Infection with Campylobacter spp. commonly precedes
Guillain-Barré syndrome (GBS). We therefore hypothesized
that GBS incidence may have followed a marked rise and
then decline in campylobacteriosis rates in New Zealand.
We reviewed records for 1988–2010: hospitalization
records for GBS case-patients and campylobacteriosis
case-patients plus notifi cations of campylobacteriosis. We
Author affi liations: University of Otago, Wellington, New Zealand
(M.G. Baker, A. Kvalsvig, J. Zhang, A. Sears, N. Wilson); and
Institute of Environmental Science and Research, Christchurch,
New Zealand (R. Lake)
identifi ed 2,056 fi rst hospitalizations for GBS, an average
rate of 2.32 hospitalizations/100,000 population/year.
Annual rates of hospitalization for GBS were signifi cantly
correlated with rates of notifi cations of campylobacteriosis.
For patients hospitalized for campylobacteriosis, risk
of being hospitalized for GBS during the next month
was greatly increased. Three years after successful
interventions to lower Campylobacter spp. contamination
of fresh poultry meat, notifi cations of campylobacteriosis
had declined by 52% and hospitalizations for GBS by
13%. Therefore, regulatory measures to prevent foodborne
campylobacteriosis probably have an additional health and
economic benefi t of preventing GBS.
Declining Guillain-Barré S yndrome
after Campylobac teriosis Control,
New Zealand, 1988–2010
Michael G. Baker, Amanda Kvalsvig, Jane Zhang, Rob Lake, Ann Sears, and Nick Wilson
226 Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 18, No. 2, February 2012
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Upon completion of this activity, participants will be able to:
• Distinguish the infection most closely associated with GBS
• Analyze the temporal relationship between campylobacteriosis and GBS
• Assess differences in the association between campylobacteriosis and GBS based on age
• Evaluate the effect of infection-control measures on rates of campylobacteriosis and GBS
P. Lynne Stockton, VMD, MS, ELS(D), Technical Writer/Editor, Emerging Infectious Diseases. Disclosure: P. Lynne Stockton,
VMD, MS, ELS(D), has disclosed no relevant fi nancial relationships.
Charles P. Vega, MD, Health Sciences Clinical Professor; Residency Director, Department of Family Medicine, University of
California, Irvine. Disclosure: Charles P. Vega, MD, has disclosed no relevant fi nancial relationships.
Michael G. Baker, MBChB, DPH, FNZCPHM; Amanda Kvalsvig, MBChB; Jane Zhang, MSc; Rob Lake, PhD; Ann Sears,
MBChB, MPH; and Nick Wilson, MBChB, MPH, FNZCPHM, have disclosed no relevant fi nancial relationships.
Guillain-Barré Syndrome and Campylobacteriosis
Patients typically describe ascending weakness and
sensory disturbance that evolve over several days; during
this acute phase, approximately one third of patients
require ventilatory support. The condition is generally self-
limiting, but for 3%–10% of patients, it is fatal (1).
An estimated 40%–70% of patients with GBS had
an infection before GBS onset; for 6%–39% of these
patients, the infection affected the gastrointestinal system
(2). Campylobacteriosis is the most commonly identifi ed
antecedent infection; several studies have shown that in
industrialized countries (Europe, North and South America,
Japan, and Australia), Campylobacter spp. infection
preceded GBS for 20%–50% of patients (3,4).
During 1980–2006 in New Zealand, incidence of
campylobacteriosis steadily increased. The notifi cation
rate in 2006 (379 cases/100,000 population) remains
the highest national rate reported in the literature
(5,6). In 2006, in response to this high incidence,
New Zealand introduced an array of voluntary and
regulatory interventions to reduce contamination of
poultry with Campylobacter spp. (7). By 2008, the rate
of campylobacteriosis notifi cations had dropped to 157
cases/100,000 population, a decrease of 59% over 2
years (7); this decline has persisted (8). Given the known
association between Campylobacter spp. infection and
GBS and the marked recent changes in reported rates of
campylobacteriosis in New Zealand, we examined GBS
hospitalization data for evidence of responsiveness to
trends in campylobacteriosis incidence.
uillain-Barré syndrome (GBS) is an autoimmune
condition that affects the peripheral nervous system.
Identifi cation of GBS Incidence
Because GBS is a serious illness that nearly always
results in hospitalization, hospitalization data provided the
most accurate available measure of GBS incidence. We
obtained national hospital discharge data for the 23-year
period 1988–2010 in New Zealand. To estimate the case-
fatality proportion, we also obtained data on deaths from
GBS for 1988–2008 (the most recent year available). Both
datasets are collated and maintained by the New Zealand
Ministry of Health.
Although hospitalization data are available for earlier
years, we used 1988 as the starting point because that is
when use of unique patient identifi ers, the National Health
Index (NHI), became universal in New Zealand. Use of
the NHI enables identifi cation and removal of repeat GBS
hospitalizations for the same patient, thereby identifying
the fi rst GBS hospitalization for each case (hereafter called
GBS hospitalization), which provides an estimate of the
number of incident cases of GBS.
We selected all cases from 1988 on that had Inter-
national Classifi cation of Diseases, 9th and 10th Revisions,
Clinical Modifi cation and Australian Modifi cation, codes
for GBS (ICD-9 CM 357.0 and ICD-10 AM G61.0)
recorded as the principal or additional diagnosis. Records
of patients who had been transferred between hospitals
were merged to create 1 hospitalization event. We identifi ed
repeat hospitalizations for the current year and for previous
years, i.e., case-patients with the same NHI number
previously admitted in the same or a previous year. Some
patients were readmitted before universal use of the NHI
in 1988, so the calculation needed to take these estimated
repeat hospitalizations into account. (See online Technical
Appendix Tables 1, 2, wwwnc.cdc.gov/EID/pdfs/11-1126-
Techapp.pdf, for a description of how estimated repeat
hospitalizations and incident cases were calculated.)
Identifi cation of Campylobacteriosis Incidence
Since 1980, campylobacteriosis has been a notifi able
disease in New Zealand. Medical practitioners are required
to report all identifi ed and suspected cases to the local
medical offi cer of health. These data are in turn collated
nationally by the Institute of Environmental Science and
Research for the New Zealand Ministry of Health. We
used published annual totals of notifi cations (9) as well as
anonymized datasets of notifi ed cases. Most cases were
culture confi rmed (>96% during 1997–2008 ), although
the case defi nition also allows for cases epidemiologically
linked to a confi rmed case.
Hospitalizations for campylobacteriosis are recorded in
hospital discharge data, which are electronically available
for a similar period. However, a specifi c diagnostic code
for Campylobacter spp. infection was not introduced until
July 1995. Hospitalizations for campylobacteriosis were
defi ned as those with ICD-9 CM code 008.43 from July
1995 on and ICD-10 AM code A04.5 from July 1999 on. To
create a dataset of incident cases, we included principal or
additional diagnoses, merged records for those transferred
with records from preceding hospitalizations, and removed
repeat hospitalizations in the current and previous years.
Analysis of Hospitalizations for GBS
To assess the association between the 2 conditions,
we investigated the incidence
patients hospitalized for campylobacteriosis. Because
campylobacteriosis was only specifi cally identifi ed in
hospitalization data from July 1995, this analysis focused
on the period starting in July 1995. To allow a follow-up
period for GBS cases to emerge, we continued the inclusion
period through December 2008.
For those cases identifi ed, we fi rst analyzed the
time from hospital admission for campylobacteriosis to
of GBS among
Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 18, No. 2, February 2012 227
admission for GBS. For epidemiologic purposes, the risk
period for GBS after Campylobacter spp. infection is ≈2
months (10); neurologic signs of GBS usually develop
1–3 weeks after a preceding infection (3). In our dataset,
a clear trend was seen toward a close temporal association
between hospitalization dates: for most (34/35, 97.1%)
patients, hospitalizations for GBS and campylobacteriosis
were concurrent (patients were discharged with a diagnosis
of both), or hospitalization for GBS occurred within 1
month of hospitalization for campylobacteriosis.
To assess the risk for GBS associated with
campylobacteriosis, we calculated GBS hospitalization
rates for comparison conditions, notably other infections
that might be associated with an elevated risk for GBS.
We used the GBS rate in the total New Zealand population
as our reference rate for calculating age-standardized
rate ratios for GBS after campylobacteriosis and other
conditions of interest.
We also evaluated which age groups might be more
vulnerable to development of GBS. To do so, we compared
the age distributions of all patients hospitalized for GBS
and those associated with campylobacteriosis with the
age distributions for those with campylobacteriosis alone
(hospitalized or with notifi ed case).
Because of marked changes in campylobacteriosis
disease incidence and some changes in case identifi cation
during the 23-year study period, some outcomes were
measured over a shorter time. The periods associated
with implementation of the Campylobacter spp. control
interventions used a baseline period similar to that used in
a previous study (7).
Data were analyzed by using Stata version 11.0
(StataCorp LP, College Station, TX, USA) and SAS
version 9.1 (SAS Institute, Cary, NC, USA). CIs are given
at the 95% level throughout. We used well-documented
methods for calculating adjusted rates, rate ratios (RRs),
and 95% CIs (11). Rates were calculated by using
mean population estimates published by Statistics New
denominators. To calculate age-standardized rates, we used
the population age structure determined by the New Zealand
2006 Census of Population and Dwellings (www.stats.govt.
This study identifi ed 2,056 fi rst hospitalizations for
GBS that occurred during 1988–2010, resulting in an
average rate of 2.32 hospitalizations/100,000 population/
year (online Technical Appendix Table 1). Incidence
was not stable over the period of the study (Figure). The
minimum recorded rate was 1.53 hospitalizations/100,000
population/year in 1989; the maximum was 2.93 in 2005.
During 1989–2008, a total of 56 deaths from GBS were
recorded; case-fatality proportion (56 deaths/1,873 cases)
Changes in GBS and Campylobacteriosis Incidence
For 1988–2010, there was a signifi cant direct
correlation between annual rates of hospitalization for
GBS and annual rates of notifi cation of campylobacteriosis
cases (Spearman ρ = 0.52, p = 0.012). During 1988–2006,
incidence of campylobacteriosis notifi cations and of
GBS hospitalizations increased (Figure; online Technical
Appendix Table 3). Subsequently, campylobacteriosis
notifi cations then decreased markedly, and GBS
hospitalizations decreased, although less dramatically.
The fall in campylobacteriosis notifi cations followed the
introduction of countrywide campylobacteriosis control
measures focused on reducing contamination levels in
fresh poultry meat (7).
228 Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 18, No. 2, February 2012
campylobacteriosis notifi cation rates,
by year, New Zealand, 1988–2010.
*Per 100,000 population.
Guillain-Barré Syndrome and Campylobacteriosis
Table 1 summarizes the changes between the 2
periods: 1) 2002–2006, the baseline period, when rising
campylobacteriosis rates became an urgent public health
concern, and 2) 2008–2010, the postintervention period,
after implementation of wide-ranging control measures.
The transition year, 2007, was excluded.
During the postintervention period, notifi cations and
hospitalizations decreased by ≈50% (online Technical
Appendix Tables 3, 4). Incidence of GBS declined by
13%, which was statistically signifi cant (RR 0.87, 95% CI
0.81–0.93), suggesting that ≈25% of GBS was caused by
GBS among Patients Hospitalized
for Campylobacteriosis or Other Conditions
During 1995–2008, among the 8,448 patients
hospitalized for campylobacteriosis, 35 were also
hospitalized for GBS. The frequency distribution of
time delays is shown in Table 2. These data show that
most (29) of these 35 patients had diagnoses of GBS and
campylobacteriosis at time of hospital discharge. Another 5
patients were hospitalized for GBS within 4 weeks of being
hospitalized for campylobacteriosis. The time difference
for the remaining patient was >1,500 days (this patient
was excluded from subsequent analyses). This striking
distribution further supports a causative association
between campylobacteriosis and GBS in New Zealand.
We calculated the rate of GBS hospitalizations among
the cohort of patients hospitalized for campylobacteriosis
and compared this with rates of GBS hospitalization among
other patient cohorts hospitalized for infectious diseases
(Table 3). This analysis used the overall rate of GBS
hospitalizations among the New Zealand population as a
reference for calculating age-standardized RRs.
The age-standardized rate of GBS was 810.0
41.4–1,578.7) in the month after hospitalization for
campylobacteriosis. The RR, compared with the rate of
GBS hospitalizations among the New Zealand population,
was 319.4 (95% CI 201.5–506.4). This rate was markedly
higher than rates for the other patient cohorts examined
Patients with GBS (median age 52.5 years)
were signifi cantly older than those hospitalized for
campylobacteriosis (median 41 years), who in turn were
signifi cantly older than those with campylobacteriosis
notifi cations (median 31 years) (Tables 4, 5). The age of
the subpopulation of patients with GBS associated with
campylobacteriosis was similar (median 54 years) to that
of the total population with GBS.
This study shows how the incidence of an acute
infectious disease, campylobacteriosis, can infl uence
incidence of a serious neurologic condition, GBS. At the
population level, hospitalizations for GBS were signifi cantly
correlated with notifi cations of campylobacteriosis for the
same year. At the individual level, compared with rates for
the New Zealand population as a whole, hospitalizations
for campylobacteriosis were associated with an almost
320-fold increased risk for subsequent hospital admission
for GBS in the next month.
Results also show that food safety measures to reduce
contamination of fresh poultry meat with Campylobacter
spp. not only reduced incidence of campylobacteriosis but
also were associated with reduced incidence of GBS. In
the 3 years after introduction of these control measures,
campylobacteriosis notifi cations and hospitalizations
decreased by ≈50%, and GBS hospitalizations dropped
by 13%. These fi ndings suggest that in New Zealand,
Campylobacter spp. infection may be responsible for
≈25% of GBS cases, which is consistent with data from
other industrialized countries (3).
A recent systematic review (12) summarized attempts
to quantify the association between campylobacteriosis
and GBS incidence. There is general agreement that
measuring GBS population rates is useful, for example,
for monitoring vaccine adverse effects (13,14). However,
Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 18, No. 2, February 2012 229
Table 1. Incidence of campylobacteriosis and GBS before and after intervention to reduce Campylobacter spp. in poultry, New
Before intervention, 2002–2006
Total no. Average/yearRate‡
GBS hospitalizations¶ 513 103 2.6
*GBS, Guillain-Barré syndrome.
†Excludes 2007, which was a transitional year.
‡Annual no. cases/100,000 person-years at risk. Denominator populations based on mean population estimates published by Statistics New Zealand
(www.stats.govt.nz/browse_for_stats/population/estimates_and_projections/national-pop-estimates.aspx). Campylobacteriosis and Guillan-Barré
syndrome hospitalizations used age-standardized rates based on the age structure of the New Zealand 2006 Census of Population and Dwellings
§Published campylobacteriosis notification data (9).
¶Hospitalization data from New Zealand Ministry of Health.
After intervention, 2008–2010†
Total no. Average/year
Rate ratio (95% CI)
<0.0001 69,207 13,841 339.4
4,669 934 23.2 1,603 534 12.2 0.53 (0.51–0.54) <0.0001
290 97 2.2 0.87 (0.81–0.93) 0.0496
to our knowledge, no similar population-based analysis
of the relationship between GBS and campylobacteriosis
has been conducted for other countries, probably because
few countries collect similarly detailed national-level
hospitalization data. An earlier population-based study
in New Zealand did not show an association between
notifi cations for campylobacteriosis and GBS incidence
(15). However, that study was over a shorter period and did
not use a correction factor to account for undetected repeat
hospitalizations in the early years of the observation period,
which would have made it harder to detect an association
between incidence rates for the 2 conditions.
Compared with global estimates, rates of GBS in
New Zealand are high. In a review of reported GBS rates
during 1980–2000, worldwide incidence varied between
1.0 and 1.8 cases/100,000 population/year (2). The average
reported rate for New Zealand during this period was at the
upper end of this range (1.8/100,000). A more recent study
from the United States estimated that annual hospitalization
rates for GBS varied between 1.65 and 1.79/100,000 during
2000–2004 (16). In New Zealand during the same period,
the annual hospitalization rates varied between 1.8 and
The 320-fold increased risk for GBS in the month after
hospitalization for campylobacteriosis found in this study
is higher than that previously reported. In a case–control
study of GBS and potential antecedent infections in the
United Kingdom, Tam et al. reported that persons with
Campylobacter enteritis had a 38-fold increased risk that
GBS would develop in the next 2 months (17). However,
when they added a correction factor to account for under-
ascertainment of campylobacteriosis, the risk increased to
60-fold. Similarly, a population-based study in Sweden
estimated that patients with laboratory-confi rmed C. jejuni
infection had a 100-fold increased risk that GBS would
develop in the next 2 months (10). We used a 1-month risk
period because the GBS cases we identifi ed subsequent to
hospitalizations for campylobacteriosis were confi ned to
this period. Using a 2-month risk period would have halved
our estimated age-standardized RR, but the elevated risk
would still be higher than that reported elsewhere.
The proportion of GBS cases attributable to preceding
Campylobacter spp. infection estimated for New Zealand
(≈25%) is within the range described elsewhere. Studies
from other countries and regions have reported serologic
evidence of previous C. jejuni infection in 13%–72%
of GBS case-patients (18). A systematic review, based
on 32 eligible studies, estimated that 31% of GBS cases
were attributable to Campylobacter spp. infection (12).
230 Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 18, No. 2, February 2012
Table 2. Hospitalization for Guillain-Barré syndrome during or
after hospitalization for campylobacteriosis, New Zealand, July
Interval, d No. (%) persons hospitalized
Concurrent 29 (82.9)
1–7 2 (5.7)
8–28 3 (8.6)
1,524 (4.2 y) 1 (2.9)
Total 35 (100)
Table 3. Incidence of GBS after hospitalization for campylobacteriosis and other infectious diseases compared with total population
incidence rate for GBS, New Zealand, July 1995–December 2008*
(ICD chapter 1)
rate¶ (95% CI)
480–488 J09–J18 250,399 19 (82) 91.1
77,793 6 (21) 93.3
Campylobacteriosis 8,448 5 (29) 710.2 810.0
population GBS rate
*GBS, Guillain-Barré syndrome; ICD, International Classification of Diseases; ICD-9, ICD 9th Revision; ICD-10, ICD 10th Revision; NA, not applicable.
†Denominator population based on either 1) incident hospitalizations for specific condition (number of acute and arranged first overnight hospitalizations
as principal or additional diagnosis); or 2) total New Zealand population person-years for July 1995– December 2008 for calculating the New Zealand
population GBS rate.
‡First hospitalization of GBS either 1) among those with a previous hospitalization in the preceding 30 d and excluding those with concurrent diagnoses
(numbers in parentheses); or 2) in the total New Zealand population for July 1995–December 2008.
§Rate per 100,000 person-years at risk. For GBS hospitalizations after specific conditions, monthly rate has been multiplied by 12 to convert to annual
¶Standard population is population of New Zealand according to the New Zealand 2006 Census of Population and Dwellings
#Excluding campylobacteriosis and salmonellosis.
Guillain-Barré Syndrome and Campylobacteriosis
The strength of the association with GBS may vary
geographically, according to the neuropathic propensity
of local Campylobacter strains. We would also expect
the percentage contribution of preceding Campylobacter
spp. infection to vary according to the incidence of this
infection in the population and the incidence of other causal
infections and exposures.
The results of our study suggest that risk for GBS may
not be uniform for different degrees of campylobacteriosis
severity. Our study found that risk for GBS was ≈1
in 1,690 (5 in 8,448) among patients hospitalized for
campylobacteriosis and that ≈25% of GBS cases were
caused by campylobacteriosis. On the basis of an annual
incidence of ≈100 GBS cases, these data suggest that
≈42,000 cases of campylobacteriosis occur each year in
New Zealand. Current estimates of total campylobacteriosis
incidence are higher. Annual notifi cations remain at ≈7,000
cases. A study from the United Kingdom estimated that 9.3
cases of campylobacteriosis occurred in the community for
every notifi ed case (19); a study from Australia estimated
this number to be 10 (20). Applied to New Zealand, these
multipliers suggest an incidence among the population of
65,000 to 70,000 cases per year. These fi ndings suggest
that the causal association between campylobacteriosis
and GBS is probably weaker for patients with less severe
infections, who do not require hospitalization.
Analysis of the age distribution of patients with
campylobacteriosis and GBS suggests that older age is a
major risk factor for more severe outcomes (hospitalization
and GBS) from this enteric infection. The rising incidence
of GBS with increasing age in New Zealand is consistent
with incidence observed in other countries (21).
One strength of this study is that it has been able to
monitor a natural experiment in which campylobacteriosis
incidence decreased by 50% within a few months, providing
an unusual opportunity to assess the effect of this change
on incidence of GBS. New Zealand’s comprehensive
recording of national hospitalization data and use of a unique
patient number also provided us with a consistent base
for estimating population rates of GBS over a prolonged
period. Although the spectrum of GBS includes extremely
mild cases, studies elsewhere indicate that only ≈3.0%–
5.8% of patients with GBS are not hospitalized (22,23). In
addition, patients with Campylobacter-associated GBS are
believed to experience more severe disease (24,25), which
would minimize the number of Campylobacter-associated
GBS cases missed by this investigation.
One limitation of this study is the group used to
compare risk for GBS: the total New Zealand population.
A variety of conditions and events have been identifi ed as
possible GBS triggers (1,24,26–29). Consequently, because
it is not possible with current knowledge to identify a
Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 18, No. 2, February 2012 231
Table 4. Distribution of campylobacteriosis and GBS cases, by age, New Zealand, July 1995–December 2008*
No. (%) Rate‡ No. (%)
<5 15,232 (11.7) 442.5 538 (6.4)
5–9 6,295 (4.9) 176.9 200 (2.4)
10–19 14,481 (11.2) 203.7 965 (11.4)
20–29 25,063 (19.3) 385.9 1,509 (17.9)
30–39 19,511 (15.0) 270.7 935 (11.1)
40–49 16,572 (12.8) 237.0 747 (8.8)
50–59 14,311 (11.0) 261.9 778 (9.2)
60–69 9,559 (7.4) 255.7 824 (9.8)
70–79 6,174 (4.8) 235.9 1,046 (12.4)
2,712 (2.1) 190.8 906 (10.7)
Total 129,910 (100.0) 270.4 8,448 (100.0)
*GBS, Guillain-Barré syndrome.
†Association with hospitalization for camplylobacteriosis. Includes subsequent and concurrent hospitalizations (campylobacteriosis and GBS diagnoses at
time of hospital discharge).
‡Average annual no./100,000 population.
GBS hospitalizations associated
Table 5. Comparison of ages of patients with campylobacteriosis and GBS, New Zealand, July 1995–December 2008*
A. Patients with
p value for age
compared with A§
Mean 33.7 43.7 <0.0001
Median 31 41 <0.0001
B. Patients hospitalized for C. Patients hospitalized
p value for age
compared with B§
D. Patients hospitalized for
GBS and campylobacteriosis†
p value for age
compared with C‡
Age, y Age, y
*GBS, Guillain-Barré syndrome.
†Includes subsequent and concurrent hospitalizations (campylobacteriosis and GBS diagnoses at time of hospital discharge).
‡Means compared with Student t-test medians compared with median 2-sample test.
reference patient population with no additional GBS risk
factors, we considered that the total population provided
the most appropriate reference rate.
The association between campylobacteriosis and GBS
in New Zealand needs further investigation. It will be useful
to continue to follow the trends identifi ed here to assess
the stability of the decrease in GBS, which will eventually
give greater precision to the estimated contribution of
campylobacteriosis. Ongoing monitoring of GBS should
be included in the comprehensive surveillance of infectious
diseases (30). The hypothesis that patients not hospitalized
for campylobacteriosis have a lower risk for GBS should
be tested by investigation of incidence of GBS among these
Our fi ndings suggest the value of further research to
identify other potentially preventable infectious causes of
GBS. Table 3 shows a markedly elevated risk for GBS
after hospitalization for infectious diseases in general.
Investigating these associations in detail may identify other
potentially preventable causes of GBS.
Findings of this study have relevant implications for
food safety programs. Although GBS is rare, the toll it
takes on the individual patient is often high (1). Even with
treatment, 9%–17% of patients die or remain disabled (31),
and repeat hospitalizations are common, representing ≈60%
of total hospitalizations (online Technical Appendix Table
1). Almost half of all patients report ongoing diffi culties
3–6 years after GBS onset (32). Consequently, ongoing
health care costs for each GBS patient are considerable.
In New Zealand during 1988–2008, the GBS case-fatality
proportion was 3.0%, and a recent article (33) estimated
that 204 (13%) of 1,568 disability-adjusted life years for
campylobacteriosis in New Zealand were caused by GBS.
This study shows that food safety programs that
successfully lower rates of campylobacteriosis might have
the additional benefi t of preventing GBS. This fi nding
adds to the health and economic arguments for such
control measures. The justifi cation for such interventions
is particularly strong where a substantial proportion of
human disease can be linked to a widely consumed food
source, such as contaminated poultry products, as it is in
New Zealand (7).
We thank 2 anonymous reviewers for considerably
improving this article.
The New Zealand Ministry of Health provided the
hospitalization and mortality data, and the Institute of Environmental
Science and Research provided the notifi cation data.
Dr Baker is an associate professor at the University of
Otago, Wellington. He is actively investigating the potential for
public health surveillance to guide more effective interventions
in a range of settings. His research includes a strong focus on
infectious diseases and their determinants, particularly the effects
of housing conditions and social and ethnic inequalities.
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Address for correspondence: Michael G. Baker, Department of Public
Health, University of Otago, Box 7343, Wellington 6242, New Zealand;
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