Infectious Disease Transmission through Cell, Tissue, and Organ Transplantation: Reducing the Risk through Donor Selection

1995 ◽  
Vol 4 (5) ◽  
pp. 455-477 ◽  
Author(s):  
Ted Eastlund

The incidence of cell transplant-transmitted infection is unknown and can only be inferred from prospective studies–that have not yet been performed and reported. The possibility of donor-to-recipient disease transmission through cell transplant therapy can be considered by reviewing the risk associated with other transplanted tissues and organs. Viral, bacterial, and fungal infections have been transmitted via transplantation of organs, tissue allografts such as bone, skin, cornea, and heart valves, and cells such as islets, hematopoietic stem cells, and semen. Several types of protozoan and worm parasites have been transferred via organ transplants. Bone allografts have transmitted hepatitis, tuberculosis, and human immunodeficiency virus (HIV-1). Corneas have transmitted rabies, Creutzfeldt-Jakob disease (CJD), hepatitis B (HBV), cytomegalovirus (CMV), herpes simplex virus (HSV), bacteria, and fungi. Heart valves have been implicated in transmitting tuberculosis and hepatitis B. HIV-1 and CMV seroconversion has been reported in patients receiving skin from seropositive donors. CJD has been transmitted by dura and pericardium transplants. Over the past several years, improvements in donor screening criteria, such as excluding potential donors with infection and those with behaviors risky for HIV-1 and hepatitis infection, and introduction of new donor blood tests have greatly reduced the risk of HIV-1 and hepatitis and may have nearly eliminated the risk of tuberculosis and CJD. Prior to use, many tissues are exposed to antibiotics, disinfectants, and sterilants, which further reduce or remove the risk of transmitted disease. Because organs, cells, and some tissue grafts cannot be subjected to sterilization steps, the risk of infectious disease transmission remains and thorough donor screening and testing is especially important.

2020 ◽  
Author(s):  
Angela Maria Cadavid Restrepo ◽  
Luis Furuya-Kanamori ◽  
Helen Mayfield ◽  
Eric J. Nilles ◽  
Colleen L. Lau

2012 ◽  
Vol 54 (1-2) ◽  
pp. 23-36 ◽  
Author(s):  
E. K. WATERS ◽  
H. S. SIDHU ◽  
G. N. MERCER

AbstractPatchy or divided populations can be important to infectious disease transmission. We first show that Lloyd’s mean crowding index, an index of patchiness from ecology, appears as a term in simple deterministic epidemic models of the SIR type. Using these models, we demonstrate that the rate of movement between patches is crucial for epidemic dynamics. In particular, there is a relationship between epidemic final size and epidemic duration in patchy habitats: controlling inter-patch movement will reduce epidemic duration, but also final size. This suggests that a strategy of quarantining infected areas during the initial phases of a virulent epidemic might reduce epidemic duration, but leave the population vulnerable to future epidemics by inhibiting the development of herd immunity.


2019 ◽  
Vol 34 (4) ◽  
Author(s):  
Amy Moran-Thomas

Long-accepted models of causality cast diseases into the binary of either “contagious” or “non-communicable,” typically with institutional resources focused primarily on interrupting infectious disease transmission. But in southern Belize, as in much of the world today, epidemic diabetes has become a leading cause of death and a notorious contributor to organ failure and amputated limbs. This ethnographic essay follows caregivers’ and families’ work to survive in-between public health categories, and asks what responses a bifurcated model of infectious versus non-communicable disease structures or incapacitates in practice. It proposes an alternative focus on diabetes as a “para-communicable” condition—materially transmitted as bodies and ecologies intimately shape each other over time, with unequal and compounding effects for historically situated groups of people. The article closes by querying how communicability relates to community, and why it matters to reframe narratives about contributing causalities in relation to struggles for treatment access.


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