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1 nd identify potential therapies for critical pertussis.
2 the possibility of host-targeted therapy for pertussis.
3 Preterm infants are most vulnerable to pertussis.
4 nated mothers required intubation or died of pertussis.
5 Infants are at greatest risk for severe pertussis.
6 nization (WHO) clinical case definitions for pertussis.
7 with cough illness that is not recognized as pertussis.
8 t protect against transmission of Bordetella pertussis.
9 ccination during pregnancy to prevent infant pertussis.
10 memory induced by natural infection with B. pertussis.
11 and Prevention case definition of "definite" pertussis.
12 f 10 infant cases qualified as having severe pertussis.
13 or reducing the morbidity and mortality from pertussis.
14 athology that promotes mortality in critical pertussis.
15 in adaptive immunological memory against B. pertussis.
16 lence of the whooping cough agent Bordetella pertussis.
17 tion requires growing large quantities of B. pertussis.
18 icient and those with pertactin-producing B. pertussis.
23 cal factor in establishing infection with B. pertussis and acts by specifically inhibiting the respon
24 ces in low-temperature adaptation between B. pertussis and B. bronchiseptica may result from selectiv
25 ely related respiratory pathogens Bordetella pertussis and Bordetella bronchiseptica Although B. pert
26 d that Bordetella bronchiseptica, Bordetella pertussis and Bordetella parapertussis have the recyclin
27 a previous report on the effect of adding a pertussis and diphtheria component to the tetanus vaccin
28 nce to support maternal immunisation against pertussis and influenza is rapidly accumulating, importa
30 panded in the lungs during infection with B. pertussis and proliferated rapidly after rechallenge of
31 n the lungs of mice during infection with B. pertussis and significantly expanded through local proli
32 l virus, sepsis-induced respiratory failure, pertussis, and "other"; and preextracorporeal membrane o
35 in Bordetella pertussis, the causal agent of pertussis, and related organisms, including the broad ho
36 ced diphtheria toxoid, and reduced acellular pertussis; and human papillomavirus vaccines) in additio
38 during 2008-2014 on the kinetics of maternal pertussis antibodies in unvaccinated women and their inf
39 increases in the prevalence of undetectable pertussis antibodies were found at 10 years after high c
40 vaccine containing diphtheria, tetanus, and pertussis antigens (DTP3) was >/=90% in 14 countries in
45 tussis (whooping cough) caused by Bordetella pertussis are on the rise, and understanding factors tha
48 ence and clinical presentation of Bordetella pertussis-associated hospitalization in perinatal HIV-ex
50 tegy in a setting such us ours to prevent B. pertussis-associated illness in women and their young in
52 at 27-36 weeks gestation had a lower risk of pertussis at <8 weeks of age than infants born to women
54 ed role in protective immunity to Bordetella pertussis, but this evidence is based largely on periphe
58 We conducted a case-control evaluation among pertussis cases <2 months old with cough onset between 1
60 Extended, retrospective analysis of reported pertussis cases between January 1, 1990, and December 31
61 g kindergarten in 2011 and 2012 and reported pertussis cases in 2012 for children in age groups 5 yea
62 and 11 statistically significant clusters of pertussis cases in children and adolescents were identif
65 We analyzed data on probable and confirmed pertussis cases reported through Enhanced Pertussis Surv
68 l terms, currently there is no evidence that pertussis causes a significant burden of disease in youn
70 er of DAP-type peptidoglycan from Bordetella pertussis, causes cytopathology in the respiratory epith
74 ovement in third dose of diphtheria- tetanus-pertussis-containing vaccine (DTP3) coverage in polio hi
76 in low- and middle-income countries (LMICs), pertussis continues to cause deaths in the youngest infa
80 ), and induced sputum, have been used for B. pertussis detection, although there is limited head-to-h
81 re admitted to hospital within 21 days of B. pertussis detection, whereas none of the 20 cases >/=2 m
83 ed knowledge gaps with respect to the infant pertussis disease burden in LMICs, and discussed propose
89 the late 2000s, when an increased burden of pertussis emerged among children 1 to 10 years old, resu
94 tely 0.1% of children who were infected with pertussis experienced a clinically significant second ep
95 unity to the respiratory pathogen Bordetella pertussis gammadelta T cells, predominantly Vgamma4(-)ga
97 es: polio, pentavalent (diphtheria, tetanus, pertussis, hepatitis B virus, and Haemophilus influenzae
98 h covers diphtheria, tetanus, and whole-cell pertussis; hepatitis B; and Haemophilus influenzae type
103 t prospective surveillance studies of infant pertussis in a developing country, we identified a moder
105 ies had geographic clusters of high rates of pertussis in children ages 10 to 14 years old, consisten
106 s gestation was more effective at preventing pertussis in infant than vaccination during the second t
109 ed as a means to reduce the burden of infant pertussis in low- and middle-income countries (LMICs), b
110 Evidence suggests that the resurgence of pertussis in many industrialized countries may result fr
111 ective strategy in reducing the incidence of pertussis in neonates prior to the onset of the primary
113 red for persistence of the human pathogen B. pertussis in the murine LRT and we provide evidence that
115 rize the available evidence of the burden of pertussis in the region, given historical data, and desc
117 g immunity may have had on the resurgence of pertussis in the United States at the community level.
121 uced responses to booster doses of acellular pertussis, inactivated polio, and diphtheria vaccines at
122 theria vaccine (diphtheria-tetanus-acellular pertussis-inactivated poliovirus/Haemophilus influenzae
123 demic pertussis since the lowest point in US pertussis incidence (after January 1, 1977), and for stu
124 onths, antenatal immunization reduced annual pertussis incidence by 60%, from 780 per 100,000 firstbo
129 unity to B. pertussis Natural immunity to B. pertussis induced by infection is considered long lastin
130 ctive cohort study design evaluating whether pertussis-infected infants born in 2011-2015 whose mothe
132 We conducted a population-based study of pertussis infection and reinfection during a 5-year peri
134 ia of respiratory illness were tested for B. pertussis infection by PCR on paired NPSs and NPAs; or p
135 eded to understand the immune response to B. pertussis infection in children vaccinated with aP vacci
136 rtactin-deficient and pertactin-producing B. pertussis infection in infants and describe correspondin
137 d children with >/=2 episodes of symptomatic pertussis infection that met the case definition were in
138 ious study used a murine model of Bordetella pertussis infection to demonstrate that treatment with t
139 ds and aP vaccine at the time of their first pertussis infection, 1 (4%) had received 1 dose, and 5 (
148 ression among Bordetella species and that B. pertussis is capable of expressing a full range of T3SS-
149 is study, a neonatal mouse model of critical pertussis is characterized, and a central role for pertu
154 ussis (whooping cough), caused by Bordetella pertussis, is resurging in the United States and worldwi
155 ged with a high dose of a highly virulent B. pertussis isolate, they were fully protected against dis
156 Molecular characterization of archived B. pertussis isolates (collected January 2007 to March 2014
160 al chemoselectivity, suggesting this E. coli pertussis-like toxin may serve as a unique tool to study
161 n spread to other bodily locations) encode a pertussis-like toxin that inhibits mammalian cell growth
164 toxin in whooping cough is well-established, pertussis-like toxins produced by other bacteria are les
165 lecular mechanism underpinning activation of pertussis-like toxins, and we also identified difference
166 mpared with B. bronchiseptica Remarkably, B. pertussis maintained the production of virulence factors
167 vaccines (tetanus, diphtheria, and acellular pertussis, measles and rubella, or measles, mumps, and r
168 IgG levels specific for diphtheria, tetanus, pertussis, measles, rubella, and Haemophilus influenzae
169 ults indicate a role for S1P signaling in B. pertussis-mediated pathology and highlight the possibili
170 ropose that the reduced plasticity of the B. pertussis membranes ensures sustained production of viru
175 ams have proven effective in reducing infant pertussis mortality in high-income countries using tetan
176 We systematically reviewed studies reporting pertussis mortality rates (PMRs) per million population,
178 y sensitivity analyses identified the infant pertussis mortality rates required to make maternal immu
179 untry, at a vaccine price of $4/dose, infant pertussis mortality would need to be 0.043 per 1000 to c
180 respiratory CD4 TRM cells in immunity to B. pertussis Natural immunity to B. pertussis induced by in
187 be a valuable tool to investigate causes of pertussis pathogenesis and identify potential therapies
189 and complications are less common among AAV pertussis patients, demonstrating that the positive impa
191 is-negative African cases in this age group, pertussis-positive cases were younger, more likely to vo
192 ls from the lungs of mice reinfected with B. pertussis produced significantly more IL-17 than gammade
194 VirB/VirD4, E. coli R388 Trw, and Bordetella pertussis Ptl systems support conjugative DNA transfer i
199 is and Bordetella bronchiseptica Although B. pertussis represents a pathogen strictly adapted to the
200 results indicate that the blunting of infant pertussis responses induced by maternal immunization, me
201 dap vaccine during pregnancy had less severe pertussis, resulting in a lower risk of hospitalization
204 hooping cough causative bacterium Bordetella pertussis Secreted as soluble protein, it targets myeloi
205 clinically significant illness, or of severe pertussis (seizure, encephalopathy, pneumonia, and/or ho
206 after January 1, 2000), endemic and epidemic pertussis since the lowest point in US pertussis inciden
209 ed pertussis cases reported through Enhanced Pertussis Surveillance (Emerging Infections Program Netw
211 receive a tetanus, diphtheria, and acellular pertussis (Tdap) vaccine at 27-36 weeks gestation during
212 o receive tetanus, diphtheria, and acellular pertussis (Tdap) vaccine at the start of the third trime
213 ct a maternal tetanus, diphtheria, acellular pertussis (Tdap) vaccine booster between 2 consecutive p
214 countries using tetanus-diphtheria-acellular pertussis (Tdap) vaccines in their maternal and infant p
215 trative coverage with 3rd dose of diphtheria-pertussis-tetanus vaccine in the 107 high-risk LGAs impr
216 e "master virulence regulator" in Bordetella pertussis, the causal agent of pertussis, and related or
218 nt nasopharyngeal colonization by Bordetella pertussis, the principal causative agent of whooping cou
219 has low detection sensitivity for diagnosing pertussis; the diagnosis is confirmed by measuring serum
221 morbidity and mortality caused by Bordetella pertussis To better inform such interventions, we conduc
222 A-produced signaling of cAMP thus enables B. pertussis to evade the key innate host defense mechanism
225 agnosis is confirmed by measuring serum anti-pertussis toxin (anti-PT) or anti-filamentous hemaggluti
227 MCs) of cord blood antibodies to recombinant pertussis toxin (PT) and filamentous hemagglutinin (FHA)
229 1143-induced AA contraction was sensitive to pertussis toxin (PTX), the LPA1&3 antagonist Ki16425, an
231 ntrast, inhibition of Galphai signaling with pertussis toxin affects speed but not the intermittent m
232 cs, and this reversal effect is inhibited by pertussis toxin and by genetic deletion of alpha-gustduc
233 propose that it is the systemic activity of pertussis toxin and not pulmonary pathology that promote
237 bitors of cAMP/PKA signaling, insensitive to pertussis toxin or beta-arrestin knock-out, and mimicked
238 ylcholine, after G-protein inactivation with pertussis toxin or in myocytes from M2- or M1/3-muscarin
239 RHGEF1, and DOCK2 is completely inhibited by pertussis toxin pretreatment, thus suggesting different
243 was also observed in neurons pretreated with pertussis toxin, an uncoupler of G proteins and MOR.
246 nist-induced rosette formation is blocked by pertussis toxin, dependent on PI3K activity and accompan
247 obulin (Ig) G specific for diphtheria toxin, pertussis toxin, filamentous hemagglutinin and pertactin
248 ect of MQC was reversed by pretreatment with pertussis toxin, indicating that FFA3 acts via the Gi/o
251 rom IL-17-activated PCs, but not ECs, induce pertussis toxin-sensitive neutrophil polarization, likel
256 with 11% lower postvaccination antibody for pertussis toxoid (GMR, 0.89; 95% CI, 0.87-0.90) and fila
261 of Tdap (tetanus, diphtheria, and acellular pertussis)-vaccinated pregnant women and 37 infants of w
264 occurred in vaccinated persons, showing that pertussis vaccination does not prevent all pertussis cas
265 s, demonstrating that the positive impact of pertussis vaccination extends beyond decreasing risk of
268 to 9 age groups corresponding to the current pertussis vaccination schedule and fit to 2012 pertussis
269 anus, reduced-dose diphtheria, and acellular pertussis vaccine (Tdap) could be an effective way of mi
270 netics of antibody responses to an acellular pertussis vaccine by a genome-wide association study in
273 analysis of published studies that evaluated pertussis vaccine efficacy or effectiveness within 3 yea
281 id, reduced diphtheria toxoid, and acellular pertussis) vaccine was recommended for women during each
282 having received an age-appropriate number of pertussis vaccines (AAV) (for persons aged >/=3 months)
283 nly (three doses of diphtheria, tetanus, and pertussis vaccines [DTP3] commencing in 1985, 1995, or 2
285 lysis of the short-term protective effect of pertussis vaccines limited to formulations currently on
287 antenatal care programs to deliver maternal pertussis vaccines, particularly with respect to infants
290 reventing hospitalization among infants with pertussis was 72% (95% confidence interval [CI], 49%-85%
293 (95% confidence interval, 4.2%-26.8%; 5/40); pertussis was identified in 3.7% of 137 in-hospital deat
294 We encountered an adult patient in whom B. pertussis was isolated by culture who previously receive
298 fy all children with 2 reported incidents of pertussis with symptom onset between 1 January 2010 and
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