Clinical Variables Associated With Adverse Maternal Outcomes in Puerperal Group A Streptococci Infection.

OBJECTIVE: To identify clinical variables associated with increased risk of composite adverse outcome in a cohort of women with puerperal group A streptococci infection. METHODS: Our prospective case registry enrolled patients between 1991 and 2017. Chart abstraction was conducted for admission demographic and clinical data in patients with culture-proven puerperal group A streptococci infection. We created a composite variable of signs of capillary leakage including pulmonary edema, pleural effusion, ascites, and abdominal distention. The composite adverse outcome included death, hysterectomy, intensive care unit admission, mechanical ventilation, and blood transfusion. Clinical characteristics were compared between those with a composite adverse outcome and those without. We fit unadjusted log-linear models with robust error variance to measure the relative risk of a composite adverse outcome associated with clinical and demographic variables among patients with group A streptococci. RESULTS: Thirty-five of 71 (49%) patients had an adverse outcome. Women who had adverse outcomes had higher admission heart rates (126±19 vs 112±22 beats per minute, P=.008) and respiratory rates (26±10 vs 20±5 breaths per minute, P=.01), lower systolic blood pressure (98±24 vs 114±19 mm Hg, P=.004), and were more likely to have signs of capillary leakage (77% vs 20%, P<.001) and symptoms of capillary leakage (dyspnea, cough, shoulder pain, abdominal bloating, and chest pain) (40% vs 17%, P=.03) compared with those without adverse outcomes. Log-linear models indicated that these clinical variables were individually associated with increased risk of a composite adverse outcome. The relative risk of an adverse outcome was 3.5 times higher among women with signs of capillary leakage (relative risk 3.67, 95% CI 1.94-6.94, P<.001). CONCLUSION: Vital sign parameters consistent with severe infection correlate with adverse outcomes in women with puerperal group A streptococci infection. Signs of capillary leakage are most strongly associated with a composite adverse outcome. These clinical characteristics, particularly signs of capillary leakage, are potentially useful to guide clinical care.

Interleukin-6 in sepsis and capillary leakage syndrome.

Bacterial sepsis is one of the most frequent and dreaded causes of death in intensive care units. According to the current understanding of sepsis, bacterial components activate innate immune responses via pattern-recognition receptors that stimulate signaling pathways, thereby leading to activation of NF-κB and the release of cytokines, alarming the organism and coordinating appropriate defense mechanisms. The resulting "cytokine storm" not only restricts bacterial invasion; it also harms the host by triggering a hemodynamic collapse with a drop in blood pressure, which could lead to death. One of the cytokines released during sepsis is interleukin-6 (IL-6). Originally described as a B-cell-stimulating factor, this cytokine has since been shown to have multiple additional functions. Interestingly, there is emerging evidence of IL-6 trans-signaling in the pathogenesis of sepsis. We review recent findings and discuss whether therapeutic interference with IL-6 trans-signaling may be beneficial in this important clinical scenario.

Toxigenic Helicobacter pylori induces changes in the gastric mucosal microcirculation in rats.

BACKGROUND AND AIMS: One of the key components of inflammation is changes in vascular structure and function. This suggests that the microcirculation may be a key target of Helicobacter pylori released factors. It has previously been shown in vivo that pooled H pylori extracts from duodenal ulcer/gastritis patients induce platelet aggregation but no leucocyte activation within rat gastric mucosal microcirculation (GMMC). However, infection with strains associated with ulcer disease as compared with gastritis may exert greater effects on the microcirculation. This study used fluorescent in vivo microscopy to determine the acute effects of extracts of genotypically different H pylori strains on the GMMC. METHODS: Three H pylori extracts, with different cagA and VacA toxigenic status, were individually administered to the gastric mucosa of anaesthetised Wistar rats. The mucosal surface was visualised via an incision made in the exteriorised stomach. Fluoroscein isothiocyanate conjugated to bovine serum albumin (FITC-BSA) or acridine orange was used to quantify macromolecular leak (MML) and leucocyte/platelet activity respectively for 120 minutes. Changes in capillary and post-capillary venule (PCV) diameters were also monitored. RESULTS: The cagA(+) VacA toxigenic strain 60190 induced significant and sustained MML by five minutes (p<0.01). Transient and less leakage was observed with its isogenic VacA(-) mutant and other non-toxigenic strains regardless of cagA status. Significant increases in leucocyte adhesion (p<0.05), platelet aggregation (p<0.05), and PCV vasoconstriction (p<0.05) were only observed with the cag A(+) and toxigenic strain. CONCLUSION: Extracts of H pylori are capable of inducing marked disturbances within the rat GMMC. These disturbances seem to be dependent on the production of an active vacuolating cytotoxin. Varying effects on the GMMC may explain the clinically diverse outcomes associated with genotypically different strains.

[Multisystemic severe infection with Chlamydia pneumoniae]. / Infection multisystémique sévère à Chlamydia pneumoniae.

Chlamydia pneumoniae (CP) is responsible for 8-10% of community acquired pneumonia. However, multiorgan disease is rare and the association with a cutaneous vasculitis has only been described once. We report a case of serious systemic CP infection with capillary leak syndrome and cutaneus vasculitis who was treated successfully with levofloxacin.

The effect of C1-esterase inhibitor in definite and suspected streptococcal toxic shock syndrome. Report of seven patients.

OBJECTIVE: To evaluate the effect of adjunctive C1-esterase inhibitor substitution therapy on clinical characteristics and outcome of patients with streptococcal toxic shock syndrome (TSS). DESIGN: Observational. SETTING: Medizinische Poliklinik, University of Bonn, Germany. PATIENTS: Seven patients with direct or indirect evidence of streptococcal TSS. INTERVENTION: In addition to conventional and supportive therapy, all patients received 2-3 single doses of C1-esterase inhibitor totaling 6,000-10,000 U within the first 24 h after admission. MEASUREMENTS AND RESULTS: All patients developed fulminant septic shock, multiorgan failure and/or capillary leak syndrome and necrotizing fasciitis within 10-72 h following the onset of first symptoms. Between 1 and 4 days following administration of C1-esterase inhibitor, a marked shift of fluid from extravascular to intravascular compartments took place in all but one patient, accompanied by a transient intra-alveolar lung edema and rapidly decreasing need for adrenergic agents. Six of seven patients survived. CONCLUSIONS: These clinical observations in a small series of patients and the favorable outcome point towards a positive effect of early and high-dose administration of C1-esterase inhibitor as adjunctive therapy in streptococcal TSS. The possible mechanism involved may be the attenuation of capillary leak syndrome (CLS) via early inactivation of complement and contact systems. Controlled studies are needed to establish an improvement of the survival rates of patients with streptococcal TSS following administration of C1-esterase inhibitor.