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Deficiency of maternal group B streptococcal (GBS) type-specific IgG increases neonatal susceptibility to GBS infection. We asked if immunization-induced maternal type III GBS opsonic antibody transferred prenatally (via placenta) or postnatally (via breast milk) would affect suckling rat survival after GBS infection. Pregnant immunized dams with type III GBS opsonic antibody (20 through 320 dil-1) and nonimmunized dams without GBS antibody were matched (n = 16). Half of each litter was cross-suckled to a matching dam creating four pup groups with different exposure to maternal type III GBS opsonic antibody: none, postnatal, prenatal, and combined (pre- and postnatal). After infection with type III GBS, group survival (n) was 41% (51), 66% (47), 98% (43), and 98% (47), respectively. Type III GBS opsonic antibody in surviving pups was directly related to their immunized dam's antibody either postnatally (R = 0.85), prenatally (R = 0.84), or combined (R = 0.81). Pups exposed postnatally to high titers (80 to 320 dilution-1) of type III GBS opsonic antibody survived more often than those exposed to low titers (20 to 40 dil-1) (p less than 0.03). Immunization-induced maternal type III GBS opsonic antibody is transferred pre- and postnatally and results in improved neonatal survival after GBS infection. Survival of pups exposed to postnatal antibody appears related to the concentration of maternal type III GBS opsonic antibody. Breast milk with high titers of GBS type-specific antibody may modify the course of GBS infection. GBS vaccines and strategies could be tested in this model.
The comparative study of different protein bases has shown that the combined base containing animal blood hydrolysate (amino peptide) and acidic casein hydrolysate, moderately cleaved, in the proportion 1:1 is a good source of nitrogen and ensures the intensive growth of streptococci. As determined by the study of the physiological parameters and growth of streptococci, the presence of fodder yeast extract, glutamine, glucose and phosphates in media containing blood hydrolysate and casein hydrolysate has been found to render a stimulating effect on the growth and multiplication of these organisms. The data thus obtained have been used as the basis for developing the formula of a dried culture medium, capable of ensuring the growth of streptococci without blood or serum added and not inferior in its quality to Todd-Hewitt Broth manufactured by Oxoid Ltd. (Great Britain) and Difco Laboratories (USA). The physico-chemical and physiological characteristics of the proposed medium have been determined. The use of the new dried culture medium in medical practice will make it possible to improve the microbiological diagnosis of streptococcal infections.
A study was done on school children infected with group A beta hemolytic streptococci to examine whether antioxidant vitamins play a role in improving the hemoglobin level. A total of 606 primary school children aged 5 to 15 years were randomly divided into two intervention groups. Group 1 (n=299) was treated with pehnoxymethyl penicillin V and group 2 (n=307) was treated with phenoxymethyl penicillin V plus antioxidant vitamins for eight weeks. From each group two blood samples were drawn in acute and convalescent (after eight weeks) states. Before treatment, mean hemoglobin values were 11.0 and 10.8 mg/dL in groups 1 and 2 respectively. After treatment hemoglobin values were 10.5 and 11.6 mg/dL respectively. Values were significantly decreased in group 1 (P=0.0001), whereas increased in group 2 (P=0.001). Adjustment for age and sex by ANCOVA confirmed the difference in hemoglobin levels between group (LS means-0.5 vs 0.8 in groups 1 and 2 respectively (P=0.0001). Hemoglobin level increases after antioxidant vitamin supplementation in children suffering from group A beta hemolytic streptococcal infection.
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STUDY OBJECTIVE: To alert practicing emergency physicians to an important and possibly increasing relationship between life-threatening group A beta-hemolytic streptococcal (GABHS) infections and children recovering from varicella. DESIGN: A case series of six patients managed from January through March 1993. SETTING: A university-affiliated pediatric specialty emergency department. TYPE OF PARTICIPANTS: Six previously healthy immunocompetent children between 1 and 5 years of age seen in our ED over a nine-week period. RESULTS: Six children had onset of varicella two days to two weeks before developing a serious life-threatening GABHS infection. Children presented with clinical symptoms of invasive GABHS infection with bacteremia (one patient); streptococcal toxic shock syndrome with negative blood culture (two), pneumonia with pleural effusion and streptococcal toxic shock syndrome (one), pneumonia with pleural effusion (one), and pyomyositis of the thigh (one). Four of six patients required intensive care admissions and aggressive support of vital signs. All six survived. CONCLUSION: Emergency physicians should be aware of the association between varicella and serious GABHS infections and be prepared to recognize and aggressively manage serious complications should they occur.
Rheumatic fever is an immunologically mediated disease that follows infection by group A beta-hemolytic Streptococcus (GABHS). In rheumatic fever, antibodies generated against GABHS cross-react with the heart, joints, skin, and other sites, inducing an inflammatory, multisystem disease. Brain tissue-specific antibodies have been demonstrated in a subset of children with Sydenham chorea (a component of the Jones criteria for the diagnosis of rheumatic fever), and most Sydenham chorea patients manifest obsessive-compulsive symptoms very similar to those in traditional obsessive-compulsive disorder. The parallels drawn from the paradigm of Sydenham's chorea to Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections (PANDAS) is an area of active controversy. Newly emerging information on the role of GABHS superantigens in the pathogenesis of rheumatic fever is of particular interest. In this article, we review the microbial characteristics of GABHS and the subsequent immune responses to GABHS as a possible etiology of PANDAS.
Infective endocarditis (IE) is a life-threatening disease most often caused by blood-borne bacteria that infect previously damaged cardiac tissue. Despite the importance of this disease, the genetic basis for IE-associated fitness remains poorly defined. Here, we present the first genome-wide in vivo analysis of bacterial fitness in a vertebrate model of IE. We identified 146 genes in Streptococcus sanguinis required for IE fitness, the majority of which had not previously been linked to endocarditis. These determinants cluster into conserved metabolic, cell envelope, transport, and regulatory pathways, representing a vast reservoir of potential targets for novel antimicrobial intervention. A subset of these genes was examined in Streptococcus mutans; all were found to be essential for IE fitness in this distantly related oral species as well, suggesting broad conservation. Using experimental evolution, we further show that disruption of key fitness pathways triggers reproducible compensatory "bypass" mechanisms. Together, these findings provide a comprehensive, genome-wide map of the bacterial niche-requirements for streptococcal infective endocarditis.
Tissue cages implanted subcutaneously were used to infect rabbits with erythrogenic toxin (ET) producing streptococci. The in-vivo production of ET was followed during the infection by immunoprecipitation analyses of the tissue cage fluid (TCF). ET types A and C were mainly detected during the first week of infection, but, as late as 4 weeks after the inoculation, ET was occasionally found in TCF. The nonspecific mitogenic activity of ET on human lymphocytes was also used as a biological marker to recognize ET in TCF. Mitogenic activity was detected in 90% of samples during the first week. In order to characterize the mitogenic material released by growing streptococci, TCF was electrofocused in polyacrylamide gel. The eluates of sliced gels were checked for mitogenic activity and compared with a purified ET preparation containing ET types A and C. It could be verified that ET type A was produced under in-vivo conditions by strains NY-5 and SF130, while ET type C was produced by strain T18. Differences between production of toxins in vitro and in vivo might be of significance for the understanding of the pathogenetic mechanisms in streptococcal infection.
Two boys developed rhythmic involuntary movements in the extremities on one side of the body after febrile illness. They also showed behavioral disturbances. In both patients, serum antistreptolysin-O and antistreptokinase titers were elevated in acute illness and decreased a few months later. One patient showed tremorous movement, and the other choreiform movement. In the former, a surface EMG showed short-duration (30 to 60 ms), highly frequent (6 to 8 Hz) and synchronous discharges of multiple muscles, including the antagonists, suggesting myoclonic jerk. In the latter, a surface EMG showed long-duration (0.5 to 1 s), repetitive (about 0.5 Hz) and synchronous or asynchronous discharges of the antagonists, suggesting choreoathetosis. In both patients, giant somatosensory evoked potentials and high-voltage slow EEG activities were observed predominantly in the hemisphere contralateral to the involuntary movement. In the myoclonic patient, long-latency EMG responses were enhanced and cortical potentials preceding the myoclonus were present by jerk-locked back averaging technique. The present data suggest that unilateral rhythmic involuntary movements occur secondary to streptococcal infection. The pathophysiology of the involuntary movements may be associated with sensorimotor cortex hyperexcitability.
Serial observations including cultures of the upper respiratory tract and of infected skin lesions and streptococcal antibody determinations were made over a two-year period in a semi-closed population of children between 10 months and 15 years of age. There was a high prevalence of group A streptococci in nose and throat cultures and of skin lesions containing these organisms. Almost 90% of the study population developed streptococcal impetigo during the study period. A slightly higher proportion of males than females developed skin infection but there was no relationship to age. Impetigo was observed throughout the calendar year, exceeding 12% of child-visits in one winter month, but was generally more common in the summer and fall. Conversely, group A streptococci were more often isolated from nose and throat cultures in the winter months. The increase in recovery of streptococci from nose and throat cultures lagged behind the increase in streptococcal impetigo and continued into the winter months, when the prevalence of impetigo had declined. Calculation of ratios for individual streptococcal serotypes isolated from different body sites revealed a clear cut distinction between "respiratory" and "impetigo" serotypes, with respect to both prevalence and acquisition rates. Respiratory serotypes were more commonly isolated in the winter and impetigo serotypes in the summer and fall. Significant antibody responses to extracellular antigens of the streptococcus were documented for pharyngeal acquisitions of both impetigo and respiratory serotypes and for skin lesions associated with impetigo serotypes. Group A streptococcal serotypes may be divided into three categories on the basis of their human pathogenicity for body sites: some with the potential for respiratory infection, others with the potential for skin infection and a few unusual serotypes with the potential for infecting both sites.
The surface M protein of group A streptococci (GAS) is one of the major virulence factors for this pathogen. Antibodies to the M protein can facilitate opsonophagocytosis by phagocytic cells present in human blood. We investigated whether pooled normal immunoglobulin G (IVIG) contains antibodies that can opsonize and enhance the phagocytosis of type M1 strains of GAS and whether the levels of these antibodies vary for different IVIG preparations. We focused on the presence of anti-M1 antibodies because the M1T1 serotype accounts for the majority of recent invasive GAS clinical isolates in our surveillance studies. The level of anti-M1 antibodies in three commercial IVIG preparations was determined by enzyme-linked immunosorbent assay (ELISA), and the opsonic activity of these antibodies was determined by neutrophil-mediated opsonophagocytosis of a representative M1T1 isolate. High levels of opsonic anti-M1 antibodies were found in all IVIG preparations tested, and there was a good correlation between ELISA titers and opsonophagocytic activity. However, there was no significant difference in the levels of opsonic anti-M1 antibodies among the various IVIG preparations or lots tested. Adsorption of IVIG with M1T1 bacteria removed the anti-M1 opsonic activity, while the level of anti-M3 opsonophagocytosis was unchanged. Plasma was obtained from seven patients with streptococcal toxic shock syndrome who received IVIG therapy, and the level of anti-M1 antibodies was assessed before and after IVIG administration. A significant increase in the level of type M1-specific antibodies was found in the plasma of all patients who received IVIG therapy (P < 0.006). The results reveal another potential mechanism by which IVIG can ameliorate severe invasive group A streptococcal infections.
Antistreptolysin antibodies were estimated in 787 normal children and young adults by latex test. This test detects titres of 200 IU/ml and above, which is the western cut off point, for diagnosis. Children below one year showed no antibodies. Unlike western studies where no antibodies are detected below the age of 3 years, our study revealed that 7.9% children between 1-3 years had significantly elevated antibodies. This epidemiological pattern is well reflected in the different clinical profile of younger children developing rheumatic heart disease in our country. Antibodies progressively increased with age--11.8% in 4-8 years group to 15.8% in 9-12 years age group. All these were from the lower socio-economic group. ASO was positive in 16.7% of young adults from lower socio-economic status while it was positive only in 9.2% in the upper socio-economic status. A total of 522 patients of rheumatic carditis were studied. Only 23.4% had no antibodies or less than 200 IU/ml, and 77% were positive (26.9% had greater than 400 IU/ml and 49.7% had 200 IU/ml). Throat swab culture and ASO antibodies were done simultaneously in 76 outdoor patients, clinically diagnosed as acute bacterial pharyngitis. Group A beta hemolytic streptococci were isolated in 64% and significant antistreptolysin antibodies were seen in 62%. School health records were scanned in more than 50,000 school children. Point prevalence of rheumatic heart disease was estimated to be 0.17% in lower and 0.05% in upper socio-economic groups. Age and socio-economic factors are important variables in epidemiology of streptococcal infection.(ABSTRACT TRUNCATED AT 250 WORDS)
OBJECTIVES: The objective of the study is to determine if the presence of antistreptokinase (ASK) antibody in the blood, leads to ineffective thrombolytic therapy with streptokinase (SK) in acute myocardial infarction (AMI) and to investigate if increased dose of streptokinase (2.5 million units) could improve the infarct-related artery (IRA) patency or the clinical outcome in these patients. METHODS: The study was conducted between 1994 and 2001 in 2 institutions; King Fahd Armed Forces Hospital, Jeddah, Saudi Arabia and in Kasr El-Aini Faculty of Medicine, Cairo, Egypt. Fifty consecutive patients with acute myocardial infarction (AMI) were included in this prospective double blind, randomized study. All patients were given the allocated streptokinase dose (1.5 or 2.5 million units) and underwent angiography within 24 hours to establish the anatomy of coronary arteries and the patency of infarct-related artery. Antistreptokinase antibody assay was carried out in a core laboratory. RESULTS: The study results showed that the presence of ASK antibody or the administration of an increased dose of SK had no effect on improving the patency rate of the infarct-related artery. CONCLUSION: The presence of a previous streptococcal infection may not necessarily reduce the effect of SK on the patency of the IRA and/or clinical outcome in patients presenting with AMI. The administration of a larger than currently recommended dose of SK (2.5 million units) did not alter the clinical outcome because it did not improve the patency rate of the IRA. However, a larger study is needed to confirm these observations.
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