Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.36 (hyaluronidase)
 4,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Group A streptococci (S. pyogenes) possess a number of capsule and cell wall associated components and release many extracellular proteins (toxins and hydrolytic enzymes) that are known or thought to contribute to the virulence and pathogenicity of the microorganism. Groupe A streptococci cause a wide array of infections, the most frequent of which are acute pharyngitis and pyoderma with two severe sequelae (acute rheumatic fever and glomerulonephritis). Other manifestations are scarlet fever and various soft tissue infections as well as sepsis and the recently characterized streptococcal toxic shock syndrome. The somatic components of group A streptococci include cell wall M protein, capsular hyaluronic acid, lipoteichoic acid, peptidoglycan, fibronectin binding protein, C5a peptidase and receptors for various human plasma proteins particularly IgA and IgG. The extracellular products are numerous and consist of among others the hemolytic toxins streptolysins S and O, hyaluronidase, streptokinase and cysteinyl proteinase as well as the superantigens erythrogenic toxins A and C also known as pyrogenic exotoxins.
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PMID:[Cellular constituents and extracellular proteins involved in the pathogenic capacity of Streptococcus group A]. 873 28

The determination of protein M and T serotypes, biotypes and pyrogenic (erythrogenic) exotoxin A (SPE A), streptolysin O (SLO), streptokinase (SK), hyaluronidase (HA) and cysteine proteinase release by 212 S. pyogenes isolates from patients with severe invasive group A streptococcal (GAS) infections, among them 74 cases of streptococcal toxic shock syndrome (STSS) has been investigated. M1 or M3 serotypes were expressed by 25% of the isolates (53/212), whereas 59% (125/212) belonged to 15 other different serotypes and 16% (34/212) were untypeable. Of the 74 isolates from STSS patients, 42% (31/74) expressed M1 and to a lesser extent M3 serotypes versus 19% of the non STSS isolates (26/138). Among the ten different biotypes known, biotypes 1 and 3 were prevalent, particularly the former in the case of STSS isolates. SPE A was detectably produced by about 25% (54/212) of the strains. However, as high as 40.5% of the STSS isolates (30/74) versus 17.4% of non STSS isolates (24/138) released SPE A. Moreover, 67% of the SPE A producing strains were of serotype M1 or M3. SK and HA were released by 71% and 10% of the isolates respectively. All strains released SLO (4 to 256 HU/ml) and 85% cysteine proteinase. No relationship between toxin or enzyme titer and the type of disease or clinical origin of the strains was found. Culture supernatants of all isolates showed moderate to high lymphocyte transforming activity with index values ranging from 14.5 to 50.3 including those strains which did not release detectable amounts of SPE A suggesting that SPE C and other mitogenic factor(s) are released by the isolates investigated.
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PMID:Streptococcal pyrogenic exotoxin A, streptolysin O, exoenzymes, serotype and biotype profiles of Streptococcus pyogenes isolates from patients with toxic shock syndrome and other severe infections. 936 88

The last decade has witnessed a remarkable change in the epidemiology of group A streptococcal infections. There has been a marked increase globally in the reporting of invasive infections caused by Streptococcus pyogenes, Lancefield group A streptococci. Many of these cases were deep-seated infections associated with shock and multi-organ failure and are defined as streptococcal toxic shock syndrome. In addition, reports of streptococcal sequelae, in particular, acute rheumatic fever, have re-emerged and remain a serious health threat in developed countries. It appears that these infections are related to the type distributions of the organism among the general population, with the re-emergence of more 'virulent' strains, such as the M1 serotype which in earlier decades was primarily seen in cases of either superficial disease or scarlet fever. Population-based surveillance studies have clearly indicated the importance and relevance of type identification for epidemiological purposes. There have also been suggestions that certain extracellular products and toxins play a major role in the so-called 'increased virulence' of the organism; these include cell surface molecules such as the M protein, opacity factor, the hyaluronic acid capsule, C5a peptidase and streptococcal inhibitor of complement (SIC), in addition to secreted proteins, pyrogenic exotoxins, cysteine proteinase, streptolysins O and S, hyaluronidase, streptokinase and other enzymes. All these factors, and events during the last decade, strongly emphasize the need for a better understanding of the epidemiology, pathogenesis, treatment and prevention of group A streptococcal infections.
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PMID:Group A streptococci in the 1990s. 1075 57

Streptococcus constellatus, S. intermedius, and S. anginosus, the three species of the S. milleri group, form part of the normal flora most commonly found in the mouth, throat, gastrointenstinal tract, and genital tract. The S. milleri group has become known as an important pathogen in abscess disease, but little attention has been paid to their role in deep neck abscesses. We have treated 9 patients with deep neck abscesses relating to the S. milleri group since 1991, and regarded this group as an important pathogen also in these abscesses. We studied the frequency of the S. milleri group isolated from deep neck abscesses in our cases and from the literature and discuss clinical significance and bacteriological pathogenesis. Cases numbered 27 treated at our facility since 1991 and 200 cases reported in the Japanese literature since 1990. Of our 9 cases, 4 originated from acute pharyngitis, 3 from peritonsillar abscesses, and 2 from odontogenic infection. Serious complications such as mediastinitis, cervical necrotizing fasciitis, sepsis accompanied by disseminated intravascular coagulation, and spondylitis of the cervical vertebrae were seen in 4 cases. Among organisms isolated, the S. milleri group appeared to be a pathogen contributing to abscess formation and to serious complications. The genus Streptococcus was most frequently isolated both in our 27 cases (66.7%) and the 200 in the literature (45.5%). Among species of the genus Streptococcus, the S. milleri group numbered the highest in our cases at 33.3% but only 8.5% in the literature. Cases in the literature, however, contained many unknown species of Streptococci--31.5% vs. 18.5% in our cases. alpha-streptococcus was frequently reported in the literature among unknown species of Streptococci--36 of 63. Culture-negative cases were also numbered more in the literature than in our case--29.0% vs. 18.5%. Special conditions and procedures are required to suitably isolate and detect the S. milleri group. Since not all facilities use identical techniques in routine bacteriological examination, a considerable number of the S. milleri group could be missed in unknown species of Streptococci or alpha-streptococcus and culture-negative cases. The detailed pathogenesis of the S. milleri group remains to be clarified. Infection by normal flora on mucosa is thought to occur due to an imbalance between organisms and host defense in deep neck abscesses. Some strains of the S. milleri group have been reported to produce many tissue-destroying enzymes such as collagenase and hyaluronidase. The co-existence of the S. milleri group with some anaerobe strains has also been suggested to accelerate inflammation. We discuss the mechanism inducing the massive release of cytokines through T cell response to certain exotoxins produced by S. milleri group, as reported in toxic shock-like syndrome due to the group A beta-streptococcus and in alpha-streptococcal shock syndrome due to viridans streptococci (alpha-streptococci).
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PMID:[Clinical and bacteriological significance of the Streptococcus milleri group in deep neck abscesses]. 1125 79

Staphylococcus aureus is a facultative, Gram-positive coccus well known for its disease-causing capabilities. In particular, methicillin and vancomycin resistant strains of S. aureus (MRSA and VRSA, respectively) isolated globally represent daunting medical challenges for the 21(st) Century. This bacterium causes numerous illnesses in humans such as food poisoning, skin infections, osteomyelitis, endocarditis, pneumonia, enterocolitis, toxic shock, and autoimmune disorders. A few of the many virulence factors attributed to S. aureus include antibiotic resistance, capsule, coagulase, lipase, hyaluronidase, protein A, fibronectin-binding protein, and multiple toxins with diverse activities. One family of protein toxins is the staphylococcal enterotoxins (SEs) and related toxic shock syndrome toxin-1 (TSST-1) that act as superantigens. There are more than twenty different SEs described to date with varying amino acid sequences, common conformations, and similar biological effects. By definition, very low (picomolar) concentrations of these superantigenic toxins activate specific T-cell subsets after binding to major histocompatibility complex class II. Activated T-cells vigorously proliferate and release proinflammatory cytokines plus chemokines that can elicit fever, hypotension, and other ailments which include a potentially lethal shock. In vitro and in vivo models are available for studying the SEs and TSST-1, thus providing important tools for understanding modes of action and subsequently countering these toxins via experimental vaccines or therapeutics. This review succinctly presents the pathogenic ways of S. aureus, with a toxic twist. There will be a particular focus upon the biological and biochemical properties of, plus current neutralization strategies targeting, staphylcoccocal superantigens like the SEs and TSST-1.
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PMID:Staphylococcus aureus: the toxic presence of a pathogen extraordinaire. 1974 26