Host-to-Host Group A
Streptococcus
Transmission Causes Infection of the Lamina Propria but not Epithelium of the Upper Respiratory Tract in MyD88-Deficient Mice
To understand protective immune responses against the onset of Group A Streptococcus respiratory infection, we investigated whether MyD88 KO mice were susceptible to acute infection through transmission. After commingling with mice that had intranasal GAS inoculation, MyD88 -/- recipient mice had increased GAS loads in the nasal cavity and throat that reached a mean throat colonization of 6.3 x 10 6 cfu/swab and mean GAS load of 5.2 x 10 8 cfu in the nasal cavity on day 7. Beyond day 7, MyD88 -/- recipient mice became moribund, with mean 1.6 x 10 7 cfu/swab and 2.5 x 10 9 cfu GAS in the throat and nasal cavity, respectively. Systemic GAS infection occurred a couple of days after the upper respiratory infection. GAS infects the lip, gingival sulcus of the incisor teeth, the lamina propria of the turbinate but not the nasal cavity and nasopharyngeal tract epithelia, and C57BL/6J recipient mice had no or low levels of GAS in the nasal cavity and throat. Direct nasal GAS inoculation of MyD88 -/- mice caused GAS infection mainly in the lamina propria of the turbinate. In contrast, C57BL/6J mice with GAS inoculation had GAS bacteria in the nasal cavity but not in the lamina propria of the turbinates. Thus, MyD88 -/- mice are highly susceptible to acute and lethal GAS infection through transmission, and MyD88 signaling is critical for protection of the respiratory tract lamina propria but not nasal and nasopharyngeal epithelia against GAS infection.