Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040425 (tonsillitis)
1,594 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nonmenstrual toxic shock syndrome (TSS) in adults has been associated with various staphylococcal respiratory tract infections, including pharyngitis, tonsillitis, pneumonia, and postinfluenza respiratory tract infections. In children, nonmenstrual TSS has also been described as a complication of bacterial tracheitis. We describe the case of a 40-year-old woman who presented with laryngotracheitis as well as clinical and laboratory evidence of TSS. Culture of her sputum samples yielded pure growth of Staphylococcus aureus, which was shown to produce TSS toxin 1 (TSST-1). The patient responded promptly to therapy with iv clindamycin. We discuss the association of TSS with staphylococcal laryngotracheitis and the role of clindamycin in the treatment of TSS. To our knowledge, there are no previous reports of TSS complicating laryngotracheitis in adults.
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PMID:Bacterial laryngotracheitis associated with toxic shock syndrome in an adult. 801 30

Erythrogenic toxin type A (ETA) is assumed to play a causative role in both scarlet fever and the streptococcal toxic shock-like syndrome (TSLS). For a molecular epidemiological analysis of the gene of erythrogenic toxin type A (speA) we used altogether 497 clinical isolates of Streptococcus pyogenes belonging to three groups: a) isolates from patients with scarlet fever, b) isolates from cases with TSLS, c) isolates from patients with other streptococcal infections (like otitis media, tonsillitis, impetigo) (general group). We found that less than 50% of the scarlet fever-associated strains possessed the speA gene as compared to 25% of the general group. Only 5 to 30% of these strains secreted the toxin under experimental conditions in very low quantities. Among strains isolated from TSLS, 67% appeared to contain the speA gene. The amount of ETA secreted into the medium was also extremely low. Southern hybridization patterns proved to be the same with an speA-specific probe in all three groups of streptococcal isolates (HaeIII, HindIII). Increased occurrence of the speA gene among scarlet fever and TSLS-associated strains does not seem to be sufficient to support the hypothesis that ETA may have a causative role in both diseases since a considerable number of strains in these groups did not possess the speA gene.
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PMID:Erythrogenic toxin type A (ETA): epidemiological analysis of gene distribution and protein formation in clinical Streptococcus pyogenes strains causing scarlet fever and the streptococcal toxic shock-like syndrome (TSLS). 821 99

Medical records of 876 servicemen of a young age who have suffered various forms of clinical diphtheria were analysed. (Lethal cases were marked in 52 cases--5.9%). A true clinical symptom complex for the diagnosis of diphtheria at pre-hospital period is as following: fever, intoxication and febrinous tonsillitis. The main cause of unfavourable outcome of the disease depends on the affection of cardiovascular, central and peripheral nerve systems by diphtheritic exotoxin. The most frequent limitations during medical care were the following: error diagnosis of angina (41%), late hospitalization and late specific treatment, insufficient doses of antidiphtheric serum, inopportune diagnosis of severe aggravations (infectious toxic shock, pneumonia).
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PMID:[The diagnostic and treatment characteristics of diphtheria in troop units and military medical institutions]. 830 51

In the present study, the gamma delta T cell content of the tonsillar T cell population has been evaluated for the first time. Flow cytometric analysis showed that 1.56% of T cells in palatine tonsils obtained from patients with recurrent tonsillitis (n = 17) expressed the gamma delta T cell receptor. Next, the tissue distribution of these cells in palatine tonsil was examined immunohistologically. Gamma delta T cell receptor positive cells and CD3 positive cells were counted in the crypt epithelium, tonsillar epithelium on the free surface and in the interfollicular space (n = 29). The gamma delta T cell content of the whole T cell population in each of these regions was calculated and compared. It was demonstrated that T cells in the crypt epithelium contained more gamma delta T cell receptor bearing cells than did T cells infiltrating the tonsillar epithelium on the free surface. T cells in the interfollicular space included even fewer gamma delta T cells. The gamma delta T cell content of tonsillar T cells showed a gradual decrease with age in each region. Then, infiltration of gamma delta T cells in the crypt epithelium was compared among recurrent tonsillitis, hypertrophic tonsil and focus tonsil (PPP) specimens. Recurrent tonsillitis showed the highest gamma delta T cell content in T cells infiltrating the crypt epithelium. There was no remarkable infiltration of these cells in the crypt epithelium of focus tonsil. Furthermore, the gamma delta T cell population was isolated from tonsillar lymphocytes and stimulated with staphylococcal enterotoxin A (SEA), staphylococcal enterotoxin B (SEB) and toxic shock syndrome toxin-1 (TSST-1).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Gamma delta T cells in the palatine tonsil--immunohistological and functional study]. 831 38

Streptococcus pyogenes may cause tonsillitis, scarlet fever and so-called "streptococcal toxic shock-like syndrome" (STSS). These streptococci produce exotoxins which are implicated as superantigens in the pathogenesis of STSS and scarlet fever. Using human peripheral blood-derived mononuclear cells in vitro, such toxins were shown to induce neopterin production and degradation of the amino acid tryptophan to metabolites such as kynurenine by activating indoleamine (2,3)-dioxygenase via interferon-gamma. We investigated the sera of seven patients with streptococcal tonsillitis and of four patients with STSS. Those with STSS showed higher serum neopterin concentrations (median: 152 nmol/l; 95th percentile in healthy controls: 8.7 nmol/l) than those with tonsillitis (median: 12 nmol/l). Similarly, kynurenine to tryptophan ratios were increased in tonsillitis and extremely high in patients with STSS. Highly increased neopterin production and tryptophan degradation in patients with STSS suggest an association between a high degree of T cell activation and the severity of the disease manifestation.
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PMID:Neopterin production and tryptophan degradation in humans infected by Streptococcus pyogenes. 1138 14

The human bacterial pathogen group A Streptococcus (GAS) causes many different diseases including pharyngitis, tonsillitis, impetigo, scarlet fever, streptococcal toxic shock syndrome, necrotizing fasciitis and myositis, and the post-infection sequelae glomerulonephritis and rheumatic fever. The frequency and severity of GAS infections increased in the 1980s and 1990s, but the cause of this increase is unknown. Recently, genome sequencing of serotype M1, M3 and M18 strains revealed many new proven or putative virulence factors that are encoded by phages or phage-like elements. Importantly, these genetic elements account for an unexpectedly large proportion of the difference in gene content between the three strains. These new genome-sequencing studies have provided evidence that temporally and geographically distinct epidemics, and the complex array of GAS clinical presentations, might be related in part to the acquisition or evolution of phage-encoded virulence factors. We anticipate that new phage-encoded virulence factors will be identified by sequencing the genomes of additional GAS strains, including organisms non-randomly associated with particular clinical syndromes.
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PMID:The fundamental contribution of phages to GAS evolution, genome diversification and strain emergence. 1241 16

An invasive beta-haemolytic Lancefield group A streptococcal (GAS) infection was diagnosed in 4 patients: a 70-year-old woman, her 71-year-old husband, a 62-year-old woman and her 43-year-old son. In the married couple the infection was caused by GAS-type TB3264M100. The woman had a pneumonia, whilst her husband developed a streptococcal toxic shock-like syndrome; he died. The other woman and her son were infected with GAS-type T6M6. The son died of a circulatory arrest due to necrotizing fascitis from a wound in his arm. His mother recovered following a severe tonsillitis. The number of invasive GAS infections has increased in the past decades. GAS infections occur mostly in isolated cases, but clusters of patients are also seen, like the two described here. The risk of an invasive GAS-infection is greatest if one has been in the neighbourhood of the index patient during the week prior to the diagnosis in that patient. According to the latest (American) guidelines, there is no reason for prophylactic treatment of the close contacts of patients.
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PMID:[Invasive infections due to group A beta-haemolytic streptococci in two families]. 1289 68

A rare case of primary peritonitis caused by group A beta-hemolytic streptococcus in previously healthy woman is presented. The entry site of infection was tonsillitis. Infection was complicated by soft-tissue infection of abdominal and thoracic wall, associated with toxic shock. Streptococcus growth was obtained in the cultures from the tonsils and blood. The patient underwent surgery: laparoscopy, laparotomy and multiple incisions in the phlegmon site. The lasting administration of penicillin caused recovery.
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PMID:[Primary peritonitis caused by group A beta-hemolytic streptococcus]. 1551 20

The grampositive bacterium S. pyogenes (beta-haemolytic group A Streptococcus) is a natural colonizer of the human oropharynx mucous membrane and one of the most common agents of infectious diseases in humans. S. pyogenes causes the widest range of disease in humans among all bacterial pathogens. It is responsible for various skin infections such as impetigo contagiosa and erysipelas, and localized mucous membrane infections of the oropharynx (e. g. tonsillitis and pharyngitis). Betahaemolytic group A Streptococcus causes also invasive diseases such as sepses including puerperal sepsis. Additionally, S. pyogenes induces toxin-mediated syndromes, i. e. scarlet fever, streptococcal toxic shock syndrome (STSS) and necrotizing fasciitis (NF). STSS and NF are severe, frequently fatal diseases that have emerged in Europe and Northern America during the last two decades. Finally, some immunpathological diseases such as acute rheumatic fever and glomerulonephritis also result from S. pyogenes infections. Most scientists recommend penicillins (benzylpenicillin, phenoxymethylpenicllin) as drugs of first choice for treatment of Streptococcus tonsillopharyngitis and scarlet fever. Erysipelas and some other skin infections should be treated with benzylpenicillin. Intensive care measurements are needed for treatment of severe toxin-mediated S. pyogenes diseases. These measurements include the elimination of internal bacterial foci, concomitant application of clindamycin and benzylpenicillin and suitable treatment of shock symptoms. Management of immunpathological diseases requires antiphlogistical therapy. Because of the wide distribution of S. pyogenes in the general population and the lack of an effective vaccine, possibilities for prevention allowing a suitable protection for diseases due to S. pyogenes are very limited.
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PMID:[Streptococcus pyogenes--much more than the aetiological agent of scarlet fever]. 1994 4

Group A streptococcus is a strict human pathogen that can cause a wide range of diseases, such as tonsillitis, impetigo, necrotizing fasciitis, toxic shock, and acute rheumatic fever. Modeling human diseases in animals is complicated, and rapid, simple, and cost-effective in vivo models of GAS infection are clearly lacking. Recently, the use of non-mammalian models to model human disease is starting to re-attract attention. Galleria mellonella larvae, also known as wax worms, have been investigated for modeling a number of bacterial pathogens, and have been shown to be a useful model to study pathogenesis of the M3 serotype of GAS. In this study we provide further evidence of the validity of the wax worm model by testing different GAS M-types, as well as investigating the effect of bacterial growth phase and incubation temperature on GAS virulence in this model. In contrast to previous studies, we show that the M-protein, among others, is an important virulence factor that can be effectively modeled in the wax worm. We also highlight the need for a more in-depth investigation of the effects of experimental design and wax worm supply before we can properly vindicate the wax worm model for studying GAS pathogenesis.
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PMID:Galleria mellonella larvae as an infection model for group A streptococcus. 2379 64


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