BACKGROUND:Donor-derived infection remains a risk in solid organ transplantation. Clinical practice guidelines inform best practices for donor evaluation and acceptance, although they vary across centers and regions. This study aimed to evaluate the quality and consistency of guidelines for the evaluation of infections in solid organ donors and to summarize their recommendations. METHODS:We searched electronic databases and websites of professional organizations for clinical practice guidelines and consensus statements on evaluating solid organ donors for the presence and risk of infection. The methodological quality was assessed using the Appraisal of Guidelines for Research and Education II tool. Textual synthesis was used to compare the recommendations and summarize their conclusions. RESULTS:We included 19 clinical practice guidelines and 19 consensus statements covering different donor types (deceased/living, adult/pediatric), solid organs (liver, kidney, lung, heart, and pancreas) and infection types (viral, bacterial, fungal, parasitic, and prion). Most guidelines focused on describing the scope and purpose, but with less emphasis on domains such as the guidelines' applicability and rigor of development. Recommendations for screening and organ acceptance were generally consistent for hepatitis B virus, hepatitis C viru, HIV, Mycobacterium tuberculosis , Toxoplasma gondii , and Treponema pallidum infections. Variations exist, especially for emerging infections or when the screening test performance was poor. Most recommendations were ungraded. CONCLUSIONS:Recommendations for common infections were mostly consistent. Where uncertainties exist, transparency in evidence synthesis and translation into recommendations is needed. Real-world evaluation of guideline implementation and its clinical impact is crucial for maximizing donor organ use while minimizing donor-derived infections.

Disseminated Lomentospora prolificans infection typically occurs in immunocompromised hosts and is almost universally fatal. We describe a case of L. prolificans native valve infective endocarditis with cerebral mycotic aneurysm after recovery from allogeneic stem cell transplant. The case is notable for minimal immunosuppression at diagnosis, and pathological evidence of infection at sites which looked normal at surgery or by imaging. With early surgery and olorofim the patient survived to 76 days after diagnosis.

Neutropenic fever is a common complication of haematology and oncology treatments and is associated with a significant risk of morbidity and mortality. Few studies report patients' and carers' understanding of neutropenic fever, including risk reduction, recognition and optimal management. This guideline aims to improve communication around prevention, recognition and management strategies for neutropenic fever in patients receiving cancer treatment. Medical specialists, allied health physicians, other key stakeholders, parents and carers, and patient consumers collaborated to develop guidelines for patients and carers on neutropenic fever. This addition to the 2024 Australasian Consensus Guidelines for the Management of Neutropenic Fever in Patients with Cancer is the first directed at healthcare workers treating paediatric and adult patients at risk of neutropenic fever.

BACKGROUND:Systems for quality and safety assurance in organ donation and transplantation are vital, especially those that seek to minimize donor disease transmission. Australia has developed a national vigilance and surveillance system to identify, review, and analyze actual and potential donor-derived infections and other disease transmissions. METHODS:The system involves notification of incidents to the Australian Organ and Tissue Authority for review by a Vigilance and Surveillance Expert Advisory Committee (VSEAC). The VSEAC grades incidents, O makes recommendations, and issues communications both publicly and to the clinical donation and transplant sector. RESULTS:Annual notifications have increased since the inception of the system in 2012 until 2022. The vast majority relate to procedural aspects including donor assessment, information/data issues, and the recovery, offer, allocation, preservation and transportation of organs. Possible donor-derived disease accounted for 19% of all notifications, and those related to possible donor-derived infection only 12%. The VSEAC, as a result of reviewing these incidents, has made recommendations resulting in revisions to donor screening, organ allocation, packaging and transportation. The review of incidents has led to changes in clinical guidance for increased viral risk donor assessment, testing, and ensuing organ utilization and recipient surveillance. Guidance has also been reviewed for other infectious risks including strongyloides, human T-lymphotropic virus, and HEV. CONCLUSION:The Australian vigilance and surveillance system has enabled national retrospective reporting and evaluation of serious adverse events or reactions to identify trends and inform processes and guidelines, therefore improving the safety of donation and transplantation.

We transplanted six solid organs from three hepatitis C virus (HCV) polymerase chain reaction (PCR)-positive donors during 2018-2023. Recipients were treated with glecaprevir/pibrentasvir or sofosbuvir/velpatasvir for 4-12 weeks, with all six achieving sustained virological response without significant adverse events. As occurs in other jurisdictions, solid organ transplants from HCR PCR-positive donors can be safely utilised in Australia.

A 64-year-old man of European descent presented to a tertiary hospital in the Northern Territory with a four-week history of fevers, headaches, coughing and dyspnoea. His background included follicular lymphoma, for which he received maintenance obinutuzumab therapy every two months, having achieved remission the previous year. He had no other medical conditions. He had received two doses of the coronavirus disease 2019 (COVID-19) vaccine, with the most recent dose 12 months prior and prophylactic tixagevimab–cilgavimab five months prior. He was febrile at 39°C and tachypnoeic at 26 breaths per minute, with a blood oxygen saturation level of 97% on room air. On chest auscultation, there were bilateral inspiratory crepitations. Blood results revealed a raised C-reactive protein concentration and a normal white cell count. Chest computed tomography scans showed bilateral pulmonary infiltrates with no pulmonary embolism. He was treated for sepsis secondary to bilateral pneumonia with piperacillin–tazobactam and vancomycin as per local guidelines. His nasopharyngeal swab for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) polymerase chain reaction (PCR) revealed a weak positive result, reflected by the high cycle threshold value of 36.9. This result prompted a search for an alternative pathogen. During treatment with broad spectrum antibiotics, he had daily fevers higher than 38°C and a worsening blood oxygen saturation level of 88% on room air, correctable with 4 L of oxygen therapy. On Day 9 and 13, sputum samples were tested for SARS-CoV-2 (PCR). The resulting cycle threshold values of 32.0 and 23.7 respectively suggested active viral replication. These results prompted a ten-day course of remdesivir and dexamethasone. Although he met the criteria for severe COVID-19, baricitinib was not initiated due to an ongoing suspicion for concomitant bacterial infection. He rapidly defervesced but remained on 4 L oxygen therapy. On Day 23, within 48 hours of COVID-19 treatment cessation, fevers higher than 38°C recurred and dyspnoea worsened. Interval chest imaging scans demonstrated progressive bilateral pulmonary infiltrates with widespread ground glass opacities. Serial samples for SARS-CoV-2 PCR demonstrated decreasing cycle threshold values while off COVID-19 treatments, suggesting recrudescence of COVID-19 pneumonitis (Box). We re-initiated treatment with remdesivir and dexamethasone, while awaiting whole genome sequencing (WGS), which identified the Omicron recombinant subvariant XBB.1.5. A literature review revealed studies demonstrating significantly reduced neutralising activity of anti-spike protein monoclonal antibodies against subvariant XBB.1.5, including tixagevimab–cilgavimab.1 We escalated concerns to the Australian Society of Infectious Diseases Ozbug community, an online platform for infectious diseases physicians to share ideas and seek help with complex cases. The consensus was for combined therapies targeting viral suppression and the inflammatory response using antiviral agents, nirmatrelvir–ritonavir and remdesivir, and immunomodulatory agents including baricitinib and dexamethasone. As he was hypogammaglobulinaemic while on B-cell depleting therapy, we also administered intravenous immunoglobulin (IVIG). Given the degree of iatrogenic immunosuppression in our already immunocompromised patient, we commenced prophylactic anti-microbial therapies to mitigate the risk of opportunistic infections (Box). During this treatment course, he defervesced at 48 hours and was weaned off oxygen. His levels of serum inflammatory markers and chest imaging scans demonstrated marked improvement. He was discharged with a negative SARS-CoV-2 PCR result on nasopharyngeal swab and has remained well in the community. We present a case of severe, prolonged COVID-19 pneumonitis in an immunocompromised patient secondary to SARS-CoV-2 Omicron subvariant XBB.1.5. infection. Increased morbidity and mortality due to COVID-19 is well described in patients suffering from an underlying haematological malignancy or receiving lymphocyte-depleting therapy, both of whom may have attenuated vaccine-induced humoral immunity.2, 3 Subvariant XBB.1.5. is categorised as a variant of interest by the Communicable Diseases Genomics Network due to enhanced pathogenicity and transmissibility. Although reduced routine testing will likely underestimate the true incidence, subvariant XBB.1.5. accounted for 4.3% of variants of interest during a 28-day period in November 2023.4 Treatment options are limited by a significant rate of viral escape to vaccine immune response and neutralising antibodies targeting the spike protein. With respect to IVIG preparations, there is evidence to suggest they may contain COVID-19 neutralising antibodies. Our use of a fresh batch of IVIG theoretically increased the probability of neutralising antibodies to currently circulating variants. IVIG may have a role in treating COVID-19 in lymphocyte-depleted patients or those who are hypogammaglobulinaemic.5 More robust studies are needed to determine the best treatment options for COVID-19 in immunocompromised patients. However, rapidly evolving variants present a challenge for researchers as ongoing efficacy of treatments is likely to be affected. We also acknowledge the discordance in cycle threshold values between sputum and nasopharyngeal sampling. Sputum sampling is more sensitive for diagnosing COVID-19 pneumonitis, and a higher sputum viral load correlates with increased disease severity.2, 3, 6 Where the diagnosis of COVID-19 pneumonitis is suspected, especially in immunocompromised patients, a SARS-Cov-2 PCR test using a sputum sample should be undertaken. WGS also plays an important role in isolating the causative subvariant and directing subsequent management. The patient provided written consent for publication. No relevant disclosures. Not commissioned; externally peer reviewed. CRP = C-reactive protein, IV = intravenous, PCR = polymerase chain reaction. COVID-19 treatment: intravenous immunoglobulin, single dose 45 g; nirmatrelvir–ritonavir, 150 mg/100 mg twice daily for 10 days; baricitinib, 4 mg once daily for 14 days; remdesivir, intravenous 200 mg loading dose, followed by 100 mg once daily for 14 days; dexamethasone, 4 mg oral once daily for 15 days. Prophylactic therapies: liposomal amphotericin B, 200 mg thrice weekly; valganciclovir, 900 mg once daily; trimethoprim–sulfamethoxazole, 800 mg/160 mg once daily.

Internal Medicine JournalVolume 54, Issue 3 p. 516-517 Letter to the Editor Pleural empyema caused by Filifactor alocis in a man with periodontitis Kok T. Tan, Kok T. Tan [email protected] orcid.org/0000-0001-9097-5802 Department of Infectious Diseases, Fiona Stanley Hospital, Perth, Western Australia, AustraliaSearch for more papers by this authorPeter Boan, Peter Boan orcid.org/0000-0002-0518-0421 Department of Infectious Diseases, Fiona Stanley Hospital, Perth, Western Australia, Australia Department of Microbiology, PathWest Laboratory Medicine, Fiona Stanley Hospital, Perth, Western Australia, AustraliaSearch for more papers by this authorChristopher H. Heath, Christopher H. Heath orcid.org/0000-0001-7850-6931 Department of Infectious Diseases, Fiona Stanley Hospital, Perth, Western Australia, Australia Department of Microbiology, PathWest Laboratory Medicine, Fiona Stanley Hospital, Perth, Western Australia, AustraliaSearch for more papers by this author Kok T. Tan, Kok T. Tan [email protected] orcid.org/0000-0001-9097-5802 Department of Infectious Diseases, Fiona Stanley Hospital, Perth, Western Australia, AustraliaSearch for more papers by this authorPeter Boan, Peter Boan orcid.org/0000-0002-0518-0421 Department of Infectious Diseases, Fiona Stanley Hospital, Perth, Western Australia, Australia Department of Microbiology, PathWest Laboratory Medicine, Fiona Stanley Hospital, Perth, Western Australia, AustraliaSearch for more papers by this authorChristopher H. Heath, Christopher H. Heath orcid.org/0000-0001-7850-6931 Department of Infectious Diseases, Fiona Stanley Hospital, Perth, Western Australia, Australia Department of Microbiology, PathWest Laboratory Medicine, Fiona Stanley Hospital, Perth, Western Australia, AustraliaSearch for more papers by this author First published: 12 March 2024 https://doi.org/10.1111/imj.16353Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat No abstract is available for this article. References 1Aja E, Mangar M, Fletcher HM, Mishra A. Filifactor alocis: recent insights and advances. J Dent Res 2021; 100: 790–797. 10.1177/00220345211000656 CASPubMedWeb of Science®Google Scholar 2Dyrhovden R, Nygaard RM, Patel R, Ulvestad E, Kommedal Ø. The bacterial aetiology of pleural empyema. A descriptive and comparative metagenomic study. Clin Microbiol Infect 2019; 25: 981–986. 10.1016/j.cmi.2018.11.030 CASPubMedWeb of Science®Google Scholar 3Gray RM, Vidwans M. Mixed anaerobic thoracic empyema: the first report of Filifactor alocis causing extra-oral disease. New Microbes New Infect 2019; 29: 100528. 10.1016/j.nmni.2019.100528 CASPubMedGoogle Scholar 4Romero-Martínez R, Maher A, Àlvarez G, Figueiredo R, León R, Arredondo A. Whole genome sequencing and phenotypic analysis of antibiotic resistance in Filifactor alocis isolates. Antibiotics (Basel) 2023; 12: 1059. 10.3390/antibiotics12061059 CASPubMedGoogle Scholar 5Dyrhovden R, Eagan TM, Fløtten Ø, Siljan W, Leegaard TM, Bø B et al. Pleural empyema caused by Streptococcus intermedius and fusobacterium nucleatum – a distinct entity of pleural infections. Clin Infect Dis 2023; 77: 1361–1371. 10.1093/cid/ciad378 PubMedWeb of Science®Google Scholar 6Kostrzewa M, Nagy E, Schröttner P, Pranada A. How MALDI-TOF mass spectrometry can aid the diagnosis of hard-to-identify pathogenic bacteria – the rare and the unknown. Expert Rev Mol Diagn 2019; 19: 667–682. 10.1080/14737159.2019.1643238 CASPubMedWeb of Science®Google Scholar 7Chaddha U, Agrawal A, Feller-Kopman D, Kaul V, Shojaee S, Maldonado F et al. Use of fibrinolytics and deoxyribonuclease in adult patients with pleural empyema: a consensus statement. Lancet Respir Med 2021; 9: 1050–1064. 10.1016/S2213-2600(20)30533-6 CASPubMedWeb of Science®Google Scholar Volume54, Issue3March 2024Pages 516-517 ReferencesRelatedInformation

Coronavirus-19 (COVID-19) mortality rates among haemopoietic stem cell transplant (HSCT) patients are high, ranging between 20% and 40%. We prospectively evaluated the mortality outcomes of COVID-19 in Western Australian HSCT patients. A total of 32/492 (6.5%) HSCT recipients contracted COVID-19 during the study, of whom 30/32 (94%) developed mild or asymptomatic disease. Two allogeneic HSCT patients were hospitalised for severe COVID-19; one patient died. Stringent healthcare, social isolation practices, aggressive vaccination programmes and rapid access to COVID-19 antivirals may have promoted mild COVID-19 illness in Western Australian HSCT patients, resulting in one of the lowest COVID-19 mortality rates in HSCT recipients worldwide.

Solid organ transplant recipients (SOTRs) have poorer coronavirus disease 2019 (COVID-19) outcomes than the general population.1 Outcomes among SOTRs are improved by vaccination,2 Omicron compared with prior variant infection,3 nonlung transplant,3 younger age,1 less comorbidity,1 tixagevimab-cilgavimab preexposure prophylaxis,4 early monoclonal antibody or antiviral treatment,2,5 and convalescent plasma.6 In the general population, prior infection provides additional protection against infection and severe infection regardless of vaccination status7; however, this has not been studied specifically in SOTRs. Solera et al8 studied severity in a vaccinated population with Omicron infection, comparing those with prior infection in wild-type/alpha/delta waves to those without prior infection. They successfully propensity matched for important confounders such as age, transplanted organ, vaccination status, and comorbidities. They showed a lower rate of hospitalization (5.8% versus 19.4%) and oxygen requirement (3.9% versus 13.6%) for those with prior infection compared with primary infection and associated correlates of lower 5-d (hypoxia driven) remdesivir use, lower dexamethasone use, and lower rate of calcineurin inhibitor dose reduction. Rates of mechanical ventilation (1% versus 2.9%) and death (1% versus 2.9%) were too low to comment on the effect of prior infection on these severe outcomes. Subgroup analysis in the prior infection group was hampered by a low number of clinical events (n = 4 requiring oxygen); however, oxygen requirement was associated with lung transplant recipients and those with severe prior infection. T- and B-cell immunity were not assessed in this study. Reference is made to some of the excellent immunological work performed through the pandemic by the same group, showing prior infection with vaccination stimulates a broader antibody and better T-cell response than vaccination alone in SOTRs.9,10 Omicron infection provides higher Omicron-specific antibody and T-cell levels.9 The study reinforces generally good outcomes in SOTRs through the Omicron wave in a vaccinated population with or without prior infection. The condition of patients hospitalized and requiring oxygen could be effectively reversed with current antivirals and immunomodulation so that severe and critical infections were avoided in both groups but for a small number of patients. The patients in this trial do not represent all SOTRs. They were young (median age ~54 y), many years from transplant, vaccinated (median 4 doses), and with median 2 comorbidities. Few had estimated glomerular filtration rate <30 mL/min/1.73 m2 (12%) or recent antithymocyte globulin (1%–2%). Some had received tixagevimab-cilgavimab that has a degree of in vivo activity against about half of the variants which caused infection (BA.2 and BA.4/5), and ~60% received early remdesivir. It seems we can worry less about some vaccinated SOTRs with prior infection and provide counsel that their risk of severe outcomes appears lower. As fewer SOTRs get testing or seek out treatment for mild symptoms, a question that is being asked at the current time is, “Are we still treating mild COVID-19 in SOTRs with antivirals?” This is particularly pertinent in those units negotiating the logistical barriers of intravenous remdesivir or nirmatrelvir/ritonavir. This question is not adequately addressed by the current literature nor specifically by this study, apart from noting that ~40% did not receive early antiviral therapy. It may be that low-risk SOTRs can be identified who indeed may not require COVID-19 antiviral therapy, and among other factors, prior infection would be considered in the evaluation. For the moment, we continue treatment with interventions proven effective in early stages of the pandemic; early antiviral therapy, and dexamethasone with hypoxia.5 For SOTRs, the role of interleukin-6 receptor/JAK inhibition and background immunosuppressant are less certain.1,5 Updated management strategies continue with the development of oral remdesivir, variant-specific vaccines and variant-specific monoclonal antibodies. There is ongoing study of the optimal approach for immunosuppressed patients with persistent/relapsing infection or post–COVID-19 symptoms. So far, Omicron strains have filled an ecological niche because of increased transmissibility and immune escape. We hope that more virulent strains do not evolve.

BACKGROUND:Western Australia (WA) was in a unique position to experience coronavirus disease 2019 (COVID-19) in a highly vaccinated and geographically isolated population.AIM:To describe the COVID-19 Omicron experience at the only quaternary hospital in WA following border opening from 3 March to 11 May 2022.PARTICIPANTS:A total of 158 adults with microbiologically confirmed COVID-19 were admitted to the respiratory or intensive care unit (ICU).OUTCOMES:Admission numbers, disease severity, prevalence of COVID-19 deterioration risk factors, immunisation status, severity of infection, immunosuppression and treatment regimen.RESULTS:One hundred fifty-eight COVID-19-positive patients were admitted to the respiratory ward (n = 123) and the ICU (n = 35) during the study period. COVID-19 infection was the primary admission reason in 32.9% of patients, 51.3% were male and the median age was 62 years. Aboriginal or Torres Strait Islanders (ATSI) were overrepresented (13.3%). Care was predominantly ward based (77.2%). Nearly half of the patients had mild COVID-19 (49.4%). Dexamethasone was the most common treatment provided to patients (58.2%). The median length of stay was 5.8 days (interquartile range, 5-15). Eight patients died during the study period (5.1%), with three of those deaths attributable to COVID-19.CONCLUSIONS:COVID-19 case numbers following WA state border opening were of lower care acuity and disease severity than predicted. Two-thirds of admissions were for other primary diagnoses, with incidental COVID detection. Hospital admissions were overrepresented by partially or unvaccinated patients and by ATSI Australians. An increase in social support along with general and geriatric medicine speciality input were required to treat hospitalised COVID-19 cases in the WA Omicron wave.

Outbreaks of viruses such as West Nile virus, Zika virus, and severe acute respiratory syndrome coronavirus 2 are a concern for donor-derived infection that may have serious manifestations in a potently immunosuppressed organ recipient. For donation and transplantation, there is a focus on whether the infection has characteristic epidemiological or clinical features to prompt diagnosis; whether there are sensitive, specific, and timely diagnostic tests; the presence and duration of infectivity from donated organs; outcomes of donor-derived infection; the success of risk mitigation strategies; and the efficacy of available treatments. With enough instances of organ utilization from infected donors, knowledge is gained to guide donation and transplantation, as has occurred for coronavirus disease 2019 infection, in which transmission seems to occur only through lung and possibly intestinal donation,1 and for hepatitis C virus infection, which can be effectively cleared after transplantation. Against the risks of donor-derived infection, the transplant community balances the individual and community risks of not proceeding to organ utilization. From January 1 to September 13, 2022, there have been 58 285 laboratory-confirmed monkeypox cases and 22 deaths in 102 Member States of the World Health Organization, with highest case numbers in Europe and the United States.2 Globally, weekly case numbers are reducing2; however, the future of the outbreak is difficult to forecast. The current outbreak has characteristic epidemiology, with 95.0% identifying as men who have sex with men (MSM) and transmission occurring through sexual contact in 90.6% to 93.9% of cases.2,3 The case fatality rate is low, and death may follow the rare development of encephalitis.4 Most HIV-positive cases have had preserved CD4+ lymphocyte count and low viral load on antiretroviral therapy,5 so we are uncertain of clinical outcomes in potently immunosuppressed people. In human studies, virus has been cultured from oropharyngeal, anal, urethral, and skin swabs. Polymerase chain reaction (PCR) is positive in blood and urine, with blood viral load highest during the prodromal and early symptomatic phases of illness.6-8 Animal studies of orthopoxvirus infection following acquisition through the respiratory route show lymphohematogenous spread to the bone marrow, spleen, liver, lungs, kidneys, heart, intestine, and other organs.9,10 Donor assessment should elicit contact with monkeypox in the prior 21 d (the upper range of the incubation period) and involve careful evaluation of donors who are MSM. Focus is on sexual behavior in MSM, increasing the risk of monkeypox infection and examination of MSM for skin lesions at genital, perianal, and oropharyngeal sites. PCR of skin lesion material (fluid, tissue, crust) from several lesions obtained through vigorous swabbing is recommended for diagnosis. It is acknowledged that donor infection in the prodromal and early clinical phase of illness might be missed and present a risk of transmission because the blood viral load is highest at this time.8-10 There is no simple method to detect and diagnose such cases, which should be rare. One hopes that they may have been identified as a close contact, and in these special cases in which there are no skin lesions, PCR of oropharynx swab, anorectal swab, and blood may be considered, although these should not be routine sample sites. With characteristic epidemiology, none of the transplantation bodies currently suggest asymptomatic donor screening, such as through oropharyngeal and/or anorectal PCR (Transplantation Society of Australia and New Zealand [TSANZ], 2022, email memorandum to members),11,12 which would predictably lead to false-positive PCR results and delays because of test turnaround. Based on current limited clinical information and positive viral culture of blood and organs in animal studies, Table 1 shows that transplantation bodies agree that donation should not proceed from actively infected donors (TSANZ),11,12 generally, until skin lesions have scabbed and skin has reepithelialized (TSANZ).12 There are no reports of donor-derived infection, but if this were to occur, treatment is recommended for immunosuppressed people. Tecovirimat has been predominately used and is well tolerated,13 and combination treatment may be considered. TABLE 1. - Management by transplantation societies of United States, United Kingdom, and Australia of solid organ donation from donors infected, recovered, or in contact with monkeypox virus AST 12 NHSBT 11 TSANZ Actively infected cases Proven cases not suitable Proven, probable, and possible cases not suitable Proven, probable, and possible cases not suitable Consideration of donation in recovered cases When all lesions scabbed and skin reepithelialized Eight weeks after recovery When released from isolation (lesions scabbed and skin reepithelialized) Donor contact with monkeypox in the previous 21 d Risk–benefit discussion if high-risk contact Medium- and high-risk contact not suitable. Low-risk contact donation can be considered Consider in exceptional circumstances if high- or medium-risk contact AST, American Society of Transplantation; NHSBT, National Health Service Blood and Transplant; TSANZ, Transplantation Society of Australia and New Zealand. Vaccination used for pre- and postexposure prophylaxis is predominately replication incompetent modified vaccinia Ankara vaccine that poses no risk of transmission from donor to recipient (available as JYNNEOS in the United States and Australia, IMVAMUNE in Canada, IMVANEX in the Europe Union). Uncommonly replication-competent vaccinia virus-based vaccines such as ACAM2000 will be used. As virus may be cultured from the inoculation site to day 42 after vaccination,14 the Food and Drug Administration suggests deferral of blood donation until the vaccine scab has spontaneously separated from the skin (which usually occurs 14–21 d after vaccination).15 The risk of transmission through organ transplantation is probably small because the orthopoxvirus seems localized in this situation, not detected in the blood of 60 vaccines in one study.14 Monkeypox occurs characteristically in MSM presenting with rash, allowing a focus on specific donors at risk for infection and a diagnostic (lesion PCR) rather than screening approach in donors. Screening routine donors without clinical features of monkeypox infection is not recommended. Transmission is unlikely through donor ACAM2000 vaccination. We should follow transplantation society guidance regarding donors infected, recovering, or who have had contact with monkeypox virus. Guidance may evolve if the monkeypox outbreak continues, and we learn from unstable waitlisted patients who receive organs from infected or recovered donors under the cover of antiviral therapy.

Patients can be immunocompromised from a diverse range of disease and treatment factors, including malignancies, autoimmune disorders and their treatments, and organ and stem-cell transplantation. Infections are a leading cause of morbidity and mortality in immunocompromised patients, and the disease treatment landscape is continually evolving. Despite being a critical but preventable and curable adverse event, the reporting of infection events in randomised trials lacks sufficient detail while inconsistency of categorisation and definition of infections in observational and registry studies limits comparability and future pooling of data. A core reporting dataset consisting of category, site, severity, organism, and endpoints was developed as a minimum standard for reporting of infection events in immunocompromised patients across study types. Further additional information is recommended depending on study type. The standardised reporting of infectious events and attributable complications in immunocompromised patients will improve diagnostic, treatment, and prevention approaches and facilitate future research in this patient group.

Background: Cytomegalovirus (CMV) is a common cause of morbidity after allogeneic haematopoietic cell transplantation (alloHCT). Pre-emptive therapy (PET) with valganciclovir (VGC) is associated with haematological toxicity. Methods: We included alloHCT patients from 2018 to 2021 where letermovir (LTV) was used for CMVPET because of cytopenias. Results: Ten patients were included. Six received VGC prior to LTV. VGC was commenced at median d42, given for median 40 days. LTV was commenced at median d90, given for median 54 days. At commencement of antiviral, CMV viral load was higher for VGC at 3.7 log10 IU/mL, compared to LTV at 2.9 log10 IU/mL. Viral load reduction occurred at 0.18 log10 IU/mL per week forVGC, compared to 0.17 log10 IU/mL per week for LTV. There was no clinically significant CMVviremia after stopping LTV. Cytopenias improved on LTV. Conclusion: LTV was effective in controlling CMVviremiawhen it was given at a lower starting CMV viral load and later post alloHCT than VGC. Further study is required of LTV as upfront PET following alloHCT.

BACKGROUND:Western Australia (WA) serves as a unique global case study on the impact of coronavirus disease 2019 (COVID-19) on an isolated, prepared and highly vaccinated population. This study builds upon the study performed by House et al. through an extended data set. AIM:To examine the impact of COVID-19 at the only quaternary hospital in WA following the border opening from 3 March to 17 July 2022. PARTICIPANTS:A total of 257 adults were admitted with COVID-19 under either respiratory or the intensive care unit (ICU). OUTCOMES:Admission numbers, disease severity, ICU admission, prevalence of COVID-19 deterioration risk factors, length of stay and mortality. RESULTS:A total of 257 patients were admitted with COVID-19, under respiratory (81.7%) and ICU (18.3%). COVID-19 was the primary reason for admission for 67.7%. Ten patients died during the study, with seven deaths attributed to COVID pneumonitis. COVID-19 severity was 37.4% mild, 37.0% moderate, 18.3% severe and 7.4% critical. Risk factors for requiring ICU included incomplete immunisation status (P = 0.011), chronic kidney disease (P = 0.008) and Aboriginal and Torres Strait Islander (ATSI) ethnicity. The WA Department of Health predicted that the number of hospitalisations and ICU cases were significantly higher than the actual number of cases. CONCLUSION:The number of hospitalisations and ICU COVID-19 cases were significantly less than predicted, likely due to high population vaccination rates prior to border opening. The main risk factors for COVID-19 severity were incomplete immunisation and ATSI ethnicity.

Hyperammonemia syndrome (HS) is a life-threatening condition occurring in solid organ transplant patients, affecting primarily lung recipients, and is associated with Mycoplasma hominis and/or Ureaplasma spp infection. The organ donor was a young man who died of hypoxic brain injury and had urethral discharge antemortem. The donor and 4 solid organ transplant recipients had infection with M hominis and/or Ureaplasma spp. The lung and heart recipients both developed altered conscious state and HS associated with M hominis and Ureaplasma spp infections. Despite treatment with antibiotics and ammonia scavengers, both the lung and heart recipients died at day +102 and day +254, respectively. After diagnosis in the thoracic recipients, screening samples from the liver recipient and 1 kidney recipient were culture positive for M hominis with or without Ureaplasma spp. Neither the liver nor kidney recipients developed HS. Our case series demonstrates the unique finding of M hominis and Ureaplasma spp dissemination from an immunocompetent donor across 4 different organ recipients. Phylogenetic whole genome sequencing analysis demonstrated that M hominis samples from recipients and donor were closely related, suggesting donor-derived infection. Screening of lung donors and/or recipients for Mycoplasma and Ureaplasma spp is recommended, as well as prompt treatment with antimicrobials to prevent morbidity.

Context/Objective Prevention of urinary tract infection (UTI) after spinal cord injury is an important goal. Intravesical hyaluronic acid with chondroitin sulphate (HA+CS) has been effective in preventing UTI in other settings. We aimed to demonstrate safety and feasibility of a standard treatment course of 7 intravesical HA+CS instillations over 12 weeks, in patients with acute (Arm A) and chronic (Arm B) spinal cord injury (SCI). Design Follow-up of adverse events, quality of life bladder management difficulty (BMD) and bladder complication (BC) T-scores at baseline (Arm B only), 12 and 24 weeks, and symptomatic urinary tract infection (UTI). Results Of 33 and 14 individuals screened, 2 and 8 participants were recruited to the study for Arm A and Arm B respectively. Of the 10 participants, 8 completed all 7 instillations. HA+CS commonly caused cloudy urine with urinary sediment which was mild and short-lived. In Arm B, a mean reduction in BMD and BC T-scores was observed from baseline (57.3 and 54.4 respectively), of 6.8 and 4.3 at 12 weeks and 1.6 and 2.8 at 24 weeks, respectively. Four participants with a history of frequent UTI in the prior 12 months did not have UTI in the 24 weeks of the study. Conclusions HA+CS was well tolerated. Recruitment was more difficult in early acute SCI; participants with chronic SCI were highly motivated to reduce UTI and manage self-administration without difficulty. Larger case-control or randomized controlled trials in patients with neurogenic bladder from SCI are warranted.

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