Search

In 1985, the authors studied the epidemiology of hepatitis B virus (HBV) in a healthy Middle Eastern population. Residents of three remote villages and urban areas of Jordan were assessed for seroprevalence of hepatitis B surface antigen (HBsAg) and HBV infection. Infection was defined as the presence of antibody to hepatitis B core antigen (total) and/or antibody to hepatitis B surface antigen, with or without HBsAg. The overall HBsAg prevalence was 9.9% and was not age-related, although significant differences were noted between the villages (range, 5.7%-12.8%). The prevalence of HBV infection was 36% and increased with age. In addition, there were differences between the villages in patterns of age-specific infection. A newly constructed socioeconomic index showed greater HBsAg prevalence in lower (14.4%) than in upper (2.4%) socioeconomic groups. A history of contact with a jaundiced person and socioeconomic status were independent risk factors for HBsAg-positive status, while contact with a jaundiced person, rural background, and age were independently related to HBV infection. There was evidence of familial clustering of HBV in two of the villages, with HBV carriers and infected children particularly aggregating around HBsAg-positive siblings. There was also a trend toward an association of HBsAg-positive children with HbsAg-positive mothers. HBV carrier prevalence correlated with family size, and HBV infection in the household increased proportionately with the number of carriers in the family. Hepatitis B e antigen was detected most frequently in children and antibody to hepatitis B e antigen in adults. Postnatal early childhood transmission through contact among children of poorer and larger families probably accounts for the high endemicity of HBV in this region.

An outbreak of type B hepatitis followed transfusion with a single lot of plasma protein fraction (PPF) at a 1200-bed hospital in June and July 1973. Of 51 recipients of the product, 31 were available as a study population and 19 (61%) had an illness compatible with hepatitis. Epidemiologic and serologic investigations provided firm evidence that this material was the vehicle for transmission of disease to its recipients. Recipients of four other PPF lots from the same manufacturer were studied. Two of these lots were also associated with extremely high clinical hepatitis attack rates (45% and 55%). The other two lots, which had been prepared from donor plasma contributing to the composition of the initially-studied PPF lot, failed to produced clinical illness, although one of these lots was associated with a high prevalence of hepatitis B seropositivity in recipients. Thus, a broad spectrum of clinical and serologic responses was evident in PPF produced from similar donor plasma and pasteurized in the same bulk container. This study is the first to incriminate heat-treated PPF in transmission of type B hepatitis and suggests the need for further studies of the effect of pasteurization cycles on inactivation of hepatitis B virus.

Sera collected in 1973-1975 from 3053 residents of 12 selected Alaskan Eskimo villages were tested for evidence of hepatitis B virus infection. Overall, hepatitis B surface antigen (HBsAg) was found in 6.4% of those tested. Evidence of hepatitis B infection (positive for HBsAg or antibody to hepatitis B surface antigen (anti-HBs] varied considerably by village, from 4.6% to 69.9%, and increased with advancing age. The proportion with HBsAg was significantly higher in those under the age of 13 years, and the male/female ratio varied from 0.9 to 1.5 to 1.5 in the prepubertal, postpubertal-premenopausal, and postmenopausal age groups, respectively. The prevalence of hepatitis B e antigen (HBeAg) in HBsAg-positive persons decreased with advancing age, and conversely, the prevalence of antibody to hepatitis B e antigen (anti-HBe) increased with age. Hepatitis B infection was found to be sporadically distributed, with great village-to-village variation and further variation by household within most villages. The high HBsAg and HBeAg seropositivity observed in children suggests that children are both more recently infected with hepatitis B and are more involved in hepatitis B transmission in these villages.

In 1982, the Centers for Disease Control, the Food and Drug Administration, and the manufacturer created a surveillance system to monitor spontaneous reports of adverse events occurring after inoculation with the new plasma-derived hepatitis B vaccine (Heptavax-B, Merck Sharp and Dohme, West Point, PA). In the three years between June 1, 1982 and May 31, 1985, an estimated 850,000 persons received the vaccine. During that period, a total of 41 reports were received for one of the following neurologic adverse events: convulsions (five cases), Bell's palsy (10 cases), Guillain-Barre syndrome (nine cases), lumbar radiculopathy (five cases), brachial plexus neuropathy (three cases), optic neuritis (five cases), and transverse myelitis (four cases). Half of these occurred after the first of three required vaccine doses. There were no deaths. Calculation of the relative risks of these illnesses after hepatitis B vaccination was highly dependent on diagnostic classification of the cases, estimates of the size of the vaccinated population, background incidence of the diseases, and the length and distribution of the hypothetical at-risk interval used in the analysis. Other factors important in judging the results of the study could not be measured, including underreporting. In some analyses, Guillain-Barre syndrome was reported significantly more often than expected (p less than 0.05, Poisson probability distribution). However, no conclusive epidemiologic association could be made between any neurologic adverse event and the vaccine. Even if such an association did exist, the preventive benefits of the vaccine in persons at high risk for hepatitis B would unequivocally outweigh the risk of any neurologic adverse event.

In 1981, a hepatitis B vaccine demonstration project was initiated among Yupik Eskimos of southwest Alaska to demonstrate that, under field conditions, the vaccine was safe, immunogenic, and efficacious. Laboratory tests for serologic markers of hepatitis B virus infection (HBsAg, anti-HBs, and anti-HBc) performed on sera collected in May 1981 from 3,988 residents of 17 remote Eskimo villages revealed that 2,645 (66.3%) had no evidence of hepatitis B virus infection. Because of a limited supply of vaccine, specific criteria for selection were used so that those at highest risk of infection would be immunized first. In November 1981, the first dose of vaccine was administered to 1,693 carefully selected individuals. The second dose was administered to 1,678 (99.1%) of those who received the first dose, and the final dose was administered to 1,630 persons (96.3%). Serologic follow-up showed the vaccine to be safe (0.4% experienced minor adverse reactions) and immunogenic (97.4% developed antibody). Vaccine-induced antibody levels were significantly higher for persons less than 30 years of age (p less than 0.001) and for females (p less than 0.001). Vaccine recipients were also protected from hepatitis B virus infection (p = 0.002). This public health measure proved to be feasible and effective in this remote arctic population despite difficult conditions for delivery and administration of this temperature-sensitive vaccine. This strategy for immunization is now being applied on a larger scale in Alaska as part of a program for the primary prevention of this infection and its sequelae.

During the 1973 summer season, 27 employees and 35 overnight guests at the North Rim, Grand Canyon National Park, Arizona, acquired febrile illnesses compatibel with relapsing fever. Sixteen cases were confirmed by finding Borrelia spirochetes in peripheral blood smears or inoculated Swiss mice. Retrospective surveys of 278 employees and 7247 guests at the park revealed that acquisition of illness was significantly associated with the persons sleeping in rustic log cabins and acquiring bites of "unknown" insects. From rodent nesting materials found in the walls and attics of cabins where cases had occurred, infective Ornithodoros hermsi ticks were recovered. Exceptional activity of ticks in human populations appeared to have resulted from a decreased population of the ticks' usual rodent hosts. Vector control activities consisted of spraying the cabins with residual insecticide, removing nesting materials, and "rodent proofing." This outbreak, the largest yet identified in North America, extends the known range of a principal vector and establishes the North Rim as an endemic source of tick-borne relapsing fever.

The occurrence of a common source hepatitis A epidemic among the residents of a New England state mental institution where hepatitis B is hyperendemic provided an opportunity to observe concurrent infections with both agents. Nine HBsAg-positive individuals developed hepatitis A infections documented by hepatitis A antibody seroconversion in eight. The incidence of hepatitis A infections in susceptible HBsAg-positive persons (67%) did not differ from that in HBsAg-negative individuals (63%). The icteric to anicteric infection ratio in the HBsAG-positives (1:1.7) was similar to that in the negatives (1:2.1), and the clinical course in the antigen positives did not differ significantly from that of the antigen negatives. In addition to confirming previous reports that the viruses of hepatitis A and B are immunologically distinct, these results document that infection with either is independent of the other, and that the morbidity from simultaneous infection is no greater than that caused by either alone.

Between June 1, 1983 and August 30, 1984, an epidemic involving 313 cases of hepatitis A occurred in Muskingum County, Ohio. One hundred ninety-seven cases occurred in the city of Zanesville, with 34.7% of cases concentrated in two neighborhoods in the eastern part of the city. Case characteristics were similar to those reported in previous community-wide outbreaks, including a maximum attack rate among 5-9-year-olds and a very low attack rate in adults over 30 years. Case households were larger, and their members were less educated than the mean for households in the city. Forty-eight per cent of the cases reported exposures to other cases which temporally could have been the source of infection. A case-control study failed to show differences in several behavioral factors between case and control households, but did confirm that lower socioeconomic status was a risk factor for the disease. Broad use of immunoglobulin was effective in preventing clinical disease among family contacts, but did not stop the outbreak. This outbreak typifies a genre of hepatitis A epidemic transmitted from person to person in which exact routes of spread are poorly understood and control is difficult. Lower socioeconomic status may be a marker for some unidentified behaviors that promote hepatitis A transmission.

In 1973, epidemiologic and serologic data related to hepatitis B infection were collected from the residents of two remote Alaskan Eskimo villages located in an area of high hepatitis incidence. A total of 418 sera were tested by solid-phase radioimmunoassay for heaptitis B surface antigen (HBsAg) and antibody to that antigen (anti-HBs). The overall infection prevalence of 54.8% in the two villages included a 13.9% prevalence of HBsAg and a 40.9% prevalence of anti-HBs. Families containing an individual with HBsAg had significantly higher infection prevalence than those without an antigen carrier. Larger households had higher proportions of infected members than smaller households. The data suggest that efficient transmission of hepatitis B virus occurs within the household setting in these villages by other than classically established parenteral routes.

To identify occupational categories and work areas of possible risk for acquisition of nosocomial hepatitis B by hospital personnel, serologic sampling for hepatitis B surface antigen (HBSAg) and antibody (anti-HBS) by radioimmunoassay was carried out in 513 employees of a large metropolitan hospital serving predominantly indigent patients. HBSAg was detected in 0.7%, HBSAg and anti-HBS in 0.4%, and anti-HBS in 13.3% of the study population. No significant difference in seropositivity was noted between sexes. Furthermore, neither exposure to patients with hapatitis nor previous blood transfusion correlated with serologic evidence of hepatitis B infection. However, frequency and intensity of exposure to blood products was associated with serologic evidence of infection: 18.9% of those with frequent blood contact were positive for HBSAg or anti-HBS, compared with 11.4% of those without blood product exposure (p less than .05). Direct patient contact, apart from blood exposure, did not appear operative as a major factor in hepatitis B transmission in this population. Accordingly, occupational categories and work areas with highest risk for acquisition of nosocomial hepatitis B were those with greatest blood exposure.

To determine if passively reported cases of acute viral hepatitis are representative of the affected population, an active surveillance system was set up that identified all persons in Pierce County, Washington, who had been diagnosed by a physician as having acute viral hepatitis in the period March 1 through August 31, 1984. In this county, this was part of an ongoing epidemiologic study of viral hepatitis that had previously included some stimulation of reporting. The active surveillance system covered all primary sources of medical care, including all private physicians who were most likely to see persons with hepatitis. Secondary sources, those that did not provide direct medical care but might be aware of new cases, were also surveyed. The results of active surveillance showed that passive reporting was about 65% complete in Pierce County. No change occurred in the number of hepatitis A cases reported, but hepatitis B cases increased by 50%, and non-A, non-B hepatitis cases increased by 138%. Most of the increase was a result of enhanced reporting from private physicians. The two risk groups most affected by underreporting were homosexual men with hepatitis B and blood transfusion recipients with non-A, non-B hepatitis. During active surveillance, the proportion of persons with hepatitis B who reported homosexual activity was 52% compared with 20% from passive surveillance. Transfusion recipients represented 24% of the non-A, non-B hepatitis reported from active surveillance compared with 9% reported from passive surveillance. Although Pierce County may not be representative of all counties in the United States, persons responsible for public health prevention programs should recognize that data acquired through passive surveillance may not accurately reflect the magnitude of the risk for specific populations or the amount of disease that can be prevented.

The cities of Portland, Oregon, and Buffalo, New York, each experienced a restaurant-associated foodborne outbreak of viral hepatitis type A during 1975. Although there were several food handlers ill with viral hepatitis A in each of the restaurants involved, each outbreak was the apparent result of food contamination by a single food handler. In the Buffalo outbreak, food contamination was documented to have occurred for a brief period of time six days prior to onset of any symptoms in the index case. These outbreaks point out the uncommon occurrence of food contamination by individuals ill with type A viral hepatitis, the usefulness of two types of food questionnaires in identifying the vehicle(s) of transmission, and the apparent lack of benefit of widespread immune serum globulin administration as a control measure in this setting.

The occurrence of a common source hepatitis A epidemic among the residents of a New England state mental institution where hepatitis B is hyperendemic provided an opportunity to observe concurrent infections with both agents. Nine HBsAg-positive individuals developed hepatitis A infections documented by hepatitis A antibody seroconversion in eight. The incidence of hepatitis A infections in susceptible HBsAg-positive persons (67%) did not differ from that in HBsAg-negative individuals (63%). The icteric to anicteric infection ratio in the HBsAG-positives (1:1.7) was similar to that in the negatives (1:2.1), and the clinical course in the antigen positives did not differ significantly from that of the antigen negatives. In addition to confirming previous reports that the viruses of hepatitis A and B are immunologically distinct, these results document that infection with either is independent of the other, and that the morbidity from simultaneous infection is no greater than that caused by either alone.

Several independent studies suggest that both hepatitis B immune globulin (HBIG) made from plasma pools containing high titers of anti-HBs and standard immunoglobulin (IG) containing some anti-HBs may be effective for pre- and post-exposure prophylaxis of hepatitis B. Based on a synthesis of current data, it seems reasonable to recommend HBIG for the post-exposure prophylaxis of individuals sustaining accidental needle stick or mucosal exposure to blood known to contain hepatitis B surface antigen (HBsAg). If HBIG is unavailable there is also reason to expect that administration of standard IG which contains some anti-HBs may confer benefit. Although available data regarding prophylaxis of infants born to mothers with HBsAg positive hepatitis at time of delivery are insufficient to warrant firm recommendations on globulin administration, a temporary set of guidelines supporting use of either HBIG or standard IG containing some anti-HBs seems warranted in view of the serious implications for induction of the HBsAg chronic carrier state in infancy. Because appropriate environmental control measures may significantly reduce the transmission of hepatitis B in certain endemic settings such as hemodialysis units or homes for the mentally retarded, IG prophylaxis in these surroundings cannot be routinely recommended. Since current data show no evidence for superiority of HBIG over standard IG in these settings, and because there is some evidence that use of lower anti-HBs titer globulins may provide for acquisition of passive-active immunity, it seems reasonable to suggest that if IG is to be used for pre-exposure prophylaxis, the material to be used should be standard IG containing some anti-HBs.

In 1981, a hepatitis B vaccine demonstration project was initiated among Yupik Eskimos of southwest Alaska to demonstrate that, under field conditions, the vaccine was safe, immunogenic, and efficacious. Laboratory tests for serologic markers of hepatitis B virus infection (HBsAg, anti-HBs, and anti-HBc) performed on sera collected in May 1981 from 3,988 residents of 17 remote Eskimo villages revealed that 2,645 (66.3%) had no evidence of hepatitis B virus infection. Because of a limited supply of vaccine, specific criteria for selection were used so that those at highest risk of infection would be immunized first. In November 1981, the first dose of vaccine was administered to 1,693 carefully selected individuals. The second dose was administered to 1,678 (99.1%) of those who received the first dose, and the final dose was administered to 1,630 persons (96.3%). Serologic follow-up showed the vaccine to be safe (0.4% experienced minor adverse reactions) and immunogenic (97.4% developed antibody). Vaccine-induced antibody levels were significantly higher for persons less than 30 years of age (p less than 0.001) and for females (p less than 0.001). Vaccine recipients were also protected from hepatitis B virus infection (p = 0.002). This public health measure proved to be feasible and effective in this remote arctic population despite difficult conditions for delivery and administration of this temperature-sensitive vaccine. This strategy for immunization is now being applied on a larger scale in Alaska as part of a program for the primary prevention of this infection and its sequelae.