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An outbreak of Hepatitis A in Jizan, 2002

On 14th March, 2002 (1st Moharram, 1423) the General Health Directorate of Jizan reported an increase in the number of children suffering from hepatitis A in a locality near Jizan In response, a team from FETP was assigned to investigate this outbreak.
All the cases had appeared in three neighboring villages: Mehlia, Omeriah and Khradla. Since there had been no recent change in the environmental and other epidemiological factors indicating the cause of this outbreak, other factors that could explain this local upsurge of disease were investigated. There was no community water supply in the area and people mainly depended on water tankers for their water needs. Otherwise, few households used bottled mineral water for drinking or household-wells for non-drinking purposes.
After assessment of the distribution of disease, a case control study was conducted to identify the risk factors. A case was defined as any person living in the catchment area of Mehlia Primary Health Care Centre and diagnosed as suffering from Hepatitis A clinically and /or confirmed by laboratory tests, since 1st December 2001. Neighborhood controls were defined as any child who lived in the same area, below 15 years of age who did not suffer from Hepatitis A clinically since 1St December 2001; confirmed by serological examination .
A structured data collection form was designed containing information on demographic data, previous history of jaundice, presence or absence of signs E and symptoms of hepatitis, possible risk factors; such as personal hygiene, eating habits and history of contact with a known case. A list of the reported cases was finalized and each case was interviewed, at times with the assistance of the mother, father or an older family member. A blood sample was drawn to test for anti HAV IgM antibodies. Neighbourhood controls were recruited following the same procedure. Blood samples were sent to the laboratory of King Fahad Hospital, Jizan.
A total of 63 cases were identified. Their symptoms and signs were fever (93.7%), malaise (93.7%), nausea (92.1%), jaundice (87.3%), headache(82.5%), skin itching (79.4%), diarrhea (73.1%), abdominal discomfort (65.1%), vomiting (63.5%), change in color of urine (44.4%) and anorexia (25.4%). All the cases were children below 12 years of age with a mean of 6.5 years (SD 7.28 years). 49.2% of cases were from Mehlia, 42.9% from Khradla and 7.9% were from Omeriah with attack rates of clinical hepatitis A of 13.4/1,000 population, 24.3/1,000 population and 2.5/1,000 population, respectively.
As shown in figure 1, the first reported case occurred on 12th December, 2001 in Mehlia. The outbreak extended to Khradla and then to Omeriah over the following 3 months, in a pattern conforming to person-to-person transmission. The cases disappeared rapidly after local health authorities held a mass campaign for passive immunization in children during the second week of March.
Out of 177 controls, 4 were positive for anti HAV IgM antibodies, reflecting recent infection, so 173 controls were compared against the 63 cases. Males constituted 41.3% of cases and 37% of controls, but the difference was not statistically significant (OR 1.2, 95% CI 0.66-2.16). Saudi nationals composed 96.8% of cases, compared to 100% of controls. 58.7% of the cases were students, compared to 81.5% of controls, indicating that attending school was significantly associated with a lower risk of disease (OR 0.32, 95% CI 0.16-0.64). Among the 146 study subjects who could recall exposure to a known case of jaundice, 43.8% of cases and 6.15% of controls reported exposure and the difference was statistically significant (OR= 11.86, 95% CI 3.0-48.0).
There was no significant difference between cases and controls regarding eating food outside the home in the previous 45 days. Eating potatoes from street vendors was associated with a higher risk of disease but was not statistically significant.
The main source of drinking water was the water tankers for 92.1% of cases and 95.4% of controls, and was associated with a lower risk of disease when compared to drinking bottled water (OR 0.56, 95% CI 0.16-2.07). As for non-drinking purposes, the tankers were the main source of water for 92.1% of cases and 89.0% of controls, and were associated with a nonsignificant increased risk of disease as compared to using water from wells in the houses (OR 1.43, 95% CI 0.474.61). A small number of households used non-drinking water for drinking purposes (4.8% of cases and 1.7% of controls), and 25.4% of cases and 19.1% of controls reported using the non-drinking water for routine kitchen work (OR 1.44, 95% CI 0.69-3.01).
Washing hands with soap after using the lavatory and before eating meals had an inverse relationship with disease.

Editorial note:

Hepatitis A is endemic in many parts of the world, including Saudi Arabia.[1,2] The epidemic curve shows that the outbreak started in Mehlia village then gradually extended to the physically contiguous villages in a pattern of person-to-person transmission. In the presence of an unidentified number of subclinical cases this curve does not represent the magnitude of the total infected persons but gives a reasonable indication of the disease progression pattern in the area.
The exact pattern of prevalence of Hepatitis A depends mainly on environmental sanitation conditions.[3] In countries with poor environmental sanitation, disease is mainly transmitted among children but is more visible in adults due to a higher proportion of subclinical cases. In this study, however, all reported cases had occurred in children below 12 years of age, which may be explained by the fact that most of the adults had already developed antibodies against HAV as a result of clinical or subclinical infection, leaving only children as the available pool of susceptible hosts.
In spite of all efforts, no source of infection that could explain a common source model was identified, whether in household or school environments. Although a person-to-person trans-mission pattern could not be established due to a high proportion of subclinical cases, the absence of facilities for HAV isolation with sub-typing, and sudden disruption of outbreak by passive immunization of most of the population by immunoglobulins, the cumulative evidence in support of person-to-person transmission is large. First, the epidemic curve exhibits multiple peaks and sequential transmission from one area to other is quite supportive to the person-to-person transmission model. Second, the children who had exposure to a known case of jaundice had a higher risk. Third, the children who had better personal hygiene practice, were at lower risk. Fourth, families which used non-drinking water were at higher risk. Although many of the associations observed were statistically not-significant but they conform with general pattern described. This outbreak can be treated as an exacerbation of the endemic person to person faeco-oral transmission of disease which is prevalent in such areas with poor water supply and low socioeconomic status. [1,4,5]
To prevent recurrence of such outbreaks and control of endemic transmission of disease, piped water supply should be provided to the community, preferably accompanied by establishment of proper sewage disposal system. In the meantime, the local municipality should do periodic monitoring of the quality of water provided by tankers. A health education campaign should be initiated to improve personal hygienic practices mainly targeting children.
  1. World Health Organization. Public health control hepatitis A. memorandums from a WHO meeting. Bull Wrld Hlth Org 1995; 73(1): 15-60.
  2. Shobokshi OA, Serebour FE. The etiology of acute viral hepatitis in the western region of Saudi Arabia. Trans Soc Trop Hyg 1987; 81: 219-21.
  3. Shapirio CN, Coleman PJ, McQuillan GM, et al Epidemiology of hepatitis A: Seroepidemiology and risk groups in the USA. Vaccine 1992; 10(1): S40.
  4. Melink JL. History and epidemiology of hepatitis A virus. J Infect Dis 1995; 171(1): S2-5.
  5. Strickland GT. Hepatitis A. Hunter's tropical medicine (7th ed.) Philadelphia: WB Saunders Co. 1991; 188-90.