Author Correction: Colonoscopy and fecal immunochemical testing versus usual care in diagnostic colorectal cancer screening: the SCREESCO randomized controlled trial.
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Published Erratum↗
Biomedical subjects
Lars Engstrand
Publications and source records attributed to Lars Engstrand.
Colonoscopy and fecal immunochemical testing versus usual care in diagnostic colorectal cancer screening: the SCREESCO randomized controlled trial.
There is a need to quantify the benefits and harms of colorectal cancer (CRC) screening using primary colonoscopy or fecal immunochemical testing (FIT) compared with usual care with no screening. Guidelines recommend screening in individuals aged 50-75 years using colonoscopy or FIT, and many screening programs use one-sample biennial FIT. Here we compare incidence of diagnosed CRCs and gastrointestinal and cardiovascular events between screening and usual care during the diagnostic phase of the SCREESCO trial. A randomized block method (no masking) assigned 278,280 individuals aged 60 years to once-only colonoscopy, 2 rounds of two-stool FIT with a low cutoff (10 μg g-1 feces) or usual care (control group) in a ratio of 1:6 for colonoscopy versus control and 1:2 for FIT versus control. In the analysis, 31,113 individuals were in the primary colonoscopy arm and 60,267 were in the FIT arm, and there were 186,671 primary colonoscopy controls, of whom 120,521 were also controls for comparison with the FIT arm. After a median follow-up of 4.8 years, the incidence rate of CRC was 107.9 in the colonoscopy arm and 99.9 in controls per 100,000 person-years (incidence rate ratio (IRR): 1.08, 95% confidence interval (CI): 0.91-1.28) and 96.0 in the FIT arm and 103.9 in controls (IRR: 0.92, 95% CI: 0.81-1.05). Rates of stage I-II CRC were higher in the colonoscopy arm (IRR: 1.38, 95% CI: 1.09-1.74) and in the FIT arm (IRR: 1.19, 95% CI: 0.99-1.43) versus controls. Rates of cardiovascular and gastrointestinal events were slightly higher in the intervention arms during the first year and were subsequently more similar to controls. Our findings of an increase in CRC detection implies a benefit of screening while the increase in adverse events suggests some initial harm. ClinicalTrials.gov: NCT02078804 .
Humans↗
Inflammatory response in patients with malignant obstructive jaundice.
OBJECTIVE: Surgery in patients with malignant obstructive jaundice is associated with increased risks for postoperative septic complications. The aim of this study was to investigate the inflammatory and the local cellular immune response in patients accepted for surgery because of tumours in the hepatic-pancreatic-biliary (HPB) tract. MATERIAL AND METHODS: Patients with obstructive jaundice (group HPB(+)) were compared with those without (HPB(-)). Patients undergoing surgery for benign abdominal disorders served as controls. Obstructive jaundice was present in 18 out of 33 HPB patients. Preoperatively, blood was analysed for bacteria, endotoxins and cytokines (TNF-alpha, IL-6 and IL-10). At operation, mesenteric lymph nodes (MLNs) were excised for bacterial cultures using standard microbiological techniques, and immunohistochemistry, using antibodies CD4 and CD8 (mainly staining T lymphocytes), CD68 (macrophages), and anti-caspase-3 (to determine the rate of apoptosis). RESULTS: Bacterial translocation was not demonstrated in any of the patients. Increased preoperative concentrations of endotoxins were found in group HPB(+). The number of macrophages and the rate of apoptosis in MLNs were increased in jaundiced patients, while the number of T lymphocytes was decreased. CONCLUSIONS: Malignant obstructive jaundice causes increased blood concentrations of endotoxins and cytokines, an increased number of macrophages in MLNs, a higher rate of apoptosis in MLNs, but a decreased number of T lymphocytes in MLNs. The lymphocyte depletion is probably due to the increased rate of apoptosis, and might reduce the ability of jaundiced patients to eradicate infection.
Adult↗
Impaired mucus-bicarbonate barrier in Helicobacter pylori-infected mice.
To resist the harsh intrinsic milieu, several lines of defense exist in the stomach. The aim of this study was to investigate the effect of the gastric pathogen Helicobacter pylori on these mechanisms in vivo. We used FVB/N mice expressing human alpha-1,3/4-fucosyl transferase (producing Lewis b epitopes) and inoculated with H. pylori 1. Mice were anesthetized with isoflurane or Hypnorm-midazolam, the stomach was exteriorized, and the surface of the corpus mucosa was exposed. Mucus thickness was measured with micropipettes, juxtamucosal pH (pH(jm)) was measured with pH-sensitive microelectrodes, blood flow was measured with laser-Doppler flowmetry, and mRNA levels of the bicarbonate transporter SLC26A9 were quantified with real-time PCR. The increase in mucosal blood flow seen in response to luminal acid (pH 1.5) in control animals (140 +/- 9% of control) was abolished in infected mice. The firmly adherent mucus layer was significantly thinner in infected mice (31 +/- 2 microm) than in control mice (46 +/- 5 microm), and no mucus accumulation occurred in infected mice. pH(jm) decreased significantly more on exposure to luminal acid in infected mice (luminal pH 1.5, pH(jm) 2.4 +/- 0.7) than in control mice (pH(jm) 6.4 +/- 0.5). Despite reduced pH(jm), SLC26A9 mRNA expression was significantly, by increased 1.9-fold, in infected mice. The reduction in pH(jm) by infection with H. pylori might be due to a reduced firmly adherent mucus layer, increased mucus permeability to H(+), and/or inhibition of bicarbonate transport. The upregulation of SLC26A9 in H. pylori-infected epithelium might be a result of continuous inhibition of the transporter, e.g., by ammonium, a H. pylori product, which has been previously shown to inhibit SLC26A9.
Animals↗
Peptic ulcer disease in a general adult population: the Kalixanda study: a random population-based study.
The authors' aim in this study was to explore the prevalence, symptomatology, and risk factors for peptic ulcer in a general adult population. Between December 1998 and June 2001, the authors surveyed a random sample (n=3,000) of the adult population (n=21,610) in two communities in northern Sweden using a validated questionnaire, the Abdominal Symptom Questionnaire (response rate=74%). A subsample (n=1,001) of the responders was randomly invited to undergo esophagogastroduodenoscopy and symptom assessment (response rate=73%). The prevalence of peptic ulcer was 4.1% (20 gastric ulcers and 21 duodenal ulcers). Nausea and gastroesophageal reflux were significant predictors of peptic ulcer disease, but epigastric pain/discomfort was not. Six persons with gastric ulcer and two persons with duodenal ulcer were asymptomatic. Eight subjects with duodenal ulcer (38%) lacked evidence of current Helicobacter pylori infection. Five (25%) of the gastric ulcers and four (19%) of the duodenal ulcers were idiopathic (no use of aspirin or nonsteroidal antiinflammatory drugs, no H. pylori infection). Smoking, aspirin use, and obesity were risk factors for gastric ulcer; smoking, low-dose (<or=160 mg) aspirin use, and H. pylori infection were risk factors for duodenal ulcer. Peptic ulcer disease often coexists with atypical symptoms or no symptoms at all, and idiopathic duodenal ulcer may be more common than anticipated.
Adult↗
An enzymatic ruler modulates Lewis antigen glycosylation of Helicobacter pylori LPS during persistent infection.
Helicobacter pylori persistently colonizes about half the human population and contributes to the development of peptic ulcer disease and gastric cancer. This organism has evolved means to structurally alter its surface characteristics to evade innate and adaptive immune responses. H. pylori produces LPS O-antigen units that can be posttranslationally fucosylated to generate Lewis antigens, structures also found on human epithelial cells. We demonstrate an extensive diversity of Lewis x and Lewis y expression in LPS O-antigen units, occurring over time and in different regions of the human stomach. Lewis expression patterns were correlated with the on/off status of the three fucosyltransferases (FucT), FutA, FutB, and FutC, which are regulated via slipped-strand mispairing in intragenic polyC tract regions of the corresponding genes. The alpha1,3-FucT, FutA and FutB, each contain a C-terminal heptad repeat region, consisting of a variable number of DD/NLRV/INY tandem repeats. Variations in the number of heptad repeats correlated to the sizes of O-antigen polymers to become decorated by fucose residues. Our data support a molecular ruler mechanism for how H. pylori varies its LPS fucosylation pattern, where one heptad repeat in the enzyme corresponds to one N-acetyl-beta-lactosamine unit in the O-antigen polysaccharide.
Amino Acid Sequence↗
Antimicrobial susceptibility of Helicobacter pylori strains in a random adult Swedish population.
BACKGROUND AND AIM: Antimicrobial resistance in Helicobacter pylori is a growing problem and has become an important factor leading to eradication failure. Information on antimicrobial susceptibility is important for selection of an optimum treatment regimen. The resistance rate in a random population has not been studied previously. METHODS: A random Swedish population sample (n = 3000, age 20-1 years) was surveyed using a mailed validated questionnaire assessing gastrointestinal symptoms (response rate of 74%). One-third of the responders was invited, in random order, and accepted an esophagogastroduodenoscopy with biopsies for H. pylori culture and histology. Subjects were not treated for their H. pylori infection but a minimum inhibitory concentration of metronidazole, clarithromycin, amoxicillin, and tetracycline for the H. pylori isolates (n = 333) was determined by agar dilution. Prescribed antibiotic in the area was recorded. RESULTS: Irrespective of symptomatology, 16.2% of the isolated H. pylori strains were resistant to metronidazole, 1.5% to clarithromycin, 0% to amoxicillin, and 0.3% to tetracycline. The antibiotic consumption was low from an international perspective. CONCLUSION: The resistance to the antibiotics was lower than expected from patient sample studies, especially for clarithromycin, most probably due to a restrictive prescription policy in the area. Introduction of a test-and-treat strategy in Sweden would only marginally affect the usage of clarithromycin.
Adult↗
Rapid detection of rifampin resistance in Mycobacterium tuberculosis by Pyrosequencing technology.
We developed an assay for rapid detection of rifampin resistance in Mycobacterium tuberculosis based on Pyrosequencing technology, involving a technique for real-time sequencing. A 180-bp region of the rpoB gene was amplified in clinical isolates of both rifampin-resistant and -susceptible M. tuberculosis. The PCR products were subjected to Pyrosequencing analysis using four different sequencing primers in four overlapping reactions. These four sequencing reactions covered the 81-bp region where > 96% of the mutations associated with rifampin resistance are located. The results were compared to those obtained with two other molecular methods, the line probe assay and cycle sequencing, and the phenotypic BACTEC method. The genotypic determination methods all detected the mutations that previously have been correlated with rifampin resistance. In addition, Pyrosequencing analysis and the two other molecular methods found additional mutations within the rpoB gene in phenotypically susceptible strains. We found that Pyrosequencing technology, in particular, offers high accuracy, short turnaround time, and a potentially high throughput in detection of rifampin resistance in M. tuberculosis.
Antibiotics, Antitubercular↗
SabA is the H. pylori hemagglutinin and is polymorphic in binding to sialylated glycans.
Adherence of Helicobacter pylori to inflamed gastric mucosa is dependent on the sialic acid-binding adhesin (SabA) and cognate sialylated/fucosylated glycans on the host cell surface. By in situ hybridization, H. pylori bacteria were observed in close association with erythrocytes in capillaries and post-capillary venules of the lamina propria of gastric mucosa in both infected humans and Rhesus monkeys. In vivo adherence of H. pylori to erythrocytes may require molecular mechanisms similar to the sialic acid-dependent in vitro agglutination of erythrocytes (i.e., sialic acid-dependent hemagglutination). In this context, the SabA adhesin was identified as the sialic acid-dependent hemagglutinin based on sialidase-sensitive hemagglutination, binding assays with sialylated glycoconjugates, and analysis of a series of isogenic sabA deletion mutants. The topographic presentation of binding sites for SabA on the erythrocyte membrane was mapped to gangliosides with extended core chains. However, receptor mapping revealed that the NeuAcalpha2-3Gal-disaccharide constitutes the minimal sialylated binding epitope required for SabA binding. Furthermore, clinical isolates demonstrated polymorphism in sialyl binding and complementation analysis of sabA mutants demonstrated that polymorphism in sialyl binding is an inherent property of the SabA protein itself. Gastric inflammation is associated with periodic changes in the composition of mucosal sialylation patterns. We suggest that dynamic adaptation in sialyl-binding properties during persistent infection specializes H. pylori both for individual variation in mucosal glycosylation and tropism for local areas of inflamed and/or dysplastic tissue.
Adhesins, Bacterial↗
Correlation of the Helicobacter pylori adherence factor BabA with duodenal ulcer disease in four European countries.
Helicobacter pylori strains harboring the vacAs1, cagA and babA2 have been associated with ulcer disease (UD). We compared the prevalence of these different genotypes and adhesive properties in H. pylori infected patients with UD in four European countries. Genomic DNA was isolated from 314 H. pylori strains: Germany (GER; n=92), Sweden (SWE, n=74), Portugal (POR, n=91) and Finland (FIN, n=57). The frequencies of babA2 genotype varied from 35% to 60%. Triple-positive strains (vacAs1+, cagA+ and babA2+) were significantly associated with UD in GER and POR and were closely correlated with UD in FIN, but not in SWE. Classification as triple-positive strains had a higher specificity for detection of UD in GER, POR and FIN than type1 or cagA+ strains. In vitro adhesion assays revealed that Swedish strains showed high adhesion properties and were thus correlated with the diagnosis of UD, although PCR detected the babA2 gene at lower frequencies and failed to show a correlation with UD. This finding appears to reflect allelic variations of the babA2 gene in SWE, although adhesive properties of the strains are retained.
Adhesins, Bacterial↗
Real-time PCR for pharmacodynamic studies of Chlamydia trachomatis.
Pharmacodynamic knowledge about Chlamydia trachomatis exposed to antibiotics is hampered due to methodological limitations. We have developed a quantitative real-time PCR method (qRT-PCR) for determination of viable C. trachomatis. The method measures specific RNA transcripts of omp2 (omcB) as an expression of viable C. trachomatis. Two clinical isolates (one strain derived from a patient with recurrent symptoms despite doxycycline treatment) were cultured in McCoy cells and exposed to doxycycline at concentrations of 0.0078-64 mg/L. MIC values were evaluated microscopically by immunofluorescence (IF) and by qRT-PCR performed on cDNA prepared from the total RNA. The MIC for two C. trachomatis strains were determined to 0.016 and 0.031 mg/L by both qRT-PCR and IF. The qRT-PCR assay enabled MIC determinations without subjective evaluation, which is a problem when visually evaluating inclusions. The presented qRT-PCR is a suitable method for MIC determination of C. trachomatis. It has the advantage of giving quantitative measurements of chlamydial RNA levels and the method is useful in pharmacodynamic studies of C. trachomatis.
Anti-Bacterial Agents↗
Clarithromycin treatment selects for persistent macrolide-resistant bacteria in throat commensal flora.
The aim of the study was to determine the effect of clarithromycin treatment on resistance development in the commensal throat flora. Alpha-haemolytic streptococci and Neisseria spp. were isolated from patients receiving clarithromycin for eradication of Helicobacter pylori. The treatment resulted in an immediate increase in the number of macrolide-resistant streptococci, which remained for one year after treatment, but declined to background level three years later. The most prevalent resistance gene was mef(A). Neisseria spp. were less affected by the treatment: the number of resistant isolates increased in only in one case during treatment. In conclusion, a one-week standard therapy with clarithromycin selects for an increased prevalence of macrolide-resistant streptococci that persisted for more than one year.
Anti-Bacterial Agents↗
Salmonella enterica SpvB-mediated ADP-ribosylation as an activator for host cell actin degradation.
The virulence-associated SpvB protein of Salmonella enterica is a mono (ADP-ribosyl)transferase defined to target mammalian actin. Exposure of Acanthamoeba rhysodes cell lysate with SpvB and [32P]nicotinamide adenine dinucleotide (NAD) was here observed to result in labeling of a protein of 43 kDa that subsequently was identified as actin by immunoprecipitation. In parallel, ADP-ribosylation promoted degradation of the protozoan actin. SpvB-mediated actin degradation occurred in the presence of the serine protease inhibitor phenylmethylsulfonylfluoride (PMSF), but was inhibited upon addition of novobiocin, an inhibitor of mono (ADP-ribosyl)transferase activity, or upon addition of EDTA. Infection of A. rhysodes with SpvB-proficient S. enterica serovariant Dublin resulted in cytotoxicity and in characteristic SpvB-mediated actin degradation. Cells infected with SpvB-deficient bacteria showed a decrease in cytotoxicity and lack of actin degradation. Combining these results show that SpvB formally can ADP-ribosylate A. rhysodes actin but that the protozoan cell has the capacity to subsequently degrade ADP-ribosyl-tagged actin. These observations illustrate a hitherto undefined consequence of actin modification, and define a new pathway in the cellular actin dynamics.
ADP Ribose Transferases↗
A negative Helicobacter pylori serology test is more reliable for exclusion of premalignant gastric conditions than a negative test for current H. pylori infection: a report on histology and H. pylori detection in the general adult population.
OBJECTIVE: Corpus-dominant gastritis, gastric mucosal atrophy and intestinal metaplasia (IM) associated with Helicobacter pylori infection are all known potential risk markers for the development of gastric cancer. As the accuracy for finding cases at risk in the general population is unknown, we aimed to determine the prevalence of current and/or past H. pylori infection and associated gastric mucosal findings by means of histological survey of a random adult population. MATERIAL AND METHODS: A random Swedish sample (n = 3000, age 20-81 years) was surveyed using a validated gastrointestinal symptom questionnaire with 74% response rate. One-third of the responders were selected at random for esophago-gastro-duodenoscopy with biopsies and H. pylori serology. RESULTS: Of those endoscoped (n = 1000, mean age 53.5, 51% women), 43.0% were H. pylori+ by serology (seropositive), 33.9% had signs of current infection on either histology or culture (gold standard+), and 9.3% were seropositive, but gold standard negative. Corpus atrophy was found in 10% and IM in 13% when gold standard positive, and in a significantly higher number (17% and 21%, respectively) of those with only a serological sign of past infection. Among those who were seronegative, values were 1% and 2%, respectively. Corpus-dominant gastritis was found in 4.1%, all seropositive. CONCLUSION: One-third had an ongoing H. pylori infection, and a further 10% had signs of past infection. Corpus-dominant gastritis was found mostly among the former, while detection of those with corpus atrophy and IM also required a test for past infection. Seronegativity almost excludes precancerous conditions in a screening situation.
Adult↗
Histology and culture results among subjects with antibodies to CagA but no evidence of Helicobacter pylori infection with IgG ELISA.
OBJECTIVE: Serological evidence of antibodies to cytotoxin-associated gene A (CagA) antigens may exist without concomitant Helicobacter pylori IgG enzyme linked immunosorbent assay (ELISA) seropositivity. In a recent case-control study, this serological pattern was strongly linked to stomach cancer, and it was hypothesized to represent "burned-out" CagA-positive infections. The aim of this analysis was to test this hypothesis. MATERIAL AND METHODS: We used data from a Swedish endoscopy clinic-based case-control study with 64 gastric cancer cases and 281 age-matched and gender-matched non-cancer patients who had other gastric diseases or normal endoscopy. HM-CAP ELISA and Helicoblot 2.0 immunoblot results were compared with culture and histology. RESULTS: Overall, 86 out of 345 (25%) subjects were CagA seropositive but ELISA seronegative. This proportion was similar among cancer and non-cancer patients. Current H. pylori infection could be verified by culture or histology in only 15% of these patients. Forty-three percent of subjects with this isolated CagA seropositivity had histological evidence of corpus and/or antral atrophy. This was higher than in those who were negative in both tests (15%), but lower than among those seropositive for both tests (53%). The percentage of isolated CagA-seropositive patients who had atrophy was similar among those with or without evidence of current infection. CONCLUSIONS: Although false-positive tests for CagA, or false-negative ELISA tests, may explain the serologic pattern in some of the subjects with isolated CagA seropositivity, healed infections are estimated to account for the majority. Unless the histology is often restituted after spontaneous disappearance of the infection, atrophy does not appear to be a mandatory intermediate step leading to this serology.
Adenocarcinoma↗
High prevalence of gastroesophageal reflux symptoms and esophagitis with or without symptoms in the general adult Swedish population: a Kalixanda study report.
OBJECTIVE: Gastroesophageal reflux disease has been reported to be a common burden on health-care resources in the Western world, but its manifestations in the general population are as yet unclear. The aim of this study was to estimate the prevalence of, and to identify the risk factors for gastroesophageal reflux symptoms (GERS) and erosive esophagitis (EE) in the adult population of two Swedish municipalities. MATERIAL AND METHODS: A random sample (n =3000) of the adult population (20-81 years of age) of two Swedish municipalities (n =21,610) was surveyed using a validated postal questionnaire assessing gastrointestinal symptoms. The response rate was 74%. A subsample (n = 1000) of the responders was subsequently invited, in random order, for esophago-gastro-duodenoscopy with evaluation of GERS, risk factors and tests for Helicobacter pylori. RESULTS: GERS were reported by 40.0% and EE was found in 15.5% of the population that had undergone endoscopy. Of those with GERS, 24.5% had EE while 36.8% of those with EE reported no GERS. Hiatus hernia and obesity remained significant risk factors for GERS and/or EE, with or without symptoms in a main effect model (OR up to 14 at EE). Those with active H. pylori infection had a higher risk of GERS without EE than those without H. pylori infection (OR = 1.71 (1.23 2.38)). CONCLUSIONS: GERS and EE (of which one-third is asymptomatic) are highly prevalent in the Swedish adult population. H. pylori infection seems to play a role in the manifestations of gastroesophageal reflux.
Adult↗
Lactobacillus gastricus sp. nov., Lactobacillus antri sp. nov., Lactobacillus kalixensis sp. nov. and Lactobacillus ultunensis sp. nov., isolated from human stomach mucosa.
In an attempt to study the composition of the Lactobacillus flora from mucosa of human stomach, 16S rRNA gene sequences of 129 isolates were analysed. For 15 of these, the results differed significantly from known sequences, and additional tests were performed to determine whether these isolates represented as yet unrecognized species. Phenotypic and genetic characteristics revealed that these isolates represented four novel Lactobacillus species. Two belong to the Lactobacillus reuteri and the other two to the Lactobacillus delbrueckii subgroup of Lactobacillus. The names Lactobacillus gastricus sp. nov., Lactobacillus antri sp. nov., Lactobacillus kalixensis sp. nov. and Lactobacillus ultunensis sp. nov. are proposed, with the respective type strains Kx156A7T (=LMG 22113T=DSM 16045T=CCUG 48454T), Kx146A4T (=LMG 22111T=DSM 16041T=CCUG 48456T), Kx127A2T (=LMG 22115T=DSM 16043T=CCUG 48459T) and Kx146C1T (=LMG 22117T=DSM 16047T=CCUG 48460T).
Bacterial Typing Techniques↗
Evaluation of western blot CagA seropositivity in Helicobacter pylori-seropositive and -seronegative subjects.
CagA seropositivity is an important risk factor for gastric adenocarcinoma and duodenal ulcer. However, CagA seropositivity is also found in Helicobacter pylori-seronegative subjects. Is CagA seropositivity in these subjects a sign of a past H. pylori infection, or does it represent a false-positive reaction? This study investigates the intensity of the CagA immune reaction and the variation in CagA seroprevalence with year of birth for 650 subjects belonging to the Malmo Preventive Medicine cohort. CagA and H. pylori seroprevalences were determined by Western blot analysis (Helicoblot 2.1) and enzyme-linked immunosorbent assay. The peak intensity of the CagA band was significantly lower in H. pylori-seronegative subjects than in those with concomitant H. pylori seropositivity. In H. pylori-seropositive subjects, peak CagA intensity had a bimodal distribution. The prevalence of CagA-seropositive but H. pylori-seronegative subjects increased successively and significantly with year of birth, in contrast to the prevalence of CagA-seropositive and H. pylori-seropositive subjects, which decreased significantly. However, within H. pylori-seropositive and -seronegative subgroups, CagA seroprevalences were constant for different birth cohorts. If CagA seropositivity in H. pylori-seronegative subjects represents a past H. pylori infection, there must have been some mechanisms of eradication that were more common in younger subjects and that were of more importance than the presence of gastric atrophy and the longer duration and higher prevalence of H. pylori infection found in older subjects. Antibiotic treatment of H. pylori was not common practice at the time of enrollment. On the other hand, a false-positive reaction would be constant and independent of birth cohorts, as with the H. pylori-seronegative subgroup of our study. Peak CagA intensity in H. pylori-seronegative subjects corresponded to the lower part of the bimodal distribution of peak CagA intensity in H. pylori-seropositive subjects. We conclude that a major proportion of CagA seropositivity in H. pylori-seronegative subjects represents a false-positive reaction. Peak CagA intensity has a bimodal distribution in H. pylori-seropositive subjects. Low-intensity CagA seropositivity in H. pylori-seropositive subjects is indeterminate, representing both false-positive and true-positive reactions.
Adult↗