An epidemic form of arthritis has been occurring in eastern Connecticut at least since 1972, with the peak incidence of new cases in the summer and early fall. Its identification has been possible because of tight geographic clustering in some areas, and because of a characteristic preceding skin lesion in some patients. The authors studied 51 residents of three contiguous Connecticut communities—39 children and 12 adults—who developed an illness characterized by recurrent attacks of asymmetric swelling and pain in a few large joints, especially the knee. Attacks were usually short (median: 1 week) with much longer intervening periods of complete remission (median: 2.5 months), but some attacks lasted for months. To date the typical patient has had three recurrences, but 16 patients have had none. A median of 4 weeks (range: 1–24) before the onset of arthritis, 13 patients (25%) noted an erythematous papule that developed into an expanding, red, annular lesion, as much as 50 cm in diameter. Only 2 of 159 family members of patients had such a lesion and did not develop arthritis (P < 0.000001). The overall prevalence of the arthritis was 4.3 cases per 1,000 residents, but the prevalence among children living on four roads was 1 in 10. Six families had more than 1 affected member. Nine of 20 symptomatic patients had low serum C3 levels, compared to none of 31 asymptomatic patients (P < 0.005); no patient had iridocyclitis or a positive test for antinuclear antibodies. Neither cultures of synovium and synovial fluid nor serologic tests were positive for agents known to cause arthritis. “Lyme arthritis” is thought to be a previously unrecognized clinical entity, the epidemiology of which suggests transmission by an arthropod vector.

Thirty-two patients with the onset of erythema chronicum migrans, Lyme arthritis, or both in mid-1976 were studied prospectively. The skin lesion (24 patients) typically lasted about 3 weeks, beginning as a red macule or papule that expanded to form a large ring with central clearing. Associated symptoms ranged from none to malaise, fatigue, chills and fever, headache, stiff neck, backache, myalgias, nausea, vomiting, and sore throat. Three patients had been bitten by ticks at the site of the initial lesion 4 to 20 days before its onset. Nineteen patients suddenly developed a monoarticular or oligoarticular arthritis 4 days to 22 weeks (median, 4 weeks) after onset of the skin lesion; eight developed arthritis without a preceding skin lesion. Seven of these 27 experienced migratory joint pains. Arthritis attacks, most commonly in the knee, were typically short (median, 8 days) but sometimes persisted for months. Other manifestations included neurologic abnormalties, myocardial conduction abnormalities, serum cryoprecipitates, elevated serum IgM levels, and elevated erythrocyte sedimentation rates. The diagnostic marker is the skin lesion; without it, geographic clustering is the most important clue.

Fourteen patients who developed B cell lymphomas or lymphoproliferative lesions after kidney, liver, heart, or heart-lung transplantation in Pittsburgh during [1981][1982][1983] had active infection with Epstein-Barr virus (EBV) of the primary (six patients), reactivated (seven patients), or chronic (one patient) type. In transplant patients without tumors, the incidence of EBV infection was 30% (39 of 128). Only three of these patients had primary infections. Thus the frequency of active infection was significantly higher in patients with tumors, and patients with primary infections were at greater risk of developing tumors. Five of 13 tumors tested contained EBV nuclear antigen (EBNA) and nine of 11 contained EBV genomes detected by DNA-DNA hybridization with BamHI K, BamHI W, or EcoRI B cloned probes. All EBNA-positive tumors, except one, were also positive by hybridization. Only one tumor was negative for both EBNA and EBV DNA. These data suggest that EBV plays an etiologic role in the development of these lesions.Epstein-Barr virus (EBV) is a human herpesvirus associated with an array of conditions that range from inapparent infection and infectious mononucleosis to lethal lymphoproliferative syndromes, nasopharyngeal carcinoma, Burkitt's lymphoma, and B cell lymphomas in immunocompromised patients [1]. The precise role of the virus in carcinogenesis is unclear, although in Burkitt's lymphoma the importance of viral transformation of infected B lymphocytes and chromosomal translocations has been emphasized [2]. It is even less clear in lymphomas and lymphoproliferative lesions arising in immuno-compromised patients, where the immunopathology may not be uniform and where chromosomal studies are largely lacking.Recently, we reported on the reversibility of lymphomas and lymphoproliferative lesions in a series of 17 transplant patients after reduction of cyclosporine and steroid immunosuppression [3]. In that preliminary report we noted that seven of these patients had evidence of primary EBV infections and eight had evidence of reactivated infection. Six tumors had evidence of EBV nuclear antigen (EBNA) and seven had evidence of EBV DNA by nucleic acid hybridization. [6] reported the results of studies on 19 renal transplant patients who developed lymphoproliferative disorders and lymphomas after transplantation. All the patients except one were receiving azathioprine, prednisone, and antithymocyte globulin. Two of their patients developed primary EBV infection, in six the infection reactivated, and 12 had evidence of EBV DNA in their tumors by hybridization studies. Bieber et al. [7] reported that five of 39 heart transplant recipients receiving cyclosporine, prednisone, and antithymocyte globulin developed lymphomas. Four tumors were positive for EBV DNA by cRNA-DNA filter hybridization, and three patients had serological evidence of EBV infection.We report here evidence for active EBV infection in all of our patients with tumors and a significantly higher frequency of primary infection than found i...

Purpose Transitioning the medical care of children with perinatally-acquired HIV from pediatric care to internal medicine practices has become increasingly important as newer therapies prolong survival. The study aims to describe challenges to caring for these adolescents and the potential barriers to transitioning them to internal medicine-based care. Methods Qualitative study in which data were gathered from open-ended interviews conducted from November 2005-April 2006 with 18 adolescents with HIV, 15 of their principal guardians, and 9 pediatric health care providers from the Yale Pediatric AIDS Care Program, New Haven, Connecticut. Results Issues of stigma played a prominent role in both the challenges to care and barriers to transitioning care. Challenges to care were: (1) poor adherence to medication regimens; (2) adolescent sexuality; and (3) disorganized social environments. Potential barriers to transitioning care were: (1) families’ negative perceptions of and experiences with stigma of HIV disease--which undermined the desire to meet new providers; (2) perceived and actual lack of autonomy-- pediatric providers feared that staff in adult clinics would demand a level of independence that adolescents did not have; and (3) difficulty letting-go of relationships-- adolescents, guardians, and providers described a familial relationship and expressed anxiety about terminating their relationships. Conclusion Understanding these challenges and barriers can inform both pediatric and adult HIV care providers and enable them to create successful transition programs, with the goal of improving retention and follow-up to care.