Brote familiar de botulismo alimentario / A family outbreak of foodborne botulism

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Cardiopatía tirotóxica reversible secundaria a tirotoxicosis facticia / Reversible thyrotoxic cardiopathy secondary to thyrotoxicosis factitia

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Influence of a vaccination schedule on viral load rebound and immune responses in successfully treated HIV-infected patients.

Vaccination is recommended for HIV-infected patients. Transient increases of viral load (VL) and risk of developing resistance to HAART have been described. In addition, VL rebounds could increase HIV-specific immune responses. Twenty-six successfully treated HIV-infected adults were randomized to receive a vaccination schedule or placebo during 12 months. Afterward, HAART was discontinued. Influences of vaccination over VL, genotypic mutations, different T cell subsets, and HIV-1-specific immune responses were evaluated. Patients did not present any secondary effect. No differences in incidence of detectable VL determinations were detected between groups [relative risk 0.54 (95% CI 0.23-1.26)]. No relevant resistance mutations were detected. The vaccinated group showed a significant drop in CD4(+) T cells (p = 0.046) associated with increases in activated T cells. HIV-1-specific lymphoproliferative responses increased more in the vaccinated group during the vaccination period. Viral rebound dynamics after interrupting HAART were similar in both groups. A vaccination schedule in successfully treated HIV patients was safe, was not associated with an increase in detectable VL, and did not increase the risk of developing resistance mutations. However, it induced an increase in T cell activation and a drop in CD4(+) T cells, although these changes did not influence the VL rebound dynamics after HAART interruption.

Orbital cellulitis and endogenous endophthalmitis secondary to Proteus mirabilis cholecystitis.

We report the first case of orbital cellulitis and endogenous endophthalmitis secondary to Proteus mirabilis bacteremia that resulted from a calculus cholecystitis. Despite resolution of the gallbladder infection with antimicrobial therapy, the patient required evisceration of the affected eye. The pathogenesis of hematogenous endophthalmitis due to Gram-negative bacilli is discussed.

Short Communication: Natural killer cells and expression of KIR receptors in chronic HIV type 1-infected patients after different strategies of structured therapy interruption.

Few data evaluating the NK cell profile during structured therapy interruption (STI) in chronic HIV-1 infection are available. Changes in NK cell percentages and KIR and NKG2A receptors were analyzed at baseline and after 2 years of follow-up in 121 patients on ART with CD4(+) >450 cells/ml and VL <200 copies/ml randomized in three arms according to the criteria employed to resume ART during STI: virological arm (VA n = 47, VL >30,000 copies/ml or CD4 <350 cells/ml), immunological arm (IA n = 37, CD4< 350 cells/ml), and a control arm (n = 37) in which ART was maintained. After 2 years of follow-up, a decrease in CD3(-)CD56(+) CD16(+) cell percentages in VA and IA patients, but not in CA patients, was observed. Those patients with higher decrease in CD3(-)CD56(+)CD16(+) cells had a higher decrease in CD4(+) cells (r = 0.35, p = 0.001) and higher increase in PVL (r = -0.26, p = 0.02). KIR and NKG2A receptor expression tended to increase in CA and decreased in the other two arms (more in IA than in VA). Patients who displayed a greater decrease in CD4(+) T cells and a greater rise in PVL after 2 years of follow-up had a significantly higher decrease in KIR and NKG2A receptors expressed in CD3(-)CD56(+) cells. Patients who presented the lowest levels of total NK cells and KIR and NKG2A receptor expression after STI showed the poorest virology or immunology outcomes. This finding suggests that STI could decrease the number of NK subsets, which is related to the worst clinical development in these patients.

Acidosis láctica grave por déficit de tiamina / Severe lactic acidosis due to deficit of thiamine

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Demencia por cuerpos de Lewy / Dementia with Lewy bodies

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