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1 ndular (25%) forms of tularemia, followed by pneumonic (12%), typhoidal (10%), oculoglandular (3%), a
2     Most patients had primary bubonic (63%), pneumonic (21%), or septicemic (5%) plague, with associa
3 ar dendritic cell subset, the tipDCs, in the pneumonic airways.
4 ogenicity, leading to protection against the pneumonic and bubonic forms of plague.
5  achieve its full pathogenic ability in both pneumonic and bubonic plague in C57BL/6J mice.
6 opositive animals detected in 9/9 versus 0/9 pneumonic and nonpneumonic populations, respectively [P
7 e in models of bubonic plague but not in the pneumonic and septicemic forms of the disease.
8 rial growth and the development of fulminant pneumonic and septicemic plague.
9 cal form of plague, 93.6% were bubonic, 5.9% pneumonic, and 0.5% septicemic with associated case fata
10              Yersinia pestis causes bubonic, pneumonic, and septicemic plague, diseases that are rapi
11 ia pestis is the causative agent of bubonic, pneumonic, and septicemic plague.
12              Yersinia pestis causes bubonic, pneumonic, and septicemic plague.
13 enic wild-type (WT) bacterium in bubonic and pneumonic animal models (mouse and rat) of plague.
14                        MCs were localised at pneumonic areas, in the granuloma periphery and particul
15                          In a mouse model of pneumonic B. mallei infection, we found that both MCP-1(
16 hanisms required to generate protection from pneumonic B. mallei infection.
17 tical chemokine required for protection from pneumonic B. mallei infection.
18 MyD88-dependent pathways may be important in pneumonic B. thailandensis infection but that MyD88-inde
19 ng a protective function of MGL1 in an acute pneumonic bacterial infection.
20                                              Pneumonic BALF, but not S. pneumoniae, induced degradati
21 presence of M. ovipneumoniae in the lungs of pneumonic bighorn sheep in this study, and M. ovipneumon
22  high-quality diagnostic specimens from nine pneumonic bighorn sheep in three populations and analyze
23 sights into the host-pathogen interaction in pneumonic Burkholderia infection.
24 icrobials, thus making it difficult to treat pneumonic Burkholderia infections.
25 ic nature of outbreaks and the low number of pneumonic cases of disease, we sought FDA approval of an
26                                    Following pneumonic challenge, the best efficacy was obtained in m
27                                              Pneumonic consolidation and mean virus titer in lung 7 d
28 here was moderate to severe inflammation and pneumonic consolidation in isolated areas at 5 and 7 day
29  patients from both outbreaks presented with pneumonic disease and although aerosol transmission has
30  Francisella tularensis causes acute, lethal pneumonic disease following infection with only 10 CFU.
31 vine respiratory tract prior to the onset of pneumonic disease is potentially due to bacterial invasi
32                                          For pneumonic disease specifically, ciprofloxacin may have s
33 ion to transmission-associated septicemic or pneumonic disease states.
34                                Patients with pneumonic disease who received ciprofloxacin had no fata
35 f serotype A1 bacteria leads to the onset of pneumonic disease.
36 ceroglandular, oropharyngeal, glandular, and pneumonic disease.
37 infection but only slight attenuation by the pneumonic-disease model, closely mimicking the virulence
38 es and rabbits against challenge with lethal pneumonic doses of fully virulent Ames strain spores.
39                               Progression of pneumonic extension >=0.5 lung fields per day compared t
40 microbiome and resistome of 38 subclinically pneumonic foals treated with either MaR (n = 19) or gall
41 horacic ultrasonography (i.e., subclinically pneumonic foals) is common in the United States.
42 ve agent of tularemia, is most deadly in the pneumonic form; therefore, mucosal immunity is an import
43 la pneumophila is the main cause of a severe pneumonic illness known as Legionnaires' disease and is
44  in the development of acute fibrinopurulent pneumonic infection in cattle.
45  immunity and IFN-gamma production following pneumonic infection with B. mallei and therefore may als
46  with the pathogen Salmonella Typhimurium or pneumonic infection with Burkholderia thailandensis, the
47 cells, NK cells, and NKT cells, during acute pneumonic infection with Klebsiella pneumoniae (KPn).
48 ng bubonic infection and in the lungs during pneumonic infection, suggesting a role for the Yaps duri
49 e of MGL1 in controlling neutrophilia during pneumonic infection, thus playing an important role in r
50 ed replication in respiratory airways during pneumonic infection.
51                  Sepsis resulting from acute pneumonic infections by Gram-negative bacteria is often
52 t can cause severe, rapidly life-threatening pneumonic infections.
53 red in the murine bubonic (subcutaneous) and pneumonic (intranasal) plague infection models.
54 89.8%) than for urine from patients with non-pneumonic invasive infection (61.5%; P<0.05).
55 pha is required for the prompt resolution of pneumonic legionellosis and point to a direct role for T
56  alone or in combination with rF1, prevented pneumonic lesions and disease pathogenesis.
57                                          The pneumonic lesions and mortality caused by Mannheimia hae
58 tory disease and macroscopic and microscopic pneumonic lesions were more severe and persistent in M.
59 examination of the lungs and live imaging of pneumonic lesions, using a bioluminescent pneumococcus,
60  children presenting with uncomplicated (non-pneumonic) LRTI in primary care, overall and in key clin
61 quency CD8(+) tetramer(+) populations in the pneumonic lung and mediastinal lymph nodes fell rapidly
62 c sequences of two bovine isolates, one from pneumonic lung and the other from healthy prepuce, have
63  was detected as a predominant member of the pneumonic lung flora in lambs with early lesions of bron
64 onse profile in both lymphoid tissue and the pneumonic lung has no obvious deleterious consequences.
65 g lesions of these cattle with a majority of pneumonic lung lobes exhibiting fibronecrotic and exudat
66 magnitude of the inflammatory process in the pneumonic lung, though replication of this influenza vir
67 ffector T cell function and pathology in the pneumonic lung.
68 aged, "high-antigen load" environment of the pneumonic lung.
69 d virus-specific CD4+ T cell response in the pneumonic lung; 2) enhanced primary antiviral Ab-forming
70 neutrophils exhibited an increased influx in pneumonic lungs of K. pneumoniae-infected mice.
71 nfluenza epitope recovered directly from the pneumonic lungs of mice, this technique determined that
72 heimia haemolytica serotype A2 isolated from pneumonic lungs of two different ruminant species, one f
73 ating cytokine expressed in the airspaces of pneumonic lungs, but its physiological significance in t
74                  A whole-body mouse model of pneumonic melioidosis was established for future evaluat
75 ts are confirmed using an experimental mouse pneumonic metastasis model.
76 eumonia but was ineffective against severely pneumonic mice, despite effective bacterial killing.
77 -dependent modifications in the airspaces of pneumonic mice, implicating a network of dispatched live
78 free beta-GlcCer accumulated in the lungs of pneumonic mice, which correlated with pulmonary NET form
79 he induction of select APPs in the livers of pneumonic mice.
80 roximately half of RSV-infected persons, and pneumonic opacities were typically small and unilateral.
81 nfected with a closely related gram-negative pneumonic organism (Klebsiella pneumoniae) suggesting th
82 echnology to render them less susceptible to pneumonic pasteurellosis and concomitant economic losses
83  One of the pathological hallmarks of bovine pneumonic pasteurellosis is an influx of neutrophils int
84 imia haemolytica is the etiological agent of pneumonic pasteurellosis of cattle and sheep; two differ
85 bronecrotic and exudative changes typical of pneumonic pasteurellosis, but other lung lobules had his
86 hospholipase products in the pathogenesis of pneumonic pasteurellosis, development and use of anti-in
87 to the pathogenesis of lung injury in bovine pneumonic pasteurellosis.
88 important role in the pathogenesis of bovine pneumonic pasteurellosis.
89 to the pathogenesis of lung injury in bovine pneumonic pasteurellosis.
90 ophysiological events associated with bovine pneumonic pasteurellosis.
91 ts in an acute respiratory disorder known as pneumonic pasteurellosis.
92                                              Pneumonic plague (PP), caused by Yersinia pestis, is the
93                                        Acute pneumonic plague accompanies the up-regulation of pro-in
94 rat as an alternative small animal model for pneumonic plague and characterized both the efficacy and
95  studying T-cell-mediated protection against pneumonic plague and demonstrates the capacity for live,
96 early host/pathogen interactions that define pneumonic plague and showcase the utility of human preci
97 ling early host/pathogen interactions during pneumonic plague and solidify the role of Pla in promoti
98 n CO92 and screened them in a mouse model of pneumonic plague at a dose equivalent to 5 50% lethal do
99 dicate that Y. pestis was capable of causing pneumonic plague before it evolved to optimally cause in
100 lly virulent in animal models of bubonic and pneumonic plague but also break through immune responses
101  is essential for Y. pestis to cause primary pneumonic plague but is less important for dissemination
102 d Yersinia pestis confers protection against pneumonic plague but is not considered safe for general
103 ation protected mice from lethal bubonic and pneumonic plague caused by CO92, a wild-type F1+ strain,
104 rt the use of gepotidacin as a treatment for pneumonic plague caused by Y. pestis.
105       Development of this new agent to treat pneumonic plague caused by Yersinia pestis depends on th
106 ation resulted in partial protection against pneumonic plague challenge with 250 MLD Y. pestis CO92,
107 responses and protection against bubonic and pneumonic plague challenges, with 80% and 90% survival,
108 o longer responsible for pandemic outbreaks, pneumonic plague continues to be a challenge for medical
109 side-ciprofloxacin group died, and secondary pneumonic plague developed in 3 patients in each group.
110 ague have highlighted a significant role for pneumonic plague during outbreaks of Y. pestis infection
111 lence testing in mouse models of bubonic and pneumonic plague found only a modest increase in surviva
112 course, severity, and difficulty of treating pneumonic plague highlight how differences in the route
113  severely attenuated Y. pestis CO92 to evoke pneumonic plague in a mouse model while retaining the re
114 ighly attenuated in evoking both bubonic and pneumonic plague in a mouse model.
115 in are fully effective treatment options for pneumonic plague in AGMs.
116               The mean lethal dose (MLD) for pneumonic plague in guinea pigs was estimated to be 1000
117               Yersinia pestis causes primary pneumonic plague in many mammalian species, including hu
118 ented Y. pestis were reported to cause fatal pneumonic plague in mice, suggesting a useful model for
119  in virulence for bubonic plague but not for pneumonic plague in mice.
120 s conferred comprehensive protection against pneumonic plague in naive recipient mice.
121                 To develop an alternative to pneumonic plague in nonhuman primates, we explored guine
122 ting type III secretion in the prevention of pneumonic plague in rats and reveal critical contributio
123                                              Pneumonic plague is a deadly respiratory disease caused
124                                        Human pneumonic plague is a devastating and transmissible dise
125               Disease progression of primary pneumonic plague is biphasic, consisting of a preinflamm
126                                              Pneumonic plague is one of the world's most deadly infec
127                             The AGM model of pneumonic plague is reproducible, well-characterized, an
128                                              Pneumonic plague is the deadliest form of disease caused
129                                     Although pneumonic plague is the deadliest manifestation of disea
130                                              Pneumonic plague is the most severe manifestation of pla
131                                      Primary pneumonic plague is transmitted easily, progresses rapid
132 Pla, its precise role in the pathogenesis of pneumonic plague is yet to be defined.
133 rovide 90 to 100% survivability to mice in a pneumonic plague model at 20 to 50 LD50.
134  double mutant was still fully virulent in a pneumonic plague model but had an approximately 90-fold
135 he Deltalpp or DeltamsbB single mutant, in a pneumonic plague model were significantly protected agai
136   Surprisingly, via intranasal instillation (pneumonic plague model), we saw a difference in the viru
137                                    In murine pneumonic plague models, passive transfer of convalescen
138  virulence of Y. pestis in either bubonic or pneumonic plague models.
139                 In a parallel study with the pneumonic plague mouse model, after 72 h postinfection,
140 tion mutant was decreased about 10-fold in a pneumonic plague mouse model.
141 also attenuated (40 to 100%) at 12 LD50 in a pneumonic plague mouse model.
142 caf mutant was as virulent as WT CO92 in the pneumonic plague mouse model; however, it was attenuated
143 mized, controlled efficacy trials in the AGM pneumonic plague nonhuman primate model together with th
144 portant role for RovA in bubonic plague than pneumonic plague or systemic infection.
145 ernative small animal model for the study of pneumonic plague pathogenesis and immunity.
146 ptb1(pYA5199) play a protective role against pneumonic plague remains unclear.
147                                              Pneumonic plague represents the most severe form of dise
148  We hypothesized that the pathophysiology of pneumonic plague resulting from expression of proteins e
149                                              Pneumonic plague resulting from Yersinia pestis induces
150 t is less important for dissemination during pneumonic plague than during bubonic plague.
151 ulence factors required for the induction of pneumonic plague that are independent of iron scavenging
152 can green monkey (AGM) inhalational model of pneumonic plague to test the efficacy of gepotidacin.
153 utant and comparing its ability in mediating pneumonic plague to that of the wild type in two animal
154 rtant new target for developing an effective pneumonic plague vaccine.
155 ary Y. pestis challenge, and we suggest that pneumonic plague vaccines should aim to induce mixed typ
156 vations strongly suggest that development of pneumonic plague vaccines should strive to prime both CD
157 To aid the development of safe and effective pneumonic plague vaccines, we are deciphering mechanisms
158 y host response during the course of primary pneumonic plague was investigated in two mouse strains,
159                             The AGM model of pneumonic plague was used to explore the effect of delay
160 illation, these rats rapidly developed fatal pneumonic plague within 2 to 4 days of infection.
161 ulmonary infection by Yersinia pestis causes pneumonic plague, a necrotic bronchopneumonia that is ra
162                     Vaccines against primary pneumonic plague, a potential bioweapon, must be tested
163  of the bacterium Yersinia pestis causes the pneumonic plague, a rapidly fatal disease.
164 ulmonary infection by Yersinia pestis causes pneumonic plague, a rapidly progressing and often fatal
165 pestis is the causative agent of bubonic and pneumonic plague, an acute and often fatal disease in hu
166 am-negative bacterium Yersinia pestis causes pneumonic plague, an acutely lethal septic pneumonia.
167 he potential virulence properties of Psa for pneumonic plague, an Escherichia coli strain expressing
168                                              Pneumonic plague, an often-fatal disease for which no va
169 on with the bacterium Yersinia pestis causes pneumonic plague, an often-fatal disease for which no va
170 ficantly affected by the Pla protease during pneumonic plague, and although A2AP participates in immu
171 ynergistically in protecting animals against pneumonic plague, and we have demonstrated an immunologi
172 onsequences of neutrophil recruitment during pneumonic plague, and we studied the susceptibility of C
173 rsinia pestis-laden aerosols that results in pneumonic plague, arming both the mucosal and systemic i
174 s protective immunity to prevent bubonic and pneumonic plague, as well as yersiniosis, in mice and wo
175 uvant to enhance protective immunity against pneumonic plague, but in a dose-dependent fashion.
176                                              Pneumonic plague, caused by inhalation of Yersinia pesti
177                                              Pneumonic plague, caused by Yersinia pestis, is a rapidl
178 is review we describe the characteristics of pneumonic plague, focusing on its disease progression an
179    Yersinia pestis, which causes bubonic and pneumonic plague, forms pigmented red colonies on Congo
180                                          For pneumonic plague, immunized mice required immunity to bo
181  deeply rooted strains of Y. pestis to cause pneumonic plague, indicating that Y. pestis was primed t
182 m-negative bacterium that causes bubonic and pneumonic plague, is able to rapidly disseminate to othe
183                    In a coinfection model of pneumonic plague, it appears that Yersinia pestis quickl
184                    Despite the importance of pneumonic plague, little is known of the early pulmonary
185 t failure defined as death, fever, secondary pneumonic plague, or alternative or prolonged plague tre
186 that protect mice against bubonic plague and pneumonic plague, suggesting that rV10 may serve as an i
187 ared to the WT bacterium in a mouse model of pneumonic plague, the Deltalpp Deltaail double mutant an
188             Additional treatment options for pneumonic plague, the most severe form of infection by Y
189 le this modification is unnecessary to cause pneumonic plague, the substitution is instead needed to
190 tis virulence in mouse models of bubonic and pneumonic plague, we characterized an msbB in-frame dele
191 sing the C57BL/6 mouse models of bubonic and pneumonic plague, we determined that all of these genes
192 produces a severe primary pneumonia known as pneumonic plague, which is contagious and highly lethal
193 esidues 271-300, elicited protection against pneumonic plague, which seemed to be based on conformati
194 , Yersinia-specific sRNA in a mouse model of pneumonic plague.
195 positive strains of Y. pestis in bubonic and pneumonic plague.
196 th Yersinia pestis, the agent of bubonic and pneumonic plague.
197 a live attenuated cell-based vaccine against pneumonic plague.
198 bt, that plays a role in the pathogenesis of pneumonic plague.
199 anism and the causative agent of bubonic and pneumonic plague.
200 for virulence in mouse models of bubonic and pneumonic plague.
201  the use of an iron dextran-treated model of pneumonic plague.
202 pigmented Yersinia pestis does not result in pneumonic plague.
203 e was no disease pathology characteristic of pneumonic plague.
204 tis primes T cells that protect mice against pneumonic plague.
205 n in virulence in mouse models of bubonic or pneumonic plague.
206  derivative, V10, to protect these rats from pneumonic plague.
207 to become the causative agent of bubonic and pneumonic plague.
208 sease that can manifest as either bubonic or pneumonic plague.
209 and F1 antigens protected mice in a model of pneumonic plague.
210 ce for the pathogenesis of plague, including pneumonic plague.
211 e cells to vaccine-primed protection against pneumonic plague.
212 . pestis infection, an experimental model of pneumonic plague.
213 terized an intranasal mouse model of primary pneumonic plague.
214 llular immunity will most effectively combat pneumonic plague.
215 fferentiation primary response 88 (MyD88) in pneumonic plague.
216 ion, protected mice in models of bubonic and pneumonic plague.
217 stis KIM, the etiologic agent of bubonic and pneumonic plague.
218 of Yersinia pestis, the agent of bubonic and pneumonic plague.
219 ormation and expansion or protection against pneumonic plague.
220 able inflammatory responses to cause primary pneumonic plague.
221 bacterium Yersinia pestis results in primary pneumonic plague.
222 m that is the causative agent of bubonic and pneumonic plague.
223  CO92 in mouse and rat models of bubonic and pneumonic plague.
224 . pestis CO92 in mouse models of bubonic and pneumonic plague.
225 dent manner in the lungs during experimental pneumonic plague.
226 able impact on the progression or outcome of pneumonic plague.
227  pestis causes the fatal respiratory disease pneumonic plague.
228 nuation at 11 or 12 LD50 in a mouse model of pneumonic plague.
229 3SS as a potential vaccine candidate against pneumonic plague.
230 icantly protected from developing subsequent pneumonic plague.
231 pha and IFN-gamma in protecting mice against pneumonic plague.
232 d for production of bubonic, septicemic, and pneumonic plague.
233 a pestis, the causative agent of bubonic and pneumonic plague.
234 mportant for development of both bubonic and pneumonic plague.
235 ing specific roles for these pathways during pneumonic plague.
236 d lethality in murine models of systemic and pneumonic plague.
237 ironment during the preinflammatory phase of pneumonic plague.
238 protease is essential for the development of pneumonic plague; however, the complete repertoire of su
239 a pestis, the causative agent of bubonic and pneumonic plagues, has undergone detailed study at the m
240 pestis is the etiologic agent of bubonic and pneumonic plagues.
241 redict the ventilatory support need based on pneumonic progression of COVID-19 on consecutive chest X
242 role of the C-type lectin receptor Mincle in pneumonic sepsis caused by K. pneumoniae.
243 uses Gram-negative lung infections and fatal pneumonic sepsis for which limited therapeutic options a
244                         In a murine model of pneumonic sepsis using pulmonary infection with Klebsiel
245 se-type lectin-1 (MGL1), a mammalian CLR, in pneumonic sepsis, a deadly immune disorder frequently as
246 e a critical cellular population to regulate pneumonic sepsis.
247 ating nociceptors promote CRKP pneumonia and pneumonic sepsis.
248 tidrug-resistant Gram-negative infection and pneumonic sepsis.
249 il sequestration and edema formation at that pneumonic site with or without pretreatment with endotox
250 e 14th century are inconsistent with direct (pneumonic) transmission.
251 onducted a case-control study of adults with pneumonic tularemia and investigated the environment to
252 on of Francisella tularensis biovar A causes pneumonic tularemia associated with high morbidity and m
253         The development of a vaccine against pneumonic tularemia has been limited by a lack of inform
254            Study of this outbreak of primary pneumonic tularemia implicates lawn mowing and brush cut
255 ated as potential vaccine candidates against pneumonic tularemia in experimental animals.
256         We now report the natural history of pneumonic tularemia in female Fischer 344 rats after nos
257                             Although primary pneumonic tularemia in humans typically occurs by inhala
258  Inhalation of Francisella tularensis causes pneumonic tularemia in humans, a severe disease with a 3
259                 Overall, the pathogenesis of pneumonic tularemia in the female F344 rat model appears
260     The only previously reported outbreak of pneumonic tularemia in the United States also occurred o
261                                              Pneumonic tularemia is a life-threatening disease caused
262                                              Pneumonic tularemia is caused by inhalation of Francisel
263                             The incidence of pneumonic tularemia is very low; therefore, it is not fe
264 n the summer of 2000, an outbreak of primary pneumonic tularemia occurred on Martha's Vineyard, Massa
265 ar results were obtained in a mouse model of pneumonic tularemia using the highly virulent F. tularen
266 mutant because this strain was attenuated in pneumonic tularemia yet induced a protective immune resp
267 profloxacin were efficacious in treatment of pneumonic tularemia, although clearance of bacteria may
268                                 Inhalational pneumonic tularemia, caused by Francisella tularensis, i
269 eyard who had symptoms suggestive of primary pneumonic tularemia, were ill between May 15 and October
270  was severely reduced in the murine model of pneumonic tularemia.
271 f chicken embryos and in the murine model of pneumonic tularemia.
272  ligand on resistance to F. novicida-induced pneumonic tularemia.
273  novicida, leading to protective immunity to pneumonic tularemia.
274 rtant role in tempering the host response to pneumonic tularemia.
275 ronment to identify risk factors for primary pneumonic tularemia.
276 th tularemia; 11 of these cases were primary pneumonic tularemia.
277 r to qualify the cynomolgus macaque model of pneumonic tularemia.
278 ting novel vaccines and therapeutics against pneumonic tularemia.
279 vere tissue damage that characterizes lethal pneumonic tularemia.
280 ompared to the wild type in a mouse model of pneumonic tularemia.
281 n of this agent with bronchopneumonia (16/34 pneumonic versus 0/17 nonpneumonic sheep were PCR positi

 
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