Disease relevance of Streptococcal Infections

• In addition, M protein/fibrinogen complexes were identified in tissue biopsies from a patient with necrotizing fasciitis and STSS, further underlining the pathogenic significance of such complexes in severe streptococcal infections [1].
• Prophylaxis of streptococcal infections and rheumatic fever: a comparison of orally administered clindamycin and penicillin [2].
• These results show that streptococcal enolase is a novel cross-reactive antigen that may play an important role in the initiation of the autoimmune diseases related to streptococcal infection [3].
• The M protein is one of the most important virulence factors of group A streptococci (Streptococcus pyogenes) and may play an important role in the first steps of streptococcal infection [4].
• In addition, there are recent reports of dystonia, chorea encephalopathy, and dystonic choreoathetosis occurring as sequelae of streptococcal infection [5].

High impact information on Streptococcal Infections

• Response to type III polysaccharide in women whose infants have had invasive group B streptococcal infection [6].
• Significant changes occurred in the spectrum of invasive group A streptococcal infections in Pima County, Arizona, between 1985 and 1990 [7].
• Excluding uncooperative patients, the rate of streptococcal infection remained less, though not statistically significant, in the clindamycin group than in the penicillin group [2].
• SDH, a major surface protein of group A streptococci, has both glyceraldehyde-3-phosphate dehydrogenase and ADP-ribosylating enzyme activities that may relate to early stages of streptococcal infection [8].
• These findings clearly suggest that SDH plays an important role in cellular communication between streptococci and pharyngeal cells that may be important in host cell gene transcription, and hence in the pathogenesis of streptococcal infection [8].

Chemical compound and disease context of Streptococcal Infections

• The efficacy of a single dose of aqueous penicillin G in preventing neonatal group-B streptococcal infections was demonstrated in a randomised study conducted over 41 months [9].
• A significant activation of the complement common pathway (from C3 to terminal components) was observed only with SK infusion and is attributable to the rapid formation of immunocomplexes between SK and anti-SK antibodies present in plasma as a consequence of previous streptococcal infections [10].
• RESULTS: Significant decreases in streptococcal infections during the study year were found with a mean of .1 (.3 SD) per subject, compared to the baseline year with 1.9 (1.2 SD) in the penicillin group and 2.4 (1.1 SD) in the azithromycin group [p<.01] [11].
• CONCLUSIONS: Penicillin and azithromycin prophylaxis were found to be effective in decreasing streptococcal infections and neuropsychiatric symptom exacerbations among children in the PANDAS subgroup [11].
• Because of the poor activities of erythromycin and azithromycin against S. pyogenes isolates from patients in southern Taiwan, these drugs should no longer be considered the drugs of choice for the management of group A streptococcal infections among patients who live in this area [12].

Biological context of Streptococcal Infections

• Contribution of protein G-related alpha2-macroglobulin-binding protein to bacterial virulence in a mouse skin model of group A streptococcal infection [13].
• Inhibition of streptokinase-induced, antibody-mediated platelet aggregation with tirofiban after exposure to streptokinase or streptococcal infection [14].
• Increased pulmonary susceptibility to streptococcal infection following inhalation of manganese oxide [15].
• The streptococcal infection cases from two outbreaks were serologically examined against two components of the streptococcal cellular wall; the M associated protein (MAP), by a latex agglutination test and the group A carbohydrate (A-CHO), by passive hemagglutination technique [16].

Anatomical context of Streptococcal Infections

• They also support the hypothesis that in susceptible persons who have ADHD or OCD, chronic or recurrent streptococcal infections are associated with structural alterations in basal ganglia nuclei [17].
• A role for C5 and C5a-ase in the acute neutrophil response to group B streptococcal infections [18].
• Protection of mice from group A streptococcal infection by intranasal immunisation with a peptide vaccine that contains a conserved M protein B cell epitope and lacks a T cell autoepitope [19].
• Myocardial infarction associated with pseudoephedrine use and acute streptococcal infection in a boy with normal coronary arteries [20].
• We studied the possibility of detecting beta-hemolytic streptococcal infections by determining antibodies against the group specific polysaccharides from streptococci of groups A, A-variant, C and G. The methods used were radio-immunoassay with these four polysaccharides and hemagglutination of group A polysaccharide sensitized erythrocytes [21].

Gene context of Streptococcal Infections

• Cytokine appearance and effects of anti-tumor necrosis factor alpha antibodies in a neonatal rat model of group B streptococcal infection [22].
• Correlation between serum TNF alpha and IL6 levels and severity of group A streptococcal infections [23].
• To investigate the immune-mediated response in TS, and its relationship with streptococcal infection, we measured serum levels of soluble intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-selectin in patients with TS, compared to healthy and diseased controls [24].
• Since streptokinase (SK) is a potent immunogen and binds to DPP IV, we speculated that patients with autoimmune diseases showed higher DPP IV autoantibody levels than healthy controls as a consequence of an abnormal immune stimulation triggered by SK released during streptococcal infections [25].
• Studies of group B streptococcal infection in mice deficient in complement component C3 or C4 demonstrate an essential role for complement in both innate and acquired immunity [26].

Analytical, diagnostic and therapeutic context of Streptococcal Infections

• In an effort to examine further whether passive immunotherapy is a useful adjunct to antimicrobial therapy for neonatal group B streptococcal disease, we evaluated human intravenous immune globulin and penicillin G, alone and in combination, for their therapeutic efficacy against experimental severe group B streptococcal infection in newborn rats [27].
• Type-specific protection of neonatal rats from lethal group B streptococcal infection by immune sera obtained from human volunteers vaccinated with type III-specific polysaccharide [28].
• Previous studies have shown that a type-specific IgA monoclonal antibody alone or in combination with fibronectin (Fn) enhances protective efficacy in two animal models of group B streptococcal infection [29].
• We studied the clinical value of Wellcogen, a latex particle agglutination test designed to diagnose rapidly Group B streptococcal infections in 620 infants [30].
• A prospective multicentre study of Italian children with acute pharyngotonsillitis was carried out to determine the incidence of beta-haemolytic streptococcal infection and its epidemiological characteristics and to evaluate the effectiveness of a recently marketed macrolide, miocamycin [31].

References