Revisiting Persistent <i>Salmonella</i> Infection and the Carrier State: What Do We Know?
One characteristic of the few <i>Salmonella enterica</i> serovars that produce typhoid-like infections is that disease-free persistent infection can occur for months or years in a small number of individuals post-convalescence. The bacteria continue to be shed intermittently which is a k...
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2021-10-01
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author | Neil Foster Ying Tang Angelo Berchieri Shizhong Geng Xinan Jiao Paul Barrow |
author_facet | Neil Foster Ying Tang Angelo Berchieri Shizhong Geng Xinan Jiao Paul Barrow |
author_sort | Neil Foster |
collection | DOAJ |
description | One characteristic of the few <i>Salmonella enterica</i> serovars that produce typhoid-like infections is that disease-free persistent infection can occur for months or years in a small number of individuals post-convalescence. The bacteria continue to be shed intermittently which is a key component of the epidemiology of these infections. Persistent chronic infection occurs despite high levels of circulating specific IgG. We have reviewed the information on the basis for persistence in <i>S</i>. Typhi, <i>S</i>. Dublin, <i>S.</i> Gallinarum, <i>S</i>. Pullorum, <i>S</i>. Abortusovis and also <i>S</i>. Typhimurium in mice as a model of persistence. Persistence appears to occur in macrophages in the spleen and liver with shedding either from the gall bladder and gut or the reproductive tract. The involvement of host genetic background in defining persistence is clear from studies with the mouse but less so with human and poultry infections. There is increasing evidence that the organisms (i) modulate the host response away from the typical Th1-type response normally associated with immune clearance of an acute infection to Th2-type or an anti-inflammatory response, and that (ii) the bacteria modulate transformation of macrophage from M1 to M2 type. The bacterial factors involved in this are not yet fully understood. There are early indications that it might be possible to remodulate the response back towards a Th1 response by using cytokine therapy. |
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spelling | doaj.art-9fc15c84e1d4403fa9bb7f48d1cdbead2023-11-22T19:33:53ZengMDPI AGPathogens2076-08172021-10-011010129910.3390/pathogens10101299Revisiting Persistent <i>Salmonella</i> Infection and the Carrier State: What Do We Know?Neil Foster0Ying Tang1Angelo Berchieri2Shizhong Geng3Xinan Jiao4Paul Barrow5SRUC Aberdeen Campus, Craibstone Estate, Ferguson Building, Aberdeen AB21 9YA, UKInstitute of Molecular Physiology, Shenzhen Bay Laboratory, Shenzhen 518055, ChinaDepartamento de Patologia Veterinária, Faculdade de Ciências Agrárias e Veterinárias, Univ Estadual Paulista, Via de Acesso Paulo Donato Castellane, s/n, 14884-900 Jaboticabal, SP, BrazilJiangsu Key Laboratory of Zoonosis, Jiangsu Co-Innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou University, Yangzhou 225009, ChinaJiangsu Key Laboratory of Zoonosis, Jiangsu Co-Innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou University, Yangzhou 225009, ChinaSchool of Veterinary Medicine, University of Surrey, Daphne Jackson Road, Guildford GU2 7AL, UKOne characteristic of the few <i>Salmonella enterica</i> serovars that produce typhoid-like infections is that disease-free persistent infection can occur for months or years in a small number of individuals post-convalescence. The bacteria continue to be shed intermittently which is a key component of the epidemiology of these infections. Persistent chronic infection occurs despite high levels of circulating specific IgG. We have reviewed the information on the basis for persistence in <i>S</i>. Typhi, <i>S</i>. Dublin, <i>S.</i> Gallinarum, <i>S</i>. Pullorum, <i>S</i>. Abortusovis and also <i>S</i>. Typhimurium in mice as a model of persistence. Persistence appears to occur in macrophages in the spleen and liver with shedding either from the gall bladder and gut or the reproductive tract. The involvement of host genetic background in defining persistence is clear from studies with the mouse but less so with human and poultry infections. There is increasing evidence that the organisms (i) modulate the host response away from the typical Th1-type response normally associated with immune clearance of an acute infection to Th2-type or an anti-inflammatory response, and that (ii) the bacteria modulate transformation of macrophage from M1 to M2 type. The bacterial factors involved in this are not yet fully understood. There are early indications that it might be possible to remodulate the response back towards a Th1 response by using cytokine therapy.https://www.mdpi.com/2076-0817/10/10/1299<i>Salmonella</i>carrier statetyphoidimmunityTyphiDublin |
spellingShingle | Neil Foster Ying Tang Angelo Berchieri Shizhong Geng Xinan Jiao Paul Barrow Revisiting Persistent <i>Salmonella</i> Infection and the Carrier State: What Do We Know? Pathogens <i>Salmonella</i> carrier state typhoid immunity Typhi Dublin |
title | Revisiting Persistent <i>Salmonella</i> Infection and the Carrier State: What Do We Know? |
title_full | Revisiting Persistent <i>Salmonella</i> Infection and the Carrier State: What Do We Know? |
title_fullStr | Revisiting Persistent <i>Salmonella</i> Infection and the Carrier State: What Do We Know? |
title_full_unstemmed | Revisiting Persistent <i>Salmonella</i> Infection and the Carrier State: What Do We Know? |
title_short | Revisiting Persistent <i>Salmonella</i> Infection and the Carrier State: What Do We Know? |
title_sort | revisiting persistent i salmonella i infection and the carrier state what do we know |
topic | <i>Salmonella</i> carrier state typhoid immunity Typhi Dublin |
url | https://www.mdpi.com/2076-0817/10/10/1299 |
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