Ornithodoros hermsi Wheeler as a Vector of Relapsing Fever in California

1936 ◽  
Vol 22 (3) ◽  
pp. 276 ◽  
Author(s):  
W. B. Herms ◽  
C. M. Wheeler
1999 ◽  
Vol 5 (S2) ◽  
pp. 1220-1221
Author(s):  
Elizabeth R. Fischer ◽  
Tom G. Schwan

Relapsing fever, a disease characterized by recurrent episodes of high fevers, is caused by geographically distinct spirochetes of the genus Borrelia,transmitted by ticks of the genus Ornithodoros. In the Northwestern United States, the soft tick Ornithodoros hermsi has been identified as the vector for the spirochete Borrelia hermsii. The life cycle of O.hermsi includes larval and multiple nymphal stages prior to full maturation into an adult male or female (Fig.1). Progression into each stage requires a blood-meal typically provided by squirrels and chipmunks, and incidentally humans. Feeding is rapid, lasting 10-60 minutes, and during this time an infected tick can transmit the agent of relapsing fever, B. hermsii. Following ingestion, spirochetes are initially found in the tick midgut. Within 1-3 weeks, they are found in other organs, including the central ganglion and salivary glands. Since saliva is the primary mode of transmission of these bacteria during tick feeding, we assessed by electron microscopy the structural and functional relationships between the spirochetes and the salivary glands.


2011 ◽  
Vol 77 (24) ◽  
pp. 8494-8499 ◽  
Author(s):  
Paul F. Policastro ◽  
Sandra J. Raffel ◽  
Tom G. Schwan

ABSTRACTThe soft tickOrnithodoros hermsi, which ranges in specific arboreal zones of western North America, acts as a vector for the relapsing fever spirocheteBorrelia hermsii. Two genomic groups (genomic group I [GGI] and GGII) ofB. hermsiiare differentiated by multilocus sequence typing yet are codistributed in much of the vector's range. To test whether the tick vector can be infected via immersion, noninfected, colony-derivedO. hermsilarvae were exposed to reduced-humidity conditions before immersion in culture suspensions of several GGI and GGII isolates. We tested for spirochetes in ticks by immunofluorescence microscopy and in mouse blood by quantitative PCR of thevtplocus to differentiate spirochete genotypes. The immersed larval ticks were capable of spirochete transmission to mice at the first nymphal feeding. Tick infection with mixed cultures of isolates DAH (vtp-6) (GGI) and MTW-2 (vtp-5) (GGII) resulted in ticks that caused spirochetemias in mice consisting of MTW-2 or both DAH and MTW-2. These findings show that this soft tick species can acquireB. hermsiiby immersion in spirochete suspensions, that GGI and GGII isolates can coinfect the tick vector by this method, and that these spirochetes can be cotransmitted to a rodent host.


Author(s):  
Tom G Schwan

Abstract The relapsing fever spirochetes Borrelia hermsii and Borrelia turicatae are each maintained and transmitted in nature by their specific tick vectors, Ornithodoros hermsi Wheeler (Acari: Argasidae) and Ornithodoros turicata (Duges), respectively. The basis for this spirochete and vector specificity is not known, but persistent colonization of spirochetes in the tick’s salivary glands is presumed to be essential for transmission by these long-lived ticks that feed in only minutes on their warm-blooded hosts. To examine this hypothesis further, cohorts of O. hermsi and O. turicata were infected with B. hermsii and examined 7–260 d later for infection in their midgut, salivary glands, and synganglion. While the midgut from all ticks of both species at all time points examined were infected with spirochetes, the salivary glands of only O. hermsi remained persistently infected. The salivary glands of O. turicata were susceptible to an early transient infection. However, no spirochetes were observed in these tissues beyond the first 32 d after acquisition. Ticks of both species were fed on mice 112 d after they acquired spirochetes and only those mice fed upon by O. hermsi became infected. Thus, the vector competency for B. hermsii displayed by O. hermsi but not O. turicata lies, in part, in the persistent infection of the salivary glands of the former but not the latter species of tick. The genetic and biochemical mechanisms supporting this spirochete and vector specificity remain to be identified.


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