Early pathogenesis of equine Streptococcus equi infection (strangles).

The research article investigates how the bacterium Streptococcus equi, the cause of equine strangles, enters and replicates in susceptible horses. Findings suggest that the bacterium quickly enters through the tonsillar tissues and travels to regional lymph nodes despite the presence of seemingly small numbers, a process that involves failure of the horses’ innate immune defenses.

Research Objective and Methods

• The main aim of the study is to identify the entry points and subsequent replication and dispersion sites of the bacterium S. equi, by examining horses at different times after intranasal infection. These results are expected to assist in designing better intranasal vaccines and understanding shedding and protective immune responses.
• Horses that had not been previously exposed to S. equi were inoculated, some with one strain of the bacteria, known as CF32, while others were given suspensions of CF32 along with its mutants lacking specific virulence factors.
• Some horses were infected via commingling exposure, being kept closely together, and then subjected to euthanasia after the onset of fever.
• Post euthanasia, their tonsils and lymph nodes were cultured for S. equi, while tissues were examined under histopathological test and fluorescent microscopy.

Results and Findings

• The research revealed that the tonsillar tissues served as the entry points of the bacterium into the horse’s body. This entry occurred rapidly, though only a few bacteria were involved initially.
• Within 3 hours of inoculation, a small number of bacteria were detected in the tonsillar crypts, adjacent subepithelial follicular tissue, and draining lymph nodes.
• After 48 hours, clusters of S. equi were visible in the lamina propria (the connective tissue layer of the mucous membrane).
• At the onset of fever, the tonsillar tissues and one or more mandibular and retropharyngeal lymph nodes were heavily infiltrated by neutrophils (a type of white blood cell) and long chains of extracellular S. equi.
• The researchers did not identify S. equi mutants lacking virulence factors in draining lymph nodes, indicating that these mutants were less successful in invading the horse’s tissues.

Conclusions and Future Directions

• The research concludes that even though the number of S. equi entering lingual and nasopharyngeal tonsils was initially small, these bacteria were carried to regional lymph nodes within a few hours.
• There was visual evidence of both intracellular and extracellular multiplication of S. equi in tonsillar lymphoid tissue and lymph nodes over the following days, indicating a failure of innate immune defenses.
• The researchers suggest that further research should be targeted towards understanding tonsillar immune mechanisms, including the identification of effector cell(s) and antigens involved.