Cutaneous manifestations of Campylobacter jejuni infection: A case report and review of the literature.

A 51 year old man with active follicular lymphoma presented with several days of erythematous skin nodules on all extremities two weeks after a self-limited diarrheal illness. All serum immunoglobulin levels were found to be low. Blood cultures grew Campylobacter jejuni. The patient was given one week of azithromycin with complete resolution of his skin nodules. The literature of skin manifestations seen in active Campylobacter jejuni infection are reviewed. The majority of cases occur in immunocompromised hosts, many with low or no serum immunoglobulin levels. Postulated mechanisms include a lack of secretory IgA in intestinal mucosa predisposing susceptible patients to translocated enteric pathogens however the precise pathogenesis underlying cutaneous manifestations are unknown.

Application of Cardiogenic Shock Working Group-defined Society for Cardiovascular Angiography and Interventions (CSWG-SCAI) Staging of Cardiogenic Shock to the Medical Information Mart for Intensive Care IV (MIMIC-IV) database.

BACKGROUND: The optimal parameters for defining stages of cardiogenic shock (CS) are not yet known. The Cardiogenic Shock Working Group-defined Society for Cardiovascular Angiography and Interventions (CSWG-SCAI) staging of CS was developed to provide simple and specific parameters for risk-stratifying patients. OBJECTIVES: The purpose of this study was to test whether the Cardiogenic Shock Working Group-defined Society for Cardiovascular Angiography and Interventions (CSWG-SCAI) staging is associated with in-hospital mortality, using the Medical Information Mart for Intensive Care IV (MIMIC-IV) database. METHODS: We utilized the open-access MIMIC-IV database, which includes >300,000 patients admitted between 2008 and 2019. We extracted the clinical profile of patients admitted with CS and stratified them into different SCAI stages at admission based on the CSWG criteria. We then tested the association between in-hospital mortality and parameters of hypotension, hypoperfusion, and overall CSWG-SCAI stage. RESULTS: Of the 2463 patients, CS was predominantly caused by heart failure (HF; 54.7 %) or myocardial infarction (MI; 26.3 %). Mortality was 37.5 % for the total cohort, 32.7 % for patients with HF, and 40 % for patients with MI (p < 0.001). Mortality was higher among patients with mean arterial pressure < 65 mmHg, lactate >2 mmol/L, ALT >200 IU/L, pH ≤ 7.2, and more than one drug/device support at baseline. Increasing CSWG-SCAI stages at baseline and maximum CSWG-SCAI stage achieved were significantly associated with in-hospital mortality (p < 0.05). CONCLUSIONS: The CSWG-SCAI stages are significantly associated with in-hospital mortality and may be used to identify hospitalized patients at risk of worsening cardiogenic shock severity. CONDENSED ABSTRACT: We analyzed data from 2463 patients with cardiogenic shock using the MIMIC-IV database to investigate the relationship between the Cardiogenic Shock Working Group-defined Society for Cardiovascular Angiography and Interventions (CSWG-SCAI) staging and in-hospital mortality. The main causes of cardiogenic shock were heart failure (54.7 %) and myocardial infarction (26.3 %). The overall mortality rate was 37.5 %, with a higher rate among patients with myocardial infarction (40 %) compared to those with heart failure (32.7 %). Mean arterial pressure < 65 mmHg, lactate >2 mmol/L, ALT >200 IU/L, and pH ≤ 7.2 were significantly associated with mortality. Increasing CSWG-SCAI stages at baseline and maximum achieved stages were strongly associated with higher mortality (p < 0.05). Therefore, the CSWG-SCAI staging system can be used to risk-stratify patients with cardiogenic shock.

Shiga toxin 2-induced intestinal pathology in infant rabbits is A-subunit dependent and responsive to the tyrosine kinase and potential ZAK inhibitor imatinib.

Shiga toxin producing Escherichia coli (STEC) are a major cause of food-borne illness worldwide. However, a consensus regarding the role Shiga toxins play in the onset of diarrhea and hemorrhagic colitis (HC) is lacking. One of the obstacles to understanding the role of Shiga toxins to STEC-mediated intestinal pathology is a deficit in small animal models that perfectly mimic human disease. Infant rabbits have been previously used to study STEC and/or Shiga toxin-mediated intestinal inflammation and diarrhea. We demonstrate using infant rabbits that Shiga toxin-mediated intestinal damage requires A-subunit activity, and like the human colon, that of the infant rabbit expresses the Shiga toxin receptor Gb(3). We also demonstrate that Shiga toxin treatment of the infant rabbit results in apoptosis and activation of p38 within colonic tissues. Finally we demonstrate that the infant rabbit model may be used to test candidate therapeutics against Shiga toxin-mediated intestinal damage. While the p38 inhibitor SB203580 and the ZAK inhibitor DHP-2 were ineffective at preventing Shiga toxin-mediated damage to the colon, pretreatment of infant rabbits with the drug imatinib resulted in a decrease of Shiga toxin-mediated heterophil infiltration of the colon. Therefore, we propose that this model may be useful in elucidating mechanisms by which Shiga toxins could contribute to intestinal damage in the human.