Plague Transmission from Corpses and Carcasses.
Ontology highlight
ABSTRACT:
SUBMITTER: Jullien S
PROVIDER: S-EPMC8314843 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:During a pneumonic plague outbreak in Moramanga, Madagascar, we identified 4 confirmed, 1 presumptive, and 9 suspected plague case-patients. Human-to-human transmission among close contacts was high (reproductive number 1.44) and the case fatality rate was 71%. Phylogenetic analysis showed that the Yersinia pestis isolates belonged to group q3, different from the previous outbreak.
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Project description:The Justinianic Plague, the first part of the earliest of the three plague pandemics, has minimal historical documentation. Based on the limited primary sources, historians have argued both for and against the "maximalist narrative" of plague, i.e. that the Justinianic Plague had universally devastating effects throughout the Mediterranean region during the sixth century CE. Using primary sources of one of the pandemic's best documented outbreaks that took place in Constantinople during 542 CE, as well as modern findings on plague etiology and epidemiology, we developed a series of dynamic, compartmental models of disease to explore which, if any, transmission routes of plague are feasible. Using expected parameter values, we find that the bubonic and bubonic-pneumonic transmission routes exceed maximalist mortality estimates and are of shorter detectable duration than described by the primary sources. When accounting for parameter uncertainty, several of the bubonic plague model configurations yielded interquartile estimates consistent with the upper end of maximalist estimates of mortality; however, these models had shorter detectable outbreaks than suggested by the primary sources. The pneumonic transmission routes suggest that by itself, pneumonic plague would not cause significant mortality in the city. However, our global sensitivity analysis shows that predicted disease dynamics vary widely for all hypothesized transmission routes, suggesting that regardless of its effects in Constantinople, the Justinianic Plague would have likely had differential effects across urban areas around the Mediterranean. Our work highlights the uncertainty surrounding the details in the primary sources on the Justinianic Plague and calls into question the likelihood that the Justinianic Plague affected all localities in the same way.
| S-EPMC7192389 | biostudies-literature
Project description:Numerous historical works have mentioned that trade routes were to blame for the spread of plague in European history, yet this relationship has never been tested by quantitative evidence. Here, we resolve the hypothetical role of trade routes through statistical analysis on the geo-referenced major trade routes in the early modern period and the 6,656 geo-referenced plague outbreak records in AD1347-1760. Ordinary Least Square (OLS) estimation results show that major trade routes played a dominant role in spreading plague in pre-industrial Europe. Furthermore, the negative correlation between plague outbreaks and their distance from major trade ports indicates the absence of a permanent plague focus in the inland areas of Europe. Major trade routes decided the major plague outbreak hotspots, while navigable rivers determined the geographic pattern of sporadic plague cases. A case study in Germany indicates that plague penetrated further into Europe through the local trade route network. Based on our findings, we propose the mechanism of plague transmission in historical Europe, which is imperative in demonstrating how pandemics were spread in recent human history.
| S-EPMC5636801 | biostudies-literature
Project description:The ability of the agent of plague, Yersinia pestis, to form a biofilm blocking the gut of the flea has been considered to be a key evolutionary step in maintaining flea-borne transmission. However, blockage decreases dramatically the life expectancy of fleas, challenging the adaptive nature of blockage. Here, we develop an epidemiological model of plague that accounts for its different transmission routes, as well as the within-host competition taking place between bacteria within the flea vector. We use this theoretical framework to identify the environmental conditions promoting the evolution of blockage. We also show that blockage is favored at the onset of an epidemic, and that the frequencies of bacterial strains exhibiting different strategies of blockage can fluctuate in seasonal environments. This analysis quantifies the contribution of different transmission routes in plague and makes testable predictions on the adaptive nature of blockage.
| S-EPMC6541909 | biostudies-literature
Project description:Yersinia pestis, the bacterial agent of plague, is enzootic in many parts of the world within wild rodent populations and is transmitted by different flea vectors. The ecology of plague is complex, with rodent hosts exhibiting varying susceptibilities to overt disease and their fleas exhibiting varying levels of vector competence. A long-standing question in plague ecology concerns the conditions that lead to occasional epizootics among susceptible rodents. Many factors are involved, but a major one is the transmission efficiency of the flea vector. In this study, using Oropsylla montana (a ground squirrel flea that is a major plague vector in the western United States), we comparatively quantified the efficiency of the two basic modes of flea-borne transmission. Transmission efficiency by the early-phase mechanism was strongly affected by the host blood source. Subsequent biofilm-dependent transmission by blocked fleas was less influenced by host blood and was more efficient. Mathematical modeling predicted that early-phase transmission could drive an epizootic only among highly susceptible rodents with certain blood characteristics, but that transmission by blocked O. montana could do so in more resistant hosts irrespective of their blood characteristics. The models further suggested that for most wild rodents, exposure to sublethal doses of Y. pestis transmitted during the early phase may restrain rapid epizootic spread by increasing the number of immune, resistant individuals in the population.
| S-EPMC9754260 | biostudies-literature
Project description:We lack a clear understanding of the enzootic maintenance of the bacterium (Yersinia pestis) that causes plague and the sporadic epizootics that occur in its natural rodent hosts. A key to elucidating these epidemiological dynamics is determining the dominant transmission routes of plague. Plague can be acquired from the bites of infectious fleas (which is generally considered to occur via a blocked flea vector), inhalation of infectious respiratory droplets, or contact with a short-term infectious reservoir. We present results from a plague modeling approach that includes transmission from all three sources of infection simultaneously and uses sensitivity analysis to determine their relative importance. Our model is completely parameterized by using data from the literature and our own field studies of plague in the black-tailed prairie dog (Cynomys ludovicianus). Results of the model are qualitatively and quantitatively consistent with independent data from our field sites. Although infectious fleas might be an important source of infection and transmission via blocked fleas is a dominant paradigm in the literature, our model clearly predicts that this form of transmission cannot drive epizootics in prairie dogs. Rather, a short-term reservoir is required for epizootic dynamics. Several short-term reservoirs have the potential to affect the prairie dog system. Our model predictions of the residence time of the short-term reservoir suggest that other small mammals, infectious prairie dog carcasses, fleas that transmit plague without blockage of the digestive tract, or some combination of these three are the most likely of the candidate infectious reservoirs.
| S-EPMC1434514 | biostudies-literature
Project description:BackgroundAlthough the linkage between climate change and plague transmission has been proposed in previous studies, the dominant approach has been to address the linkage with traditional statistical methods, while the possible non-linearity, non-stationarity and low frequency domain of the linkage has not been fully considered. We seek to address the above issue by investigating plague transmission in pre-industrial Europe (AD1347-1760) at both continental and country levels.MethodsWe apply Granger Causality Analysis to identify the casual relationship between climatic variables and plague outbreaks. We then apply Wavelet Analysis to explore the non-linear and non-stationary association between climate change and plague outbreaks.ResultsOur results show that 5-year lagged temperature and aridity index are the significant determinants of plague outbreaks in pre-industrial Europe. At the multi-decadal time scale, there are more frequent plague outbreaks in a cold and arid climate. The synergy of temperature and aridity index, rather than their individual effect, is more imperative in driving plague outbreaks, which is valid at both the continental and country levels.ConclusionsPlague outbreaks come after cold and dry spells. The multi-decadal climate variability is imperative in driving the cycles of plague outbreaks in pre-industrial Europe. The lagged and multi-decadal effect of climate change on plague outbreaks may be attributable to the complexity of ecological, social, or climate systems, through which climate exerts its influence on plague dynamics. These findings may contribute to improve our understanding of the epidemiology of plague and other rodent-borne or flea-borne infectious diseases in human history.
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Project description:It is important for the poultry industry to maximize product safety and quality by understanding the connection between bacterial diversity on chicken carcasses throughout poultry processing to the end of shelf life and the impact of the local processing environment. Enumeration of total aerobic bacteria, Campylobacter and Pseudomonas, and 16S rRNA gene amplicon sequencing were used to evaluate the processing line by collecting 10 carcasses from five processing steps: prescald, postplucker, pre- and post-immersion chill, and post-air chill. The diversity throughout a 12-day shelf life was also determined by examining 30 packaged carcasses. To identify the sources of possible contamination, scald water tank, immersion chilling water tank, air samples, and wall surfaces in the air-chill room were analyzed. Despite bacterial reductions on carcasses (>5 log10 CFU/ml) throughout the process, each step altered the bacterial diversity. Campylobacter was a minor but persistent component in the bacterial community on carcasses. The combination of scalding, defeathering, and plucking distributed thermophilic spore-forming Anoxybacillus to carcasses, which remained at a high abundance on carcasses throughout subsequent processes. Pseudomonas was not isolated from carcasses after air chilling but was abundant on the wall of the air-chill room and became the predominant taxon at the end of shelf life, suggesting possible contamination through air movement. The results suggest that attention is needed at each processing step, regardless of bacterial reductions on carcasses. Changing scalding water regularly, maintaining good hygiene practices during processing, and thorough disinfection at the end of each processing day are important to minimize bacterial transmission.IMPORTANCE Culture-based and culture-independent approaches were utilized to reveal bacterial community changes on chicken carcasses at different processing steps and potential routes from the local processing environment. Current commercial processing effectively reduced bacterial loads on carcasses. Poultry processes have similar processes across facilities, but various processing arrangements and operating parameters could impact the bacterial transmission and persistence on carcasses differently. This study showed the use of a single tunnel incorporating scalding, defeathering and plucking may undesirably distribute the thermoduric bacteria, e.g., Campylobacter and Anoxybacillus, between the local environment and carcasses, whereas this does not occur when these steps are separated. The length of immersion and air chilling also impacted bacterial diversity on carcasses. Air chilling can transfer Pseudomonas from wall surfaces onto carcasses; this may subsequently influence chicken product shelf life. This study helps poultry processors understand the impact of current commercial processing and improve the chicken product quality and safety.
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Project description:OBJECTIVES:In Madagascar, plague (Yersinia pestis infection) is endemic in the central highlands, maintained by the couple Rattus rattus/flea. The rat is assumed to die shortly after infection inducing migration of the fleas. However we previously reported that black rats from endemic areas can survive the infection whereas those from non-endemic areas remained susceptible. We investigate the hypothesis that lineages of rats can acquire resistance to plague and that previous contacts with the bacteria will affect their survival, allowing maintenance of infected fleas. For this purpose, laboratory-born rats were obtained from wild black rats originating either from plague-endemic or plague-free zones, and were challenged with Y. pestis. Survival rate and antibody immune responses were analyzed. RESULTS:Inoculation of low doses of Y. pestis greatly increase survival of rats to subsequent challenge with a lethal dose. During challenge, cytokine profiles support activation of specific immune response associated with the bacteria control. In addition, F1 rats from endemic areas exhibited higher survival rates than those from non-endemic ones, suggesting a selection of a resistant lineage. In Madagascar, these results support the role of black rat as long term reservoir of infected fleas supporting maintenance of plague transmission.
| S-EPMC6295079 | biostudies-other
Project description:The flea's lumen gut is a poorly documented environment where the agent of flea-borne plague, Yersinia pestis, must replicate to produce a transmissible infection. Here, we report that both the acidic pH and osmolarity of the lumen's contents display simple harmonic oscillations with different periods. Since an acidic pH and osmolarity are two of three known stimuli of the OmpR-EnvZ two-component system in bacteria, we investigated the role and function of this Y. pestis system in fleas. By monitoring the in vivo expression pattern of three OmpR-EnvZ-regulated genes, we concluded that the flea gut environment triggers OmpR-EnvZ. This activation was not, however, correlated with changes in pH and osmolarity but matched the pattern of nutrient depletion (the third known stimulus for OmpR-EnvZ). Lastly, we found that the OmpR-EnvZ and the OmpF porin are needed to produce the biofilm that ultimately obstructs the flea's gut and thus hastens the flea-borne transmission of plague. Taken as a whole, our data suggest that the flea gut is a complex, fluctuating environment in which Y. pestis senses nutrient depletion via OmpR-EnvZ. Once activated, the latter triggers a molecular program (including at least OmpF) that produces the biofilm required for efficient plague transmission.
| S-EPMC6842400 | biostudies-literature