DH-VIDB-16-1-web - PDF

Victorian Infectious
Diseases Bulletin
ISBN 1 441 0575 Volume 16 Issue 1 March 2013
Contents
Hepatitis B surveillance in Victoria: are we missing newly acquired
cases? 2
Invasive pneumococcal infection in Victoria, 2008–2012: serotype
changes following the introduction of a 13-valent vaccine 9
Outbreak of Q fever related to changed farming practices, Victoria,
Australia 15
Reports of blood stream infections and meningitis to the Victorian
Hospital Pathogen Surveillance Scheme, July–December 2012 20
Immunisation program report, Victoria, March 2013 24
Communicable disease surveillance, Victoria,
October–December 2012 27

2 Victorian Infectious Diseases Bulletin Volume 16 Issue 1 March 2013
Hepatitis B surveillance in Victoria:
are we missing newly acquired cases?
Nasra Higgins, Jessica Rotti and Emma Clements
Communicable Disease Prevention and Control Unit, Department of Health, Victoria
In Victoria, an average of 2000 Hepatitis B cases are notified each year. Surveillance comprises passive reporting upon
diagnosis and selective enhanced surveillance focusing on potential newly acquired infections or where the notification
indicates a possible public health risk. Case ascertainment is important for preventing further transmission and to assess
and improve control and prevention efforts such as vaccination, contact tracing and outbreak investigation. However active
follow up of all hepatitis B notifications requires considerable expenditure of time and resources. We evaluated the Victorian
surveillance process for hepatitis B to determine if the current system was missing any newly acquired cases and to inform
hepatitis B surveillance practice in Victoria. The active surveillance process of this study identified only one additional case
and therefore suggests that the current surveillance system and selective follow-up poses minimal risk of missing any newly
acquired cases.
Introduction
Identifying newly acquired cases
of hepatitis B can be problematic
as a high proportion of cases are
asymptomatic, obtaining previous
negative testing history in the past
24 months is difficult and the required
specific laboratory tests are not
always done. Case ascertainment
is important for preventing further
transmission and to assess and
improve control and prevention efforts
such as vaccination, contact tracing
and outbreak investigation. It also
provides a mechanism for longer term
monitoring of both the epidemiology
and transmission of newly acquired
hepatitis B−whether through the more
common modes of transmission,
injecting drug use and sexual
contact1
, or less common exposures
including blood products, medical/
surgical procedures or tattooing−to
identify who is at risk of infection
and, emerging trends of public health
importance.
In Victoria, surveillance of hepatitis B
consists of two systems: 1) passive
surveillance, whereby diagnosing
doctors and laboratories are legally
required (under the Public Health
Wellbeing Regulations 2009) to
notify all diagnoses (presumptive or
confirmed) of hepatitis B infection
to the Department of Health within
five days of diagnosis; and 2)
enhanced surveillance, which involves
Communicable Disease Prevention
and Control Unit (CDPCU) staff
contacting the notifying doctors
to obtain additional demographic
information, risk factors, reason for
testing and time of infection applicable
to each person notified. These
surveillance systems are designed
to meet the hepatitis B surveillance
objectives in Victoria (Box 1).
Notified cases of hepatitis B are
classified as either newly acquired
or unspecified based on laboratory
evidence, in accordance with nationally
agreed case definitions (Box 2)2
.
On average, 2,000 cases of hepatitis
B notifications are received annually in
Victoria3
by the Department of Health.
Given the high volume of hepatitis B
notifications it is impossible to follow
up every single notification. Therefore,
since 2004, a selective follow-up
has been implemented focussing on
potential newly acquired infections or
those where the information provided
by the notifying doctor suggests
public health risk (Box 3).
In September 2009, a project was
undertaken to evaluate the surveillance
process for hepatitis B: 1) to determine
if the current hepatitis B surveillance
system was missing any newly
acquired cases, and 2) to inform the
current hepatitis B surveillance practice
in Victoria.
Box 1: Objectives of hepatitis B surveillance
• Guide immediate action for cases of public health importance to prevent
further transmission
• To identify cases in health care workers, cases potentially associated with
nosocomial transmission, transmission through other skin penetration
practices, and clusters of cases
• Monitor trends with respect to time, population groups, geography and
other risk factors
• Guide the planning and implementation of policy, service provision,
prevention strategies and other public health interventions
• Provide a basis for epidemiological research
• Monitor and evaluate the impact of interventions

Victorian Infectious Diseases Bulletin Volume 16 Issue 1 March 2013 3
Methods
Hepatitis B notifications received
by the Department of Health for the
month of September 2009 were
included in the study. Notifications
from Department of Immigration and
Citizenship (DIAC) were excluded
(n=18). These notifications arose from
the health-undertaking requirements
for overseas people migrating to
Victoria. Testing is mostly done
overseas and as newly arrived
migrants, these people often do not
yet have a general practitioner with
whom the department can follow
up. Furthermore, when DIAC notified
cases have been followed up in
the past, most notifications are for
persons with chronic hepatitis B.
During the study period, notifications
were screened to identify potential
missed newly acquired cases in those
not usually followed up further. Those
notifications that met the criteria for
newly acquired infection (Box 3) were
followed up by a public health officer
within three to five working days, as
per the hepatitis B disease follow up
protocol (routine surveillance) using a
structured questionnaire (Attachment
1). All remaining notifications were
analysed to determine those that
were potentially newly acquired
cases. Laboratory notifications from
a pathology service that indicated a
negative anti-HBc IgM result were
classified as hepatitis B unspecified
and excluded, according to case
definitions (Box 2).
Remaining notifications were
followed up as outlined below:
• The diagnosing laboratory was
contacted to obtain previous
testing history and current anti-HBc
IgM.
• If no previous testing history or
current anti-HBc IgM was available,
the diagnosing doctor was
contacted for more information on
the notified case.
• If the doctor believed the case
was newly acquired (<24 months)
and had not ordered anti-HBc
IgM, the test was ordered by the
Department of Health.
• If the doctor believed the case was
not newly acquired (≥24 months
duration) no further follow-up was
conducted.
If a case was notified by both the
diagnosing doctor and laboratory,
these notifications were matched
and followed up as outlined above. In
cases where there was no matching
laboratory notification for a doctor-
notified case, results were obtained
from the laboratory specified on
the doctor notification (Enhanced
surveillance form).
Qualitative and quantitative data
were collected by the public health
officer regarding the amount of time
required, number of phone calls, and
other practical aspects of the active
surveillance process conducted as
part of the study.
No ethics approval was required for
this study. Hepatitis B is a scheduled
notifiable infectious disease under the
legislation; the study was conducted
as a public health activity to evaluate
the surveillance of hepatitis B infection
and therefore was exempt from ethics
approval.
Data were managed and analysed
using Microsoft Excel.
Box 3: Hepatitis B notification – follow-up criteria
• Doctor notifications where doctor notifies as acute or newly acquired.
• Laboratory notifications with a positive hepatitis B surface antigen together
with positive core IgM.
• Laboratory notification with a positive PCR together with positive core IgM.
• Laboratory/doctor notifications indicating a previous negative hepatitis B
surface antigen testing history in the last 24 months.
• Doctor notifications indicating public health risk (e.g. tattooing in the last
two years)
• Doctor notifications indicating hepatitis B in a health care worker.
Box 2: Communicable Diseases Network Australia (CDNA) case definitions for
hepatitis B
Hepatitis B – newly acquired
• Detection of hepatitis B surface antigen (HBsAg) in a patient shown to be
negative within the last 24 months OR
• Detection of hepatitis B surface antigen (HBsAg) and IgM to hepatitis B
core antigen (anti-HBc IgM), in the absence of prior evidence of hepatitis B
virus infection OR
• Detection of hepatitis B virus by nucleic acid testing, and anti-HBc IgM, in
the absence of prior evidence of hepatitis B virus infection.
Hepatitis B – unspecified
• Detection of hepatitis B surface antigen (HBsAg), or hepatitis B virus by
nucleic acid testing, in a patient with no prior evidence of hepatitis B virus
infection AND that the case does not meet any of the criteria for a newly
acquired case.

Results
A total of 161 cases of hepatitis B
were notified to the Department
in September 2009, similar to
the number of cases notified in
September 2007 and 2008 (Figure 1).
During 2009 there were an average
of 166 cases of hepatitis B notified
monthly of which seventy per cent
were notified by the laboratory only.
Routine surveillance
Thirteen notifications met the criteria
for newly acquired hepatitis B and all
were followed-up according to the
routine hepatitis B disease notification
protocol. Ten were laboratory
notifications, and investigation
confirmed that these were newly
acquired hepatitis B cases. Three
cases were notified as newly acquired
by doctors; follow up of these cases
revealed that only one of the three
cases met the case definition for
newly acquired hepatitis B, bringing
the total number of newly acquired
hepatitis B cases identified through
the routine surveillance system in
September 2009 to 2011.
Enhanced surveillance
Of the 148 remaining hepatitis B
notifications, 98 were classified as
unspecified, based on anti-HBc
results and did not require further
follow-up (Table 1). The remaining 50
notifications without an anti-HBc result
were followed up with the laboratory
and/or doctor. This activity identified
that test types ordered for hepatitis B
varied between laboratories.
This newly applied active surveillance
process in the month of September
resulted in one additionally identified
newly acquired case.
The combined routine and enhanced
surveillance identified 12 cases of
newly acquired hepatitis B, with
one detected through the additional
procedures applied during the study.
This was higher than the number of
cases notified in September 2008
and September 2007 and was the
second highest monthly total for 2009
overall (Figure 2). On average there
were seven cases of hepatitis B newly
acquired infections identified monthly
in 2009 which was similar to 2008
and 2007.
Surveillance resource
allocation
Time
Follow-up with the notifying doctor or
laboratory by the public health officer
took approximately five to 10 minutes
for each notification, depending on
complexity of the case. A total of 180
minutes (three hours) were required
Figure 1: Notified cases of hepatitis B, by month of notification, January to
September, 2007–2009
Table 1: Number of notified cases and type of tests, by type of follow-up
Type of tests done
Active
surveillance
Routine
surveillance Total
HBsAg and anti-HBc IgM only 80 7 87
All tests (HBsAg, anti-HBc total, anti-HBc IgM, and anti-HBs) 18 5 23
HBsAg and total anti-HBc only 27 1 28
HBsAg with another marker (including e antigen) 16 0 16
HBsAg only 7 0 7
Total 148 13 161
Figure 2: Newly acquired hepatitis B, by month of notification, January to
September, 2007–2009
0
40
80
120
160
200
January February March April May June July August September
Month of notification
Numberofnotifiedcases
2007 2008 2009
January February March April May June July August September
Month of notification
2007 2008 2009
0
2
4
6
8
10
12
14
16
18
Numberofnotifiedcases

to follow up the 13 cases that were
identified via routine surveillance.
Follow-up of cases identified as
potentially newly acquired through
active surveillance required a total of
877 minutes (14.62 hours). Although
the 98 notifications classified as
hepatitis B unspecified did not qualify
for follow-up according to the design
of the study. An average of 2.2
minutes was spent per notification,
which included sorting and matching
of doctor and laboratory notifications,
which brought total time for this
process to 217 minutes (3.62 hours).
Phone calls
Thirty-one calls were made following
up the 13 notifications identified from
routine surveillance. A total of 143
phone calls were made to laboratories
or doctors regarding notifications
that required active surveillance.
The number of calls required varied
according to case, ranging from one
to six phone calls. Nine calls made
related to notifications that did not
require any further follow-up such as
querying on names and or date of
birth and other information.
The public health officer reported that
no difficulties were encountered when
approaching laboratories for previous
negative test results or other testing
history and all results were made
available as requested. There was
occasional reluctance from doctors
and clinics due to time constraints
and as a result multiple call-backs
were sometimes required to obtain
the required information.
Discussion
This study identified only one
additional newly acquired case
of hepatitis B that would have
been missed through the routine
surveillance process. The lack of
notification of this case resulted from
a combination of oversights; the
diagnosing doctor did not indicate
the hepatitis B markers clearly on the
laboratory request slip, the laboratory
indicated that it was missed from the
system due to a technical error, and
the diagnosing doctor did not notify
to the Department of Health. If one of
these systems had not failed, the case
would have been detected through
the routine surveillance process.
Identifying newly acquired cases of
hepatitis B can be problematic as
infection is often asymptomatic or
produces non-specific symptoms.
Differentiation between newly-
acquired and non-newly acquired
hepatitis B is dependent on serology,
specifically the presence of anti-HBc
IgM and or previous negative testing
history in the past 24 months. The
practice of testing for core IgM when
incident hepatitis B is suspected
varied between laboratories; however
during the study period 15 of the
19 laboratories that performed
hepatitis B testing performed anti-
HBc IgM on all the tests performed.
Implementation of routine inclusion
of core IgM (as well as the standard
HBsAg, total anti-HBc, and HBsAb)
when acute hepatitis B is suspected
on clinical or biochemical grounds
could improve case ascertainment for
newly acquired cases and reduce the
time spent following up notifications
for further test results. Clinicians’
lack of knowledge in identification of
newly acquired cases highlights the
importance of clinician education in
understanding of the disease.
The variation and heterogeneity of the
specific tests requested by diagnosing
doctors (Table 1) indicated that
clinician education should emphasise
the importance of ordering a complete
panel of tests to establish the natural
history of hepatitis B infection, in
line with the policies outlined in
Australia’s National Hepatitis B Testing
Policy3
and the recommendations
on HepBHelp4
, a website hosted
by the Victorian Infectious Diseases
Reference Laboratory designed to
assist clinicians with the diagnosis
and management of people living with
hepatitis B.
The workload for the public health
officer generated by active follow up
is an important issue. Although it took
five to 10 minutes per notification
on average, the active follow up
process corresponded to 15 extra
hours for the whole month, which was
equivalent to 10 per cent of the public
health officer’s equivalent full time. The
study suggested that if active follow
up was to continue as part of the
routine surveillance, the workload and
time commitment would be similar to
that in the study period.
The study was conducted for a period
of one month only, so the findings
may not be generalisable to the
long-term hepatitis B surveillance. As
shown in Figures 1 and 2, the monthly
number of hepatitis B notifications
varies. This investigation ascertained
the adequacy of case finding during
routine surveillance only and it is not
known how this would apply to newly
acquired hepatitis B case finding
during an outbreak or cluster setting.
Doctors notified only thirty per
cent of cases, even though it is a
legal requirement. The clinical and
demographic data only available
from clinicians (including risk factors,
country of birth, Aboriginal and
Torres Strait Islander status, and
reason for testing) provides essential
epidemiological information that not
only helps determine appropriate
follow-up, but also allows the
assessment of trends and risk factors
for hepatitis B in Victoria, which in
turn informs prevention and control
initiatives. More work is required
to encourage and support doctors
to notify infectious diseases (not

just hepatitis B), and to explain the
importance of the information gained
through clinician notification over
and above that available from testing
laboratories.
It should be noted that this study was
examining only the benefit of active
follow-up of hepatitis B notifications
from the perspective of identifying
previously unsuspected cases of
newly acquired infection. This does
not assess any other potential
benefits of follow-up of people notified
with unspecified or chronic hepatitis
B, such as supporting testing or
vaccination of contacts, ensuring
those notified receive information
regarding their condition, and that
they and their clinicians are linked
with other necessary services
following diagnosis with a treatable
communicable disease5,6
which is
contributing to the fastest increasing
cause of cancer death of Australians7
.
Conclusions and
recommendations
Active follow up of hepatitis B
notifications requires considerable
expenditure of time by the public
health officer, and in this study, only
found one additional case. These
results suggest that the current
surveillance system poses minimal
risk of missing newly acquired
hepatitis B infections.
Further issues for consideration
include encouraging routine testing
with a full panel of hepatitis B serology
as recommended in the National HBV
Testing Policy3
; routine addition of
anti-HBc IgM in any patient in whom
newly acquired infection is suspected;
encouraging notification of all cases
of hepatitis B by the diagnosing
clinician, in addition to the testing
laboratory; and consideration of the
broader public health and clinical
benefits that can be obtained by
informing and assisting clinicians and/
or people notified, over and above
considerations of determination of the
acuity of infection.
Acknowledgements
The authors wish to thank Ben
Cowie, Medical Epidemiologist
(Victorian Infectious Disease Reference
Laboratory, Royal Melbourne
Hospital and Department Health) for
his guidance and assistance in the
development of this manuscript. In
addition we would like to acknowledge
staff of the Communicable Disease
Prevention and Control Section of the
Department of Health.
References
1. National Centre in HIV Epidemiology
and Clinical Research. HIV/
AIDS, viral hepatitis and sexually
transmissible infections in Australia:
Annual Surveillance Report 2011
[report on the Internet]. Sydney
(AUST): Kirby Institute, The
University of New South Wales;
2011 [cited 2013 Feb 01]. Available
from: http://www.med.unsw.edu.au
2. Australian National Notifiable
Disease Surveillance System
Surveillance Case Definitions for
the Australian National Notifiable
Diseases Surveillance System, 1
January 2004 to 1 January 2011,
Available at: http://www.health.gov.
au/casedefinitions, Accessed 01
November 2012
3. National HBV Testing Policy,
Available at: http://testingportal.
ashm.org.au/hbv, Accessed 17
November 2012
4. Welcome to HepBHelp, Available
at: http://www.hepbhelp.org.au,
Accessed 17 November 2012
5. Williams S, Vally H, Fielding J
and Cowie B. Chronic hepatitis B
surveillance in Victoria, 1998–2008:
instituting a 21st century approach
to an old disease. ANZJPH 2011;
35:16–21
6. Williams S, Vally H, Fielding J,
Cowie B. Hepatitis B prevention
in Victoria, Australia – the
potential to protect. Euro Surveill.
2011;16(22):pii
7. MacLachlan J. and Cowie
B. Liver cancer is the fastest
increasing cause of cancer death
in Australians. MJA 2012; 197(9):
492–493

Enhanced Surveillance form used for the follow-up of hepatitis B
Hepatitis B September 2012 page 1 of 2
Communicable Disease Prevention and Control
Enhanced Surveillance Form
Hepatitis B
If you require help completing this form or have any other
enquiries please call 1300 651 160. Please send completed
forms to: Communicable Disease Prevention & Control,
Department of Health, Reply Paid 65937, Melbourne VIC
8060 (no stamp required), or fax to 1300 651 170.
PHESS ID
DEPARTMENT USE ONLY
PHESS completed DD / MM / YYYY by (initials)
3 2 0
Case details
Family name First name(s)
Residential address
Suburb/town State/Territory Postcode Country
Tel (home) Tel (work) Tel (mobile)
Parent/Guardian name (if applicable)
Sex
Male
Female
Not stated
Date of birth
DD / MM / YYYY
Age Is the case of Aboriginal or Torres Strait Islander origin
Yes, Aboriginal No
Yes, Torres Strait Islander Unknown
Yes, both Aboriginal and Torres Strait Islander
Occupation
Country of birth
Australia
Overseas  specify country and year of arrival in Australia
Language spoken at home
English
Other  specify
Is the case alive Alive
Died due to hepatitis B 
Died due to other causes 
Unknown
Date of death DD / MM / YYYY
Notifying doctor
Name of treating doctor
Address
Suburb/town State/territory Postcode Tel
Details of person completing this form (if different to notifier)
Name Tel Position
Further information
May the Department contact your patient if necessary. Yes
No

Hepatitis B September 2012 page 2 of 2
PHESS ID 3 2 0
Clinical summary
Case definition
Hepatitis B (Newly Acquired) –
meets at least one of the following criteria
• Detection of hepatitis B surface antigen (HBsAg) in a patient
shown to be negative within the past 24 months
• Detection of hepatitis HBsAg and IgM to hepatitis B core
antigen, in the absence of prior evidence of hepatitis B virus
infection
• Detection of hepatitis B virus by nucleic acid testing and IgM
to hepatitis B core antigen, in the absence of prior evidence of
hepatitis B virus infection.
Hepatitis B Unspecified Case – detection of hepatitis B surface
antigen (HBsAg) or hepatitis B virus by nucleic acid testing in a
patient with no prior evidence of hepatitis B infections AND does
not meet any of the criteria for a newly acquired case.
Date of current positive result DD / MM / YYYY
Hepatitis B surface antigen
(HBsAg) Detected Not detected Unknown
Hepatitis B core Igm
(HBcIgM) Detected Not detected Unknown
Has the case had a negative hepatitis B surface antigen
(HBsAg) test within the past 24 months
Yes 
No
Unknown
Last negative test DD / MM / YYYY
Laboratory Laboratory ID
Reason for testing May tick more than one
Patient request
Antenatal screening
Postnatal screening in a child to HBV positive mother
Prison screening
Screening due to drug and/or alcohol use
Blood or organ donor screen
Occupational exposure  Source person
Exposed person
Abnormal liver function test
Other medical problem
Asymptomatic sexual contact of HBV positive case
Asymptomatic household contact of a HBV positive case
Investigation of symptomatic hepatitis
STI screen
Peri operative
Research or study
Health care worker screening
Other, specify
Has the case had symptoms of acute hepatitis within the past
two years
Yes 
No
Unknown
Date of onset of symptoms DD / MM / YYYY
Bilirubin in urine
Jaundice – result
ALT – result Upper limit
Date DD / MM / YYYY
Has the case been hospitalised due to this infection
Yes 
No
Admitted DD / MM / YYYY
Discharged DD / MM / YYYY
Hospital
Has the case been tested for hepatitis C
Yes 
No
Unknown
Hepatitis C antibodies / PCR
Detected Not detected Unknown
Test date DD / MM / YYYY
History of illness/clinical comments include any relevant
comments, such as possible source of infection, others with similar
illness, etc.
Risk factors
Does the patient have a history of injecting drug use
Yes  Was this within the past 2 years Yes No
No history of injecting drug use
Unknown
In the past 2 years, has the patient had
Sexual partner of opposite sex
with HBV Yes No Unknown
Sexual partner of same sex
with HBV Yes No Unknown
Household contact with hepatitis B Yes No Unknown
Perinatal transmission Yes No Unknown
Imprisonment Yes No Unknown
Tattoos Yes No Unknown
Ear or body piercing Yes No Unknown
Acupuncture Yes No Unknown
Surgical procedure Yes No Unknown
Major dental surgery Yes No Unknown
Haemodialysis Yes No Unknown
Blood/blood products/tissue
in Australia Yes No Unknown
Blood/blood products/tissue overseas Yes No Unknown
Organ transplantation in Australia Yes No Unknown
Organ transplantation overseas Yes No Unknown
Health care worker with no
documented exposure Yes No Unknown
Occupational needlestick/biohazardous
injury in health care worker Yes No Unknown
Occupational needlestick/biohazardous
injury in a non health care worker Yes No Unknown
Non-occupational or unspecified
needlestick / biohazardous injury Yes No Unknown
Other risk  specify
Risk unable to be determined Yes
If answered yes above, please provide details
Privacy Legislation Commonwealth and State privacy legislation does not negate the responsibility to notify the specified conditions nor
to provide the information requested on this form. Doctors have a responsibility to inform their patients that their information is being provided
to the Department of Health. The Department is committed to protecting the confidentiality of the information it receives and is bound by
legislation and maintains strict privacy policies. Further information about privacy and notifiable conditions is available from
www.health.vic.gov.au/ideas/notifying/privacy.

Invasive pneumococcal infection in Victoria, 2008–2012:
serotype changes following the introduction of a 13-valent
vaccine
Janet Strachan and Marion Easton
Microbiological Diagnostic Unit Public Health Laboratory, The University of Melbourne
We report trends in the serotypes and antibiotic susceptibilities of pneumococcal strains from blood and cerebrospinal
fluid (CSF) culture positive infections in Victoria, Australia from 2008 to 2012, the period before and after introduction of the
13-valent conjugate pneumococcal vaccine (PCV13) into the national childhood immunisation schedule in July 2011. Overall,
the number of infections remained fairly stable from 2008 to 2012, with an average annual rate of 6.7 per 100 000 population.
Cases involving serotypes from the earlier 7-valent vaccine (PCV7) slowly decreased from 2008 to 2011, with a slight increase
in 2012 in those over 65 years of age. The number of infections with PCV7 serotypes in 2012 was almost 60 per cent less
than in 2008. In contrast, infections due to PCV13-nonPCV7 serotypes slowly rose from 2008 to 2010, and decreased slightly
thereafter, largely due to changes in the number of infections caused by serotype 19A, particularly in children under five years
of age. As serotype 19A was the strain most commonly associated with reduced penicillin and third generation cephalosporin
susceptibility, decreasing numbers of this serotype contributed to the fall in prevalence of resistance to these antibiotics from
2008 to 2012. Infections with non-vaccine serotypes rose over the time period, most notably serotype 6C. Ongoing surveillance
of the serotypes and antimicrobial susceptibilities of isolates causing invasive pneumococcal disease is essential as non-vaccine
serotypes, often with increased antimicrobial resistance, are emerging.
Introduction
Streptococcus pneumoniae (the
pneumococcus) is a major cause of
morbidity and mortality worldwide,
affecting mainly the very young and
the elderly. There are over 90 different
pneumococcal serotypes.
A 23-valent polysaccharide vaccine
(PPV23) has been available in Australia
since 1983 and publicly funded for
those aged 65 years and older in
Victoria since 1998. The 7-valent
pneumococcal conjugate vaccine
(PCV7) first became available for
private purchase in 2001. It was
added to the federally funded national
childhood immunisation schedule in
2005, with a catch-up program for
children born after 1 January 2003. A
13-valent pneumococcal conjugate
vaccine (PCV13) with an additional
six serotypes replaced PCV7 for all
Australian states and territories except
the Northern Territory on 1 July 2011
(Table 1).
Infant pneumococcal vaccination
programs have been associated with
declines in invasive pneumococcal
disease (IPD)1,2,3
, but incidence of
infection with non-vaccine serotypes,
often with increased antimicrobial
resistance, has risen. We have
reported previously on the immediate
impact of PCV7 on the serotypes
causing IPD in Victoria from 2003
to 20074
. After the addition of PCV7
to the immunisation schedule, IPD
due to vaccine serotypes was greatly
reduced, particularly among young
children. While overall rates of IPD
decreased, rates of disease due to
non-PCV7 serotypes doubled.
In this paper we report on trends
in the serotypes and penicillin and
third-generation cephalosporin (3GC)
susceptibilities of pneumococcal
strains from blood and cerebrospinal
fluid (CSF) culture positive infections
within the Victorian population from
2008 to 2012.
Methods
Since 1988 Victorian laboratories
have been voluntarily contributing
information on blood and CSF isolates
to the Victorian Hospital Pathogen
Surveillance Scheme (VHPSS) co-
Table 1: Serotypes included in pneumococcal vaccines
Vaccine
type
PCV7 4, 6B, 9V, 14, 18C, 19F, 23F
PCV13 1,3, 4, 5, 6A, 6B, 7F, 9V, 14, 18C, 19A, 19F, 23F
PPV23
1, 2, 3, 4, 5, 6B, 7F, 8, 9N, 9V, 10A, 11A, 12F, 14, 15B, 17F, 18C, 19A, 19F, 20, 22F,
23F, 33F
Table 2: Penicillin and 3GC MIC breakpoint interpretive criteria (mg/L)
Penicillin 3GC
Meningitis Non-meningitis Meningitis Non-meningitis
Susceptible <=0.06 <=2 <=0.5 <=1
Resistant > 0.06 >2 >0.5 >1

ordinated by the Microbiological
Diagnostic Unit Public Health
Laboratory (MDU PHL). Data collected
includes patient demographics and
antimicrobial susceptibilities of isolates
as determined by the submitting
laboratory. In conjunction with the
Victorian Department of Health,
cultures are sought for all reported IPD
cases. We analysed VHPSS reports
of S. pneumoniae from samples
collected between January 2008 and
December 2012. Only the first invasive
isolate within a fourteen-day period
was included.
We contacted submitting laboratories
to obtain available penicillin and third
generation cephalosporin (3GC)
susceptibilities and minimum inhibitory
concentrations (MICs) if they were not
provided on the VHPSS report.
Diagnostic laboratories use one
of several available antimicrobial
susceptibility testing standards,
which provide MIC breakpoints for
susceptibility categories (typically
susceptible, intermediate and
resistant) for most bacterial species.
Pneumococcal breakpoints for
penicillin and 3GC differ for meningitis
and non-meningitis clinical syndromes
(Table 2)5
. When laboratories do not
know the clinical syndrome of an IPD
case and the penicillin or 3GC MIC is
greater than the susceptible breakpoint
for meningitis (0.06 and 0.5 mg/L
respectively) they report the MIC value
alone without a susceptibility category.
These are recorded in VHPSS as a
“non-interpretable” category.
Pneumococcal serotyping was
performed at the MDU using the
Quellung method with antisera
produced by the Statens Serum
Institute in Denmark as previously
described6
.
Australian Bureau of Statistics mid-
year population figures were used to
calculate rates7
.
Results
From 2008 to 2012, there were
1,840 reports to the VHPSS of S.
pneumoniae isolated from blood
and CSF samples (1,796 and
44 respectively). Serotypes were
determined for 1,823 (99.1 per cent)
isolates. Four strains were not-typable
and typing could not be performed on
an additional thirteen strains due to
loss of viability.
Overall, the number of IPD infections
reported to the VHPSS remained
stable from 2008 to 2012 (Figure 1),
with an average annual rate of 6.7 per
100,000 population, being 9.6, 4.0
and 18 per 100,000 population for
those aged under five, five to sixty-four,
and over sixty-five years respectively.
The annual IPD rate was slightly higher
in males than females, 7.4 compared
with 6.0 per 100,000. The gender
difference was most marked in children
under five years of age, where the
male:female ratio was 1.6:1.
Cases involving PCV7 serotypes slowly
decreased from 2008 to 2011, with
a slight increase in 2012 (Figure 1).
The number of infections with these
serotypes in 2012 was almost 60 per
cent less than in 2008. In children
aged less than five years, there were
only twelve infections with PCV7
serotypes over the time period under
review, and eight of those were due
to serotype 19F (Table 3). In those
aged five years or more, the number
of PCV7 serotypes causing infection
more than halved from 2008 to 2012,
although for those aged 65 years or
more the rate increased slightly from
2011 to 2012 (Table 3).
In contrast, infections due to PCV13-
nonPCV7 serotypes slowly rose from
2008 to 2010, and decreased slightly
thereafter, largely due to changes in
the number of infections with serotype
19A. These had risen to a peak of
95 cases in 2011 and then fell to
63 in 2012 (Table 3), with the most
dramatic reduction in those aged
less than five years. The number of
infections with serotype 7F grew each
year from 13 in 2008 to 67 in 2012,
with most occurring in the older age
groups (Table 3). Serotype 6A which
also occurred almost exclusively
in those aged more than five years
decreased over time, with no cases
among those aged 65 and older
in 2011 and 2012. There were no
serotype 3 infections in children less
than five years of age in 2012.
Among PPV23 non-PCV13 serotypes
there was little change (Table 4) in the
overall incidence of infections, with
only small annual fluctuations.
Non-vaccine serotypes accounted
for 20 per cent of pneumococcal
Figure 1: Annual rate of IPD per 100,000 population, VHPSS, 2008–2012
Rateper100000population
Year
0
2
4
6
8
20122011201020092008
PCV13: PCV7 serotypes PCV13: non-PCV7 serotypes
PPV23: non-PCV13 serotypes Non-vaccine serotypes Annual rate

Table 3: PCV13 serotypes of Victorian IPD isolates, VHPSS, 2008–2012
Age Less than five years Five to 64 years 65 years and older
TotalYear 2008 2009 2010 2011 2012 Total 2008 2009 2010 2011 2012 Total 2008 2009 2010 2011 2012 Total
PCV13: PCV7 types
4 1 - - - - 1 10 10 7 1 4 32 3 4 6 - 1 14 47
6B 1 - - - - 1 4 1 - 1 1 7 9 1 3 1 2 16 24
9V - - - - - 0 8 4 5 5 2 24 5 1 1 2 2 11 35
14 1 - - - - 1 5 6 3 6 2 22 3 4 - 2 - 9 32
18C 1 - - - - 1 4 1 3 1 - 9 2 3 - - - 5 15
19F - 2 4 1 1 8 6 5 10 3 7 31 3 4 - 2 5 14 53
23F - - - - - 0 - 3 1 1 1 6 4 5 1 1 1 12 18
Sub total 4 2 4 1 1 12 37 30 29 18 17 131 29 22 11 8 11 81 224
Rate per
100 000
1.2 0.6 1.2 0.3 0.3 0.7 0.9 0.7 0.7 0.4 0.4 0.6 4.1 3 1.5 1 1.4 2.1 0.8
PCV13: non-PCV7 types
1 - - - 2 - 2 8 8 8 1 1 26 - 1 - - - 1 29
3 2 3 2 3 - 10 16 19 16 20 15 86 13 12 12 11 16 64 160
5 - - - - - 0 - - - 1 - 1 - - - - - 0 1
6A - - - 1 - 1 6 1 4 2 2 15 5 4 5 - - 14 30
7F 2 2 4 2 2 12 8 19 31 47 50 155 3 3 6 10 15 37 204
19A 17 25 28 22 7 99 26 35 39 40 30 170 22 27 24 33 26 132 401
Sub total 21 30 34 30 9 124 64 82 98 111 98 453 43 47 47 54 57 248 832
Rate per
100 000
6.3 8.8 9.8 8.5 2.5 7.2 1.5 1.9 2.2 2.5 2.2 2.1 6 6.4 6.2 7 7.1 6.6 3.1
Total PCV13
serotypes
25 32 38 31 10 136 101 112 127 129 115 584 72 69 58 62 68 329 1056
Rate per
100 000
7.5 9.4 11 8.8 2.8 7.9 2.4 2.6 2.9 2.9 2.6 2.7 11 9.4 7.7 8 8.4 8.7 3.9
Table 4: PPV23 non-PCV13 serotypes of Victorian IPD isolates, VHPSS, 2008–2012
Age 0–4 years 5–64 years 65 years and older
8 - - - - 1 1 3 7 3 8 3 24 1 3 1 2 1 8 33
9N - 1 2 - - 3 6 2 3 2 8 21 - 2 2 3 4 11 35
10A 2 1 1 2 - 6 1 7 2 - 2 12 2 1 - 2 2 7 25
11A 1 1 - - - 2 2 5 5 3 3 18 3 2 2 5 9 21 41
12F - - - - 1 1 1 - 2 1 1 5 - - - - - 0 6
15B 1 - 1 1 1 4 1 1 2 2 - 6 4 1 2 1 2 10 20
17F 1 1 - - - 2 2 3 - 1 4 10 2 1 1 2 - 6 18
20 1 - - - - 1 3 - 1 - 4 8 - - - - 1 1 10
22F 3 - 2 2 6 13 12 13 16 14 19 74 15 15 18 16 10 74 161
33F 2 1 2 1 1 7 5 4 6 6 4 25 7 3 6 3 - 19 51
Total 11 5 8 6 10 40 36 42 40 37 48 203 34 28 32 34 29 157 400
Rate per
100 000
3.3 1.5 2.3 1.7 2.8 2.3 0.9 1 0.9 0.8 1.1 0.9 4.8 3.8 4.2 4 3.6 4.2 1.5
isolates over the five-year period
with a 62 per cent increase from
2008 to 2012 (Table 5). The number
of serotype 6C infections more
than doubled over the five-year
period. There were no serotype 15A
infections in 2008, but the numbers
slowly rose from 2009 to 2012.
Nearly half (14) of the 31 serotype
23B infections occurred in 2011.
Penicillin and third generation
cephalosporin resistance
Penicillin susceptibilities were available
for 1,823 (99 per cent) of the 1,840
VHPSS reports during this five-year
period, of which 1,246 reports provided
MICs. Twenty-three of those with MICs
(1.8 per cent) had a penicillin MIC ≥
2mg/L; the annual proportion, zero,
1.5, 1.4, 3.2 and 2.9 for 2008 to 2012
respectively. Nearly half (11 isolates) of
these strains with high level resistance
were serotype 19A.

Using the MIC breakpoint categories
as submitted by the laboratories, 1743
isolates were allocated a susceptibility
category and 80 isolates (4.3 per cent)
were reported as not interpretable.
The overall proportion of isolates
reported to be PNSP was 8.4 per
cent: 11.8, 7.7, 5.9, 6.7 and 6.4 per
cent for 2008 to 2012 respectively.
Serotype 19A was the most commonly
reported PNSP (67 of 134 isolates; 19
per cent) (Table 6), but the serotype
which was most frequently penicillin
non-susceptible was 9V (13 of 32
isolates; 40.6 per cent). PNSP strains
accounted for ten per cent of PCV13
serotypes (101 of 1056 isolates),
three per cent of PPV23 non-13PCV
serotypes and five per cent of non-
vaccine serotypes (18 of 367 isolates).
Two of the four not-typable isolates
were PNSP, and twelve of the thirteen
strains not available for serotyping
were reported as PNSP.
3GC MIC susceptibility categories
were available for 1730 isolates (94 per
cent). The prevalence of 3GC non-
susceptibility was 1.5 per cent overall:
1.6, 1.5, 1.7, 1.6 and 0.6 in for 2008
to 2012 respectively. Again the most
commonly isolated non-susceptible
serotype was 19A (9 of 25 with
available data) (Table 6). Serotype 23B
was most frequently non-susceptible
to 3GC, although the number of
isolates was very small (two of 29;
6.9 per cent). One not-typable isolate
was 3GC non-susceptible. Only two
isolates (serotypes 19A and 19F) had
reported 3GC MICs ≥ 2mg/L.
Discussion
Data from Victoria reported in this
paper, show early trends similar to
those seen elsewhere after PCV13
introduction1,2
. There were declining
rates of infection with PCV13-
nonPCV7 types, mainly due to the
reduction in the number of 19A
infections, particularly in children under
five years of age. As serotype 19A
was the serotype most commonly
associated with reduced penicillin
and 3GC susceptibility, decreasing
numbers of this type contributed to
the fall in rates of PNSP and 3GC from
2008 to 2012.
Infections with non-vaccine serotypes,
particularly serotype 6C, rose over
the time period. Serotype 6C was first
described in 2007 and is an antigenic
variant of serotype 6A8
. Cooper et
al.9
showed that immunisation with
PCV13 may induce cross-protective
responses to some related serotypes
not included in the vaccine. Rates
of serotype 6A began to slowly
decline after the introduction of
PCV7, probably due to cross-reaction
with the serotype 6B component of
PCV710
. It is thought that rates of
infection with serotype 6C will also fall
Table 5: Non-vaccine serotypes of Victorian IPD isolates, VHPSS, 2008–2012
Age 0–4 years 5–64 years 65 years and older
6C 3 - 1 2 1 7 2 9 13 6 8 38 7 5 13 18 20 63 108
6D - - - - - 0 - - - - 1 1 - - - - - 0 1
7B - - - - - 0 - - - 1 - 1 - - 1 - - 1 2
7C - - - - - 0 - 1 - - 1 2 - - - 2 2 4 6
10F - - - - - 0 - 1 - - - 1 - - - - - 0 1
13 - - - - - 0 1 - - 1 - 2 - - - - - 0 2
15A - - 1 - - 1 - 1 1 2 6 10 - 2 4 5 11 22 33
15C - 1 - 1 1 3 - - - 3 3 6 3 1 - - 1 5 14
16F - - - 1 - 1 2 2 2 4 - 10 4 2 2 3 2 13 24
18B - - 1 - - 1 - - - - - 0 - - - - - 0 1
21 - - - - - 0 - 1 - - - 1 - - - 1 - 1 2
22A - - - - - 0 1 - - - 1 2 2 2 - 1 1 6 8
23A 1 - - - - 1 5 6 4 2 1 18 4 3 1 6 5 19 38
23B 1 - 1 - 1 3 - 2 1 7 1 11 - 4 3 7 3 17 31
29 - - - - - 0 - - - 1 - 1 1 - - - - 1 2
31 - - - - - 0 - - - 2 - 2 1 1 1 1 2 6 8
34 - - - - - 0 1 - 2 1 3 7 1 1 - - 1 3 10
35B 1 1 - 2 3 7 3 1 5 4 3 16 6 4 2 6 2 20 43
35F 1 - - 1 - 2 - 1 1 - - 2 1 1 5 3 3 13 17
37 - - - - - 0 - 1 - - 1 2 1 - - - - 1 3
38 1 1 1 1 - 4 1 2 - - 2 2 1 4 2 3 1 11 17
Total 8 3 5 8 6 30 16 26 29 34 31 135 32 30 34 56 54 206 367
Rate per
100,000
2.4 0.9 1.4 2.3 1.7 1.7 0.4 0.7 0.7 0.8 0.7 0.6 4.5 4.1 4.5 7 6.7 5.4 1.3

after the implementation of PCV13
immunisation programs, due to cross-
reaction with serotype 6A9
, although as
yet this has not occurred in Victoria.
Herd immunity, whereby reductions
in IPD and pneumonia occur in
non-immunised age cohorts, has
been seen in other populations with
childhood pneumococcal conjugate
vaccine programs11,12
. From 2008 to
2012 rates of infection with some, but
not all, PCV7 serotypes declined in
Victorians over five years of age.
The increase in IPD due to non-
vaccine serotypes such as that
seen in Victoria is also occurring
elsewhere1,2,3
. There were several
IPD serotypes detected from 2008
to 2012 which were not detected in
the previous five year period, namely
serotypes 6D, 7B, 10F, 15A, 21, 31
and 37. For most of these serotypes
the numbers of isolates were small.
However, serotypes 31 and 15A both
appear to be rising in prevalence, with
15A being of particular concern due
to the high proportion with increased
penicillin and 3GC resistance.
The emergence of non-vaccine
serotypes is believed not be due to
genetic serotype switching events13
,
but expansion of existing clones
sometimes with modification of
capsular polysaccharides14
. Specific
protein vaccines, which potentially
cover all pneumococci, regardless of
serotype, are under development13
.
From 2008 to 2012 there were
1945 Victorian IPD notifications
to the National Notifiable Disease
Surveillance Scheme15
compared with
1840 from VHPSS data. Differences
between NNDSS and VHPSS figures
are due in part to the differing dates
used to define reporting periods for
each system. The VHPSS uses date
of collection of sample, whereas the
NNDSS uses the date of notification.
Also, the latter scheme includes
invasive infections other than
bacteraemia and meningitis and IPD
cases confirmed by polymerase chain
reaction (PCR) alone are included in
NNDSS data, but are not reported to
VHPSS.
In their 2007 national survey of
pneumococcal susceptibilities, the
Australian Group on Antimicrobial
Resistance (AGAR) found a prevalence
of 0.9 per cent of high level (≥2 mg/L)
penicillin non-susceptibility16
. This is
somewhat lower than the percentage
of strains (1.8 per cent) with penicillin
MIC ≥2 mg/L among the Victorian
isolates for the period 2008 to 2012,
although interestingly our data
showed no strains with high-level
penicillin resistance in 2008. The
higher prevalence overall however
may be explained by the high number
of resistant isolates found among the
differing serotypes causing IPD in older
Victorian patients. The AGAR figures
are based on sentinel surveillance of a
number of sites throughout Australia,
including several large paediatric
hospitals.
Table 6: IPD serotypes with reported penicillin and 3GC resistance, VHPSS, 2008–2012
Serotype
Number of
isolates
Isolates with
interpretable
penicillin result PNSP
Percentage
PNSP
Isolates with
interpretable
3GC result 3GC resistant
Percentage
3GC resistant
19A* 401 353 67 19 380 9 2.4
9V* 35 32 13 40.6 33 2 6.1
15A 33 23 9 39.1 30 1 3.3
14* 32 29 6 20.7 30 2 6.7
19F* 53 48 5 10.4 51 3 5.9
6A* 37 37 3 8.1 35 - -
6B* 24 23 3 13 22 1 4.5
11A 41 37 3 8.1 38 1 2.6
15B 20 19 3 15.8 19 - -
23A 38 37 3 8.1 37 - -
35B 43 38 3 7.9 41 1 2.4
4* 47 46 2 4.3 44 - -
10A 25 25 2 8 25 - -
23B 31 30 2 6.7 29 2 6.9
23F* 18 17 2 11.8 18 1 5.6
33F 51 48 2 4.2 51 - -
12F 6 6 1 16.7 6 - -
15C 14 14 1 7.1 12 - -
17F 18 18 1 5.6 18 1 5.6
20 10 10 1 10 10 - -
Total 1840 1743 146 8.4 1730 25 1.5
*PCV13 serotypes

Conclusion
Ongoing surveillance of the serotypes
and antimicrobial susceptibilities of
isolates causing IPD is essential. As
shown by the Victorian data presented
here, IPD due to the serotypes
contained within conjugate vaccines
has been reduced, but non-vaccine
serotypes, often with increased
antimicrobial resistance are emerging.
The development of non-serotype
dependent vaccines is required to
prevent IPD in the future.
Acknowledgements
We thank Samantha Tawil, May
Chai, Despina Stylianos and
Joanne Stylianopoulos for technical
assistance, Victorian diagnostic
laboratories for submitting isolates,
and the Australian Government
Department of Health and Ageing for
funding serotyping. We acknowledge
We gratefully acknowledge the
Victorian Department of Health for
their support of VHPSS and their role
in IPD surveillance and Artemesia
Green, Juvelee Marzan, Wendy Siryj
and Eleanor Latomanski for data
management.
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Introduction
Q fever is a zoonotic disease caused
by the bacterium Coxiella burnetii.
It was first recognised as a specific
pathogen in 1937 when it was
isolated in specimens from northern
Australian abattoir workers.1,2
A wide
range of wild and domestic animals
(including arthropods, birds, rodents,
dogs, cats and livestock) serve as a
natural reservoir for the pathogen.
Cattle and small ruminants have been
associated with large outbreaks in
humans. A whole-cell inactivated
vaccine for Q fever, developed and
licensed for use in Australia in 1989,
is targeted at individuals working in
high-risk occupations.3
A human case of Q fever is a
notifiable condition in Victoria. The
Communicable Diseases Network of
Australia’s case definition for confirmed
acute Q fever requires laboratory
definitive evidence or laboratory
suggestive evidence in the setting of
a clinically compatible illness.4
Typical
clinical features can include fever,
chills, headache, myalgia and cough.
Profound fatigue is often a feature and
pneumonia can occur. However acute
infection can be asymptomatic or non-
specific in up to half of cases.5
Laboratory definitive evidence involves
the detection of Coxiella burnetii by
nucleic acid testing or culture, or
seroconversion to (or fourfold rise
in antibody titre to) Phase II antigen
in paired sera tested in parallel
in the absence of recent Q fever
vaccination. Laboratory-suggestive
evidence is defined as detection of
specific IgM to phase II antigens
in the absence of recent Q fever
vaccination.
In September 2011, the Victorian
Government Department of Health
was notified of a case of Q fever in
a staff member of a horse and cattle
farm in rural northern Victoria.
Outbreak investigation
Following the initial notification and
diagnosis of Q fever, the farm manager
arranged for all eight farm staff to
attend for Q fever vaccination. Medical
assessment prior to vaccination
against Q fever is required to exclude
those previously exposed to Q
fever, given the possibility of vaccine
hypersensitivity reactions in these
patients.6
On clinical review prior to
vaccination, the GP noted that half of
the staff had experienced symptoms
possibly consistent with Q fever.
Serological testing
Blood samples were obtained from
all staff to assess for recent infection
with Q fever. The serum samples
were tested at different pathology
laboratories using different serological
techniques. Quantitation of titres was
not available for baseline serolology
in some individuals. Interpretation
of thresholds for positive tests
were as per reporting from testing
laboratories.
Case interviews
The Department conducted interviews
with the five staff members with
positive serology on testing (the five
listed in Table 1, four of whom had
clinical illness). The remaining three
staff members were not interviewed
as they had not experienced a
clinically compatible illness and had
negative Q fever serology when tested
prior to vaccination.
Environmental assessment
A description of the farm layout
and detail of work practices was
conducted. Weather information
(rainfall and average temperature)
was obtained from the Bureau of
Meteorology.7,8
Outbreak of Q fever related to changed farming practices,
Victoria, Australia
Leah N Gullan1
, Benjamin C Cowie1–4
and Lucinda J Franklin1
1. Communicable Diseases Prevention and Control Unit, Department of Health, Victoria, Australia
2. Victorian Infectious Diseases Reference Laboratory, Victoria, Australia
3. Royal Melbourne Hospital, Victoria, Australia
4. University of Melbourne, Victoria, Australia
During September and October 2011, an outbreak of Q fever occurred at a farm in rural Victoria. Five out of eight employees
had evidence of recent infection with Coxiella burnetii. The outbreak appeared to be related to an increased number of calves
born on the farm and a change of practice in the handling of birth products from the livestock motivated by sustainable/
organic farming practices. Q fever is a zoonosis with considerable impact on those working in high-risk occupations and
where process changes can result in increased likelihood of infection. Consideration should be given to specific education
targeted to animal farm owners and workers regarding Q fever and the factors associated with increased risk of infection,
plus the availability of vaccination.

Results
Setting
The property where the outbreak
occurred is situated on 500 acres,
located approximately 120 km north
of Melbourne, Victoria. The farm
backs onto a river and the landscape
comprises mostly cleared woodland/
wetland with clay-based silts and
soils (Figure 1)9
. Average rainfall for
October in the region is 100mm per
month and the average temperature
for the six months from September
2011 to February 2012 was between
19 and 21 degrees Celsius.7,8
The property is a mixed-farming
operation with horse stud and beef
cattle production. The eight full-time
staff included three horse handlers,
two gardeners, two general farm
hands and a manager. The horse
handlers had little involvement with
the cattle operation, which was
operated by the farm hands and
farm manager. The gardeners’ main
responsibilities were to maintain
the gardens around the main farm
buildings, mostly adjacent to the
horse enclosure. One of the three
horse handlers lived on the property.
A schematic of the property is
included in Figure 2.
Case interviews
The initial case, also a 45-year-old
male, developed symptoms including
headache, chills and sweats, in
particular night sweats, from the 29
August 2011; he was ill for about one
week. He did not present to a GP,
believing he had a flu or cold. This
case worked as the farm manager of
the property.
The second case, a 49-year-old
female, developed fever, severe
headache, chills, sweats, and myalgia
on the 8 September 2011. She also
did not see a GP, however, was
away from work for five days. She
presumed she had a cold or influenza.
This case worked as a horse handler
at the same property.
The third case was the 45-year-old
male first notified to the department.
He developed symptoms of fever,
headache, chills, sweats, malaise,
myalgia and weakness on 18
September 2011. He presented to his
GP on 27 September 2011 and was
referred to a local hospital the same
day. He was admitted for two nights
and responded well to treatment with
doxycycline. His blood tests showed
abnormal liver function, which was
attributed to Q fever. He worked as a
general farm hand at the property.
The fourth case, a 47-year-old female,
worked at the property as a gardener
and occasionally as a farm hand.
She developed severe headaches,
chills, malaise, myalgia and general
weakness on the 23 September 2011
and was ill for about seven days.
Figure 1: Location of the farm in Victoria, Australia
Figure 2: Schematic representation of farm layout at the time of the outbreak

The fifth case, a 39-year-old female,
lived on the property and worked
closely with the horses. She did not
recall experiencing any symptoms
of Q fever but was later serologically
confirmed as having recently been
exposed to Q fever.
Although all four symptomatic cases
reported feeling seriously unwell
and considered presentation to
hospital, only the third case required
hospitalisation. The remaining three
employees from the farm were
reported by the farm manager to
have negative serology results and
were subsequently offered Q fever
vaccination.
Serology results
Interpretation of serology results in
this outbreak were complicated by
different laboratories using different
methodologies (including enzyme
immunoassay, immunofluorescence,
and immunochromatography).
Furthermore, quantitation of titres for
positive results were not available
for baseline serology tests in some
individuals.
Despite this, the serology results for
all five cases were suggestive of acute
infection with Q fever (Table 1), as;
• All cases were positive for Q fever
phase II IgM and IgG on initial
testing, with only the first patient
affected (case 1) positive for phase
I IgM at a lower titre;
• Both individuals (cases 1 and 3)
with antibody titres available at
baseline demonstrated a fourfold
rise in phase II IgM and/or IgG
between tests when tested by the
same laboratories in parallel
• All individuals had high IgG and
(where performed) IgM titres on
follow-up serology, with phase
II titres substantially higher than
phase I titres where the latter were
detectable
Risk factors
Two main risk factors were identified
during the investigation: a high calving
season and changed practices in
handling placentas.
A higher than usual number of calves
had been born on the property
during the 2011 calving season.
The season began with the first calf
born on the 6 February 2011, with a
further 26 calves born during 2011.
Some of the cattle that had calved
had recently been purchased from
a source in New South Wales (the
State bordering Victoria to the north).
The farm manager (case 1) and farm
hand (case 3) had had close contact
with birthing fluids from assisting with
calving. The foaling season ran from
July to August 2011 with 12 foals
born. One of the horse handlers (case
5) lived at the property and had close
contact with the horses and their
foals as her main role during July and
August was to assist with foaling.
The farm had implemented a new
practice at the beginning of the
calving season of placing placental
tissue from both cattle and horses
on an open composting pile, to be
used in the farm’s gardens as part of
organic gardening processes. The
large compost heap was situated
on top of a hill overlooking the horse
stables, main farm buildings and
gardens (Figure 2). Until this change
was implemented, it was usual for
the placental tissues to be buried or
left out for the foxes to consume. It
was early spring at the time of the
Table 1: Symptom onset date and serology results for cases linked to the
outbreak
Case Details#
Onset
day*
Test 1
day* Phase II Phase I
Test 2
day*
Phase
II Phase I
1
Male
45 yrs
Cattle
0 42
IgA -
<1:10
IgM +
1:640
IgG +
1:640
IgA -
<1:10
IgM +
1:160
IgG -
< 1:10
49
IgA +
t=25
IgM +
t>=3200
IgG +
t>=3200
IgA +
t=25
IgM +
t=200
IgG +
t=100
2
Female
49 yrs
Horses
10 39
IgM +
IgG +
ND 49
IgA +
t=25
IgM +
t=200
IgG +
t=1800
IgA -
IgM -
IgG -
3
Male
45 yrs
Cattle
20 31
IgM +
IgG +
t=64
ND 43
IgM +
IgG>512
ND
4
Female
47 yrs
Garden
25 39
IgM +
IgG +
ND 49
IgA -
IgM +
t>=3200
IgG +
t>=3200
IgA -
IgM +
t=400
IgG -
5
Female
39 yrs
Horses
N/A 39
IgM +
IgG +
ND 49
IgA +
t=25
IgM +
t=400
IgG +
t=400
IgA -
IgM +
t=50
IgG -
#
Sex, age and area of farm where individual spent most of their time during the exposure period.
* days after onset in 1st
case.

outbreak and the gardener (case 4)
had been handling the compost in
order to prepare the garden beds.
Following the department’s
investigation, the farm ceased the
practice of placing placental tissue
from the cattle and horses on the
compost pile and reverted to the
previous practice of burying. They
also covered the pile and employees
were told not to use the compost.
At the time of the outbreak, none
of the staff reported having been
aware of Q fever, and none had
been vaccinated for Q fever. The
farm manager arranged for three
employees whose serology results
were negative to be offered Q fever
vaccination and implemented a policy
to have new employees screened
prior to employment.
Discussion
In this report, we describe an
outbreak of Q fever among workers
on a rural property that appears to
have occurred through environmental
exposure to placental material
from cattle. The suspected mode
of transmission was either direct
contact with the material, or airborne
transmission from the compost heap
following the introduction of these
materials into composting practices.
Based on serological evidence, five
out of eight employees were infected;
four developed clinical illness of
variable severity.
The property was a mixed farming
operation, with eight full-time
staff: three horse handlers, two
gardeners, two general farm hands
and a farm manager. Intriguingly,
one from each of these occupational
groups did not develop symptoms
and were found to be negative on
serology. While the horse handlers
had little involvement with the cattle
operation, the gardeners’ worked
primarily in the gardens around the
main farm buildings adjacent to
the horse enclosure. At the time of
the outbreak, it was reported that
the gardeners had been spreading
compost on the garden beds. To our
knowledge this is the first report of a
Q fever outbreak related to a change
in practice motivated by sustainable/
organic farming principles.
One limitation of this study is the
variable testing of those affected in
different pathology laboratories using
different serological techniques.
Furthermore, testing was not
undertaken in most cases until
10 days to six weeks after onset
of clinical symptoms, and the
time elapsed between initial and
subsequent blood tests was short
(7–12 days).
In Victoria, Q fever has been a
notifiable disease in humans since
1991.10
Since 2005, there were an
average of 25 cases notified to the
Victorian Government Department of
Health each year, with a total of 20
confirmed cases of Q fever notified
in 2011. Most notified cases are
sporadic and the majority are linked
to high-risk occupational exposures
(Table 2). For example, of the cases
notified in 2011 (inclusive of the
outbreak described in this report),
12 were in full-time employment with
details regarding their work available;
nine were linked to farms, one was
a veterinarian, one was a gardener
on an agricultural property and one
was a tradesperson who worked in
abattoirs.
The 2011 outbreak was the first
reported in Victoria since 2006, when
there were two abattoir-associated
outbreaks (one involving infections
among people using a walking track
adjacent to an abattoir, the other
among employees at a separate
abattoir). There were four outbreaks
in 2005 and one each in 2003 and
2002. The largest outbreak ever
reported in Victoria occurred in 2002
and involved 28 Q fever infections in
abattoir employees.
Similar to the outbreak described
in this report, one of the outbreaks
in 2005 involved a change in work
practice, although this occurred at
a cosmetic company. The company
used animal-birth-products in the
production of facial powders and
health products for export, and
implemented a change in procedure
so that frozen animal-birth-products
were thawed before being boiled.
Previously the birth products had
been boiled directly from a frozen
state. Four staff working with these
Table 2: Notified cases of Q fever by occupational category, Victoria,
2000–2011
Year Cases
Number of cases
where occupation
was stated
Number of cases
who work in a high-
risk occupation
% high risk
occupation
2000 23 0 NA NA
2001 55 51 45 88%
2002 76 72 63 87.5%
2003 17 17 15 88%
2004 26 21 16 76%
2005 31 27 22 81.5%
2006 32 23 13 57%
2007 34 24 18 75%
2008 21 18 12 67%
2009 23 22 17 77%
2010 19 15 13 87%
2011 20 12 10 83%

products developed Q fever following
this process change.11
While animals infected with Q fever
rarely show any symptoms, they can
shed the bacteria in large numbers in
urine, faeces, milk and birth products.
The bacteria are resistant to heating,
drying and sunlight, and can survive
for more than a year in a dried
state. Q fever is commonly spread
by inhalation of infected material,
particularly from placental tissue and
fluids, or being splashed with infected
urine or blood. Indirect contact with
infected animals or contaminated
straw, manure, wool, hair, hides, dust
or clothing, or drinking unpasteurised
milk can also result in the spread of
the disease.12
Q fever vaccination is the primary
preventive measure for those at
occupational risk. Although infection
with Q fever in Victoria has previously
been most common in abattoir
workers, notifications among animal
farmers and farm workers are
now more common. None of the
individuals infected in this outbreak
had previously been vaccinated,
nor heard of Q fever. Consideration
should be given to specific education
regarding Q fever and the factors
associated with increased risk of
infection, plus the availability of
vaccination, targeted to animal farm
owners and workers.
Acknowledgements
The authors wish to thank the staff on
the property involved in the outbreak
for their enthusiasm and willingness
to share information for the purposes
of this outbreak investigation. In
addition, we wish to thank Roger
Paskin at The Department of Primary
Industries (Victoria) for his assistance
in the veterinary epidemiology aspects
of the investigation, and finally, the
laboratories who undertook the
testing for these cases: The Australian
Rickettsial Reference Laboratory,
Institute of Medical and Veterinary
Science, South Australia (IVMS),
Healthscope and the Victorian
Infectious Diseases Reference
Laboratory (VIDRL).
References
1. Derrick EH. “Q” fever, a new fever
entity: clinical features, diagnosis
and laboratory investigation.
MJA.1937; 2:281–299
2. Burnet FM, Freeman M.
Experimental studies on the virus of
“Q” fever. MJA.1937; 2:299–305
3. Brotherton J, Wang H, Schaffer
A, Quinn H, et al. Vaccine
Preventable Diseases and
Vaccination Coverage in Australia,
2003 to 2005. Commun Dis Intell.
2007;31(Supplement): S65–68
4. Communicable Diseases
Network of Australia. Australian
national notifiable diseases case
definitions. Australian Government
Department of Health and Ageing.
2004. Accessed on 21 March
2012. Available at: http://www.
health.gov.au/internet/main/
publishing.nsf/Content/cdna-
casedefinitions.htm
5. American Public Health Association
(APHA). Control of Communicable
Diseases Manual. Heymann
DL (ed), 19th
Edition. 2008;
Washington DC: APHA.
6. Australian Technical Advisory
Group on Immunisation (ATAGI).
The Australian Immunisation
Handbook, Ninth edition. 2008;
Canberra: Australian Government
Department of Health and Ageing
7. Australian Government Bureau
of Meteorology (2012) Victorian
Rainfall Totals (mm) for Victoria:
October 2011. Product of the
National Climate Centre. Accessed
on: 20 February 2012. Available at:
http://www.bom.gov.au/jsp/awap/
rain/index.jsp?colour=colour&time=
history%2Fvc%2F2011110120111
130&step=12&map=totals&period
=month&area=vc
8. Australian Government Bureau of
Meteorology (2012). Six-monthly
mean temperature for Victoria: 1
September 2011 to 29 February
2012. Product of the National
Climate Centre.Accessed on: 20
February 2012. Available at: http://
www.bom.gov.au/jsp/awap/temp/
index.jsp?colour=colour&time=hist
ory%2Fvc%2F2011090120120229
&step=8&map=meanave&period=6
month&area=vc
9. Department of Natural Resources
and Environment. Vegetation
Profile for the Euroa-Nagambie
Wetlands and Gilgai Plains. 2000.
Melbourne: State Government of
Victoria. Accessed on 7 February
2011. Available at: http://www.
gbcma.gov.vic.au/revegetation
10. National Notifiable Diseases
Surveillance System Annual Report
Writing Group. Australia’s notifiable
disease status, 2009: Annual report
of the National Notifiable Diseases
Surveillance System. Commun Dis
Intell, 2011. 35(2):61–131
11. Wade AJ, Cheng AC, Athan E,
Molloy JL, Harris OC, Stenos J,
Hughes AJ. Q Fever Outbreak
at a Cosmetics Supply Factory.
Clinical Infectious Diseases 2006;
42:e50–2
12. Nugent T. Vaccinate to prevent
Q-fever. Farming Ahead.2003;
140:72

Reports of blood stream infections and meningitis to the
Victorian Hospital Pathogen Surveillance Scheme, July–
December 2012
Marion Easton
Microbiological Diagnostic Unit – Public Health Laboratory, The University of Melbourne, Victoria
This account describes reports of blood stream infections and meningitis to the Victorian Hospital Pathogen Surveillance
Scheme (VHPSS) for the second half of 2012, and provides a brief summary of 2012 data and comparison with recent years.
The VHPSS provides voluntary, laboratory-based surveillance of bacterial and fungal agents of blood stream infections and
meningitis in Victoria. Although not all laboratories participate, the data are broadly representative and readily interpretable to
provide insights into the wider population.
Surveillance case definitions
A case of bacteraemia or meningitis
is defined as the first isolation of
a clinically significant bacterium
or fungus from the blood or
cerebrospinal fluid (CSF) of a person
in a 14-day period. When more
than one species of bacteria/fungi
are reported from a blood culture
or CSF each isolate are counted
as a separate case. The reporting
period is defined by specimen
collection dates. An organism
may sometimes be identified
and reported by the diagnostic
laboratory only to the level of genus
or may be incompletely speciated
(where definitive identification is
unnecessary for patient care).
Therefore some organism categories,
such as coagulase-negative
Staphylococcus and Staphylococcus
epidermidis overlap. For this
report all Staphylococcus species
that are not S. aureus have been
categorised as coagulase-negative
Staphylococcus. Previous VHPSS
accounts have included the species
of Staphylococcus as reported
by the laboratories and as such
the counts of coagulase-negative
Staphylococcus are lower than in this
report. Five year comparative data for
Staphylococcus species have also
been re-categorised for this report.
Variable reporting of suspected
contaminants may also affect counts.
Summary of the
important agents of
bloodstream infection
and meningitis, July–
December 2012
Cases reported to the VHPSS
during this six-month period were
diagnosed by 18 laboratories and
were associated with 99 Victorian
hospitals. There were 3,658 reports
(3,639 bloodstream and 19 CSF
isolates) of 243 species/types of
bacteria and fungi. The twenty most
common organisms accounted for 82
per cent of reports (Table 1).
The ranking of the 20 most common
isolate types remain relatively stable,
with E coli and S. aureus the most
common (28 per cent and 14 per
cent of all reports respectively).
Coagulase-negative Staphylococcus
is the third most common organism
for this period. The increase in
report numbers from the January
to June period (71 – ranked ninth)
was due to the incorporation of all
non-S. aureus staphylococci into
one category. Both Streptococcus
mitis and Streptococcus mitis group
are among the most common
isolates. The S. mitis group includes
a number of species that are related
to S. mitis and, due to the use of
different identification protocols, not
all laboratories fully speciate these
viridans streptococci. Changes in
laboratory protocols may have led
to an increase in the number of
isolates included in the S. mitis group
as compared to the previous five
year average. Descriptions of some
isolates of interest are included in the
later section of this report.
Reported antimicrobial
resistance of some invasive
bacterial pathogens, July–
December 2012
In the second half of 2012 the
proportion of S. aureus isolates that
were methicillin-resistant was lower
than the previous five-year average
(Table 2). The level of resistance
has remained at less than 20 per
cent since the July to December
period of 2008.1
The proportion of
resistance varies with the length of
hospital duration prior to specimen
collection. Resistance is more
common among S. aureus isolates
from specimens collected after seven
days of hospitalisation (22 per cent)
than among those collected between
two and seven days hospitalisation
(14 per cent) and prior to three
days hospitalisation (16 per cent).
There were no reports of S. aureus
isolates with reduced susceptibility to
vancomycin during this period.
Twelve isolates of S. pneumoniae
were reported to be penicillin non-
susceptible (PNSP) in this period.

Table 2: Prevalence of key antimicrobial resistances of S. aureus, S. pneumoniae and enterococci, July–December 2012
Period
Staphylococcus aureus
Streptococcus
pneumoniae Enterococcus faecalis Enterococcus faecium
Methicillin
resistant (%)
Isolates
tested (n)
Penicillin non-
susceptible (%)
Isolates
tested (n)
Vancomycin
resistant (%)
Isolates
tested (n)
Vancomycin
resistant (%)
Isolates
tested (n)
Jul–Dec 2012 16% 523 6% 211 0 127 54% 97
Mean Jul–Dec
(2007–2011)
18% 449 9% 211 1% 113 48% 71
Nine PNSP reports included minimum
inhibitory concentration (MIC) data
for penicillin; MIC values ranging
between 0.25mg/L and 4mg/L. A
further 15 isolates with penicillin
MICs ranging from 0.125mg/L to
2mg/L were reported without a
susceptibility category (susceptible
or non-susceptible) as the patients
clinical syndrome (meningitis or
non-meningitis), which defines the
susceptibility category, was unknown
to the laboratory.2
All twelve confirmed
PNSP cases were in adults aged
between 36 and 88 years, with
a median age of 57 years. The
confirmed PNSP were four serotype
19A, three serotype 15A, two serotype
11A and one each of serotypes 15C,
23A and 9V. Most S. pneumoniae
reports (92 per cent) included
susceptibilities for either cefotaxime or
ceftriaxone; one of the twelve PNSP
isolates had reduced sensitivity to
cefotaxime.
There were no reports of vancomycin-
resistant E. faecalis in the second
half of 2012. Thirty-nine of the 52
reports of vancomycin-resistant E.
faecium included results of van gene
PCR testing; all isolates were vanB
positive.
Reports of the susceptibility of
E. coli to amoxicillin, ceftazidime,
ciprofloxacin and gentamicin were
available for 98 per cent, 56 per
cent, 86 per cent and 99 per cent of
isolates respectively. Among E. coli
isolates with susceptibility data, 52
per cent were resistant to amoxicillin,
eight per cent to ceftazidime, 10 per
cent to ciprofloxacin and seven per
cent to gentamicin. Among isolates
with adequate data 59 (six per
cent) isolates were resistant to both
amoxicillin and gentamicin and eight
(1.5 per cent) were resistant to all four
of these antimicrobial agents.
Summary of the
important agents of
bloodstream infection
and meningitis in 2012
Cases reported to the VHPSS
during 2012 were diagnosed by 20
laboratories and were associated with
120 Victorian hospitals. In 2012 there
were 7152 reports (7120 bloodstream,
and 32 CSF isolates) of 327 species/
types of bacteria and fungi.
The 20 most common organisms
reported for 2012 were the same
Table 1: Twenty most common isolates reported to VHPSS, July–December
2012
Organism name
Total
Jul–Dec
2012
Mean
Jul–Dec
(2007–2011)
Total
2012
Annual
mean
(2007–2011)
Escherichia coli 980 759 1983 1514
Staphylococcus aureus 523 449 1033 882
Coagulase negative Staphylococcus 281 290 560 540
Streptococcus pneumoniae 227 219 372 356
Klebsiella pneumoniae 150 131 298 280
Enterococcus faecalis 128 113 231 221
Enterococcus faecium 97 71 147 135
Pseudomonas aeruginosa 82 84 212 177
Group B Streptococcus 73 50 135 97
Enterobacter cloacae 59 55 136 118
Group A Streptococcus 58 52 113 98
Klebsiella oxytoca 52 51 116 101
Haemophilus influenzae 48 28 63 48
Proteus mirabilis 43 45 89 89
Group G Streptococcus 35 25 61 54
Candida albicans 34 33 77 69
Streptococcus mitis group 33 11 60 23
Bacteroides fragilis 32 22 57 45
Serratia marcescens 29 22 56 49
Streptococcus mitis 25 24 42 48
Total of top 20 isolate types 2989 - 5841 -
Total of other isolate types 669 - 1311 -
Total of all isolates 3658 3056 7152 6030
Total isolate types 243 - 299 -

as those reported in the second
half of the year (Table 1) though the
ranking of some organisms was
slightly different. Counts of some of
the moderately common, typically
healthcare-associated, Gram-negative
isolates fluctuate; these may reflect
clusters of cases in particular settings.
The 20 most common organisms
accounted for 82 per cent of all
reports to VHPSS in 2012. The overall
number of reports in 2012 was 19 per
cent more than the average for the
previous five years. This increase was
evident for the majority of common
organisms with E. coli having the
greatest increase (31 per cent).3
The number of reports of S.
pneumoniae to VHPSS in 2012
was only marginally higher than the
five-year average for 2007 to 2011
(372 and 356 respectively). Following
an increase in report numbers from
281 in 2007 to 406 in 2011 the
number declined to 372 in 2012.
This was mostly due to the decline
in isolates with serotypes included
in the 13-valent conjugate vaccine
(13vPCV) introduced into the National
Immunisation Programme in July
2011.4
The number of 13vPCV
isolates declined from 222 in 2011
to 193 in 2012, mostly due to a
decrease in serotype 19A among
children aged less than five years.
In 2012 there were 26 reports of
invasive pneumococcal disease from
children aged less than five years. Ten
isolates were serotypes included in
the 13vPCV vaccine; seven serotype
19A, two 7F and one 19F. There
were 16 isolates of serotypes not
included in the 13-valent vaccine.
One hundred and fifty-one isolates
of S. pneumoniae reported in 2012
were from adults aged 65 years or
more, 97 (64 per cent) were serotypes
included in the 23-valent vaccine.
The predominant serotypes in this
age group were 23-valent vaccine
serotypes 19A, 3 and 7F (26, 16 and
15 isolates respectively) and non-
vaccine serotype 6C (20 isolates).
There were 63 reports of H. influenzae
in 2012. Of the 62 with typing data,
54 (87 per cent) were non-typeable.
The eight typeable isolates comprised
three type b (one case of meningitis
in a 49 year old and two cases in
children aged three months and
12 years with no reported clinical
syndrome), four type f (persons aged
two months, 29, 34 and 58 years)
and one type e (aged 81 years).
Twenty-three cases of invasive
meningococcal disease were reported
to VHPSS in 2012. Isolates of N.
meningitidis comprised 19 serogroup
B (two infants aged less than one
year, a further three aged less than
five years, three adolescents 17, 18
and 18 years and 10 adults aged 21
to 82 years (median 31 years)) and
four serogroup Y (persons aged three
months, 32, 51 and 70 years).
In 2012 there were 32 reports of
isolates from CSF, which comprised
14 species of bacteria and yeasts.
The five most common species were
coagulase negative Staphylococcus
(seven isolates of which six were
healthcare-acquired), and the
typically community-acquired isolates
Streptococcus pneumoniae (six
isolates), Neisseria meningitidis (four
isolates), Listeria monocytogenes
(four isolates) and Haemophilus
influenzae (three isolates).
Reported antimicrobial
resistance of some
invasive bacterial
pathogens, 2012
The proportion of S. aureus isolates
manifesting methicillin resistance was
the same as 2011 and lower than
the previous five-year average (18
per cent) (Table 3). Seventy-five (47
per cent) of the 159 reports of MRSA
included data on six key antimicrobial
agents (ciprofloxacin, erythromycin,
fusidic acid, gentamicin, rifampicin
and tetracycline). Fifty-seven (76
per cent) of these isolates were
non-multiresistant MRSA (nmMRSA
– resistant to methicillin and agents
from no more than two other
antimicrobial agents). Forty of 47
bacteraemic nmMRSA isolates with
reported case admission dates were
Table 3: Prevalence of key antimicrobial resistances in S. aureus, S. pneumoniae and enterococci, 2007–2012
Year
Staphylococcus aureus Streptococcus Pneumoniae Enterococcus faecalis Enterococcus faecium
Methicillin
resistant
(%)
Isolates
tested
(n)
Penicillin non-
susceptible
(%)
Isolates
tested
(n)
Vancomycin
resistant
(%)
Isolates
tested
(n)
Vancomycin
resistant
(%)
Isolates
tested
(n)
2007 23% 841 7% 280 2% 176 35% 92
2008 19% 893 12% 348 1% 207 34% 134
2009 16% 943 9% 349 2% 241 48% 152
2010 19% 844 9% 382 6% 227 55% 156
2011 15% 889 7% 379 0% 252 52% 139
2012 15% 1033 7% 372 0% 231 54% 147

from specimens collected less than
three days into hospitalisation and
therefore suggestive of community-
acquired MRSA.
Twenty-four isolates of penicillin non-
susceptible S. pneumoniae (PNSP)
were reported to VHPSS in 2012 with
MIC values between 0.125mg/L and
4.0mg/L. Eleven (46 per cent) of the
PNSP isolates were serotype 19A.
The other PNSP isolates comprised
seven serotypes; six serotype 15A,
two serotype 9v and one each of 11A,
12F, 15C, 19F and 23A. A further
25 isolates with MICs ranging from
0.125mg/L to 2mg/L were reported
without a susceptibility category
(susceptible or non-susceptible)
as the patients clinical syndrome
(meningitis or non-meningitis), which
defines the susceptibility category,
was unknown to the laboratory.
In 2012 two PNSP were reported
from children aged less than five
years (serotype 19A – included in the
13-valent vaccine, and 12F). Of the
nine PNSP isolates from adults aged
65 years or more five were serotypes
included in the 23-valent vaccine
(three 19A and one each of 11A
and 9V) and four were non-vaccine
serotypes (three 15A and one 23A).
There were no reports of vancomycin-
resistant E. faecalis to VHPSS in
2012. Fifty-seven of the 79 reports
of vancomycin-resistant E. faecium
included van gene PCR results. Fifty-
five isolates were vanB gene positive,
one was vanA gene positive and the
other contained both vanA and vanB
genes.
In 2012 there were seven
reports of carbapenem resistant
Enterobacteriaceae (CRE), all of which
were resistant to meropenem. Five
of the 200 Klebsiella pneumoniae
isolates with reported carbapenem
susceptibilities were resistant. The
other two CRE were an Escherichia
coli and a Proteus mirabilis (1,233
and 50 reports respectively included
susceptibility data).
Acknowledgments
We gratefully acknowledge the
confidential contributions of Victorian
laboratories to VHPSS, the support
provided by the Victorian Department
of Health, and data management by
Wendy Siryj and Eleanor Latomanski.
Data include reports received by
1 March 2012, and are subject to
revision.
References
1. Easton M, Veitch M. Ten years
of Staphylococcus aureus
bloodstream and cerebrospinal
fluid isolates in Victoria: reports to
the Victorian Hospital Pathogen
Surveillance Scheme, 1999–2008.
Victorian Infectious Diseases
Bulletin. 2010;13(1):2–6
2. Clinical and Laboratory Standards
Institute. Performance standards
for antimicrobial susceptibility
testing; Twenty-third Informational
Supplement. CLSI document
M100–S23; 2013
3. Easton M, Hogg G. Ten years of
Escherichia coli bacteraemia and
meningitis in Victoria; reports to
the Victorian Hospital Pathogen
Surveillance Scheme, 2002–2011.
Victorian Infectious Diseases
Bulletin 2012 (in publication)
4. Australian Government Department
of Health and Ageing (2013).
The Australian Immunisation
Handbook, 10th edition, Australian
Government, Canberra

Immunisation program report, Victoria, March 2013
Helen Pitcher, Department of Health, Victoria
Immunisation report
The local government area
immunisation coverage table for the
three measured cohorts of children
up to five years of age can once
again be provided in this and future
reports. The coverage data provided
quarterly by the Australian Childhood
Immunisation Register (ACIR) has
been withheld since June 2012. The
Commonwealth Government recently
determined that the coverage data
can now be released under the Health
Insurance Act 1973.
Immunisation coverage data cited
in this report are based on the ACIR
coverage report. Table 1 presents
immunisation coverage at 30
September 2012 for children aged
12–<15 months, 24–<27 months and
60–<63 months of age. These data
were processed at 31 December
2012. Only those immunisation
services a child has received up to 12
months, 24 months and 63 months
of age are included in this table. ACIR
reported immunisation coverage
against individual vaccines for each
local government area are available
upon request from the Immunisation
Section, Department of Health, Victoria
(immunisation@health.vic.gov.au).
The ACIR report measures vaccine
coverage for diphtheria, tetanus,
pertussis, poliomyelitis, hepatitis B,
Haemophilus influenzae type b,
measles, mumps, and rubella
vaccines. The report does not
measure vaccine coverage for:
• hepatitis B vaccine given at birth
• rotavirus vaccine given at two, four
and six months of age
• pneumococcal vaccine given at
two, four and six months of age
• meningococcal C (MenCCV)
vaccine given at 12 months of age
• varicella vaccine given at 18
months of age.
Data are presented for three cohorts.
For each cohort it is assumed that all
previous vaccinations were received.
Children aged 12–<15 months
(cohort one) have received their third
vaccination for diphtheria, tetanus,
pertussis, poliomyelitis, hepatitis B
and Haemophilus influenzae type b,
all prior to the age of one year.
(cohort two) have received their third
vaccination for diphtheria, tetanus,
pertussis, poliomyelitis, hepatitis B
and their fourth dose of Haemophilus
influenzae type b and their first
vaccination for measles, mumps and
rubella, all prior to the age of two
years.
(cohort three) have received their
fourth vaccination for diphtheria,
tetanus, pertussis, poliomyelitis and
their second vaccination for measles,
mumps and rubella, all prior to the
age of five years.
In cohort one, 84 per cent (67 of
79) of LGAs achieved immunisation
coverage greater than or equal to 90
per cent. Victoria achieved 91.84 per
cent coverage in cohort one compared
to the Australian coverage of 91.49
per cent. Victoria ranked fourth behind
Tasmania (92.43 per cent), ACT (92.41
per cent) and Queensland (92.32
per cent) in the coverage for this age
group. Mansfield and Mount Alexander
LGAs reported coverage between 80
to less than 85 per cent in cohort one.
In cohort two, 94 per cent (74 of
coverage greater than or equal to 90
per cent. State coverage for cohort
two was 92.68 per cent compared to
the Australian coverage of 92.20 per
cent. Victoria ranked fourth behind
Tasmania (94.90 per cent), NT (93.12
per cent), and ACT (92.86 per cent)
in the coverage for this age group.
Mount Alexander LGA reported a
coverage rate between 80 to less
than 85 per cent in cohort two.
In cohort three, 93 per cent (73 of
coverage greater than or equal to
90 per cent. State coverage for
cohort three was 92.88 per cent
compared to the Australian coverage
of 91.76 per cent. Victoria ranked
second behind ACT (93.67 per cent)
in the coverage for this age group.
Melbourne and Port Phillip LGAs
reported coverage between 80 to less
than 85 per cent in cohort three.
Buloke and Queensliffe LGAs
reported 100 per cent coverage for all
three cohorts for this coverage period.

Table1: Immunisation coverage by local government area (LGA), July–September 2012, Victoria
Age group
% fully
immunised Local government area (LGA)
Total LGAs
(% LGA’S)
12–<15
months
(Cohort 1)
100 Buloke, Hindmarsh, Queenscliffe, West Wimmera 4 (5)
95+
Alpine, Colac-Otway, Golden Plains, Horsham, Southern Grampians, Wangaratta, Warrnambool,
Wodonga, Yarra
9 (11)
90–<95
Ararat, Ballarat, Banyule, Bass Coast, Baw Baw, Bayside, Benalla, Boroondara, Brimbank,
Campaspe, Cardinia, Casey, Central Goldfields, Corangamite, Darebin, East Gippsland, Frankston,
Glen Eira, Greater Geelong, Greater Shepparton, Hepburn, Hobsons Bay, Hume, Kingston, Knox,
Latrobe, Macedon Ranges, Manningham, Maribyrnong Maroondah, Melbourne, Melton, Mildura,
Mitchell, Moira, Monash, Moonee Valley, Moorabool, Moreland, Mornington Peninsula, Moyne,
Murrindindi, Northern Grampians, Port Phillip, South Gippsland, Stonnington, Strathbogie, Surf
Coast, Towong, Wellington, Whitehorse Whittlesea, Wyndham, Yarra Ranges
54 (68)
85–<90
Gannawarra, Glenelg, Greater Bendigo, Greater Dandenong, Indigo, Loddon, Nillumbik, Pyrenees,
Swan Hill, Yarriambiack
10 (13)
80–<85 Mansfield, Mount Alexander 2 (3)
24–<27
months
(Cohort 2)
100 Buloke, Central Goldfields, Glenelg, Hindmarsh, Pyrenees, Queenscliffe Yarriambiack 7 (9)
95+
Alpine, Ararat, Baw Baw, Benalla, Casey, Colac-Otway, East Gippsland Gannawarra, Greater
Bendigo, Greater Shepparton, Horsham, Latrobe Mildura, Mitchell, Northern Grampians, Swan Hill,
Wangaratta, Warrnambool, Whittlesea, Wodonga
20 (25)
90–<95
Ballarat, Banyule, Bass Coast, Bayside, Boroondara, Brimbank, Campaspe, Cardinia, Corangamite,
Darebin, Frankston, Glen Eira, Golden Plains, Greater Dandenong, Greater Geelong, Hobsons
Bay, Hume, Kingston, Knox, Loddon, Macedon Ranges, Manningham, Mansfield, Maribyrnong,
Maroondah, Melton, Moira, Monash, Moonee Valley, Moorabool, Moreland, Mornington Peninsula,
Moyne, Murrindindi, Nillumbik, Port Phillip, South Gippsland, Southern Grampians, Stonnington,
Strathbogie, Surf Coast, Towong, Wellington Whitehorse, Wyndham, Yarra, Yarra Ranges
47 (60)
85–<90 Hepburn, Indigo, Melbourne, West Wimmera 4 (5)
80–<85 Mount Alexander 1 (1)
60–<63
months
(Cohort 3)
100 Buloke, Queenscliffe, Strathbogie, Towong, West Wimmera, Yarriambiack 6 (8)
95+
Alpine, Campaspe, Casey, Central Goldfields, Colac-Otway, Corangamite, Glenelg, Horsham, Indigo,
Latrobe, Macedon Ranges, Mansfield, Maribyrnong, Mitchell, Moorabool, Northern Grampians,
Pyrenees, Wellington, Wodonga
19 (24)
90–<95
Ararat, Ballarat, Banyule, Bass Coast, Baw Baw, Bayside, Benalla Boroondara, Brimbank, Cardinia,
Darebin, East Gippsland, Frankston, Gannawarra, Glen Eira, Golden Plains, Greater Bendigo, Greater
Dandenong, Greater Geelong, Hepburn, Hindmarsh, Hobsons Bay, Hume, Kingston, Knox, Loddon,
Manningham, Maroondah Melton, Mildura, Moira, Monash, Moonee Valley, Moreland, Mornington
Peninsula, Mount Alexander, Nillumbik, South Gippsland, Southern Grampians, Stonnington, Surf
Coast, Wangaratta, Warrnambool, Whitehorse, Whittlesea, Wyndham, Yarra, Yarra Ranges
48 (61)
85–<90 Greater Shepparton, Moyne, Murrindindi, Swan Hill 4 (5)
80–<85 Melbourne, Port Phillip 2 (2)

Vaccination program updates
Prevenar 13®
supplementary
dose
The free single supplementary
dose of Prevenar 13®
, a 13-valent
(13vPCV) for children aged between
12 and 35 months inclusive, ended
on 30 September 2012. Since
1 October 2011, the Commonwealth
Government has provided the
time-limited supplementary dose
of Prevenar 13®
to eligible children
who had routinely received a course
or partial course of the seven valent
(7vPCV) Prevenar®
. Children who
receive the additional six strains in
the Prevenar 13®
vaccine will benefit
from the extra protection against
pneumococcal bacteria.
Prevenar®
was replaced with Prevenar
13®
in July 2011 on the National
Immunisation Program schedule.
Prevenar 13®
is routinely scheduled
for an infant at two (which can start
from six weeks of age), four and six
months of age. The pneumococcal
bacteria strains in Prevenar 13®
are 1,
3, 4, 5, 6A, 6B, 7F, 9V, 14, 18C, 19A,
19F and 23F.
HPV vaccine – free for boys
from 2013
On 12 July 2012, the Minister for
Health, the Hon Tanya Plibersek
MP announced funding for the HPV
vaccine Gardasil®
under the National
Immunisation Program schedule from
2013.
Year 7 secondary school boys –
ongoing program
From 2013 the HPV vaccine program
will target boys in Year 7 of secondary
school as an ongoing program
to complement the girls’ Year 7
secondary school program.
Year 9 secondary school boys –
time-limited program
For a two year period a catch-up HPV
vaccine program for Year 9 secondary
school boys will be offered at the
same time as the introduction of the
Year 7 boys’ program. This two-year
time-limited program begins in 2013
and runs again in 2014.
Boys who are age equivalent in the
funded years can also receive a free
course of Gardasil®
vaccine at their
doctor or local council immunisation
service. A Year 7 student is about
12 to 13 years of age and a Year 9
student is about 14 to 15 years of age.
Gardasil®
vaccine for boys and girls
is administered as a three-dose
course, with two months’ spacing
between doses one and two and
four months spacing between doses
two and three. All three doses are
required for protection – if a dose is
missed it should be given as soon as
practicable.
Adolescents will get the greatest
protection from the HPV types 6,
11, 16 and 18 if they are vaccinated
before becoming sexually active.
HPV types 6 and 11 protect against
90 per cent of genital warts. Type
16 protects males from about 90
per cent of cancers caused by HPV,
which include penile, anal, and
oropharyngeal cancers. HPV types 16
and 18 protect females against 70 to
80 per cent of cervical cancers.
For more information visit the Australia
government website australia.gov.au/
hpv or the Cancer Council website
www.hpvvaccine.org.au.
Hepatitis B vaccine ceasing in
secondary schools from 2013
2013 is the final year of the hepatitis B
vaccine program for Year 7 secondary
school students or age equivalent 12–
13 year olds. Most Year 7 students
will have had the hepatitis B vaccine
course as infants. Those students
who have not completed a course of
hepatitis B vaccine can still receive
the course of vaccine for free from a
doctor or local council immunisation
service in 2013. From 2014, Year 7
students will no longer be eligible for
free hepatitis B vaccine.
2013 seasonal influenza
vaccine
The Australian Influenza Vaccine
Committee (AIVC) selected influenza
viruses for the composition of the
trivalent influenza vaccines for 2013.
The expert committee reviewed and
evaluated the surveillance data related
to: epidemiology; antigenic and genetic
characteristics of recent influenza
isolates circulating in Australia and
the Southern Hemisphere; serological
responses to 2011–2012 vaccines and
the availability of candidate vaccine
viruses and reagents.
The Therapeutic Goods
Administration (TGA) accepted the
recommendations of the AIVC. For
more information visit: www.tga.gov.
au/about/committees-aivc.htm
The composition of the influenza virus
vaccine in 2013 was:
• A (H1N1): an A/California/7/2009
(H1N1) – like virus
• A (H3N2): an A/Victoria/361/2011
(H3N2) – like virus
• B: a B/Wisconsin/1/2010 – like
virus.

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