Blood borne transit of CJD from brain to gut at early stages of infection
<p>Abstract</p> <p>Background</p> <p>In Creutzfeldt-Jakob disease (CJD) and other related transmissible spongiform encephalopathies it is critical to understand the various pathways by which the infectious agent spreads to different organs.</p> <p>Methods<...
| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
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BMC
2001-10-01
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| Series: | BMC Infectious Diseases |
| Online Access: | http://www.biomedcentral.com/1471-2334/1/20 |
| _version_ | 1811265687429054464 |
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| author | Martin Daniel Chernyak Mark Radebold Klaus Manuelidis Laura |
| author_facet | Martin Daniel Chernyak Mark Radebold Klaus Manuelidis Laura |
| author_sort | Martin Daniel |
| collection | DOAJ |
| description | <p>Abstract</p> <p>Background</p> <p>In Creutzfeldt-Jakob disease (CJD) and other related transmissible spongiform encephalopathies it is critical to understand the various pathways by which the infectious agent spreads to different organs.</p> <p>Methods</p> <p>We injected a CJD agent into mice, either intracerebrally (ic) or intraperitoneally (ip) and monitored the progressive appearance of abnormal PrP in peripheral tissues over time.</p> <p>Results</p> <p>Abnormal PrP was detected in lymphoreticular tissues of the gastrointestinal tract as early as 28 to 32 days after infection by both routes. This change persisted until the terminal stages of disease. In contrast, abnormal PrP was not detected in brain or spinal cord until 80 to 120 days after ic inoculation, or until 170 days after ip inoculation.</p> <p>Conclusions</p> <p>Brain lacks significant lymphatic drainage, and has little infectivity before 40 days, even after ic inoculation. Thus the infectious inoculum must spread to the gut by a vascular route, a direction opposite to that generally assumed. This interpretation is consistent with previous studies demonstrating white blood cell infectivity as well as perivascular PrP accumulations in CJD. Notably, enteric infection at early as well as later stages of disease, and regardless of the route of agent entry, implicates potential environmental spread by fecal matter.</p> |
| first_indexed | 2024-04-12T20:28:29Z |
| format | Article |
| id | doaj.art-9c28e3f2d9fc4a8a80700765bd15a05e |
| institution | Directory Open Access Journal |
| issn | 1471-2334 |
| language | English |
| last_indexed | 2024-04-12T20:28:29Z |
| publishDate | 2001-10-01 |
| publisher | BMC |
| record_format | Article |
| series | BMC Infectious Diseases |
| spelling | doaj.art-9c28e3f2d9fc4a8a80700765bd15a05e2022-12-22T03:17:48ZengBMCBMC Infectious Diseases1471-23342001-10-01112010.1186/1471-2334-1-20Blood borne transit of CJD from brain to gut at early stages of infectionMartin DanielChernyak MarkRadebold KlausManuelidis Laura<p>Abstract</p> <p>Background</p> <p>In Creutzfeldt-Jakob disease (CJD) and other related transmissible spongiform encephalopathies it is critical to understand the various pathways by which the infectious agent spreads to different organs.</p> <p>Methods</p> <p>We injected a CJD agent into mice, either intracerebrally (ic) or intraperitoneally (ip) and monitored the progressive appearance of abnormal PrP in peripheral tissues over time.</p> <p>Results</p> <p>Abnormal PrP was detected in lymphoreticular tissues of the gastrointestinal tract as early as 28 to 32 days after infection by both routes. This change persisted until the terminal stages of disease. In contrast, abnormal PrP was not detected in brain or spinal cord until 80 to 120 days after ic inoculation, or until 170 days after ip inoculation.</p> <p>Conclusions</p> <p>Brain lacks significant lymphatic drainage, and has little infectivity before 40 days, even after ic inoculation. Thus the infectious inoculum must spread to the gut by a vascular route, a direction opposite to that generally assumed. This interpretation is consistent with previous studies demonstrating white blood cell infectivity as well as perivascular PrP accumulations in CJD. Notably, enteric infection at early as well as later stages of disease, and regardless of the route of agent entry, implicates potential environmental spread by fecal matter.</p>http://www.biomedcentral.com/1471-2334/1/20 |
| spellingShingle | Martin Daniel Chernyak Mark Radebold Klaus Manuelidis Laura Blood borne transit of CJD from brain to gut at early stages of infection BMC Infectious Diseases |
| title | Blood borne transit of CJD from brain to gut at early stages of infection |
| title_full | Blood borne transit of CJD from brain to gut at early stages of infection |
| title_fullStr | Blood borne transit of CJD from brain to gut at early stages of infection |
| title_full_unstemmed | Blood borne transit of CJD from brain to gut at early stages of infection |
| title_short | Blood borne transit of CJD from brain to gut at early stages of infection |
| title_sort | blood borne transit of cjd from brain to gut at early stages of infection |
| url | http://www.biomedcentral.com/1471-2334/1/20 |
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