Abstract
Cross-species transfers of pathogens (zoonoses) cause some of the most virulent diseases, including anthrax, hantavirus and Q fever. Zoonotic infections occur when a pathogen moves from its reservoir host species into a secondary host species. Similarly, commensal infections often have a primary reservoir location within their hosts' bodies from which they rarely cause disease symptoms, but commensals such as Neisseria meningitidis cause severe disease when they cross into a different body compartment from their normal location. Both zoonotic and commensal infections cause either mild symptoms or severe disease, but rarely intermediate symptoms. We develop a mathematical model for studying three factors that affect the probability of severe disease: the size of the inoculum, the route of inoculation and the frequency of naturally occurring infections that do not cause symptoms but do induce protective immunity (vaccinating inoculations). With a single route of infection, increasing pathogen density causes inoculations to develop more often into disease rather than asymptomatic vaccinations that provide protective immunity. With two routes of infection, it may happen that a lower density of a pathogen or of a particular antigenic variant leads to a relatively higher frequency of disease-inducing versus vaccinating inoculations. This reversal occurs when one route of infection tends to vaccinate against relatively common pathogens but less often vaccinates against relatively rare pathogens, whereas the other route of infection is susceptible to disease-inducing inoculation even at relatively low pathogen density.
Full Text
The Full Text of this article is available as a PDF (198.9 KB).
Selected References
These references are in PubMed. This may not be the complete list of references from this article.
- Anderson R. M., May R. M. Coevolution of hosts and parasites. Parasitology. 1982 Oct;85(Pt 2):411–426. doi: 10.1017/s0031182000055360. [DOI] [PubMed] [Google Scholar]
- Frank S. A. Models of parasite virulence. Q Rev Biol. 1996 Mar;71(1):37–78. doi: 10.1086/419267. [DOI] [PubMed] [Google Scholar]
- Gyimah J. E., Panigrahy B. Immunogenicity of an Escherichia coli (serotype O1) pili vaccine in chickens. Avian Dis. 1985 Oct-Dec;29(4):1078–1083. [PubMed] [Google Scholar]
- Levin B. R., Bull J. J. Short-sighted evolution and the virulence of pathogenic microorganisms. Trends Microbiol. 1994 Mar;2(3):76–81. doi: 10.1016/0966-842x(94)90538-x. [DOI] [PubMed] [Google Scholar]
- Menon J. N., Bretscher P. A. Parasite dose determines the Th1/Th2 nature of the response to Leishmania major independently of infection route and strain of host or parasite. Eur J Immunol. 1998 Dec;28(12):4020–4028. doi: 10.1002/(SICI)1521-4141(199812)28:12<4020::AID-IMMU4020>3.0.CO;2-3. [DOI] [PubMed] [Google Scholar]
- Messier S., Quessy S., Robinson Y., Devriese L. A., Hommez J., Fairbrother J. M. Focal dermatitis and cellulitis in broiler chickens: bacteriological and pathological findings. Avian Dis. 1993 Jul-Sep;37(3):839–844. [PubMed] [Google Scholar]
- Panigraphy B., Gyimah J. E., Hall C. F., Williams J. D. Immunogenic potency of an oil-emulsified Escherichia coli bacterin. Avian Dis. 1984 Apr-Jun;28(2):475–481. [PubMed] [Google Scholar]
- Sandhu T. S., Layton H. W. Laboratory and field trials with formalin-inactivated Escherichia coli (O78)-Pasteurella anatipestifer bacterin in white pekin ducks. Avian Dis. 1985 Jan-Mar;29(1):128–135. [PubMed] [Google Scholar]
- Sjögren I., Sutherland I. Studies of tuberculosis in man in relation to infection in cattle. Tubercle. 1975 Jun;56(2):113–127. doi: 10.1016/0041-3879(75)90022-7. [DOI] [PubMed] [Google Scholar]