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Chapter 44 : Animal Models of Experimental Infection

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Abstract:

This chapter discusses experimental models of infections, including toxic shock, sepsis, endocarditis, colonization of joints and bones, mastitis, eye and skin infections, and septic arthritis. It concentrates on models that provide an insight into the pathogenesis of . As an example of a model for studying staphylococcal disease, the chapter presents the murine model of septic arthritis and sepsis and discusses how models such as this might be used to formulate treatment and prophylaxis regimens. The various disease entities associated with infections and some proposed animal models are listed in a table. Cytokines play a critically important role in the pathogenesis of infection, and the modulation of specific cytokines is attracting substantial interest as a means of treating disease. The emergence of antibiotic-resistant staphylococci and in particular the methicillin-resistant strains has stimulated a resurgence in the development of new antibiotics with antistaphylococcal activities and alternatives to classical antibacterial therapies. During the last decade, the use of experimental models of staphylococcal infections has clarified the involvement of several bacterial virulence factors as well as many hematopoietic cell types and their products in the pathogenesis of infection. Animal models that mimic the etiology, progression, and pathology of the disease in the natural host are a crucial component in the development of therapeutic strategies.

Citation: Collins L, Tarkowski A. 2006. Animal Models of Experimental Infection, p 535-543. In Fischetti V, Novick R, Ferretti J, Portnoy D, Rood J (ed), Gram-Positive Pathogens, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816513.ch44

Key Concept Ranking

Toxic Shock Syndrome Toxin 1
0.515625
Major Histocompatibility Complex Class II
0.43584833
0.515625
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Figures

Image of FIGURE 1
FIGURE 1

() Early and persistent infiltrations of inflammatory cells during dermatitis. The micrograph shows the inflammatory infiltrate in mouse skin that was inoculated intracutaneously with 2 × 10 CFU of LS-1: after 6 h (A), 48 h (B), and 1 week (C). The inflammatory infiltrate, which mainly contains macrophages, peaks at 48 h and starts to disappear 2 weeks after the inoculation (from reference ).

Citation: Collins L, Tarkowski A. 2006. Animal Models of Experimental Infection, p 535-543. In Fischetti V, Novick R, Ferretti J, Portnoy D, Rood J (ed), Gram-Positive Pathogens, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816513.ch44
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Image of FIGURE 2
FIGURE 2

ClfA influence on septic arthritis. Development of arthritis in NMRI mice that were inoculated i.v. with 1.4 to 1.9 × 10 CFU of wild-type strain Newman, mutant DU5876 (), complemented mutant strain DU5898 ( mutant + ), or mutant with vector plasmid strain DU5899 ( mutant + empty vector). Circles and squares show the median, and whiskers show the arthritic index. Two sets of statistical tests were performed: the wildtype and DU5876-infected mice were compared, and the DU5898- and DU5899-infected mice were compared. * <0.001. The severity of arthritis is markedly reduced in mice challenged i.v. with the mutant, compared with mice infected with the wild-type strain (from reference ).

Citation: Collins L, Tarkowski A. 2006. Animal Models of Experimental Infection, p 535-543. In Fischetti V, Novick R, Ferretti J, Portnoy D, Rood J (ed), Gram-Positive Pathogens, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816513.ch44
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Image of FIGURE 3
FIGURE 3

Effect of sortase mutation on the ability of to cause septic arthritis. Severity of arthritis in NMRI mice inoculated with 6 × 10 CFU of Newman or its isogenic sortase-deficient mutant, strain SKM3 (10 mice/group). Data shown are median and interquartile range for each group of mice. Comparisons were made using the Mann-Whitney Utest. values are for the comparison between the wild-type Newman strain and the sortase mutant strain SKM3. N.S., not significant. The results show that the sortase loss significantly reduces the arthritogenicity of strain Newman (from reference ).

Citation: Collins L, Tarkowski A. 2006. Animal Models of Experimental Infection, p 535-543. In Fischetti V, Novick R, Ferretti J, Portnoy D, Rood J (ed), Gram-Positive Pathogens, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816513.ch44
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Image of FIGURE 4
FIGURE 4

Mucosal administration of SEA protects against SEA-induced death. Mice were given SEA, recombinant nonsuperantigenic SEA (rSEA), or ovalbumin (OVA) intranasally three times 1 week apart, and challenged intraperitoneally with SEA + LPS 1 week later. Data are expressed as survival of OVA-tolerized (■), rSEA-tolerized (Δ), and SEA-tolerized (□) C57BL/6 (A) and BALB/c (B) mice during the first 70 h post-SEA challenge. **, <0.01; ***, <0.001 compared to OVA-tolerized animals. The data show that mice that receive SEA intranasally are protected against a subsequent lethal SEA challenge (from reference ).

Citation: Collins L, Tarkowski A. 2006. Animal Models of Experimental Infection, p 535-543. In Fischetti V, Novick R, Ferretti J, Portnoy D, Rood J (ed), Gram-Positive Pathogens, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816513.ch44
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Tables

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TABLE 1

Experimental animal models used to study diseases associated with infection

Citation: Collins L, Tarkowski A. 2006. Animal Models of Experimental Infection, p 535-543. In Fischetti V, Novick R, Ferretti J, Portnoy D, Rood J (ed), Gram-Positive Pathogens, Second Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816513.ch44

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