Infectious diseases

To the Editor: The incidence of syphilis is dramatically rising in Australia. As such, previously rare sequelae like syphilitic hepatitis are occurring more frequently, supported by a growing number of case reports in the literature.1 We present a typical case of syphilitic hepatitis and review the evolving at‐risk populations, to raise awareness of this potentially fatal yet highly treatable disease. A 34‐year‐old Caucasian man presented with a maculopapular rash over the trunk and limbs associated with abdominal discomfort, anorexia and fatigue. He had been treated for early syphilis 2 years previously, with serological evidence of response. He had no history of human immunodeficiency virus infection. He was married with children and denied other sexual relationships. Aside from the aforementioned rash, his examination was unremarkable. His alkaline phosphatase level was 684 U/L (reference interval [RI], 50–130 U/L), γ‐glutamyl transpeptidase was 942 U/L (RI, < 55 U/L), alanine aminotransferase was 429 U/L (RI, < 45 U/L), and aspartate aminotransferase was 181 U/L (RI, 5–35 U/L); bilirubin was 18 μmol/L (RI, < 20 μmol/L) and C‐reactive protein (CRP) was 55 mg/L (RI, < 5 mg/L). Abdominal ultrasound and extensive liver screen results were normal. Treponema pallidum particle agglutination assay and rapid plasma reagin test results were reactive at a 1:32 titre, prompting a diagnosis of syphilitic hepatitis. He was administered 2.4 million units of benzathine benzylpenicillin intramuscularly once‐weekly for 3 weeks. His rash, symptoms and liver function tests resolved within 6 weeks. The Australian notification rate of syphilis increased from 5.0 to 18.3 per 100 000 population between 2010 and 2017. Women aged 15–19 years experienced a tenfold increase in incidence over this period. In 2017, women from remote areas were 27.3 times more likely to contract syphilis than those from major cities, while Aboriginal and Torres Strait Islander people were 6.6 times more likely to contract syphilis than non‐Indigenous Australians.2 Despite this disproportionate rise in vulnerable populations, rates remain highest among men who have sex with men and those with human immunodeficiency virus infection.3,4 Re‐infection is common, as was found in our patient. Described as the “great imitator”, secondary syphilis can be difficult to diagnose; consequently, the true incidence of syphilitic hepatitis is not known. While our case illustrates a typical presentation, cases of fulminant liver failure have been described.5 Rash (78%), anorexia (57%) and fatigue (57%) are the most common presenting symptoms.1 Marked elevation of alkaline phosphatase and γ‐glutamyl transpeptidase, coupled with milder elevation of alanine aminotransferase and aspartate aminotransferase are the most common laboratory findings, with hyperbilirubinaemia present only in severe cases. A liver biopsy is not essential for diagnosis, but may reveal inflammatory infiltration of the bile duct, hepatic granulomas or, less commonly, intrahepatic spirochetes via immunohistochemical staining.1 It is imperative that clinicians consider ordering treponemal serology in high risk patients fitting this presentation, as prompt treatment with penicillin leads to rapid disease resolution and aversion of tertiary complications, including death.

Matthew Smale · William R Connell · Julien D Schulberg

To the Editor: A 35‐year‐old man born in Dire Dawa, Ethiopia, with childhood exposure to swimming in rivers, migrated to Australia 18 years ago. He presented with recurrent gastrointestinal bleeding. His index gastroscopy revealed portal hypertensive gastropathy and large oesophageal varices with high risk stigmata of recent bleeding requiring banding. Abdominal ultrasonography and transient elastography excluded liver cirrhosis. Six weeks later, he re‐presented with recurrent severe haematemesis associated with dark maroon rectal bleeding. Repeat urgent gastroscopy and flexi‐sigmoidoscopy revealed oesophageal varices without active bleeding. On sigmoidoscopy, a large amount of dark blood was seen, presumed to be related to rapid transit from recent oesophageal variceal bleeding. In the next 48 hours, a repeat colonoscopy was performed. Colonoscopy identified yellowish nodules throughout the colon with diffuse telangiectasia (Box, A and B). Mucosa was oedematous and friable. Aphthous ulcers were seen in the transverse colon and biopsies were obtained. No polyps or focal source of colonic bleeding were evident. Histopathology confirmed the presence of cystic ova resembling Schistosoma in the lamina propria immediately adjacent to crypts. Although classical granuloma formation was absent, aggregation of eosinophils was seen around a ruptured ovum (Box, C and D). Indirect assay via serology testing was positive for Schistosoma mansoni antibody (titre of 1:640). His eosinophil count was normal and stool microscopy was negative. He was treated with praziquantel. Four months later, a follow‐up gastroscopy revealed stable appearance of grade 1 oesophageal varices without high risk features. Routine variceal surveillance had been organised but not further colonoscopies. Schistosomiasis affects over 200 million people worldwide but is not acquired in Australia. In a national survey in Ethiopia, 37.3 million individuals were living in endemic areas.1 Schistosoma mansoni is the commonest species to cause intestinal and hepatic schistosomiasis. In the 2016 national census, there were 11 795 people in Australia who were born in Ethiopia, 64.3% (7584) of whom were Australian citizens.2 Most screening data for schistosomiasis in Australia are based on African refugees, with 37% in Newcastle, 38% in Hobart and 12% in Melbourne.3 Despite anecdotal knowledge, there are no published cases of non‐cirrhotic portal hypertension related to schistosomiasis in Australia. As a multiracial country with high immigration and tourism, increased recognition in Australia is paramount. Box – Colonoscopy showing widespread yellowish nodules (arrows) with oedematous and friable mucosa (A) and diffuse telangiectasia (B); and histopathology showing aggregation of eosinophils surrounding a Schistosoma ovum(C) and a cross‐sectional image of a Schistosoma ovum (D)

Julia Lim · Shweta Sharma · Damian Dowling

To the Editor: We read with interest the article by Kault,1 who carried out an analysis on superspreaders, asymptomatic cases, and coronavirus disease 2019 (COVID‐19) elimination. Although all efforts made for preventing or containing the COVID‐19 pandemic are certainly welcome, we raise doubts on some basic aspects used for constructing the prediction model and which do not seem to be evidence‐based. In the risk model of COVID‐19 re‐emergence after release of restrictive measures (eg, lockdowns), Kault made some erroneous assumptions, including the fact that asymptomatic subjects may be as infectious as symptomatic patients with COVID‐19.1 This hypothesis seems to be contradicted by several lines of evidence. First, a meta‐analysis published in 2020 concluded that the rate of asymptomatic transmission of severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infection is 35% lower compared with COVID‐19 patients with symptomatic illness.2 This has also been clearly explained in a seminal study showing that the viral load is the highest in concomitance with symptoms onset, so that the infectiousness of pre‐symptomatic or asymptomatic individuals is probably low.3 Notably, the impact of pre‐symptomatic SARS‐CoV‐2 transmission seems also rather limited, whereby the secondary attack rate was found to account for only 15% of all secondary COVID‐19 cases.4 A second aspect that needs to be highlighted is that presuming that 50% of SARS‐CoV‐2‐positive patients are asymptomatic may also be formally incorrect. Beside the fact that the asymptomatic SARS‐CoV‐2‐positive rate varies greatly depending on many genetic, demographic (ie, age, sex and ethnic origin) and even clinical (eg, time course of disease, comorbidities) variables, an analysis in the official database of the Italian National Institute of Health reveals, for example, that the rate of asymptomatic subjects with SARS‐CoV‐2 infection approximates 70%.5 Combined with lower infectiousness, the high prevalence of asymptomatic subjects bearing SARS‐CoV‐2 infection after release of restrictive practices (eg, lifting of lockdowns) would persuade us to conclude that the possible impact of asymptomatic superspreaders on SARS‐CoV‐2 transmission would be low and perhaps insufficient to influence or guide future policies aimed at restricting individual freedom.

Camilla Mattiuzzi · Giuseppe Lippi

The Olympic Games raise many infection control, health security and ethical challenges

Craig B Dalton · Joanne Taylor

Developing a pathway to prioritise clinical research and prepare for future pandemics remains an urgent need

Asha C Bowen · Steven YC Tong · Joshua S Davis

The research response in Australia has been rapid, but better coordination is imperative

Anna Lene Seidler · Mason Aberoumand · Jonathan G Williams · Aidan Tan · Kylie E Hunter · Angela Webster

Vaccination delivery was generally resilient in a period of unprecedented social and health care disruption

Brynley P Hull · Alexandra J Hendry · Aditi Dey · Kerin Bryant · Catherine Radkowski · Stephen Pellissier · Kristine Macartney · Frank H Beard

To the Editor: The toll of group A Streptococcus is dramatically unappreciated, despite increasing evidence of its burden.1 In Australia and New Zealand, we recently demonstrated that group A streptococcal throat and skin infections cause a sizable burden at the population level — cellulitis is the main contributor to the total burden of all group A streptococcal diseases and acute rheumatic fever and rheumatic heart disease contribute disproportionately relative to their frequency of occurrence.2,3 At a global level, the burden of group A Streptococcus is not abating. Global Burden of Disease data suggest that incident cases and deaths due to rheumatic heart disease alone have surpassed those of meningitis (Box). In 2019, more than 85% of rheumatic heart disease cases occurred among people aged under 35 years.4 No other group A streptococcal‐specific endpoints are available from the Global Burden of Disease data, yet all‐cause cellulitis was ranked the 24th most frequently occurring condition in high income countries in 2019.4 Group A Streptococcus causes outbreaks of poststreptococcal glomerulonephritis, contributing to the burden of chronic renal disease, and it is estimated to be the fifth most lethal pathogen on the planet, behind the human immunodeficiency virus (HIV), Mycobacterium tuberculosis, Plasmodium falciparum and S. pneumoniae, yet expenditure on vaccine development is only 0.17% of that spent on vaccines for HIV infection, malaria and tuberculosis.5 The divergence in numbers of cases and deaths due to group A Streptococcus compared with meningitis partially demonstrates the value of vaccination. Another major benefit of vaccination is a substantial reduction in antibiotic consumption. Indeed, pharyngitis is a major driver of antibiotic consumption globally, and an estimated 17% of antibiotic prescriptions for pharyngitis among children in the United States could be prevented by a group A Streptococcus vaccine.6 Two major initiatives aim to progress vaccine development. The Australian Strep A Vaccine Initiative (ASAVI) and the Strep A Vaccine Global Consortium (SAVAC) are addressing technical and investment barriers and leading at least one of the current vaccine candidates to an efficacy trial for pharyngitis prevention by 2024.5 An effective vaccine may prevent health and economic burdens due to the full range of group A streptococcal diseases and associated antibiotic consumption. Box – Estimated number of new cases (left) and deaths (right) due to meningitis and rheumatic heart disease globally* * Data obtained from the Global Burden of Disease study 2019.4

Jeffrey W Cannon · Julie Bennett · Michael G Baker · Jonathan R Carapetis

To the Editor: In their article, Blakely and colleagues1 describe an infectious disease model for simulating the effect of a lockdown on the transmission of severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2). Although we cannot say this work determined pandemic policy, two of the authors have described their close collaboration with the Victorian Government, culminating in the release of a road map to reopening2 based directly on, and released alongside, their modelling.3 The model is stochastic and agent‐based, with 2500 individuals moving around a model space. When both an infected and a susceptible person land on the same patch, there is a probability of transmission. Some individuals are marked as being essential workers; population homogeneity is otherwise assumed.4 Models are necessarily abstractions from reality; it is neither possible nor relevant to include every population group. The question is whether the model effectively captures the dynamics of infection. The combination of model type and population structure has a surprising result. People in the model can only be infected by moving around, and a lockdown is simulated by a reduction in the pace and frequency of movement. At a technical level, the model’s mechanics guarantee the effectiveness of a population‐wide lockdown because it most extensively reduces movement. It is hardly surprising that Blakely and colleagues refer to a lockdown as an “opportunity”.1 The assumption of population homogeneity is robust to exceptions, but only to a point. Using official data, we estimate that, in Victoria, the odds of an aged care worker becoming infected were almost 12 times that of the general population (odds ratio [OR], 11.81; 95% CI, 11.76–11.87). For health care workers, the odds were more than three times higher (OR, 3.19; 95% CI, 3.14–3.23).5 At this level of contact and risk heterogeneity, the model cannot reflect the true virus dynamics. Throughout the period covered by the model predictions, interventions targeted at health care settings were implemented. These interventions, such as closing hospital tea rooms and changing aged care working conditions, cannot be factored into the model predictions because health and aged care workers are not included in the model. By failing to specifically consider the populations that drove the epidemic or the interventions targeted at those populations, any ultimate concurrence between the actual and predicted numbers can only be attributable to chance.

Bradley R Crammond · Vishaal Kishore

On 23 May 2019, the Central Queensland Public Health Unit received a confirmed laboratory notification of a dengue virus serotype‐2 (DENV‐2) infection in a Rockhampton resident. On 5 May, a 71‐year‐old man without a history of travel overseas or to Far North Queensland had developed symptoms consistent with a zoonotic disease, and presented later that month to his general practitioner because his symptoms had not abated. Between 23 May and 7 October 2019, 21 locally acquired cases of DENV‐2 were identified in Rockhampton: 13 laboratory‐confirmed cases and eight probable cases detected by active surveillance. This was the first outbreak of locally acquired dengue in Central Queensland for 65 years.1 In 14 cases (67%), the infected persons sought medical attention; two required hospitalisation. A formal outbreak response was initiated by the Central Queensland Public Health Unit on 23 May 2019, including extensive mosquito surveillance and active and passive human surveillance within 200 metres of the residences of each identified infected person. Particular attention was directed to surveying locations that might facilitate increased dengue transmission in the community (such as schools, a plant nursery, and aged care facilities) for artificial and natural containers that could serve as breeding areas for infected mosquitoes (Aedes aegypti). Such containers were either removed or emptied of residual water and treated with pellets of the insect growth regulator (S)‐methoprene, and the premises and buildings were sprayed inside and out with the residual insecticide Temprid 75 (Bayer; includes imidacloprid and β‐cyfluthrin). In addition to the house‐to‐house human surveillance, a novel “lure and kill” approach was adopted for vector control: lethal ovitraps were deployed within 200 metres of the residence of any person with a probable or confirmed infection. Ae. aegypti was found in 105 of 1107 inspected residential premises (9.5%), or more than half of the 205 premises found to contain mosquitoes. Enhanced serological surveillance was undertaken to detect patients with viraemia early, enabling prompt public health and mosquito control interventions. The complete DENV‐2 genome sequence (GenBank accession number, MN982899.1) indicated that the implicated virus was most closely related to Southeast Asian strains of DENV‐2. Given the presence of Ae. aegypti in Central Queensland and the increasing numbers of travellers and visitors returning from countries in which dengue is endemic, it is important that Rockhampton be recognised as a dengue‐receptive area. As locally acquired cases of dengue are being reported outside Far North Queensland, the state map of dengue‐receptive areas2 should be updated; specifically, the broad geographic area from Townsville south to Rockhampton should be considered dengue‐receptive.

Jacina Walker · Alyssa Pyke · Paul Florian · Rachael M Rodney Harris · Gulam Khandaker

Overlooking the potential for airborne transmission of SARS-CoV-2 leaves Australia vulnerable to outbreaks

Zoë Hyde · David Berger · Andrew Miller

Clinical record A 44‐year‐old male health care worker presented with fevers, fatigue and head “fogginess” with abdominal discomfort and increased bowel frequency 8 days after receiving his first dose of the COVID‐19 vaccine (ChAdOx1‐S [recombinant]) (AstraZeneca). He was previously well, with a past history of depression and was only taking escitalopram. He had no prior thrombosis or exposure to heparin. The low platelet count, 70 × 109/L (reference range, 150–400 × 109/L), and markedly elevated D‐dimer, 114 mg/L (upper limit of normal, 0.5 mg/L), with vague abdominal pains prompted a computed tomography (CT) venogram of the abdomen, which demonstrated thrombosis with complete occlusion of the portal and splenic veins and protrusion of a tongue of thrombus into the superior mesenteric vein (Box 1). CT venogram of the head did not show central venous sinus thrombosis. The rest of the full blood count and the blood film showed no features of microangiopathic haemolytic anaemia. The prothrombin time, activated partial thromboplastin and fibrinogen levels, liver and renal function tests were all normal. Antiphospholipid antibodies were negative and a heterozygous prothrombin G20210A mutation was identified. Antibodies to the severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) nucleocapsid protein and the respiratory polymerase chain reaction (PCR) test for coronavirus disease 2019 (COVID‐19) were negative, ruling out active COVID‐19 infection as a potential thrombosis aetiology. Antibodies to the heparin–platelet factor 4 (PF4) complex in the patient’s plasma was strongly positive (optical density, 1.94) by enzyme‐linked immunosorbent assay (ELISA)‐based test (Asserachrom HPIA IgG; Stago). Three functional assays, including serotonin release assay (SRA; Hidex 300 SL, Hydex), multiple electrode aggregometry (MEA; Roche Diagnostics) and flow cytometry (BD Fortessa, ETH Zürich; procoagulant assay) all detected heparin‐independent PF4 antibody complexes that activated donor platelets.1 Immediate anticoagulation was started with the anti‐factor Xa agent fondaparinux 10 mg (weight, 105 kg) subcutaneously every 24 hours and intravenous immunoglobulin (1 g/kg) administered on days 2 and 3, and repeated on days 7 and 8 after admission. Despite achieving the anti‐factor Xa fondaparinux level 6 hours after receiving a dose of 0.94 U/mL (target range, 0.50–1.20 U/mL), the platelets remained between 6 × 109/L and 20 × 109/L for the initial 6 days. The patient subsequently developed an acute abdomen clinically and a repeat CT scan showed extension and occlusive thrombus into the superior mesenteric vein with venous outlet obstruction and bowel ischaemic features. He underwent an immediate laparotomy with resection of 1.8 m of ischaemic bowel. Contemporaneously, given clot extension had occurred on fondaparinux, anticoagulation was changed to thrombin inhibitor bivalirudin, which had a short half‐life (25 minutes) that allowed for titratable perioperative anticoagulation and an intravenous pulse of methylprednisolone 1 g administered to augment PF4 antibody immunosuppression. The patient returned to the theatre 48 hours after the first laparotomy, where further compromised bowel was resected. Methylprednisolone 1 g daily was reinstituted for 4 days, with an immediate platelet peak to 385 × 109/L at completion of this 4‐day pulse. He was discharged after 34 days without further complications. He has transitioned to warfarin and continues to be well while monitored in the haematology outpatient clinic. Box 2 summarises the time course of treatment and response. Discussion In March 2021, Australia began the roll‐out of the COVID‐19 vaccine (ChAdOx1‐S [recombinant]) to combat the COVID‐19 pandemic. In Europe, where more than 20 million doses of this vaccine had been administered by mid‐March 2021, there were case reports of thrombosis at unusual sites associated with thrombocytopenia, which occurred at day 4–28 after vaccination and had a mortality rate of up to 25%, at an estimated rate of 1:100 000.2 In Australia, the COVID‐19 vaccine (ChAdOx1‐S [recombinant]) was initially offered to people working in high risk professions without age restrictions. By the end of March 2021, about 350 000 first doses of the COVID‐19 vaccine (ChAdOx1‐S [recombinant]) had been administered Australia‐wide. This is the first reported case of thrombosis at an unusual site with thrombocytopenia following vaccination with the COVID‐19 vaccine (ChAdOx1‐S [recombinant]) in Australia. The temporal association, the detection of anti‐PF4 antibodies with platelet activation in the absence of heparin, which is neutralised at high dose heparin, is consistent with the most recent reports.3 This entity, currently labelled as vaccine‐induced thrombotic thrombocytopenia (VITT) — also known as thrombosis with thrombocytopenia syndrome (TTS) — has pathological similarity to autoimmune heparin‐induced thrombocytopenia but without prior heparin exposure. More evidence is needed to demonstrate if the serum of patients with VITT contains antibodies that can bind to PF4 independent of heparin following vaccination for COVID‐19. Furthermore, the mechanism responsible for profound platelet activation following vaccination with the COVID‐19 vaccine (ChAdOx1‐S [recombinant]), as evidenced by ELISA high optical densities, remains to be established.3 While the COVID‐19 vaccine (ChAdOx1‐S [recombinant]) is delivered via adenovirus vector, to the best of our knowledge, there are no reported VITT cases associated with mRNA COVID‐19 vaccines. It is doctrine in the management of heparin‐induced thrombocytopenia that, in addition to immediate cessation of all heparins, a non‐heparin anticoagulant is commenced to prevent (further) thrombosis. Given the pathogenic similarities of VITT cases to heparin‐induced thrombocytopenia, we initially used fondaparinux, as our patient was clinically stable with normal renal function at presentation. It is unclear if the clinical deterioration in our patient, despite achieving favourable therapeutic fondaparinux drug level, was resultant of anti‐factor Xa drugs non‐efficacy and/or because of the severity of the venous outflow obstruction with compromised ischaemic small bowel. In principle, the surgical removal of any ischaemic tissue would be associated with clinical improvement. The benefit of intravenous immunoglobulin remains debatable, but in vitro spiking experiments and observation of platelet increment after its administration suggest that there may be a role.3,4 It is possible that intravenous immunoglobulin displaces the binding of anti‐PF4 antibody complex to FcgammaRIIA (an Fc receptor for IgG) receptors on platelets.5 In our patient, it is difficult to ascribe a specific clinical and platelet recovery to intravenous immunoglobulin solely given the simultaneous timing of surgical removal of ischaemic intestine, the commencement of alternate anticoagulation with bivalirudin, and pulsed high dose steroids. It is noted that pulsed methylprednisolone was prescribed in the majority of recently reported cases.3 In line with evolving guidance documents, clinicians assessing patients who present with organ‐specific thrombotic symptoms 4–28 days following vaccination with the COVID‐19 vaccine (ChAdOx1‐S [recombinant]) should look for any combination of thrombocytopenia and elevated D‐dimer, and/or low fibrinogen, with a low threshold for requesting imaging of the appropriate organ — in particular, the brain central venous sinus and abdominal splanchnic venous systems — for thrombosis plus anti‐PF4 ELISA testing in consultation with haematology. Lessons from practice Vaccine‐induced immune thrombotic thrombocytopenia (VITT) is rare but potentially life‐threatening. VITT should be considered when patients present at day 4–28 after vaccination with unusual site thrombosis: splanchnic and/or central venous sinus thrombosis, or thrombocytopenia (or falling platelets) and markedly elevated D‐dimer. Specific testing to detect anti‐platelet factor 4 (PF4) antibody is needed to support VITT. Treat with non‐heparin anticoagulation, intravenous immunoglobulin, and consider pulsed methylprednisolone. Avoid platelet transfusions. Box 1 – Computed tomography venogram at presentation showing (A) a filling defect of portal vein, contrast in superior mesenteric vein and its tributaries (arrow, coronal plane) and (B) a thrombus in the superior mesenteric vein (the arrow shows the contrast, axial plane) Box 2 – Time course and management IV = intravenous; IVIg = intravenous immunoglobulin; SC = subcutaneous.

Jay Hocking · Sanjeev D Chunilal · Vivien M Chen · Tim Brighton · James Nguyen · Jocelyn Tan · Stephen B Ting · Huyen Tran

Is a policy of mandatory vaccination for health care workers permissible under Australian law?

Dev AS Kevat · Danielle CA Panaccio · Sam C Pang · Jessica M Dean · Caitlin C Farmer · Patrick D Mahar

National surveillance would facilitate strategies for preventing or managing conditions that predispose people to severe streptococcal disease

Jeffrey W Cannon · Asha C Bowen

The social determinants of incidence should be addressed, and other relevant host, pathogen, and health system factors investigated

Cameron M Wright · Rachael Moorin · Glenn Pearson · John R Dyer · Jonathan R Carapetis · Laurens Manning

When SARS-CoV-2 prevalence is low, a risk-based approach to screening could improve testing efficiency and reduce resource needs

Eloise Williams · Katherine Bond · Deborah A Williamson

Novel PPE, such as 3D printed face shields, must be compliant with regulatory requirements and a clinical evaluation protocol should be developed

Mathilde R Desselle · Marianne Kirrane · Ian T Chao · Jasamine Coles Black · Maria A Woodruff · Jason Chuen · Clair Sullivan

Genomic surveillance enhances detection and response to emerging SARS-CoV-2 variants

Patiyan Andersson · Norelle L Sherry · Benjamin P Howden

A 64-year-old woman presented to the emergency department with 7 days of right ankle pain

Peter Bradhurst · Carlos El‐Haddad · John Ng · Nicolás Urriola

Navigating parenthood and pandemics: uncertainty is the new normal

Jacqueline Fleetwood

The psittacosis epidemic of 1929–1930, spread by the Australian budgie, provides lessons for the COVID- 19 pandemic

Robert M Kaplan

Onsite “buddies” are not always available to monitor the donning and doffing of personal protective equipment (PPE) in hospitals, especially during a pandemic, potentially leading to poor PPE compliance and increased risk of health care infections.1,2 We therefore compared monitoring of PPE donning/doffing procedures in a standard critical care setting3,4 by remote buddies with monitoring by onsite buddies. We designed 30 procedural scenarios (15 donning, 15 doffing) that included random errors in some procedural steps (online Supporting Information). Four buddies (two onsite, two remote), unaware of the number and type of errors in each scenario, concurrently viewed and assessed each step. The remote buddies viewed the procedures via videoconferencing on their computers. The camera of the transmitting laptop computer was positioned so that the entire body of the person donning or doffing PPE could be seen. Procedures were live‐streamed to the remote buddies via the hospital Wi‐Fi network. The buddies were not permitted to communicate with each other or with the person donning or doffing PPE. The study was approved by the Melbourne Health Human Research Ethics Committee (QA2020104). Sensitivity (correctly identifying correct procedure) was 100% for both onsite and remote buddies; specificity (correctly identifying incorrect procedure) was 98.9% for onsite buddies and 94.5% for remote buddies; overall accuracy was respectively 99.7% and 98.7% (Box). Concordance between assessments by onsite and remote buddies (κ = 0.95), by the two onsite buddies (κ = 0.97), and by the two remote buddies (κ = 0.98) was very good. The most frequent error was remote buddies missing chin exposure below the mask, probably because of the two‐dimensional view provided by the camera. Paying specific attention to the mask position when the donner turns side on in front of the camera might prevent this error. Practical considerations for remote buddies include the need for reliable hospital network and internet connections, or a wired hardware system, to avoid disruption of monitoring. As the remote buddy is unable to physically intervene when they identify an error, clear verbal communication is important. The psychological effect of having an onsite buddy was not characterised, but may influence user acceptability of remote buddies. All buddies were very experienced in providing observation feedback, but we did not assess their proficiency. Their accuracy may also have reflected greater vigilance while being observed (the Hawthorne effect). Finally, we did not weight the donning and doffing steps according to their importance for safety. Having a trained observer monitor PPE compliance is important for health care safety. The high level of accuracy and the agreement between onsite and remote buddies were encouraging. Apart from identifying errors, remote buddies could also provide step‐by‐step instruction in donning and doffing procedures, which could improve compliance and minimise contamination.5 Using remote buddies may help preserve PPE supplies and ensure reliable access to monitoring, even when PPE supply or onsite staff numbers are limited, while also reducing the infection exposure risk for the monitoring observers. Box – Personal protective equipment (PPE) monitoring assessment accuracy by onsite and remote buddies Scenario outcome* Buddy outcome* Pass Fail Onsite buddies (390 tests) Pass 298 1 PPV, 99.7% Fail 0 91 NPV, 100% Sensitivity, 100% Specificity, 98.9% Overall accuracy, 99.7% Remote buddies (383 tests†) Pass 292 5 PPV, 98.3% Fail 0 86 NPV, 100% Sensitivity, 100% Specificity, 94.5% Overall accuracy, 98.7% PPV = positive predictive value; NPV = negative predictive value. * For each step of each PPE donning/doffing procedure: pass = correctly performed; fail = not correctly performed. † Seven assessments were missing because of internet interruptions.

Reny Segal · William PL Bradley · Daryl Williams · Romulo Correa de Araujo Nunes · Irene Ng

A 67-year-old woman was referred to our ear, nose and throat department with confirmed cerebrospinal fluid (CSF) rhinorrhoea

Sandeep G Mistry · Wallace Walker · James Earnshaw · Anders Cervin