Carditis

Abstract: To assess the incidence of Lyme borreliosis in Central Europe, a 12-month, prospective, population-based surveillance study of Lyme borreliosis was conducted in the Wurzburg region of central Germany, following an aggressive awareness campaign. The diagnosis of Lyme borreliosis required the presence of (i) erythema migrans (diameter ≥5 cm); (ii) lymphocytoma; or (iii) another specific manifestation including Lyme arthritis, neuroborreliosis, carditis or acrodermatitis chronica atrophicans in conjunction with serological confirmation. A total of 313 cases of Lyme borreliosis was diagnosed, giving an incidence of 111 cases/100 000 inhabitants, the highest rates occurring in children and elderly adults living in wooded as opposed to agricultural areas. The incidence in city dwellers and inhabitants of rural areas was not significantly different. Erythema migrans was the only manifestation in 279 (89%) patients. Of the 34 patients with manifestations other than erythema migrans alone, 15 had arthritis, nine neuroborreliosis, six lymphocytoma, four acrodermatitis chronica atrophicans and one carditis. Children were more likely than adults to have manifestations other than erythema migrans alone. Lyme borreliosis was very common in central Germany, and one of the most frequent bacterial infections. The observation of more cases of arthritis than neuroborreliosis was similar to that in the USA. These results may be representative for many parts of central Europe and suggest the need for development of a vaccine against borreliosis caused by European strains of Borrelia species.

Abstract: Information about 261 cases of Kawasaki disease (KD) was reported to the Center for Disease Control (CDC) between July 1976 and July 1978. KD occurred at all times of the year in young, previously healthy children throughout the United States. KD was more common in infants and toddlers, males, and Asian and part-Asian children. The illness was characterized by acute onset of prolonged high fever; maculopapular or scarlatiniform rash; adenopathy; injection of the conjunctival and mucous membranes of the upper respiratory tract; redness of the palms and soles; indurative edema of the extremities; desquamation, arthralgias; and elevated white blood cell count, erythrocyte sedimentation rate, and platelet count. Complications included gallbladder disease and carditis; 2.8% died. Surviving patients were hospitalized for a mean of 8.9 days.

Abstract: Rheumatic fever (RF) is an autoimmune disease caused by the gram-positive bacteria Streptococcus pyogenes that follows a nontreated throat infection in susceptible children. The disease manifests as polyarthritis, carditis, chorea, erythema marginatum, and/or subcutaneous nodules. Carditis, the most serious complication, occurs in 30% to 45% of RF patients and leads to chronic rheumatic heart disease (RHD), which is characterized by progressive and permanent valvular lesions. In this review, we will focus on the genes that confer susceptibility for developing the disease, as well as the innate and adaptive immune responses against S. pyogenes during the acute rheumatic fever episode that leads to RHD autoimmune reactions. The disease is genetically determined, and some human leukocyte antigen class II alleles are involved with susceptibility. Other single nucleotide polymorphisms for TNF-alpha and mannan-binding lectin genes were reported as associated with RF/RHD. T cells play an important role in RHD heart lesions. Several autoantigens were already identified, including cardiac myosin epitopes, vimentin, and other intracellular proteins. In the heart tissue, antigen-driven oligoclonal T cell expansions were probably the effectors of the rheumatic heart lesions. These cells are CD4+ and produced inflammatory cytokines (TNFα and IFNγ). Molecular mimicry is the mechanism that mediated the cross-reactions between streptococcal antigens and human proteins. The elucidation of chemokines and their receptors involved with the recruitment of Th1, Th2, and Th17 cells, as well as the function of T regulatory cells in situ will certainly contribute to the delineation of the real picture of the heart lesion process that leads to RHD.

Abstract: The evolution of Lyme borreliosis was examined in genetically resistant C.B.-17 and susceptible C3H/He(C3H) mice homozygous for the severe combined immune deficiency (scid) gene, or their immunocompetent counterparts. The C.B-17, C.B-17-scid, C3H, and C3H-scid mice were inoculated intradermally with 104 Borrelia burgdorferi and examined on days 14, 21, 30, 45, and 60 after inoculation. Spirochetemia was detected through 30 days, but was cleared in all groups by 45 days. Kidney and brain were inconsistently culture positive, but spleen and ear punch samples were positive in most mice. Immunocompetent C.B-17 and C3H mice seroconverted with equivalent IgG titers to B. burgdorferi, while C.B-17-scid and C3H-scid mice did not seroconvert. Arthritis occurred in nearly all joints examined in all genotypes on day 14, was of equal severity among C.B-17, C.B-17-scid, and C3H mice, but was more severe in C3H-scid mice. By days 30 and 45, arthritis began to resolve in immunocompetent mice, with C3H mice having more severe disease than C.B-17 mice. Arthritis persisted in C.B-17-scid and C3H-scid mice. Carditis occurred to an equal degree in all groups on day 14, remained active in scid mice, but regressed in immunocompetent mice at later intervals. Many spirochetes were visualized with silver stain in inflamed synovial tissues of scid mice, and were present in other tissues in smaller numbers. These studies show that specific immunity is not involved in arthritogenesis or genetically determined susceptibility to arthritis, but is involved in arthritis and carditis regression.