marker germ, which creates the anaerobic environment necessary for the settlement of the main periodontal germs via the metabolism of residual sugar in the sulcus or in the forming periodontal pocket. Pi uses steroid hormones as growth factors, and therefore occurs more often in pregnant women.

Treatment

Pi with increased germ counts can not be treated by means of scaling/root planing. Nitromidazole preparations (e.g. metronidazole) are the antibiotics of choice. Isolated penicillinase-related penicillin resistance is known; Other than anaerobic beta-lactam antibiotics (e.g, penicillin G, ampicillin, amoxicillin). The efficacy of clindamycin (resistance) and tetracycline varies; Aminoglycosides are always ineffective.

Literature

Potempa, M., Potempa, J., Kantyka, T., Nguyen, KA., Wawrzonek, K., Manadhar, S.P., Popadiak, K., Riesbeck, K., Eick, S. and Blom, A.M., 2009. Interpain A, a Cysteine Protease from Prevotella intermedia Inhibits Complement by Degrading Complement Factor 3. PLoS Pathogens, 5 (2), e1000316.

Riggio, M.P., Lennon, A. and Roy, K.M., 1998. Detection of Prevotella intermedia in subgingival plaque of adult periodontitis patients by polymerase chain reaction. Journal Periodontal Research, 33 (6), 369-376.

Yamanaka, T., Yamane, K., Furukawa, T., Matsumoto-Mashimo, C., Sigimori, C., Obata, N., Walker, C.B., Leung, K.P. and Fukushima, H., 2011. Comparision oft he virulence of exopolysaccharide- producing Prevotella intermedia to exopolysaccharide non- producing perodontoipathic organism. BMC Infection Disease, 11, 228-237

Nomenclature

Treponema denticola (Td)

Characteristics

Short, strictly anaerobic gram-negative spirochaete

Pathogenicity

Strongly pathogenic

Virulence factors

Tissue-destroying proteases, hyaluronidases, phosphatases and phospholipases. Stimulates formation of IL-1 alpha and TNF-alpha.

Occurrence

Is associated with periodontal destruction (advanced periodontitis), necrotising ulcerative gingivitis/periodontitis.

Treatment

It is useful as a marker in the evaluation of treatment success (scaling/root planing) in therapy refractory pockets. Antibiotics of choice, if necessary, are metronidazole or ornidazole.

Literature

Asai, Y., Jinno, T., Igarashi, H., Ohyama, Y. and Ogawa, T., 2002. Detection and Quantification of Oral Treponemes in Subgingival Plaque by Real-Time PCR. Journal of Clinical Microbiology, 40 (9), 3334-3340.

Dashper, S.G., Seers, C.A., Tan, K.H. and Reynolds, E.C., 2011. Virulence Factors oft he Oral Spirochete Treponema denticola. Journal Dent. Research, 90 (6), 691-703.

Pandit, N., Gugnani, S., Sushil, D. and Bali, D., 2016. Treponema denticola: A teammate in periodontal progression. Journal of ICDRO, 8 (1), 58-62.

Sela, M.N., 2001. Role of Treponema denticola in periodontal diseases. Crit Rev Oral Biol Med, 12 (5), 399-413.

Nomenclature

Porphyromonas gingivalis (Pg)

Characteristics

Gram-negative strict anaerobe

Pathogenicity

Highly pathogenic

Virulence factors

Membrane-associated proteases, which, for example, split fibrinogen, which leads to bleeding on probing (BOP), releases haemin and iron and at the same time leads to further propagation of the germ as a food source. Lipopolysaccharides, exopolysaccharides, OMP (outer membrane proteins), collagenase, trypsin-like protease, gelatinase, aminopeptidase.

Occurrence

The germ does not belong to the "normal" oral flora; the immune system is unable to completely control an infection. It occupies the periodontal area more uniformly than A. actinomycemtemcomitans, which is more likely to occur in isolated areas.

Treatment

Can usually be removed with root planing. If it is nevertheless detected after this treatment, reintervention with curettage or surgery is indicated. If Pg and Aa are present in larger quantities, antibiotics must be prescribed in addition to scaling/root planing. Antibiotics of choice are metronidazole or ornidazole + amoxicillin.

Literature

How, K.Y., Song, K.P.and Chan, K.G., 2016. Porphyromonas gingivalis: An Overview of Periodontopathic Pathogen below the Gum Line. Frontiers in Microbiology, 7 (53).

Lyons, S.R., Griffen, A.L. and Leys, E.J., 2000. Quantitative Real-Time PCR for Porphyromonas gingivalis and Total Bacteria. Journal of Clinical Microbiology, 38 (6), 2362-2365.

Mysak, J., Podzimek, S., Sommerova, P., Lyuya-Mi, Y., Bartova, J., Janatova, T., Prochazkova, J. and Duskova, Jana, 2014. Porphyromonas gingivalis: Major Periodontopathic Pathogen Overview. Journal of Immunology Research, ID 476068, 8.

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