Medlab Central (New Zealand)

ABSTRACT Bat boxes can be employed to provide short-term mitigation for the loss of trees with bat roost potential. Traditionally bat box utilisation (by long-tailed bats) has been difficult to confirm in NZ, partly due to a lack of published survey techniques to confirm bat box utilisation when bats are not present at the time of sampling. While environmental deoxyribonucleic acid (eDNA) has been widely applied as a biomonitoring tool, it has not been used previously in the context of bat box surveys in New Zealand. Here we present a method for collecting eDNA from bat boxes using swabs and test the efficacy of eDNA in validating bat box utilisation as confirmation of roosting. Bat boxes were deployed by the Hamilton City Council as part of the bat mitigation strategy for the Southern Links Project in southern Hamilton. The eDNA method confirmed a total of 25 boxes out of the 73 (34%) included in this study were being utilised by long-tailed bats. The results indicate that eDNA can be applied with confidence to demonstrate box use, even at very low and infrequent occupancy rates.

BackgroundFemales of reproductive age with concussion report a greater number of symptoms that can be more severe and continue for longer than age matched males. Underlying mechanisms for sex differences are not well understood. Short non-coding Ribonucleic Acids (sncRNAs) are candidate salivary biomarkers for concussion and have been studied primarily in male athletes. Female sex hormones influence expression of these biomarkers, and it remains unclear whether a similar pattern of sncRNA expression would be observed in females following concussion. This study aims to evaluate recovery time, the ratio of salivary sncRNAs and symptom severity across different hormone profiles in females presenting to emergency departments (ED) with concussion and, to investigate the presence of low energy availability (LEA) as a potential modifier of concussion symptoms.MethodsThis prospective cohort study recruits participants from New Zealand EDs who are biologically female, of reproductive age (16–50 years) and with a confirmed diagnosis of concussion from an ED healthcare professional. Participants are excluded by ED healthcare professionals from study recruitment as part of initial routine assessment if they have a pre-diagnosed psychiatric condition, neurological condition (i.e., epilepsy, cerebral palsy) or more than three previously diagnosed concussions. Participants provide a saliva sample for measurement of sncRNA’s, and online survey responses relating to hormone profile and symptom recovery at 7-day intervals after injury until they report a full return to work/study. The study is being performed in accordance with ethical standards of the Declaration of Helsinki with ethics approval obtained from the Health and Disability Ethics Committee (HDEC #2021 EXP 11655), Auckland University of Technology Ethics Committee (AUTEC #22/110) and locality consent through Wellington hospital research office.DiscussionIf saliva samples confirm presence of sncRNAs in females with concussion, it will provide evidence of the potential of saliva sampling as an objective tool to aid in diagnosis of, and confirmation of recovery from, concussion. Findings will determine whether expression of sncRNAs is influenced by steroid hormones in females and may outline the need for sex specific application and interpretation of sncRNAs as a clinical and/or research tool.Trial registrationAustralian New Zealand Clinical Trials Registry (ANZCTR) registration number ACTRN12623001129673.

Clostridioides difficile infection (CDI) is a form of antibiotic-associated infectious diarrhoea resulting in significant morbidity and mortality. Community-acquired disease in low-risk individuals is increasingly recognised. There are limited New Zealand data published. To determine the incidence and location of onset of CDI cases in the Manawatu region, and further describe the demographics, risk factors and prevalent C. difficile ribotypes of the population. We performed an incidence case-control study of CDI in the Manawatu region between September 2018 and September 2019. Cases were matched to controls with a negative test for C. difficile. Demographic and comorbidity data, location of onset, drug exposure, disease recurrence and 30-day mortality were collected. Ribotype analysis was performed on C. difficile isolates. Thirty-two specimens tested toxin positive over 12 months, yielding an incidence of 18.3 cases per 100 000 person-years. Twenty-five percent of cases had community onset disease. Cases were more likely to have had amoxicillin/clavulanate or ceftriaxone prescribed. Elevated blood white cell count and lower HbA1c were significantly associated with CDI. The dominant ribotype was 014/020. Two cases were RT 023. Our data are similar to previous national data. RT 023 has not been previously reported in New Zealand and has been associated with severe colitis. We demonstrated a significant proportion of community-acquired cases and the true incidence might be higher. Vigilance for community onset disease is required. These data may allow observation of temporal changes in incidence and infection patterns of CDI in New Zealand.

Severe COVID-19 has been associated with many risk factors including aging and underlying chronic diseases such as obesity, diabetes, hypertension, chronic lung disease and chronic liver disease [1]. Satapathy et al. demonstrated that liver chemistry abnormalities (LCA) including aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase and bilirubin were associated with the severity of COVID-19 [2]. Furthermore, LCA were linked to chronic liver disease but not with other risk factors of severe COVID-19, indicating chronic liver disease is an independent indicator of severe COVID-19. However, the mechanisms could be complex as hepatocytes do not express ACE2, suggesting direct hepatic injury by the virus is minor. We posit that the gut–liver axis could play a key role in LCA/chronic liver disease-associated severe COVID-19. The gut–liver axis represents bidirectional interactions between gut microbiota and liver physiology. Whilst chronic liver disease can affect gut microbiota composition, dysregulation of gut microbiota (gut dysbiosis) can cause liver inflammation through biliary tract, portal vein and systemic circulation [3]. Gut dysbiosis has been associated with chronic liver disease through promoting inflammation and reducing anti-inflammatory mechanisms [1,3]. LCA, an indicator of the extent of hepatic pathogenic changes, have been associated with inflammatory status, particularly with the cytokine storm in COVID-19 [4]. In COVID-19 patients with chronic liver disease, gut microbiota could be highly disturbed. The infections of the intestines by SARS-CoV-2 viruses, which are common in COVID-19, can directly aggravate pre-existing gut dysbiosis in chronic liver disease [1]. Gut dysbiosis can result in intestinal and hepatic inflammation through translocation of endotoxins and bacteria due to increased intestinal permeability. Endotoxin and bacteria in the liver can activate Kuffer cells, macrophages and dendritic cells to produce high levels of proinflammatory cytokines. Recently, several studies reported that gut dysbiosis also caused proinflammatory types of T cells and B cells in the liver [3,5]. In addition, gut dysbiosis reduces the production of commensal bacterial metabolites, which have anti-inflammatory effects such as butyrate, indole and bile acid derivatives [1]. The gut dysbiosis-caused hepatic inflammation together with other pathogenic changes caused by SARS-CoV-2 such as inflammatory cytokines from the lung and local blood vessel endothelial cell infections by SARS-CoV-2 viruses lead to severe COVID-19 and increased mortality. Incorporation of the gut–liver axis could better elucidate the pathogenesis of chronic liver disease-associated severe COVID-19 and have therapeutic implications. Acknowledgements None. Conflicts of interest There are no conflicts of interest.

SummaryCoronavirus disease 2019 (Covid‐19), caused by severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infection, is now pandemic. While most Covid‐19 patients will experience mild symptoms, a small proportion will develop severe disease, which could be fatal. Clinically, Covid‐19 patients manifest fever with dry cough, fatigue and dyspnoea, and in severe cases develop into acute respiratory distress syndrome (ARDS), sepsis and multi‐organ failure. These severe patients are characterized by hyperinflammation with highly increased pro‐inflammatory cytokines including IL‐6, IL‐17 and TNF‐alpha as well as C‐reactive protein, which are accompanied by decreased lymphocyte counts. Clinical evidence supports that gut microbiota dysregulation is common in Covid‐19 and plays a key role in the pathogenesis of Covid‐19. In this narrative review, we summarize the roles of intestinal dysbiosis in Covid‐19 pathogenesis and posit that the associated mechanisms are being mediated by gut bacterial metabolites. Based on this premise, we propose possible clinical implications. Various risk factors could be causal for severe Covid‐19, and these include advanced age, concomitant chronic disease, SARS‐CoV‐2 infection of enterocytes, use of antibiotics and psychological distress. Gut dysbiosis is associated with risk factors and severe Covid‐19 due to decreased commensal microbial metabolites, which cause reduced anti‐inflammatory mechanisms and chronic low‐grade inflammation. The preconditioned immune dysregulation enables SARS‐CoV‐2 infection to progress to an uncontrolled hyperinflammatory response. Thus, a pre‐existing gut microbiota that is diverse and abundant could be beneficial for the prevention of severe Covid‐19, and supplementation with commensal microbial metabolites may facilitate and augment the treatment of severe Covid‐19.

The recent lowering of the World Health Organisation (WHO) haemoglobin (Hb) and haematocrit (HCT) thresholds for diagnosis of polycythaemia vera (PV) has markedly increased the proportion of complete blood counts (CBC) that could be referred for haematologist review for comment, including advice on JAK2 V617F mutation analysis. The utility of an algorithm based on CBC indices and immature platelet fraction (IPF) to select cases for haematologist review was investigated. IPF analysis was performed on 22 patients with known JAK2 V617F mutation and 41 patients who were negative for this mutation previously tested because of suspicion of PV. A reference range study for IPF was performed on 102 normal patients. The algorithm was applied to data from 163358 CBC analyses to identify those most likely to have PV for review by a haematologist. The CBC algorithm and IPF requirement were satisfied by 47 patients (0.03%), eight of whom were known to have myeloproliferative disorders; the remaining 39 were referred for haematologist review. Utilising the algorithm enables identification of patients with a high likelihood of PV for haematological review. Large numbers are able to be screened efficiently and cost-effectively. Some patients with masked PV are able to be detected before clinical presentation.

BackgroundThe incidence of oropharyngeal cancer (OPC) in New Zealand (NZ) has more than doubled over the last 14 years with 126 cases in 2010. Overseas studies have shown that human papillomavirus (HPV) plays a significant role in the development of these cancers. However, the role of HPV in OPC and the burden on the NZ health system is unclear.AimThe aim of the study was to determine the prevalence and the genotypes of HPV associated with OPC in New Zealand.MethodsIn this study, 621 OPC were identified from cancer registry data from 1996–98, 2003–05, and 2010–12. Biopsies of 267 cases were then retrieved from laboratories throughout New Zealand. p16 immunohistochemistry and a human beta globin PCR were performed on all specimens. HPV genotyping was performed on all beta globin positive specimens using real-time PCR with melt analysis.ResultsUsing a p16/PCR algorithm, 77.9% (95% CI: 71.1–83.5%) of cases were attributable to HPV. Of these, 98.5% were HPV 16 positive. There was also one case each of HPV 33 and 35. The percentage of HPV positive cases increased from 61.9% (95% CI: 40.9%– 79.2%) in 1996–98 to 87.5% (95% CI: 79.8%– 92.5%) in 2010–12. Results from the multivariable model, adjusted for sex and ethnicity found statistically significant associations between HPV positivity and timeframe (OR: 5.65, 95% CI: 2.60–12.30, 2010–12 vs 1996–98), and between HPV positivity and patient age (OR: 0.55, 95% CI: 0.33–0.99, ≥61 years vs ≤60 years).ConclusionsThis data is consistent with data from other developed countries showing an increase in cases of HPV positive OPC in New Zealand, and the majority of cases being attributable to HPV 16. These results support the recent inclusion of males into the nationally funded immunization schedule for Gardasil® 9.

Energy resolving performance of spectral CT systems is influenced by the accuracy of the detector's energy calibration. Global energy calibration maps a given threshold to the average energy response of all pixels of the detector. Variations arising from CMOS manufacturing processes and properties of the sensor cause different pixels to respond differently to photons of the same energy. Threshold dispersion adversely affects spectral imaging by degrading energy resolution, which contributes to blurring of the energy information. In this paper, we present a technique for per-pixel energy calibration of photon-counting x-ray detectors (PCXDs) that quantifies the energy response of individual pixels relative to the average response. This technique takes advantage of the measurements made by an equalized chip. It uses a known global energy map to quantify the effect of threshold dispersion on the energy response of the detector pixels across an energy range of interest. The proposed technique was assessed using a MARS scanner with an equalized Medipix3RX chip flip-bonded to 2 mm thick CdTe semiconductor crystal at a pitch of 110 μ m. Measurements were made of characteristic x-rays of a molybdenum foil. Results were compared between the case that the global calibration was used on its own and the case of using it in conjunction with our per-pixel calibration technique. The proposed technique quantified up to 1.87 keV error in energy response of 100 pixels of a selected region of interest (ROI). It made an improvement of 28.3% in average FWHM. The additional information provided by this per-pixel calibration technique can be used to improve spectral reconstruction.