This is the html version of the file http://www.cda.gov.au/pubs/cdi/1996/cdi2019/cdi2019c.pdf.

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gene which, unlike high level resistance mediated by the
van A gene, is difficult to detect.
Efforts to contain VRE and prevent its spread to others is
necessary for the management of patients colonised with
this organism. Affected patients should be isolated and
standard infection control principles adhered to. Particu-
lar attention should be paid to the decontamination and
disinfection of the environment around the patient. The
patient should remain in isolation while colonised with
VRE or if readmitted without VRE ’clearance’. The patient
may be ’delisted’ if rectal and lesion swabs for VRE are
persistently negative (three cultures on consecutive
weeks) in hospital.
A record of VRE cases should be kept for the epidemiologi-
cal tracking of cases including their location, antibiotic
history and risk factors. Vancomycin use should be re-
served for specific conditions and hospitals should de-
velop guidelines for the proper use of vancomycin
5
.
References
1.
Neu HC. Antimicrobial agents. Role in preosocomial infections.
In Wenzel RP. Prevention and control of nosocomial infections.
Baltimore: Williams and Wilkins 2nd ed., 1993.
2.
French GL, Phillips J. Antimicrobial resistance in hospital flora
and nosocomial infections. In CG Mayhall, ed. Hospital epidemiol-
ogy and infection control. Baltimore: Williams and Wilkins, 1996.
3.
Landman D, Quale JM, Oydna E et al. Comparison of five selec-
tive media for identifying faecal carriage of VRE. J Clin Micro
1996;34:751-752.
4.
Centers for Disease Control and Prevention. Addressing emerging
infectious disease threats, a prevention strategy for the United States.
Atlanta: United States Department of Health and Human Serv-
ices, Public Health Service, 1994.
5.
HospitaL Infection Control Practices Advisory Committee. Rec-
ommendations for preventing the spread of vancomycin
resistance.
Infection Control Hospital Epidemiology 1995;16:105-113.
ACUTE FLACCID PARALYSIS SURVEILLANCE IN AUSTRALIA:
THE FIRST YEAR
Ana Herceg
1,4
, Margery Kennett
2,4
, Jayne Antony
3,4
and Helen Longbottom
1,4
Abstract
Surveillance for acute flaccid paralysis commenced through the Australian Paediatric Surveillance
Unit in March 1995. Thirty-five cases were reported in the first year, giving an estimated incidence
of 0.90 cases per 100,000 children under the age of 15 years. Nearly half the cases were Guillain-
Barre syndrome. No cases of poliomyelitis were identified. This surveillance scheme will assist in
the process of certification of the eradication of poliomyelitis in Australia and the World Health
Organization Western Pacific Region. Comm Dis Intell 1996;20:403-405.
Introduction
The World Health Organization (WHO) aims to eradicate
poliomyelitis from the world by the year 2000
1
. Poliomye-
litis has already been eradicated from the Americas
2
. For
a country to be declared polio free it needs to meet a
number of requirements, including polio vaccination cov-
erage of more than 80%, no confirmed poliomyelitis cases
for three years and adequate surveillance and investiga-
tion of suspected poliomyelitis cases.
Australia has not had any poliomyelitis cases reported
through the National Notifiable Diseases Surveillance
System since one case was reported in 1986, one case in
1978 and two cases in 1977
3
. The WHO however considers
the detection and investigation of all cases of acute flaccid
paralysis (AFP) as an essential and sensitive method of
detecting wild poliovirus.
The differential diagnosis of acute flaccid paralysis in-
cludes Guillain-Barre syndrome, transverse myelitis and
traumatic paralysis
4
. Other viruses (for example en-
terovirus types 70 and 71) may mimic polio. All these
events are rare and little is known about the incidence,
clinical course and outcomes of AFP in Australia.
In March 1995, surveillance of acute flaccid paralysis com-
menced through the Australian Paediatric Surveillance
Unit (APSU). The aims of the study were to describe the
incidence, causes and clinical picture of AFP cases in
Australia and to determine whether any cases of AFP are
caused by paralytic ’wild’ poliovirus.
Methods
A case of acute flaccid paralysis was defined as a child
aged less than 16 years with:
acute onset of flaccid paralysis in one or more limbs
or
acute onset of bulbar paralysis.
The Australian Paediatric Surveillance Unit (a unit of the
Australian College of Paediatrics) conducts active, pro-
spective national surveillance of selected rare paediatric
CDI 16 September 1996
403
Vol 20/No. 19
1.
Department of Health and Family Services, MDP 15, GPO Box 9848 Canberra ACT 2601.
2.
National Polio Reference Laboratory, Victorian Infectious Diseases Reference Laboratory, Fairfield, Vic.
3.
New Children’s Hospital, Westmead, NSW.
4.
Australian Paediatric Surveillance Unit Acute Flaccid Paralysis Study Group.
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conditions by sending a reply-paid report card each month
to over 900 paediatricians in Australia. Paediatricians are
asked whether or not they have seen any of a number of
conditions listed on the card. Over 90 per cent of paedia-
tricians return the card each month. Acute flaccid
paralysis was included on the APSU card from March
1995.
In addition to returning the APSU card, paediatricians
were asked to report cases by telephone to the principal
investigator. This was so that paediatricians could be re-
minded of the WHO requirements for stool testing and
asked to comply with them.
Paediatricians were asked to collect two stool specimens
from the case, preferably 24 hours apart, within 14 days of
the onset of paralysis. Specimens were then sent for viral
culture, in particular looking for poliovirus. If poliovirus
was isolated, it was sent to the National Polio Reference
Laboratory in Melbourne for characterisation as wild or
vaccine-like. This protocol has recently changed slightly
(see Box).
A two-page questionnaire on the clinical features, labora-
tory investigations and final diagnosis of the case was sent
to reporting paediatricians and was followed by a second
questionnaire at 60 days asking about any residual paraly-
sis.
Data analysis was performed using Epi Info version 6
5
.
Cases were classified according to WHO criteria
6
as:
Poliomyelitis:
an AFP case with wild poliovirus iso-
lation.
Non-polio AFP:
an AFP case with adequate stool
specimen testing negative, or with no
residual paralysis except if wild virus
is isolated, or
Polio-compatible:
an AFP case with residual paralysis or
who died or was lost to follow-up and
for whom stool specimens were either
not taken or were inadequate.
Results
There were 35 cases of AFP with onset dates between
March 1995 and February 1996, reported by 49 paediatri-
cians. The 35 cases in 12 months corresponded to an
incidence of 0.90 per 100,000 children under the age of 15
years.
Nineteen initial reports (54%) were by telephone. Com-
pleted questionnaires containing clinical information
were provided for 29 cases. The diagnosis alone was pro-
vided for four cases and no information at all was available
for two cases. Reports were for cases from all States and
Territories except the Australian Capital Territory (Table
1).
Of the 33 cases for which information was provided, 18
cases were male and 15 female. Their ages ranged from
two months to 12 years. There was no seasonal distribu-
tion of cases. Their reported diagnoses are described in
Table 2. Forty-eight per cent of cases were diagnosed as
having Guillain-Barre syndrome. No cases of poliomyeli-
tis were identified.
One case with a diagnosis of transverse myelitis had been
vaccinated with oral polio vaccine seven days prior to
developing paralysis; poliovirus type 3 (Sabin-like) was
identified from his stool. In addition, the case had a dem-
onstrated seroconversion to poliovirus type 3.
Thirty-two cases were hospitalised and 11 required inten-
sive care admission. Nineteen cases had paralysis of all
four limbs, six had paralysis of two limbs, one had paraly-
sis of one limb and no information was reported for seven
cases. Six cases had bulbar paralysis and six had respira-
tory depression. Nine cases had cranial nerve
involvement. Eighteen cases had residual paralysis at 60
days. There were no deaths.
Only eight cases had two stool samples taken and tested
according to WHO criteria. A further four cases had one
stool sample taken. As a result, of the 35 total cases, 17 were
classified as non-polio and 18 were classified as polio
compatible.
Discussion
The first year of surveillance of acute flaccid paralysis in
Australia has supported the presumption that Australia is
free of wild poliomyelitis. The estimated incidence of 0.90
cases of AFP per 100,000 children under the age of 15 years
is close to the one case per 100,000 expected for a polio-
myelitis-free country. Surveillance of AFP in the Americas
found an annual incidence of 1.4 cases per 100,000 children
State/Territory
Number of
cases
ACT
0
NSW
14
NT
1
Qld
9
SA
2
Tas
2
Vic
3
WA
4
Diagnosis
Number of cases
Guillain-Barre syndrome
16
Transverse myelitis
5
Demyelination
3
Encephalomyelitis
2
Trauma
2
Hypotensive brainstem necrosis or
demyelination
1
Lumbar radiculopathy
1
Post drug polyneuromyopathy
1
Infant botulism
1
Table 2.
Diagnosis for 33 cases of acute flaccid
paralysis, Australia, March 1995 -
February 1996
Table 1.
Acute flaccid paralysis cases reported by
State and Territory, March 1995 -
February 1996
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Page 3
under the age of 15
in 1991, the year in which the last case
of polio occurred
7
. In the United Kingdom, the rate is
approximately one case per 100,000 children under the age
of 16 years
8
. The three cases of AFP identified in Victoria
are fewer than the expected nine cases for that population
and indicate there may be under-reporting in that State. In
other States and Territories, the numbers of cases were as
expected.
No cases of poliomyelitis were identified by this surveil-
lance system. Although according to WHO criteria, 18 of
the cases of AFP would be classified as polio compatible,
most cases had multiple investigations and were treated
by paediatric neurologists. In these circumstances it is
unlikely that the diagnoses reported are incorrect. Paedi-
atricians are encouraged however to continue stool testing
to exclude not only poliomyelitis but other viral causes of
paralysis. In one case during this study the testing identi-
fied an echovirus type 9 as the probable cause of the illness.
The causes of AFP identified in this study are consistent
with the experience of similar surveillance in the United
Kingdom, with 48% of cases being Guillain-Barre syn-
drome and 15% transverse myelitis
8
. While no definite
vaccine-associated paralysis was identified, one case with
a diagnosis of transverse myelitis did have Sabin-like
poliovirus type 3 identified from his stool and docu-
mented seroconversion to the same virus. It is estimated
that one case of vaccine-associated paralysis will occur
with every 2.5 million doses of oral polio vaccine distrib-
uted
9
. Surveillance of AFP would be expected to
occasionally identify these cases.
Australia will shortly be undergoing scrutiny to determine
whether wild poliovirus exists in this country, as part of
the process of certification of poliomyelitis-free status in
the Western Pacific Region of the World Health Organiza-
tion. A Regional Commission for the Certification of
Poliomyelitis Eradication met for the first time in April
1996. Surveillance of cases of AFP will provide informa-
tion to assist in certifying Australia and the Region
polio-free.
While it is unlikely that Australia does have indigenous
wild poliovirus, the potential for importation of the virus
from other countries is still high. In 1992 in the Nether-
lands a wild poliovirus type 3 strain introduced from India
was responsible for a large outbreak of poliomyelitis in a
community opposed to immunisation
10
. In 1993 the same
virus was identified in Canada through active surveillance
in a linked community
11
. Continued high rates of routine
vaccination against polio are still required in Australia to
prevent similar importation. Surveillance for poliomyeli-
tis is also important so that if imported poliomyelitis does
occur, an immediate public health response can be com-
menced.
Acknowledgements
The APSU is funded by the Financial Markets Foundation
for Children and the Department of Health and Family
Services. The National Polio Reference Laboratory re-
ceives funding from the National Centre for Disease
Control of the Department of Health and Family Services,
and the Victorian Department of Human Services. We
would also like to thank the individual paediatricians and
laboratories who have contributed to this study.
References
1. World
Health
Assembly.
Global eradication of poliomyelitis by the
year 2000. Geneva: World Health Organization, 1988 (Resolution
WHA11.28).
2.
Centers for Disease Control and Prevention. Certification of po-
liomyelitis eradication - the Americas, 1994. MMWR Morb Mort
Wkly Rep 1994;13:720-722.
3.
Hall R. Notifiable Diseases Surveillance, 1917 to 1991. Comm Dis
Intell 1993:17:226-236.
4.
Benenson AS, editor. Control of Communicable Diseases Manual,
Sixteenth Edition. Washington: American Public Health Associa-
tion 1995.
5.
Dean AG, Dean JA, Coulombier D et al. Epi Info, Version 6: a word
processing, database, and statistics program for epidemiology on
microcomputers. Atlanta: Centers for Disease Control, 1994.
6.
Report of the Interim Meeting of the Technical Advisory Group
on the EPI and Poliomyelitis Eradication in the Western Pacific
Region, Beijing, October 29-November 2 1994. Report series num-
ber RS/94/GE/40 (CHN).
7.
Andrus JK, de Quadros CA, Olive J-M. The surveillance chal-
lenge: final stages of eradication of poliomyelitis in the Americas.
MMWR Morb Mort Wkly Rep CDC Surveill Summ 1992:41:21-26.
8.
Salisbury DM, Begg NT. Surveillance of poliomyelitis in the
United Kingdom. Public Health Rev 1993-4;21:35-40.
9.
Strebel PM, Sutter RW, Cochi SL, et al. Epidemiology of polio-
myelitis in the United States one decade after the last reported
case of indigenous wild virus-associated disease. Clin Inf Dis
1992;14:568-579.
10. Oostvogel PM, Van Wijngaarden JK, Van der Avoort HGAM et
al. Poliomyelitis outbreak in an unvaccinated community in the
Netherlands, 1992-93. Lancet 1994;344:665-70.
11. Health and Welfare Canada. Wild poliovirus isolated in Alberta,
1993. Canada Comm Dis Rep 1993;19:57-58.
Reporting cases of acute flaccid paralysis
Paediatricians should report cases of acute flaccid paraly-
sis to the Australian Paediatric Surveillance Unit (APSU),
and by telephone to Dr Ana Herceg on (06) 289 8638.
Stool specimen testing
Two stool specimens from every case of AFP should be
collected, preferably 24 hours apart, within 14 days of the
onset of paralysis. Following a World Health Organization
Technical Advisory Group meeting in Canberra in April
1996, the laboratory protocol for testing stool specimens
for AFP has changed. The WHO states that specimens
should be tested in a WHO certified laboratory. In Austra-
lia, only the National Polio Reference Laboratory is
certified.
All stool specimens should now be sent directly to the
National Polio Reference Laboratory in Melbourne, not to
the State or Territory virology laboratory as previously
requested. Laboratories can obtain information on speci-
men transport from Mrs Margery Kennett on (03) 9280
2397. The National Polio Reference Laboratory will pay for
specimen transport.
CDI 16 September 1996
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Vol 20/No. 19

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