Plague in the Western Part of the United States: Infection in Rodents, Experimental Transmission by Fleas, and Inoculation Tests for Infection

Eskey, C. R.; Haas, Victor H.

doi:10.2307/4582984

Cited by 32 publications

(25 citation statements)

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“…If such a high bacteremia level is required for rodent blood to be infectious for feeding fleas, it is unlikely that the rodent will survive its infection. Other researchers 27,31 believe that fleas are unlikely to become infected by feeding on chronically infected or resistant hosts, or hosts with mild, sub-acute infections. Our findings agree with these hypotheses and seem to contradict later studies that look to the importance of resistant or chronically infected rodent reservoirs, which may have a low level of bacteremia over a long period of time.…”

Section: Preparation Of Y Pestis Cells Expressing Green Fluorescent mentioning

confidence: 99%

Quantitative competitive PCR as a technique for exploring flea-Yersina pestis dynamics.

Engelthaler

Hinnebusch²,

Rittner³

et al. 2000

The American Journal of Tropical Medicine and Hygiene

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Abstract. We used a quantitative competitive polymerase chain reaction assay to quantify Yersinia pestis loads in fleas and bacteremia levels in mice that were used as sources of infectious blood meals for feeding the fleas. Xenopsylla cheopis, the Oriental rat flea, achieved higher infection rates, developed greater bacterial loads, and became infectious more rapidly than Oropsylla montana, a ground squirrel flea. Both flea species required about 10 6 Y. pestis cells per flea to be able to transmit to mice. Most fleas that achieved these levels, however, were incapable of transmitting. Our results suggest that at the time of flea feeding, host blood must contain Ն10 6 bacteria/ml to result in detectable Y. pestis infections in these fleas, and Ն10 7 bacteria/mL to cause infection levels sufficient for both species to eventually become capable of transmitting Y. pestis to uninfected mice. Yersinia pestis colonies primarily developed in the midguts of O. montana, whereas infections in X. cheopis often developed simultaneously in the proventriculus and the midgut. These findings were visually confirmed by infecting fleas with a strain of Y. pestis that had been transformed with the green fluorescent protein gene.

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Section: Preparation Of Y Pestis Cells Expressing Green Fluorescent mentioning

confidence: 99%

Quantitative competitive PCR as a technique for exploring flea-Yersina pestis dynamics.

Engelthaler

Hinnebusch²,

Rittner³

et al. 2000

The American Journal of Tropical Medicine and Hygiene

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“…9,10 Such transmission is most effective for many flea species within the first few days after taking an infectious host blood meal, and later for a smaller number of flea species in which midgut blockage occurs. [9][10][11][12][13][14][15] Plague bacteria also may survive outside living hosts on carcasses or in the soil, but only limited evidence exists to suggest that such mechanisms are important for long-term survival in nature. 9,16,17 Plague likely evolved in Asia, 9,18,19 and has since spread broadly by various means, 18 including the transport of infected hosts and fleas along overland trade routes or aboard rat-infested ships during the three historically documented pandemics.…”

Section: Introductionmentioning

confidence: 99%

Range-wide Determinants of Plague Distribution in North America

Maher

Ellis²,

Gage³

et al. 2010

The American Society of Tropical Medicine and Hygiene

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Abstract. Plague, caused by the bacterium Yersinia pestis , is established across western North America, and yet little is known of what determines the broad-scale dimensions of its overall range. We tested whether its North American distribution represents a composite of individual host-plague associations (the "Host Niche Hypothesis"), or whether mammal hosts become infected only at sites overlapping ecological conditions appropriate for plague transmission and maintenance (the "Plague Niche Hypothesis"). We took advantage of a novel data set summarizing plague records in wild mammals newly digitized from paper-based records at the Centers for Disease Control and Prevention to develop range-wide tests of ecological niche similarity between mammal host niches and plague-infected host niches. Results indicate that plague infections occur under circumstances distinct from the broader ecological distribution of hosts, and that plagueinfected niches are similar among hosts; hence, evidence coincides with the predictions of the Plague Niche Hypothesis, and contrasts with those of the Host Niche Hypothesis. The "plague niche" is likely driven by ecological requirements of vector flea species.

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“…For example, the Rocky Mountain spotted fever can be transmitted by several different tick species, including Dermacentor variabilis and Dermacentor andersoni [20]. The sylvatic plague in prairie dogs can be transmitted by multiple flea species (Oropsylla hirsuta and Oropsylla tuberculata cynomuris) and through multiple manners (by blocked fleas and also through transition immediately following an infected blood meal) [28,77,78]. Let N N), where θ is called the Allee threshold (see [29]).…”

Section: Time T: N I (T) = S I (T) + I I (T) + R I (T)mentioning

confidence: 99%

“…Transmission dynamics are not well understood and plague dynamics among prairie dogs do not directly follow plague dynamics among fleas [76]. 'Blocked' infected fleas (referred to as such due to the formation of biofilm in their gut) were traditionally believed to be the primary transmission route to prairie dogs [28]. However, the specific flea species commonly found on prairie dogs seldom become blocked (1 out of 10 for O. t. cynomuris and 3 out of 70 for O. hirsuta; see [28]).…”

Section: Prairie Dog Modelmentioning

confidence: 99%

“…'Blocked' infected fleas (referred to as such due to the formation of biofilm in their gut) were traditionally believed to be the primary transmission route to prairie dogs [28]. However, the specific flea species commonly found on prairie dogs seldom become blocked (1 out of 10 for O. t. cynomuris and 3 out of 70 for O. hirsuta; see [28]). Another transmission route is through 'unblocked fleas', immediately following a blood meal from an infectious prairie dog [78] …”

Section: Prairie Dog Modelmentioning

confidence: 99%

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A seasonal SIR metapopulation model with an Allee effect with application to controlling plague in prairie dog colonies

Ekanayake¹,

Ekanayake²

2014

Journal of Biological Dynamics

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For wildlife species living among patchy habitats, disease and the Allee effect (reduced per capita birth rates at low population densities) may together drive a patch's population to extinction, particularly if births are seasonal. Yet local extinction may not be indicative of global extinction, and a patch may become recolonized by migrating individuals. We introduce deterministic and stochastic susceptible, infectious, and immune epidemic models with vector species to study disease in a metapopulation with an Allee effect and seasonal birth and dispersal. We obtain conditions for the existence of a strong Allee effect and existence and stability of a disease-free positive periodic solution. These general models have application to many wildlife diseases. As a case study, we apply them to evaluate dynamics of the sylvatic plague in prairie dog colonies interconnected through dispersal. We further evaluate the effects of control of the vector population and control by immunization on plague eradication.

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Plague in the Western Part of the United States: Infection in Rodents, Experimental Transmission by Fleas, and Inoculation Tests for Infection

Cited by 32 publications

References 0 publications

Quantitative competitive PCR as a technique for exploring flea-Yersina pestis dynamics.

Quantitative competitive PCR as a technique for exploring flea-Yersina pestis dynamics.

Range-wide Determinants of Plague Distribution in North America

A seasonal SIR metapopulation model with an Allee effect with application to controlling plague in prairie dog colonies

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