SUSCEPTIBILITY OF PEOPLE VACCINATED AGAINST S. PNEUMONIAE TO SARS-COV-2 – MECHANISMS OF NON-SPECIFIC ACTION OF PNEUMOCOCCAL VACCINE

The review provides data showing the nonspecific effect of preventive vaccines, such as pneumococcus, tuberculosis, and influenza, on the parameters of innate and adaptive immunity, which is reflected in a reduction of susceptibility not only to vaccine antigens, but also to other infectious pathogens. It is also discussed possible variants of immune mechanisms activation after the receiving a pneumococcal vaccine, especially conjugated polysaccharide vaccine, and their role in the interaction between the organism and the new SARS-CoV-2 coronavirus. Three variants of the nonspecific action of the vaccine are considered as the most probable: antigen mimicry, nonspecific activation and trained immunity.

Sarcoidosis in A. C. Milan (1899)?

The pathogenesis, diagnosis and therapy of sarcoidosis as an autonomous disease are subjects of spirited discussions, which haven’t found definitive conclusion yet. Distinguishing between sarcoidosis and sarcoid-like reactions (sarcoid - type granulomas) is not currently a medical “gold standard” and is not implemented in clinical practice. This leads to 1) misinterpretation of numerous available data; 2) difficulty in the interpretation of other unverified data, which is often followed by 3) inappropriate or inadequate therapeutic approach. Similarly to many other diseases, in sarcoidosis and sarcoid - types of reactions the concept of personalised approach and therapy should also be introduced. This methodology of clinical guidance is difficult, complex and not always achievable in the current medical status and relations (doctor-patient relationship; financial factor; time factor). It is appropriate to note that in some cases the guidelines or the so-called standards are neglected or not possible to put into practice with the aim of better therapeutic practices and strategies, as well as the achievement of optimal final clinical results (especially in patients with sarcoid granulomas). The sarcoid granuloma, even when it is sterile, should not be considered as the equivalent of sarcoidosis, i.e., sarcoidosis as an autonomous disease. Sure enough, exactly because of this fact, the personalised approach should not be an exception, but it has to gradually become a rule in medical practice. When clinical decisions are conformed to some of the latest modern concepts, officialised in the international databases, often the achieved results can be much better.We present a patient with a tattoo of AC Milan (1899) on his right arm, who subsequently developed localised sterile sarcoid granulomas in the area of the tattoo. Later the process became generalised on his whole body’s skin, lungs and lymph nodes. It is unclear for the moment whether this condition should be interpreted as sarcoidosis as an autonomous disease or, instead, as a sarcoidal type of reaction with subsequent generalisation due to cross-reactivity against antigens present in other tissues with similarities to the exogenous pigments. Following the modern concepts regarding the pathogenesis of these two conditions, we introduced, in this case, an innovative, non-standard approach: 1) systemic and local immunosuppressive therapy, combined with 2) recommеndation for immediate surgical excision of the tattoo to remove the possible trigger of molecular and antigen mimicry.

Seborrheic Pemphigus, Antigen Mimicry and the Subsequent-Wrong Diagnostic and Therapeutic Approach?

It is well-established that drugs could be leading cause of occurrence of numerous diseases, including pemphigus, being either inducer or triggering factor of the autoimmunity. Despite medications, it should be kept in mind that chronic or acute infections are also capable of being a trigger in various types of cutaneous eruptions, including pemphigus. The rapidly obtained and uncompleted history for accompanied medication leads to general mistakes in the subsequent treatment approach, as the first step in such cases is discontinuation of the drug-inductor. The absence of this information guaranties the fail of the treatment. On the other hand, the lack of performed screening for chronic or acute hepatitis and tuberculosis is not the only mistake, regarding the high dosage of immunosuppressors that have been planned as regiment and the possible fatal effect on the infection’s spread or exacerbation, but also because of the possible triggering ability of chronic or acute infection, which may play also a key role in the generation of antigen- or molecular- mimicry, as a potential source of antibodies reactive with various tissue antigens. It turns out that although the diagnosis of pemphigus in regular cases is usually not a challenge, the treatment occasionally could be, just because of a simple pitfall in anamnesis and screening, as in the presented case. Herein, we present a case of a patient with seborrheic pemphigus, which is strongly demonstrative for these statements, as we want to emphasise the importance of the first and the most powerful clinician’s weapons – the patient’s history and thorough examination.

Antigen mimicry followed by epitope spreading: a pathogenetic trigger for the clinical morphology of lichen planus and its transition to Graham Lassueur Piccardi Little Syndrome and keratosis lichenoides chronica - Medical hypotheses or reality?

Literature data analysis, providing an exact explanation of the lichen planus pathogenesis, as well as its transition into other rare forms such as Keratosis lichenoides chronica or Graham Lassueur Piccardi Little Syndrome are scant, or totally missing. The chronological course of the disease, known in the literature as lichen planus, varies. Some patients develop Lichen planus or lichen nitidus and there is no logical explanation why. It is also not clear why single patients initially develop ulcerative lesions in the area of the mucosa and only in a few of them these lesions affect the skin. Antigen Mimicry and Epitope Spreading could be the possible pathogenic inductor in cases of lichenoid dermatoses, as well as the cause for their transition into ulcerative, exanthematous or other rare forms. The Epitope Spreading is probably not the leading pathogenetic factor in lichen planus but a phenomenon which occurs later. This manuscript analyzes some basic pathogenic aspects and presents some possible medical hypotheses regarding the heterogenic clinical picture and pathogenesis of lichen planus and lichenoid like pathologies of the skin which, in the near future should be analyzed in details in order to clarify several dilemmas the clinical dermatologist has to face.