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| Journal of the New Zealand Medical Association,
21-June-2002, Vol 115 No 1156
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Geographically separate outbreaks of shigellosis in Auckland,
New Zealand, linked by molecular subtyping to cases returning from
Samoa
Philip C Hill, John Hicking, Jennifer M Bennett, Azeem
Mohammed, Joanna M Stewart, Greg Simmons,
Shigella spp. are
responsible for less than 5% of bacterial food borne notifications in New
Zealand. However, outbreaks of shigellosis are difficult to control because of
the low infectious dose of the inoculum.1
Usually due to S. sonnei in developed
countries,2 they have been reported most
commonly among children at summer camps for the developmentally
disabled3 and at daycare
facilities.4
In February 2001, Auckland District Public Health Unit (PHU)
was notified of two outbreaks of Shigella
sonnei Biotype a gastroenteritis. One was at a health camp for socially
deprived children commencing on 16 January and running for six weeks. The second
involving two cases was at a 28-room elderly care facility with 21 residents and
sixteen staff on the other side of the city (40 km away) from the camp. This
report describes the investigations into these two outbreaks and into a possible
link between them and sporadic cases elsewhere in New Zealand over a four-month
period.
MethodsOutbreak
1 – health camp. A case was defined as any person who attended the
camp suffering from diarrhoea of at least one day’s duration. Diarrhoea
was defined as the occurrence of at least three loose stools over a 24 hour
period. A shigellosis case questionnaire was administered by investigators from
the PHU and included possible risk factors identified through open-ended
interviews and a site visit. Cases were matched for a three day incubation
period with two controls, staff with staff, children with children. Exposure to
faeces was defined as physical contact with faecal matter.
All cases were asked to submit two faecal specimens. The camp swimming pool was tested for faecal indicators and the presence of Shigella species. Shigella isolates were biotyped by the Institute of Environmental Science and Research (ESR). Outbreak control measures were put in place and an environmental investigation was conducted. A multivariate analysis was conducted by conditional logistic regression using SAS software.5 Differences in attack rates and frequency of symptoms were assessed using a chi-squared test. Outbreak 2 - rest home. A case was defined in residents and staff as in outbreak 1. Separate questionnaires were prepared and administered to staff and residents. Faecal specimens were requested and processed as in outbreak 1. An environmental inspection was undertaken. Investigation of a possible link between outbreaks. The index cases of both outbreaks were questioned extensively to find a common source. Other notified cases of S. sonnei Biotype a gastroenteritis were investigated and laboratories were contacted to identify non-notified cases. Restriction digestion of total genomic DNA was performed using standard methods.6 Gels were run and restriction patterns were compared visually and interpreted in accordance with principles suggested by Tenover et al.7 ResultsOutbreak
1 - health camp. 94 of 96 (98%) camp staff and students were interviewed.
Fifteen students and fifteen staff fitted case criteria (Table 1). Nine (60%) of
the students and none of the staff submitted faecal specimens within one week of
illness onset; eight were positive for
Shigella sonnei Biotype a. The attack
rates in students (37%) and staff (28%), were not statistically different
(p=0.4). The majority of students were males (68%), whereas most staff were
females (79%). While 74% of the staff were Europeans, over 60% of the students
were Maori or Pacific Islanders. A higher percentage of students than staff (60%
versus 20%) had vomiting as part of their illness (p=0.03). The first student
became unwell on the 28th of January; no staff member was unwell until over 2
weeks later (Figure 1). On follow-up at one week, only one family member of a
student became unwell.
Thirteen students and 14 staff cases were matched with
controls. The only variable that could be demonstrated to be associated with the
risk of illness in the combined analysis (Table 2) was exposure to human faeces
(OR 4.0, 95% confidence interval 1.0-16.3; p=0.05). Although ethnicity as a
whole was not shown to be related to illness, there was an indication of a
difference between Pacific Islanders and Europeans. For staff there was also an
indication of an association of eating camp food with illness (OR 6.9, 1.0-5.0;
p=0.06). One of the kitchen workers became unwell during the outbreak, but not
until the 16th of February.
Problems in food inspection, storage and handling, and with
wastewater discharge from the sluice were found. It was noted that the swimming
pool had turned green in early February, suggesting contamination at that time.
A sample of pool water as negative for Shigella spp.
Outbreak 2 - rest home.
Over eleven days, four staff and four residents developed illness, with
an attack rate of 24%. All were females, with an age range of 29 to 66 years for
staff, and 70 to 92 years for residents. Apart from the two notified cases only
one other person who had been ill had a positive faecal specimen. The median
duration of symptoms was 3 ½ days (range 0.5 to 9 days). All cases, after
the first one, could be explained by person to person transmission through close
contact. No other risk factors were found. Opportunities for minor improvements
in cleaning and disinfection were identified.
Table 1. Characteristics of those interviewed at the
health camp.
*median(range);†one or more of: fever, headache,
nausea, abdominal cramps.
 Figure 1. Epidemic curve for health camp
outbreak.
Link investigation.
The index case at the health camp, an eight year old Pacific Island boy,
became unwell on the evening that he returned from a weekend at home. Two other
members of the household developed gastroenteritis within three days. The index
case at the elderly care facility, a female resident, was cared for by a staff
member who also became unwell and often purchased fruit for her. Both the
boy’s mother and the staff member of the elderly care facility bought
apples, packed by hand into plastic bags, from the same fruit shop in the few
days before the outbreaks began. No other potential common source was
identified.
Table 2. Assessment of risk factors for illness at the
health camp.
*confidence interval; calculated from Odds
Ratio.
During January and February, 21 people had stool specimens
positive for S. sonnei Biotype a in
Auckland and sixteen (76%) of these were notified. Two were flight attendants on
the same flight from Samoa in early January. At least three other flight
attendants on the flight had gastroenteritis. All had stayed at the same hotel.
A questionnaire was circulated by mail among the flight attendants and no
obvious link with outbreak 1 or 2 was established. During the period 1 January
through to 30 April there were five isolates from cases of
Shigella sonnei Biotype gastroenteritis
in people living outside Auckland. Two of these were known to have had recent
overseas travel to Samoa, and one reported staying at the implicated
hotel.
The isolates of children from the health camp, flight
attendants, two travellers from Samoa who returned to cities outside Auckland,
and another case from outside Auckland no travel details available), were
identical (Figure 2). The patterns of the isolates from residents at the elderly
care facility differed by only one band suggesting that they were also the same
strain.7
DiscussionWe have described two
geographically distinct outbreaks of Shigella
sonnei Biotype a gastroenteritis that started within two days of each
other. Consideration of a common exposure eventually led to a fruit shop and
molecular subtyping confirmed that they were related to one another, to other
cases in and outside Auckland, and ultimately to a source in Samoa. At the
health camp, the inexperience of the new management, the social background of
the children, and the lack of adequate hygienic measures all conspired to
facilitate the propagation of the outbreak and the high attack rate among both
children and staff. However, the attack rate of 24% at the elderly care facility
illustrates that even when hygienic practices are relatively good,
Shigella infection can spread within an
institutional setting.
Exposure to human faeces as a risk factor for illness at the
health camp can be interpreted as at least a marker for close contact, and
eating camp food as a risk factor for staff suggests some hygienic breakdown at
mealtimes. For the initial control of the health camp outbreak, several
procedures were undertaken with handwashing being by far the most important of
these. The role of antimicrobials in control of
Shigella outbreaks is controversial,
and we did not use them as a control measure. Antimicrobials are not a
substitute for hygienic measures, such as hand washing with soap and water and
thorough drying, in reducing the secondary spread of shigellosis. It can be
argued that antimicrobials should be reserved for treatment of patients only
when clinically indicated8 since this practice
can lead to the development of resistant that complicate
therapy.9
Figure 2. Restriction patterns for S.
sonnei Biotype a isolates.
 Lane 1: DNA size marker. Lane 2: Child from health camp. Lane 3. Child from health camp. Lane 4: Child from health camp. Lane 5: Resident of elderly care facility. Lane 6: Resident of elderly care facility. Lane 7: DNA size marker. Lane 8: Flight attendant. Lane 9: Flight attendant. Lane 10: Recent traveller from Samoa to city outside Auckland. Lane 11: Recent traveller from Samoa to city outside Auckland (stayed at implicated hotel). Lane 12: Case from outside Auckland, travel history not known. Lane 13: Case from outside Auckland, travel history not known. Lane 14: Isolate from New Zealand reference culture collection. Pulsed-field gel electrophoresis (PFGE) has been used to
link separate restaurant outbreaks of S.
sonnei infection in the United States.10
Isolates from those outbreaks had two closely related restriction
patterns that differed only by a single band. The epidemiological investigation
implicated parsley imported from a farm in Mexico as the source of the
outbreaks. Similarly, we have used PFGE to link two geographically separate
outbreaks in Auckland to a source in Samoa.
While a history of overseas travel is recorded routinely for
cases of notifiable disease in New Zealand, the contribution of imported
infections to the overall burden of disease and outbreaks in the country has not
been quantified. Furthermore, feedback concerning imported cases to the
respective public health authorities in other countries rarely occurs. The
Samoan Public Health Authorities were alerted on this occasion. This particular
strain entered New Zealand intermittently over at least the four months of
January to April in 2001. The ongoing transmission makes it less likely that one
particular person was the source, and a more fundamental problem with water
supply or some other breakdown in hygiene may have occurred.
This investigation provides one example of how molecular
laboratory techniques can be utilised in public health investigations. In order
to take full advantage of advances in both information and molecular technology,
New Zealand needs electronically transmitted direct laboratory notification of
positive specimens and an expanded molecular subtyping capacity. This would lead
to the identification of all specimen positive cases (only 76% were notified in
Auckland) and much earlier notification, and would enable more outbreaks and the
linkages between them to be identified. A model for this has been developed by
Bender et al11,12 who perform routine rapid
molecular subtyping of selected organisms. This model has revolutionised
outbreak investigation and has been shown to be cost
effective.13 This approach could be adopted in
New Zealand, increasing the detection of regional and inter-regional outbreaks
of infection and the identification of infectious sources.
Author Information:
Philip C Hill, Public Health Physician; John Hicking, Health Protection Officer,
Public Health Protection, Auckland, District Health Board, Auckland; Jennifer M
Bennett, Scientist, Institute of Environmental Science and Research, Porirua;
Azeem Mohammed, Health Protection Officer, Public Health Protection,Auckland
District Health Board, Auckland; Joanna M Stewart, Statistician, Department of
Community Health, University of Auckland; Greg Simmons, Public Health Physician,
Public Health Protection, Auckland District Auckland.
Acknowledgements: We
thank Basker Nadarajah and Jane Gower for their work in the investigation; Kathy
Pritchard for her guidance; Dr’s Nick Jones, Lester Calder, Phyllis Taylor
and Robert Scragg for expert advice.
Correspondence: Dr
Greg Simmons, Public Health Protection Unit, Auckland District Health Board,
Private Bag 92605, Symonds St, Auckland 1001. Fax: (09) 630 7431; email: gregs@adhb.govt.nz
References:
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