Epidemiological studies on a HEV epidemic in Xijiang province between 1986 and 1988

Outline

From September 1986 to April in 1988, a hepatitis E epidemic occurred in the southern region of Xinjiang province — Hetian, Kashi and Kizilsu three regions, involving 23 counties and cities, which lasted for 20 months and experienced two prevalent periods with a total of 119,280 cases. The attack rate was 2.96%, and there were 705 deaths with a 0.59% mortality rate. The highest attack rate was 33.02% in a village with a mortality rate of 0.53%. The incidence cases were mainly young adults, and Uygur farmers accounted for the majority of the cases with an obvious familial aggregation. Women, maternal women in particular, had much higher rates of incidence and mortality than men. The latency was 19-75 days with an average of 42 days. The disease had similar symptoms and signs with other types of acute hepatitis and showed strong self-limited features. The ratio of clinical infection to sub-clinical infection was 1:2.56, but for children younger than 9 years old, this ratios was 1:13. The infection in children had no difference from that in adults but was mainly of subclinical type. Studies on the role of excreted virus in stools showed that a large amount of virus was excreted in the end of latency and early acute phase. And no more viruses were found two weeks after the onset of this disease. Thus, the isolation period for the disease was 2-3 weeks after the onset of this disease. This epidemic was caused by contamination of drinking water sources, and a close contact of healthy people with the patients played an important role in the continuous long-term prevalence. At present there is no effective, either active or passive, immunization approach, and comprehensive preventive measures are mainly to cut off the transmission route, which appears to be the most effective prevention and control means at the present time.

1. Epidemic history of Hepatitis E

From December 1^st 1955 to January 20^th, 1956, an outbreak of viral hepatitis occurred in the New Delhi State, which was caused by contamination of pipeline water source[1]. In 1980, through serological excluding tests, Wong D.C. confirmed that the virus that caused this epidemic was non-A, non-B hepatitis (EHN ANB) [2]. In September 1989, in an international academic meeting held in Tokyo on the non-A and non-B hepatitis and blood-borne diseases, this disease and its virus were officially named as the hepatitis E (HE) and hepatitis E virus (HEV), respectively. The epidemic in New Delhi State of India was the first report on the epidemic of this disease worldwide. So far, it has been identified that this disease has been prevalent in many countries in the world but mainly in Asia, including Mongolia, China, Afghanistan, Indonesia peninsula, Myanmar, Thailand, India, Kashmir, Nepal, Pakistan, Indonesia, and some Central Asian Republics in CIS; it also occured in Africa, including Algeria, Tunisia, Ethiopia, Sudan, Somalia, Chad and Ivory Coast as well as in Central America, at least in
Mexico; in Europe, some disease with the same characteristics of this disease occurred in the middle of this century; in some developed countries, such as the United States, Britain, France, and Japan, there were some sporadic cases. In China, a large-scale epidemic occurred in the southern region of Xinjiang province between 1986 and 1988, and its prevalence intensity and involvement of areas and duration were the largest worldwide to date[3]. In September 1986, this epidemic started from Luopu County in Hetian prefecture. At that time, there was no specific laboratory diagnostic method, except for serological methods of exclusion tests that ere used to establish the diagnosis of non-A and non-B hepatitis in combination of the findings of enteric transmission and epidemiological studies. However, because there were no effective preventive measures, the number of cases rapidly increased, leading to continuous epidemic progresson and a large-scale epidemic involving three prefectures (states), 23 counties and cities that lasted for 20 months. In addition, small-scale epidemics occurred in Liaoning, Jilin, Hebei, Shandong, Inner Mongolia and other provinces or autonomous regions, mostly sporadic cases.

2. Clinical features

2.1 Latency investigation

This investigation was conducted in epidemic areas where it was confirmed that daily living contact was the main route of transmission [4]. Using case investigation methods, follow-ups were conducted on healthy people (potential cases) with a single potential transmission factor who only contacted one case (primary cases) in the infectious period. The criteria for identifying potential cases were as follows: (1) having some daily living contact history with primary cases in the infectious period before the onset of this disease. (2) The possibility of the same source of infection with primary cases was ruled out. (3) Infection from other sources was excluded. (4) Diagnosed with the same standards for the primary case. Therefore, from the contact date of potential cases with the primary cases to the onset date of potential cases, the interval was considered as the latency period of this case. The median of latency of all new cases was taken as the overall latency. The results showed that the overall latency of this disease was 42 days, the longest and shortest latency period were 19 and 75 days, respectively.

2.2 Clinical manifestations

The prevalent rates of symptoms and signs of acute hepatitis E are shown in Table 8.1. The patients had a rapid onset and similar clinical features to that of other acute hepatitis. The average period for ALT (please spell this out the first time it was used) reaching the peak was 7.5 days, and ALT abnormal duration was 3-48 days with an average of 16.5 days. The average period for serum bilirubin reaching the peak was 9.13 days. Severe hepatitis accounted for 1.67% of the total number of acute cases. The disease was strong self-limited and most cases can be cured by having some rest, enhanced nutrition and proper treatment. The mortality of severe hepatitis was up to 61.5%-66.7% without chronic turnover.

2.3 Sub-clinical infection

During the period of hepatitis E epidemic, epidemiological investigation
and clinical observations were conducted on families with and without the disease [5]. In the investigated population, the ratio of clinical infection to sub-clinical infection was 1:2.56, but, for children younger than 9 years old, this ratios was 1:13. Clinicaltype cases were mainly confined to young adults, but the infection of hepatitis E in children had no difference from that in adults but was mainly of the sub-clinical type. The infection rate of sub-clinical type in families with the incidence of this disease was higher than families without the incidence (Table 8.2, Table 8.3 ). This indicated that affected children were more susceptible to hepatitis E with the subclinical type, but their attack rate of the clinical type was significantly lower than the rate of adults.

Table 8.1 Prevalent rates of major symptoms and signs in cases with acute hepatitis E^*

Symptoms and signs	Occurrence rate	Symptoms and signs	Occurrence rate
Loss of appetite	70.4	Spleen enlargement	23.5
Oil disgust	59.2	Jaundice	76.8
Nausea	88.2	Port colored urine	81.6
Vomiting	44.8	Broken skin itching	28.7
Abdominal distension	60.8	Fever	33.6
Diarrhea	11.2	Chill	14.4
Stomach discomfort	53.6	Cough	5.6
Pain in right upper abdomen	23.2	Pharyngodynia	14.4
Fatigue and weakness	86.4	Nasal congestion	7.2
Pain in liver	49.6	Joint pain	8.8
Liver enlargement	81.6	Rashes	0.8
Pressing pain in liver	96.8
^*Modified from reference 3

Table 8.2 Age distribution of infection frequency of hepatitis E in different groups^*

Age group	Families with the incidence of HE			Families without the incidence of HE			Total
Age group	Tested number	Anti-HEV positive number	%	Tested number	Anti-HEV positive number	%	Tested number	Anti-HEV positive number	%
0˜	9	5	55.6	6	1	16.7	15	6	40.0
5˜	11	8	72.7	15	5	33.3	26	13	50.0
10˜	13	7	53.8	8	3	37.5	21	10	47.6
15˜	54	35	64.8	44	17	38.6	98	52	53.1
50˜	11	5	45.5	11	3	27.3	22	8	36.4
Total	98	60	61.2	84	29	34.3	182	89	48.9
Between all age groups χ²=2.75, P>0.05
Between children younger than 9 years old in families with and without the incidence of HE χ²=5.47, P<0.05
^*Modified from reference 5.

2.4 Infectious phase and isolation phase

Acute cases with typical clinical symptoms were selected and a series of stool specimens before and after the
incidence were collected. Using immunoelectronic microscopy method to examine the virus particles, we investigated the role of virus particle excreted in the stools of patients (Table 8.4 ) [6]. The duration of excretion of virus particles varied from 3 to 12 days among all cases. There were 17 of 60 specimens (28.3%) showing positive results in the excretion of virus particles. The peak of virus discharge was between 1 – 4 days before the onset of the disease and one week after the onset of the disease. Subsequently, positive detection rates decreased along with the disease incidence course, and there were no virus particles discharged two weeks after the onset of the disease. Based on these facts, the infectious phase of this disease was between the end of latency phase and two weeks after the onset of this disease, and the isolation phase was defined from the onset date to 2-3 weeks after the onset of this disease.

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