ライフサイエンスコーパス: sputum

1 tic and viscous moduli compared with healthy sputum.

2 ceptibility analyses on M. tuberculosis from sputum.

3 on down to 43 cfu/mL of MTB bacilli from raw sputum.

4 ls, suggesting heterogeneous growth rates in sputum.

5 ssify these sounds to detect the presence of sputum.

6 nsitivity and specificity for urine, pus and sputum.

7 e adverse events and bacterial resistance in sputum.

8 erial translational activity in expectorated sputum.

9 the surface of eosinophils and mast cells in sputum.

10 nce and the neutrophil activation pathway in sputum.

11 umbers of neutrophils and lymphocytes in the sputum.

12 dia, bronchoalveolar lavage (BAL) fluid, and sputum.

13 y-seven subjects were recruited and provided sputum (83 asthmatics; 14 healthy subjects), with 29 als

14 erculosis (TB) usually require collection of sputum, a viscous material derived from human airways.

15 elationship between demographic features and sputum ACE2 and TMPRSS2 gene expression in asthma.Method

16 We compared sputum ACE2 expression in patients with COPD stratified

17 Pathogenicity of detected sputum ANCA was assessed using in vitro degranulation as

18 In addition, 16 of 17 (94%) of sputum ANCA(+) patients had clinical manifestations of s

19 ere asthma compared with 3 of 6 (50%) in the sputum ANCA(-) subset (P = 0.04).

20 mined the presence and clinical relevance of sputum ANCAs in the serum ANCA(-) patients with eGPA.

21 urable levels of nicotine were detectable in sputum and BAL, which corresponded to the half-maximal e

22 alyzed the nicotine concentration in induced sputum and BAL.

23 IL33 levels are elevated in sputum and bronchial biopsies of patients with asthma.

24 enes from lower respiratory tract specimens (sputum and bronchoalveolar lavage [BAL] fluid).

25 Although sputum and bronchoalveolar lavage samples provide the hi

26 uencing to identify the dominant bacteria in sputum and compositional data analysis to determine asso

27 portion of fungal taxa in common between the sputum and EDC samples was significantly higher when pat

28 d by risk of frequent exacerbations, airway (sputum and mucosal) neutrophilia, decreased lung microbi

29 We sought to determine sputum and oral microbiota relationships to clinical or

30 Novel associations of sputum and oral microbiota to immunologic features were

31 microbiota profiles were analyzed in induced sputum and oral wash samples from 32 subjects with mild

32 Induced sputum and peripheral blood obtained after each MT were

33 Sputum and serum PZP was measured by validated ELISA.

34 d on eosinophils and mast cells in asthmatic sputum and targeting Siglec-8 with an antibody is a plau

35 patients also have increased eosinophils in sputum and this may be reflected by increased blood eosi

36 rough screening HIV-positive inpatients with sputum and urine diagnostics in Malawi and South Africa

37 lture positivity (fluid, biopsy specimen, or sputum) and/or pleural biopsy histopathology (termed def

38 more abundant from bronchoscopy samples than sputum, and differentially more abundant in asthma than

39 Metabolites in nasal lining fluid, sputum, and plasma from patients with N-ERD (n = 15) and

40 r non-TB diseases, but who could expectorate sputum, and were then evaluated by smear microscopy, BAC

41 Among them, deep throat saliva and induced sputum are desired for RT-qPCR test or other early detec

42 oral swabs may become useful supplements to sputum as samples for diagnosis of pulmonary TB in child

43 t nucleic acids directly in blood, urine and sputum at sub-femtomolar concentrations, and microorgani

44 f eosinophils, monocytes, and ECP in induced sputum at V3 compared with V1.

45 However, mycobacterial sputum bacillary load and clinical characteristics, incl

46 Sputum bacterial burden inversely associated with bronch

47 s in lung inflammatory mediators and reduced sputum bacterial diversity.

48 ficity than smear microscopy-the most common sputum-based diagnostic test.

49 Sputum-based diagnostics are challenging to implement an

50 Current sputum-based diagnostics are specific but lack sensitivi

51 Organization target product profiles for non-sputum-based tests.

52 ies on primary clinical specimens, including sputum, blood cultures, and pus, bacteria from 5 differe

53 s included IFN-response markers in serum and sputum, blood leucocyte counts and serum inflammatory cy

54 Sputum can be difficult and hazardous to collect and cha

55 counts, IL-1beta protein levels (ELISA), and sputum cell gene expression (Nanostring nCounter).

56 Network analysis of sputum cell transcriptome expression data from 84 subjec

57 rences in ACE2 or TMPRSS2 gene expression in sputum cells among patients with asthma may identify sub

58 es: To define the transcriptional profile of sputum cells and its implication in the pathogenesis of

59 1) (rhinovirus receptor as a comparator) in sputum cells from 330 participants in SARP-3 (Severe Ast

60 : We performed single-cell RNA sequencing of sputum cells from nine subjects with CF and five healthy

61 used to characterize Siglec-8 expression in sputum cells from stable asthma.

62 iptomic analysis of bronchial epithelial and sputum cells has identified a Type 2 high inflammation c

63 Gene expression for Siglec-8 is increased in sputum cells in asthma and correlates with gene expressi

64 cteristics, inflammatory phenotypes based on sputum cells, as well as eicosanoid levels in induced sp

65 Baseline TB severity, sputum conversion, and treatment outcomes (cure, failure

66 isk of progression from LTBI to ATB prior to sputum conversion.

67 00 cells/mul), sputum Xpert, and/or a single sputum culture among consecutive people living with HIV

68 fungal sensitization and/or positive fungal sputum culture and markers of asthma severity in childre

69 ated 5 different diagnostic strategies using sputum culture as a reference standard (Xpert alone, LAM

70 Q total score, and Pseudomonas aeruginosa in sputum culture at baseline.

71 ss the impact of PZA gDST and MIC on time to sputum culture conversion (SCC) and treatment outcome in

72 second-line tuberculosis drugs with time to sputum culture conversion (tSCC) and treatment outcome i

73 We compared time to sputum culture conversion (TSCC) using Kaplan-Meier curv

74 Adjusted rates of sputum culture conversion at 2 months (67% vs 47%, respe

75 Adjusted rates of sputum culture conversion at two months (67 vs. 47%, p=0

76 Median time to sputum culture conversion did not differ between the two

77 everity, higher bacterial burden and delayed sputum culture conversion in pulmonary tuberculosis (PTB

78 The primary and secondary outcomes were the sputum culture conversion rate at the end of 8 weeks and

79 butol that is continued for 12 months beyond sputum culture conversion to negative.

80 rug regimen, 80% of participants experienced sputum culture conversion within 6 months.

81 All patients achieved sputum culture conversion within a mean of 71 days (26-1

82 All patients achieved sputum culture conversion within a mean of 71 days (26-1

83 hic severity of disease, the longest time to sputum culture conversion, and the highest rates of trea

84 egimens were associated with higher rates of sputum culture conversion, more favorable outcomes, and

85 tcome was daily percentage change in time to sputum culture positivity (TTP) in liquid medium over da

86 h the presence of filamentous fungi positive sputum culture.

87 rial load (>=10(7) cfu/g) using quantitative sputum culture.

88 ment, as well as sputum-smear microscopy and sputum-culture positivity at 2 and 6 months.

89 oduct of PZA, directly in the supernatant of sputum cultures by detecting a color change following th

90 Diagnosis requires 2 or more positive sputum cultures or 1 bronchoscopic specimen culture.

91 Overnight sputum cultures were collected daily.

92 Monthly sputum cultures, minimal inhibitory concentration testin

93 Sputum deposition blocks the airways of patients and lea

94 Sputum differential cell count and IS supernatant (ISS)

95 2, airway inflammation was measured based on sputum differential cell counts, IL-1beta protein levels

96 mong these patients, 22 were able to produce sputum during "stable" or pulmonary "exacerbation" perio

97 Due to low numbers of bacteria present in sputum during early infection, diagnosis does not usuall

98 Sputum eDNA in asthma was associated with airway neutrop

99 omparison of results in patients with a high sputum eosinophil level and those with a low level.

100 ter stability was associated with changes in sputum eosinophil percentages (P = .045).

101 The identification of sputum eosinophilia indicating corticosteroid responsive

102 High sputum eosinophilia was in line with higher pro-inflamma

103 m miR-1 levels had inverse correlations with sputum eosinophilia, airway obstruction, and number of h

104 antibody is a plausible strategy to decrease sputum eosinophils and inhibit lung mast cells in asthma

105 Increased blood and sputum eosinophils are associated with more frequent exa

106 Combined elevated sputum eosinophils+neutrophils in asthma associated with

107 easurements and Main Results: Bronchiectasis sputum exhibited increased percent solids, total and ind

108 In sputum-expectorating hospitalized patients with advanced

109 rmed a post hoc analysis of 561 HIV-infected sputum-expectorating patients (median CD4 count of 130 c

110 h COPD who were taking ICSs also had reduced sputum expression of ACE2.

111 s with and without TB among those submitting sputum for diagnosis.

112 ened with CAD4TB and simultaneously provided sputum for Xpert MTB/RIF testing.

113 Pneumococcal lysates and the sputum fraction were separately evaluated by MIA with a

114 e bacterial load, bacterial eradication from sputum, frequency of exacerbations, time to first exacer

115 We obtained sensitization data and/or sputum from 175 children: 99 with chronic asthma, 39 wit

116 bosomal RNA gene sequencing was performed on sputum from 253 clinically stable COPD patients (4-year

117 whether an S8mAb can decrease eosinophils in sputum from asthma patients ex vivo.

118 ase activity within the extracellular DNA of sputum from cystic fibrosis patients.

119 me-wide analysis of microRNA and mRNA in the sputum from patients with asthma and correlated expressi

120 S8mAbs decrease eosinophils in sputum from patients with asthma and inhibit FcepsilonR1

121 stigate the number of persistent bacteria in sputum from tuberculosis patients compared to in vitro a

122 disease, which can be differentiated by the sputum gammaP:F ratio.

123 A sputum gene expression signature of 6 biomarkers (6-gene

124 atory-diagnosed TB, the diagnostic yields of sputum GeneXpert (1 sample per subject) and OSA (2 sampl

125 from South African adult subjects, including sputum GeneXpert MTB/RIF (GeneXpert)-confirmed TB patien

126 (GeneXpert)-confirmed TB patients (n = 138), sputum GeneXpert-negative but culture-positive TB patien

127 a combined sensitivity of 92.8% relative to sputum GeneXpert.

128 Conclusions: The microbiome profile of sputum in AECOPD is associated with 1-year mortality and

129 ic lung disease influences the microbiota of sputum in patients with CAP.

130 ated with increased neutrophil counts in the sputum in response to ozone exposure.

131 Sputum induction is a non-invasive method to evaluate th

132 of exhaled nitric oxide (Fe(NO)) spirometry, sputum induction, and gave a blood sample.

133 ents with aspirin hypersensitivity underwent sputum induction.

134 Clinical characteristics and sputum inflammatory mediators were compared across the c

135 can be a surrogate marker for recognition of sputum inflammatory phenotypes.Methods: We conducted a p

136 ween the two types of agents in the baseline sputum inflammatory profiles, but OA caused by HMW agent

137 cobacterium tuberculosis (MTB) directly from sputum is challenging for three primary reasons.

138 Induced sputum is indeed not widely available and markers of neu

139 Induced sputum (IS) allows to measure mediators of asthmatic inf

140 Induced sputum (IS) was collected from patients with NERD (n = 2

141 Oral swabs and induced sputum (IS) were collected from 201 South African childr

142 First, the sample matrix, sputum, is highly viscous and heterogeneous, posing a ch

143 identified inhA, katG, and rpoB mutations in sputum isolates using the Hain MTBDRplus line probe assa

144 Simultaneous sputum liquefaction, bacteria heat inactivation (99 degr

145 Sputum macrophage number and the ES for most macrophage

146 d we confirmed our findings by using induced sputum macrophages isolated from healthy human volunteer

147 were confirmed by using DEP-exposed induced sputum macrophages isolated from healthy volunteers, dem

148 cells grown on lysogeny broth or artificial sputum medium.

149 otype in 104 patients, and the corresponding sputum MIA showed concordant results with additional mul

150 most prevalent serotype detected only by the sputum MIA.

151 Differences in sputum microbial profiles at acute exacerbation of airwa

152 rmed to assess the effect of azithromycin on sputum microbiology from participants of the AMAZES (Ast

153 Our aim was to investigate the COPD sputum microbiome and its association with inflammatory

154 sought to determine the relationship between sputum microbiome at the time of AECOPD hospitalization

155 The sputum microbiome has a potential role in disease phenot

156 The sputum microbiome is associated with clinical and inflam

157 This suggests that the sputum microbiome may serve as a biomarker for better ch

158 o identify severe asthma phenotypes based on sputum microbiome profiles and assess their stability af

159 We hypothesized that sputum microbiomic clusters exist in stable airways dise

160 Differences in specific sputum microbiota also associated with T2-low asthma phe

161 , Zimbabwe, we determined the association of sputum microbiota composition (using 16S ribosomal RNA V

162 Cell-free products of HMN sputum microbiota induced features of epithelial disrupt

163 with asthma, the compositional structure of sputum microbiota showed greater deviation from baseline

164 res identified four compositionally distinct sputum microbiota structures.

165 Patients whose sputum microbiota was dominated by Haemophilus, Moraxell

166 Thus, HIV-positive children harbor distinct sputum microbiota, with those dominated by Haemophilus,

167 jects with asthma.Conclusions: This study of sputum microRNA and mRNA expression from patients with a

168 ic regression models adjusting for sex, age, sputum microscopy, and HIV status.

169 taxa at the species level were identified in sputum, most at low relative abundance.

170 Sputum multiplex PCR could become a useful diagnostic to

171 coccus pneumoniae urinary antigen detection, sputum mycobacterial culture and Xpert MTB/RIF, and naso

172 cylcarnitines were increased in macrophages, sputum, nasal lining fluid, and plasma of patients with

173 ex raw samples, such as human blood, saliva, sputum, nasal swabs, urine, and plant tissues.

174 observing tissue infection by, SARS-CoV-2 in sputum, nasopharyngeal or oropharyngeal, urine, stool, b

175 ID-19 status was confirmed by PCR testing of sputum, nasopharyngeal swabs, or throat swabs.

176 before symptom onset, and these were largely sputum negative at diagnosis.

177 k sensitivity resulting in treatment of many sputum negative cases.

178 rmal lung function, separated by contrasting sputum neutrophil and macrophage percentages after CS tr

179 ings, AGER expression correlated with higher sputum neutrophil counts and more severe AHR in COPD pat

180 With both brensocatib doses, sputum neutrophil elastase activity was reduced from bas

181 rate of exacerbations (secondary end point), sputum neutrophil elastase activity, and safety were ass

182 ples and significantly associated with a low sputum neutrophilia.

183 UFP alone, caused a significant increase in sputum neutrophils and circulating leucocytes.

184 ential locations, percentage of blood and/or sputum neutrophils and macrophages, lung spirometry resu

185 le-cell transcriptome characterization of CF sputum.Objectives: To define the transcriptional profile

186 ene signatures of macrophage subtypes in the sputum of 104 asthmatics and 16 healthy volunteers from

187 taphylococcus species were isolated from the sputum of an individual with Cystic Fibrosis and assembl

188 -seq and microscopy and then apply it to the sputum of asthmatic patients to find known and novel rel

189 gainst Bcc and B. gladioli isolated from the sputum of individuals with CF; however, 10% of the isola

190 : Identify microRNA and mRNA networks in the sputum of patients with asthma.Methods: We conducted a g

191 ng neutrophil elastase, are increased in the sputum of patients with bronchiectasis at baseline and i

192 r of formation of Creola bodies found in the sputum of patients with severe asthma and could be a bio

193 egulator of the TLR and Th17 pathways in the sputum of subjects with asthma.Conclusions: This study o

194 serotype-specific detection of S. pneumoniae Sputum optimization involved liquefaction and fractionat

195 hether microbiome characteristics of induced sputum or oral samples demonstrate unique relationships

196 ally based on the presence of neutrophils in sputum, or the absence (or normal levels) of eosinophils

197 The shedding of viral RNA from sputum outlasted the end of symptoms.

198 evels) of eosinophils or other T2 markers in sputum (paucigranulocytic), airway biopsies or in blood.

199 Sputum percent solid concentrations, total and individua

200 Within subjects with bronchiectasis, sputum percent solids correlated inversely with FEV(1) a

201 We found that 66/109 (61%) TB patients were sputum positive at diagnosis, and 10/109 (9%) were HIV p

202 tic classifier identified breath sounds with sputum present with a sensitivity of 93.36% and a specif

203 rsistent bacteria between in vitro and human sputum prior to chemotherapy was quantified using differ

204 oea score (1.32, 1.25-1.39; p<0.0001), daily sputum production (1.16, 1.03-1.30; p=0.013), and radiol

205 Sputum production or chest congestion was associated wit

206 Chronic cough and sputum production poorly correlate with the presence of

207 oms such as dyspnea, the amount of cough and sputum production, and how often a patient experiences a

208 constellation of symptoms, including cough, sputum production, and shortness of breath.

209 aracterized by airway mucus accumulation and sputum production, but the role of mucus concentration i

210 tography/mass spectrometry was performed for sputum protein profiling of patients with bronchiectasis

211 lectively detect the intensity of ROS in the sputum sample (with a volume of less than 500 mul).

212 Tuberculosis (TB) diagnosis relies on a sputum sample, which cannot be easily obtained from all

213 based real-time tracing of COVID-19 from the sputum sample.

214 bacterial and viral respiratory pathogens on sputum samples (spontaneous or induced) from a prospecti

215 culosis and rifampicin resistance (Xpert) in sputum samples (standard of care) versus sputum Xpert co

216 RNA sequencing (RNA-seq) of sputum samples can be challenging to interpret due to th

217 and untreated (live) fractions of BCG and TB sputum samples for 42 days.

218 ) of Mycobacterium tuberculosis from patient sputum samples for clinical diagnosis of drug-resistant

219 t and validation of applying MIA directly to sputum samples for the serotype-specific detection of S.

220 Methods: We used sputum samples from 102 patients hospitalized because of

221 sified all nasopharyngeal, oropharyngeal and sputum samples from 75 patients with COVID-19 and 75 hea

222 We analysed sputum samples from 77 patients and found a Streptococcu

223 Most cases were identified from sputum samples of individuals with underlying lung disea

224 o compare microbial communities from EDC and sputum samples of patients according to type 2 (T2)-asth

225 unodeficiency virus, those unable to produce sputum samples or with extrapulmonary TB, household cont

226 um smear positive patients (n = 25) provided sputum samples prior to onset of chemotherapy.

227 n an experimental otitis media model, and in sputum samples recovered from cystic fibrosis patients t

228 this longitudinal multicenter cohort study, sputum samples were collected for microbiome profiling f

229 Sputum samples were collected from 63 subjects with seve

230 rconcentration and disease severity.Methods: Sputum samples were collected from subjects with bronchi

231 Sputum samples were cultured with PZA for up to 21 days

232 served lower survival among patients in whom sputum samples were negative for Veillonella (HR, 13.5;

233 ar lavage specimens, tracheal aspirates, and sputum samples) in addition to serum samples were submit

234 Mycobacterial culture was done on 2 sputum samples, blood cultures, and relevant extrapulmon

235 n" periods and had complete pairs of EDC and sputum samples, both collected and analyzed.

236 lmette-Guerin (BCG) cultures and TB-positive sputum samples, we show that boiling for 20 min at 80, 8

237 is viability loss was replicated in clinical sputum samples, with the bacterial load dropping by 0.65

238 for S. pneumoniae) for clinical metagenomic sputum samples.

239 rapy, many centers no longer collect induced sputum samples.

240 towards detection of filamentous fungi from sputum samples.

241 of Mycobacterium tuberculosis culture on two sputum samples.

242 o determine PZA susceptibility directly from sputum samples.

243 abundance identified in direct sequencing of sputum samples; importantly, culture enrichment identifi

244 adding urine-based tuberculosis screening to sputum screening for hospitalised patients with HIV.

245 ur DNA samples extracted from smear-positive sputum sediments, previously sequenced using the Deeplex

246 Positive sputum smear and cavitary disease, correlates of disease

247 A cohort of newly diagnosed, sputum smear and culture positive adult individuals with

248 offered intensified active case-finding with sputum smear and culture testing monthly for 6 months an

249 TB was diagnosed based on sputum smear and sensitive molecular and microbial tests

250 Patients aged 18 years or older with sputum smear grade 1+ or higher were eligible for enrolm

251 t predictors were pulmonary tuberculosis and sputum smear grade, age, and the maximum number of hours

252 There was no difference in sputum smear grading and pulmonary cavitation.

253 t group vs 16.38 per 100 person-years in the sputum smear group) for HIV-positive patients (hazard ra

254 Sputum smear microscopy and BD MAX were performed on a s

255 e programmatic active case-finding entailing sputum smear microscopy and clinical assessment.

256 Tests that can replace sputum smear microscopy have been identified as a top pr

257 Sputum smear positive patients (n = 25) provided sputum

258 of 127; p=0.03), and were more likely to be sputum smear-negative (33 [62%] of 53 vs 62 [35%] of 179

259 e linked in the network, while patients with sputum smear-positive disease were less likely to be lin

260 esign of diagnostic test accuracy studies of sputum smear-replacement tests.

261 e first 9 months of TB treatment, as well as sputum-smear microscopy and sputum-culture positivity at

262 TB cases were positive for acid-fast bacilli sputum smears and 43% had cavitary disease; at study ent

263 Archived Ziehl-Neelsen-stained sputum smears were used to conduct microbead-based spoli

264 ince many patients are not able to produce a sputum specimen, and traditional diagnostics are costly

265 d an MDR-TB risk factor and a smear-positive sputum specimen, but had PSQ performed on a culture isol

266 s were very proficient at collecting induced sputum specimens for the diagnosis of Pneumocystis jirov

267 ompared pathogen yields from NP/OP swabs and sputum specimens from patients >=18 years hospitalized w

268 The pathogen yields from NP/OP against sputum specimens have not been extensively explored, esp

269 differentiation of carbapenemase genes from sputum specimens in patients with a clinical diagnosis o

270 A total of 301 sputum specimens were collected and tested.

271 In a case-control cohort diagnostic study, sputum specimens were collected from 308 patients (aged

272 ected respiratory specimens (846 BAL and 836 sputum specimens) evaluated with the PN panel were also

273 CRE detection and identification directly in sputum specimens.

274 gets using BAL specimens and for 10/24 using sputum specimens.

275 k clinical samples (infection-negative human sputum spiked with 0 to 10(5) Mycobacterium bovis BCG ce

276 ebo-treated and 69 AZM-treated patients) had sputum stored for quantitative PCR of 6GS markers at bas

277 lls, as well as eicosanoid levels in induced sputum supernatant (ISS) and urine were extracted for th

278 y was used to profile eicosanoids in induced sputum supernatant (ISS).

279 Sputum T2 gene expression was characterized by an immune

280 ent symptom screenings, chest radiographies, sputum TB bacteriologies, TB infection (TBI) testing (tu

281 of the microRNA-mRNA networks present in the sputum that contribute to airway inflammation in asthma

282 Given the complex nature of sputum (the primary specimen type used for pulmonary TB)

283 g PD-1 expression negatively correlates with sputum TNF-alpha concentrations.

284 ion, and LFA amplification in a multisample, sputum-to-genotype system.

285 P < 0.001; H. influenzae, P < 0.0001) and in sputum-type specimens (S. aureus, P < 0.05).

286 acterial culture or Xpert MTB/RIF testing of sputum, urine, or blood.

287 ance, mortality, adherence to treatment, and sputum volume; safety endpoints were adverse events and

288 The persistent bacteria in sputum was 17% of the in vitro levels, suggesting a diff

289 The isolation rate of filamentous fungi from sputum was higher in children with acute compared with c

290 Induced sputum was obtained 3.5 h after exposure.

291 lture of contemporaneously collected patient sputum was variable.

292 din (PVL)-negative MRSA isolate from patient sputum, we show that linezolid therapy significantly imp

293 lymphocytes and in situ hybridization of the sputum were used to identify the cellular sources of mic

294 py and BD MAX were performed on a single raw sputum, which was then processed for culture and phenoty

295 in sputum samples (standard of care) versus sputum Xpert combined with a lateral flow assay for M tu

296 mic outcomes of three testing strategies: 1) sputum Xpert MTB/RIF (Xpert); 2) sputum Xpert plus urine

297 In the facility-based screening arm, sputum Xpert MTB/RIF was performed on all patients prese

298 ategies: 1) sputum Xpert MTB/RIF (Xpert); 2) sputum Xpert plus urine AlereLAM (Xpert+AlereLAM); 3) sp

299 ert plus urine AlereLAM (Xpert+AlereLAM); 3) sputum Xpert plus urine FujiLAM (Xpert+FujiLAM).

300 urine TB-LAM (if CD4 count <=100 cells/mul), sputum Xpert, and/or a single sputum culture among conse