Cutaneous tuberculosis (CTB) is the result of a chronic infection by Mycobacterium
tuberculosis, M. ovis and occasionally by the Calmette-Guerin bacillus. The clinical
manifestations are variable and depend on the interaction of several factors
including the site of infection and the host's immunity. This article revises the
current knowledge about this disease's physiopathology and immunology as well as
detailing the possible clinical presentations.
The evolution in the knowledge of tuberculosis' physiopathology allowed not only
a better understanding of the immunological factors involved in the disease
process, but also the development of new laboratory tests, as well as the
establishment of a histological classification that reflects the host's ability
to contain the infectious agent. At the same time, the increasing bacilli
resistance led to alterations in the basic tuberculosis treatment scheme in
2009. This article critically examines laboratory and histological
investigations, treatment regimens for tuberculosis and possible adverse
reactions to the most frequently used drugs.
The disease caused by the new coronavirus (COVID-19) has many systemic manifestations affecting the upper airways, lungs, gastrointestinal tract and inducing hematological repercussions. With the evolution of the pandemic, skin lesions were observed. However, there is little information about the evolution of the lesions at this moment. The authors report a case of a patient who had more than one exposure to the coronavirus during the evolution of the disease and manifested different types of edematous lesions. The lesions started in the prodromal period and changed their presentation and localization during the evolution of COVID-19. The lesions regressed quickly with the use of corticoid cream and antihistamine. Viral skin lesions are frequent causes of exanthema. However, viral etiology is not always investigated in acute urticarial and atypical erythematous-edematous conditions. The immunological basis of acute urticaria has points in common with COVID-19, justifying the appearance of lesions. Investigation of viral etiology should always be remembered in acute urticarial and edematous conditions.
Bullae autoimmune diseases can be induced by environmental factors in a genetically susceptible individual, and viruses may be important triggers for this process. Coronavirus disease 2019 (COVID-19) is a multisystemic disease known for developing many types of skin lesions. However, little is known about post-COVID-19 manifestations. A previous healthy male patient, 43 years old, with resistant mediastinal Hodgkin's lymphoma stage II diagnosed in 2019, without treatment at the moment, developed monomorphic flaccid bullae on the trunk 40 days after testing positive for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Although he had risk factors for IgA and paraneoplastic pemphigus, there were no elements for these diseases. The investigation confirmed a pemphigus vulgaris (PV). PV had a good response to treatment with prednisolone 1 mg/kg per day, and methotrexate 15 mg subcutaneously was added per week. The patient was discharged with oral methotrexate and prednisolone at the same dose. Prednisolone was decreased by 20 mg per day during the follow-up. Viruses such as herpesvirus, cytomegalovirus, and varicela zoster can act as triggers for PV. This process is not immediate after the infection because it depends on the change in antibodies initially produced against the virus that start to identify antigens present in the skin's anchoring structures. SARS-CoV-2 can induce autoimmunity, as seen in Guillán-Barré syndrome and in Kawasaki disease. It is a highly immunogenic virus that is the perfect agent for triggering PV. This case can be considered a cutaneous autoimmune post-COVID-19 manifestation.
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