To the Editor: A previously healthy young man with a 1-day history of fever and a rash receives a clinical diagnosis of chickenpox from his general practitioner. Should he be treated with an antiviral drug such as aciclovir?

Following the inclusion of a single dose of varicella vaccine in the National Immunisation Program Schedule in 2005, the incidence of varicella (chickenpox) and its complications appears to be declining, with the total number of hospitalisations per year in Australia probably now around 400–500.1 Similar trends have been observed
in the United States. In spite of the immunisation program, around
5%–10% of adults in Australia remain non-immune to varicella infection. The disease may lead to significant morbidity and mortality in otherwise healthy adolescents and adults. The main potentially serious complication is pneumonitis, particularly in people who smoke and pregnant women.

There is anecdotal evidence that otherwise healthy adolescents and adults presenting to emergency departments (EDs) with varicella are likely to receive an antiviral drug,
but the same is not true in general practice. In the latest version of Therapeutic guidelines: antibiotic there is no recommendation for early (oral) antiviral therapy for all adults with varicella.2 This is of concern if one considers the fact that antiviral therapy is most effective when started early in the course of varicella and is likely to reduce the rate and severity of complications.3 Guidelines in the US and the United Kingdom, on the other hand, recommend antiviral therapy for early, uncomplicated varicella in adolescents and adults.4–6 Additional benefits of treating varicella potentially include reducing demands on EDs, decreasing the risk of transmission to nonimmune individuals (particularly immuno-compromised patients) and a cost-benefit to the taxpayer.

The Pharmaceutical Benefits Scheme indications for aciclovir (or the alternative antiviral drugs) in its various orally active forms do not include varicella. Aciclovir is expensive in Australia when purchased at retail pharmacies without an authority prescription, costing $85–$135 for 35 generic aciclovir 800 mg tablets.

A formal Australian recommendation for antiviral therapy without the backing of public funding would likely compromise GP management of acute varicella
cases. Given the low and decreasing incidence of varicella in the adolescent and adult population, a funded recommendation would lead to little overall cost incurred by the taxpayer — but would possibly save several Australian lives each year.

One of the most concerning emerging resistance traits among gram-negative bacteria is the ability of these organisms to produce carbapenem-hydrolysing β-lactamases, which confer resistance to almost all β-lactams.1 Carbapenem-resistant Enterobacteriaceae (CRE) are increasing in prevalence worldwide, causing growing concern, as they are often combined with non-β-lactam resistance to produce isolates that are multidrug resistant, have few treatment options available and are associated with high mortality rates.2

Although multiple resistance mechanisms have been identified, carbapenem resistance is often plasmid-encoded, allowing gene dissemination and a propensity to cause nosocomial outbreaks.3–6

We describe a CRE outbreak due to the presence of the metallo-β-lactamase gene blaIMP-4 in an intensive care unit (ICU) associated with contaminated sinks. This report highlights the key role of bacterial environmental contamination and sink design and usage in the propagation of CRE outbreaks.

Dandenong Hospital is a 440-bed tertiary referral hospital in Melbourne, Australia. The ICU has a 14-bed capacity, admitting both medical and surgical patients and averaging 1400 admissions yearly.

Ten ICU patients were found to have clinical specimens with Enterobacteriaceae harbouring the blaIMP-4 gene between November 2009 and July 2012. The ICU routinely screens for vancomycin-resistant enterococci (VRE) carriage using rectal swabs on admission, weekly and on discharge. During the 4-week period from 6 September to 4 October 2012, CRE screening was performed in addition to the routine screen for VRE.

Environmental screening for CRE targeting all 28 wet area locations (including 11 sinks and taps, as well as water fountains and ice machines) was performed. Samples were recollected from CRE positive locations after successive decontamination attempts. A total of 97 samples were collected from taps, water, grates and drains (10 cm down and above the water trap interface where biofilm may be expected to persist).

All environmental and patient screening swabs were cultured onto chromogenic agar (Brilliance CRE Agar, Oxoid). Suspect colonies were further characterised using the modified Hodge test and VITEK 2 (Biomérieux). All isolates with a meropenem minimum inhibitory concentration (MIC) ≥ 0.25 mg/L and a positive modified Hodge test result were forwarded for confirmation by polymerase chain reaction and molecular sequencing. Molecular typing using pulsed field gel electrophoresis (PFGE) was conducted on clinical and environmental isolates and interpreted as per the reference guidelines.7

Guidelines on ICU handwashing sink styles were reviewed to establish whether sinks met clinical design standards.8

Ten clinical isolates (Klebsiella pneumoniae [n = 5], Serratia marcescens [n = 4] and Enterobacter cloacae [n = 1]) and one screening isolate (Escherichia coli) containing the blaIMP-4 gene were detected over the 30-month period. There were four distinct CRE clusters, commencing with three cases of K. pneumoniae in November 2009, followed by two cases of S. marcescens 6 months later, three cases (two S. marcescens and one E. cloacae) after another 11 months, and three cases of K. pneumoniae in July 2012.

Clinical characteristics, patient demographics and ICU admission details of all 11 patients are summarised in Box 1. Patients acquired CRE after a median length of stay in ICU of 10 days (range, 3–134 days). No patient died due to clinical CRE infection. Patient 1 had a prolonged CRE bacteraemia that responded to removal of a central venous catheter, the presumed source of infection.

A total of 111 rectal swabs were collected from 71 patients. Only one patient (Patient 11) was CRE-positive with an E. coli isolate detected.

Antibiotic resistance profiles of clinical isolates indicated resistance to β-lactams and meropenem with MICs ≥ 1 mg/L. All S. marcescens clinical isolates were sensitive to piperacillin/tazobactam, ciprofloxacin and amikacin, while K. pneumoniae and E. coli were only sensitive to amikacin. S. marcescens environmental isolates showed a higher meropenem MIC of ≥ 16 mg/L.

S. marcescens was the only species recovered from environmental samples and was isolated persistently, even after six attempts to decontaminate the grates and drains of eight of the 11 central sinks in the ICU. Tap spout and water cultures were negative for CRE.

Three of the four S. marcescens clinical isolates from 2010 and 2011 were indistinguishable or closely related by PFGE to four isolates from sinks. S. marcescens was isolated from an intercostal catheter swab of Patient 4, matching two sink isolates; Patient 5 had an endotracheal aspirate identical to two different sink locations; and the urine isolate from Patient 6 was closely related to a different sink. The isolate from Patient 7 was unable to be typed by PFGE.

Sink inspection revealed aged and deteriorating porcelain, even though sinks were only installed in 2005. Sink design did not comply with Australasian clinical design standards,8 with a small, shallow sink and a tap that directed water over the drain (Box 2). The design of the ICU sinks led to poor use for hand hygiene (although measured hand hygiene compliance using alcoholic hand rub was around 70% within the unit) and the potential for organisms residing down the drain to be splashed back onto staff hands or contaminate patient areas. It was also revealed that the handwashing sinks had been used incorrectly, with staff disposing clinical waste and residual antibiotics directly into drains. Further enquiry also revealed that a single brush had been used to clean down the drains of all sinks in the ICU without disinfection between sinks.

Cleaning was attempted in an effort to rid the organisms from the sinks. First, cleaning of grates and drains using single-use, soft brushes was attempted, but repeat screening revealed continued CRE growth. Next, in addition to the brushes, hypochlorite deep cleaning was used after the scrub; however, heavy CRE growth was again evident 1 week later. Finally, an attempt using pressurised steam decontamination (Jetsteam Maxi with plunger tool attachment, Duplex) for 1 minute at 170°C on grates and drains appeared to eradicate almost all CRE at Day 1 (one sink remained colonised); however, repeat testing 3 days after steam treatment showed re-emergence of CRE in all previously affected sinks.

We report an outbreak of CRE in an ICU with identical organisms isolated from patients and an environmental source (sinks).

Dissemination of carbapenemase-resistant bacteria has been reported previously in an ICU in Australia, with 62 patients infected or colonised with gram-negative bacteria from multiple genera containing the blaIMP-4 gene.9 The gene is carried on a highly mobile plasmid making it efficient for nosocomial transmission. The gene can reside in multiple genera of hardy environmental organisms that can establish a reservoir within biofilm.

Identifying the outbreak using molecular methods allowed us to establish clonality between clinical and environmental isolates and to propose a mechanism whereby patient contamination may have occurred. Although we cannot prove that the sinks were the source of patient infection, the persistence of the organism within the environment was a concern. Attempts at sink sterilisation were futile, and complete eradication will require future sink removal and replacement with appropriately designed sinks.

Others have reported outbreaks of multiresistant bacteria such as extended-spectrum β-lactamase-producing K. pneumoniae linked to imperfect sink design requiring sink cleaning, replacement and/or improved sink practices to successfully control the outbreaks.10

Our data should act as a reminder on the importance of appropriate hospital design, adequate environmental cleaning and antimicrobial stewardship in the hospital setting.

2 Existing design of intensive care unit sink compared with a design that complies with Australasian standards8

A: Existing sink, showing water spray directly over drain. B: Compliant sink design, showing larger basin and less forceful water flow directed away from drain, to prevent splash back and contamination with drain contents.

Randomised controlled trials (RCTs) are accepted as the best type of study to assess the effects of health care interventions and therefore have a pivotal role in evidence-based medicine.1 A new paradigm is emerging whereby RCTs are now being undertaken by a network of clinicians.2

Clinician-initiated RCTs have several features that differentiate them from industry-sponsored studies. They are more likely to compare generically available, off-patent medications, or to study processes of care or non-pharmacological interventions. As clinician-initiated trials are financially independent of industry, with their funding source being governmental research organisations (eg, the National Health and Medical Research Council [NHMRC]), the results are viewed by clinicians as more credible.3 The NHMRC has already demonstrated a willingness to fund clinician-initiated RCTs, as shown by the success of networks such as the Australian and New Zealand Intensive Care Society Clinical Trials Group.4–7 The impact of their successfully completed trials on practice change, cost savings and improved patient outcomes has not been formally measured but is likely to be significant.

Another key advantage is that clinician-initiated RCTs tend to investigate issues that clinicians find most important and relevant to their practice. Moreover, the process of engagement with other clinicians is a crucial one. If investigator-initiated studies are to successfully recruit patients, there needs to be an appreciation by other clinicians that the studies have realistic comparators and clinically significant end points.

To facilitate physician engagement and training in clinical trials methodology, the Australasian Society for Infectious Diseases Clinical Research Network (ASID CRN) was established in 2009. This report summarises the results of an online survey of infectious diseases physicians, conducted by the ASID CRN, to establish its research priorities.

In 2012, a self-reported online questionnaire-based survey was administered on behalf of the steering group of the ASID CRN. The survey was developed by the ASID CRN steering group, who compiled a list of more than 100 potential studies: 42 potential randomised controlled trials, 20 epidemiological studies and 40 observational studies/registries. These studies pertained to bacterial infections (69 of the nominated studies), viral infections (18), fungal infections (10), mycobacterial infections (3) and general aspects of clinical infectious diseases practice (3).

A “short list” of these studies was selected by the ASID CRN steering group to be sent to the entire community of members of ASID, comprising most practising infectious diseases physicians in Australia and New Zealand. The ASID members were asked to rate the proposed studies within each group: (a) RCTs, (b) epidemiological studies, and (c) registries of specific infectious diseases, using a numerical scale (with 1 being of little likely clinical significance and 5 being of greatest clinical significance).

To determine the feasibility of the proposed studies, the physicians were also asked to estimate the number of patients seen at their hospital in the past year with each of the conditions relevant to the proposed clinical trial. Additionally, they were asked to describe barriers to enrolment of study patients at their hospital.

Of the 550 clinicians approached online, 122 (22%) responded to the survey. The RCTs ranked by the ASID members as having most potential clinical significance are listed in Box 1. Foremost among these were RCTs investigating prosthetic joint infections, native joint septic arthritis or osteomyelitis, Staphylococcus aureus bloodstream infections, foot infection in diabetes and serious infections due to gram-negative bacilli. Clinician estimates of case loads per annum, and hence the number of subjects eligible for recruitment into these studies, ranged from 600 to 700 for the studies on prosthetic joint infection and gram-negative bacilli; 1000 to 2000 for those on native joint infections; and 2700 for foot infections in diabetes.

The surveyed clinicians also supported further study of emerging infections (eg, multi- or extensively drug-resistant tuberculosis or unexplained encephalitis) by way of registries or epidemiological studies.

Barriers to performance of clinician-initiated studies are listed in Box 2. The most commonly perceived barrier was lack of funding for conducting studies, followed by absence of infrastructure or study personnel, and lack of time owing to clinical commitments.

A number of features dominated the research preferences of Australian and New Zealand infectious diseases physicians. RCTs investigating optimal treatment of commonly encountered infections were highly ranked, highlighting the lack of well conducted RCTs in this area. Investigations into optimal therapy of antibiotic-resistant organisms were also identified as a priority.

Clinician-initiated research presents a number of advantages over research sponsored by pharmaceutical companies. The primary focus of clinician-initiated research is to answer problems of direct clinical relevance, while that of pharmaceutical companies is to obtain regulatory approval for new, patented products. Additionally, the impact of clinician-focused research is, in many cases, cost-savings to the health care system, while that of company-initiated research is the introduction of new and often expensive drugs or devices. As an example, the four highest-ranked RCTs proposed by Australian and New Zealand infectious diseases physicians dealt with reducing the duration of courses of intravenous antibiotics (Box 1). RCTs whereby medications are used less are unlikely to be of interest to industry. RCTs that allow the rigorous evaluation of recommendations in guidelines are likely to be of particular value to clinicians, and those that reduce the duration of intravenous antibiotic courses are likely to reduce costs for governments and, potentially, reduce adverse events for patients.

Steering groups, comprising both researchers and clinicians, have now been established to develop protocols, seek funding for the trials and initiate the studies most highly ranked by clinicians.

Could the methodology and results of our survey of infectious diseases physicians be of use to other clinicians? More than 90 research networks of collaborating clinicians currently exist in Australia (http://australianclinicaltrials.gov.au/). Some of these networks are well established and have been highly productive, completing a number of high-impact studies.4–9 Others are nascent, like our own, and may seek to replicate our methodology.

There are significant challenges in the initiation and conduct of clinician-initiated studies. Foremost of these is funding, which was regarded in our survey as the single largest barrier to studies being conducted. Other potential difficulties included time-consuming processes for (and cost of) ethical approval, and lack of support and infrastructure in cash-strapped hospital systems. Innovative solutions to these barriers should be sought — other research networks (eg, Australian and New Zealand Intensive Care Society Clinical Trials Group) have received funding from foundations and the NHMRC. In addition, the private hospital system may be an untapped resource for clinician and administrative support.

A limitation of our study was the low response rate of 22%. This is to be expected given the nature of online surveys. The research priorities chosen may not necessarily reflect those of all members of ASID.

We have described here a method for giving practising clinicians a central role in the selection of clinical studies. We hope that this will facilitate not just the planning and conduct of these studies, but also their rapid implementation into clinical practice.

Hepatitis C virus (HCV) has emerged worldwide as a major infectious disease. An estimated 221 000 Australians (about 1% of the population) were living with chronic hepatitis C by the end of 2010, and HCV infection is now the most common indication for liver transplantation.1,2 While HCV diagnosis rates have declined nationally over the past 10 years, the persistence of risk behaviours, and the relatively limited uptake of HCV treatment (only 3760 Australians were treated for HCV infection in 2010) suggest that the epidemic is ongoing.1

Public health measures to curb HCV infection in Australia have focused on harm reduction. Injecting drug use (IDU) remains the predominant risk factor,3 but there has been accumulating evidence of sexual (permucosal) transmission over the past decade. Two per cent of the 899 newly acquired Australian cases from 1997 to 2000 were considered related to sexual contact,4 and more recent recognition of HCV–HIV co-infection in men who have sex with men (MSM) has prompted reconsideration of what constitutes blood-to-blood contact.5–7 Several studies of HIV-infected MSM have identified specific risk factors for HCV transmission: group sex, unprotected intercourse, fisting (inserting a hand into the rectum), non-injecting (ie, nasal or rectal) drug use, use of sex toys, and concurrent genital ulceration.6,8–10 Notably, reports of sexually transmitted HCV in HIV-negative MSM remain rare. Nonetheless, with the accelerated progression of liver fibrosis in patients co-infected with HCV–HIV now well established, co-infection has become a key issue, with liver disease-related mortality ranking as one of the leading causes of death among HIV-infected individuals in the developed world.11,12

The prevalence of HCV co-infection in Australians living with HIV was estimated at 13.1% in 2002 and 9.9% in 2010, with most co-infected individuals reporting IDU as a risk factor.1,13 One Melbourne sexual health clinic, however, identified 24 patients with newly acquired HCV without a history of IDU among 620 HIV-infected MSM over an 8-year period up to March 2010.14 We aimed to examine HCV acquisition among HIV-infected MSM in Victoria and to determine the relevance of novel risk factors within this group.

We undertook a retrospective review of all cases of HCV notified to the Victorian Department of Health from 1 April 2010 to 30 June 2011. The investigation began in April 2011, with subsequent cases examined prospectively. Hepatitis C is a nationally notifiable disease; in Victoria, medical practitioners and laboratories are legally required to notify the Department of Health. From these notifications we delineated a case series of newly acquired HCV infection in MSM infected with HIV (Box 1).

High-caseload centres were the focus of our investigation, including general practitioner clinics specialising in HIV medicine and infectious diseases services. All notifications from these centres were crosschecked with the Victorian HIV Registry (Centre for Population Health, Burnet Institute, Melbourne) to identify patients with co-infection. We undertook the same process for any doctors’ notifications where MSM behaviour was indicated. A standard definition of newly acquired HCV was used, based on any one of: antibody seroconversion in the previous 24 months, new viraemia with a negative antibody test in the previous 24 months, or unexplained alanine aminotransaminase (ALT) elevation (at least 350 U/L; reference interval, 5–50 U/L) at first positive antibody or HCV RNA detection.15

For these patients, we gathered epidemiological data from the following sources:

• Enhanced surveillance data from notifications of hepatitis C by clinicians;16

• The Victorian Infectious Diseases Reference Laboratory (VIDRL) for HCV genotyping, HIV viral loads, CD4+ lymphocyte counts and results of syphilis serology. We defined recent HIV monitoring as any results within 3 months of HCV diagnosis. We looked for syphilis serology results indicating infectiousness (a fourfold or greater rise in rapid plasma reagin titre plus a reactive specific treponemal test);
• The Department of Health Notifiable Infectious Diseases Surveillance database, to identify sexually transmitted infection (STI) notifications in the 12 months before hepatitis C notification;
• A cluster-specific questionnaire examining risk factors for HCV acquisition, which was designed by the authors, the Sexual Health and Viral Hepatitis team at the Department of Health, and the Partner Notification Officers (PNOs). Patients were first contacted by their treating doctor to seek informed consent. The PNOs then conducted the questionnaire by telephone with consenting patients who had been de-identified.

To examine whether specific strains of HCV were being transmitted, VIDRL staff performed sequence analysis of HCV isolates from a random selection of patients. The HCV genotype and subtype of samples were determined using a commercially available assay, VERSANT Hepatitis C Virus Genotype Assay (LiPA) version 2.0 (Siemens Healthcare Diagnostics). Further discrimination was carried out by sequence analysis of the HCV core region.17 Sequences were aligned with references using ClustalW and BioEdit (http://www.mbio. ncsu.edu/BioEdit/bioedit.html).

This study was approved as an investigation into an emerging outbreak of HCV in Victoria under the direction of the then Deputy Chief Health Officer (RL) in accordance with the Public Health and Wellbeing Act 2008 (Vic).

Newly acquired HCV co-infection in MSM was identified in 31 patients (Box 1). Demographics of this group are shown in Box 2. The median ALT level at diagnosis was 580 U/L (range, 52 –1715 U/L). Nineteen patients (61%) had HCV antibody seroconversion, all within 18 months; six patients (19%) had positive polymerase chain reaction (PCR) test results for HCV with a concurrent negative antibody test consistent with newly acquired HCV; and six patients (19%) tested positive for HCV antibodies, with markedly elevated ALT levels. Of the 29 patients who had their HIV viral load measured around the time of HCV diagnosis, 13 (45%) had a detectable HIV viral load. Intercurrent STI diagnoses are listed in Box 3. The distribution of cases over time is shown in Box 4.

Fourteen patients completed the questionnaire. These patients had similar demographics and clinical characteristics to the total group. Frequencies of traditional and novel risk factors for HCV transmission are shown in Box 5. IDU was confirmed to be a risk factor in the minority (five patients), compared with potential sexual modes of transmission (at least 10 patients). Only five patients had been aware of the potential for HCV to be sexually transmitted before their diagnosis with HCV. Twelve patients reported changing their sexual practices since being diagnosed.

HCV genotyping results were available for 29 patients. Genotype 1a was identified in 21 patients, genotype 3a in seven, and one patient had spontaneous clearance of virus. Nine test samples (six HCV genotype 1a and three genotype 3a) were further characterised by sequencing of the HCV core region. Nucleotide sequence alignments showed that two of the HCV 1a samples shared 100% identity with each other, as did the three HCV 3a isolates. At least one patient within each cluster participated in our questionnaire and had not injected drugs in the 12 months before diagnosis with HCV.

This study described the epidemiology of acute HCV in HIV-infected MSM in Victoria and confirmed the importance of transmission risk factors other than IDU. This has direct relevance to testing strategies and prevention messages for HIV-infected MSM.

The 31 cases of newly acquired HCV co-infection represent a relatively small proportion (0.9%) of the total HCV cases statewide. However, among the estimated 5722 Victorians living with HIV at the end of 2010 (about 0.1% of the population), 31 cases of HCV is disproportionately high.18,19 While other Australian studies have reported instances of HIV–HCV co-infection — particularly the Australian Trial in Acute Hepatitis C (ATAHC), with 50 cases nationwide, 23 in MSM with sexual exposure20 — the density of cases in our study’s single jurisdiction is concerning. The sequencing results support the hypothesis that overlapping risk factors contributed to HCV transmission, and related sequences suggest that at least two common lineages of HCV are circulating in this group.

Within this case series, IDU was a relatively uncommon risk factor for HCV acquisition, with 39% of the 31 men reporting any previous history of IDU, and five of 14 patients interviewed confirming IDU in the 12 months before HCV diagnosis. Conversely, sexual risk factors were highly prevalent. Inconsistent condom use with multiple sexual partners was universal among the men who completed the questionnaire, and correlates with the high proportion of STIs in the cluster (15/31 patients). Unprotected sex has become the paradoxical reaction to the success story of anti-retroviral therapy (ART).21 Potentially traumatic sexual practices combined with non-injecting drug use were frequently reported and were probably synergistic in HCV transmission.6 While it is likely that IDU introduces HCV into a sexual network, there is now evidence that sexual transmission in HIV-infected MSM does occur, irrespective of CD4+ lymphocyte counts.9,10,20,22 Serosorting, or selection of sexual partners on the basis of their HIV status, then concentrates HCV transmission within this population.

This study reaffirms the need for periodic HCV testing in HIV-infected MSM, particularly where history-taking reveals high-risk sexual behaviours. Based on our study, we would also argue that any diagnosis of STI in this group should prompt discussion around HCV transmission. Most cases were identified because abnormal LFTs were detected during routine management of ART. Given that HCV infection is commonly asymptomatic, there may be more MSM in the community with undiagnosed HCV who are not aware of the risk to sexual partners. Further, there is a risk of HCV re-infection after treatment or spontaneous clearance, necessitating continued HCV RNA testing to detect possible re-infection.23 This highlights the need for effective education campaigns to circumvent repeated courses of therapy that are both toxic and expensive. There is a much higher response to early treatment with current HCV therapy even in HIV co-infected patients, which again emphasises the need for frequent testing and timely identification and treatment.24

This study has a number of limitations. It is possible that the case-finding strategy may have missed potential patients who underwent their HCV testing elsewhere. The increase in notifications of cases may have been the result of increased testing. An alert was issued by the Chief Health Officer advising of an increase in hepatitis C in HIV-positive men in May 2011, which may have contributed to this.25 The retrospective 12-month period of interest used for the questionnaire may have introduced error resulting from inaccuracy in patients’ recollections of activities undertaken. Finally, only 14 patients participated in the questionnaire. While this group was representative of the cluster on demographic variables, we can only assume that this also applied to sexual risk factors.

There is a pressing need for the development and rollout of health promotion strategies to increase awareness of HCV sexual transmission and risk mitigation in Australia, in conjunction with the affected community. This is particularly important given that we as practitioners have previously generally delivered a message that HCV was not effectively sexually transmitted. We have continued to monitor the incidence of HCV–HIV co-infection in Victoria, and are aware of at least 13 further cases in the second half of 2011 (data not shown). Prospective data collection should measure changes in risk behaviours in response to prevention campaigns. Without intervention, however, the tide of HCV–HIV co-infection has the potential to erode the revolutionary gains made in the health of HIV-infected men.

1 Process of identifying cases of newly acquired hepatitis C virus (HCV) in
HIV-infected men who have sex with men (MSM) in Victoria from 1 April 2010 
to 30 June 2011

* We searched for previous HCV antibody results at four Victorian pathology services and the Victorian Infectious Diseases Reference Laboratory. † Two patients had false-positive results of polymerase chain reaction (PCR) tests with normal liver function tests; the remaining 25 patients
did not meet the seroconversion or alanine aminotransaminase (ALT) criteria.

4 Distribution of cases of newly acquired hepatitis C virus (HCV) infection in
HIV-infected men who have sex with men in Victoria by month of notification from 1 April 2010 to 30 June 2011

To the Editor: I read with great interest the recent article by Knox and Marshall.1 Chromoblastomycosis may result in a number of rare systemic complications that may be associated with significant morbidity.

For instance, chromoblastomycosis may affect the cornea. This usually follows cataract surgery. Cladophialophora carrionii is the aetiological agent involved in corneal chromoblastomycosis.2 Keratitis occurs, resulting in ocular pain and decreased visual acuity. Topical and systemic antifungal therapy may be successful in treating the condition, but usually surgical procedures such as penetrating keratoplasty are required.

Rarely, malignancies such as squamous cell carcinomas may develop in the affected area. This is more common in the extremities and in men over the age of 60 years. Rarely, amputation may be required in this scenario. This complication usually affects patients with a 20–30-year history of chronic untreated or undertreated chromoblastomycosis.3

Chromoblastomycosis may also affect the genitalia, resulting in genital elephantiasis. Chromoblastomycosis may rarely affect the skeletal system, resulting in osteomyelitis.4 Septic arthritis has also been reported. Treatment requires arthrotomy and debridement followed by antimycotic therapy.

Chromoblastomycosis may also affect the central nervous system. For instance, mycotic granulomas in the medullary region of the brain have been reported.5 This is usually seen in intravenous drug users and may be fatal.

These examples clearly illustrate the necessity of identifying and treating chromblastomycosis in a timely manner.