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)

Azithromycin (AZM), a new macrolide antibiotic, in fine granules and in capsules was studied for pharmacokinetic and clinical evaluations. 1. Antibacterial activities. MIC profile of AZM was as follows: 0.78 approximately 1.56 micrograms/ml against Staphylococcus aureus, < or = 0.025 approximately 0.10 microgram/ml against Streptococcus pyogenes, 0.10 approximately 0.39 and 6.25 micrograms/ml against Streptococcus pneumoniae, < or = 0.025 approximately 0.39 microgram/ml against Moraxella(Branhamella) catarrhalis, 0.39 approximately 3.13 micrograms/ml against Haemophilus influenzae, and 0.20 approximately 6.25 micrograms/ml against Haemophilus parainfluenzae. 2. Absorption and excretion. The elimination half-life of AZM after its administration at 10 mg/kg/day for three days was 28.1 approximately 46.1 hours. The cumulative urinary excretion rate in the first 120 hours after start of treatment was 4.01 approximately 8.47%. 3. Clinical evaluation. AZM was given to 76 pediatric patients to treat following infections: pharyngitis in seven, tonsillitis in 11, bronchitis in 11, pneumonia in 19, Mycoplasma pneumonia in eight, scarlet fever in 13, infective enteritis in one, SSTI in four, and otitis media in two. Effectiveness of AZM was assessed in 75 patients and the drug was rated "excellent" or "good" in 71 resulting in an efficacy rate of 94.7%, 87.0% of the 46 cases indicated that AZM had eradicated bacteria identified before the treatment. One patient complained of moderate diarrhea which disappeared after treatment of anti-diarrheic. Abnormal laboratory changes were reported in 12 patients in the following: decreased leukocytes in eight, increased eosinophils in two, increased platelet count in one, and increased GPT in one. All cases of abnormality was deemed mild in severity and clinically insignificant.
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PMID:[Pharmacokinetic and clinical evaluation of azithromycin using fine granules or capsules in the pediatric patients]. 898 10

The presence of gene encoding erythrogenic toxin type A (spe A) was determined by the polymerase chain reaction (PCR) to target specific sequences in 72 strains of Streptococcus pyogenes representative T type strains, which were associated with scarlet fever, impetigo, tonsillitis, isolated between the years 1980-1982 and in 1995 by carriers. Isolates showed statistically significant differences in the presence of spe A. With scarlet fever the strains had a 22.22% association, with impetigo had a 8.33% association. With tonsillitis' and with carriers had a low association, 5.55% and 6.9% respectively. The analysis of the data indicated that strains with certain T type surface antigens showed a higher (such as T-1, T-2, T-5) or lower (such as T-4, T-13, T-27) tendency to contain the spe A gene were more likely to be associated with scarlet fever and impetigo than with other types of diseases.
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PMID:Streptococcal erythrogenic toxin spe A gene detection by polymerase chain reaction in strains isolated in Albania. 974 27

Infection with group A beta-hemolytic streptococci (GABHS) is the most common bacterial cause of acute pharyngitis and tonsillitis beyond infancy. We report on two patients with scarlet fever associated with hepatitis. The patients (boys aged 6 and 7 years) both presented with a scarlatiniform rash, dark urine and light-colored stools. Laboratory studies revealed elevated liver transaminases and negative antibody tests against hepatitis viruses A, B and C, cytomegalovirus and Epstein-Barr virus. Both patients were treated with antibiotics and recovered completely within a few days. Although the association between scarlet fever and hepatitis has been known for many decades, the pathogenesis is still unknown. Physicians treating patients with group A beta-hemolytic streptococcal infections should be aware of possible hepatic involvement.
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PMID:Scarlet fever associated with hepatitis--a report of two cases. 1096 36

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

In the German Health Interview and Examination Survey for Children and Adolescents (KiGGS), which was conducted from 2003 to 2006, data on acute/infectious and chronic diseases were collected from a population-based sample of 17,641 subjects aged 0 to 17 years. The annual prevalence rates among acute diseases vary widely. Children and adolescents are most frequently affected by acute (infectious) respiratory conditions. 88.5 % of the surveyed children and adolescents experienced at least one episode of common cold within the last 12 months. Among the other acute respiratory infections, bronchitis and tonsillitis were the most frequently encountered conditions with 19.9 % and 18.5 %, respectively. The 12-month prevalence of otitis media and pseudocroup was 11 % and 6.6 %, respectively. 1.5 % of the children and adolescents experienced an episode of pneumonia. Apart from respiratory infections, gastrointestinal infections were very frequently stated as reasons for acute illness. Furthermore, 12.8 % of the children and adolescents experienced a herpetic infection, 7.8 % a conjunctivitis and 4.8 % a urinary tract infection. Lifetime prevalence rates of infectious diseases were as follows: pertussis 8.7 %, measles 7.4 %, mumps 4.0 %, rubella 8.5 %, varicella 70.6 %, scarlet fever 23.5 %. The various chronic somatic diseases in children and adolescents had different lifetime prevalence rates. Most frequently, children and adolescents were affected by obstructive bronchitis (13.3 %), neurodermatitis/atopic eczema (13.2 %) and hay fever (10.7 %). Scoliosis and asthma had been diagnosed by a doctor in 5.2 % and 4.7 % of subjects aged 0-17 years, respectively. The lifetime prevalence rates of the remaining diseases varied between 0.14 % for diabetes mellitus and 3.6 % for convulsions/epileptic fits. For the first time ever, these survey results provide nationwide representative information on the prevalence rates of acute/infectious and chronic diseases in children and adolescents which is based on a population-representative sample.
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PMID:[Prevalence of somatic diseases in German children and adolescents. Results of the German Health Interview and Examination Survey for Children and Adolescents (KiGGS)]. 1751 53

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

Scarlet fever, an infection caused by toxin-producing strains of Streptococcus pyogenes, was associated with high levels of morbidity and mortality when epidemics were common in the 18th and 19th centuries throughout Europe and the USA.1 Although this disease nearly disappeared during the 20th century, several countries, including the UK, have recently experienced a re-emergence of scarlet fever.1-3 However, the reason for these new outbreaks remains unclear.1,4 Despite a general move to reduce the use of antibiotics for many mild self-limiting infections (e.g. tonsillitis, sinusitis), national guidance recommends treating people with scarlet fever with antibiotics regardless of severity of illness to speed recovery, to reduce the length of time the infection is contagious and to reduce the risk of complications.5,6 Here, we discuss the management of scarlet fever in the UK.
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PMID:Managing scarlet fever. 2888 51

Tonsillitis is an extremely common condition, usually it is self-limiting, of viral origin, and managed conservatively in general practice. Rarely patients require inpatient management, usually when bacterial infection is present or when the cause is virulent organisms such as Epstein Barr virus. Complications can be divided into non-suppurative; sepsis, scarlet fever, rheumatic fever, glomerulonephritis and Lemierres disease, and suppurative; quinsy, parapharyngeal abscess and retropharyngeal abscess, respectively. Anecdotally, there is concern that modern medical practice that counsels vigilance against overuse of antibiotics, could lead to increased complications of tonsillitis. We report a case of an otherwise healthy man who presented with dysphagia, odynophagia and neck pain following a sore throat. Despite antibiotic treatment he developed an intramural oesophageal abscess, to our knowledge, an unreported complication of tonsillitis.
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PMID:Intramural oesophageal abscess: an unusual complication of tonsillitis. 3073 46

Stuttering is one of the most well-known speech disorders, but the underlying neurological mechanisms are debated. In addition to genetic factors, there are also major non-genetic contributions. It is here proposed that infection with group A beta-hemolytic streptococcus (GAS) was a major underlying cause of stuttering until the mid-1900s when penicillin was introduced in 1943. The main mechanism proposed is an autoimmune reaction from tonsillitis, targeting specific molecules, for example within the basal ganglia. It is here also proposed that GAS infections may have continued to cause stuttering to some extent, to the present date, though more rarely. If so, early diagnosis of such cases would be of importance. Childhood cases with sudden onset of stuttering after throat infection may be particularly important to assess for possible GAS infection. The support for this hypothesis primarily comes from three lines of argument. First, medical record data from the 1930s strongly indicates that there was one type of medical event in particular that preceded the onset of childhood stuttering with unexpected frequency: diseases related to GAS throat infections. In particular, this included tonsillitis and scarlet fever, but also rheumatic fever. Rheumatic fever is a childhood autoimmune sequela of GAS infection, which was a relatively widespread medical problem until the early 1960s. Second, available reports of changes of the childhood prevalence of stuttering indicate striking parallels between stuttering and the incidence of rheumatic fever, with: (1) decline from the early 1900s; (2) marked decline from the introduction of penicillin in the mid 1940s; and (3) reaching a more stable level in the 1960s. The correlations between the data for stuttering and rheumatic fever after the introduction of penicillin are very high, at about 0.95. Third, there are established biological mechanisms linking GAS tonsillitis to immunological effects on the brain. Also, a small number of more recent case reports have provided further support for the hypothesis linking stuttering to GAS infection. Overall, it is proposed that the available data provides strong evidence for the hypothesis that GAS infection was a major cause of stuttering until the mid-1900s, interacting with genetic predisposition.
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PMID:Streptococcal Infection as a Major Historical Cause of Stuttering: Data, Mechanisms, and Current Importance. 3330 52


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