Expression of virulence factors in non-typhoidal Salmonella enterica depends on a wide variety of general and specific transcriptional factors that act in response to multiple environmental signals. Expression of genes for cellular invasion located in the Salmonella pathogenicity island 1 (SPI-1) is tightly regulated by several transcriptional regulators arrayed in a cascade, while repression of this system is exerted mainly by H-NS. In SPI-1, H-NS represses the expression mainly by binding to the regulatory region of hilA and derepression is exercised mainly by HilD. However, the possible regulatory role of H-NS in genes downstream from HilD and HilA, such as those regulated by InvF, has not been fully explored. Here the role of H-NS on the expression of sopB , an InvF dependent gene encoded in SPI-5, was evaluated. Our data show that InvF is required for the expression of sopB even in the absence of H-NS. Furthermore, in agreement with previous results on other InvF-regulated genes, we found that the expression of sopB requires the InvF/SicA complex. Our results support that SicA is not required for DNA binding nor for increasing affinity of InvF to DNA in vitro . Moreover, by using a bacterial two-hybrid system we were able to identify interactions between SicA and InvF. Lastly, protein-protein interaction assays suggest that InvF functions as a monomer. Derived from these results we postulate that the InvF/SicA complex does not act on sopB as an anti-H-NS factor; instead, it seems to induce the expression of sopB by acting as a classical transcriptional regulator.

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Relapsing fever (RF) borreliosis is a neglected disease in Mexico. A retrospective serological survey using diagnostic antigens GlpQ and BipA from Borrelia turicatae was performed to evaluate human exposure to RF borreliae. Seventy serum samples were used from a cohort of patients with undifferentiated febrile illness in Mexico. Four samples were positive to GlpQ and three to BipA. Results indicate that RF borreliae continue to circulate in regions of Mexico and pose a risk to human health.

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Magnusiomyces capitatus (also denominated “Geotrichum capitatum” and “the teleomorph stage of Saprochaete capitata”) mainly affects immunocompromised patients with hematological malignancies in rare cases of invasive fungal infections (IFIs). Few cases have been reported for pediatric patients with acute lymphoblastic leukemia (ALL), in part because conventional diagnostic methods do not consistently detect M. capitatus in infections. The current contribution describes a systemic infection in a 15-year-old female diagnosed with ALL. She arrived at the Children’s Hospital of Mexico City with a fever and neutropenia and developed symptoms of septic shock 4 days later. M. capitatus ENCB-HI-834, the causal agent, was isolated from the patient’s blood, urine, bile, and peritoneal fluid samples. It was identified with matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS) and a phylogenetic reconstruction using internal transcribed spacer (ITS) and 28S ribosomal sequences. The phylogenetic sequence of M. capitatus ENCB-HI-834 clustered with other M. capitatus-type strains with a 100% identity. In vitro antifungal testing, conducted with the Sensititre YeastOne susceptibility system, found the following minimum inhibitory concentration (MIC) values (μg/mL): posaconazole 0.25, amphotericin B 1.0, fluconazole > 8.0, itraconazole 0.25, ketoconazole 0.5, 5-flucytosine ≤ 0.06, voriconazole 0.25, and caspofungin > 16.0. No clinical breakpoints have been defined for M. capitatus. This is the first clinical case reported in Mexico of an IFI caused by M. capitatus in a pediatric patient with ALL. It emphasizes the importance of close monitoring for a timely and accurate diagnosis of neutropenia-related IFIs to determine the proper treatment with antibiotics, antifungals, and chemotherapy for instance including children with ALL.