In March 2017, a patient became febrile within 4 days after visiting a rustic conference center in Austin, Texas, USA, where Austin Public Health suspected an outbreak of tickborne relapsing fever a month earlier. Evaluation of a patient blood smear and molecular diagnostic assays identified Borrelia turicatae as the causative agent. We could not gain access to the property to collect ticks. Thus, we focused efforts at a nearby public park, <1 mile from the suspected exposure site. We trapped Ornithodoros turicata ticks from 2 locations in the park, and laboratory evaluation resulted in cultivation of 3 B. turicatae isolates. Multilocus sequencing of 3 chromosomal loci (flaB, rrs, and gyrB) indicated that the isolates were identical to those of B. turicatae 91E135 (a tick isolate) and BTE5EL (a human isolate). We identified the endemicity of O. turicata ticks and likely emergence of B. turicatae in this city.

A 40-year-old woman, gravida 2 para 1, with monochorionic diamniotic (MCDA) twin pregnancy was diagnosed with twin-to-twin transfusion syndrome (TTTS) Quintero stage I at 19 + 4 weeks' gestation. In the umbilical artery of the donor twin we observed a pattern of intermittent isolated episodes of reversed end-diastolic velocity every five to six cardiac cycles (Figure 1). No Doppler abnormality was seen in the middle cerebral artery or ductus venosus, and no cardiac rhythm abnormality was seen in either twin. The abnormal Doppler pattern in the umbilical artery was not observed in subsequent follow-up visits. The TTTS remained stable for the rest of the pregnancy and both neonates were live-born following vaginal delivery at 36 + 4 weeks' gestation. The birth weight of the recipient twin was 2860 g and that of the donor twin was 2580 g. Placental studies using colored-dye injection demonstrated the presence of two large arterioarterial (AA) anastomoses (Figure 2). The Doppler findings in the umbilical cord of the donor twin reported herein may represent intermittent isolated episodes of reversal of blood flow from the recipient to the donor twin through the large AA placental anastomoses. Evidence that supports our theory is the observation of Wee et al.1 who reported an association between the presence of large AA placental anastomoses and periods of intermittent reversed end-diastolic flow in the smaller twin in MCDA twin pregnancies. Similarly, Gratacós et al.2 reported the presence of large AA placental anastomoses in all cases with intermittent periods of absent or reversed end-diastolic flow in the umbilical artery but in only 3.6% of MCDA twins without this finding. The Doppler findings in our case of TTTS are different from the patterns described by Wee et al.1 and Gratacós et al.2 as we observed intermittent isolated episodes of reversed end-diastolic velocity every five to six cardiac cycles, however the presence of large AA placental anastomoses was a common finding. In MCDA twin pregnancies complicated by twin arterial reversed perfusion (TRAP), the Doppler hallmark is the presence of reversed arterial flow in the recipient twin. In MCDA twins with large AA placental anastomoses, it is possible that the presence of large communicating arterial conduits between the umbilical arteries of both twins enables intermittent reversal of blood flow from the larger to the smaller twin. The Doppler patterns described here, as well as those described by others2,3, may represent episodes of intermittent reversed arterial perfusion between both twins. Owing to the similarities with TRAP sequence, we propose the term transient TRAP (TTRAP) to describe these Doppler patterns. We speculate that intermittent reversal of the transfusion pattern from the recipient to the donor twin in TTTS (or from the larger to the smaller twin in the absence of TTTS) may have a protective effect in MCDA twin pregnancies. Sporadic reversal of the disease process may prevent development or further deterioration of TTTS, as seen in our case. We propose that these transient Doppler patterns should not automatically lead to upstaging of the TTTS, as this may result in unnecessary intervention. In the absence of progressive disease, these intermittent Doppler findings may be a sign of a protective compensatory mechanism at work. J. Espinoza*†, A. Shamshirsaz†, R. Ruano†, S. Ledet‡ and M. Belfort† †Department of Obstetrics and Gynecology, Division of Maternal-Fetal Medicine, Baylor College of Medicine and Texas Children's Hospital Pavilion for Women, 6651 Main Street, Suite 1020, Houston, TX, USA; ‡Seton Medical Center, Pathology Department, Austin, TX 77030, USA *Correspondence. (e-mail: jimmy.espinoza@bcm.edu)

Dengue is caused by infection with any of four mosquito-transmitted dengue viruses (DENV-1-4) and is characterized by fever, headache, myalgia, and leukopenia. Hemophagocytic lymphohistiocytosis (HLH) is a potentially fatal hyperinflammatory syndrome that can be familial or acquired, and is characterized by persistent fever, pancytopenia, hepatosplenomegaly, and increased serum ferritin. Acquired HLH is most frequently associated with Epstein Barr virus infection but also has been associated with dengue. This report describes a fatal case of acquired HLH that was apparently triggered by infection with DENV-3. The patient developed an acute febrile illness in August 2012 during a 1-month vacation in New Mexico. After returning to her home in Texas, she was initially diagnosed with West Nile virus (WNV) infection, developed pancytopenia, liver failure, and disseminated intravascular coagulopathy, and died. DENV-3 was detected in a premortem bone marrow biopsy in which erythrophagocytosis was evident. This case underscores the need for clinicians in the United States to be vigilant for dengue and request diagnostic testing for suspected cases, which should be reported to public health authorities.

[Centers for Disease Control and Prevention. Update: Clostridium novyi and unexplained illness among injecting-drug users—Scotland, Ireland, and England, April-June 2000. MMWR Morb Mortal Wkly Rep. 2000;49(24):543-545.]