This report summarizes the preliminary results of the outbreak investigation. Aflatoxin poisoning likely will continue to be a public health problem until culturally appropriate storage methods for dry maize are implemented by the local population. In addition, enhanced surveillance for human aflatoxin poisoning and testing of commercially sold maize for aflatoxin levels will lead to long-term improvements in public health

Centers for Disease Control and Prevention

Gieseker, Karen E.

English

Georgia State University

Georgia State University
ScholarWorks @ Georgia State University
Public Health Faculty Publications School of Public Health
9-3-2004
Outbreak of Aflatoxin Poisoning - Eastern and
Central Provinces, Kenya, January - July 2004
Karen E. Gieseker
Georgia State University, kgieseker@gsu.edu
Centers for Disease Control and Prevention
Follow this and additional works at: https://scholarworks.gsu.edu/iph_facpub
Part of the Public Health Commons
This Article is brought to you for free and open access by the School of Public Health at ScholarWorks @ Georgia State University. It has been accepted
for inclusion in Public Health Faculty Publications by an authorized administrator of ScholarWorks @ Georgia State University. For more information,
please contact scholarworks@gsu.edu.
Recommended Citation
Gieseker, Karen E. and Centers for Disease Control and Prevention, "Outbreak of Aflatoxin Poisoning - Eastern and Central Provinces,
Kenya, January - July 2004" (2004). Public Health Faculty Publications. 3.
https://scholarworks.gsu.edu/iph_facpub/3
790 MMWR September 3, 2004
Outbreak of Aflatoxin Poisoning —
Eastern and Central Provinces,
Kenya, January–July 2004
In May 2004, CDC Kenya, trainees of the CDC-
supported Field Epidemiology and Laboratory Training Pro-
gram (FELTP) in Kenya, the World Health Organization, and
CDC were invited by the Kenya Ministry of Health (KMOH)
to participate in the investigation of an outbreak of jaundice
with a high case-fatality rate (CFR) in the districts of Makueni
and Kitui, Eastern Province. Preliminary laboratory testing of
food collected from the affected area revealed high levels of
aflatoxin, suggesting that the outbreak was caused by afla-
toxin poisoning, as was a previous outbreak in the same area
in 1981 (1). In the United States, aflatoxin concentrations are
limited to 20 parts per billion (ppb), a level also adopted by
Kenyan authorities. The 2004 outbreak resulted from wide-
spread aflatoxin contamination of locally grown maize, which
occurred during storage of the maize under damp conditions.
Urgent replacement of the aflatoxin-contaminated maize with
noncontaminated maize proved to be a critical intervention;
however, as of July 21, a limited number of new cases contin-
ued to be detected. This report summarizes the preliminary
results of the outbreak investigation. Aflatoxin poisoning likely
will continue to be a public health problem until culturally
appropriate storage methods for dry maize are implemented
by the local population. In addition, enhanced surveillance
for human aflatoxin poisoning and testing of commercially
sold maize for aflatoxin levels will lead to long-term improve-
ments in public health.
Joint KMOH and CDC teams conducted patient interviews
and reviewed medical records dating back to January 1, in
three health facilities in the Makueni and Kitui districts.
Additional case finding was conducted through similar
patient interviews and retrospective record reviews in seven
health facilities in adjacent districts of Eastern Province
(Machakos, Embu, Mbeere, and Mwingi districts) and Cen-
tral Province (Thika district) and at Kenyatta National Hos-
pital in Nairobi (Figure 1). Large-scale active surveillance
occurred from early May to late June. As of July 21, three
health facilities in Makueni and Kitui districts continued to
be monitored for new cases. A convenience sample of 20
patient households was visited to assess the occurrence of jaun-
dice in nonhospitalized household members and to
inspect food quality and storage. In this investigation, a case
of suspected aflatoxin poisoning was defined as a case of acute
jaundice that occurred after January 1, in a resident of East-
ern or Central Province or a case diagnosed at Kenyatta
National Hospital in a patient who was not known to have
chronic liver disease or any other cause of jaundice.
As of July 20, a total of 317 cases had been reported, with
125 deaths (CFR = 39%). An increase in case reports began
in the third week of April, with new cases continuing to occur
through mid-July (Figure 2). Of the 308 patients for whom
age data were available, 68 (22.1%) were aged <5 years; 90
(29.2%) were aged 5–14 years, and 150 (48.7%) were aged
>15 years. Of the 317 total patients, 178 (56.2%) were male,
and 280 (88.3%) resided in four districts: Makueni (148
[46.7%]), Kitui (101 [31.8%]), Machakos (19 [6.0%]), and
Thika (12 [3.8%]). The remaining 37 (11.7%) patients had
aflatoxicosis diagnosed at Kenyatta National Hospital in
Nairobi or at health facilities in Embu, Mbeere, or Mwingi
districts. CFR was significantly higher in Makueni district
(CFR = 49.3%) than in Kitui district (CFR = 23.7%) (CFR
ratio = 2.1; 95% confidence interval [CI] = 1.4–3.1).
Preliminary results from a case-control study that compared
40 case-patients with 80 well controls matched by village in
Makueni and Kitui districts demonstrated a statistically sig-
nificant association between the development of jaundice and
several risk factors or markers, including 1) reported consump-
tion of cooked maize kernels (odds ratio [OR] = 8.0; 95% CI
= 1.7–37.1), 2) reported possession of homegrown maize that
was discolored or visibly contaminated with mold (OR = 5.9;
95% CI = 1.9–18.2), 3) consumption of homegrown maize
(OR = 3.0; 95% CI = 1.0–8.8), 3) storage of damp maize
(OR = 3.5; 95% CI = 1.2–10.3), 4) inside storage of maize
rather than outside granary storage (OR = 12.0; 95% CI =
1.5–95.7), and 5) reported deaths of dogs or livestock (OR =
3.3; 95% CI = 1.2–9.1).
Food samples collected from household visits during May
10–19 included maize flour, maize grains, dry maize cobs,
muthokoi (i.e., maize in which the outer hulls have been
removed), millet, sorghum, and beans. A total of 31 samples were
FIGURE 1. Districts affected by aflatoxicosis outbreak — Eastern
and Central Provinces, Kenya, January–July 2004
Thika
Nairobi
Machakos
Makueni
Kitui
Mwingi
Mbeere
Embu
KENYA
Vol. 53 / No. 34 MMWR 791
tested by the Kenya National Public Health Laboratory Services,
and 15 had >20 ppb aflatoxin B1 (range: 20–8,000 ppb).
A representative survey of maize products from agricultural
markets and outlets (Figure 3) in Makueni, Kitui, Thika, and
Machakos districts was conducted to assess the extent and mag-
nitude of aflatoxin contamination in the sampled maize.
Preliminary results indicated widespread, high-level aflatoxin
contamination. A total of 182 (53.2%) of 342 samples had >20
ppb of aflatoxin. In addition, a substantial percentage of samples
from each district had aflatoxin levels
>1,000 ppb: Makueni (12.1%), Kitui
(9.6%), Thika (3.9%), and Machakos
(2.9%).
The government of Kenya is provid-
ing replacement food in the most
heavily affected districts: Makueni dis-
trict (population: 771,545) and Kitui
district (population: 515,422). Resi-
dents of affected districts have been
advised to avoid consumption of maize
or other foods suspected to be moldy
or appearing discolored. In addition,
food inspections by public health
authorities are being conducted, and
suspect food is being seized, destroyed,
and replaced. Surveillance for possible
aflatoxin poisoning in humans has been
extended to other parts of Kenya by
MOH, and aflatoxin screening of maize
has been increased.
Reported by: J Nyikal, A Misore, C Nzioka,
C Njuguna, E Muchiri, J Njau, S Maingi,
J Njoroge, J Mutiso, J Onteri, A Langat,
IK Kilei, J Nyamongo, G Ogana, B Muture,
Aflatoxin Task Force, Kenya Ministry of
Health; P Tukei, C Onyango, W Ochieng,
Kenya Medical Research Institute; C Tetteh,
S Likimani, P Nguku, T Galgalo, S Kibet,
A Manya, A Dahiye, J Mwihia, I Mugoya,
Kenya Field Epidemiology and Laboratory
Training Program/Kenya Ministry of
Health. J Onsongo, A Ngindu, World Health
Organization Kenya Country Office.
KM DeCock, K Lindblade, L Slutsker,
P Amornkul, D Rosen, D Feiken, T Thomas,
CDC Kenya. P Mensah, N Eseko, A Nejjar,
World Health Organization Regional Office
for Africa. M Onsongo, F Kessel, Foreign
Agricultural Svc, U.S. Dept of Agriculture.
H Njapau, DL Park, Center for Food Safety
and Applied Nutrition, Food and Drug
Administration. Div of International Health,
Epidemiology Program Office; L Lewis, G Luber, H Rogers, L Backer,
C Rubin, National Center for Environmental Health; KE Gieseker,
E Azziz-Baumgartner, W Chege, A Bowen, EIS officers, CDC.
Editorial Note: Evidence that this outbreak resulted from
aflatoxin poisoning included 1) high levels of aflatoxin (up to
8,000 ppb) in maize samples collected from patient house-
holds, 2) a clinical illness consistent with acute aflatoxin poi-
soning, 3) clustering of cases among residents of the same
household, and 4) reports of deaths among animals known to
FIGURE 3. A posho (maize flour) mill — Makueni district, Eastern Province, Kenya, 2004
Photo/CDC
FIGURE 2. Number of aflatoxicosis cases, by date of reporting — Eastern and Central
Provinces, Kenya, January–July 2004
0
2
4
6
8
10
12
14
16
1 8 15 22 29 5 12 19 26 4 11 18 25 1 8 15 22 29 6 13 20 27 3 10 17 24 1 8 15
Jan Feb Mar Apr May Jun Jul
Day and month
Active surveillance
Nu
m
be
r
792 MMWR September 3, 2004
have eaten the same maize as the patients during the same
period. Serum specimens from a convenience sample of seven
patients were tested for differential viral etiologies. All seven
patients had negative serologic tests for yellow fever, dengue,
West Nile virus, Rift Valley fever, Chikungunya and
Bunyamwera viruses, acute hepatitis A, acute hepatitis B, and
hepatitis C.
Aflatoxins are a group of metabolic products formed by two
species of fungus, Aspergillus flavus and A. parasiticus, in sev-
eral agricultural commodities, including corn or maize. Two
structural types of aflatoxins are known (B and G types), of
which aflatoxin B1 is considered the most toxic and was the
type most commonly found in Kenya during this outbreak.
Exposure to aflatoxins occurs primarily through ingestion of
contaminated foods (2) and can cause hepatic and gastrointes-
tinal injury and have immunosuppressive, teratogenic, and
oncogenic effects. Chronic low-level aflatoxin exposure can
increase the risk for hepatocellular carcinoma (3). Severe, acute
liver injury with high morbidity and mortality has been asso-
ciated with high-dose exposures to aflatoxins (4). Ingestion of
2–6 mg/day of aflatoxin for a month can cause acute hepatitis
and death (5,6).
The largest reported outbreak of aflatoxicosis to date
occurred in western India in 1974, resulting in 397 recog-
nized cases and 106 deaths (6). The ongoing epidemic in Kenya
already has resulted in 125 recognized deaths. Because of the
remoteness of villages in the affected districts in Kenya and
the large geographic area involved, case finding has been lim-
ited to medical facilities. In addition, because some persons
might not have been able to reach health-care facilities for
diagnosis and treatment, the true magnitude of this outbreak
is likely to be considerably greater than reported.
An outbreak of acute aflatoxicosis (20 cases; CFR = 60%)
was reported previously in Makueni district, Eastern Prov-
ince, Kenya, in 1981 (1). Patients were clustered in family
groups that shared meals consisting of aflatoxin-contaminated
maize (1,600–12,000 ppb). Acute hepatitis associated with
consumption of moldy grains also has been reported in other
areas in Africa, Western India, and Malaysia (6–8), where
affected persons came from areas prone to drought and mal-
nutrition and unseasonable rains forced the harvest of grains
before adequate drying had occurred. Typically,
increased reports of jaundice and hepatitis followed within
weeks of such harvests (6–8). Locally produced maize associ-
ated with this outbreak was harvested in February during peak
rains, and the first illnesses were reported in Makueni district
in late March and early April.
For every symptomatic case of aflatoxicosis identified,
several other persons likely were exposed to unsafe levels of
aflatoxin and might face future adverse health consequences.
In addition, individual cases or clusters of aflatoxin poisoning
likely occur regularly but are not recognized. Efforts should
focus on the prevention of aflatoxin exposure by implement-
ing extensive food replacement, without which, the epidemic
can be expected to continue. Longer-term requirements
include strengthened surveillance; increased food inspections
to ensure food safety; and local education and assistance to
ensure that maize is harvested correctly, dried completely, and
stored properly.
This report describes the first investigation by the Kenya
FELTP, a partnership of CDC, KMOH, and Jomo Kenyatta
University of Agriculture and Technology intended to build
public health, epidemiologic, and laboratory capacity in Kenya.
This investigation provided field experience to these Kenyan
public health workers in training and exemplified collabora-
tion between different national and international agencies and
among various sectors and disciplines, including health, agri-
culture, food safety, nutrition, and humanitarian relief.
Increased collaboration between the health sector and others
involved in food security and safety could enable early warn-
ing of high levels of aflatoxins.
As a result of widespread drought, Kenya faces an acute
food shortage, with nearly 1.8 million persons in 26 districts
vulnerable to food insecurity (9), including persons in the
area most heavily affected by the aflatoxicosis outbreak.
Because an estimated 166,000 metric tons of food will be
required to meet the requirements of emergency and school
feeding programs during August 2004–January 2005, public
health officials should be vigilant to a possible wider
aflatoxicosis outbreak resulting from the large-scale storage
and distribution of certain emergency food supplies.
Acknowledgments
The findings in this report are based, in part, on contributions
by Makindu Sub-District Hospital, Makueni district, Mutomo
Mission Hospital, Kitui district, other health facilities, staff at the
National Public Health Laboratory Svcs, Kenya.
References
1. Ngindu A, Kenya PR, Ocheng DM, et al. Outbreak of acute hepatitis
by aflatoxin poisoning in Kenya. Lancet 1982;319:1346–8.
2. Fung F, Clark RF. Health effects of mycotoxins: a toxicological over-
view. J Toxicol Clin Toxicol 2004;42:217–34.
3. Peraica M, Radic B, Lucic A, Pavlovic M. Toxic effects of mycotoxins in
humans. Bull World Health Organ 1999;77:754–66.
4. Chao TC, Maxwell SM, Wong SY. An outbreak of aflatoxicosis and
boric acid poisoning in Malaysia: a clinicopathological study. J Pathol
1991;164:225–33.
5. Patten RC. Aflatoxins and disease. Am J Trop Med Hyg 1981;30:422–5.
6. Krishnamachari KA, Nagaarajan V, Bhat RV, Tilak TB. Hepatitis due to
aflatoxicosis—an outbreak in Western India. Lancet 1975;305:1061–3.
Vol. 53 / No. 34 MMWR 793
7. Krishnamachari KA, Bhat RV, Nagarajan V, Tilak TBG. Investigations
into an outbreak of hepatitis in parts of Western India. Indian J Med
Res 1975;63:1036–49.
8. Lye MS, Ghazali AA, Mohan J, Alwin N, Nair RC. An outbreak of
acute hepatic encephalopathy due to severe aflatoxicosis in Malaysia.
Am J Trop Med Hyg 1995;53:68–72.
9. USAID Famine Early Warning Systems Network (Kenya), World Food
Program, Kenya Ministry of Agriculture. Kenya food security report—
August 9, 2004. Available at http://www.fews.net/centers/files/
Kenya_200407en.pdf.
An Outbreak of Norovirus
Gastroenteritis at a Swimming
Club — Vermont, 2004
John Snow’s historic investigation of a severe epidemic of
cholera traced the cause of infection to a common water source
(1). Today, 150 years later, waterborne diseases remain a pub-
lic health problem, and similar investigations are used to iden-
tify the source of infection. On February 3, 2004, the Vermont
Department of Health (VDH) was notified of an outbreak of
acute gastroenteritis among children whose only common
exposure was attendance at a swimming club the previous
weekend (January 31–February 1). This report summarizes
the results of an investigation conducted by VDH and CDC,
which determined the cause of the outbreak to be a combina-
tion of stool contamination, a blocked chlorine feed tube, and
multiple lapses of pool-maintenance procedures. The find-
ings underscore the importance of correct pool maintenance
for rapid identification of water-quality problems to prevent
outbreaks of swimming pool–associated
illness.
Pool attendance records were avail-
able for review for the period from Fri-
day evening, January 30, to Monday
noon, February 2, 2004. During this
time, seven private groups used the
pool, including three mother-infant
swimming classes, two groups from a
local girls’ organization, a birthday party
of children aged 5–10 years, and a pre-
school class. In addition, members of
the club used the pool during two de-
fined open-swim sessions. The seven
private groups ranged in size from four
to 31 persons. The group leader for each
event provided a roster of attendees. An
adult in each household was contacted
by telephone and asked to identify fam-
ily members who attended events at the
swimming club and to question them about recent gastrointes-
tinal illness by using a standardized questionnaire. Family
members who reported recent gastrointestinal illness were
asked to submit stool specimens for laboratory testing. Re-
spondents also were asked to describe the appearance of the
pool water at the time of their visit. A case was defined as
vomiting or diarrhea (i.e., >3 loose stools within a 24-hour
period) that occurred in a person within 72 hours of visiting
the swimming club.
Of the 189 persons for whom information was collected
and who visited the pool during the outbreak period, median
age was 13 years (range: 5 months–73 years); 53 (28%)
reported an illness consistent with the case definition. Among
these 53 persons, onset of symptoms began a median of 30
hours (range: 8–62 hours) after attending an event at the club
and included vomiting (89%), diarrhea (50%), nausea (77%),
stomach cramps (68%), chills (58%), and a fever of >100.4º
F (>38º C) (53%). The median age of patients was 7 years
(range: 5 months–61 years); 31 (58%) were female. Six per-
sons (five children and one adult) sought medical care from
their physicians, and one adult was hospitalized with severe
vomiting. Of the 10 stool specimens tested, five were positive
for norovirus by reverse transcription-polymerase chain reac-
tion (RT-PCR). Three strains were characterized further and
determined to share identical nucleotide sequences. The high-
est attack rates were observed among persons who visited the
pool on Saturday or Sunday (Figure). No one who attended
Friday’s event became ill, and by Sunday afternoon, the attack
FIGURE. Number of well and ill persons and attack rates of acute gastroenteritis, by
exposure group and day — Vermont, January 30–February 2, 2004
0
10
20
30
40
Nu
m
be
r o
f p
er
so
ns
0
20
40
60
80
100
Attack rate (%)
Girls
group
Friday
Infant
swim
Infant
swim
Infant
swim
Open
swim
Birthday Open
swim
Sunday
Girls
group
Preschool
MondaySaturday
Group and day of exposure
Chlorine added
Cloudy water noted; no action taken 120
50
Broken chlorinator
tube found and
repaired
Ill (n = 53)
Well (n = 136)
Attack rate



Outbreak of Aflatoxin Poisoning - Eastern and Central Provinces, Kenya, January - July 2004

ScholarWorks @ Georgia State University

Georgia State UniversityScholarWorks @ Georgia State UniversityPublic Health Faculty Publications School of Public Health9-3-2004Outbreak of Aflatoxin Poisoning - Eastern andCentral Provinces, Kenya, January - July 2004Karen E. GiesekerGeorgia State University, kgieseker@gsu.eduCenters for Disease Control and PreventionFollow this and additional works at: https://scholarworks.gsu.edu/iph_facpubPart of the Public Health CommonsThis Article is brought to you for free and open access by the School of Public Health at ScholarWorks @ Georgia State University. It has been acceptedfor inclusion in Public Health Faculty Publications by an authorized administrator of ScholarWorks @ Georgia State University. For more information,please contact scholarworks@gsu.edu.Recommended CitationGieseker, Karen E. and Centers for Disease Control and Prevention, "Outbreak of Aflatoxin Poisoning - Eastern and Central Provinces,Kenya, January - July 2004" (2004). Public Health Faculty Publications. 3.https://scholarworks.gsu.edu/iph_facpub/3790 MMWR September 3, 2004Outbreak of Aflatoxin Poisoning —Eastern and Central Provinces,Kenya, January–July 2004In May 2004, CDC Kenya, trainees of the CDC-supported Field Epidemiology and Laboratory Training Pro-gram (FELTP) in Kenya, the World Health Organization, andCDC were invited by the Kenya Ministry of Health (KMOH)to participate in the investigation of an outbreak of jaundicewith a high case-fatality rate (CFR) in the districts of Makueniand Kitui, Eastern Province. Preliminary laboratory testing offood collected from the affected area revealed high levels ofaflatoxin, suggesting that the outbreak was caused by afla-toxin poisoning, as was a previous outbreak in the same areain 1981 (1). In the United States, aflatoxin concentrations arelimited to 20 parts per billion (ppb), a level also adopted byKenyan authorities. The 2004 outbreak resulted from wide-spread aflatoxin contamination of locally grown maize, whichoccurred during storage of the maize under damp conditions.Urgent replacement of the aflatoxin-contaminated maize withnoncontaminated maize proved to be a critical intervention;however, as of July 21, a limited number of new cases contin-ued to be detected. This report summarizes the preliminaryresults of the outbreak investigation. Aflatoxin poisoning likelywill continue to be a public health problem until culturallyappropriate storage methods for dry maize are implementedby the local population. In addition, enhanced surveillancefor human aflatoxin poisoning and testing of commerciallysold maize for aflatoxin levels will lead to long-term improve-ments in public health.Joint KMOH and CDC teams conducted patient interviewsand reviewed medical records dating back to January 1, inthree health facilities in the Makueni and Kitui districts.Additional case finding was conducted through similarpatient interviews and retrospective record reviews in sevenhealth facilities in adjacent districts of Eastern Province(Machakos, Embu, Mbeere, and Mwingi districts) and Cen-tral Province (Thika district) and at Kenyatta National Hos-pital in Nairobi (Figure 1). Large-scale active surveillanceoccurred from early May to late June. As of July 21, threehealth facilities in Makueni and Kitui districts continued tobe monitored for new cases. A convenience sample of 20patient households was visited to assess the occurrence of jaun-dice in nonhospitalized household members and toinspect food quality and storage. In this investigation, a caseof suspected aflatoxin poisoning was defined as a case of acutejaundice that occurred after January 1, in a resident of East-ern or Central Province or a case diagnosed at KenyattaNational Hospital in a patient who was not known to havechronic liver disease or any other cause of jaundice.As of July 20, a total of 317 cases had been reported, with125 deaths (CFR = 39%). An increase in case reports beganin the third week of April, with new cases continuing to occurthrough mid-July (Figure 2). Of the 308 patients for whomage data were available, 68 (22.1%) were aged <5 years; 90(29.2%) were aged 5–14 years, and 150 (48.7%) were aged>15 years. Of the 317 total patients, 178 (56.2%) were male,and 280 (88.3%) resided in four districts: Makueni (148[46.7%]), Kitui (101 [31.8%]), Machakos (19 [6.0%]), andThika (12 [3.8%]). The remaining 37 (11.7%) patients hadaflatoxicosis diagnosed at Kenyatta National Hospital inNairobi or at health facilities in Embu, Mbeere, or Mwingidistricts. CFR was significantly higher in Makueni district(CFR = 49.3%) than in Kitui district (CFR = 23.7%) (CFRratio = 2.1; 95% confidence interval [CI] = 1.4–3.1).Preliminary results from a case-control study that compared40 case-patients with 80 well controls matched by village inMakueni and Kitui districts demonstrated a statistically sig-nificant association between the development of jaundice andseveral risk factors or markers, including 1) reported consump-tion of cooked maize kernels (odds ratio [OR] = 8.0; 95% CI= 1.7–37.1), 2) reported possession of homegrown maize thatwas discolored or visibly contaminated with mold (OR = 5.9;95% CI = 1.9–18.2), 3) consumption of homegrown maize(OR = 3.0; 95% CI = 1.0–8.8), 3) storage of damp maize(OR = 3.5; 95% CI = 1.2–10.3), 4) inside storage of maizerather than outside granary storage (OR = 12.0; 95% CI =1.5–95.7), and 5) reported deaths of dogs or livestock (OR =3.3; 95% CI = 1.2–9.1).Food samples collected from household visits during May10–19 included maize flour, maize grains, dry maize cobs,muthokoi (i.e., maize in which the outer hulls have beenremoved), millet, sorghum, and beans. A total of 31 samples wereFIGURE 1. Districts affected by aflatoxicosis outbreak — Easternand Central Provinces, Kenya, January–July 2004ThikaNairobiMachakosMakueniKituiMwingiMbeereEmbuKENYAVol. 53 / No. 34 MMWR 791tested by the Kenya National Public Health Laboratory Services,and 15 had >20 ppb aflatoxin B1 (range: 20–8,000 ppb).A representative survey of maize products from agriculturalmarkets and outlets (Figure 3) in Makueni, Kitui, Thika, andMachakos districts was conducted to assess the extent and mag-nitude of aflatoxin contamination in the sampled maize.Preliminary results indicated widespread, high-level aflatoxincontamination. A total of 182 (53.2%) of 342 samples had >20ppb of aflatoxin. In addition, a substantial percentage of samplesfrom each district had aflatoxin levels>1,000 ppb: Makueni (12.1%), Kitui(9.6%), Thika (3.9%), and Machakos(2.9%).The government of Kenya is provid-ing replacement food in the mostheavily affected districts: Makueni dis-trict (population: 771,545) and Kituidistrict (population: 515,422). Resi-dents of affected districts have beenadvised to avoid consumption of maizeor other foods suspected to be moldyor appearing discolored. In addition,food inspections by public healthauthorities are being conducted, andsuspect food is being seized, destroyed,and replaced. Surveillance for possibleaflatoxin poisoning in humans has beenextended to other parts of Kenya byMOH, and aflatoxin screening of maizehas been increased.Reported by: J Nyikal, A Misore, C Nzioka,C Njuguna, E Muchiri, J Njau, S Maingi,J Njoroge, J Mutiso, J Onteri, A Langat,IK Kilei, J Nyamongo, G Ogana, B Muture,Aflatoxin Task Force, Kenya Ministry ofHealth; P Tukei, C Onyango, W Ochieng,Kenya Medical Research Institute; C Tetteh,S Likimani, P Nguku, T Galgalo, S Kibet,A Manya, A Dahiye, J Mwihia, I Mugoya,Kenya Field Epidemiology and LaboratoryTraining Program/Kenya Ministry ofHealth. J Onsongo, A Ngindu, World HealthOrganization Kenya Country Office.KM DeCock, K Lindblade, L Slutsker,P Amornkul, D Rosen, D Feiken, T Thomas,CDC Kenya. P Mensah, N Eseko, A Nejjar,World Health Organization Regional Officefor Africa. M Onsongo, F Kessel, ForeignAgricultural Svc, U.S. Dept of Agriculture.H Njapau, DL Park, Center for Food Safetyand Applied Nutrition, Food and DrugAdministration. Div of International Health,Epidemiology Program Office; L Lewis, G Luber, H Rogers, L Backer,C Rubin, National Center for Environmental Health; KE Gieseker,E Azziz-Baumgartner, W Chege, A Bowen, EIS officers, CDC.Editorial Note: Evidence that this outbreak resulted fromaflatoxin poisoning included 1) high levels of aflatoxin (up to8,000 ppb) in maize samples collected from patient house-holds, 2) a clinical illness consistent with acute aflatoxin poi-soning, 3) clustering of cases among residents of the samehousehold, and 4) reports of deaths among animals known toFIGURE 3. A posho (maize flour) mill — Makueni district, Eastern Province, Kenya, 2004Photo/CDCFIGURE 2. Number of aflatoxicosis cases, by date of reporting — Eastern and CentralProvinces, Kenya, January–July 200402468101214161 8 15 22 29 5 12 19 26 4 11 18 25 1 8 15 22 29 6 13 20 27 3 10 17 24 1 8 15Jan Feb Mar Apr May Jun JulDay and monthActive surveillanceNumber792 MMWR September 3, 2004have eaten the same maize as the patients during the sameperiod. Serum specimens from a convenience sample of sevenpatients were tested for differential viral etiologies. All sevenpatients had negative serologic tests for yellow fever, dengue,West Nile virus, Rift Valley fever, Chikungunya andBunyamwera viruses, acute hepatitis A, acute hepatitis B, andhepatitis C.Aflatoxins are a group of metabolic products formed by twospecies of fungus, Aspergillus flavus and A. parasiticus, in sev-eral agricultural commodities, including corn or maize. Twostructural types of aflatoxins are known (B and G types), ofwhich aflatoxin B1 is considered the most toxic and was thetype most commonly found in Kenya during this outbreak.Exposure to aflatoxins occurs primarily through ingestion ofcontaminated foods (2) and can cause hepatic and gastrointes-tinal injury and have immunosuppressive, teratogenic, andoncogenic effects. Chronic low-level aflatoxin exposure canincrease the risk for hepatocellular carcinoma (3). Severe, acuteliver injury with high morbidity and mortality has been asso-ciated with high-dose exposures to aflatoxins (4). Ingestion of2–6 mg/day of aflatoxin for a month can cause acute hepatitisand death (5,6).The largest reported outbreak of aflatoxicosis to dateoccurred in western India in 1974, resulting in 397 recog-nized cases and 106 deaths (6). The ongoing epidemic in Kenyaalready has resulted in 125 recognized deaths. Because of theremoteness of villages in the affected districts in Kenya andthe large geographic area involved, case finding has been lim-ited to medical facilities. In addition, because some personsmight not have been able to reach health-care facilities fordiagnosis and treatment, the true magnitude of this outbreakis likely to be considerably greater than reported.An outbreak of acute aflatoxicosis (20 cases; CFR = 60%)was reported previously in Makueni district, Eastern Prov-ince, Kenya, in 1981 (1). Patients were clustered in familygroups that shared meals consisting of aflatoxin-contaminatedmaize (1,600–12,000 ppb). Acute hepatitis associated withconsumption of moldy grains also has been reported in otherareas in Africa, Western India, and Malaysia (6–8), whereaffected persons came from areas prone to drought and mal-nutrition and unseasonable rains forced the harvest of grainsbefore adequate drying had occurred. Typically,increased reports of jaundice and hepatitis followed withinweeks of such harvests (6–8). Locally produced maize associ-ated with this outbreak was harvested in February during peakrains, and the first illnesses were reported in Makueni districtin late March and early April.For every symptomatic case of aflatoxicosis identified,several other persons likely were exposed to unsafe levels ofaflatoxin and might face future adverse health consequences.In addition, individual cases or clusters of aflatoxin poisoninglikely occur regularly but are not recognized. Efforts shouldfocus on the prevention of aflatoxin exposure by implement-ing extensive food replacement, without which, the epidemiccan be expected to continue. Longer-term requirementsinclude strengthened surveillance; increased food inspectionsto ensure food safety; and local education and assistance toensure that maize is harvested correctly, dried completely, andstored properly.This report describes the first investigation by the KenyaFELTP, a partnership of CDC, KMOH, and Jomo KenyattaUniversity of Agriculture and Technology intended to buildpublic health, epidemiologic, and laboratory capacity in Kenya.This investigation provided field experience to these Kenyanpublic health workers in training and exemplified collabora-tion between different national and international agencies andamong various sectors and disciplines, including health, agri-culture, food safety, nutrition, and humanitarian relief.Increased collaboration between the health sector and othersinvolved in food security and safety could enable early warn-ing of high levels of aflatoxins.As a result of widespread drought, Kenya faces an acutefood shortage, with nearly 1.8 million persons in 26 districtsvulnerable to food insecurity (9), including persons in thearea most heavily affected by the aflatoxicosis outbreak.Because an estimated 166,000 metric tons of food will berequired to meet the requirements of emergency and schoolfeeding programs during August 2004–January 2005, publichealth officials should be vigilant to a possible wideraflatoxicosis outbreak resulting from the large-scale storageand distribution of certain emergency food supplies.AcknowledgmentsThe findings in this report are based, in part, on contributionsby Makindu Sub-District Hospital, Makueni district, MutomoMission Hospital, Kitui district, other health facilities, staff at theNational Public Health Laboratory Svcs, Kenya.References1. Ngindu A, Kenya PR, Ocheng DM, et al. Outbreak of acute hepatitisby aflatoxin poisoning in Kenya. Lancet 1982;319:1346–8.2. Fung F, Clark RF. Health effects of mycotoxins: a toxicological over-view. J Toxicol Clin Toxicol 2004;42:217–34.3. Peraica M, Radic B, Lucic A, Pavlovic M. Toxic effects of mycotoxins inhumans. Bull World Health Organ 1999;77:754–66.4. Chao TC, Maxwell SM, Wong SY. An outbreak of aflatoxicosis andboric acid poisoning in Malaysia: a clinicopathological study. J Pathol1991;164:225–33.5. Patten RC. Aflatoxins and disease. Am J Trop Med Hyg 1981;30:422–5.6. Krishnamachari KA, Nagaarajan V, Bhat RV, Tilak TB. Hepatitis due toaflatoxicosis—an outbreak in Western India. Lancet 1975;305:1061–3.Vol. 53 / No. 34 MMWR 7937. Krishnamachari KA, Bhat RV, Nagarajan V, Tilak TBG. Investigationsinto an outbreak of hepatitis in parts of Western India. Indian J MedRes 1975;63:1036–49.8. Lye MS, Ghazali AA, Mohan J, Alwin N, Nair RC. An outbreak ofacute hepatic encephalopathy due to severe aflatoxicosis in Malaysia.Am J Trop Med Hyg 1995;53:68–72.9. USAID Famine Early Warning Systems Network (Kenya), World FoodProgram, Kenya Ministry of Agriculture. Kenya food security report—August 9, 2004. Available at http://www.fews.net/centers/files/Kenya_200407en.pdf.An Outbreak of NorovirusGastroenteritis at a SwimmingClub — Vermont, 2004John Snow’s historic investigation of a severe epidemic ofcholera traced the cause of infection to a common water source(1). Today, 150 years later, waterborne diseases remain a pub-lic health problem, and similar investigations are used to iden-tify the source of infection. On February 3, 2004, the VermontDepartment of Health (VDH) was notified of an outbreak ofacute gastroenteritis among children whose only commonexposure was attendance at a swimming club the previousweekend (January 31–February 1). This report summarizesthe results of an investigation conducted by VDH and CDC,which determined the cause of the outbreak to be a combina-tion of stool contamination, a blocked chlorine feed tube, andmultiple lapses of pool-maintenance procedures. The find-ings underscore the importance of correct pool maintenancefor rapid identification of water-quality problems to preventoutbreaks of swimming pool–associatedillness.Pool attendance records were avail-able for review for the period from Fri-day evening, January 30, to Mondaynoon, February 2, 2004. During thistime, seven private groups used thepool, including three mother-infantswimming classes, two groups from alocal girls’ organization, a birthday partyof children aged 5–10 years, and a pre-school class. In addition, members ofthe club used the pool during two de-fined open-swim sessions. The sevenprivate groups ranged in size from fourto 31 persons. The group leader for eachevent provided a roster of attendees. Anadult in each household was contactedby telephone and asked to identify fam-ily members who attended events at theswimming club and to question them about recent gastrointes-tinal illness by using a standardized questionnaire. Familymembers who reported recent gastrointestinal illness wereasked to submit stool specimens for laboratory testing. Re-spondents also were asked to describe the appearance of thepool water at the time of their visit. A case was defined asvomiting or diarrhea (i.e., >3 loose stools within a 24-hourperiod) that occurred in a person within 72 hours of visitingthe swimming club.Of the 189 persons for whom information was collectedand who visited the pool during the outbreak period, medianage was 13 years (range: 5 months–73 years); 53 (28%)reported an illness consistent with the case definition. Amongthese 53 persons, onset of symptoms began a median of 30hours (range: 8–62 hours) after attending an event at the cluband included vomiting (89%), diarrhea (50%), nausea (77%),stomach cramps (68%), chills (58%), and a fever of >100.4ºF (>38º C) (53%). The median age of patients was 7 years(range: 5 months–61 years); 31 (58%) were female. Six per-sons (five children and one adult) sought medical care fromtheir physicians, and one adult was hospitalized with severevomiting. Of the 10 stool specimens tested, five were positivefor norovirus by reverse transcription-polymerase chain reac-tion (RT-PCR). Three strains were characterized further anddetermined to share identical nucleotide sequences. The high-est attack rates were observed among persons who visited thepool on Saturday or Sunday (Figure). No one who attendedFriday’s event became ill, and by Sunday afternoon, the attackFIGURE. Number of well and ill persons and attack rates of acute gastroenteritis, byexposure group and day — Vermont, January 30–February 2, 2004010203040Number of persons020406080100Attack rate (%)GirlsgroupFridayInfantswimInfantswimInfantswimOpenswimBirthday OpenswimSundayGirlsgroupPreschoolMondaySaturdayGroup and day of exposureChlorine addedCloudy water noted; no action taken 12050Broken chlorinatortube found andrepairedIll (n = 53)Well (n = 136)Attack rate

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Outbreak of Aflatoxin Poisoning - Eastern and Central Provinces, Kenya, January - July 2004

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