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PubMed1974

Cellular reactivity studies to streptococcal antigens. Migration inhibition studies in patients with streptococcal infections and rheumatic fever.

The question of whether hypersensitivity to streptococcal antigens plays a role in the pathogenesis of the nonsuppurative sequelae of streptococcal infections remains at present unclear. As a first step in the approach to this question, the degree of cellular reactivity of peripheral blood leucocytes to streptococcal antigens was investigated in a number of rheumatic fever patients, patients with uncomplicated streptococcal infections, as well as normal healthy subjects. Using the in vitro technique for the inhibition of capillary migration of peripheral blood leucocytes as an index of the degree of sensitivity to streptococcal antigens, the results indicate that patients with acute rheumatic fever exhibit an exaggerated cellular reactivity to these antigens and in particular to streptococcal cell membrane antigens. This abnormal response to streptococcal membrane antigens appears to persist in rheumatic subjects for at least 5 yr after the initial attack of rheumatic fever. Only Group A streptococcal membrane antigens elicited this unusual response in rheumatic subjects, since the cellular reactivity to Group C and D streptococcal membranes was the same in all groups. Patients with evidence of valvular disease exhibited the same degree of cellular reactivity to these antigens as did patients without clinical evidence of rheumatic heart disease. The nature of the antigens responsible for the observed cellular response remains unknown. Enzymatic treatment of streptococcal cell walls and membranes designed to remove type-specific M proteins did not alter the observed cellular reactivity to the streptococcal antigens. The finding that an abnormal cellular response to certain streptococcal antigens is present only in rheumatic patients suggests that cell-mediated factors may play an important role in the disease process.

Animals↗
PubMed2003

The Treatment of Severe Group A Streptococcal Infections.

Group A streptococci can cause a variety of diseases ranging from uncomplicated superficial infections to severe systemic infections associated with high morbidity and mortality. Since the late 1980s a drastic resurgence of highly aggressive invasive streptococcal infections, including streptococcal toxic shock syndrome and necrotizing fasciitis, have been noted worldwide. This has prompted intense research in the field and important new information has been gained regarding the pathogenesis and treatment of life-threatening invasive group A streptococcal infections. Exotoxins with superantigenic activities have been identified as central mediators of the systemic effects seen in streptococcal toxic shock syndrome. Novel therapeutic strategies include agents that can inhibit these superantigens, and one promising candidate is intravenous polyspecific immunoglobulin that contains neutralizing antibodies against a wide spectrum of streptococcal superantigens. Intravenous immunoglobulin adjunctive therapy was shown in a case-control study to reduce mortality in patients with streptococcal toxic shock syndrome.

Journal Article↗
PubMed1995

Kawasaki disease associated with streptococcal infection within a family.

OBJECTIVE: To describe the illness occurring in four members of a family, which had clinical and laboratory features of Kawasaki disease and streptococcal infection. METHODOLOGY: A retrospective report of three siblings and an adult male living in one household. The children had serology, blood counts, cultures and echocardiography performed and were treated with antibiotics and gammaglobulin infusions. RESULTS: The patients developed clinical, and exhibited laboratory, features suggesting streptococcal infection and 4/5 criteria suggesting the diagnosis of Kawasaki disease. All made a good clinical recovery but the youngest developed a coronary artery aneurysm. CONCLUSIONS: It may be difficult to distinguish streptococcal infection and Kawasaki disease. It is possible that some cases of Kawasaki disease are precipitated by streptococcal infection.

Adult↗
PubMed1992

Invasive group A streptococcal infections.

Beginning in the mid-1980s and continuing to the present, there has been an apparent increase in the number of severe group A streptococcal infections and their suppurative and nonsuppurative sequelae. The reasons for this epidemiologic change remain incompletely explained. At present, the data seem to suggest that this change is related to the reappearance in the population of not only "new" serotypes, but most likely virulent strains of these serotypes. This has been suggested by available epidemiologic surveys. The pathogenetic mechanism by which these virulent strains cause an increased severity of disease is also incompletely understood. It has been suggested that certain of the streptococcal pyrogenic exotoxins (pyrogenic exotoxin A or B) are associated with strains isolated from severe cases of systemic group A streptococcal infections, but the data conflict in many instances. Clinically, this is an extraordinarily virulent syndrome often leading to the death of the patient within a matter of hours or days. This is despite what would seem to be adequate and appropriate antimicrobial therapy with agents which are effective in vitro against the offending group A streptococcus. Therapy therefore is still based on appropriate antibiotic therapy and support of other systemic manifestations with appropriate medical therapy. At present, prevention of these suppurative and nonsuppurative sequelae is impractical simply because the initial streptococcal infection or colonization is rarely recognized. These events of the last half decade strongly support the need for additional understanding of the epidemiology, pathogenesis, treatment, and prevention of serious group A beta-hemolytic streptococcal infections.

Bacterial Toxins↗
PubMedDate not supplied

[Dynamics of streptococcal infections and prevention of post-streptococcal diseases in children's communities of Timişoara].

An analysis was carried out of the dynamics of circulation of the beta-haemolytic streptococcus in pre-school and in school children in the first two years of primary school. The study was performed simultaneously in two groups of children (an experimental and a control group) and allowed, after confrontation of the results obtained, to evaluate correctly the investigations performed, that is the detection of the acute disease and of healthy carriers by bacteriological examinations and early detection of post-streptococcal complications with the aid of serologic examinations (ASLO). The importance is stressed, of living conditions in the family and at school, as well as of individual factors (hereditary, hormonal, immunologic, etc.) in the development of late complications. Thus the measures proposed by the authors are aimed not only at the medical aspects, but also to the social-organizatoric ones.

Age Factors↗
PubMed1976

[Comparison of value of four immunological methods (AST, ADNase B, AHy, ANADase) by A-streptococcal infections and their significance in the routine diagnostic (author's transl)].

In the sera of approximately 600 patients of all age groups, who were on clinical suspicion of an A-streptococcal infection, AST, ADNase B, AHy and ANADase were determined. The ANADase alone detects 90% of the acute A-streptococcal infections, the AHy and the ADNase B 80% and the ASO 50%. In skin infections superinfected by A-streptococci, the AHy is positive in 85%, the ANADase in 80%, the ADNase B in 75% and the AST in 40% of the cases. The most frequent A-streptococcal infection, Angina tonsillaris, is determined in the best manner possible through the combination ADNase B + ANADase + AHy. According to the statistical evaluation, the ADNase B and the ANADase are the most reliable tests. The age group of the 4 to 15 year-olds reaches for ASO, ADNase B and AHy a percentage of highly increased titers twice as high in comparison with the adult group. In no case does one test determine 100% of the collective; therefore, a combination of several antibody reactions is desirable for the diagnosis. Increased titers should be checked every four weeks, also normal titers with patients, who continue on the clinical suspicion of having an A-streptococcal infection, because their blood sample may have been taken before the immune reaction occurred.

Adolescent↗
PubMed2002

Is parental report of upper respiratory infection at the onset of obsessive-compulsive disorder suggestive of pediatric autoimmune neuropsychiatric disorder associated with streptococcal infection?

The diagnosis of pediatric autoimmune neuropsychiatric disorder associated with streptococcal infection (PANDAS) requires a prospectively determined association between group A beta-hemolytic streptococcal (GABHS) infection and obsessive-compulsive disorder (OCD) or tic disorder. Screening for GABHS infection imposes a significant burden on both patient and clinician. To heighten the index of suspicion for PANDAS, it would be useful to know if parent-reported upper respiratory infection (URI) is associated with PANDAS symptoms or associated characteristics. Eighty-three consecutive, clinically referred patients aged 6 to 17 years with a primary diagnosis of OCD and their primary caregivers were asked about URI signs and symptoms at the time of OCD onset, PANDAS symptoms, OCD and tic symptoms, comorbidity, and putative PANDAS risk factors. Specific inquiry regarding URI symptoms proved more informative than general inquiry. In the URI present versus URI absent group, more patients experienced a sudden rather than insidious onset of symptoms. Additionally, more patients with a URI plus sudden onset exhibited a comorbid tic disorder. Until validated biomarkers permit retrospective diagnosis, a history that OCD began around the time of a URI should clue the clinician to look prospectively for PANDAS. Additional research is required to define the boundaries of PANDAS and to develop psychometrically reliable and valid diagnostic strategies.

Adolescent↗
PubMed1988

Perinatal group B streptococcal infections across intact amniotic membranes.

We reviewed the perinatal mortality due to group B streptococcal infection over a three-year period at a tertiary center. In 6 of 16 perinatal deaths due to group B Streptococcus, representing a range of gestational ages, infection occurred with the membranes intact. A review of reports from the obstetric and pediatric literature revealed that 10-50% of group B streptococcal infections occur in this manner. Several investigators of both animals and humans have demonstrated the pathophysiology of an ascending transamniotic infection. The current series emphasized this mode of infection in group B streptococcal disease.

Adult↗
PubMed1978

Overwhelming postoperative streptococcal infection.

Fulminant postoperative group A beta-hemolytic streptococcal infections present a serious and potentially lethal threat to children. Three children with severe postoperative streptococcal wound infections are presented. Each child developed high fever within the first 24 hr after surgery, followed shortly by signs of septic shock. In all patients, the clinical appreciation of wound infection became apparent late in the course of the illness. All three children had white blood cell counts below 6000/cu mm. One child developed crepitus in the incision; another showed radiographic evidence of free air in the soft tissues. The only survivor received antibiotics immediately following the initial fever along with re-exploration and drainage of the operative wound.

Anti-Bacterial Agents↗
PubMedDate not supplied

[Improvement of rapid laboratory methods for the diagnosis of streptococcal infections].

In 1975, clinical and epidemiological investigations were carried out on streptococcal infections, affecting 261 persons in a children's community. Rapid laboratory tests were used, employing commercial sodium amyl polyethylen microtablets. Of the total persons investigated 24.5% (64) presented primary streptococcal infections and 0.3% (1) complications. Environmental complications was 5% greater in the communities with scarlet fever foci than in the intact communities. The absence of late manifestations in the 1--4 year-old children attests to the effectiveness of the preventive measures taken.

Adult↗
PubMed2001

Paediatric autoimmune neuropsychiatric disorders associated with streptococcal infection (PANDAS).

The evidence to date, both published and unpublished, which addresses the validity of the proposed unique subgroup of children with early and abrupt onset of obsessive--compulsive disorder (OCD) and/or tic disorders subsequent to streptococcal infections was reviewed. The aetiology of OCD and tic disorders is unknown, although it appears that both disorders may arise from a variety of genetic and environmental factors. Post-streptococcal autoimmunity has been postulated as one possible mechanism for some. The acronym PANDAS (for paediatric autoimmune neuropsychiatric disorders associated with streptococcal infections) has been given to a subgroup of paediatric patients who meet five inclusionary criteria: presence of OCD and/or tic disorder, pre-pubertal symptom onset, sudden onset or episodic course of symptoms, temporal association between streptococcal infections and neuropsychiatric symptom exacerbations, and associated neurological abnormalities. The proposed model of pathophysiology provides for several unique treatment strategies, including the use of antibiotic prophylaxis to prevent streptococcal-triggered exacerbations, and the use of immunomodulatory interventions (such as intravenous immunoglobulin or therapeutic plasma exchange) in the treatment severe neuropsychiatric symptoms. For the latter study group, long-term (2--5 yr) follow-up revealed continued symptom improvement for the majority of patients, particularly when antibiotic prophylaxis had been effective in preventing recurrent streptococcal infections. In addition, the episodic nature of the subgroup's illness provides for opportunities to study brain structure and function during health and disease, as well as allowing for investigations of the aetiologic role of anti-neuronal antibodies and neuroimmune dysfunction in both OCD and tic disorders. Although much research remains to be done, an increasing body of evidence provides support for the postulate that OCD and tic disorders may arise from post-streptococcal autoimmunity. The unique clinical characteristics of the PANDAS subgroup, the presence of volumetric changes in the basal ganglia, and the dramatic response to immunomodulatory treatments, suggest that symptoms arise from a combination of local, regional and systemic dysfunction. Ongoing research is directed at understanding the nature of the abnormal immune response, as well as identifying at-risk children, in order to provide for novel strategies of prevention and treatment.

Age of Onset↗
PubMed1992

Outbreak of group A streptococcal infection in a day-care center.

During an outbreak of streptococcal infections in a day-care center it is often difficult to determine the source and extent of the outbreak and the optimal means of management. An intervention strategy based on repeated throat cultures and initial antibiotic treatment of culture-positive individuals was used during an outbreak of respiratory tract infections with Group A streptococci at a day-care center. The spread of streptococci carriers was studied. Two weeks after the diagnosis of the index case, 61% of the 30 children were colonized with Group A streptococci. From 20 to 30% of the children remained streptococcal carriers, but they did not give rise to secondary cases. Initially the environment was heavily contaminated with Group A streptococci. Damp material might constitute a potential source of streptococcal spread. All Group A streptococcal strains belonged to the same serotype, T12M12. Prompt recognition and intervention are important to prevent spread of streptococcal infection to many day-care attenders.

Child↗
PubMed2000

Inverse relation between disease severity and expression of the streptococcal cysteine protease, SpeB, among clonal M1T1 isolates recovered from invasive group A streptococcal infection cases.

The streptococcal cysteine protease (SpeB) is one of the major virulence factors produced by group A streptococci (GAS). In this study we investigated if differences exist in SpeB production by clonally related M1T1 clinical isolates derived from patients with invasive infections. Twenty-nine of these isolates were from nonsevere cases and 48 were from severe cases, including streptococcal toxic shock syndrome (STSS) and necrotizing fasciitis (NF) cases. The expression and amount of the 28-kDa SpeB protein produced were determined by quantitative Western blotting, and protease activity was measured by a fluorescent enzymatic assay. A high degree of variation in SpeB expression was seen among the isolates, and this variation seemed to correlate with the severity and/or clinical manifestation of the invasive infection. The mean amount of 28-kDa SpeB protein and cysteine protease activity produced by isolates from nonsevere cases was significantly higher than that from STSS cases (P = 0.001). This difference was partly due to the fact that 41% of STSS isolates produced little or no SpeB compared to only 14% of isolates recovered in nonsevere cases. Moreover, the cysteine protease activity among those isolates that expressed SpeB was significantly lower for STSS isolates than for isolates from nonsevere cases (P = 0.001). Increased SpeB production was also inversely correlated with intact M protein expression, and inhibition of cysteine protease activity blocked the cleavage of the surface M protein. Together, the data support the existence of both an "on-off" and a posttranslational regulatory mechanism(s) controlling SpeB production, and they suggest that isolates with the speB gene in the "off" state are more likely to spare the surface M protein and to be isolated from cases of severe rather than nonsevere invasive infection. These findings may have important implications for the role of SpeB in host-pathogen interactions via regulation of the expression of GAS virulence genes and the severity of invasive disease.

Antigens, Bacterial↗
PubMed2004

Inhibition of streptokinase-induced, antibody-mediated platelet aggregation with tirofiban after exposure to streptokinase or streptococcal infection.

STUDY OBJECTIVE: To evaluate the effect of tirofiban (a glycoprotein IIb-IIIa inhibitor) in preventing streptokinase-induced, antibody-mediated platelet aggregation after administration of streptokinase or development of a streptococcal infection. DESIGN: Prospective analysis. SETTING: Research center of a Canadian hospital. PARTICIPANTS: Forty-five healthy volunteers, 45 patients who had received streptokinase within the past 3 years, and 13 patients who had a severe streptococcal infection also within the past 3 years. INTERVENTION: Blood samples were drawn to measure the extent of inhibition of streptokinase-induced, antibody-mediated platelet activation and aggregation by tirofiban. MEASUREMENTS AND MAIN RESULTS: Platelet aggregation was measured by using a turbidimetric method. The extent of inhibition by tirofiban was measured by incubating tirofiban for 2 minutes before adding streptokinase 5000 U/ml. Also, tirofiban was added 2 minutes before adding adenosine 5'-diphosphate (ADP) 2 microM/L into the last tube as a comparison. Strepto-kinase-induced, antibody-mediated platelet aggregation was observed in 10 (22%) of the 45 patients treated with streptokinase, in 3 (23%) of the 13 patients with streptococcal infection, and in none of the 45 healthy volunteers. Tirofiban inhibited streptokinase-induced, antibody-mediated platelet aggregation by 89 +/- 14% (p<0.001). Similarly, ADP-induced platelet aggregation was inhibited by 92 +/- 6% (p<0.001) with tirofiban. CONCLUSION: Streptokinase-induced, antibody-mediated platelet aggregation occurred in 13 (22%) of 58 patients who received streptokinase or were exposed to a streptococcal infection in the past 3 years. Such patients may not benefit from streptokinase therapy. In these patients, tirofiban significantly decreased the extent of antistreptokinase antibody-mediated platelet aggregation. Hence, patients undergoing streptokinase therapy may benefit from tirofiban as adjunctive therapy.

Adult↗
PubMed1992

Clusters of invasive group A streptococcal infections in family, hospital, and nursing home settings.

The spread of group A streptococcal infection to close contacts of infected persons is well recognized. With the resurgence of invasive group A streptococcal infections, there is an increased potential for clusters of patients with invasive disease. We reviewed data collected since December 1988 at the Centers for Disease Control (Atlanta) to identify clusters of infection in which one or more patients had invasive disease. Twelve family clusters were identified. Infection in index cases included the toxic shock-like syndrome and septicemia. Infection in family contacts included invasive infections, pharyngitis, or asymptomatic carriage. Most invasive disease occurred in adults, while the majority of noninvasive infections were in children. Five nosocomial clusters with spread of infection from patients to hospital personnel were documented. All index patients had the toxic shock-like syndrome; secondary infections included the toxic shock-like syndrome, pneumonia, bullous cellulitis, lymphangitis, and pharyngitis. Clusters of invasive infections also were identified in five nursing homes. Pneumonia, cutaneous infections, and the toxic shock-like syndrome occurred most commonly. Clustering by nursing home unit occurred in three outbreaks. In hospitals and nursing homes, improved infection control will likely decrease secondary spread; in families, spread of disease may be prevented by identifying and treating those harboring the organism or by chemoprophylaxis. Studies that characterize the rate of secondary infection are needed before definitive recommendations can be made.

Adult↗