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PubMed1990

Spirochetal infection of the central nervous system.

Four spirochetal diseases frequently involve the central nervous system: syphilis, leptospirosis, relapsing fever, and Lyme borreliosis. In particular, syphilis and Lyme borreliosis are increasing problems. During the spirochetemic phase there is seeding of the nervous system. After a quiescent latent period, there may be late disease flareups producing a variety of neurologic syndromes. Cerebrospinal fluid examination is very helpful in these infections.

Central Nervous System Diseases↗

PubMed1996

Ticks and Borrelia: model systems for investigating pathogen-arthropod interactions.

Blood-feeding arthropods transmit numerous types of infectious agent and parasite that have a tremendous impact on human health and mortality throughout the world. These vector-borne pathogens display a wide array of evolutionary patterns that allow them to infect and to be successfully transmitted by ticks, mites, and hematophagous insects. The vector's method of feeding, type of development, and host preference are also critical factors for the transfer of zoonotic agents from wild animal reservoirs to susceptible humans. Ticks are obligate blood-feeders in all life stages and biologically transmit many infectious agents. In North America, two ticks that are involved in the maintenance and transmission of pathogenic spirochetes include Ixodes scapularis (family Ixodidae) and Ornithodoros hermsi (family Argasidae). These ticks are the respective vectors of the Lyme disease spirochete Borrelia burgdorferi and a relapsing fever spirochete, Borrelia hermsii. Little is known concerning how these and related species of Borrelia adapt to successfully alternate between warm-blooded vertebrates and ticks; however, the possibility that borrelial surface proteins are differentially expressed in their different hosts is an exciting area of current research.

Animals↗

PubMed1997

A mouse model of Borrelia meningitis after intradermal injection.

Both young and adult C3H/HeN mice developed meningitis within 3 weeks of intradermal inoculation with a newly identified uncultivable Borrelia species, an agent of human relapsing fever. Meningoencephalitis with perivascular infiltrates and plexitis developed at approximately 25 days after inoculation. Infiltrates were composed of B and plasma cells and monocytes. This model recreated the meningitis associated with spirochetal infections through an intradermal route of infection.

Aging↗

PubMed1999

The body louse as a vector of reemerging human diseases.

The body louse, Pediculus humanus humanus, is a strict human parasite, living and multiplying in clothing. Louse infestation is associated with cold weather and a lack of hygiene. Three pathogenic bacteria are transmitted by the body louse. Borrelia recurrentis is a spirochete, the agent of relapsing fever, recently cultured on axenic medium. Historically, massive outbreaks have occurred in Eurasia and Africa, but currently the disease is found only in Ethiopia and neighboring countries. Bartonella quintana is now recognized as an agent of bacillary angiomatosis bacteremia, trench fever, endocarditis, and chronic lymphadenopathy among the homeless. Rickettsia prowazekii is the agent of epidemic typhus. The most recent outbreak (and the largest since World War II) was observed in Burundi. A small outbreak was also reported in Russia in 1997. Louse infestation appears to become more prevalent worldwide, associated with a decline in social and hygienic conditions provoked by civil unrest and economic instability.

Animals↗

PubMed1985

Glucose and insulin homeostasis during the Jarisch-Herxheimer reaction.

Plasma concentrations of glucose and insulin were measured in ten patients during the Jarisch-Herxheimer reaction of tetracycline-treated louse-borne relapsing fever. Plasma glucose fell significantly in eight of the ten patients associated with the peak of the reaction, but plasma insulin remained low. Glucoregulation by insulin was therefore normal. This evidence questions the role of macrophage mediator-induced pancreatic insulin release in causing hypoglycaemia in borreliosis or bacterial endotoxicosis.

Adolescent↗

PubMed1999

Identification of a novel strain of Borrelia hermsii in a previously undescribed northern California focus.

An epizootiologic investigation testing for the presence of tick-borne relapsing fever spirochetes in rodent and tick hosts was conducted at Eagle Lake in Lassen County, California. Six of 211 O. hermsii ticks and none of 180 rodents were polymerase chain reaction (PCR)-positive for Borrelia spirochetes. Sequencing of the PCR-amplified flagellin gene fragment suggests that the spirochetes from Eagle Lake represent a previously undescribed strain of Borrelia hermsii.

Animals↗

PubMed2005

The versatile roles of antibodies in Borrelia infections.

Antibodies are the primary weapons of the mammalian immune system that are used against the tick-borne borreliae, the causative agents of relapsing fever and Lyme disease worldwide. Some antibody responses have 'traditional' functions, whereas others are more versatile and have novel functions and modes of action. At a time when the multiple functions of antibodies are being increasingly recognized and passive immunization is being revived as therapy for infectious and other diseases, the versatile nature of the antibody response to the borreliae fits well with this antibody renaissance.

Animals↗

PubMed1976

Clinical pathology of the Jarisch-Herxheimer reaction.

The Jarisch-Herxheimer reaction is a complication that can follow treatment of several infectious diseases. Its most severe form is in louse-borne relapsing fever; in this syndrome the reaction can cause death. Information from studies in Ethiopia during the past eight years is presented, and clinical, physiological, pathological, and immunological features of the reaction are described. Possible causative mechanisms of the reaction are discussed, especially in relation to the role of endotoxin, and an attempt is made to consider this reaction in relation to other endotoxin-associated states.

Adult↗

PubMed2001

Testicular damage by microcirculatory disruption and colonization of an immune-privileged site during Borrelia crocidurae infection.

The agent of African relapsing fever, Borrelia crocidurae, causes reversible multiple organ damage. We hypothesize that this damage is caused when the spirochete forms aggregate with erythrocytes in vivo, creating rosettes that plug the microcirculatory system. To test this hypothesis, we compared testicular microcirculation over an extended time period in two groups of rats: one experimentally inoculated with B. crocidurae, the other with the nonerythrocyte rosette-forming Borrelia hermsii. In the B. crocidurae group, erythrocyte rosettes formed during spiro-chetemia blocked precapillary blood vessels and reduced the normal pattern of microcirculatory blood flow. After spirochetemia, erythrocyte rosettes disappeared and flow was normalized. Decreased blood flow and focal vascular damage with increased permeability and interstitial bleeding adjacent to the erythrocyte microemboli induced cell death in seminiferous tubules. Interestingly, we found that B. crocidurae could penetrate the tubules and remain in the testis long after the end of spirochetemia, suggesting that the testis can serve as a reservoir for this bacteria in subsequent relapses. The group infected with B. hermsii displayed normal testicular blood flow and vasomotion at all selected time points, and suffered no testicular damage. These results confirmed our hypothesis that the erythrocyte rosettes produce vascular obstruction and are the main cause of histopathology seen in model animal and human infections.

Animals↗

PubMed1994

Predictive value of serology in diagnosing Lyme borreliosis.

AIMS: To compare the predictive value of immunoblotting and enzyme linked immunosorbent assay (ELISA) in diagnosing Lyme borreliosis. METHODS: An ELISA using a whole cell sonicate of the B31 strain of Borrelia burgdorferi was used to screen samples submitted for Lyme borreliosis serology. A total of 1222 serum samples reactive in the ELISA were tested by immunoblotting also using the B31 strain. Patients with other spirochaetal diseases were tested by both methods to assess specificity, while those with erythema migrans were used to evaluate sensitivity. Subjects with different clinical conditions, which may have been associated with Lyme borreliosis, were tested using both techniques. RESULTS: Only 16.3% of serum samples from patients submitted for Lyme borreliosis serology which were reactive by ELISA were confirmed as positive by immunoblotting. This is unlikely to represent a sensitivity problem as 51% of samples from 53 patients with erythema migrans were detected by immunoblotting compared with only 28% by ELISA. Patients whose samples were negative by ELISA were also negative by immunoblotting. Serum samples from patients with relapsing fever were reactive in both ELISA and by immunoblotting, but for other test groups immunoblotting offered increased specificity. CONCLUSIONS: Not all ELISA results could be confirmed by immunoblotting. Yet immunoblotting was both more sensitive and specific than ELISA techniques. As a result of these observations all ELISA results should be serologically confirmed by immunoblotting. Though immunoblotting is not suited to large scale screening of samples, it can be used satisfactorily in conjunction with ELISA methods to improve the predictive value of serological tests for Lyme borreliosis.

Cross Reactions↗

PubMed1980

Phagocytosis of Borrelia recurrentis by blood polymorphonuclear leukocytes is enhanced by antibiotic treatment.

The removal of Borrelia spirochetes from the blood in relapsing fever was studied by examining patients' blood phagocytic cells with the Dieterle silver stain. Polymorphonuclear leukocytes ingested Borrelia at increased rates for several hours after antibiotic treatment, during which time the total numbers of circulating plasma spirochetes were decreasing. Incubation of infected blood at 37 degrees C for 2 h resulted in a progressive increase in phagocytosis. Addition of penicillin G and tetracycline to infected blood caused a further enhancement of phagocytosis. Electron microscopy of polymorphonuclear leukocytes revealed spirochetes in phagosomes. These results indicated that blood polymorphonuclear leukocytes have a prominent role in removing Borrelia from the plasma and suggested that antibiotics act by altering the surface of spirochetes to render them more susceptible to phagocytosis.

Adult↗

PubMed1983

Detection of Borrelia in acridine orange-stained blood smears by fluorescence microscopy.

Tick-borne borreliosis (relapsing fever) can be an important, unsuspected cause of febrile illness. The diagnosis is generally made by identifying Borrelia spirochetes in stained peripheral blood smears. Since Borrelia may be difficult to detect with Romanowsky stains, an alternative method, using acridine orange (AO), was used to screen blood smears. Duplicate blood smears of seven patients were examined with the AO technique and Romanowsky stains. In all seven cases spirochetes were easily identified with the AO-stained smears compared with only five cases with Romanowsky stains. In a double-blind laboratory experiment, six of ten duplicate smears from a single patient with mild spirochetemia were positive by AO, whereas only two of ten were positive by Romanowsky stain. We concluded that the AO stain is simple, rapid and more sensitive than Romanowsky methods for detecting cases of low-level spirochetemia.

Acridine Orange↗

PubMed2000

Structural characterization of the inflammatory moiety of a variable major lipoprotein of Borrelia recurrentis.

Louse-borne relapsing fever, caused by Borrelia recurrentis, provides one of the best documented examples of the causative role of tumor necrosis factor (TNF) in the pathology of severe infection in humans. We have identified the principal TNF-inducing factor of B. recurrentis as a variable major lipoprotein (Vmp). Here we report the complete gene sequence of Vmp, including its lipoprotein leader sequence. Using metabolically labeled forms of the native Vmp we confirm that the TNF inducing properties are associated with the lipid portion of the molecule. Quadrupole orthogonal time of flight mass spectrometry unequivocally locates the lipidic moiety at the NH(2)-terminal cysteine of the native polypeptide, and indicates the existence of three forms which are consistent with the structures C16:0, C16:0, C16:0 glyceryl cysteine; C18:1, C16:0, C16:0 glyceryl cysteine; and C18:0, C16:0, C16:0 glyceryl cysteine. These data provide the first direct evidence that the TNF inducing lipid modification of native Borrelia lipoproteins is a structural homologue of the murein lipoprotein of Escherichia coli.

Antigens, Surface↗

PubMed2000

Vector-host interactions in disease transmission.

Tick-borne spirochetes include borreliae that cause Lyme disease and relapsing fever in humans. They survive in a triangle of parasitic interactions between the spirochete and its vertebrate host, the spirochete and its tick vector, and the host and the tick. Until recently, the significance of vector-host interactions in the transmission of arthropod-borne disease agents has been overlooked. However, there is now compelling evidence that the pharmacological activity of tick saliva can have a profound effect on pathogen transmission both from infected tick to uninfected host, and from infected host to uninfected tick. The salivary glands of ticks provide a pharmacopoeia of anti-inflammatory, anti-haemostatic and anti-immune molecules. These include bioactive proteins that control histamine, bind immunoglobulins, and inhibit the alternative complement cascade. The effect of these molecules is to provide a privileged site at the tick-host interface in which borreliae and other tick-borne pathogens are sheltered from the normal innate and acquired host immune mechanisms that combat infections. Understanding the key events at the tick vector-host interface, that promote spirochete infection and transmission, will provide a better understanding of the epidemiology and ecology of these important human pathogens.

Animals↗

PubMed1996

A glyceraldehyde-3-phosphate dehydrogenase homolog in Borrelia burgdorferi and Borrelia hermsii.

A polyreactive monoclonal antibody recognized a 38.5-kDa polypeptide with amino-terminal sequence identity to conserved regions of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) in Borrelia burgdorferi, the Lyme disease agent, and Borrelia hermsii, an agent of American relapsing fever. This monoclonal antibody also recognized GAPDH from other pathogenic spirochetes and other prokaryotes and eukaryotes as well. GAPDH activity was detected in sonicates of both B. burgdorferi and B. hermsii but not in live, intact organisms, indicating the possibility of a subsurface localization for the Borrelia GAPDH activity. Degenerate primers constructed from highly conserved regions of gapdh of other prokaryotes successfully amplified this gene homolog in both B. burgdorferi and B. hermsii. Nuclei acid and deduced amino acid sequence analysis of the 838-bp probes for each borrelia indicated 93.9% identity between B. burgdorferi and B. hermsii at the amino acid level. Amino acid identities of B. burgdorferi and B. hermsii with Bacillus stearothermophilus were 59.2% and 58.8% respectively. Southern hybridization studies indicated that the gene encoding GAPDH is located on the chromosome of each borrella. In other bacterial species, GAPDH has other functions in addition to its traditional enzymatic role in the glycolytic pathway. GAPDH may play a similar role in borrelias.

Amino Acid Sequence↗

PubMed1996

In vivo activities of ceftriaxone and vancomycin against Borrelia spp. in the mouse brain and other sites.

Borrelia burgdorferi, the agent of Lyme disease, and B. turicatae, a neurotropic agent of relapsing fever, are susceptible to vancomycin in vitro, with an MIC of 0.5 microgram/ml. To determine the activity of vancomycin in vivo, particularly in the brain, we infected adult immunocompetent BALB/c and immunodeficient CB-17 scid mice with B. burgdorferi or B. turicatae. The mice were then treated with vancomycin, ceftriaxone as a positive control, or normal saline as a negative control. The effectiveness of treatment was assessed by cultures of blood and brain and other tissues. Ceftriaxone at a dose of 25 mg/kg of body weight administered every 12 h for 7 to 10 days eliminated cultivable B. burgdorferi or B. turicatae from all BALB/c or scid mice in the study. Vancomycin at 30 mg/kg administered every 12 h was effective in eliminating infection from immunodeficient mice if treatment was started within 3 days of the onset of infection. If treatment with vancomycin was delayed for 7 days or more, vancomycin failed to eradicate infection with B. burgdorferi or B. turicatae from immunodeficient mice. The failure of vancomycin in eradicating established infections in immunodeficient mice was associated with the persistence of viable spirochetes in the brain during antibiotic treatment.

Animals↗

PubMed1982

Interaction of Borrelia spirochetes with human mononuclear leukocytes causes production of leukocytic pyrogen and thromboplastin.

Relapsing fever caused by Borrelia spirochetes is characterized by episodes of spirochetemia, fever, and DIC. We examined the ability of Borrelia hermsii to induce production of leukocytic pyrogen and thromboplastin from human blood leukocytes in vitro. Organisms were found devoid of endotoxin by the Limulus assay. Human peripheral blood leukocytes were separated into MNC and PMN fractions and were incubated with two to five spirochetes per cell in 10% human serum. Supernatant fluids from MNC-spirochete mixtures produced mean increases in the temperature of rabbits of 0.80 degree to 1.35 degrees C, which were significantly higher than those caused by supernatant fluids of MNC or spirochetes alone (p less than 0.05). MNC-spirochete mixtures possessed seven to 15 times the thromboplastic activity of MNC suspensions alone, assayed with a modified one-stage prothrombin time. Supernatant fluids of PMNs and spirochetes, on the other hand, did not contain leukocytic pyrogen, and PMN suspensions did not produce thromboplastin. Cycloheximide (10 micrograms/ml), and inhibitor of protein synthesis, completely suppressed both pyrogen and thromboplastin production. Although intracellular spirochetes were observed within phagosomes of blood monocytes by electron microscopy, the production of leukocytic pyrogen and thromboplastin was not significantly altered by serum opsonins or by the inhibitors of phagocytosis cytochalasin B (5 micrograms/ml) or phenylbutazone (2 mg/ml). These results showed that Borrelia spirochetes stimulated human MNCs to produce increased amounts of leukocytic pyrogen and thromboplastin and that this stimulation required de novo synthesis of protein, was not mediated by endotoxin, and was not prevented by omitting opsonic proteins or by inhibiting phagocytosis.

Borrelia↗

PubMed2006

The mammalian host response to borrelia infection.

Tick-borne relapsing fever (RF) and Lyme disease (LD) are spirochetal infections of humans caused by different Borrelia species in endemic areas throughout the world. Our laboratory is studying the response of mammalian hosts to borrelia infection in RF and LD. For this, we use mice and non-human primates infected with B. burgdorferi sensu stricto strain N40 (N40) and the Oz1 strain of Borrelia turicatae (Bt), agents of LD and RF in North America, respectively. Our results have revealed that outbred non-human primates are significantly less susceptible than outbred mice to persistent infection with N40. In contrast, the majority of mice inoculated with the RF agent B. turicatae clear the infection, with the notable exception of residual brain or blood infection in up to 25% of cases. Little if any tissue injury occurs in immunocompetent animals with either LD or RF. In contrast, impairment of specific antibody production results in significant tissue injury, most notably in the heart, in both LD and RF. The inflammatory infiltrate is rich in plasma cells, activated macrophages and T cells, and there is significant deposition of antibody and complement, including membrane attack complex, in inflamed tissues and spirochetes. Significant loss of cardiomyocytes with apoptosis and caspase activation was observed in the heart of immunosuppressed non-human primates infected with N40 and in B cell-deficient mice infected with B. turicatae. Unlike the heart, the brain of B cell-deficient mice infected with B. turicatae showed prominent microglial activation but no detectable tissue injury. Tissues from immunosuppressed non-human primates infected with N40 produce large amounts of immunoglobulin and the B cell chemokine CXCL13, both of which significantly correlate with the spirochetal load. We conclude that the main response of mammalian hosts in LD and RF is the production of specific antibody to clear the infection. Failure of this response leads to persistent infection, which can lead to tissue injury, most notably in the heart.

Animals↗