![]()
|
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
A descriptive epidemiology of giardiasis in New Zealand and
gaps in surveillance data
Ekramul Hoque, Virginia Hope, Robert Scragg, Michael Baker,
Rupendra Shrestha
Public health interest in
Giardia is increasing because of the
growing recognition of its role as a cause of disease outbreaks in a range of
settings.1–3
Giardia duodenalis is now the most
widespread human intestinal parasite in the world. Approximately 200 million
people are infected with the parasite globally, with 500,000 new cases reported
annually.4 Giardiasis occurs throughout
tropical and temperate regions. In developed countries,
Giardia has the distinction of being
the most commonly reported human parasite.5 The
prevalence of the disease varies from 2%–5% to 20%–30% in developed
and developing countries respectively.6,7
A prevalence of 2%–7% has been reported for most
developed countries, including North America, Australia, and New
Zealand.8 Most infected persons will remain
asymptomatic, thus acting as a source of infection for other persons in the
community.9
Giardiasis has been a notifiable disease in New Zealand
since 1 July 1996. Before then, surveillance data were collected on an ad hoc
basis.10 Giardiasis is the third-most commonly
notified communicable disease in New Zealand, after campylobacteriosis and
salmonellosis. Between 1500 and 2200 cases of
Giardia infection are notified each
year. The incidence rate in New Zealand in 2002 was 41.4 per 100,000
population11 and is thought to be one of the
highest among developed countries.10
This paper aims to describe the epidemiology of giardiasis
in New Zealand based on the first 4 years of notification data. It also applies
a number of analytical approaches to evaluate the quality of surveillance data
and to detect spatial and temporal trends.
MethodsGiardiasis notifications for
New Zealand for the 4-year period July 1996 to June 2000 were collected from the
national notifiable disease database, EpiSurv, operated by Environmental Science
and Research (ESR) Ltd. Population data were accessed from Supermap, which was
based on the 1996 New Zealand census.
The New Zealand surveillance data were checked for
consistency and validity, and logical values were introduced as necessary. The
surveillance data were grouped by age, gender, ethnicity, Local Authority (as
area of residence) and reporting month and year. Ethnicity was categorised into
four groups: Pakeha/European, Maori, Pacific people, and Asian/others. Crude
annual infection rates for these groups were calculated and adjusted for age,
gender, ethnicity, and area of residences (as appropriate) using a direct
standardised method.
Giardia
infection rates, both crude and adjusted, were calculated and plotted
geographically using ArcView 3.0 GIS,12 to
compare the distribution of cases by Local Authority (LA) and Health District
(HD). A spatial map of New Zealand was initially divided by LA boundaries.
Blocks of LAs were merged together to define Health District boundaries.
Notification rates were converted separately into ArcView shape files for LAs
and HDs, which were then overlaid on the respective maps. To highlight the rate
differences between geographic areas, infection rates were expressed in groups
and in descending order.
Overseas data were collected from the surveillance
networks of Australia (NSW Health, Victoria Health), Canada (Canada Com Dis
Report), the United Kingdom (PHLS), and the United States (CDC). Their data were
available for periods of 2 to 9 years, depending on jurisdiction. The
denominator populations used were those from the census data published by the
respective government census authorities.
ResultsBetween July 1996 and June 2000,
there were 7818 notifications throughout New Zealand. There were three missing
cases for age. Gender was recorded for 99% of cases. Of these, half (50.10%)
were females. There was no significant difference in age between genders
(Chi²=1.04).
The mean age for giardiasis cases was 26.0 (SE 0.23) years.
Rates showed a bimodal pattern, peaking in children under 5 years of age and in
the 25–44 years age group. The infection pattern did not change after
adjusting for ethnicity, gender, or area of residence in combination or
separately. Notification rates were higher among male children in the 1–4
years age group, whereas females had higher rates in the 25–34 years age
group (Figure 1).
The completeness of information varied by Public Health Unit
(PHU) and time. Ethnicity was recorded for 82% of cases. Of these, most were of
Pakeha/European origin. Maori and Asian/others shared equal proportions of
notifications, whereas Pacific people accounted for only 1%. The incidence of
giardiasis varied significantly between ethnic groups (Chi² 2133, df 5,
p<0.0001). The Asian/other category had a two-fold increased risk of
infection compared with Europeans, whereas Pacific people and Maori rates were
lower than for Europeans (Figure 2).
The proportion of age specific notifications across the
ethnic groups was similar other than for the Maori population who were
distributed more towards the younger (<10 years) age group (Table1). A
significant difference in mean age among ethnic groups was also observed
(F=18.2, p<0.0001). The mean age was higher for females than for males in
each ethnic group other than for Asian/others, for whom the opposite was true.
The Local Authority (LA) was used as the unit for residence.
Notification data from 73 LAs were analysed; no notifications were from the
Chatham Islands. Infection rates varied widely across the boundaries of LAs from
7.86/100,000 (Stratford, Taranaki) to 117.03/100,000 (Hurunui, Canterbury).
Notification rates for the North and South Islands were 57 and 42 cases per
100,000 population, respectively. This variation was statistically significant
(Chi²=534.08, p<0.0001).
Analysis of unadjusted giardiasis rates by LA showed high
notification rates (>100/100,000) in parts of the East and West Coasts of the
South Island and in one area of the central North Island. Moderately high
notification rates (>60/100,000) were also found in the West Coast, central
Canterbury, the south of the South Island, the central North Island, Gisborne,
Hastings, Rotorua, Waikato, Auckland, and Wellington. When these rates were
adjusted for age, gender and ethnicity, the notification rates in
‘moderately high’ areas actually increased.
Local Authorities (LAs) were further aggregated to form the
24 Health Districts (HDs). Information on ethnicity was incomplete for a number
of HDs, mostly in the North Island, including (in descending order) Taupo,
Hawke’s Bay, Tauranga, Ruapehu, Auckland, and Rotorua (Figure 3). The
proportion of missing information on ethnicity was statistically significant for
these HDs separately compared to total cases. For example, Auckland Health
District (chi²=1685.08, p<0.0001), Rotorua and Taupo (chi²=345.37,
p<0.0001), and Tauranga (chi²=956.33, p<0.0001) all had significantly
high proportions of undocumented ethnicity in case notifications.
Notification rates were low in a number of HDs but remained
high for many others compared to the national rate of
46/100,000,13 including the West Coast,
Wellington, Waikato and Tauranga (Table 2). When infection rates were adjusted
for age, gender, and ethnicity, no additional changes were observed except for
the West Coast (of the South Island). This variation disappeared when ethnicity
was removed from controlling factors, suggesting a confounding effect.
The proportion of change in notification rate was calculated
for each HD for the most recent year compared to previous years by using the
formula: {(CR÷PR-1)×100}, where CR denotes current rate and PR denotes
the average rate for previous years. A substantial reduction (50%) in infection
rates was found in Wanganui and Gisborne (Figure 4). Rates were higher in the
Wairarapa, central Auckland, Hawke’s Bay, and in the Ruapehu region; rates
remained unchanged in north-west Auckland, and in Taupo.
Analysing giardiasis notification rates by Health District
‘evened-out’ the range of rates to some extent. The notification
rates for Auckland, central Canterbury, and southeastern Otago dropped from the
>60/100,000 to <60/100,000 category (Figure 5). However, some areas of the
North Island increased their rates at the expense of adjacent zones; for
example, Tauranga rates increased compared to the comparable LA
distribution.
A significant seasonal variation of Giardia notification was
observed (Edward’s test: Chi²=15.0, df=2. p<0.001), peaking in
late summer and early autumn. This varied by age group with, for example, the
10-19 year group rate peaking in autumn (Edward’s Chi ²=5.30, df=2,
p=0.07), and a sustained high in late summer, autumn and in winter in the 1-4
(Edward’s Chi ²=36.99, df=2, p<0.0001) and 25-44 (Edward’s
Chi ²=17.62, df=2, p<0.0001) year group rates.
DiscussionThis study provides the first
comprehensive review of national giardiasis notification data since the disease
became notifiable in June 1996. It describes the main epidemiological
characteristics of the disease in New Zealand, and also highlights potential
improvements to the quality of surveillance data.
Giardiasis notifications were evenly distributed between
genders in this study. This is inconsistence with one earlier GP-based active
surveillance study which reported a higher proportion of cases for females than
males at a regional level.14 However, the
gender difference was not statistically significant in either study. An overseas
prevalence study, however, reported a significant increase in infection rates
for females.15
The mean age for all cases nationally (and by gender) was
consistent with other published reports where the means for females were
slightly higher than for males but not significantly
so.14 This finding was also consistent with our
study of Auckland notification data.10 A higher
mean age in females of childbearing age may reflect closer association with
children, resulting in person-to-person transmission. However, an increased rate
of Giardia infection in females is not
universal either in developed8 or developing
countries.16 The gender difference, therefore,
could be biased by presenting behaviour, ethnicity and socioeconomic conditions.
A pattern of transmission typical of developing countries is not uncommon among
minorities or economically disadvantaged
groups.10,17 The bimodal pattern of infection
peaking in children under 5 years old and in adults 20–40 years is common,
especially in developed countries.8,14,18,19
Cross-sectional studies in Australian Aborigines, and in Africa and Asia found
the highest incidence in those among under 15 years, especially in the
6–14 years age group.17,20,21
Infection rates in children may be confounded by ethnicity.
Ethnicity differences in the under 5 age group were highly significant
(chi²=474.05 df=4, p<0.0001). Australian data indicated a higher
proportion of Giardia infection among
Aborigine children.17 However, a US survey of
pre-school children attending early childhood education facilities reported an
eight-fold lower infection rate in children of African (Black) descendants
compared with their White counterparts.22 Very
high rates of notifications observed for some ethnic groups in a number of HDs
could be due to misclassification error or unreported outbreaks; for example,
the high rates among Asians in the West Coast and elsewhere or the unknown
ethnic group in Tauranga (Table 2).
The pattern of
Giardia infection has remained
relatively similar over the years, but variations in rates persist between the
areas. Although infection rates decreased in most areas, they have increased in
five areas (representing 30% of the national population). No specific reasons
for these changes have been promoted. Random variation in yearly rate could be a
possibility. However, anecdotal reports suggest that enhanced surveillance,
better provision of drinking water, and health promotion are likely to have
contributed to these changes in some
areas,10—eg, in the West Coast (Humphrey
A, Canterbury Health, NZ – personal communication). Nevertheless,
reductions in giardiasis notifications of up to 50% in a number of HDs, compared
to the previous rates, warrants further investigation.
Infection rates in the South Island were lower than in the
North Island compared to the national average
rate.11 Among the 12 PHUs reporting average
annual infection rates above the national average for 2000, two were in the
South Island, and the remainder from the North Island. Of the 12 PHUs, the West
Coast (of the South Island) had the highest infection rate (93.2/100,000),
followed by Wellington (83.5/100,000). Three out of four regions of Auckland had
notification rates of more than 60 cases per 100,000 population. A similar
higher infection pattern has been reported from the metropolitan regions of
Victoria, Australia, with an average rate of 20 cases per 100,000 population for
the region23—although their rate was
one-third that of Auckland rates.
Giardiasis surveillance in England and Wales has also
highlighted a regional trend, where one-quarter of cases are reported from the
South-East regions.24 Regional high
Giardia infection rates have also been
reported from the US but at much lower rates than in New Zealand. Giardia
infection rates in the US varied from 0.9 to 42.3 cases per 100,000 with a
national average of 9.5 cases per 100,000
population.25 Out of 43 states reporting
giardiasis regularly, 10 states reported more than 20 cases per 100,000,
including New York State (20.3/100,000), with Vermont (42.3/100,000) being the
highest. Unlike New Zealand, these American states have active surveillance
systems in place for giardiasis.
The seasonal distribution of giardiasis cases over the years
showed a consistent pattern of peaking in late summer and early autumn, and low
incidence in winter and early spring. This finding was consistent with other
giardiasis studies.8,10,18,19 The summer peak
possibly reflects enhanced outdoor activities and more contact with contaminated
water, or could be a result of more personal contact between friends and family
during summer vacations. However, it is difficult to explain why the 10–19
years age group, which would be expected to be most exposed to recreational
water during the summer, had the lowest reported infection rate. This group also
showed a weak seasonal distribution peaking slightly in early autumn, as also
reported elsewhere.18
In contrast, the age-group with the highest reported
infection rate, 1–4 year old children, showed a significant seasonal
variation with sustained peak periods in both late summer and autumn, and in the
winter, suggestive of recreational exposure to contaminated water during summer
vacation.19 Increased family activities and
contact during the vacation season has been reported to favour person to person
transmission of giardiasis.18
The winter peak in 1-4 year old children could be due to
indoor confinement especially in institutional care or the presence of nappy
wearing toddler/s in the family26—an
ideal situation for person to person transmission of
Giardia parasites. The same seasonal
variation of infection was seen in the 22–44 years age group but to a
lesser degree, suggestive of similar external environmental exposures and
person-to-person contacts. Although it is not clear why the usual incidence peak
continues to be in autumn,19 one explanation
could be the long incubation period of
Giardia infection combined with the
complacency of infected person for weeks or months at the end of their holidays,
before acting on symptoms and then visiting a local GP for diagnosis and
subsequent notification.
Cases of enteric diseases are suspected to be grossly
under-reported in the national surveillance data. The main reason could be that
most people with gastroenteritis do not consult a doctor. A large prospective
study of infectious intestinal disease in England found that only half of
community cases of giardiasis presented to a
GP.27 However, even when diagnosed on the basis
of laboratory tests, subsequent notification to health authorities is not
guaranteed.
It is likely that the clinical diagnosis of
Giardia infection will vary by
attending GP and according to local environmental situations and presentations
of disease.18,28 The rate of notification
varies with the degree of severity of the
disease.29 The frequency of notification of the
disease also depends on GPs’ perceptions of the importance of the disease
and the severity of illness in presenting patients as GPs do not request stool
tests for most patients presenting with
diarrhoea.28
An early laboratory-based study observed that GPs missed 66%
of giardiasis cases due to not requesting stool examinations for patients with
gastrointestinal complaints.30 In addition,
data sampling and recording was performed by various people and was not uniform.
Thus, adequate training on data management and the coding method is useful for
maintaining a quality data collection
process.31
A major weakness in ethnicity information on
Giardia infection in New Zealand was
data incompleteness. Unknown ethnicity in this study was considered to be high
at 18% of cases. This was reminiscent of the previous study on Auckland
notification data.10 Unlike laboratory based
reported cases,32 notified giardiasis cases are
usually investigated by local public health units, where recording ethnicity is
a routine step in epidemiological investigation in a multiethnic population.
Incomplete ethnicity information has been reported in other
notifiable disease surveillance studies in multiethnic communities. The CDC has
reported that 37-40% of case notifications do not identify the ethnicity of
cases.32,33 Variation in the completeness of
ethnicity reporting may reflect differences in sources of notification and the
frequency of case investigation by the local health
department.32 Reporting may also be influenced
by disease priority.34
Overseas experiences suggest that the completeness of
diagnosis and reporting is reduced in vulnerable ethnic groups due to cultural
complexities and economic difficulties.35
Under-representation in GP visits among socially deprived communities, which are
often ethnic minority groups in New Zealand, has been observed
elsewhere.27 Information gaps in ethnic data in
the present study are age-group sensitive. Given the lowest rates of ethnicity
recording are in areas with high proportions of mixed ethnic groups (such as
Auckland, Rotorua), this information could be influenced by cultural
factors.
Under-diagnosis and the data gaps limit our capacity to
estimate the true burden of giardiasis in New Zealand as well as hampering an
effective and meaningful analysis of risk factors for the disease. Nevertheless,
we were able to compare the information with exposure information collected from
external sources.
The spatial depiction of data in the present study has
helped to identify areas with high rates of notification. Descriptive analysis
using GIS could be useful for the monitoring of surveillance performance and/or
the need for enhancement. Superimposing multi-layer information, and displaying
it simultaneously by the administrative boundaries of an area, can facilitate
the step from descriptive to analytical epidemiological work and raise
hypotheses about associations.
Analysis of spatial information is critically dependent on
the accuracy of the source data and technology-driven which implies additional
cost and skilled manpower. ‘Point data’, which identify individuals
by residential address, are desirable for investigating causal relationships or
for longitudinal studies and to maximise the benefits of GIS in public health
studies, although they may not be accessible due to perceptions of the ethical
considerations of personal privacy.36
Information from LAs on area and population could not be
correlated with exposure factors because of incomplete supporting data, such as
lack of street addresses. Due to such data restrictions, aggregated point data
was used in this study. This has restricted the capacity to manipulate
information.
Lastly, further investigation of reasons for variation in
reported rates could promote better understanding of the transmission of this
disease in New Zealand and assist in the development of intervention
strategies.
Author information:
M Ekramul Hoque, Research Fellow, Section of Epidemiology & Biostatistics,
School of Population Health, University of Auckland, Auckland; Virginia T Hope,
Senior Lecturer, Section of Epidemiology & Biostatistics, School of
Population Health, University of Auckland—and Auckland Regional Public
Health Services, Auckland; Robert Scragg, Associate Professor, Section of
Epidemiology & Biostatistics, School of Population Health, University of
Auckland, Auckland; Michael Baker, Public Health Medicine Specialist, ESR
Ltd, Porirua (currently Senior Lecturer, Department of Public Health, Wellington
School of Medicine and Health Sciences, University of Otago, Wellington);
Rupendra Shrestha, PhD Candidate, Environmental Health Group, National
Centre for Epidemiology and Population Health, Australian National University,
Canberra, Australia
Acknowledgements: We
thank staff at ESR (for sharing giardiasis surveillance data) and Amanda
Scoggins at NIWA (for helping with GIS mappings).
Correspondence: Dr M
Ekramul Hoque, Section of Epidemiology & Biostatistics, School of Population
Health, University of Auckland, Private Bag 92019, Auckland. Fax: (09) 373 7503;
email: e.hoque@auckland.ac.nz
References:
|
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Current
issue | Search journal |
Archived issues | Classifieds
| Hotline (free ads) Subscribe | Contribute | Advertise | Contact Us | Copyright | Other Journals |