Borrelia turicatae

Borrelia turicatae is a bacterial species of the spirochaete class of the genus Borrelia. It is one of the relapsing fever spirochaetes, which are globally distributed yet understudied agents of tick-borne relapsing fever. The tick vector Ornithodoros turicata transmits B. turicatae, which causes relapsing fever, an arthropod-borne infection of humans and other mammals caused by different Borrelia species. B. turicatae is long and spiral-shaped, as is typical for all spirochaetes. It is a Gram-negative bacterium and visible with light microscopy. Few epidemiological studies have been performed and few molecular data exist for B. turicatae and its arthropod vector O. turicata. B. turicatae is predominant in the Southwestern United States. Endemic foci for B. turicatae occur in Texas and Florida, where clinical isolates have been obtained from sick dogs, suggesting a role for wild canids in the maintenance of the spirochaetes in nature. O. turicata has also been reported to be distributed in Mexico and Central and South America, yet given the absence of Latin American isolates for B. turicatae, the identification of endemic foci is unclear. Currently, the only known isolates of B. turicatae originate from argasid soft ticks and sick dogs, although the mammalian hosts for most species of relapsing fever spirochaetes include rodents and insectivores. The epidemiological evidence for B. turicatae causing human infections is strong. B. turicatae was first described by Émile Brumpt in 1933 and later described by Edward Arthur Steinhaus in his book Insect Microbiology, published in 1946. Its vector O. turicata was first described by Eugenio Dugès in 1876. Along with fever, patients may experience an incredible range of nonspecific symptoms. The clinical features of relapsing fever may include recurring febrile episodes, chills, nausea, headache, muscle and joint aches, vomiting, lethargy, thrombocytopenia, spirochetemia, anemia, facial paralysis, neutrophilia, lymphopenia, anorexia, dry cough, light sensitivity, rash, neck pain, eye pain, confusion, dizziness, eosinopenia, myocarditis, dermatitis, brain infection, lymphoid hyperplasia, and pregnancy complications. The neurological complications of Borrelia infections are referred to as neuroborreliosis, and the most common manifestations of neuroborreliosis in relapsing fever include meningitis, facial nerve palsy, radiculitis, and encephalopathy. The severity of the disease depends on the infecting serotype. The incubation period typically lasts 7 days, while the symptomatic periods tend to last 3 days, and the afebrile periods tend to last 7 days. Each febrile episode ends with a sequence of symptoms collectively known as a 'crisis'. During the 'chill phase' of the crisis, which lasts 10 to 30 minutes, patients develop very high fever (up to 106.7 °F or 41.5 °C) and may become delirious, agitated, tachycardic, and tachypneic. This phase is followed by the 'flush phase', characterized by drenching sweats and a rapid decrease in body temperature and transient hypotension. Generally, patients who are not treated will experience one to four episodes of fever before illness resolves. TBRF contracted during pregnancy can cause spontaneous abortion, premature birth, and neonatal death. The maternal-fetal transmission of Borrelia is believed to occur either transplacentally or while traversing the birth canal. In general, pregnant women have higher spirochaete loads and more severe symptoms than nonpregnant women. The definitive diagnosis of TBRF is based on the observation of Borrelia spirochaetes in smears of peripheral blood, bone marrow, or cerebrospinal fluid in a symptomatic person. B. turicatae is best seen by dark-field microscopy, but the organisms can also be detected using acridine orange or Wright's stain. The organisms are best detected in blood obtained while a person is febrile. With subsequent febrile episodes, the number of circulating spirochaetes decreases, making detecting spirochetes on a peripheral blood smear more difficult. Even during the initial episode, spirochaetes can only be seen 70% of the time. Especially in resource-poor areas, people continue to be afflicted by undiagnosed febrile illnesses, which pose a significant health burden. However, the ecology, pathogenesis, and distribution of B. turicatae remains understudied, and regions of endemicity not previously known to exist continue to be identified. Because relapsing fever has such nonspecific clinical manifestations, the disease is likely underreported, thus improved diagnostic tools for relapsing fever spirochaetes are needed to better identify the endemic foci and to ensure proper treatment. A limitation in defining the distribution of B. turicatae has been the absence of diagnostic antigens specific for the species. A spirochaete antigen designated the Borrelia immunogenic protein A (BipA) has been identified in B. turicatae. As antibody responses generated against recombinant BipA appear to be unique to infections caused by B. turicatae, these immune responses generated against BipA suggest that it may be a species-specific antigen that could be used to identify additional vertebrate hosts, define endemic foci for B. turicatae, and increase the awareness of the disease to improve healthcare.