Sensitivity and specificity of bacterial culture, qPCR, and somatic cell count for detection of goats with Staphylococcus aureus intramammary infection using Bayesian latent class models.

Staphylococcus aureus (S. aureus) is an important udder pathogen affecting goat milk production. The ability to detect goats with subclinical mastitis caused by S. aureus is essential in udder health control programs. In Norway, the industry recommends using somatic cell count (SCC) as a screening tool, and conventional bacterial culture (BC) as a confirmatory test for goat milk samples, but a commercial qPCR, Mastitis 4 qPCR (DNA Diagnostics, Risskov, Denmark) is also available. However, few studies have validated the use of these methods for the detection of goats with S. aureus intramammary infection (IMI). Therefore, the objective of this retrospective study was to estimate the diagnostic sensitivity and specificity of BC, qPCR, and SCC for the detection of goats with IMI caused by S. aureus using Bayesian latent class analysis. We analyzed the BC and qPCR results of aseptically collected milk samples and SCC results from milk recording samples from 319 goats from three herds using different SCC cut-offs. At a SCC cut-off of 2000,000 cells/mL, the estimated median prevalence in each herd was 12.7% (95% highest posterior density credible interval [CI] 6.5-19.8), 15.7% (95% CI 9.3-23.0), and 1.5% (95% CI 0.0-4.3). The median sensitivity was 93.0% (95% CI 80.2-100), 93.6% (95% CI 82.3-100) and 78.2% (95% CI 62.3-91.2) for BC, qPCR, and SCC, respectively. The estimated median specificity of BC was 99.5% (99% CI 98.4-100), for qPCR, 98.9% (95% CI 97.5-100), and for SCC 61.5% (95% CI 56.0-67.1). The results show that BC, which is today's standard method for diagnosing IMI, has a high accuracy for detection of goats with S. aureus IMI, but qPCR had a sensitivity and specificity similar to BC, and may act as an alternative.

Simulated effects of increasing salmonid production on sea lice populations in Norway.

Norway produces more than one million tonnes of salmonids every year, almost exclusively in open-water net pens. In 2014, the Norwegian government announced plans to increase salmonid production. However, increasing the number of farmed salmonids can have negative effects on the marine environment that threaten the industry's sustainability. In particular, production growth can lead to an increase in density-dependent diseases, including parasitic sea lice. The aim of this study was to simulate the effects of increased salmonid production on sea lice abundance using different scenarios for increasing the number of fish and for the management of sea lice. We used a previously developed, partly stage-structured model based on Norwegian production and environmental data to simulate the different scenarios. Our results show that increasing the marine farmed salmonid population at a national level by two or five times the current production leads to an increase in the sea lice abundance by 3.5% and 7.1%, respectively. We also found that by lowering the maximum allowable level of sea lice to an average of 0.049 adult females per fish, weekly treatments can be used to control sea lice population growth with a five times increase in production. However, this increases the number of farms treating per week by as much as 281.3%, which can lead to high costs and increased mortality among farmed salmonids. Overall, the results from our study shed light on the effects of increasing salmonid production in Norway with respect to the ongoing threat of sea lice infestations.

Realtime case study simulations of transmission of Pancreas Disease (PD) in Norwegian salmonid farming for disease control purposes.

Pancreas Disease (PD) is a viral disease caused by Salmonid Alphavirus (SAV). It affects farmed salmonids in the North Atlantic, and leads to reduced feed intake and increased mortality with reduced production and welfare as a consequence. In 2013, the estimated cost of an outbreak on an average salmon farm was about 6.6 mil €. In Norway, PD has been notifiable since 2008, and regulations to mitigate disease spread are in place. However, despite the regulations, 140-170 farms are affected by PD every year. The aquaculture industry is growing continuously, introducing farms in new geographical areas, and fish are moved between hydrographically separated zones for trade and slaughter. All such movements and relocations need to be approved by the competent authorities. Thus, there is a demand for support to farmers and competent authorities when making decisions on disease management and especially on the effect of moving infected fish. We have used a disease-transmission model for outbreak-simulation in real time for assessing the probability of disease transmission from a farm that gets infected with PD. We have also simulated the effects of three different control-regimes: no stamping-out, delayed stamping-out or immediate stamping-out, on the transmission of PD to surrounding farms. Simulations showed that the immediate stamping out of an infected farm led to effective containment of an outbreak. No stamping out led to up to 32.1% of farms within 100 km of the index farm to become effected. We have used real production data for the model building and the scenario simulations, and the results illustrate that a risk assessment of horizontal disease transmission must be undertaken on a case-by-case basis, because the time and place of the outbreak has a large influence on the risk of transmission.

The influence of temperature on the seasonality of historical plague outbreaks.

Modern plague outbreaks exhibit a distinct seasonal pattern. By contrast, the seasonality of historical outbreaks and its drivers has not been studied systematically. Here, we investigate the seasonal pattern, the epidemic peak timing and growth rates, and the association with latitude, temperature, and precipitation using a large, novel dataset of plague- and all-cause mortality during the Second Pandemic in Europe and the Mediterranean. We show that epidemic peak timing followed a latitudinal gradient, with mean annual temperature negatively associated with peak timing. Based on modern temperature data, the predicted epidemic growth of all outbreaks was positive between 11.7°C and 21.5°C with a maximum around 17.3°C. Hence, our study provides evidence that the growth of plague epidemics across the whole study region depended on similar absolute temperature thresholds. Here, we present a systematic analysis of the seasonality of historical plague in the Northern Hemisphere, and we show consistent evidence for a temperature-related process influencing the epidemic peak timing and growth rates of plague epidemics.

Factors associated with baseline mortality in Norwegian Atlantic salmon farming.

In 2019, it was estimated that more than 50 million captive Atlantic salmon in Norway died in the final stage of their production in marine cages. This mortality represents a significant economic loss for producers and a need to improve welfare for farmed salmon. Single adverse events, such as algal blooms or infectious disease outbreaks, can explain mass mortality in salmon cages. However, little is known about the production, health, or environmental factors that contribute to their baseline mortality during the sea phase. Here we conducted a retrospective study including 1627 Atlantic salmon cohorts put to sea in 2014-2019. We found that sea lice treatments were associated with Atlantic salmon mortality. In particular, the trend towards non-medicinal sea lice treatments, including thermal delousing, increases Atlantic salmon mortality in the same month the treatment is applied. There were differences in mortality among production zones. Stocking month and weight were other important factors, with the lowest mortality in smaller salmon stocked in August-October. Sea surface temperature and salinity also influenced Atlantic salmon mortality. Knowledge of what affects baseline mortality in Norwegian aquaculture can be used as part of syndromic surveillance and to inform salmon producers on farming practices that can reduce mortality.

Significant reduction of vancomycin resistant E. faecium in the Norwegian broiler population coincided with measures taken by the broiler industry to reduce antimicrobial resistant bacteria.

Vancomycin resistant enterococci (VRE) belong to the most common causes of nosocomial infections worldwide. It has been reported that use of the glycopeptide growth promoter avoparcin selected for a significant livestock-reservoir of VRE in many European countries, including Norway. However, although avoparcin was banned as a feed-additive in 1995, VRE have for unknown reasons consistently been reported in samples from Norwegian broilers. When avoparcin was banned, broiler-feed was supplemented with the polyether ionophore narasin in order to control the diseases coccidiosis and the frequent sequela necrotic enteritis. A potential link between transferrable vancomycin resistance and reduced susceptibility to narasin was recently reported. The use of narasin as a feed additive was abolished by the Norwegian broiler industry in 2016 and since then, broilers have been reared without in-feed antibacterial supplements. In this study, we demonstrate that all VRE isolates from Norwegian broilers collected in 2006-2014 displayed reduced susceptibility to narasin. Surveillance data collected two years after the narasin abolishment show a significant reduction in VRE, below the detection limit of the surveillance method, and a concurrent marked reduction in Enterococcus faecium with reduced susceptibility to narasin. The significant decline of E. faecium with reduced susceptibility to these antimicrobial compounds also coincided with an increased focus on cleaning and disinfection between broiler flocks. Furthermore, data from a controlled in vivo experiment using Ross 308 broilers indicate that the proportion of E. faecium with reduced susceptibility to narasin was heavily reduced in broilers fed a narasin-free diet compared to a diet supplemented with narasin. Our results are consistent with that the abolishment of this feed additive, possibly in combination with the increased focus on cleaning and disinfection, has had a substantial impact on the occurrence of VRE in the Norwegian broiler population.

Human plague system associated with rodent diversity and other environmental factors.

Plague remains a threat to public health and is considered as a re-emerging infectious disease today. Rodents play an important role as major hosts in plague persistence and driving plague outbreaks in natural foci; however, few studies have tested the association between host diversity in ecosystems and human plague risk. Here we use zero-inflated generalized additive models to examine the association of species richness with human plague presence (where plague outbreaks could occur) and intensity (the average number of annual human cases when they occurred) in China during the Third Pandemic. We also account for transportation network density, annual precipitation levels and human population size. We found rodent species richness, particularly of rodent plague hosts, is positively associated with the presence of human plague. Further investigation shows that species richness of both wild and commensal rodent plague hosts are positively correlated with the presence, but only the latter correlated with the intensity. Our results indicated a positive relationship between rodent diversity and human plague, which may provide suggestions for the plague surveillance system.

Historical and genomic data reveal the influencing factors on global transmission velocity of plague during the Third Pandemic.

Quantitative knowledge about which natural and anthropogenic factors influence the global spread of plague remains sparse. We estimated the worldwide spreading velocity of plague during the Third Pandemic, using more than 200 years of extensive human plague case records and genomic data, and analyzed the association of spatiotemporal environmental factors with spreading velocity. Here, we show that two lineages, 2.MED and 1.ORI3, spread significantly faster than others, possibly reflecting differences among strains in transmission mechanisms and virulence. Plague spread fastest in regions with low population density and high proportion of pasture- or forestland, findings that should be taken into account for effective plague monitoring and control. Temperature exhibited a nonlinear, U-shaped association with spread speed, with a minimum around 20 °C, while precipitation showed a positive association. Our results suggest that global warming may accelerate plague spread in warm, tropical regions and that the projected increased precipitation in the Northern Hemisphere may increase plague spread in relevant regions.

The Third Plague Pandemic in Europe.

Plague has a long history on the European continent, with evidence of the disease dating back to the Stone Age. Plague epidemics in Europe during the First and Second Pandemics, including the Black Death, are infamous for their widespread mortality and lasting social and economic impact. Yet, Europe still experienced plague outbreaks during the Third Pandemic, which began in China and spread globally at the end of the nineteenth century. The digitization of international records of notifiable diseases, including plague, has enabled us to retrace the introductions of the disease to Europe from the earliest reported cases in 1899, to its disappearance in the 1940s. Using supplemental literature, we summarize the potential sources of plague in Europe and the transmission of the disease, including the role of rats. Finally, we discuss the international efforts aimed at prevention and intervention measures, namely improved hygiene and sanitation, that ultimately led to the disappearance of plague in Europe.

Epidemiology of a bubonic plague outbreak in Glasgow, Scotland in 1900.

On 3 August 1900, bubonic plague (Yersinia pestis) broke out in Glasgow for the first time during the Third Pandemic. The local sanitary authorities rigorously tracked the spread of the disease and they found that nearly all of the 35 cases could be linked by contact with a previous case. Despite trapping hundreds of rats in the area, there was no evidence of a rat epizootic and the investigators speculated that the outbreak could be due to human-to-human transmission of bubonic plague. Here we use a likelihood-based method to reconstruct transmission trees for the outbreak. From the description of the outbreak and the reconstructed trees, we infer several epidemiological parameters. We found that the estimated mean serial interval was 7.4-9.2 days and the mean effective reproduction number dropped below 1 after implementation of control measures. We also found a high rate of secondary transmissions within households and observations of transmissions from individuals who were not terminally septicaemic. Our results provide important insights into the epidemiology of a bubonic plague outbreak during the Third Pandemic in Europe.

Human ectoparasites and the spread of plague in Europe during the Second Pandemic.

Plague, caused by the bacterium Yersinia pestis, can spread through human populations by multiple transmission pathways. Today, most human plague cases are bubonic, caused by spillover of infected fleas from rodent epizootics, or pneumonic, caused by inhalation of infectious droplets. However, little is known about the historical spread of plague in Europe during the Second Pandemic (14-19th centuries), including the Black Death, which led to high mortality and recurrent epidemics for hundreds of years. Several studies have suggested that human ectoparasite vectors, such as human fleas (Pulex irritans) or body lice (Pediculus humanus humanus), caused the rapidly spreading epidemics. Here, we describe a compartmental model for plague transmission by a human ectoparasite vector. Using Bayesian inference, we found that this model fits mortality curves from nine outbreaks in Europe better than models for pneumonic or rodent transmission. Our results support that human ectoparasites were primary vectors for plague during the Second Pandemic, including the Black Death (1346-1353), ultimately challenging the assumption that plague in Europe was predominantly spread by rats.