Serum mannose-binding lectin deficiency is associated with cryptosporidiosis in young Haitian children.

BACKGROUND: Mannose-binding lectin (MBL) is a component of the innate immune response and binds microbial surfaces through carbohydrate recognition domains. MBL deficiency may contribute to susceptibility to a variety of infectious diseases, particularly in young children. MBL binds to the Cryptosporidium sporozoite and may be important in resistance to cryptosporidiosis. METHODS: We studied the association of serum MBL levels and cryptosporidiosis in a case-control study of young Haitian children with cryptosporidiosis versus children who were control subjects. RESULTS: Ninety-nine children were enrolled, as follows: 49 children with cryptosporidiosis, 41 healthy controls, and 9 children with diarrhea from other causes. Case children were more malnourished than controls, and 49% had persistent or chronic diarrhea. At enrollment, mean serum MBL levels were markedly lower in children with cryptosporidiosis (P = .002), as was the number of children with an MBL deficiency of < or = 70 ng/mL (P = .005). In multivariate analysis, the association of cryptosporidiosis and MBL deficiency persisted (P = .002; adjusted odds ratio, 22.4), as did the association of cryptosporidiosis with general malnutrition. The subset of children with cryptosporidiosis and MBL deficiency were more likely to be male (P = .025). CONCLUSIONS: MBL may be an important component of innate immune protection against Cryptosporidium infection in young children. Additional studies are necessary to determine whether MBL intestinal losses, deficient epithelial expression, and/or genetic polymorphisms in the MBL gene contribute to MBL deficiency in cryptosporidiosis and other enteric infections in young children.

African trypanosomiasis in two travelers from the United States.

African trypanosomiasis is a rare but well-documented cause of fever in United States travelers returning from areas where it is endemic. We report two recently diagnosed cases that involved tourists who went on safari in Tanzania. Review of these and 29 other published cases indicates that disease in returning United States travelers is nearly always of the East African form, a fulminant illness for which prompt diagnosis is necessary. In the United States, timely and appropriate therapy for this disease has resulted in favorable outcomes for most patients. Chemoprophylaxis for East African trypanosomiasis is not recommended, but travelers visiting areas of endemicity should practice appropriate preventive measures to prevent tsetse fly bites.

Service delivery for patients with HIV in a rural state: the Vermont model.

The incidence of human immunodeficiency virus (HIV) infection is increasing rapidly in rural areas of the United States. Barriers to health-care delivery for this patient population include the complexity of this rapidly changing field, inexperienced rural physicians, long travel distances to receive expert care, lack of psychosocial support systems, and concerns about confidentiality. Models of HIV care for rural areas have not been developed that remove these barriers. We present the philosophy, structure, implementation, and services of a model of care in Vermont that is designed to remove many of these barriers and bring HIV expertise into the rural areas of the state. Three HIV specialty clinics have been developed in regional hospitals throughout the state. The clinic team includes an HIV-trained nurse practitioner and social worker from the hospital, a client consultant from the regional AIDS service organization, and an infectious disease specialist who travels to each of the clinics monthly. Patient care will be centralized in these regionally located clinics. The dispersion of HIV care among numerous and inexperienced rural providers will be obviated. Confidentiality will be emphasized within the hospital environment. The model has the potential to provide a complete continuum of medical care and psychosocial case management, integrate patient care and regional provider education, and increase community awareness. Patients will be able to receive their care in their own community, avoiding long travel distances. This may encourage patients to seek care earlier in their illness. The model may be adaptable to other rural areas of the United States.

Extracellular matrix heparan sulfate modulates endothelial cell susceptibility to Staphylococcus aureus.

The ability of extracellular matrix heparan sulfate to alter the susceptibility of human endothelial cells to S. aureus was investigated. Endothelial cells grown on extracellular matrix synthesized by S. aureus-infected endothelial cells were more susceptible to subsequent staphylococcal infection than endothelial cells grown on the extracellular matrix synthesized by untreated endothelial cells. Endothelial cells were more susceptible to S. aureus infection when 1) grown on heparitinase-treated extracellular matrix that removed heparan sulfate chains, 2) grown on extracellular matrix produced by chlorate-treated endothelial cells that reduced sulfation in the matrix heparan sulfate proteoglycans, 3) grown on heparan sulfate purified from extracellular matrix elaborated by infected endothelial cells, and 4) endothelial cells were chlorate-treated and therefore expressed desulfated cellular heparan sulfate proteoglycans. Extracellular matrix produced by S. aureus-infected endothelial cells contained heparan sulfate proteoglycans with reduced sulfation. The altered extracellular matrix with reduced sulfated heparan sulfate proteoglycans signalled the uninfected endothelial cells to produce under sulfated cellular heparan sulfate proteoglycans that increased S. aureus adherence to the endothelial cells.

Complicated soft tissue infection with prepatellar bursitis caused by Paecilomyces lilacinus in an immunocompetent host: case report and review.

Documented Paecilomyces lilacinus infections are quite rare. Most reports involve immunocompromised patients or implanted objects. We report the first case of complicated soft tissue infection caused by P. lilacinus in an immunocompetent host. The spectrum of infections involving this fungus is reviewed.