Vector interactions and molecular adaptations of lyme disease and relapsing fever spirochetes associated with transmission by ticks. (1/47)

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.  (+info)

Savignygrin, a platelet aggregation inhibitor from the soft tick Ornithodoros savignyi, presents the RGD integrin recognition motif on the Kunitz-BPTI fold. (2/47)

Savignygrin, a platelet aggregation inhibitor that possesses the RGD integrin recognition motif, has been purified from the soft tick Ornithodoros savignyi. Two isoforms with similar biological activities differ because of R52G and N60G in their amino acid sequences, indicating a recent gene duplication event. Platelet aggregation induced by ADP (IC50, 130 nm), collagen, the thrombin receptor-activating peptide, and epinephrine was inhibited, although platelets were activated and underwent a shape change. The binding of alpha-CD41 (P2) to platelets, the binding of purified alpha(IIb)beta3 to fibrinogen, and the adhesion of platelets to fibrinogen was inhibited, indicating a targeting of the fibrinogen receptor. In contrast, the adhesion of osteosarcoma cells that express the integrin alpha(v)beta3 to vitronectin or fibrinogen was not inhibited, indicating the specificity of savignygrin toward alpha(IIb)beta3. Savignygrin shows sequence identity to disagregin, a platelet aggregation inhibitor from the tick Ornithodoros moubata that lacks an RGD motif. The cysteine arrangement of savignygrin is similar to that of the bovine pancreatic trypsin inhibitor family of serine protease inhibitors. A homology model based on the structure of the tick anticoagulant peptide indicates that the RGD motif is presented on the substrate-binding loop of the canonical BPTI inhibitors. However, savignygrin did not inhibit the serine proteases fXa, plasmin, thrombin, or trypsin. This is the first report of a platelet aggregation inhibitor that presents the RGD motif using the Kunitz-BPTI protein fold.  (+info)

Diagnosis of epizootic bovine abortion in Nevada and identification of the vector. (3/47)

In the 43 years since the first description in California, epizootic bovine abortion (EBA) has been considered but not definitively diagnosed as a cause of late-term abortions on Nevada ranches. Examination of aborted full-term bovine fetuses obtained from Nevada ranches revealed gross abnormalities consistent with EBA (enlarged lymph nodes, petechial hemorrhages of the oral mucosa and conjunctiva, ascites, and splenohepatomegaly), and EBA was confirmed by histologic examination of fetal tissues. The histologic thymic changes were characteristic of EBA and included severe histocytic thymusitis with depletion of thymocytes, interlobular hemorrhage, and fibrinocellular exudation. The gross enlargement of lymph nodes was the result of cortical follicular hyperplasia and histiocytic lymphadenitis. In addition, widespread, predominately nonsuppurative histologic lesions typical of EBA were observed in most organs, including the brain, lung, heart, liver, and spleen. Furthermore, the presence of Ornithodorus coriaceus, the argasid tick vector of EBA, was established by tick collection using CO2 traps. The tick was identified on ranches and in geographic areas (northern and northwestern counties of Nevada) coincident with diagnosis of multiple cases of EBA. This study establishes the presence of EBA as a cause of late-term abortion in Nevada. Additionally, identification of the EBA tick vector, O. coriaceus, in the same areas as the abortions provides strong evidence that the disease is endemic.  (+info)

The epidemiology of tick-borne relapsing fever in the United States. (4/47)

Each year, many residents of and visitors to endemic regions of the western United States are exposed to the vector of tick-borne relapsing fever (TBRF), an underrecognized and underreported disease. Through review of report forms and literature review, we identified 450 cases of TBRF acquired in the United States in 11 western states (and in British Columbia by a U.S. resident) from January 1977 to January 2000. Exposure sites were in forested areas, at varying elevations, in mountainous regions (Cascade, Rocky Mountain, San Bernardino, and Sierra Nevada ranges) of the United States and Canada and in limestone caves in central Texas. Only 13 counties accounted for approximately 50% of all cases. Forty percent of the cases were not residents of the state where TBRF exposure occurred, including 7% from 11 states where TBRF is not endemic. TBRF is endemic in the United States and is a disease affecting travelers, who may return home with the disease to areas where physicians are not familiar with it.  (+info)

The major tick salivary gland proteins and toxins from the soft tick, Ornithodoros savignyi, are part of the tick Lipocalin family: implications for the origins of tick toxicoses. (5/47)

The origins of tick toxicoses remain a subject of controversy because no molecular data are yet available to study the evolution of tick-derived toxins. In this study we describe the molecular structure of toxins from the soft tick, Ornithodoros savignyi. The tick salivary gland proteins (TSGPs) are four highly abundant proteins proposed to play a role in salivary gland granule biogenesis of the soft tick O. savignyi, of which the toxins TSGP2 and TSGP4 are a part. They were assigned to the lipocalin family based on sequence similarity to known tick lipocalins. Several other tick lipocalins were also identified using Smith-Waterman database searches, bringing the tick lipocalin family up to 20. Phylogenetic analysis showed that most tick lipocalins group within genus-specific clades, suggesting that gene duplication and divergence of tick lipocalin function occurred after tick speciation, most probably during the evolution of a hematophagous lifestyle. TSGP2 and TSGP3 show high sequence identity and group terminal to moubatin, an inhibitor of collagen-induced platelet aggregation from the tick, O. moubata. However, no platelet aggregation inhibitory activity is associated with the TSGPs using ADP or collagen as agonists, suggesting that TSGP2 and TSGP3 duplicated after divergence of O. savignyi and O. moubata. This timing is supported by the absence of TSGP2-4 in the salivary gland extracts of O. moubata. The absence of TSGP2 and TSGP4 in salivary gland extracts from O. moubata correlates with the nontoxicity of this tick species. The implications of this study are that the various forms of tick toxicoses do not have a common origin, but must have evolved independently in those tick species that cause pathogenesis.  (+info)

Tickborne relapsing fever outbreak after a family gathering--New Mexico, August 2002. (6/47)

On August 2, 2002, the New Mexico Department of Health (NMDOH) and the Indian Health Service (IHS) were notified of a tickborne relapsing fever (TBRF) outbreak after a 1-day family gathering held in late July at a remote, previously uninhabited cabin located in a mountainous region of northern New Mexico (elevation: approximately 8,000 feet). Approximately 40 persons attended the event; at least half slept overnight in the cabin. This report summarizes the investigation of this outbreak, which indicates that prompt diagnosis and collaboration among clinicians and public health authorities can reduce morbidity associated with TBRF. Persons living in areas where TBRF is endemic should avoid sleeping in rodent-infested buildings, rodent-proof susceptible buildings, and consider fumigation of buildings that harbor rodents.  (+info)

Tick-borne relapsing fever caused by Borrelia hermsii, Montana. (7/47)

Five persons contracted tick-borne relapsing fever after staying in a cabin in western Montana. Borrelia hermsii was isolated from the blood of two patients, and Ornithodoros hermsi ticks were collected from the cabin, the first demonstration of this bacterium and tick in Montana. Relapsing fever should be considered when patients who reside or have vacationed in western Montana exhibit a recurring febrile illness.  (+info)

African swine fever virus multigene family 360 genes affect virus replication and generalization of infection in Ornithodoros porcinus ticks. (8/47)

Recently, we reported that African swine fever virus (ASFV) multigene family (MGF) 360 and 530 genes are significant swine macrophage host range determinants that function by promoting infected-cell survival. To examine the function of these genes in ASFV's arthropod host, Ornithodoros porcinus porcinus, an MGF360/530 gene deletion mutant (Pr4Delta35) was constructed from an ASFV isolate of tick origin, Pr4. Pr4Delta35 exhibited a significant growth defect in ticks. The deletion of six MGF360 and two MGF530 genes from Pr4 markedly reduced viral replication in infected ticks 100- to 1,000-fold. To define the minimal set of MGF360/530 genes required for tick host range, additional gene deletion mutants lacking individual or multiple MGF genes were constructed. The deletion mutant Pr4Delta3-C2, which lacked three MGF360 genes (3HL, 3Il, and 3LL), exhibited reduced viral growth in ticks. Pr4Delta3-C2 virus titers in ticks were significantly reduced 100- to 1,000-fold compared to control values at various times postinfection. In contrast to the parental virus, with which high levels of virus replication were observed in the tissues of infected adults, Pr4Delta3-C2 replication was not detected in the midgut, hemolymph, salivary gland, coxal gland, or reproductive organs at 15 weeks postinfection. These data indicate that ASFV MGF360 genes are significant tick host range determinants and that they are required for efficient virus replication and generalization of infection. The impaired virus replication of Pr4Delta3-C2 in the tick midgut likely accounts for the absence of the generalized infection that is necessary for the natural transmission of virus from ticks to pigs.  (+info)