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1 e neuropsychiatric disorders associated with streptococcal infection)].
2 of CpsY-dependent regulation during systemic streptococcal infection.
3 ppressed transcription of these genes during streptococcal infection.
4 nique susceptibility of the human species to streptococcal infection.
5 the intranasal route protected mice against streptococcal infection.
6 nant of host species specificity for group A streptococcal infection.
7 nic choreoathetosis occurring as sequelae of streptococcal infection.
8 sually serologic) evidence of recent group A streptococcal infection.
9 lines focus solely on group A beta-hemolytic streptococcal infection.
10 ADEM) associated with Group A beta hemolytic streptococcal infection.
11 d no effect of cysteine protease on invasive streptococcal infection.
12 disease is an autoimmune sequela of group A streptococcal infection.
13 ) and/or tics believed to be associated with streptococcal infection.
14 the hypothesis of an autoimmune response to streptococcal infection.
15 sive disorder (OCD) may be sequelae of prior streptococcal infection.
16 such as rheumatic heart disease and invasive streptococcal infection.
17 iation of the autoimmune diseases related to streptococcal infection.
18 emic manifestations associated with invasive streptococcal infection.
19 play an important role in the first steps of streptococcal infection.
20 sceptibility to this complication of group A streptococcal infection.
21 ctivities that may relate to early stages of streptococcal infection.
22 nscription, and hence in the pathogenesis of streptococcal infection.
23 some patients with severe, invasive group A streptococcal infection.
24 ion of bacterial adaptations during systemic streptococcal infection.
25 nd contribute to the pathogenesis of group A streptococcal infections.
26 accine candidates to protect against group A streptococcal infections.
27 tic disorders occurring in association with streptococcal infections.
28 e neuropsychiatric disorders associated with streptococcal infections.
29 accounted for 20 percent of all 7867 group B streptococcal infections.
30 n important component of vaccines to prevent streptococcal infections.
31 IVIG can ameliorate severe invasive group A streptococcal infections.
32 as an important virulence factor in group A streptococcal infections.
33 he pathogenesis of severe staphylococcal and streptococcal infections.
34 e useful in the treatment of severe invasive streptococcal infections.
35 clonal basis for the resurgence of invasive streptococcal infections.
36 obic infections (13/28 [46%]), compared with streptococcal infection (23/137 [17%]) and infection inc
38 tary recruits who were evaluated for group A streptococcal infection and acute rheumatic fever betwee
39 ed on murine plasma at different times after streptococcal infection and compared with uninfected mic
40 lso several environmental factors, including streptococcal infection and stress, that affect the onse
41 shorter latency period between the inciting streptococcal infection and the onset of arthritis, a hi
42 xins, LTA-Hb interactions could occur during streptococcal infections and might result in a profound
45 f the host influence the outcome of invasive streptococcal infection, and demonstrate the underlying
46 er understanding the epidemiology of group A streptococcal infections, and for the development and us
48 s who have ADHD or OCD, chronic or recurrent streptococcal infections are associated with structural
49 ironmental triggers, such as beta-haemolytic streptococcal infections, are major determinants of dise
51 retory IgA may play a key role in preventing streptococcal infection at mucosal surfaces by blocking
52 ontribute to host susceptibility to invasive streptococcal infection but do not modulate disease outc
53 ted with increased risks, although less than streptococcal infections for OCD and any mental disorder
55 pes, its role in the pathogenesis of group A streptococcal infections has not been previously investi
59 trains, the dental clinician has to consider streptococcal infection in the differential diagnosis of
60 ed from two temporally distinct epidemics of streptococcal infections in the former East Germany foun
62 re there was active surveillance for group B streptococcal infection, including all births in which t
66 diatric autoimmune disorders associated with streptococcal infections) is the acronym applied to a su
68 pidemiology and severity of invasive group A streptococcal infections occurred in the 1980s, and the
71 monary hypertension in newborns with Group B streptococcal infection opens new avenues for therapeuti
74 lnesses secondary to group A beta-haemolytic streptococcal infections present with motor and psychiat
75 icularly with confirmed or suspected group A streptococcal infection, should be regarded as an obstet
76 -1980s, numerous reports of invasive group A streptococcal infections suggested that "highly virulent
78 tic shock; for 16 (50%) women with a group A streptococcal infection there was <2 h-and for 24 (75%)
79 butes to differences in severity of invasive streptococcal infections through their ability to regula
80 in rheumatic heart disease caused by group A streptococcal infection, valve tissues from rheumatic pa
81 cephalitis lethargica-like illness following streptococcal infection was reported, and unusual adult-
83 H binding in vivo (i.e., for pathogenesis of streptococcal infections), we used our recent finding th
84 hether previously reported associations with streptococcal infection were obscured by the presence of
85 rea is a CNS disorder and sequela of group A streptococcal infection where deposition of Abs in brain
86 describe a mechanism that underpins epidemic streptococcal infections, which have affected many milli
87 ent concepts in the pathogenesis of invasive streptococcal infection will be presented, with emphasis
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