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PubMed1978

Tick-borne relapsing fever in the Eastern United States.

Tick-borne relapsing fever is endemic in the western part of the United States, but it has not been reported east of the Mississippi River. Sporadic cases have been reported in the eastern part of the United States, but travel to the West during the incubation period appeared to provide the source of infection. In the fall of 1975, a case of relapsing fever was diagnosed in Cincinnati in a child who had not traveled outside of Ohio, indicating the presence of Borrelia in this area. Serial serological studies indicated that B turicatae was the species involved. The occurrence of this case suggests that relapsing fever may exist in the eastern part of the United States, but its presence may not be appreciated because of the rarity of the disease and the difficulty in confirming the diagnosis.

Anti-Bacterial Agents↗
PubMed1991

Molecular biology of antigenic variation in Lyme borreliosis and relapsing fever: a comparative analysis.

Lyme borreliosis and relapsing fever are human diseases caused by different members of the genus Borrelia. Antigenic variation has been a well-known feature of the pathogenesis of relapsing fever for decades. More recently it has been recognized that Borrelia burgdorferi, the agent of Lyme borreliosis, also can vary its surface antigens. In this review the biology and molecular biology of antigenic variation of the pathogens in these two disorders are compared.

Antigenic Variation↗
PubMed2002

Tick-borne relapsing fever caused by Borrelia turicatae.

Tick-borne relapsing fever manifests as relapsing episodes of fever with significant morbidity and mortality. We report a case of Borrelia turicatae disease in a 13-year-old male youth with outdoor exposures in Texas. After multiple clinic visits the diagnosis was made, and treatment was initiated. The patient did well without long term sequelae.

Adolescent↗
PubMed1991

Can protracted relapsing fever resemble Lyme disease?

We report the case of a Protestant missionary who contracted tick-borne relapsing fever in 1979 while serving in the Sudan. Despite tetracycline treatment, his acute illness ran a protracted course, with migratory polyarthralgias lasting approximately 10 months. Symptoms recurred in 1984 and have persisted. At regular intervals, the patient has experienced recurrent episodes of fever, generalized fatigue, bilateral upper and lower extremity muscle weakness, and asymetric large joint polyarthralgia. Indirect fluorescent antibody testing of sera demonstrated titers of 1:16 for B. burgdorferi and 1:64 for B. hermsii, and immunoblotting confirmed past exposure to relapsing fever, but not Lyme disease. It is hypothesized that this individual's chronic symptoms have been related to relapsing fever, and that in certain situations or in select individuals, relapsing fever can be capable of producing a chronic clinical picture analogous to Lyme disease.

Adult↗
PubMed1998

Cloning and molecular characterization of a multicopy, linear plasmid-carried, repeat motif-containing gene from Borrelia turicatae, a causative agent of relapsing fever.

Borrelia turicatae is one of several spirochete species that can cause relapsing fever. Here, we describe the identification and characterization of a gene from B. turicatae and other relapsing-fever spirochetes that exhibits homology with the rep+ and ORF-E gene families of the Lyme disease spirochetes. This gene, which we have designated repA, encodes a putative protein of 30.2 kDa with an isoelectric point of 4.69. The central region of RepA harbors a series of amino acid repeat motifs which exhibit homology with casein kinase 2 phosphorylation sites. Through Southern hybridization analyses, we demonstrate that repA (or a closely related sequence) is multicopy in the relapsing-fever spirochetes and is carried on variably sized linear plasmids in both Borrelia parkeri and B. turicatae. Transcriptional analyses demonstrate that repA is expressed, albeit at low levels, during in vitro cultivation of B. turicatae. Transcriptional start site analysis revealed that repA is preceded by a consensus ribosomal binding site and an appropriately spaced promoter element. The sequence conservation, unique features, and multicopy status of repA and its homologs suggest that RepA may play an important genus-wide role in the biology of the Borrelia.

Amino Acid Sequence↗
PubMedDate not supplied

[Current status of the foci and morbidity of tick-borne relapsing fever in Uzbekistan].

The contemporary state of settlement nidi of tick-borne relapsing fever is discussed on the material collected in the Namanganskaya and Andizhanskaya regions of Uzbek SSR. Despite the control measures and rise of the sanitary culture of population the conditions are still preserved for the maintenance of nidi. As in ancient estates, classical nidi of tick-borne relapsing fever, so in modern ones there are preserved conditions for existence of flourishing populations of vectors, i.e. favourable habitats and the availability of hosts. The analysis of factors is given affecting the contemporary level of sick-rate with tick-borne relapsing fever. Within the limits of the distribution area of the vector a higher sick-rate should be expected than it is registered.

Animals↗
PubMed2000

The relapsing fever spirochete Borrelia hermsii contains multiple, antigen-encoding circular plasmids that are homologous to the cp32 plasmids of Lyme disease spirochetes.

Borrelia hermsii, an agent of tick-borne relapsing fever, was found to contain multiple circular plasmids approximately 30 kb in size. Sequencing of a DNA library constructed from circular plasmid fragments enabled assembly of a composite DNA sequence that is homologous to the cp32 plasmid family of the Lyme disease spirochete, B. burgdorferi. Analysis of another relapsing fever bacterium, B. parkeri, indicated that it contains linear homologs of the B. hermsii and B. burgdorferi cp32 plasmids. The B. hermsii cp32 plasmids encode homologs of the B. burgdorferi Mlp and Bdr antigenic proteins and BlyA/BlyB putative hemolysins, but homologs of B. burgdorferi erp genes were absent. Immunoblot analyses demonstrated that relapsing fever patients produced antibodies to Mlp proteins, indicating that those proteins are synthesized by the spirochetes during human infection. Conservation of cp32-encoded genes in different Borrelia species suggests that their protein products serve functions essential to both relapsing fever and Lyme disease spirochetes. Relapsing fever borreliae replicate to high levels in the blood of infected animals, permitting direct detection and possible functional studies of Mlp, Bdr, BlyA/BlyB, and other cp32-encoded proteins in vivo.

Amino Acid Sequence↗
PubMed1980

Tick-borne relapsing fever in the Pacific Northwest: an underdiagnosed illness?

Some 30 cases of tick-borne relapsing fever due to Borrelia are known to have occurred between 1965 and 1978 in the Pacific Northwest. This disease was found more frequently in young men with a history of wilderness exposure during the summer months. Recurrent fever was the most common symptom with temperatures reaching higher than 39.5 degrees C (103.1 degrees F) in all cases, and many patients had three or more febrile episodes. Splenomegaly was the second most common finding reported. Diagnosis of relapsing fever was made in 20 cases by identifying spirochetes on peripheral blood smears. In ten remaining cases the diagnosis was made on clinical and epidemiologic grounds.Information regarding therapy was available in 21 cases. Ten patients received a tetracycline drug and all had a prompt response without relapse. Two of the patients died, a 68-year-old woman with possible myocardial involvement and a newborn infant with infection acquired in utero and meningeal involvement. The diagnosis was often delayed in spite of outpatient evaluation and admittance to hospital, probably because borreliosis was not considered in the differential diagnosis. Because tick-borne relapsing fever is eventually a self-limited disease in most patients, it is probably not recognized often enough. Awareness of this disease and examination of the peripheral blood smear for spirochetes will lead to earlier diagnosis. Prompt initiation of tetracycline therapy should reduce morbidity associated with borreliosis.

Adult↗
PubMed1999

Erythrocyte-aggregating relapsing fever spirochete Borrelia crocidurae induces formation of microemboli.

The African relapsing fever spirochete Borrelia crocidurae forms aggregates with erythrocytes, resulting in a delayed immune response. Mice were infected with B. crocidurae and monitored during 50 days after infection. Spirochetes were observed extravascularly at day 2 after infection. Two days later, inflammatory responses, cell death, and tissue damage were evident. The pathologic responses in lungs and kidneys were similar, whereas the symptoms in the brains were delayed, with a less pronounced inflammatory response. Microemboli were found in the blood vessels, possibly a result of the erythrocyte aggregation. The B. crocidurae invasion emerged more rapidly than has been described for Lyme disease-causing Borrelia species. In addition to erythrocyte rosetting, the presence of extravascular B. crocidurae indicates a novel route for these bacteria to propagate and cause damage in the mammalian host. The histopathologic findings in this study may explain the clinical manifestations of human relapsing fever.

Animals↗
PubMed1993

Epidemic of louse-borne relapsing fever in Ethiopia.

During summer 1991 an outbreak of louse-borne relapsing fever occurred simultaneously in two transit camps established for prisoners of war being returned from Eritrea at the end of the Ethiopian civil war. Only antibiotic treatment was given at the Bahr Dar camp where the frequency of cases increased for 20 days. Vector control by delousing in addition to antibiotics was given at Mekele camp where the frequency of cases fell over a similar period. This difference was significant (p < 0.001). Furthermore, there was a significant correlation between the decreasing proportion of camp inhabitants that had not been deloused at Mekele camp each day and the numbers of patients with fever (r = 0.89, p < 0.001). Taken together, these results confirm that effective control of an epidemic of louse-borne relapsing fever is dependent on efficient vector control in addition to antibiotic treatment.

Adolescent↗
PubMed1998

The spirochete Borrelia crocidurae causes erythrocyte rosetting during relapsing fever.

Several species of the genus Borrelia exhibit antigenic variation of variable major proteins on their surface during relapsing fever. We have investigated the African relapsing fever species Borrelia crocidurae during infections in mice and compared it with the thoroughly studied North American species Borrelia hermsii. A major difference between the two species is that B. crocidurae can bind and become completely covered with erythrocytes. In addition, B. crocidurae causes a prolonged spirochetemia which coincides with a delayed appearance of antiborrelial antibodies. We show that the antibody response against an unrelated antigen is not delayed and that antibiotic treatment, which dissociates rosettes and inhibits the spirochetes, also leads to an early antibody response. Taken together, the erythrocyte aggregation and prolonged spirochetemia hint at a new mode of immune evasion where erythrocyte-covered spirochetes may avoid contact with the phagocytic cells and B cells of the immune system, thereby delaying the onset of a specific immune response.

Animals↗
PubMed1973

Human serological response to louse-borne relapsing fever.

Serological response to louse-borne relapsing fever in Ethiopia was determined by immobilization tests using Borrelia recurrentis cultures. Isolates from 26 patients tested with autologous convalescent sera showed from 90 to 100% of the organisms had been immobilized. Sera from thirteen patients were tested with autologous and heterologous strains. Several reacted with the majority and two showed high titers against all strains tested. Screening of day 2 and day 8 sera frequently showed heterologous antibody present before autologous antibody appeared, suggesting multiple antigenic challenge to infected patients. Some strains appeared to be antigenically related, but because of the wide diversity of serological responses, no definite serological groupings could be ascertained.

Animals↗
PubMedDate not supplied

Relapsing fever and its serological discrimination from Lyme borreliosis.

Patients with Borrelia-caused relapsing fever produce cross-reacting antibodies to Borrelia burgdorferi, the anti-genetically related causative agent of Lyme borreliosis. The antibody response of the serum of a patient (acute and convalescent) with relapsing fever was analysed by the immunoblot technique using Borrelia hermsii and B. burgdorferi as antigens. The diagnosis was established by microscopic detection of spirochetes in the patient's blood. The patient's serum showed significantly elevated titers of IgG and IgM in a B. burgdorferi indirect immunofluorescence assay. Immunoblot analysis indicated the presence of cross-reacting antibodies directed to B. burgdorferi antigens with apparent molecular weights of 60, 41, 40, 36, 30 and 20 kDa.

Antibodies, Bacterial↗
PubMed1993

Louse-borne relapsing fever in Ethiopian children: a clinical study.

An outbreak of louse-borne relapsing fever, caused by the return to their original recruitment areas of soldiers at the end of 30 years of fighting in northern Ethiopia, was reported in the Arsi region. We studied 103 infants and children with louse-borne relapsing fever who were admitted to Asella Hospital between 1 May 1991 and 30 April 1992. Twenty-one per cent of the patients had a clear history of contact with sick ex-soldiers; 42% were students admitted to the hospital following the re-opening of schools after the summer vacation. The common clinical features of the disease were fever in 100%, headache in 84.5%, chills in 74%, abdominal pain in 51%, epistaxis in 20%, hepatomegaly in 26%, splenomegaly in 14%, petechial rash in 34% and jaundice in 10%. Differences in symptoms and signs according to age are described. Observed complications were pneumonia in 14% and central nervous system involvement in 10%. Four children went into deep coma, and two of them died. Severe disease was associated with a high density of spirochaetes in blood smears. Patients were treated with two low doses of penicillin or one dose of penicillin followed by, according to age, chloramphenicol or tetracycline, and with intravenous fluids. The case fatality rate was 1.9%. Jarisch-Herxheimer reactions occurred in 61% of patients. There were relapses in 2.9% of treated patients.

Adolescent↗
PubMed1992

Detection of plasma tumor necrosis factor, interleukins 6, and 8 during the Jarisch-Herxheimer Reaction of relapsing fever.

The Jarisch-Herxheimer Reaction (J-HR) is a clinical syndrome occurring soon after the first adequate dose of an antimicrobial drug to treat infectious diseases such as Lyme disease, syphilis, and relapsing fever. Previous attempts to identify factors mediating this reaction, that may cause death, have been unsuccessful. We conducted a prospective trial in Addis Ababa, Ethiopia on 17 patients treated with penicillin for proven louse-borne relapsing fever due to Borrelia recurrentis to evaluate the association of symptoms with plasma levels of tumor necrosis factor (TNF), interleukins 6, and 8 (IL-6 and -8). 14 of the 17 (82%) patients experienced a typical J-HR consisting of rigors, a rise in body temperature (1.06 +/- 0.2 degrees C) peaking at 2 h, leukopenia (7.4 +/- 0.6 x 10(-3) cells/mm3) at 4 h, a slight decrease, and then rise of mean arterial blood pressure. Spirochetes were cleared from blood in 5 +/- 1 h after penicillin. There were no fatalities, but constitutional symptoms were severe during J-HR. Plasma TNF, IL-6, and -8 were raised in several patients on admission, but a seven-, six-, and fourfold elevation of these plasma cytokine concentrations over admission levels was detected, respectively, occurring in transient form coincidental with observed pathophysiological changes of J-HR. Elevated plasma cytokine levels were not detected in the three patients who did not suffer J-HR. We conclude that the severe pathophysiological changes characterizing the J-HR occurring on penicillin treatment of louse-borne relapsing fever are closely associated with transient elevation of plasma TNF, IL-6, and -8 concentrations.

Adolescent↗
PubMed2002

Vector interactions and molecular adaptations of lyme disease and relapsing fever spirochetes associated with transmission by ticks.

Pathogenic spirochetes in the genus Borrelia are transmitted primarily by two families of ticks. The Lyme disease spirochete, Borrelia burgdorferi, is transmitted by the slow-feeding ixodid tick Ixodes scapularis, whereas the relapsing fever spirochete, B. hermsii, is transmitted by Ornithodoros hermsi, a fast-feeding argasid tick. Lyme disease spirochetes are generally restricted to the midgut in unfed I. scapularis. When nymphal ticks feed, the bacteria pass through the hemocoel to the salivary glands and are transmitted to a new host in the saliva after 2 days. Relapsing fever spirochetes infect the midgut in unfed O. hermsi but persist in other sites including the salivary glands. Thus, relapsing fever spirochetes are efficiently transmitted in saliva by these fast-feeding ticks within minutes of their attachment to a mammalian host. We describe how B. burgdorferi and B. hermsii change their outer surface during their alternating infections in ticks and mammals, which in turn suggests biological functions for a few surface-exposed lipoproteins.

Animals↗
PubMed1977

Louse-borne relapsing fever: I. A clinical and laboratory study of 363 cases in the Sudan.

Louse-borne relapsing fever seems to have become endemic in the southern Sudan. The epidemic history of the disease in the Sudan is reviewed. We have studied 363 Sudanese patients involved in an outbreak of louse-borne relapsing fever in Khartoum (Sudan) between January and June 1974. 318 of the 363 patients were new immigrants from the soughern Sudan to Khartoum. The clinical presentation varied. The common clinical fetures of the disease were: fever (94%), headache (85%), hepatosplenomegaly (74%), body and joint pains (66%), abdominal pain and tenderness (63%), jaundice (46%) and epistaxis (40%). Thrombocytopenia was common. Biochemical evidence of hepatocellular and renal damage was present in most patients. The mortality rate was 5-5% with treatment. Post-mortem examination was performed on six cases. The organs predominantly involved were the liver, spleen, brain and lungs. The common causes of death were severe hepatic damage, lobar pneumonia, subarachnoid haemorrhage and splenic rupture.

Adolescent↗
PubMed1999

Short report: Diagnosis of tick-borne relapsing fever by the quantitative buffy coat fluorescence method.

The quantitative buffy coat (QBC) parasite detection method is a sensitive and specific tool for the diagnosis of malaria parasites. It is also useful for the diagnoses of other hemoparasites, including Trypanosoma, Babesia, and Leptospira. We report a case of relapsing fever diagnosed by this technique in a short-term traveler from Senegal. The diagnosis was confirmed by the standard Giemsa hemoscopy and by the identification of significant titers of antibodies to Borrelia spp. of tick-borne relapsing fevers by specific immunofluorescence and Western blot tests. The QBC technique seems to be useful in the diagnosis of tick-borne relapsing fever in blood samples and should be included in the management of fever in the traveler returning from tropical regions.

Blood↗