Early pathogenesis of equine Streptococcus equi infection (strangles).
BACKGROUND
Little is known about entry and subsequent multiplication of Streptococcus equi following exposure of a susceptible horse. This information would have value in design of intranasal vaccines and understanding of shedding and protective immune responses.


OBJECTIVE
To determine entry points and sites of subsequent replication and dispersion of S. equi at different times after intranasal infection or commingling exposure.


METHODS
Previously unexposed horses and ponies were subjected to euthanasia 1, 3, 20 or 48 h following intranasal inoculation with biotin labelled or unlabelled S. equi CF32. Some ponies were inoculated with suspensions of equal numbers of CF32 and its mutants lacking capsule, S. equi M-like protein or streptolysin S. Others were infected by commingling exposure and subjected to euthanasia after onset of fever. Tonsils and lymph nodes were cultured for S. equi and tissues sectioned for histopathological examination and fluorescent microscopy.


RESULTS
Tonsillar tissues of both the oro- and nasopharynx served as portals of entry. Entry was unexpectedly rapid but involved few bacteria. Small numbers of organisms were detected in tonsillar crypts, in adjacent subepithelial follicular tissue and draining lymph nodes 3 h after inoculation. By 48 h, clumps of S. equi were visible in the lamina propria. At onset of fever, tonsillar tissues and one or more mandibular and retropharyngeal lymph nodes were heavily infiltrated by neutrophils and long chains of extracellular S. equi. Mutant S. equi lacking virulence factors were not seen in draining lymph nodes.


CONCLUSIONS
Although very small numbers of S. equi entered the lingual and nasopharyngeal tonsils, carriage to regional lymph nodes occurred within hours of inoculation. This observation, together with visual evidence of intracellular and extracellular multiplication of S. equi in tonsillar lymphoid tissue and lymph nodes over the following days, indicates involvement of potent antiphagocytic activity and failure of innate immune defences.


CONCLUSIONS
Future research should logically address the tonsillar immune mechanisms involved including identification of effector cell(s) and antigens.
Timoney
J F
JF
Gluck Equine Research Center, University of Kentucky, Lexington, Kentucky 40546-0099, USA.
Kumar
P
P
D000818:Animals; D015169:Colony Count, Microbial / Q000662:veterinary; D006734:Horse Diseases / Q000276:immunology / Q000382:microbiology* / Q000517:prevention & control; D006736:Horses; D007113:Immunity, Innate; D008198:Lymph Nodes / Q000276:immunology / Q000382:microbiology; D009504:Neutrophils / Q000276:immunology; D014066:Palatine Tonsil / Q000276:immunology* / Q000382:microbiology*; D012141:Respiratory Tract Infections / Q000276:immunology / Q000382:microbiology / Q000517:prevention & control / Q000662:veterinary*; D013290:Streptococcal Infections / Q000276:immunology / Q000382:microbiology / Q000517:prevention & control / Q000662:veterinary*; D018502:Streptococcus equi / Q000472:pathogenicity*