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We report an immunocompromised patient in Alabama, USA, 75 years of age, with relapsing fevers and pancytopenia who had spirochetemia after a tick bite. We identified Borrelia lonestari by using PCR, sequencing, and phylogenetic analysis. Increasing clinical availability of molecular diagnostics might identify B. lonestari as an emerging tickborne pathogen.

Molecular methods can enable rapid identification of Bartonella spp. infections, which are difficult to diagnose by using culture or serology. We analyzed clinical test results of PCR that targeted bacterial 16S rRNA hypervariable V1-V2 regions only or in parallel with PCR of Bartonella-specific ribC gene. We identified 430 clinical specimens infected with Bartonella spp. from 420 patients in the United States. Median patient age was 37 (range 1-79) years; 62% were male. We identified B. henselae in 77%, B. quintana in 13%, B. clarridgeiae in 1%, B. vinsonii in 1%, and B. washoensis in 1% of specimens. B. quintana was detected in 83% of cardiac specimens; B. henselae was detected in 34% of lymph node specimens. We detected novel or uncommon Bartonella spp. in 9 patients. Molecular diagnostic testing can identify Bartonella spp. infections, including uncommon and undescribed species, and might be particularly useful for patients who have culture-negative endocarditis or lymphadenitis.

Genetic variants in apolipoprotein L1 (APOL1), a protein that protects humans from infection with African trypanosomes, explain a substantial proportion of the excess risk of chronic kidney disease affecting individuals with sub-Saharan ancestry. The mechanisms by which risk variants damage kidney cells remain incompletely understood. In preclinical models, APOL1 expressed in podocytes can lead to significant kidney injury. In humans, studies in kidney transplant suggest that the effects of APOL1 variants are predominantly driven by donor genotype. Less attention has been paid to a possible role for circulating APOL1 in kidney injury. Using liquid chromatography-tandem mass spectrometry, the concentrations of APOL1 were measured in plasma and urine from participants in the Seattle Kidney Study. Asymmetric flow field-flow fractionation was used to evaluate the size of APOL1-containing lipoprotein particles in plasma. Transgenic mice that express wild-type or risk variant APOL1 from an albumin promoter were treated to cause kidney injury and evaluated for renal disease and pathology. In human participants, urine concentrations of APOL1 were correlated with plasma concentrations and reduced kidney function. Risk variant APOL1 was enriched in larger particles. In mice, circulating risk variant APOL1-G1 promoted kidney damage and reduced podocyte density without renal expression of APOL1. These results suggest that plasma APOL1 is dynamic and contributes to the progression of kidney disease in humans, which may have implications for treatment of APOL1-associated kidney disease and for kidney transplantation.

Syphilis with Recombination of T. pallidum StrainsA patient with poorly controlled HIV infection was found to have two different strains of Treponema pallidum. Careful evaluation showed evidence for recombination between these two organisms.

Plasmodium ookinetes traverse midgut epithelial cells before they encounter the complement system in the mosquito hemolymph. We identified a heme peroxidase (HPX2) and NADPH oxidase 5 (NOX5) as critical mediators of midgut epithelial nitration and antiplasmodial immunity that enhance nitric oxide toxicity in Anopheles gambiae. We show that the two immune mechanisms that target ookinetes—epithelial nitration and thioester-containing protein 1 (TEP1)–mediated lysis—work sequentially, and we propose that epithelial nitration works as an opsonization-like system that promotes activation of the mosquito complement cascade.

We identified 34 patients with Coxiella burnetii infection using PCR; 31 (86%) cases were diagnosed from cardiac specimens. Nearly half (15/31, 48%) of those cases were not reported to any channel of national disease surveillance, indicating substantial underreporting for diseases identified using molecular methods at noncommercial laboratories.

Isolation of Cokeromyces recurvatus , a dimorphic mucormycete fungus, from clinical specimens poses a diagnostic challenge to physicians and laboratorians as this organism may represent a rare colonizer or true pathogen. Here, we report a case of Cokeromyces recurvatus present in a circumferential duodenal lesion. The patient is a 64-year-old with no past medical history, admitted with a three-week history of left upper quadrant abdominal pain. Computerized tomography scan identified duodenitis with significant gastric outlet obstruction, confirmed by the presence of a partially obstructing non-bleeding duodenal ulcer on upper endoscopy. Histology showed variably sized spherical structures without nuclei, reproductive tracts, or alimentary tracts. Small, clustered spherules representing putative endospores were observed within the larger structures and in the exudate. Based on the histology, the differential included Coccidioides spp, Emmonsia spp, or Chrysosporium spp. Additionally, gastric biopsies revealed concurrent Helicobacter pylori gastritis. The fungus was identified as C. recurvatus by broad-range fungal polymerase chain reaction performed on formalin-fixed paraffin-embedded biopsy tissue, as well as morphology and DNA sequencing of the cultured isolate. The fungus had low MICs to all major antifungal classes; however, in the context of the Helicobacter pylori infection, the patient was only treated with amoxicillin and clarithromycin with improvement in his symptoms before hospital discharge. Only three cases of Cokeromyces recurvatus isolated from the GI tract have been reported; this case highlights a unique clinical presentation in the small bowel in a patient without underlying medical conditions.

Of 604 Treponema pallidum (syphilis) strains sampled from 13 U.S. states, Washington, D.C., and two Canadian provinces from 2017 through 2023, a total of 599 (99.2%) had genotypic resistance to azithromycin.