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Giardiasis is the most common enteric protozoan infection notifiable in New South Wales (NSW), Australia. Surveillance by NSW Health had shown a steady increase (prior to the COVID-19 pandemic) in the number of cases reported since 2012 and the reasons for this currently remain unknown. This study aimed to investigate the occurrence of Giardia intestinalis assemblages causing human infection in NSW. Individual faecal specimens were collected from participating hospitals and private laboratories, and the presence of Giardia and co-infections was confirmed by real-time multiplex-polymerase chain reaction (PCR). Samples were genotyped by sequence analysis of the triose phosphate isomerase (tpi) gene and the small subunit rDNA. Combined genotyping showed that most samples belong to assemblage B, and only a small percentage were infected with only assemblage A. Mixtures of assemblages A and B in individuals were relatively common. Co-infections were observed in ∼ half of the cases, with the most common co-infection being Blastocystis hominis and Dientamoeba fragilis. Although giardiasis was more prevalent in males, the assemblage distribution between the sexes appeared uniform. The age distribution was bimodal, with peaks in 0–15-year-olds and in adults in their 30s. The overall largest number of cases was collected from patients aged 30–49 years. Interestingly, females aged 5 years old and under had a greater risk of assemblage B infection than their male counterparts. No significant correlation was found between assemblage and clinical symptoms. This study provides new insights into the molecular diversity of giardiasis in NSW and helps inform enhanced surveillance and prevention strategies in Sydney.
Non-suicidal self-injury (NSSI) is associated with mental disorders, yet work regarding the direction of this association is inconsistent. We examined the prevalence, comorbidity, time–order associations with mental disorders, and sex differences in sporadic and repetitive NSSI among emerging adults.
Methods
We used survey data from n = 72,288 first-year college students as part of the World Mental Health-International College Student Survey Initiative (WMH-ICS) to explore time–order associations between onset of NSSI and mental disorders, based on retrospective age-of-onset reports using discrete-time survival models. We distinguished between sporadic (1–5 lifetime episodes) and repetitive (≥6 lifetime episodes) NSSI in relation to DSM-5 mood, anxiety, and externalizing disorders.
Results
We estimated a lifetime NSSI rate of 24.5%, with approximately half reporting sporadic NSSI and half repetitive NSSI. The time–order associations between onset of NSSI and mental disorders were bidirectional, but mental disorders were stronger predictors of the onset of NSSI (median RR = 1.94) than vice versa (median RR = 1.58). These associations were stronger among individuals engaging in repetitive rather than sporadic NSSI. While associations between NSSI and mental disorders generally did not differ by sex, repetitive NSSI was a stronger predictor for the onset of subsequent substance use disorders among females compared to males. Most mental disorders marginally increased the risk for persistent repetitive NSSI (median RR = 1.23).
Conclusions
Our findings offer unique insights into the temporal order between NSSI and mental disorders. Further work exploring the mechanism underlying these associations will pave the way for early identification and intervention of both NSSI and mental disorders.
Background: Carbapenem-resistant Enterobacterales (CRE) are reportable statewide with required isolate submission to the Minnesota Department of Health (MDH) Public Health Laboratory (PHL), where carbapenemase production and mechanism identification is confirmed. MDH reviews all detected carbapenemase-producing organisms (CPOs) for potential transmission. Suspected transmission clusters are assessed for relatedness using whole genome sequencing (WGS). In 2022, increased detection of multiple bacterial genera of Klebsiella pneumoniae carbapenemase (KPC)-CRE occurred at acute care hospital-A, (ACH-A) and in 2023 the increase in KPC-CRE was accompanied by an increase in New Delhi metallo-β-lactamase (NDM)-CRE detection. Methods: MDH partnered with ACH-A to review increased CPO detection. MDH-PHL conducted WGS including multilocus sequence typing (MLST) and single nucleotide polymorphism (SNP) analysis on isolates. WGS suggested clusters of relatedness spanning multiple years and epidemiologic data revealed common room occupancy. Infection prevention and control (IPC) principles were reinforced in cluster areas and audits verified adherence, prompting consideration of an environmental reservoir. An environmental screening plan was developed focusing on sink drains from common rooms. In May 2024, 94 swabs from sink drains were collected and CPO culture-based screening was conducted using selective media followed by molecular testing of bacterial growth by MDH-PHL. Results: There was detection of CPOs from 28 of 94 (29.8%) sink drains. Eight environmental KPC-CRE isolates and one NDM-CRE isolate appeared genetically related to 22 unique patients over a 10-year period (Figure 1). Three sink drain isolates showed genetic similarity to each other, but not to patient isolates. Three CPO clusters, representing 14 patients, had genetically similar isolates without an associated environmental isolate. However, isolates were collected over months to years suggesting an undetected reservoir. In August 2024, ACH-A initiated mitigation strategies to prevent CPO transmission from environmental reservoirs, including modification of sink plumbing, maintaining a splash zone, refraining from disposal of bodily fluids in sinks, optimizing sink hygiene, and monthly screening of inpatients in units with known CPO sink contamination. From August to December 2024, 325 patients were screened with 1.2% of specimens detecting KPC-CRE colonization. Conclusion: Sink drains containing CPOs on multiple hospital units that correlated with patient cases were identified at ACH-A. WGS suggests intermittent transmission of different CPOs over 10 years, and clusters of transmission appear to be related to environmental sources. Strict implementation and adherence to IPC measures, including those that minimize the spread of CPOs from facility premise plumbing, are critical to prevent CPO transmission despite widespread premise plumbing contamination.
Dispelling the myth that the discipline is intimidating, Introduction to Epidemiology for the Health Sciences is approachable from start to finish, providing foundational knowledge for students new to epidemiology. Its focus on critical thinking allows readers to become competent consumers of health literature, equipping them with skills that transfer to various health sciences and other professional workplaces. The text is structured to take the reader on a journey: each chapter opens with a scientific question before exploring the epidemiological tools available to address it. A conversation tool with representative students clarifies common points of confusion in the classroom, encouraging learners to ask questions to deepen their understanding. Example boxes feature contemporary local and global cases, often with step-by-step workings, while explanation boxes provide further clarification of complex topics. Authored by epidemiology and public health educators, this engaging textbook provides all readers with the skills they need to develop their own epidemiology toolkit.
In the study approaches we have looked at, the main purpose of investigation has been to understand and quantify relationships – relationships between exposures and outcomes, or between interventions and effects. And, just like the common plot line of a romantic tale, in this chapter we will consider how we can work out if those relationships are the ‘real deal’. How do we know we have measured what we think we have (is this really love?) and how much of the effect we have measured is entirely due to the exposure or intervention (or just a holiday thing)?
In epidemiology, we are interested in conducting studies to measure disease occurrence and look for causes of disease. Such studies can be applied to public health, allowing us to modify the causes for disease prevention. In the previous chapters, we learned about several commonly used public health measures and routine collections of health data. They form the basis of descriptive epidemiology and enable us to describe the frequency and patterns of health-related issues in relation to person, place and time characteristics. It is important to note that descriptive studies cannot be used to establish causal relationships but are useful for generating hypotheses. These hypotheses need to be tested in analytical studies to determine whether the ‘exposure’ of interest is associated with the changes in disease morbidity or mortality to search for the possible causes of the disease.
Importantly, the journey of learning epidemiology is like equipping you with knowledge and skills essential to critical thinking and problem-solving in your study or future career. The knowledge and skills will help you make scientifically informed decisions to improve population health. They include designing a study and applying quantitative research methods to collect data and identify ‘problems’. The data collected in the process will allow you to assess the measures of disease morbidity and mortality and make comparisons across populations, geographic locations, or different time points. Such comparisons allow us to determine potential ‘health problems’ in a relative way, which leads to further epidemiological investigations to search for possible ‘clues’ for ‘problem-solving’. In this chapter, we will explore this basic function of epidemiology: describing patterns of health problems, which is known as descriptive epidemiology.
For a case-control study to be a suitable design, we need a good idea about the outcome of interest (or condition) described by a strong case definition. But what if we know quite a bit about the exposures we are interested in, but we are a little hazy on the potential outcomes associated with those exposures? If we consider a scientific question like the one posed in this chapter – What happens if you eat pizza and chips every day?’ – we have specifically identified the exposures of interest, but can only guess what the outcomes might be. Okay, we could probably make fairly educated guesses about some of the potential outcomes (weight gain being foremost among these), but there remains a level of uncertainty about their timing, magnitude and variety. What is really needed to answer a question like this is a ‘cohort study’, a type of observational study in which ‘cohorts’ of people (population groups who share certain characteristics, such as being in the same work environment, or who are born in the same year) are sorted into groups on the basis of whether they have or have not been exposed to specific health-related factors.
In Chapter 6 we heard about how we can identify and quantify associations between exposures and health outcomes within populations, and even between countries. We learnt how useful cross-sectional studies were for looking at a range of risk factors and outcomes as they exist in a defined population at a particular point in time. While they have a great number of advantages, it can sometimes be difficult to sort out the direction of the relationships identified using cross-sectional approaches – that is, current risk factors or exposures may not necessarily have caused current outcomes or diseases. If we want to move towards thinking about potential causal relationships, we need an approach that allows us to determine the relative strength of relationships between exposures and outcomes and provide some hints about temporality – that is, to give us a start on determining if the exposure preceded the health event. We will need this type of study to address question posed for this chapter – what might be causing all those headaches that health science students seem to complain about.
When students are asked about the difficulties they experience in their epidemiology classes, one of the biggest barriers they report is the language their teachers use to describe the concepts being explained (note, it is the language rather than the concepts themselves). And here’s the thing: it is epidemiologists who are largely to blame, not the teachers! Being a relatively young discipline, it is not unusual to come across different words being used to describe the same concept, or the same word being used to describe different concepts – sometimes fundamentally different. Confusing, right?
A fundamental problem in descriptive epidemiology is how to make meaningful and robust comparisons between different populations, or within the same population over different periods. The problem has several dimensions. First, the data we have to work with (e.g. incident and prevalent cases, and deaths) is rarely usable in its raw form. We must therefore transform it in some way before undertaking the comparison itself. Second, our data usually tells us about fundamentally different attributes of the populations we are seeking to compare. If we are only ever interested in comparing any one of these attributes at a time (mortality, for example), then one of several simple and well-established transformations is all that is typically required. Increasingly, however, epidemiologists are being asked to bring these attributes together into more integrated and meaningful comparisons.
As we progress through this part and the next, you will be introduced to the different ways in which epidemiologists go about analysing the factors that are associated with people becoming ill or getting better. Each of these has a role to play in building up our knowledge about what influences human health. Our objective here is to provide an overview of the range of techniques that are available and to develop your understanding of which of these might be more appropriate in any given situation. One way to think about these techniques is as a set of tools for tackling a range of problems, much as a carpenter has a box full of tools for tackling different aspects of building a house. No one tool is useful in every situation, and some are more useful at certain stages of the construction process than others. Some even have features that make them useful in a variety of situations. Of course, context is everything, so even when a tool might not look like it’s the ‘right’ one in a particular situation, if the results are robust and reliable then that might be all that matters.