False-Positive Human Immunodeficiency Virus Screening Results in Pregnancy During the Coronavirus Disease 2019 (COVID-19) Pandemic.

False-positive human immunodeficiency virus (HIV) test results are rare but have been documented in the setting of certain underlying conditions such as Epstein-Barr virus, metastatic cancer, and certain autoimmune conditions. A retrospective cohort study in a large hospital system was conducted to compare the occurrence of false-positive HIV fourth-generation test results before and after the coronavirus disease 2019 (COVID-19) pandemic in a population of pregnant patients (N=44,187; 22,073 pre-COVID and 22,114 during COVID). The COVID cohort had a significantly higher frequency of false-positive HIV test results compared with the pre-COVID cohort (0.381 vs 0.676, P =.002). Within the COVID cohort, 25% of patients had a positive polymerase chain reaction test result for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) preceding their false-positive HIV test results. When this subgroup was excluded, the difference in frequency of false-positive HIV test results between the cohorts was no longer significant (0.381 vs 0.507, P =.348). Our findings suggest that SARS-CoV-2 seropositivity was associated with an increased frequency of false-positive HIV test results in the pregnant population.

Partial Molar Pregnancy Presenting as a Tubal Ectopic Pregnancy.

Background: Tubal molar pregnancy is extremely rare, with no more than 200 cases reported in the literature. The incidence is approximated at 1.5 per 1,000,000 pregnancies. Case: We report the case of a 22-year-old woman with an overall initial stable clinical presentation who was noted to have a ruptured ectopic pregnancy. She was surgically treated, and pathology revealed partial hydatidiform molar ectopic pregnancy. At the time of surgical intervention, the treating physicians had not considered molar ectopic pregnancy within the differential diagnosis, since this is a very rare presentation. Once the pathology was discovered, the patient was contacted to be scheduled for close follow-up and counseling to reduce progression to choriocarcinomas. Conclusion: This case report highlights the importance of sending, reviewing, and following up on pathologic specimens for all patients undergoing surgical intervention for presumed ectopic pregnancy and ensuring that appropriate follow-up is in place for those patients.

Acinetobacter baumannii Genes Required for Bacterial Survival during Bloodstream Infection.

Acinetobacter baumannii is emerging as a leading global multiple-antibiotic-resistant nosocomial pathogen. The identity of genes essential for pathogenesis in a mammalian host remains largely unknown. Using transposon-directed insertion-site sequencing (TraDIS), we identified A. baumannii genes involved in bacterial survival in a leukopenic mouse model of bloodstream infection. Mice were inoculated with a pooled transposon mutant library derived from 109,000 mutants, and TraDIS was used to map transposon insertion sites in the genomes of bacteria in the inoculum and of bacteria recovered from mouse spleens. Unique transposon insertion sites were mapped and used to calculate a fitness factor for every insertion site based on its relative abundance in the inoculum and postinfection libraries. Eighty-nine transposon insertion mutants that were underrepresented after experimental infection in mice compared to their presence in the inocula were delineated as candidates for further evaluation. Genetically defined mutants lacking feoB (ferrous iron import), ddc (d-ala-d-ala-carboxypeptidase), and pntB (pyridine nucleotide transhydrogenase subunit) exhibited a fitness defect during systemic infection resulting from bacteremia. In vitro, these mutants, as well as a fepA (ferric enterobactin receptor) mutant, are defective in survival in human serum and within macrophages and are hypersensitive to killing by antimicrobial peptides compared to the survival of the parental strain under these conditions. Our data demonstrate that FepA is involved in the uptake of exogenous enterobactin in A. baumannii. Genetic complementation rescues the phenotypes of mutants in assays that emulate conditions encountered during infection. In summary, we have determined novel A. baumannii fitness genes involved in the pathogenesis of mammalian infection. IMPORTANCE A. baumannii is a significant cause of bacterial bloodstream infection in humans. Since multiple antibiotic resistance is becoming more common among strains of A. baumannii, there is an urgent need to develop novel tools to treat infections caused by this dangerous pathogen. To develop knowledge-guided treatment approaches for A. baumannii, a thorough understanding of the mechanism by which this pathogen causes bloodstream infection is required. Here, using a mouse model of infection, we report the identification of A. baumannii genes that are critical for the ability of this pathogen to cause bloodstream infections. This study lays the foundation for future research on A. baumannii genes that can be targeted to develop novel therapeutics against this emerging human pathogen.

Genome-wide detection of fitness genes in uropathogenic Escherichia coli during systemic infection.

Uropathogenic Escherichia coli (UPEC) is a leading etiological agent of bacteremia in humans. Virulence mechanisms of UPEC in the context of urinary tract infections have been subjected to extensive research. However, understanding of the fitness mechanisms used by UPEC during bacteremia and systemic infection is limited. A forward genetic screen was utilized to detect transposon insertion mutants with fitness defects during colonization of mouse spleens. An inoculum comprised of 360,000 transposon mutants in the UPEC strain CFT073, cultured from the blood of a patient with pyelonephritis, was used to inoculate mice intravenously. Transposon insertion sites in the inoculum (input) and bacteria colonizing the spleen (output) were identified using high-throughput sequencing of transposon-chromosome junctions. Using frequencies of representation of each insertion mutant in the input and output samples, 242 candidate fitness genes were identified. Co-infection experiments with each of 11 defined mutants and the wild-type strain demonstrated that 82% (9 of 11) of the tested candidate fitness genes were required for optimal fitness in a mouse model of systemic infection. Genes involved in biosynthesis of poly-N-acetyl glucosamine (pgaABCD), major and minor pilin of a type IV pilus (c2394 and c2395), oligopeptide uptake periplasmic-binding protein (oppA), sensitive to antimicrobial peptides (sapABCDF), putative outer membrane receptor (yddB), zinc metallopeptidase (pqqL), a shikimate pathway gene (c1220) and autotransporter serine proteases (pic and vat) were further characterized. Here, we report the first genome-wide identification of genes that contribute to fitness in UPEC during systemic infection in a mammalian host. These fitness factors may represent targets for developing novel therapeutics against UPEC.