Skip to main content

Hepatitis "A" outbreak at Al-Berk, Asir region, 2004

On 08/03/1425H (28/4/2004), the General Health Directorate of Asir region reported to the Communicable Disease Department, Ministry of Health, that an unusually large number of hepatitis A (HAV) cases were being diagnosed from different villages of Alberk area, in Alberk Hospital and primary health care centers. Alberk area is located in Asir region, south of Saudi Arabia, about 200 kilometers away from Abha, with total population of 15000. An investigative team from the Field Epidemiology training program (FETP) visited Asir region to investigate the outbreak. However, by the time the team had arrived to Asir region, a mass vaccination campaign with IG had already been carried out.
The team conducted a case-control study to identify the risk factors associated with the occurrence of the disease. A case was defined as any person living in the catchments areas (Alberk governorate) and presented to any of the health facilities with jaundice, and/or diagnosed as suffering from hepatitis A clinically and/or confirmed by laboratory tests, during the period of 30/11/1424 (1st January 2004) to 30/3/1425 (19 May 2004). A control was defined as any person who lived in the same area who never had jaundice symptoms (did not suffer from hepatitis A clinically) before 30/03/1425 (19 May 2004). One control was selected for each case. The controls were divided into two major groups according to school attendance. For those cases attending school, one classmate control was selected giving priority to those who sat to the right, left, front, then back of the case respectively. For cases not attending school, controls were selected from the nearest neighbor of the case, and if not available the next neighbor.
We were able to identify and interview 110 cases and 110 controls. All were Saudis. The ages of the cases ranged from 2 to 35 years with mean (±SD) of 9.1 (±6.5) years. There were 54 males (49.1%), and 56 females (50.9%). The symptoms reported by the cases were yellowish discoloration of eyes (jaundice) (99.1%), dark urine (92.7%), abdominal pain (87.3%), anorexia (87.3%), fever (77.3%), vomiting (74%), malaise (68.2%), nausea (59.1%), headache (58.2%), arthralgia (42.7%), diarrhea (33.6%), and itching (15.5%).
Among the 110 cases, 74 (67.3%) reported having contact with a known case of jaundice. Contact with a known case of HAV was identified to have a three times risk to acquire infection (OR= 3.2, 95% CI=1.8-5.56) and this was statistically significant. The risk of acquiring HAV was much higher when the cases lived in the same household (OR=11.70, 95% CI= 4.47-31.85), which was also statistically significant. There was no difference between those who attended school and those who did not, regarding acquiring HAV (OR=0.74, 95%CI=0.42-1.31), and this was not statistically significant. Washing hands with water and soap before eating and after going to toilet gave protection against acquiring HAV (OR= 0.20, 95% CI= 0.05-0.74; and OR= 0.26, 95% CI= 0.1-0.68 respectively), and both were statistically significant.
The majority of controls (90%) had received the vaccine, and 82 of the cases (74.5%) had also been vaccinated but had received the vaccine after acquiring the infection, therefore those controls who received the vaccine were protected against infection (OR= 0.39, 95% CI = 0.14-0.73).
There was no community water supply to all the 19 villages where the cases were reported. People depended on tank vehicle for their water supply, brought from either desalinated water pump or from wells There was no general sewage system in these villages; each house had its own sewage system like: bayara or dug-well, and the type of sewage disposal were not a risk factor for acquiring the infection (OR= 0.99, 95% CI = 0.7-1.41) for those who used bayara, and (OR= 1.07, 95% CI = 0.65-1.65) for those who used well-hole.
Leaking sewage outside houses was reported by 14 cases (12.7%) compared to 7 controls (6.4%), giving a clue that this may play a role in acquiring infection (OR = 2.14, 95% CI = 0.83-5.54).

Editorial note:

Hepatitis A, one of the oldest diseases known to mankind, is a self-limited disease which results in fulminant hepatitis and death in a proportion of patients. It is a significant cause of morbidity and socioeconomic losses in many parts of world.[1] HAV has a worldwide distribution and like other enteric infectious diseases, it is classically an infection of childhood and is related to conditions of sanitation and hygiene.[2]
It is acquired primarily by the fecal-oral route by either person to person contact or ingestion of contaminated food or water. It may also be acquired from faecally contaminated food or water and from wastewater-contaminated drills or water supplies.[1,3] Hepatitis A occurs sporadically and epidemically worldwide, with a tendency to cyclic recurrences.[3] Several countries around the world have reported cyclic communitywide outbreaks of hepatitis A every 5 to 10 years, such as the United States, where from 1980 through 2001, an average of 25,000 cases have been reported to the Centers for Disease Control and Prevention (CDC) each year.
Hepatitis A is endemic in many parts of the world, including Saudi Arabia,[4,5] where it is a major cause of morbidity. In 1997, the overall seroprevalence of HAV was determined in the Riyadh area to be 30.2% (range 12.5%-48.6%) among children aged 6 months to 15 years. The seroprevalence was found to be higher (39%) among rural children than urban (28%) or Bedouin (26%) children.[6]
General measures for hepatitis A prevention include hygienic and sanitary measures. In household settings, good personal hygiene, including good hand-washing practices and attention to proper food preparation are important in reducing the risk of transmission. At the community level, provision of safe drinking water and proper disposal of sanitary waste will reduce the incidence of hepatitis A. Passive immunization with immunoglobulin is the first choice in prevention and control of HAV epidemics and as post exposure prophylaxis.[7]
  1. 1. Hollinger FB and Ticehurst JR. Hepatitis A virus. In: Fields Virology. Fields BN, Knipe DM, Howley PM (eds.). 3rd ed. Philadelphia, Lippincott €” Raven, 1996, pp 735-782.
  2. 2. Feinstone S. Hepatitis A: epidemiology and prevention. Eur J Gastroenterol Hepatol 1996; 8: 300-305.
  3. 3. Lemon SM. Hepatitis A virus. In: Encyclopedia of Virology. Webster RG & Granoff A (eds.). London, Academic Press Ltd, 1994; pp 546-554.
  4. 4. World Health Organization. Public health control hepatitis A: Memorandums from a WHO meeting. Bull Wrld Hlth Org 1995; 73(1): 15-60.
  5. 5. 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.
  6. 6. Mbithi JN, Springthrope VS, Boulet JR, Sattar SA. Survival of hepatitis A virus on human hands and its transfer on contact with animate and inanimate surfaces. J Clin Microbiol 1992; 30-75.
  7. 7. Koff RS. Hepatitis A. Lancet 1998; 341:1643-1649.