The effects of cortisone on bacterial infection; group A hemolytic streptococcal infection in rabbits.
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Neonatal group B streptococcal infection is frequent and may be responsible for lethal neonatal septicaemia. Its preventive treatment is still hotly debated. Digestive and genital tracts colonization is frequent in mother (15-20% of the cases) but it is unstable. About one out of two infants born of a colonized woman becomes colonized or infected. Neonates can also be colonized during their stay in maternity hospitals. Colonization is much more frequent than infection which strikes 0.2 to 0.6 per cent of neonates (at a very early period in two-thirds of the cases), but it jeopardizes their prognosis for life and later their functional prognosis. Prematurity and chorioamnionitis are the two main infection facilitating factors. Some of the various measures proposed to prevent infection in neonates, such as antibiotic therapy of colonized mothers during pregnancy and of symptomatic colonized neonates, do not seem to be effective, but others are interesting, including administration of antibiotics to mothers during delivery in high-risk situations, combined with early detection and immediate bactericidal treatment of neonatal infections.
Neonatal group B streptococcal infection is the primary cause of neonatal morbidity related to infection. It can often be prevented by identifying and treating pregnant women who carry group B streptococci or who are at highest risk of transmitting the bacteria to newborns. Increasing evidence and expert opinion support intrapartum treatment of women at relatively high risk of delivering an infant with group B streptococcal infection. Such women can be identified through the use of an anogenital culture for group B streptococci obtained at 35 to 37 weeks of gestation and by the presence of at least one of many risk factors associated with neonatal infection. These risk factors include preterm labor or rupture of the membranes at less than 37 weeks of gestation, previous delivery of an infant with invasive group B streptococcal disease, group B streptococcal bacteriuria during the present pregnancy, maternal intrapartum fever of 38 degrees C (100.4 degrees F) or higher and rupture of the fetal membranes for 18 hours or more. The recommended agent for intrapartum chemoprophylaxis is intravenous penicillin G; clindamycin is used in penicillin-allergic women. The use of risk markers alone to guide the administration of intrapartum antibiotics is much more cost-effective than other preventive strategies, but it exposes more women and infants to antibiotic-associated risks. Management of the infants of treated mothers is empiric and is currently guided by expert opinion.
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Group A streptococcal infection is associated with the occurrence of acute glomerulonephritis (AGN) and rheumatic fever (RF). A surveillance study in the Saga area, in northern Kyushu, Japan, showed a small variation in the reported number of group A streptococcal infections in the period 1988-94. However, of the AGN cases reported in this period, more than half were observed in 1992. In order to examine whether some change had occurred in the serotype distribution of Streptococcus pyogenes during the period, patients in the Saga area diagnosed as having group A streptococcal infection and patients with AGN or RF were analyzed. Serological T-typing of S. pyogenes was carried out for patients with group A streptococcal infections, and the association between the occurrence of AGN or RF and the distribution of each different T subtype was analyzed. M-typing of S. pyogenes was also carried out and the correlation between T and M types was examined. From 1988 to 1994, the annual number of patients with group A streptococcal infections in the Saga area showed a small variation, range 65-100 patients/year. Of the 42 patients with AGN and three with RF observed in this period, 27 with AGN (64%) and one with RF (33.3%) were detected in 1992. Only the T1 subtype increased in 1992; the other T subtypes showed little variation in incidence. The number of patients with the T1 subtype was significantly correlated with the occurrence of AGN by regression analysis (P < 0.01). Of the 170 subjects tested for both T and M subtypes, 44 of the 45 T1-typed subjects had the M1 protein. Our epidemiological study suggested that the T1 subtype of streptococcal infection was associated with an outbreak of AGN in 1992 in the Saga area.
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The frequency and severity of streptococcal infections and their sequelae have declined dramatically in the past century, yet the prevalence of streptococcal infections is still high. The reasons for this decline must be intimately related to host resistance, virulence of the agent, and environmental factors, especially crowding. Close examination of these fundamental influences does not reveal any evidence that humans have become less resistant to streptococcal infections, but they react less violently. There is some evidence that the agent may have lost a degree of its virulence. The decline in morbidity and mortality due to streptococcal infections began long before antibiotics, especially penicillin, were available. However, penicillin has proved to be an important factor in prevention of streptococcal infections, especially in rheumatic fever prophylaxis. There are certain indications that repeated streptococcal infections due to similar M types, occurring in young children over the past several decades, have resulted in some degree of immunity as well as the possible evolution of less virulent, but not less infectious, strains of group A streptococci. Also, a decrease in crowding would be expected to result in fewer streptococcal infections. Although there are more people in the world than at any other time in the history of man, urban population density in the western world, at least, is less than in the late 1800s and early 1900s.
Invasive group A streptococcal (GAS) infections have been of increasing concern worldwide during the past 15 years. Spread of group A streptococci to contacts with resulting invasive infection has been reported in families, in residential nursing homes, and even from patients to health care workers. We report an instance of temporally related life-threatening group A streptococcal infection in a husband and 2 weeks later in his wife. This example further emphasizes the need for careful observation among family members and other close contacts of patients with invasive group A streptococcal infection. Although at present there are no universal recommendations for monitoring or for antibiotic prophylaxis of close contacts of persons with invasive GAS infection, when added to existing literature, this report suggests additional consideration is required.
OBJECTIVE: To study recurrent group B streptococcal infection in adults. DESIGN: Patients with more than one reported group B streptococcal infection were identified through active surveillance for this infection. Sterile-site group B streptococcal isolates were evaluated for serotype and molecular subtyping using restriction endonuclease analysis of chromosomal DNA (REAC). SETTING: All acute-care hospitals in Maryland. PATIENTS: Nonpregnant residents of Maryland 18 years of age or older. RESULTS: 22 adults had at least two group B streptococcal episodes that were separated by 2 to 95 weeks (mean, 24 weeks). Of 395 patients with invasive group B streptococcal infection who survived the first episode and were followed for at least 1 year, 17 (4.3% [95% CI, 2.6% to 6.9%]) had more than one episode. Several patients were found to have endocarditis or osteomyelitis during the second episode. Group B streptococcal isolates from both episodes were obtained from 18 of 22 patients. Of the 18 isolate pairs, 13 (72% [CI, 46% to 90%]) had identical REAC patterns; the probability that at least 13 matches would be found by chance alone was less than 0.000001. Among patients with recurrent infection caused by the same strain, the interval between episodes was shorter (mean, 14 weeks) than that among patients with recurrent infection caused by another strain (mean, 43 weeks; P = 0.05). CONCLUSIONS: Recurrent group B streptococcal infection is common among adults and in most cases appears to be caused by relapse. The optimal management of adults with a first episode of group B streptococcal infection needs to be further defined to minimize the likelihood of recurrent disease.
From the mid-1980s, numerous reports of invasive group A streptococcal infections suggested that "highly virulent clones" were responsible. However, there have been virtually no extensive reports and comparisons of diverse temporal and geographic community isolates from uncomplicated throat infections to confirm the hypothesis. A unique collection of such "control" strains allowed in-depth assessment of association of M serotypes 1, 3, and 28 "clones" with invasive infections. Clones were defined by using small-fragment chromosomal restriction-enzyme analysis, pulsed-field gel electrophoresis, and M protein gene (emm) sequencing. After comparison with controls, no clone within these M serotypes had statistically increased association with invasive infections. The prevalence of specific virulence-associated clones appeared to essentially reflect their normal population prevalence. Although this does exclude other potential streptococcal factors, these findings suggest that host factors including individual and population-based immunity must also be significant in influencing infection potential.
UNLABELLED: We measured anti M protein antibody (AMPA) titres in children with idiopathic mitral regurgitation (MR), streptococcal infection, rheumatic fever (RF), post-streptococcal acute glomerulonephritis (AGN) and normal healthy children. We investigated the association of MR with streptococcal infection and whether high AMPA titres can be used as persisting evidence of previous streptococcal infection. AMPA titres were measured with an enzyme-linked immunosorbent assay. We found significantly higher antibody titres in patients with MR and in streptococcal infection, RF, and AGN than in healthy controls. In the MR group (n = 15), 54% patients had AMPA titres above the 90th percentile value that was found in normal controls. An elevated AMPA titre persisted for a long period even when the anti-streptolysin O titres had declined to normal in RF patients. Our data suggest that the high AMPA titres in MR should be further investigated to clarify the probable association with previous streptococcal infection. CONCLUSION: High AMPA titre is a risk factor for developing complications after streptococcal infection. Our serological evidence suggests that in some patients, MR may be related to previous streptococcal infection.
We explored the relationship between mutans streptococcal infection and the development of salivary IgA antibody during initial colonization. Repetitive swabbing (n = 292) of the teeth of 33 children revealed that 45% became infected with mutans streptococci between 13 and 36 months of age. In contrast, mutans streptococci could not be detected in 18 children whose last sample was taken at 39-81 months of age (median age = 62 months). During the period of mutans streptococcal infectivity, immunoglobulin A (IgA) antibody to several mutans streptococcal antigens appeared in most children, whether or not infection had been demonstrated. Robust responses to mutans streptococcal components occurred during or shortly after, but not before the period of mutans streptococcal infectivity. No consistent differences were observed among the summarized patterns of response of infected and uninfected groups of children, although the IgA Western blot patterns of individual subjects were often quite distinct. For example, sets of siblings, who would be presumed to be challenged with similar maternal mutans streptococcal clonotypes, were shown to develop qualitatively different salivary IgA responses to mutans streptococcal components. These results support a discrete period for mutans streptococcal infection and may suggest that the level of maternal infection is a factor in the success of infection of the child during this period. The data also suggest that exposure to mutans streptococci is a sufficient condition for robust mucosal IgA responses to mutans streptococcal antigens during the period of infectivity and that these responses may be different, even among siblings.
The research of antibodies for group A streptococcal polysaccharide (MSK) is affirming itself more and more for its value among serological researches of the streptococcal infection. Present work offers a compared evaluation between antipolysaccharidic C and antistreptolisinic titres, revealed during acute streptococcal infections, in paediatric practice. The study regards a group of a hundred children admitted in hospital for symptoms relating to streptococcal infection or upper respiratory tract infections of viral etiology (control group). The research of antipolysaccharidic C titer resulted positive in 88% of the streptococcal infection cases, against the positivity of 62% of ASO. The determination of MSK, already well-known for its quick reply, has shown its full value between the age-range of 1-3: in half of the cases regarding children below the age of 3, the ASO titer remained negative, instead there was a quick reply of MSK in all the cases: it is confirmed the utility of inserting the MSK among the screening tests of fever diseases of suspected bacterial nature in children.
Group B streptococcal infection has recently been recognised as an important and apparently increasingly common cause of invasive disease in nonpregnant adults. The annual incidence of invasive disease has been estimated at 4.4 per 100,000 nonpregnant adults and is highest among adults over 60 years of age. The most common clinical diagnoses include skin and soft-tissue infections, bacteraemia with no identified source, osteomyelitis, urosepsis and pneumonia. Other important but less common infections include peritonitis, infectious arthritis, meningitis and endocarditis. The majority of adults with group B streptococcal infections have underlying diseases including diabetes mellitus, malignant neoplasms and liver disease. Nosocomial infection and polymicrobial bacteraemia occur in a significant proportion of patients with invasive group B streptococcal disease. Mortality from invasive disease is particularly high in the elderly. For treatment of serious group B streptococcal infections, high doses of benzylpenicillin (penicillin G) are recommended because of the somewhat higher minimal inhibitory concentrations. In addition to parenteral antibiotic therapy surgical management may be required for successful treatment, particularly in the case of soft-tissue or bone infection. Invasive group B streptococcal infection is a major problem in elderly adults and those with chronic diseases, and efforts should be made to identify and treat such infections early. Future approaches may include vaccine prevention of serious group B streptococcal infection in adults at highest risk.
Most serious neonatal streptococcal infections are caused by group-B streptococci. The pattern of serious group-B neonatal disease in Britain resembles that described in other countries; both "early-onset" and "late-onset" forms are seen, but reliable incidence rates have not yet been determined. Serological-type III strains predominate in neonatal meningitis in Britain, but not so markedly as in some parts of the U.S.A. A deficiency of group-II strains in meningitis is, however, apparent in both countries. Present information about the carriage of group-B streptococci suggests that antibiotic prophylaxis administered to mothers or infants is unlikely to reduce greatly the frequency of "early-onset" disease. The continuous presence of a suitable chemical disinfectant in the vagina during labour might be more effective. Insufficient is known about the epidemiology of "late-onset" neonatal disease for rational preventive measures to be designed. More information is required about the postnatal acquisition of group-B streptococci by neonates and its sources, and about passive transfer of type-specific antibody from the mother to her child.
Streptococcal infection in children is usually benign and self-limited. In a small percentage of children, prominent neurologic and/or psychiatric sequelae can occur. Sydenham chorea is the best defined and best recognized. PANDAS (pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection) is a well-defined syndrome in which tics (motor and/or vocal) and/or obsessive-compulsive disorder consistently exacerbate in temporal correlation to a group A beta-hemolytic streptococcal infection. PANDAS constitutes a subset of children with tics, Tourette syndrome, and obsessive-compulsive disorder. In addition to strictly defined PANDAS, we and others have recognized several PANDAS variants, including adult-onset variant, a dystonic variant, a myoclonic variant, and a "chronic" PANDAS variant. The nosology and classification of these entities are rapidly evolving. The recognition that some pediatric neurobehavioral syndromes have infectious and/or immunologic triggers points to important new avenues of disease treatment. In this review, we summarize this complex and rapidly evolving area of clinical research.
The relationship between streptococcal infection and renal disease has been object of multiple studies. Streptococcal infection may induce acute glomerulonephritis or interstitial nephritis. We report a patient with a streptococcal infection who developed acute renal failure. The renal biopsy showed an acute interstitial nephritis, with an interstitium infiltrate with a significant number of eosinophils. We review the causes of acute renal failure associated with streptococcal infection, specially acute interstitial nephritis.
INTRODUCTION: Streptokinase use, in acute myocardial infarction, is hindered by failure to reperfuse (60%) and early reocclusion (16%). This phenomenon may, among other causes, be due to systemic inactivation of streptokinase, as well as streptokinase-induced platelet aggregation and clot propagation from antibodies to streptokinase produced after streptokinase administration or streptococcal infections. The purpose of this study was to determine the incidence of streptokinase-induced, antibody-mediated, platelet activation and aggregation after administration of SK or development of a streptococcal infection. MATERIALS AND METHODS: We included 45 normal volunteers (Control group), as well as 45 patients who had received streptokinase (Streptokinase group) and 13 who had suffered a severe streptococcal infection (Streptococcal infection group) within the past 3 years. Extent of streptokinase-induced, antibody-mediated, platelet activation and aggregation, as well as anti-streptokinase antibody and streptokinase resistance titers (lowest streptokinase concentration to cause clot lysis within 10 min) were measured. RESULTS: Whereas streptokinase-induced, antibody-mediated, platelet activation was observed in 49% of streptokinase patients and in only 17% and 15% of streptococcal infection patients and normal volunteers (p<0.05 Streptokinase vs. Control and Streptokinase vs. Streptococcal infection), streptokinase-induced platelet aggregation was observed in 23% of streptokinase patients and streptococcal infection patients, and in none of the control patients (p<0.05). CONCLUSIONS: Streptokinase-induced, antibody-mediated, platelet activation and aggregation occur in patients with high titers of anti-streptokinase antibody and may play a role in failure of streptokinase therapy. Streptococcal infection patients behave like streptokinase patients in terms of the reactivity of their platelets to subsequent streptokinase dose in vitro.