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At least 19 recordsLinked to original sources
PubMed1999

Survey of three bacterial louse-associated diseases among rural Andean communities in Peru: prevalence of epidemic typhus, trench fever, and relapsing fever.

Typhus and other louse-transmitted bacterial infections in Peruvian sierra communities are known to occur but have not recently been assessed. In this study, 194 of 1,280 inhabitants of four villages in Calca Province in the Urubamba Valley were included. Thirty-nine (20%) of the 194 volunteers had antibodies to Rickettsia prowazekii, whereas 24 (12%) had antibodies to Bartonella quintana and 2 against Borrelia recurrentis. There was a significant correlation between the presence of infesting ectoparasites and antibodies to R. prowazekii, as well as between antibodies to R. prowazekii and ectoparasite infestation and fever in the previous 6 months. The proportion of inhabitants infested with ectoparasites was significantly higher in the highest-altitude village than in the other three villages. Two volunteers' antibody levels suggested a recent typhus infection, but only B. quintana DNA was amplified from lice. Epidemic typhus remains extant in the area, and B. quintana infections were encountered and documented for the first time in South America.

Adult↗
PubMed2005

Typing African relapsing fever spirochetes.

Relapsing fever Borrelia spp. challenge microbiologic typing because they possess segmented genomes that maintain essential genes on large linear plasmids. Antigenic variation further complicates typing. Intergenic spacer (IGS, between 16S-23S genes) heterogeneity provides resolution among Lyme disease-associated and some relapsing fever spirochetes. We used an IGS fragment for typing East African relapsing fever Borrelia spp. Borrelia recurrentis and their louse vectors showed 2 sequence types, while 4 B. duttonii and their tick vectors had 4 types. IGS typing was unable to discriminate between the tick- and louseborne forms of disease. B. crocidurae, also present in Africa, was clearly resolved from the B. recurrentis/B. duttonii complex. IGS analysis of ticks showed relapsing fever Borrelia spp. and a unique clade, distant from those associated with relapsing fever, possibly equivalent to a novel species in ticks from this region. Clinical significance of this spirochete is undetermined.

Animals↗
PubMed2006

Possibilities for relapsing fever reemergence.

Relapsing fever Borrelia infections have attracted little attention in recent years; however, where endemic, these infections still result in considerable illness and death. Despite the marked antimicrobial drug susceptibility of these organisms, therapy is often delayed through lack of clinical suspicion. With increasing travel, infections may be imported, through exotic relapsing fever infection or through resurgence of infected disease vectors. Although louseborne relapsing fever is now geographically limited, it was once of global importance. The possibility for reemergence was recently highlighted by the probable reemergence of louseborne relapsing fever in homeless persons from France. Host limitations enforced through louseborne transmission are less applicable for the tickborne forms of relapsing fever. Although the latter have reduced potential for epidemic spread, they have the ability to infect diverse hosts, thus establishing reservoirs of infection and presenting greater challenges for their control.

Animals↗
PubMed1974

Lipid catabolism of relapsing fever borreliae.

Relapsing fever borreliae require lipid compounds for growth in vitro. In this study, the major pathways of lipid catabolism in three species of tick-borne relapsing fever borreliae were investigated. Thin-layer chromatography was used to compare chloroform-methanol extracts of fresh culture media with extracts of exhausted culture media after organisms were removed by centrifugation. The chromatographic data demonstrated that lysolecithin was removed from the culture media during growth of the spirochetes, whereas lecithin, sphingomyelin, triglycerides, and cholesterol esters were not affected by growth of the organisms. Sonic extracts of the organism were tested for the presence of specific enzymes of lipid catabolism. Lysolecithinase, glycerophosphorylcholine diesterase, and acid phosphatase activities were demonstrated. Thus, these organisms can sequentially dissimilate lysolecithin to fatty acids, choline, inorganic phosphate, and glycerol. Assays for phospholipases A, C, and D, alpha-glycerophosphate dehydrogenase, alkaline phosphatase, and lipase were negative.

Acid Phosphatase↗
PubMed2006

Persistent brain infection and disease reactivation in relapsing fever borreliosis.

Relapsing fever, an infection caused by Borrelia spirochetes, is generally considered a transient, self-limiting disease in humans. The present study reveals that murine infection by Borrelia duttonii can be reactivated after an extended time as a silent infection in the brain, with no bacteria appearing in the blood and spirochete load comparable to the numbers in an infected tick. The host cerebral gene expression pattern is indistinguishable from that of uninfected animals, indicating that persistent bacteria are not recognized by the immune system nor cause noticeable tissue damage. Silent infection can be reactivated by immunosuppression, inducing spirochetemia comparable to that of initial densities. B. duttonii has never been found in any host except man and the tick vector. We therefore propose the brain to be a possible natural reservoir of the spirochete. The view of relapsing fever as an acute disease should be extended to include in some cases prolonged persistence, a feature characteristic of the related spirochetal infections Lyme disease and syphilis.

Animals↗
PubMed1994

Activation of a vmp pseudogene in Borrelia hermsii: an alternate mechanism of antigenic variation during relapsing fever.

The relapsing fever agent, Borrelia hermsii, undergoes multiphasic antigenic variation to evade its host's immune response. A frequently observed switch is serotype 7 to 26. Unlike silent vmp genes previously characterized, the transcriptionally silent vmp26 sequence was a pseudogene in lacking a start codon. In serotype 7 the location of the silent vmp26 sequence just downstream of vmp7 on the expression plasmid, as well as on the silent plasmid, was also unique. The demonstration of a predicted circular recombination product in serotype 7 but not serotype 21 populations indicates that the pseudogene was activated by an intramolecular recombination producing a deletion of DNA between 20-nucleotide direct repeats in vmp7 and psi vmp26.

Amino Acid Sequence↗
PubMed2006

Complications of pregnancy and transplacental transmission of relapsing-fever borreliosis.

Relapsing-fever borreliosis caused by Borrelia duttonii is a common cause of complications of pregnancy, miscarriage, and neonatal death in sub-Saharan Africa. We established a murine model of gestational relapsing fever infection for the study of the pathological development of these complications. We demonstrate that B. duttonii infection during pregnancy results in intrauterine growth retardation, as well as placental damage and inflammation, impaired fetal circulation, and decreased maternal hemoglobin levels. We show that spirochetes frequently cross the maternal-fetal barrier, resulting in congenital infection. Furthermore, we compared the severity of infection in pregnant and nonpregnant mice and show that pregnancy has a protective effect. This model closely parallels the consequences of human gestational infection, and our results provide insight into the mechanisms behind the complications of pregnancy that have been reported in human relapsing-fever infection.

Animals↗
PubMed2006

Dual role of MyD88 in rapid clearance of relapsing fever Borrelia spp.

Relapsing fever Borrelia spp. undergo antigenic variation, achieve high levels in blood, and require rapid production of immunoglobulin M (IgM) for clearance. MyD88-deficient mice display defective clearance of many pathogens; however, the IgM response to persistent infection is essentially normal. Therefore, MyD88(-/-) mice provided a unique opportunity to study the effect of nonantibody, innate host defenses to relapsing fever Borrelia. Infected MyD88(-/-) mice harbored extremely high levels of B. hermsii in the blood compared to wild-type littermates. In the comparison of MyD88(-/-) mice and B- and T-cell-deficient scid mice, two features stood out: (i) bacterial numbers in blood were at least 10-fold greater in MyD88(-/-) mice than scid mice, even though the production of IgM still occurred in MyD88(-/-) mice; and (ii) many of the MyD88(-/-) mice were able to exert partial clearance, although with delayed kinetics relative to wild-type mice, a feature not seen in scid mice. Further analysis revealed a delay in the IgM response to lipoproteins expressed by the original inoculum; however, by 6 days of infection antibodies were produced in MyD88(-/-) mice that could clear spirochetemia in scid mice. While these results indicated that the production of IgM was delayed in MyD88(-/-) mice, they also point to a second, antibody-independent role for MyD88 signaling in host defense to relapsing fever Borrelia. This second defect was apparent only when antibody levels were limiting.

Animals↗
PubMed2004

Isolation and characterization of Borrelia hermsii associated with two foci of tick-borne relapsing fever in California.

Relapsing fever, caused by the spirochete Borrelia hermsii and transmitted by the soft tick Ornithodoros hermsi, is endemic in many rural mountainous areas of California. Between 1996 and 1998, 12 cases of relapsing fever associated with two exposure sites in northern California were investigated. Follow-up at exposure sites included collection of soft ticks and serum specimens from sylvatic rodents. Attempts to cultivate spirochetes were made through inoculation of patient blood into mice and by feeding Ornithodoros ticks on mice. Three isolates of B. hermsii were recovered from two blood specimens and one pool of ticks. The protein and plasmid profiles of the three isolates were comparable to those of previous B. hermsii isolates from the western United States. Western immunoblotting of patient sera demonstrated an expanding immunologic response to antigens within four distinct molecular weight regions by 3 to 4 weeks postonset. Antibody to B. hermsii was detected in sera from 4 of 11 yellow-pine chipmunks (Tamias amoenus); no other rodent species collected were seropositive.

Adult↗
PubMed2005

Tick-borne relapsing fever.

Tick-borne relapsing fever is characterized by recurring fevers separated by afebrile periods and is accompanied by nonspecific constitutional symptoms. It occurs after a patient has been bitten by a tick infected with a Borrelia spirochete. The diagnosis of tick-borne relapsing fever requires an accurate characterization of the fever and a thorough medical, social, and travel history of the patient. Findings on physical examination are variable; abdominal pain, vomiting, and altered sensorium are the most common symptoms. Laboratory confirmation of tick-borne relapsing fever is made by detection of spirochetes in thin or thick blood smears obtained during a febrile episode. Treatment with a tetracycline or macrolide antibiotic is effective, and antibiotic resistance is rare. Patients treated for tick-borne relapsing fever should be monitored closely for Jarisch-Herxheimer reactions. Fatalities from tick-borne relapsing fever are rare in treated patients, as are subsequent Jarisch-Herxheimer reactions. Persons in endemic regions should avoid rodent- and tick-infested areas and use insect repellents and protective clothing to prevent tick bites.

Animals↗
PubMed1997

A focus of tick-borne relapsing fever in southern Zaire.

Relapsing fevers occur worldwide and are characterized by recurrent episodes of fever and spirochetemia. In central, eastern, and southern Africa, the disease is often caused by Borrelia duttonii, which is transmitted by the soft tick Ornithodors moubata. We conducted a field investigation in September 1994 at a hospital in Mitwaba, southern Zaire, which was the only medical facility within 150 km. The introduction of a rapid blood-smear staining technique allowed us to demonstrate that 4.3%-7.4% of the 25-50 new outpatients seen each day had relapsing fever. Because of the absence of malaria in this area, these patients account for most of the febrile patients. The incidence of relapsing fever among all pregnant women in the maternity ward was estimated to be 6.4%, and this condition often led to maternal death or to spontaneous abortion. The 16S rRNA gene of B. dutonii was sequenced after the spirochete was isolated from patients' blood samples and directly from Ornithodoros tick vectors. In this region of Africa, relapsing fever should now be considered an important public health priority.

Animals↗
PubMed2002

Tick-borne relapsing fever in North America.

Relapsing fever is characterized by recurring episodes of fever and nonspecific symptoms (e.g., headache, myalgia, arthralgia, shaking chills, and abdominal complaints). The illness is caused by an infection from the Borrelia species (spirochetes) that may be acquired through the bite of an infected tick (Ornithodoros species) or contact with the hemolymph of an infected human body louse (Pediculus humanus). In North America, most cases have been acquired in the western United States, southern British Columbia, and few cases have been reported from Mexico. Most cases have been acquired from exposure to rustic tick-infested cabins and caves. This article reviews relapsing fever, especially tick-borne relapsing fever in North America.

Anti-Bacterial Agents↗
PubMed2000

Variable small protein (Vsp)-dependent and Vsp-independent pathways for glycosaminoglycan recognition by relapsing fever spirochaetes.

Tick-borne relapsing fever, caused by pathogenic Borrelia such as B. hermsii and B. turicatae, features recurrent episodes of bacteraemia, each of which is caused by a population of spirochaetes that expresses a different variable major protein. Relapsing fever is also associated with the infection of a variety of tissues, such as the central nervous system. In this study, we show that glycosaminoglycans (GAGs) mediate the attachment of relapsing fever spirochaetes to mammalian cells. B. hermsii strain DAH bound to immobilized heparin, and heparin and dermatan sulphate blocked bacterial binding to host cells. Bacterial binding was diminished by inhibition of host cell GAG synthesis or sulphation, or by the enzymatic removal of GAGs. GAGs mediated the attachment of relapsing fever spirochaetes to potentially relevant target cells, such as endothelial and glial cells. B. hermsii was able to attach to GAGs independently of variable major proteins, because strains expressing the variable major proteins Vsp33, Vlp7 or no variable major protein at all each recognized GAGs. Nevertheless, we found that a variable major protein of B. turicatae directly promoted GAG binding by this relapsing fever spirochaete. B. turicatae strain Oz1 serotype B, which expresses the variable major protein VspB, bound to GAGs more efficiently than did B. turicatae Oz1 serotype A, which expresses VspA. Recombinant VspB, but not VspA, bound to heparin and dermatan sulphate. Previous studies have shown that strain Oz1 serotype B grows to higher concentrations in the blood than does Oz1 serotype A. Thus, relapsing fever spirochaetes have the potential to express Vsp-dependent and Vsp-independent GAG-binding activities and, for one pair of highly related B. turicatae strains, differences in GAG binding correlate with differences in tissue tropism.

Animals↗
PubMedDate not supplied

[West African tick-borne relapsing fever].

West African tick-borne relapsing fever is an endemic disease due to Borrelia crocidurae. The tick Alectorobius sonrai is the only known vector of this bacterium. Several species of rodents and insectivores may be reservoir for this spirochete. The geographic distribution of Borrelia crocidurae is not well known. The zone where the presence of the vector has been recorded is situated in Sahelian regions, from Mauritania and northern Senegal up to Chad. In Senegal, it has been shown that the persistence of drought is responsible for a considerable spread of tick-borne relapsing fever to the south. Few epidemiological data are available about West African tick-borne relapsing fever. In Senegal, epidemiological investigations indicate that Borrelia crocidurae is a major cause of morbidity (annual incidence rate of 5.1%). The relapsing nature of tick-borne borreliosis depends on Borrelia's antigenic variability. Except relapsing febrile episodes, this illness presents no pathognomonic signs. Borrelia crocidurae relapsing fever is generally benignant but neurologic or ocular complications can occur. The diagnosis of tick-borne relapsing fever is made by demonstrating the presence of Borrelia in peripheral blood in thick smear, by intraperitoneal inoculation of mice or more recently with quantitative buffy coat method (QBC test). The best treatment for relapsing fever is tetracycline or doxycycline. When tetracyclines are contraindicated, the alternative is erythromycin. In neurologic complications, the effective treatment is intravenous penicillin G or ceftriaxone. West African tick-borne relapsing fever must be systematically mentioned in case of fever in a patient returning from the endemic area.

Africa, Western↗
PubMed1998

Bloodstream- versus tick-associated variants of a relapsing fever bacterium.

The relapsing fever spirochete, Borrelia hermsii, alternates infections between a mammal and a tick vector. Whether the spirochete changes phenotypically in the different hosts was examined by allowing the tick vector Ornithodoros hermsi to feed on mice infected with serotype 7 or serotype 8 of B. hermsii. Upon infection of ticks, the spirochetal serotype-specific variable major proteins (Vmps) 7 and 8 became undetectable and were replaced by Vmp33. This switch from a bloodstream- to tick-associated phenotype could be induced in culture by a decrease in temperature. After tick-bite transmission back to mice, the process was reversed and the spirochetes resumed expression of the same Vmp present in the previous infectious blood meal.

Animals↗