This work was undertaken to determine whether Acanthamoeba could play a role in the survival and transmission of coxsackieviruses and focused on in vitro interactions between Acanthamoeba castellanii and coxsackie B3 viruses (CVB-3). Residual virus titer evaluations and immunofluorescence experiments revealed a remarkable CVB-3 adsorption on amoeba surfaces and accumulation inside cells. The survival of viruses was independent of the dynamics of amoeba replication and encystment. In addition, our results indicated that virus-infected amoebas can release infectious viruses during interaction with human macrophages. On the basis of these data, Acanthamoeba appears to be a potential promoter of the survival of coxsackieviruses and their transmission to human hosts.Free-living amoebas of the genus Acanthamoeba are ubiquitous in nature (34); they have been isolated from air (19, 32, 33), soil (2, 3, 6, 29), and water environments, including chlorinated swimming pools (10), drinking water (17, 28), cooling towers (5), natural thermal water (31), hospital water networks (35), and marine water (4). Acanthamoeba is characterized by a feeding and replicating trophozoitic stage which under adverse conditions can develop to a dormant cyst stage (34). Cysts are highly resistant forms capable of withstanding disinfection, desiccation, and extremes of temperature. When favorable conditions occur, the cysts hatch and the trophozoites emerge to feed and replicate. Acanthamoeba species are not parasites, as they do not require the infection of a host organism to complete their life cycles (11, 37). However, these amoebae can infect a variety of mammals, including humans, thereby producing severe and often fatal diseases. They act as opportunistic as well as nonopportunistic pathogens, are the causative agents of granulomatous amoebic encephalitis and amoebic keratitis, and have been associated with cutaneous lesions and sinusitis (18,20,(37)(38)(39). Both trophozoites and cysts have been shown to be resistant to chlorination used for disinfecting water systems (30,35,36).In addition, Acanthamoeba amoebas play a role as reservoirs for Legionella pneumophila and other amoeba-resistant microorganisms that include bacteria, fungi, and viruses (15).Enteroviruses (polioviruses, coxsackieviruses, echoviruses, and newer enteroviruses) are naked small RNA viruses of the Picornaviridae family. They are important human pathogens often causing mild febrile illness, but clinical manifestations of enterovirus infections also include meningitis, encephalitis, paralysis, and myocarditis (16,27). Gastrointestinal involvement may also result. Transmission from person to person proceeds through the fecal-oral route. These viruses are widespread in marine water and also may be acquired by eating contaminated aquatic organisms (14). Although labile, they may persist in free-flowing estuarine or marine waters for several months and in some cases during the winter months (21). Although their life span in water may be prolonged by the influence of estu...
Bullous pemphigoid (BP) is an autoimmune bullous disease caused by circulating autoantibodies toward the hemidesmosomal antigens BP180 and BP230. Cases of BP have been described following vaccinations against tetanus, poliomyelitis, diphtheria, influenza, pneumococcus, meningococcus, hepatitis B and rabies. The putative mechanism by which COVID-19-vaccines may induce BP has not been clarified. An Italian multicentre study was conducted to collect clinical, histopathological and immunopathological data of patients with BP associated with COVID-19-vaccines. Twenty-one cases were collected, including 9 females and 12 males (M/F = 1.3) with a median age at diagnosis of 82 years. Seventeen patients received the COMIRNATY Pfizer-BioNTech vaccine, two the Moderna mRNA-1273 vaccine, one the ChAdOx1/nCoV-19-AstraZeneca/ Vaxzevria vaccine and one received the first dose with the ChAdOx1/nCoV-19-AstraZeneca/Vaxzevria vaccine and the second dose with the COMIRNATY Pfizer-BioNTech vaccine. Median latency time between the first dose of anti-SARS-CoV-2 vaccine and the onset of cutaneous manifestations was 27 days. Median BPDAI at onset was 42. Eleven out of seventeen patients (65%) had positive titres for anti-BP180 antibodies with a median value of 106.3 U/mL on ELISA; in contrast, only five out of seventeen (29%) were positive for anti-BP230 antibodies, with a median of 35.3 U/mL. In conclusion, in terms of mean age, disease severity at diagnosis and clinical phenotype vaccine-associated BP patients seem to be similar to idiopathic BP with an overall benign course with appropriate treatment. On the other hand, the slight male predominance and the reduced humoral response to BP230 represent peculiar features of this subset of patients.
Pemphigus is a group of blistering disorders characterized by the formation of intraepithelial blisters in skin and mucous membranes induced by the binding of circulating autoantibodies to intercellular adhesion molecules. The pathogenesis is complex and not fully understood; however, genetic predisposition and various triggers are widely accepted as key factors in pemphigus development. A few cases of new‐onset pemphigus following coronavirus disease 2019 (COVID‐19) vaccination have already been published. The present paper reports a total of two cases of pemphigus foliaceous and three cases of pemphigus vulgaris that occurred following vaccinations against COVID‐19, with anamnestic, clinical, and diagnostic data collection suggesting assumptions over a possible causal correlation.
Management of cutaneous lupus erythematosus (CLE) involves a combination of preventive measures, topical and systemic drugs, fairly similar for the different subtypes. Although guidelines exist, to date, no specific drugs have been specifically licensed for CLE. Antimalarials remain the first-line systemic treatment, but many patients do not respond, making refractory lupus a challenge for clinicians. The choice of alternative medication should be based on effectiveness, safety and cost. Most of the available drugs for CLE have been adapted from systemic lupus erythematosus (SLE) treatment but the existing literature is limited to small studies and evidence often lacks. As knowledge of pathogenesis of both CLE and SLE is improving, promising new therapies are emerging. In this review, we discuss the available medications, focusing on the novelties under development for CLE.
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