Visceral leishmaniasis in a lung transplant recipient: usefulness of highly sensitive real-time polymerase chain reaction for preemptive diagnosis.

We report the case of a lung transplant recipient in whom the diagnosis of visceral leishmaniasis (VL) was made by detection of parasites in a peripheral blood smear when the parasite load already reached 8.9 × 103 parasites/mL. We demonstrated that the VL diagnosis could have been done months before the development of symptoms by the use of Leishmania-specific real-time polymerase chain reaction (PCR), suggesting the role of preemptive PCR-based diagnosis in transplant recipients at risk for VL.

Incidence and outcomes of respiratory viral infections in lung transplant recipients: a prospective study.

BACKGROUND: The incidence and outcomes of respiratory viral infections in lung transplant recipients (LTR) are not well defined. The objective of this prospective study conducted from June 2008 to March 2011 was to characterise the incidence and outcomes of viral respiratory infections in LTR. METHODS: Patients were seen in three contexts: study-specific screenings covering all seasons; routine post-transplantation follow-up; and emergency visits. Nasopharyngeal specimens were collected systematically and bronchoalveolar lavage (BAL) was performed when clinically indicated. All specimens underwent testing with a wide panel of molecular assays targeting respiratory viruses. RESULTS: One hundred and twelve LTR had 903 encounters: 570 (63%) were screening visits, 124 (14%) were routine post-transplantation follow-up and 209 (23%) were emergency visits. Respiratory viruses were identified in 174 encounters, 34 of these via BAL. The incidence of infection was 0.83 per patient-year (95% CI 0.45 to 1.52). The viral infection rates upon screening, routine and emergency visits were 14%, 15% and 34%, respectively (p<0.001). Picornavirus was identified most frequently in nasopharyngeal (85/140; 60.7%) and BAL specimens (20/34; 59%). Asymptomatic viral carriage, mainly of picornaviruses, was found at 10% of screening visits. Infections were associated with transient lung function loss and high calcineurin inhibitor blood levels. The hospitalisation rate was 50% (95% CI 30% to 70.9%) for influenza and parainfluenza and 16.9% (95% CI 11.2% to 23.9%) for other viruses. Acute rejection was not associated with viral infection (OR 0.4, 95% CI 0.1 to 1.3). CONCLUSIONS: There is a high incidence of viral infection in LTR; asymptomatic carriage is rare. Viral infections contribute significantly to this population's respiratory symptomatology. No temporal association was observed between infection and acute rejection.

Effects of damage in the articular surface on the cartilage response to injurious compression in vitro.

Macroscopic structural damage to the cartilage articular surface can occur due to slicing in surgery, cracking in mechanical trauma, or fibrillation in early stage osteoarthrosis. These alterations may render cartilage matrix and chondrocytes susceptible to subsequent mechanical injury and contribute to progression of degenerative disease. To examine this hypothesis, single 300 microm deep vertical slices were introduced across a diameter of the articular surface of osteochondral explant disks on day 6 after dissection. Then a single uniaxial unconfined ramp compression at 7 x 10(-5) or 7 x 10(-2) s(-1) strain rate to a peak stress of 3.5 or 14 MPa was applied on day 13 during which mechanical behavior was monitored. Effects of slices alone and together with compression were measured in terms of explant swelling and cell viability on days 10 and 17. Slicing alone induced tissue swelling without significant cell death, while compression alone induced cell death without significant tissue swelling. Under low strain rate loading, no differences in the response to injurious compression were found between sliced and unsliced explants. Under high strain rate loading, slicing rendered cartilage more easily compressible and appeared to slightly reduce compression-induced cell and matrix injury. Findings highlight microphysical factors important to cartilage mechanical injury, and suggest ways that macroscopic structural damage may accelerate or, in certain cases, possibly slow the progression of cartilage degeneration.