Cutaneous complication after BCG vaccination: case report and review of the literature.
ABSTRACT The bacille Calmette-Guérin (BCG) vaccination protects against tuberculosis (TB)-related meningitis and disseminated tuberculosis. While severe complications after BCG vaccination are relatively rare, different cutaneous reactions have been reported. We report a patient with a 7-mm erythematous nodule at a distance of 4 cm from the BCG injection site. Histopathologically, a necrotizing granulomatous reaction pattern was seen in the dermis. Although complementary stainings did not detect acid fast bacilli, we suspected the lesion was caused by the attenuated strains of Mycobacterium bovis from the vaccine. This specific complication is called BCG-itis in the literature. After the excisional biopsy, the lesion disappeared and further treatment was not necessary. In defining the best treatment for this boy, we discovered a lack of knowledge on BCG-related lesions and their subsequent treatment options in the literature. We will list existing literature on this topic and demonstrate that treatment of BCG-related complications is poorly defined.
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ABSTRACT: Patients with chronic granulomatous disease (CGD) lack generation of reactive oxygen species (ROS) through the phagocyte NADPH oxidase NOX2. CGD is an immune deficiency that leads to frequent infections with certain pathogens; this is well documented for S. aureus and A. fumigatus, but less clear for mycobacteria. We therefore performed an extensive literature search which yielded 297 cases of CGD patients with mycobacterial infections; M. bovis BCG was most commonly described (74%). The relationship between NOX2 deficiency and BCG infection however has never been studied in a mouse model. We therefore investigated BCG infection in three different mouse models of CGD: Ncf1 mutants in two different genetic backgrounds and Cybb knock-out mice. In addition, we investigated a macrophage-specific rescue (transgenic expression of Ncf1 under the control of the CD68 promoter). Wild-type mice did not develop severe disease upon BCG injection. In contrast, all three types of CGD mice were highly susceptible to BCG, as witnessed by a severe weight loss, development of hemorrhagic pneumonia, and a high mortality (∼50%). Rescue of NOX2 activity in macrophages restored BCG resistance, similar as seen in wild-type mice. Granulomas from mycobacteria-infected wild-type mice generated ROS, while granulomas from CGD mice did not. Bacterial load in CGD mice was only moderately increased, suggesting that it was not crucial for the observed phenotype. CGD mice responded with massively enhanced cytokine release (TNF-α, IFN-γ, IL-17 and IL-12) early after BCG infection, which might account for severity of the disease. Finally, in wild-type mice, macrophages formed clusters and restricted mycobacteria to granulomas, while macrophages and mycobacteria were diffusely distributed in lung tissue from CGD mice. Our results demonstrate that lack of the NADPH oxidase leads to a markedly increased severity of BCG infection through mechanisms including increased cytokine production and impaired granuloma formation.PLoS Pathogens 09/2014; 10(9):e1004325. DOI:10.1371/journal.ppat.1004325 · 8.14 Impact Factor
PLoS Pathogens 09/2014; · 8.06 Impact Factor
09/2013; 23(4). DOI:10.1684/ejd.2013.2101