Transmission of
            <i>Anaplasma marginale</i>
            by
            <i>Boophilus microplus</i>
            : Retention of Vector Competence in the Absence of Vector-Pathogen Interaction

Futse, James E.; Ueti, Massaro W.; Knowles, Donald P.; Palmer, Guy H.

doi:10.1128/jcm.41.8.3829-3834.2003

Cited by 110 publications

(71 citation statements)

References 21 publications

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“…In contrast, strain B (yellow circles), encoding a unique variant repertoire, will establish infection in the population as the existing persistently infected animals also represent a susceptible population and transmission results in strain superinfection (green circles). The assumptions of the model regarding infection prevalence within endemic regions, equal quantitative transmissibility of strains, and the resistance to superinfection of genetically similar strains are based on both field and experimental studies of A. marginale transmission (20,21,26).…”

Section: Discussionmentioning

confidence: 99%

“…Calves were infected by tick feeding using 6DE (n ϭ 4), EM⌽ (n ϭ 4), or St. Maries (n ϭ 8) strain-infected Reynolds Creek D. andersoni. The level of A. marginale bacteremia during persistent infection was determined by quantitative real-time PCR assay for the single copy gene msp5 (26). The expression of complex mosaic variants during persistent infection was confirmed by sequencing of the expression site as described (18).…”

Section: Methodsmentioning

confidence: 99%

“…The complexity of the HVR was quantified as described (18) Cohorts of these infected ticks were identically fed on uninfected, naïve calves at the same time to confirm tick transmission of each strain to cattle. For discrimination between the St. Maries and 6DE strains, the msp1␣ sequence was amplified by using previously reported strain-common primers (26). The St. Maries and EM⌽ strains were differentiated by using strain-specific msp1␣ primers (St. Maries, forward 5Ј-CAGCAGAGTATGTGTCCTCC-3Ј and reverse, 5Ј-CATTGGAGCGCATCTCTTGC-3Ј; EM⌽, forward 5Ј-TGTTAGCAGAGTGTGTGT CCG-3Ј and reverse, 5Ј-GCCTGACCGCTTTGAGATGA-3Ј).…”

Section: Methodsmentioning

confidence: 99%

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Superinfection as a driver of genomic diversification in antigenically variant pathogens

Futse

Brayton

Dark

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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A new pathogen strain can penetrate an immune host population only if it can escape immunity generated against the original strain. This model is best understood with influenza viruses, in which genetic drift creates antigenically distinct strains that can spread through host populations despite the presence of immunity against previous strains. Whether this selection model for new strains applies to complex pathogens responsible for endemic persistent infections, such as anaplasmosis, relapsing fever, and sleeping sickness, remains untested. These complex pathogens undergo rapid within-host antigenic variation by using sets of chromosomally encoded variants. Consequently, immunity is developed against a large repertoire of variants, dramatically changing the scope of genetic change needed for a new strain to evade existing immunity and establish coexisting infection, termed strain superinfection. Here, we show that the diversity in the alleles encoding antigenic variants between strains of a highly antigenically variant pathogen was equal to the diversity within strains, reflecting equivalent selection for variants to overcome immunity at the host population level as within an individual host. This diversity among strains resulted in expression of nonoverlapping variants that allowed a new strain to evade immunity and establish superinfection. Furthermore, we demonstrated that a single distinct allele allows strain superinfection. These results indicate that there is strong selective pressure to increase the diversity of the variant repertoire beyond what is needed for persistence within an individual host and provide an explanation, competition at the host population level, for the large genomic commitment to variant gene families in persistent pathogens.antigenic variation ͉ genomic diversity ͉ population immunity

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Superinfection as a driver of genomic diversification in antigenically variant pathogens

Futse

Brayton

Dark

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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“…The small genome size of A. marginale (1.2 Mb) allowed us to use a bacterial artificial chromosome (BAC)-based strategy to obtain the genome sequence without substantial purification of the organism from the host cell. We report here the complete genome sequence of the St. Maries strain of A. marginale, originally isolated from an animal with severe acute anaplasmosis and shown to be efficiently transmitted by both Dermacentor andersoni and Boophilus microplus (8,9). The completion of this sequence and the E. ruminantium sequence (7) allows comparative genomics to identify conserved genes and pathways associated with transmission.…”

mentioning

confidence: 99%

Complete genome sequencing of Anaplasma marginale reveals that the surface is skewed to two superfamilies of outer membrane proteins

Brayton¹,

Kappmeyer²,

Herndon³

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

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248

301

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The rickettsia Anaplasma marginale is the most prevalent tick-borne livestock pathogen worldwide and is a severe constraint to animal health. A. marginale establishes lifelong persistence in infected ruminants and these animals serve as a reservoir for ticks to acquire and transmit the pathogen. Within the mammalian host, A. marginale generates antigenic variants by changing a surface coat composed of numerous proteins. By sequencing and annotating the complete 1,197,687-bp genome of the St. Maries strain of A. marginale, we show that this surface coat is dominated by two families containing immunodominant proteins: the msp2 superfamily and the msp1 superfamily. Of the 949 annotated coding sequences, just 62 are predicted to be outer membrane proteins, and of these, 49 belong to one of these two superfamilies. The genome contains unusual functional pseudogenes that belong to the msp2 superfamily and play an integral role in surface coat antigenic variation, and are thus distinctly different from pseudogenes described as byproducts of reductive evolution in other Rickettsiales.rickettsiales ͉ bacterial artificial chromosome ͉ St. Maries strain

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“…Samples were washed in 1ϫ PBS (pH 7.2), washed in water, and dehydrated in a graded ethanol series (25%, 50%, 75%, 95%, 100%, 100%), infiltrated in HM-20 acrylic resin (Electron Microscopy Sciences), and UV cured at Ϫ10°C for 48 h. Cured resin blocks were trimmed, ultrathin sectioned, and collected on Ni-coated Formvar 400-mesh grids (Electron Microscopy Sciences). Ultrathin sections were immunolabeled at room temperature as follows: grids were treated with 200 mM NH 4 (25). Cells were scraped from a heavily infected 25-cm 2 cell culture flask and passed 20 times through a 20-gauge needle prior to injection.…”

Section: Methodsmentioning

confidence: 99%

Reduced Infectivity in Cattle for an Outer Membrane Protein Mutant of Anaplasma marginale

Crosby

Brayton

Magunda

et al. 2015

Appl Environ Microbiol

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Anaplasma marginale is the causative agent of anaplasmosis in cattle. Transposon mutagenesis of this pathogen using the Himar1 system resulted in the isolation of an omp10 operon insertional mutant referred to as the omp10::himar1 mutant. The work presented here evaluated if this mutant had morphological and/or growth rate defects compared to wild-type A. marginale. Results showed that the morphology, developmental cycle, and growth in tick and mammalian cell cultures are similar for the mutant and the wild type. Tick transmission experiments established that tick infection levels with the mutant were similar to those with wild-type A. marginale and that infected ticks successfully infected cattle. However, this mutant exhibited reduced infectivity and growth in cattle. The possibility of transforming A. marginale by transposon mutagenesis coupled with in vitro and in vivo assessment of altered phenotypes can aid in the identification of genes associated with virulence. The isolation of deliberately attenuated organisms that can be evaluated in their natural biological system is an important advance for the rational design of vaccines against this species.A naplasma marginale is a tick-associated bacterium and the etiologic agent of bovine anaplasmosis, a disease that causes considerable losses to both dairy and beef industries worldwide (1, 2). Although organisms of this species are principally pathogenic to cattle, they are also found in other ruminants, such as water buffalo and deer (3).The transmission cycle of A. marginale has been well documented and indicates that the success of this pathogen depends on its ability to adapt to its invertebrate and vertebrate hosts. In the tick, during its transit from the midgut to the salivary glands, A. marginale has to overcome different tissue barriers and defense mechanisms in order to ensure its transmission to the vertebrate host (4-7). In cattle, A. marginale replicates within mature erythrocytes, producing an acute disease characterized by hemolytic anemia. However, one of the most important features of the biology of these bacteria is the lifelong persistent infection of its ruminant host, achieved by evasion of the immune system using a mechanism of antigenic variation in which different variants of outer membrane proteins Msp2 and Msp3 are expressed. These persistently infected cattle remain a reservoir of A. marginale organisms for continued tick transmission (8-11).The ability of A. marginale to thrive in such diverse environments is mediated by differential gene transcription (12). Hence, the identification and characterization of these genes using recombinant DNA technologies is not only central to understanding the biology and pathogenesis of these organisms but also for the development of drug therapies and vaccines for the control of anaplasmosis. Recently, the use of transposon mutagenesis in the A. marginale Virginia strain to create insertional mutations was demonstrated (13). Delivery of a plasmid containing the Himar1 transposon and the A7 transpo...

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Transmission of Anaplasma marginale by Boophilus microplus : Retention of Vector Competence in the Absence of Vector-Pathogen Interaction

Cited by 110 publications

References 21 publications

Superinfection as a driver of genomic diversification in antigenically variant pathogens

Superinfection as a driver of genomic diversification in antigenically variant pathogens

Complete genome sequencing of Anaplasma marginale reveals that the surface is skewed to two superfamilies of outer membrane proteins

Reduced Infectivity in Cattle for an Outer Membrane Protein Mutant of Anaplasma marginale

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