Clinical Lecture on Some Points in the Pathology and Treatment of Headache
Authors: W. H. Day
Journal: BMJ (1878)

<h3>OBJECTIVE</h3> To identify clinical and serological differences of patients with reactive arthritis after infection with Lancefield group A β-haemolytic streptococci (GAS), compared with non-group A—that is, group C or G streptococci (NGAS:GCS/GGS), and a group of culture negative or unidentified streptococci (GUS). <h3>METHODS</h3> A prospective study of consecutive patients with reactive arthritis after serologically or culture confirmed infection with β-haemolytic streptococci, presenting to the outpatient department of rheumatology from January 1992 until January 1998. Alternative causes for reactive arthritis were excluded. Main outcome measures were clinical and serological characteristics including antistreptolysine-O (ASO) and antideoxyribonuclease-B (antiDNase-B) antibody titres. <h3>RESULTS</h3> 41 patients (female/male ratio 22/19; mean (SD) age 38 (13) years) with reactive arthritis were included. Culture of throat swab was positive in 13 cases (32%): 6 (15%) GAS, 7 NGAS (17%), that is, 5 (12%) GCS, 2 (5%) GGS. In 28 cases throat culture remained negative resulting in a group of unidentified streptococci; antibiotic pre-treatment had been given by the general practitioner in 18 cases (64%). Arthritis was non-migratory, the number of arthritic joints in GAS and NGAS was similar, whereas in NGAS patients fewer joints were involved than in GUS: mean (SEM) 36 swollen joint index: 3.3 (1.0) in NGAS<i>v</i> 5.6 (1.0) in GUS (p&lt;0.005); 28 swollen joint index: 2.9 (1.0) in NGAS <i>v</i> 4.3 (0.8) in GUS (p&lt;0.05). Extra-articular manifestations—that is, erythema nodosum/ multiforme, AV conduction block or hepatitis—were observed after GAS or GUS infection, but not after NGAS infection. ASO and/or antiDNase-B rose significantly in all patients. The maximal titres for ASO and antiDNase-B in 41 PSRA patients were: mean (SEM) 1242 (232) U/l and 890 (100) U/l respectively; the maximal ASO titres were similar in the three groups: mean (SEM) 1125 (185) in GAS, 625 (160) in NGAS (GAS <i>v</i> NGAS: p=0.17), and 1430 (320) U/l in GUS (NGAS <i>v</i> GUS: p=0.10). AntiDNase-B titres were: mean (SEM) 1075 (180) in GAS, 375 (105) in NGAS (GAS <i>v</i> NGAS: p&lt;0.01), and 995 (125) U/l in GUS (NGAS <i>v</i> GUS: p&lt;0.005). ASO: antiDNase-B ratios were: mean (SEM) 0.89 (0.21) in GAS, 2.60 (0.76) in NGAS (GAS <i>v</i> NGAS: p&lt;0.05), and 1.43 (0.28) in GUS (NGAS <i>v</i> GUS: p=0.12). <h3>CONCLUSION</h3> Post-streptococcal reactive arthritis occurs not infrequently. Differentiation of PSRA based on the causative streptococcal strain is frequently thwarted by negative throat cultures. Sometimes extra-articular manifestations are present that exclude NGAS as the causative organism. Serologically, lower antiDNase-B titres may be indicative for primary NGAS infection; the ASO/antiDNase-B ratio may be of additive value for differentiation in cases of a negative throat culture: the higher ASO/antiDNase-B ratios suggesting primary NGAS infection. In reactive arthritis, serological monitoring consisting of a simultaneous titration of antiDNase-B and ASO, seems to be of clinical importance to trace GAS induced cases, especially when throat cultures remain negative.