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PubMed1992

Identification of the tick-borne relapsing fever spirochete Borrelia hermsii by using a species-specific monoclonal antibody.

Borrelia hermsii causes a relapsing fever in humans and is one of several species of tick-borne spirochetes known to occur in the western United States. Spirochetes observed in the peripheral blood of patients acutely ill have been presumptively identified in the past by the geographic location of exposure and the probable species of tick vector. We describe a monoclonal antibody (H9826) that bound to the flagellar protein of B. hermsii but not to those of any of the other species tested, which included B. parkeri, B. turicatae, B. coriaceae, B. anserina, B. burgdorferi, and Leptospira interrogans serovar ballum. This antibody bound efficiently to B. hermsii in an indirect immunofluorescence assay and was used to rapidly detect and identify this spirochete in the peripheral blood of experimentally infected mice and in the central ganglia of Ornithodoros hermsi ticks. H9826 can rapidly confirm the identification of B. hermsii to increase our understanding concerning the geographic distribution, vector specificity, and epidemiological significance of this zoonotic human pathogen.

Antibodies, Bacterial↗
PubMed1997

The effect of antibody against TNF alpha on cytokine response in Jarisch-Herxheimer reactions of louse-borne relapsing fever.

Severe Jarisch Herxheimer reaction (J-HR) precipitated by antibiotic treatment of louse-borne relapsing fever (LBRF) is associated with a transient, marked rise in circulating tumour necrosis factor alpha (TNF alpha), interleukin 6 (IL-6) and interleukin 8 (IL-8). Ovine polyclonal anti-TNF alpha antibody fragments (Fab) were used in a randomized double blind placebo controlled trial in an attempt to prevent this reaction. Within 4 h after penicillin, in controls (n = 29), a several-fold rise in cytokines occurred, concomitant with a fall in spirochaetes and maximal clinical manifestations of the J-HR. An intravenous infusion of anti-TNF alpha Fab, 30 min before penicillin in 20 patients reduced peak plasma levels of IL-6 and IL-8 (but not IL-1 beta) compared with controls (p = 0.01 and < 0.001, respectively) and the incidence of the J-HR, indicating some neutralization of TNF alpha. An apparent fall in TNF alpha reflected interference of anti-TNF alpha in the immunoassay.

Adolescent↗
PubMed2001

In vitro and in vivo neutralization of the relapsing fever agent Borrelia hermsii with serotype-specific immunoglobulin M antibodies.

The antigenic variation of the relapsing fever agent Borrelia hermsii is associated with changes in the expression of the Vlp and Vsp outer membrane lipoproteins. To investigate whether these serotype-defining proteins are the target of a neutralizing and protective antibody response, monoclonal antibodies were produced from spleens of infected mice just after clearance of serotype 7 cells from the blood. Two immunoglobulin M monoclonal antibodies, H7-7 and H7-12, were studied in detail. Both antibodies specifically agglutinated serotype 7 cells and inhibited their growth in vitro. Administered to mice before or after infection, both antibodies provided protection against infection or substantially reduced the number of spirochetes in the blood of mice after infection. Whereas antibody H7-12 bound to Vlp7 in Western blotting, enzyme-linked immunosorbent assay, and immunoprecipitation assays, as well as to whole cells in other immunoassays, antibody H7-7 only bound to wet, intact cells of serotype 7. Antibody H7-7 selected against cells expressing Vlp7 in vitro and in vivo, an indication that Vlp7 was a conformation-sensitive antigen for the antibody. Vaccination of mice with recombinant Vlp7 with adjuvant elicited antibodies that bound to fixed whole cells of serotype 7 and to Vlp7 in Western blots, but these antibodies did not inhibit the growth of serotype 7 in vitro and did not provide protection against an infectious challenge with serotype 7. The study established that a Vlp protein was the target of a neutralizing antibody response, and it also indicated that the conformation and/or the native topology of Vlp were important for eliciting that immunity.

Agglutination Tests↗
PubMed1998

Tick-borne relapsing fever in the northwestern United States and southwestern Canada.

Records from 182 cases of tick-borne relapsing fever (TBRF) were reviewed. In confirmed cases, there was febrile illness, and spirochetes were identified on peripheral blood preparations. In probable cases, there were clinical features of TBRF and either the same exposure as a confirmed case or serological (indirect fluorescent antibody test and western blotting [WB]) evidence of infection with Borrelia hermisii. Sera also were tested for antibody to Borrelia burgdorferi. We identified 133 confirmed and 49 probable cases of TBRF. A Jarisch-Herxheimer reaction was reported in 33 (54.1%) of 61 cases for which this information was available. Most patients who had antibodies to B. hermsii were serologically positive for B. burgdorferi, and WB demonstrated false positivity of testing for B. burgdorferi. Thirty-five (21%) of 166 cases were unreported to public health authorities. In 52 cases, there were more than two relapses before the diagnosis. This study demonstrates that TBRF is underrecognized and underreported and may be falsely identified as Lyme disease.

Adolescent↗
PubMed1998

Tick-borne relapsing fever in British Columbia, Canada: first isolation of Borrelia hermsii.

The spirochete that causes tick-borne relapsing fever, Borrelia hermsii, was isolated in pure culture during 1995 and 1996 from three acutely ill human patients infected in southern British Columbia, Canada. The geographic area of exposure is a known focus of this disease dating back to 1930 when the first case was recognized in a human. Analyses of plasmid DNA, protein profiles, and reactivity with a species-specific monoclonal antibody identified the new isolates of spirochetes as B. hermsii, all of which were most similar to an isolate of this spirochete from northern California described previously. These are the first reported isolates of B. hermsii from Canada.

Adult↗
PubMedDate not supplied

[How the epidemics of typhus and relapsing fever were stopped in Serbia in 1915 year].

Eighty years are passed after the catastrophic epidemics of Typhus and Relapsing Fever in 1915 in Serbia was stopped and put under control. This remarkable achievment was realized in cooperation of the British Military Mission and Serbian health services, one month before the usual seasonal maximum of epidemic wave. The cutting of epidemics was made possible by introducing famous "Serbian barrel" (constructed by Dr Stammers). However, the epidemics of Typhus fever present in the same time in several european countries lasted throughout the whole First World War.

Disease Outbreaks↗
PubMed2005

Variable tick protein in two genomic groups of the relapsing fever spirochete Borrelia hermsii in western North America.

Borrelia hermsii is the primary cause of tick-borne relapsing fever in North America. When its tick vector, Ornithodoros hermsi, acquires these spirochetes from the blood of an infected mammal, the bacteria switch their outer surface from one of many bloodstream variable major proteins (Vmps) to a unique protein, Vtp (Vsp33). Vtp may be critical for successful tick transmission of B. hermsii; however, the gene encoding this protein has been described previously in only one isolate. Here we identified and sequenced the vtp gene in 31 isolates of B. hermsii collected over 40 years from localities throughout much of its known geographic distribution. Seven major Vtp types were found. Little or no sequence variation existed within types, but between them significant variation was observed, similar to the pattern of diversity described for the outer surface protein C (OspC) gene in Lyme disease spirochetes. The pattern of sequence relatedness among the Vtp types was incongruent in two branches compared to two genomic groups identified among the isolates by multilocus sequence typing of the 16S rRNA, flaB, gyrB, and glpQ genes. Therefore, both horizontal transfer and recombination within and between the two genomic groups were responsible for some of the variation observed in the vtp gene. O. hermsi ticks were capable of transmitting spirochetes in the newly identified genomic group. Therefore, given the longevity of the tick vector and persistent infection of spirochetes in ticks, these arthropods rather than mammals may be the likely host where the exchange of spirochetal DNA occurs.

Amino Acid Sequence↗
PubMed1999

Tick-borne relapsing fever imported from West Africa: diagnosis by quantitative buffy coat analysis and in vitro culture of Borrelia crocidurae.

West African tick-borne relapsing fever (TBRF) is difficult to diagnose due to the low number of spirochetes in the bloodstream of patients. Previously, the causative microorganism, Borrelia crocidurae, had never been cultured in vitro. TBRF was rapidly diagnosed for two patients returning from western Africa with fever of unknown origin by quantitative buffy coat (QBC) analysis. Diagnosis was confirmed by intraperitoneal inoculation of blood specimens from patients into laboratory mice. In vitro experiments showed that QBC analysis may be as much as 100-fold more sensitive than thick smear. Spirochetes were also cultured from blood samples from both patients in modified Kelly's medium and were identified as B. crocidurae by partial sequencing of the PCR-amplified rrs gene.

Acridine Orange↗
PubMed2001

Platelet activation by a relapsing fever spirochaete results in enhanced bacterium-platelet interaction via integrin alphaIIbbeta3 activation.

Borrelia hermsii, a spirochaete responsible for relapsing fever in humans, grows to high density in the bloodstream and causes thrombocytopenia. We show here that B. hermsii binds to human platelets. Extended culture in bacteriological medium resulted in both diminished infectivity in vivo and diminished platelet binding in vitro. Platelet binding was promoted by the platelet integrin alphaIIbbeta3: the bacterium bound to purified integrin alphaIIbbeta3, and bacterial binding to platelets was diminished by alphaIIbbeta3 antagonists or by a genetic defect in this integrin. Integrin alphaIIbbeta3 undergoes a conformational change upon platelet activation, and bacteria bound more efficiently to activated rather than resting platelets. Nevertheless, B. hermsii bound at detectable levels to preparations of resting platelets. The bacterium did not recognize a point mutant of alphaIIbbeta3 that cannot acquire an active conformation. Rather, B. hermsii was capable of triggering platelet and integrin alphaIIbbeta3 activation, as indicated by the expression of the platelet activation marker P-selectin and integrin alphaIIbbeta3 in its active conformation. The degree of platelet activation varied depending upon bacterial strain and growth conditions. Prostacyclin I2, an inhibitor of platelet activation, diminished bacterial attachment, indicating that activation enhanced bacterial binding. Thus, B. hermsii signals the host cell to activate a critical receptor for the bacterium, thereby promoting high-level bacterial attachment.

Animals↗
PubMed1977

Louse-borne relapsing fever: II. Combined penicillin and tetracycline therapy in 160 Sudanese patients.

One hundred and sixty patients with louse-borne relapsing fever were treated with a combination therapy of procaine penicillin and tetracycline. Fortified procaine penicillin B.P. was given as 400,000 units in the first day. This was followed the next day by 2 g tetracycline orally in divided doses for seven days. A mild rise in temperature was observed in 22 (13-7%) patients within four hours of administering penicillin. Rigors and hypotension occurred in one patient. Relapse occurred in two patients, of whom one had concomitant typhoid and one visceral leishmaniasis. The combined therapy has been found to be effective and safe. It lacks the disadvantages of penicillin (relapses) and tetracycline (severe reaction), when each drug is used alone.

Adolescent↗
PubMed1993

Louse-borne relapsing fever. A clinical and an epidemiological study of 389 patients in Asella Hospital, Ethiopia.

An outbreak of louse-borne relapsing fever, due to the return of soldiers to their original recruitment areas, after the end of thirty years of fighting in northern Ethiopia, was reported in Arsi region, southern Ethiopia. The epidemic spread to different members of the community and eventually the schools. We studied 389 patients affected by the epidemic and who were admitted to Asella Hospital between June 1991 and May 1992. Twenty-seven per cent of the patients were ex-soldiers; 28% were students, who were admitted to the hospital since the schools were opened after the summer vacations. The common clinical features of the disease were fever (99%), headache (92%), hepatosplenomegaly (66%), myalgia (55%), arthralgia (51%), petechial rash (43%), epistaxis (24%) and jaundice (23%). Observed complications were pneumonia (10%), pulmonary edema (6%), myocarditis (3%) and 6 abortions in 15 pregnancies. Patients were treated with low dose penicillin and i.v. fluids. The in-hospital case fatality rate was 3.6%. Jarisch-Herxheimer reaction occurred in 43% of the patients. 1.8% of the patients had relapses after treatment.

Adolescent↗
PubMed1974

Experimental louse-borne relapsing fever in the grivet monkey, Cercopithecus aethiops. II. Pathology.

Nineteen grivet monkeys, Cercopithecus aethiops, were infected with the spirochete of louse-borne relapsing fever, Borrelia recurrentis, and killed at various intervals following inoculation: 4 during the initial spirochetemia; 4 during remission; 3 during relapse; 2 that were dying following severe relapses; and 6 during convalescence. The histologic changes of histiocytic myocarditis, multiple microabscesses replacing the nodular white pulp of the spleen, and hepatitis with foci of midzonal necrosis were similar to those seen in humans. These changes are rarely seen in other infectious diseases and suggest a specific toxic effect.

Animals↗
PubMed1980

Louse-borne relapsing fever in the Sudan. A historical review and a clinico-pathological study.

A small outbreak of louse-borne relapsing fever in Khartoum (May-June 1974) provided material for a clinico-pathological study. The history of the disease in the Sudan is reviewed and the clinical and laboratory findings in 32 patients are presented. Fever, headache, jaundice, epistaxis and hepatosplenomegaly were the commonest clinical findings; thrombocytopenia was detected in 93% of cases. Although elevated levels of fibrin degradation products were found in most patients, disseminated intravascular coagulation could not be diagnosed. Hepatocellular derangement was found in 68% of cases, while 78% had high blood urea. In five autopsied bodies there was bronchopneumonia, interstitial edema with focal myocardial fibrosis, hepatic necrosis, splenic infarcts, increase in size and cellularity of the glomeruli and brain edema and congestion. Intracranial haemorrhage was found in three of the autopsied cases.

Female↗
PubMed1996

Relapsing fever: a differential diagnosis to malaria.

A 20-year-old man who had spent several weeks in Asia suffered several attacks of fever, each lasting 1 day in a cyclic pattern. Initially he was suspected to have malaria, but no parasites were found in a blood smear. When he was readmitted to the hospital with high fever and shivering. Borrelia spirochaetes were detected in a blood smear, leading to a diagnosis of relapsing fever. He recovered immediately when treated with tetracyclin.

Adult↗