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Lipid-Based Nanocarriers for the Treatment of Infected Skin Lesions
Published in Andreia Ascenso, Sandra Simões, Helena Ribeiro, Carrier-Mediated Dermal Delivery, 2017
Sandra Simöes, Manuela Carvalheiro, Maria Manuela Gaspar
In Fig. 11.1 is shown a scheme of possible progression of BU infection after exposure to M. ulcerans in the environment. In some conditions, people exposed to M. ulcerans do not develop BU disease or even lesions may heal spontaneously depending on the host immunity. In case of progression, the infection is primarily related with two properties of M. ulcerans: the low optimal temperature of growth, favoring the development of lesions in cooler tissues particularly the skin and subcutaneous tissue, and production of a macrolide toxin, the mycolactone, being responsible for the toxic effects observed in BU lesions [14]. Mycolactones are secreted and diffuse into infected tissues. BU presents different clinical forms that can be dramatic if untreated. The first clinical presentation is non-ulcerative characterized by papules (skin lesions with a diameter inferior tocm), nodules (extension into subcutaneous tissue, diameter inferior to 2 cm), plaques (lesions with diameter superior tocm) and edema forms distributed mainly on limbs [15]. Figure 11.2 shows a schematic representation of BU pathogenesis progression from pre-ulcerative to ulcerative laceration stage.
Pharmacologic management of Mycobacterium ulcerans infection
Published in Expert Review of Clinical Pharmacology, 2020
Tjip S Van Der Werf, Yves T Barogui, Paul J Converse, Richard O Phillips, Ymkje Stienstra
Mycolactone has three different important effects that impact on the pathogenesis of M. ulcerans infection – first, necrosis, and apoptosis of an array of host cells [51], including immune cells. Partly as a result of apoptotic pathways switched on in immune cells, and probably also, by a mechanism whereby mycolactone interacts with Sec61, a second effect, a down-regulation occurs in the overall immune defense [52,53]. Third, there is impairment of sensitivity (i.e., pain sensation) mediated by different mechanisms, including impaired nerve conduction of sensory nerves [54], through the interaction of mycolactone with AT2 R [55,56], as well as an impact on host Schwann cells, resulting in nerve damage [57–59].
Vaccination efforts for Buruli ulcer
Published in Expert Review of Vaccines, 2022
Vivek P. Chavda, Melina Haritopoulou-Sinanidou, Rajashri Bezbaruah, Vasso Apostolopoulos
The mode of transmission of M. ulcerans to humans remains unknown but there have been speculations of zoonotic transmission [1,6,7,9]. Laboratory tests in West Africa have revealed that M. ulcerans is present in the salivary glands of aquatic insects, which points toward transmission through insect bites [12,13]. Further testing in Australia showed that Buruli ulcer disease is also present in horses, dogs, foxes, alpacas, koalas, indicating that it might be transmitted through insects, particularly mosquitoes, via these animals [9,14]; however, more recently it was reported that possums were the main carriers of M. ulcerans. The incubation period of this bacteria is variable and it has been estimated to be between four weeks to nine months [15]. The first sign of infection is the appearance of a painless nodule (swelling of the skin) that is commonly mistaken for an insect bite. These lesions can form in groups, and they may appear anywhere on the body, but are usually detected on the limbs [1,6,7,9,15,16]. If the subject does not seek medical treatment at these early stages, the disease will progress and the nodule will ulcerate within 4 weeks and lead to necrosis of the skin (Figure 1) [6,7]. In advanced stages, extensive scarring may result in deformities, limb contractures, bone infection, and secondary skin infection of lesions which can cause pain and fever. These further implications increase the burden of the disease and may lead to death [1,14]. Mycolactone is responsible for the pathogenic events of Buruli ulcer development. Thus, complete elimination of the M. ulcerans load may not be required for clinical cure or appropriate therapy, at least not in the immunocompetent host. Halting mycolactone development may be adequate, but it takes many days for mycolactone to be eradicated from host cells infected with M. ulcerans [17].