Peter Boan

Mycobacterium chimaera colonisation of heater–cooler units (HCU) in western australia, 2015: Investigation of possible iatrogenic infection using whole genome sequencing

Following the reported link between heater–cooler unit (HCU) colonisation with Mycobacterium chimaera and endocarditis, mycobacterial sampling of all HCUs in use in Western Australia was initiated from August 2015, revealing M. chimaera colonisation in 10 of 15 HCUs. After M. chimaera was isolated from a pleural biopsy from a cardiothoracic patient who may have been exposed to a colonised HCU, a whole genome sequencing investigation was performed involving 65 specimens from 15 HCUs across five hospitals to assess if this infection was related to the HCU. Genetic relatedness was found between the 10 HCU M. chimaera isolates from four hospitals. However the M. chimaera isolate from the cardiothoracic patient was not genetically related to the HCU M. chimaera isolates from that hospital, nor to the other HCU isolates, indicating that the HCUs were not the source of the infection in this patient.

Penicillium marneffei infection in a lung transplant recipient.

Penicillium marneffei is a thermally dimorphic fungus that can cause severe opportunistic infections in endemic regions of Southeast Asia, particularly in individuals infected with human immunodeficiency virus‐1, but has rarely been reported in solid organ transplant recipients. Herein, we report the first case, to our knowledge, of P. marneffei infection in a lung transplant recipient, occurring in a 41‐year‐old woman 28 months post lung transplantation, after recent travel to Vietnam. We have reviewed the literature to derive some management principles for this rare infection in this clinical context. The number of P. marneffei infections in transplant recipients may increase, as a result of increasing rates of transplantation and travel to endemic areas.

Refractory Arthrographis kalrae native knee joint infection.

Rare reports of infection with Arthrographis kalrae have often demonstrated a protracted clinical course. We describe refractory infection of the native knee with Arthrographis kalrae after a penetrating injury and Yttrium synovectomy, finally controlled with two stage joint revision and combination antifungal therapy. The paucity of worldwide data about such uncommon invasive fungal infections contributes to the diagnostic and therapeutic challenges of these cases.

False positive hepatitis B virus core and surface antibodies due to intravenous immunoglobulin

A 60-year-old man was diagnosed in October 2014 with chronic inflammatory demyelinating polyneuropathy. Initially, he had a partial clinical response to intravenous immunoglobulin (IVIg) therapy and high-dose oral prednisolone (1 mg/kg per day). However, by August 2015 he had relapsed and remained bed bound despite ongoing treatment with IVIg and corticosteroids. Given the pressing need to start additional immunosuppression and in order to expedite glucocorticoid weaning, 1000 mg monthly cyclophosphamide was commenced. As per expert guidelines, he was considered to be at moderate risk of hepatitis B virus (HBV) reactivation if present. HBV screening was performed by Abbott Architect assays on the Abbott i1000SR instrument (Abbott Australasia, Sydney, NSW, Australia), which was performed 13 days following the most recent IVIg infusion (Table 1, Sample:cutoff values >1 are positive). As he tested HB core antibody (HBcAb) positive, lamivudine antiviral prophylaxis was commenced as suggested by the American Gastroenterological Association Institute guidelines 2015, regardless of the plasma HBV DNA result (which was negative in this case). Using stored patient serum from June 2015, we were able to demonstrate that the patient was HBcAb negative, prior to the Batch A IVIg infusion. Subsequent testing in August and September 2015 revealed a decrease in HBcAb levels, suggesting Batch A of IVIg was primarily responsible for the positive HBcAb result from August. Our laboratory’s HBcAb assay does not give a fully quantitative result. However, we felt our hypothesis was strengthened by the reduction of the HBcAb sample:cutoff ratio congruent with the expected half-life of immunogloblin G. Accordingly, lamivudine was ceased. We suspect HB surface antibody (sAb) was also transfused from IVIg as the patient tested HBsAb negative in 2009, had no history of HBV vaccination, and (like HBcAb) the titre reduced appropriately following Batch A IVIg. We confirmed that the IVIg infused contains HBsAb and HBcAb (Table 1). IVIg is made from over 1000 pooled human donors containing a heterogeneous mixture of naturally occurring antibodies, including autoantibodies and antibodies active against infectious agents. As IgG1 typically has a half-life of 18–23 days (with subclass variation), patients may develop transient detectable antibodies to a range of infectious agents, including hepatitis A, B and C viruses; cytomegalovirus; varicella zoster virus; EpsteinBarr virus; parvovirus B19; Treponema pallidum and Borrelia burgdorferi. In Australia, blood products including IVIg undergo mandatory testing that includes HBV surface antigen, antibodies to human immunodeficiency virus (HIV) and hepatitis C and nucleic acid testing for hepatitis A, B, C and HIV. There is currently no requirement to test for HBcAb as its presence alone does not imply an infection risk. As we have demonstrated, a study from the United Kingdom also reported detectable HBV core antibody in commercial preparations of IVIg. In our case, misinterpretation of passive transfusion of HBcAb resulted in the inappropriate prescription of lamivudine, in another reported case a liver biopsy was performed. Based on our experience, prior to commencing IVIg we advocate hepatitis virus screening and storage of serum in case retrospective infectious diseases antibody testing is required. Clinicians need to be aware of the potential for false positive infectious serologies and autoantibodies after IVIg, which may lead to unnecessary investigation and

Neisseria meningitidis porA, fetA and fHbp gene distribution in Western Australia 2000 to 2011

BackgroundPorA, fetA and fHbp are three antigen encoding genes useful for meningococcal typing and FHbp is an important component of meningococcal B vaccines.MethodsWe performed sequence analysis of meningococcal porA, fetA and fHbp genes on 128 isolates from Western Australia, relating results to age, gender, race and geographic region.ResultsWe found predominantly PorA subtypes P1.22,14-16 (n = 23) and P1.7-2,4 (n = 19); FetA subtypes F1-5 (n = 41), F3-6 (n = 11), F5-1 (n = 10), F5-2 (n = 9), F5-5 (n = 8), F3-3 (n = 8); and FHbp variant groups 1 (n = 65) and 2 (n = 44). PorA P1.22,14-16 and FHbp variant group 2 were associated with younger age and aboriginality.ConclusionsFHbp modular groups of the bivalent recombinant FHbp vaccine and the multicomponent 4CMenB vaccine make up 8.3% and 47.7% respectively of the examined serogroup B isolates from 2000–2011, however to estimate vaccine efficacy requires an account of all vaccine antigens and their levels of expression.

Analysis of the QuantiFERON-CMV assay, CMV viraemia and antiviral treatment following solid organ transplantation in Western Australia

Prevention of cytomegalovirus (CMV) infection remains an important aspect of improving long term outcomes of solid organ transplantation and currently relies on prophylactic antiviral medication and early detection of viraemia or disease. Uptake of diagnostic tools to personalise assessment of CMV immunity and guide interpretation of viral testing remains low. We assessed the QuantiFERON-CMV assay in 54 Western Australian recipients of renal, heart, lung or liver allografts to determine the relationship between CMV-specific immunity, viraemia and disease following cessation of antiviral prophylaxis. We carried out an initial validation study which demonstrated that the QuantiFERON-CMV assay is highly precise and strongly correlated with CMV-specific antibodies in 30 healthy blood donors (sensitivity 82%, specificity 95%). In the solid organ transplant recipients we examined, the prevalence of asymptomatic CMV viraemia was high at 61% but only two patients ultimately developed CMV disease, both of whom had negative QuantiFERON-CMV responses, indicating lack of CMV T-cell immunity. The vast majority (94%) of patients who had spontaneous resolution or stability of asymptomatic CMV viraemia without any antiviral treatment had positive QuantiFERON-CMV responses. Positive QuantiFERON-CMV responses at cessation of antiviral prophylaxis were significantly associated with pre-transplant CMV seropositivity and the development of asymptomatic viraemia post-transplantation. Overall, 27% of patients were recommenced on antiviral therapy because of asymptomatic CMV viraemia. Patients with non-reactive QuantiFERON-CMV responses had earlier onset, higher level CMV viraemia compared to those with positive QuantiFERON-CMV responses, although the difference did not reach statistical significance. QuantiFERON-CMV results may contribute to decision making in concert with the serological risk profile, net state of immunosuppression and CMV viral load.

Mould meningitis associated with intravenous drug use

Fungal meningitis is most commonly causes by Cryptococcus species and dimorphic fungi. We present a rare case of mould meningitis, ventriculitis and subependymal nodules in an immunocompetent patient, having likely seeded the meninges and ventricular system through intravenous drug use. The causative mould remains undetermined. The case highlights the poor sensitivity of CSF culture and the need to consider surgical biopsy where there is diagnostic difficulty and fungal infection is being considered.

Infectious complications in indigenous renal transplant recipients in Western Australia: Infection in indigenous renal transplants

Infectious complications remain a significant risk following renal transplantation.