Antistreptococcal Antibodies Research Articles

Increased Antistreptococcal Antibody Titers and Anti—Basal Ganglia Antibodies in Patients With Tourette Syndrome: Controlled Cross-Sectional Study

The association between Tourette syndrome, attention-deficit hyperactivity disorder (ADHD), and obsessive-compulsive disorder following streptococcal infections has been documented, but with conflicting reports. We thus felt it was important to investigate this association in a group of Italian patients not previously documented. We took blood on 69 patients with Tourette syndrome and 72 age- and sex-matched tic-free controls. Laboratory staff were blind to the diagnostic status of the subjects. Evidence of recent streptococcal infection was defined using antistreptolysin titers. Anti-basal ganglia antibodies were determined using human basal ganglia sections. Statistical analysis was conducted using analysis of variance and chi-square tests. Raised antistreptolysin titers were found in 41 of 69 (59%) patients with Tourette syndrome and 14 of 72 (19%) controls (P = .000). Positive anti-basal ganglia antibodies were found in 22 of 69 (32%) subjects with Tourette syndrome compared with 7 of 72 (10%) controls, which was also significant (P = .002). Raised antistreptolysin titers were detected in 18 of 22 (82%) patients with Tourette syndrome with positive anti-basal ganglia antibodies and 22 of 47 (47%) patients with negative anti-basal ganglia antibodies (P = .01). These results support the reported association between streptococcal infection and anti-basal ganglia antibodies and some patients with Tourette syndrome.

Effects of Probiotic Diet Supplements on Disease Resistance and Immune Response of Young Nile Tilapia, Oreochromis niloticus

Probiotic microbial feed supplements are gaining wide acceptance in livestock production, and may be applicable to aquaculture production systems. In two experiments, fry of Nile tilapia, Oreochromis niloticuswere fed a basal diet supplemented with commercially-available probiotic microorganisms. Survival, growth, disease resistance, and immunological parameters were monitored for a maximum of 94 days. Bacterial populations were higher in the digestive tracts of tilapia receiving probiotic diets, and colony morphology suggested that viable probiotic bacteria persisted up to 48 hours after feeding. Survival was higher after 39–63 days in fish receiving the Bioplus probiotic, Bacillus spp. There was no difference in growth, lysozyme, total serum immunoglobulin, complement, specific anti-streptococcal antibody levels, or mortality due to Streptococcus iniae infection either before or after disease challenge. The results suggest that these commercially-available probiotic microorganisms do not provide beneficial effects in young Nile tilapia.

Anti-streptococcal antibodies in the diagnosis of acute and poststreptococcal disease: streptokinase versus streptolysin O and deoxyribonuclease B

To establish population normal values and compare the diagnostic value of antibodies against streptokinase (ASK), streptolysin O (ASO) and deoxyribonuclease B (ADNaseB) singularly and in combinations in acute and post-streptococcal disease. A retrospective analysis of serological results was performed to define population norms. Subjects with acute culture-confirmed infection and post-streptococcal disease were assessed using population norms, as were matched controls. The sensitivity and specificity of each antibody assay and of combinations of the different assays were calculated. Age specific population normal values were derived from 2,321 specimens. None of the three antibodies alone or in combination was a reliable marker of acute streptococcal infection. The sensitivity and specificity of a single antibody titre in post-streptococcal disease ranged from 70.5 to 72.7% and 86.4 to 93.2%, respectively. The combination of ASO and ADNaseB was the most sensitive and specific combination for identifying post-streptococcal disease (sensitivity 95.5%, specificity 88.6%). In the diagnosis of acute and post-streptococcal disease, the addition of ASK does not increase the sensitivity or specificity of serological testing. A combination of ASO and ADNaseB is required in post-streptococcal disease to achieve maximum sensitivity and specificity.

An early favorable outcome of streptococcal toxic shock syndrome may require a combination of antimicrobial and intravenous gamma globulin therapy together with activated protein C

Streptococcal toxic shock syndrome (STSS) associated with a group A beta hemolytic streptococcal infection was described 18 y ago. Since then, although the pathophysiology of the syndrome has been clarified, mortality can be as high as 80%. A middle-aged female developed STSS associated with a group A streptococcal pneumonia. Laboratory studies confirmed respiratory and renal failure as well as disseminated intravascular coagulation with a striking reduction in endogenous procoagulants. The patient, probably due to her HLA DRB1*14 haplotype was unable to generate anti-streptococcal antibodies. She was treated with appropriate antimicrobial therapy together with intravenous gamma globulin and drotrecogin or activated protein C. Her response to this combined therapy was accompanied by a rapid resolution of the multiorgan failure and correction of the accompanying disseminated intravascular coagulation. This rapid response to treatment supports the hypohesis that several host factors including the immune response and loss of procoagulants determine the development and severity of the toxic shock syndromes. Further studies with this combined approach appear warranted.

Soluble adhesion molecules in Gilles de la Tourette's syndrome

To investigate the immune-mediated response in TS, and its relationship with streptococcal infection, we measured serum levels of soluble intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-selectin in patients with TS, compared to healthy and diseased controls. Soluble VCAM-1 and sE-selectin were significantly elevated in children and adults with TS, and sVCAM-1 was higher among anti-basal ganglia antibodies (ABGA)-positive adults with TS. No correlation of adhesion molecule levels to clinical severity or anti-streptococcal antibodies was observed. Children with Sydenham's chorea and paediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS) showed an increased level of sICAM-1, but not sVCAM-1 and sE-selectin. These results provide initial evidence for a role of adhesion molecules and systemic inflammation in TS, and support the hypothesis of an ongoing immune-mediated process in this condition.

The efficacies of affected-limb care with penicillin, diethylcarbamazine, the combination of both drugs or antibiotic ointment, in the prevention of acute adenolymphangitis during bancroftian filariasis

Repeated attacks of adenolymphangitis (ADL) contribute significantly to the progression of chronic lymphoedema in lymphatic filariasis. They are a cause of stigma and, since they may prevent work and require treatment for which payment must be made, of economic loss. The aim of the present study was to improve the treatment of ADL attacks, which is currently mostly empirical. In a double-blind, placebo-controlled, clinical study, 150 subjects who had each suffered at least two ADL attacks in the preceding year were enrolled and randomly allocated to a programme of self-care of the affected limb (after an intensive training programme) and one of five treatments for 12 months. The subjects were supplied with tablets and ointment so that they could take oral penicillin (800 mg/day), oral diethylcarbamazine (DEC; 1 mg/kg.day) or both of these drugs (at the same doses), or apply framycetin ointment to the affected limb, or just take placebo tablets and apply placebo (zinc-oxide) ointment. Placebo tablets and placebo ointment were used so that neither the subjects nor those assessing the responses to treatment were aware of the treatment arm to which each subject had been assigned. The subjects were requested to continue with the affected-limb care after they had stopped taking the tablets and applying the cream, and were followed-up for 24 months from the first treatment.Overall, the mean incidence of ADL attacks decreased from 2.7 episodes/person-year in the pre-treatment year to just 0.38 episode/person-year during the treatment year (P< 0.01). The greatest reduction in incidence was seen in the 58 subjects who received penicillin (with or without DEC). Even in the placebo group, however, the incidence of ADL in the treatment year was significantly lower than that seen in the pre-treatment year, indicating that affected-limb care on its own helps to prevent some attacks. In all groups except the placebo, the incidence of ADL attacks in the year post-treatment exceeded that seen in the treatment year, indicating that chemoprophylaxis needs to be continued for more than a year if such attacks are to be prevented. In most (84%) of the attacks recorded, titres of anti-streptococcal antibodies were seen to be elevated (compared with those recorded during convalescence),indicating that streptococci have a role in the aetiology of ADL. It is recommended that a combination of penicillin prophylaxis and affected-limb care be incorporated into filariasis-control programmes, to decrease morbidity.

A boy with a mediastinal mass

A 17-year-old boy presented in March, 2003, with a fever, sore throat and dysphagia. His general practitioner diagnosed pharyngitis and gave him oral cephalosporin (cefaclor 1 g twice daily). No pharyngeal swab was taken. The boy started treatment after a delay of 2 days and stopped it after another 3 days since his pain and fever subsided rapidly. 2 weeks later, he was admitted to a local hospital with severe abdominal pain, fatigue and pallor. Doctors there documented proteinuria, haematuria, an elevated systolic blood pressure (149 mm Hg), and anti-streptococcal antibodies, and suspected that the boy had post-streptococcal glomerulonephritis. No microbiological cultures were taken. They started treatment with intravenous penicillin, but because C-reactive protein (CRP) concentrations remained high, his treatment was changed to cefuroxime and gentamicin for a total of 12 days. Nevertheless, CRP increased to 249 mg/L. On day 12, the patient became febrile and complained of severe chest pain. Radiographs of the chest showed widening of the mediastinum and CT (figure, A) showed a mass between the brachiocephalic vein and superior vena cava, spreading paratracheally to the posterior mediastinum. His doctors suspected that he had a lymphoma and referred him to us.

Antistreptococcal, neuronal, and nuclear antibodies in Tourette syndrome

Previous studies have suggested associations between Tourette syndrome and attention-deficit–hyperactivity disorder and antistreptococcal antibodies and between Tourette syndrome and antinuclear antibodies. In this study, antistreptolysin O, antideoxyribonuclease B, antinuclear, and antineuronal antibodies were measured in 41 children with Tourette syndrome and 38 controls, selected without regard to history of streptococcal infection. Results revealed that mean antistreptococcal titers did not differ between diagnostic groups. In addition, multiple regression analysis was unable to predict antistreptococcal antibody titers according to age and diagnosis. The frequency of elevated antistreptolysin O titers, based on a cutoff of 1:240, was significantly higher ( P = 0.04) in patients with attention-deficit–hyperactivity disorder (64%) than in the group without attention-deficit–hyperactivity disorder (34%) but not when dichotomized according to age-matched normal values. No analysis of antideoxyribonuclease B titers identified any differences between groups. Antinuclear antibody titers were at least 1:160 in three of 33 Tourette syndrome patients; only one subject manifested a homogeneous staining pattern. Multiple regression analyses were unable to predict antinuclear, antineuronal, or anti-HTB-10 antibody titers according to the combination of age, diagnosis, and antistreptococcal titer. We suggest that longitudinal rather than single-point-in-time laboratory measurements be evaluated before definitive conclusions are drawn on associations between the diagnosis of Tourette syndrome, attention-deficit–hyperactivity disorder, or obsessive-compulsive disorders and antistreptococcal or antinuclear antibody titers.

Poststreptococcal glomerulonephritis

Poststreptococcal glomerulonephritis is a nonsuppurative sequela of streptococcal infection that occasionally complicates pregnancy. Although group A beta-hemolytic streptococci are responsible for the majority of cases, multiple groups of streptococci can cause postinfectious glomerulonephritis. Infection of the skin or pharynx with streptococci typically precedes kidney involvement by 6 days to 2 weeks. The risk of developing acute nephritis after streptococcal infection ranges from 1–15%. This disorder usually affects children, and is more frequent in males. Poststreptococcal glomerulonephritis is considered an immune complex disease because interactions between antigen–antibody complexes and the complement system result in glomerular injury. Patients present with a wide range of complaints including hematuria, edema, malaise, lethargy, nausea, fever, weakness, anorexia, cough, and dyspnea. The most common exam findings include hypertension, edema, and hematuria. The differential diagnosis includes multisystem disease, other primary glomerular diseases, nonstreptococcal postinfectious glomerulonephritis, and urinary tract infection. The diagnosis is confirmed by the detection of antistreptococcal antibodies, and renal biopsy showing hypercellularity and proliferation. Treatment is supportive, and renal function tends to improve rapidly. Antibiotics are indicated if the patient is concurrently infected. Penicillin is the drug of choice, but erythromycin can be used in the penicillin-allergic patient. Immunity is lifelong, but recurrences may develop after infection with a different nephritogenic strain. If signs of irreversible kidney damage are present, the disease is considered chronic. Presentation in pregnancy may be confused with preeclampsia as hypertension, edema, and proteinuria are presenting signs in both entities. Poststreptococcal glomerulonephritis may lead to preterm delivery but typically has a successful outcome.

Obsessive-compulsive disorder and immunocompetence.

A postinfectious, autoimmune response may be associated with the development of pediatric obsessive-compulsive disorder (OCD). According to this model, antistreptococcal antibodies cross-react with basal ganglia neurons following streptococcus infection. This autoimmune reaction disrupts a basal ganglia-thalamocortical circuit and generates obsessive-compulsive symptoms. One implication of this model is that prolonged immunologic stress may be a risk factor for OCD. That is, immunologic stress may compromise the blood-brain barrier and permit the influx of antistriatal antibodies into the central nervous system. This article explores one part of this putative relationship by investigating whether adult OCD patients, compared to members of other psychiatric groups, demonstrate a higher incidence of recurrent infections and other conditions suggestive of compromised immune function. To test this hypothesis, we conducted a medical records review of 100 consecutive patients evaluated at a private psychiatric clinic specializing in the treatment of anxiety disorders. Sixty-five patients met diagnostic criteria for an Axis-I syndrome. Primary diagnoses included OCD, posttraumatic stress disorder, social anxiety disorder, generalized anxiety disorder, panic disorder with agoraphobia, and dysthymic disorder. Each medical record was reviewed for the presence of target syndromes or presenting symptoms suggestive of compromised immune function. Chart review revealed an increased rate of immune-related symptoms and syndromes among OCD patients in comparison to other anxiety and mood disorder groups. Groups did not differ significantly in the incidence of non-immune symptoms and syndromes. Adult OCD patients appear to have an increased rate of immune-related diseases above and beyond that seen in other psychiatric disorders.

Molecular analysis of cross-reactive anti-myosin/ anti-streptococcal mouse monoclonal antibodies

Nucleotide sequences of VH- and VL-genes of anti-myosin/ anti-streptococcal monoclonal antibodies (mAbs) were analyzed and compared with their highly detailed antigen binding reactivities. Antigen-specificities of the cross-reactive mAbs included myosin, streptococcal M-protein, actin, keratin, N-acetyl-β- d-glucosamine, vimentin, DNA, tropomyosin, troponin, and laminin as previously described. After nucleotide sequence analysis, homology indicated that some of the V gene sequences aligned with antibodies recognizing gangliosides and blood group antigens glycophorin M and N. Therefore, mAb reactivity with gangliosides and glycophorin M and N was identified. The cross-reactive mAbs utilized a heterogeneous group of germline V-heavy genes comprised of nine J558-, four 7183- and two Q52-family VH-genes. Germline V-light genes utilized by the mAbs included six Vκ4/5-, three Vκ8-, two Vκ10-, three Vκ19- and one Vκ23-family VL-genes. No preferential VH/ VL-chains correlated with any of the 12 different antigen reactivities, even for mAbs with nearly identical cross-reactivities. However, we did find that the cross-reactive mAb germline genes within a V gene family shared more homology among themselves than with other germline genes within their V gene families, suggesting convergent mutation. Cross-reactive mAbs with the highest relative avidity for myosin were found in the VH7183 family which contained two cytotoxic mAbs. Antibodies with V gene sequences most homologous to those of our cross-reactive anti-myosin/ anti-streptococcal mAbs had specificities for laminin, DNA, carbohydrates, or blood group antigens and were reported to cause autoimmune disease in mice.

Cytotoxic mAb from rheumatic carditis recognizes heart valves and laminin.

Anti-streptococcal antibodies cross-reactive with N-acetyl-betaD-glucosamine (GlcNAc) and myosin are present in the sera of patients with rheumatic fever (RF). However, their role in tissue injury is not clear. In this study, we show that anti-GlcNAc/anti-myosin mAb 3.B6 from a rheumatic carditis patient was cytotoxic for human endothelial cell lines and reacted with human valvular endothelium and underlying basement membrane. Reactivity of mAb 3.B6 with the valve was inhibited by human cardiac myosin > laminin > GlcNAc. The mAb 3.B6 epitopes were localized in fragments of human cardiac myosin, including heavy meromyosin (HMM), the S1 subfragment, and two light meromyosin (LMM) peptides containing amino acid sequences KEALISSLTRGKLTYTQQ (LMM 1) and SERVQLLHSQNTSLINQK (LMM 33). A novel feature of mAb 3.B6 was its reactivity with the extracellular matrix protein laminin, which may explain its reactivity with the valve surface. A laminin A-chain peptide (HTQNT) that includes homology to LMM33 inhibited the reactivity of mAb 3.B6 with human valve. These data support the hypothesis that cross-reactive antibodies in rheumatic carditis cause injury at the endothelium and underlying matrix of the valve.

Increased anti-streptococcal antibodies in patients with Tourette’s syndrome

Infection or postinfectious phenomena have been postulated to play a role in the pathogenesis of children afflicted with the typical symptoms of Tourette’s syndrome (TS). We investigated whether an increase of titers of antistreptococcal antibodies can be reproduced in our children with TS, and whether this increase is restricted to children. We examined the titers of two different antistreptococcal antibodies, antistreptolysin (ASL) and antiDNase B, both in children and adults. Titers of ASO and antiDNase B were measured (1) in 13 children/adolescents suffering from TS and in an age-matched comparison group; (2) in 23 adult patients, a comparison group of 23 age-matched controls, and in another group of 17 age-matched, non-medicated acute schizophrenics. ASO and antiDNase B titers were determined by laser nephelometry using a commercially available kit. Two antistreptococcal cut-off levels were compared (>250 U/ml and >400 U/ml). As expected, increased ASO titers (>400 IU/ml) were found in a higher proportion of children/adolescents with TS compared to healthy controls. In parallel, high antiDNase titers (>250 U/ml or >400 U/ml) were also observed in significantly more children/adolescents with TS compared to controls. Regarding adults, titers >250 U/ml for both antistreptococcal antigens were found in significantly more TS patients than in schizophrenic patients or healthy control subjects. The mean values of ASO and antiDNase titers were significantly higher in both groups of TS patients compared to control children/adolescents, to the comparison groups of healthy adults and to schizophrenics. No difference in antistreptococcal titers was found between schizophrenics and the group of healthy adults. TS patients exhibited higher antistreptococcal titers than age-matched comparison groups of both children/adolescents and adults using different types of calculation. Our findings support the theory that a postinfectious immune mechanism may play a role in the pathogenesis of TS. The mechanism still needs to be elucidated.

Preliminary Findings of Antistreptococcal Antibody Titers and Basal Ganglia Volumes in Tic, Obsessive-compulsive, and Attention-Deficit/Hyperactivity Disorders

Previous studies have provided preliminary serological evidence supporting the theory that symptoms of tic disorders or obsessive-compulsive disorder (OCD) may be sequelae of prior streptococcal infection. It is unclear, however, whether previously reported associations with streptococcal infection were obscured by the presence of diagnostic comorbidities. It is also unknown whether streptococcal infection is associated in vivo with anatomical alterations of the brain structures that have been implicated in the pathophysiology of these disorders. Antistreptococcal antibody titers were measured in 105 people diagnosed as having CTD, OCD, or attention-deficit/hyperactivity disorder (ADHD) and in 37 community controls without a disorder. Subjects were unselected with regard to their history of streptococcal exposure. Basal ganglia volumes were measured in 113 of these subjects (79 patients and 34 controls). A DSM-IV diagnosis of ADHD was associated significantly with titers of 2 distinct antistreptococcal antibodies, antistreptolysin O and anti-deoxyribonuclease B. These associations remained significant after controlling for the effects of CTD and OCD comorbidity. No significant association was seen between antibody titers and a diagnosis of either CTD or OCD. When basal ganglia volumes were included in these analyses, the relationships between antibody titers and basal ganglia volumes were significantly different in OCD and ADHD subjects compared with other diagnostic groups. Higher antibody titers in these subjects were associated with larger volumes of the putamen and globus pallidus nuclei. These findings suggest that the prior reports of an association between antistreptococcal antibodies and either CTD or OCD may have been confounded by the presence of ADHD. They also support the hypothesis that in susceptible persons who have ADHD or OCD, chronic or recurrent streptococcal infections are associated with structural alterations in basal ganglia nuclei.

MRI Shows Changes in Strep-Associated Tics or OCD

Interest has grown in the possible association between antineuronal antibodies (due to the interaction of antistreptococcal antibodies with neuronal

Microalbuminuria as renal marker in recurrent acute tonsillitis and tonsillar hypertrophy in children

Raised levels of microalbuminuria pointing out glomerular abnormality and indicate renal damage. Glomerulonephritis is caused by immune reaction leading to the formation of circulating immune complexes that are deposited on the basal membrane of the glomerulus. The time course and the appearance of antibodies against infectious agents both play very important roles in its clinical presentation. Antibodies against streptococci have not a protective role, but offers a useful marker of the presence or absence of recent infection. This work studies the presence of microalbuminuria and circulating anti-streptococcal antibodies, namely, anti-streptolysin O and anti-deoxyribonuclease B antibodies in ninety children which underwent tonsillectomy due to infectious and obstructive tonsillar pathology. These children were divided in recurrent acute tonsillitis ( n=34), recurrent tonsillitis with tonsillar hypertrophy ( n=26), and tonsillar hypertrophy ( n=30). It was found in recurrent acute tonsillitis a moderate correlation between microalbuminuria and anti-streptolysin O, and a weak correlation between microalbuminuria and anti-deoxyribonuclease B antibodies. It was also found significant differences of the levels of anti-streptococcal antibodies between the three groups of pathologies. It is proposed the determination of microalbuminuria, an inexpensive and harmless test, as an indicator of possible renal damage in recurrent acute tonsillitis.

Risk factors in the pathogenesis of invasive group A streptococcal infections: role of protective humoral immunity.

An impressive change in the epidemiology and severity of invasive group A streptococcal infections occurred in the 1980s, and the incidence of streptococcal toxic shock syndrome cases continues to rise. The reason for the resurgence of severe invasive cases remains a mystery-has there been a change in the pathogen or in host protective immunity? To address these questions, we have studied 33 patients with invasive infection caused by genotypically indistinguishable M1T1 strains of Streptococcus pyogenes who had different disease outcomes. Patients were classified as having severe (n = 21) and nonsevere (n = 12) invasive infections based on the presence or absence of shock and organ failure. Levels of anti-M1 bactericidal antibodies and of anti-streptococcal superantigen neutralizing antibodies in plasma were significantly lower in both groups than in age- and geographically matched healthy controls (P < 0.01). Importantly, the levels of these protective antibodies in plasma samples from severe and nonsevere invasive cases were not different. Together the data suggest that low levels of protective antibodies may contribute to host susceptibility to invasive streptococcal infection but do not modulate disease outcome. Other immunogenetic factors that regulate superantigen responses may influence the severity of systemic manifestations associated with invasive streptococcal infection.

B lymphocyte antigen D8/17 and repetitive behaviors in autism.

Monoclonal antibody D8/17 identifies a B lymphocyte antigen with expanded expression in rheumatic fever, Sydenham's chorea, and subgroups of obsessive-compulsive disorder and Tourette's syndrome with repetitive behaviors. The authors examined the rate of D8/17 expression in children with autism and its correlation with severity of repetitive behaviors. Blood samples from 18 patients with autism and 14 comparable medically ill children were evaluated for percentage of D8/17-positive B cells by immunofluorescence and for streptococcal antibodies. Severity of repetitive behaviors was also determined. The frequency of individuals with > or =11% D8/17-positive cells was significantly higher in the autistic patients (78%) than the comparison subjects (21%), severity of repetitive behaviors significantly correlated with D8/17 expression, and D8/17-positive patients had significantly higher compulsion scores than D8/17-negative patients. D8/17 expression is high in patients with autism and may serve as a marker for compulsion severity within autism.

Applications of thrombolytic therapy.

Formation of a thrombus involves the aggregation of platelets, precipitation of fibrinogen into a fibrin meshwork and subsequent trapping of red blood cells. The coagulation cascades ensure that this process is initiated in response to a wide range of stimuli including local vessel trauma, endothelial damage and systemic inflammation. Fortunately, the body also possesses a mechanism for dissolving thrombi, mediated by plasmin, a naturally occurring proteolytic enzyme that breaks down fibrin into soluble fibrin degradation products (Fig. 1). Plasmin is formed from the proenzyme plasminogen via the activity of plasminogen activators. Thrombolytic therapy exploits this naturally occurring system, such that the dynamic balance between thrombus formation and dissolution is tilted in favour of the latter. The four principal thrombolytic agents currently in use are streptokinase (SK), tissue plasminogen activator (tPA), reteplase and urokinase (UK) [1]. Streptokinase is a non-enzymic protein extracted from cultures of group A [5-haemolytic streptococci. It acts by forming a stable complex with plasminogen, which generates active plasmin. Streptokinase is antigenic, being associated with fever, rash (5 % of patients) and anaphylaxis (< 0.1% of patients). Its action is reduced by anti-streptococcal antibodies already present. Although SK has a half-life of around 25 min, its fibrinolytic effect can last up to 6 h [2].

Filariasis and Erisipela in Santo Domingo

This study examined acute-convalescent changes in diagnostic anti-streptococcal antibodies by the anti-streptolysin O (ASO) and anti-DNAase B (ADAB) tests among patients (n 28) with lymphedema and recurrent erisipela of the lower limb, comparing them with endemic normal control residents (n=25). The study was based in Villa Francisca, an urban focus of Bancroftian filariasis in eastern Santo Domingo, capital of the Dominican Republic. The acute signs and symptoms of erisipela were consistent with a diagnosis of bacterial cellulitis. The ASO test was especially successful at demonstrating a rise in mean titer during convalescence, whereas the ADAB produced about the same frequency of significant increases (0.2 log titer) as did the ASO. When subjects were scored as responders if mounting a minimal titer increase by either test, patients were found more frequently positive than were controls (chi2=5.3, P=0.02). About half (54%) of all patients mounted at least a minimal antibody increase. Filaria-specific IgG4 antibodies were absent from all sera of 20 residents of a nonendemic Dominican mountain town but appeared in about two-thirds of the sampled residents of the endemic barrio. Notably however, levels did not change between the acute phase and convalescence. These findings are consistent with the hypothesis that recurrent streptococcal invasion of the lymphatics may be a significant factor triggering or amplifying lymphedema and elephantiasis in patients with chronic filariasis.