Preface

 This report summarizes information from state health departments, university investigators,

virology laboratories, and other pertinent sources, domestic and foreign, about acute viral hepatitis.

Much of the information is preliminary. It is intended primarily for persons responsible for disease

control. Contributions to the Hepatitis Surveillance Report are most welcome; send them to:

Chief, Viral Hepatitis Surveillance

Hepatitis Branch

Division of Viral and Rickettsial Diseases

National Center for Infectious Diseases

Centers for Disease Control and Prevention

Atlanta, GA 30333

Suggested Citation

Hepatitis Surveillance Report No. 56.

Atlanta: Centers for Disease Control and Prevention, 1995. 36 p.

Centers for Disease Control and Prevention David Satcher, M.D., Ph.D., Director

National Center for Infectious Diseases James M. Hughes, M.D., Director

Division of Viral and Rickettsial Diseases Brian W. J. Mahy, Ph.D., Sc.D., Director

Hepatitis Branch and World Health

 Organization Collaborating Center for

 Reference and Research on Viral Hepatitis Harold S. Margolis, M.D., Chief

Epidemiology Section Miriam J. Alter, Ph.D., Chief

 Surveillance Activity Patrick J. Coleman, Ph.D., Chief

Publications & Graphics Activity John O’Connor, Technical Editor

Anne Mather, Editor

 Patricia A. Tyson, Computer Specialist

DVRD Biometrics Activity Karoyle L. Colbert, Graphics Specialist

Epidemiology Program Office Steven B. Thacker, M.D., M.Sc.,Director

Division of Surveillance and Epidemiology Donna Stroup, Ph.D., Director

Statistics & Surveillance Branch G. David Williamson, Ph.D., Chief

Systems Operations and Information Branch Kathy Rufo, Chief

 Acknowledgments: Special contributions to this report were made by Frank Mahoney, M.D.,

Miriam Alter, Ph.D., and Elisabeth Loos. Special thanks to Mr. Carlisle Quantrell for programming

and computer support.
HEPATITIS

Surveillance

Contents

Page

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1

Issues and Answers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3

What is the risk of acquiring hepatitis C for health-care workers and what are

the recommendations for prophylaxis and follow-up after occupational exposure

to hepatitis C virus? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3

Is the recent increase in the reported cases of hepatitis C/non-A, non-B hepatitis

a real increase? . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6

New Horizons . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9

Evaluating the effectiveness of the programs to prevent hepatitis B virus transmission 

in the United States . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9

Trends Based on Reporting to National Morbidity Reporting System, 1993 . . . . . . . . . . . . 15

Hepatitis A . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16

Hepatitis B . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18

Non-A, Non-B Hepatitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20

Viral Hepatitis Surveillance Program, 1993 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21

Case Definition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22

Use of Serologic Tests for Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23

Demographic Characteristics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23

Epidemiologic Characteristics . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24

Discussion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31

Appendix

Hepatitis Surveillance iii

Introduction

Viral hepatitis in the United States has been a major

public health problem for many years, with estimated

medical treatment costs in the hundreds of millions of

dollars annually. The long-term consequences of many

of these viral infections are only now becoming apparent to many infected patients and their families. Infections caused by the hepatitis C virus (HCV), in

particular, effectively resist the body’s attempts to develop immunity, leading to persistent infection and

chronic liver disease in a large percentage of those

infected.

Thus, the declines in the incidence of hepatitis types

A, B, and C reported in recent years are encouraging.

This report summarizes surveillance data collected during 1993 for acute viral hepatitis. Reported cases of viral hepatitis in 1993 continued their overall downward

trends with one exception. Hepatitis A increased by 5%

from 1992 to 1993, and preliminary data for 1994-95

suggest that this increase will continue into 1996.

The objective of national surveillance of viral hepatitis is to provide serologic, demographic, and

epidemiologic information that will aid in formulating

strategies and policies for the prevention and control of

these diseases. The hepatitis surveillance report interprets and disseminates this information, presents new

developments in the field, and clarifies issues related to

viral hepatitis. Nationwide information on hepatitis is

obtained by two surveillance systems. In one, incidence data are collected from cases reported to the Centers for Disease Control and Prevention (CDC)

National Notifiable Diseases Surveillance System

(NNDSS) by each state and territory. The etiologic classification is made by physician diagnosis; confirmation

by serologic testing is not required. The number of

cases and date reported of each type of hepatitis appear in the Morbidity and Mortality Weekly Report

(MMWR) and the MMWR Annual Summary of Notifiable Diseases, and are summarized in this report as

well.

In the other system, clinical, serologic and

epidemiologic data pertaining to risk factors of disease

acquisition are obtained from the Viral Hepatitis Surveillance Program (VHSP), a separate reporting system

operated by the Hepatitis Branch, Division of Viral and

Rickettsial Diseases, National Center for Infectious Diseases, CDC, Atlanta, Georgia. The VHSP obtains its information from the viral hepatitis case record, a copy

of which appears in the appendix. The case record was

revised in 1989. By 1993, 95% of cases were reported

with the revised form. This form (CDC 53.1) can be obtained from the Hepatitis Branch. In addition, in 1991

several states began submitting their case reports via

electronic surveillance through the National Electronic

Telecommunications System for Surveillance (NETSS).

For states interested in using NETSS to report hepatitis

cases, the Hepatitis Branch and CDC’s Epidemiology

Program Office will provide technical support.

A third surveillance system referenced in this report

is the Sentinel Counties Study of Acute Viral Hepatitis,

a more intensive study of viral hepatitis in six counties

representative of the United States as a whole. This surveillance system has provided nationally representative data on acute viral hepatitis since 1982, and

has been a resource for detecting emerging infections

and performing more in-depth studies.

Surveillance data such as those reported here are dependent on the cooperation of state and local health departments, public health practitioners, and medical

care persons, reporting the diseases from their hospitals, clinics, and offices. In recent years there has been a

decline in both the frequency of states reporting, and

the number of viral hepatitis cases reported to CDC

through the VHSP. Since 1989, the number of states reporting to the VHSP most (75%-100%) of the cases they

reported to NNDSS declined from 28 to 21, and an increasing number of states have stopped reporting altogether (see table on p. 22). In addition, the number of

reports received by VHSP of those reported to the

NNDSS has declined from 50% to 36%. The percentage

of NNDSS cases reported to the VHSP has dropped

particularly for hepatitis B and non-A,non-B (NANB)

hepatitis. For symptomatic serologically confirmed

hepatitis B, the VHSP received reports on only 26% of

the hepatitis B cases reported to NNDSS, and for symptomatic, serologically confirmed NANB hepatitis, the

VHSP received reports on only 18% of the cases reported to NNDSS.

CDC’s ability to accurately analyze and interpret nationwide trends and patterns, identify high-risk

groups, and determine mechanisms of transmission for

each type of hepatitis depends on the cooperation of

the state and local health departments in reporting

laboratory and epidemiologic data to the VHSP. Key to

these tasks is the accurate determination of the specific

agent causing the viral hepatitis. Six distinct agents are

responsible for viral hepatitis worldwide; four have

been identified as endemic in the United States: hepatitis types A, B, C, and D. In 1993, hepatitis A accounted

for 56% of reported cases; hepatitis B, 31%, hepatitis

C/NANB, 11%; and hepatitis unspecified, 1%. Delta

hepatitis is not a reportable disease in the United

States, and occurs as a coinfection or superinfection

with hepatitis B.

The etiology of viral hepatitis cannot be determined

by clinical or epidemiologic characteristics alone. The

wide availability of diagnostic tests to characterize

Hepatitis Surveillance 1
hepatitis A, hepatitis B, and hepatitis C makes the reporting of etiologic classification based on clinical and

epidemiologic characteristics obsolete and hinders the

clinical and public health management of patients with

these diseases. However, there are several limitations

of the serologic assay for HCV infection; some cases

caused by HCV may not develop antibody to HCV

(anti-HCV). Also, because patients with acute hepatitis

C may take 6 to 9 months to become anti-HCV positive, and because the anti-HCV assay does not distinguish between acute and chronic infection, diagnosis of

hepatitis C and NANB hepatitis both require serologic

exclusion of acute hepatitis A and hepatitis B. Reporting of NANB hepatitis should not be dependent on testing for anti-HCV. 

Disease under reporting and inaccurate diagnosis

impede the public health community’s ability to develop guidelines for preventing and controlling hepatitis and to assess the impact of these prevention

strategies. We thank those who have been actively contributing to our program and encourage others to

participate.

2 Introduction
Issues and Answers

What is the risk of acquiring hepatitis C for health care workers and

what are the recommendations for prophylaxis and

follow-up after occupational exposure to hepatitis C virus?

Hepatitis C virus (HCV) is most efficiently transmitted by large or repeated percutaneous exposures to

blood, such as through the transfusion of blood or

blood products from infectious donors and sharing of

contaminated needles among injection drug users.

Other blood-borne viruses, such as the hepatitis B virus

(HBV), are transmitted not only by overt percutaneous

exposures, but by mucous membrane and inapparent

parenteral exposures. Although these types of exposures are prevalent among health-care workers, the

risk factors for HCV transmission in this occupational

setting are not well-defined. 

Occupational Transmission

A case-control study of patients with acute non-A,

non-B hepatitis, conducted prior to the discovery of

HCV, found a significant association between acquiring disease and health-care employment, specifically

patient care or laboratory work (1). Seroprevalence

studies have reported antibody to HCV (anti-HCV)

rates of 1% among hospital-based health-care workers

in western countries (2). In the one study that assessed

risk factors for infection, a history of accidental needle

sticks was independently associated with anti-HCV positivity (3). Case reports have documented the transmission of HCV infection from anti-HCV positive patients

to health-care workers as a result of accidental needle

sticks or cuts with sharp instruments (2), and one reported the transmission of HCV from a blood splash to

the conjunctiva (4). In follow-up studies of health-care

workers who sustained percutaneous exposures to

blood from anti-HCV positive patients, the incidence

of anti-HCV seroconversion (based on second-generation testing) averaged 3.5% (range, 0%-7%) (5-9); in the

one study that used polymerase chain reaction (PCR)

to measure HCV infection by detecting HCV RNA, the

incidence was 10% (5). 

Nosocomial Transmission

Nosocomial transmission of HCV is also possible if

breaks in technique occur or disinfection procedures

are inadequate and contaminated equipment is shared

between patients. Hospitalized patients may serve as a

reservoir for transmission; the prevalence of anti-HCV

among such patients has been reported to range from

2% to 18% (10-12). Case control studies have not found

an association between standard medical care procedures and transmission of HCV in the United States

(1,13). However, in one report from Greece, 6 patients

with acute non-A, non-B hepatitis (5 of whom were

anti-HCV positive) all had onset of their disease within

a 9 day period, and all had been hospitalized 2 to 3

months previously at the same hospital; none had received transfusions or undergone surgery (14). In Australia, four patients who underwent outpatient surgery

on the same day became infected with HCV of the

same genotype as a chronically infected patient who

underwent surgery just prior to the cases (15). The factors responsible for transmission could not be identified, and none of the surgical personnel were anti-HCV

positive. In a report from Spain, however, five open

heart surgery patients with documented acute HCV infection appeared to have acquired their infection from

a cardiovascular surgeon with chronic hepatitis C (16).

By sequence analysis, a high degree of homology was

demonstrated between the virus of the surgeon and

those of the patients. The factors responsible for transmission were not identified.

Postexposure Prophylaxis

Unfortunately, postexposure prophylaxis with immune globulin does not appear to be effective in preventing hepatitis C. Historically, several studies have

attempted to assess the value of prophylaxis with immune globulin for the prevention of posttransfusion

NANB hepatitis, but the results are difficult to compare and interpret because of lack of uniformity in diagnostic criteria, mixed sources of donors (volunteer

and commercial), and different study designs (some

lack blinding and placebo controls). In some of these

studies, immune globulins seemed to reduce the rate of

clinical disease although not overall infection rates; in

one, patients receiving immune globulin were less

likely to develop chronic hepatitis. None of these data

have been reanalyzed since anti-HCV testing became

available, and in only one study was the first dose of

immune globulin given after, rather than before, the exposure, making it difficult to assess its value for postexposure prophylaxis. 

At least 85% of persons with HCV infection become

chronically infected, and chronic liver disease with persistently elevated liver enzymes develops in an average

of 67% (2). These extraordinarily high rates of chronic

Hepatitis Surveillance 3
disease and persistent viremia in humans, as well as

animal transmission experiments demonstrating the

failure of antibody elicited by infection with one genotype to cross-neutralize either heterologous genotypes

or closely related but heterogeneous species within the

same genotype, indicate the absence of an effective neutralizing immune response (17,18). Furthermore, immune globulin is now manufactured from plasma that

has been screened for anti-HCV. A recently conducted

experimental study in chimpanzees found that immune globulin manufactured from screened plasma administered 1 hour after exposure to HCV did not

prevent infection or disease (19). In February 1994, the

Immunization Practices Advisory Committee reviewed

the available data and concluded that there was no support for the use of immune globulin for postexposure

prophylaxis of hepatitis C (CDC, unpublished data).

There is no information regarding the use of anti-viral

agents, such as alpha interferon, in the postexposure

setting, and such treatment is not recommended.

Issues Regarding Follow-Up After Exposure

In the absence of postexposure prophylaxis, multiple issues need to be considered in deciding if there

should be a defined protocol for the follow-up of

health-care workers for HCV infection after occupational exposures. These areas include the limited data

on the risk of transmission, the limitations of available

serologic testing for detecting infection and determining infectivity, the poorly defined risk of transmission

by sexual, household, and perinatal exposures, the limited benefit of therapy for chronic disease, the cost of

follow-up, and the medical-legal implications. 

Although it seems clear that needle-stick exposure

to infectious blood is a risk factor for hepatitis C, and

that this risk appears to be intermediate between that

of HBV and human immunodeficiency virus, the data

are limited or nonexistent on the risk of transmission

associated with other types of occupational exposure.

This makes it difficult to provide health-care workers

who sustain such exposures with a meaningful estimate of their chances of developing HCV infection.

Testing methods readily available in the clinical setting

also have limitations. With the commercially manufactured enzyme immunoassays (EIAs) that detect antiHCV, there may be a prolonged interval between

exposure and seroconversion, although the average

time period is 8-10 weeks. In many populations, including health-care workers, the rate of false positivity for

anti-HCV is high, and supplemental assays should always be used to judge the validity of repeatedly reactive EIA results. About 5% to 10% of infections will not

be detected unless PCR is used to detect HCV RNA. Although such assays for HCV RNA are available from

several commercial laboratories on a research-use basis, they are not standardized and the cost is high,

about $200 per test. Both false-positive and false-negative results can occur from improper handling and storage or contamination of the test samples. In addition,

the detection of HCV RNA may be intermittent, and

the meaning of a single negative PCR test result is not

conclusive.

All anti-HCV-positive persons should be considered

potentially infectious, however, neither the presence of

antibody nor the presence of HCV RNA is a direct

measure of infectivity in settings where inapparent parenteral or mucosal exposures occur. Epidemiologic

studies have implicated exposure to infected sexual

and household contacts as well as to multiple sexual

partners in the transmission of HCV (1,13). Serologic

studies of the long-term sexual and household contacts

of patients with chronic hepatitis C have found evidence of HCV infection in an average of 5% of sexual

partners and in an average of 3% of children (2). Studies of infants born to anti-HCV-positive mothers have

reported rates of perinatal transmission ranging from

0% to 13% (average 6%); in two small studies, only

mothers with “high” titers of HCV RNA transmitted

HCV to their infants (20,21). The inconsistent results of

these as well as studies that looked for HCV RNA in

body fluids other than serum and plasma may reflect

different concentrations of virus in the infected persons

sampled. The risk that an HCV-infected individual will

transmit the virus may be related to the type and size

of the inoculum and the route of transmission, as well

as the titer of virus, but data on the threshold concentration of virus needed to transmit infection are insufficient. In the absence of such data and standardized

tests to measure infectivity, it is difficult to counsel antiHCV-positive persons about their risk of transmission

to others (22). Because the risk of HCV transmission between long-term steady sexual partners appears to be

low, there are no recommendations for changes in sexual practices for persons with a steady sexual partner,

although infected persons should be informed of the

possible risk so they can decide if they wish to take precautions. Household articles such as toothbrushes and

razors should not be shared. There are no data to support discouraging either pregnancy or subsequent

breast feeding (see reference 22 for further details on

counseling)

The most obvious benefit from a follow-up protocol

would appear to be the opportunity for the health-care

worker to seek evaluation for chronic liver disease and

treatment, if eligible. Studies have shown that alpha interferon therapy may have a beneficial effect among

some patients (23). In these studies, however, the patients were highly selected and therapy resulted in sustained improvement in 20% or fewer of those treated;

no clinical, demographic, serum biochemical, serologic

or histologic features have been identified that reliably

predict which patients will respond to treatment and

sustain a long-term remission. The nationwide cost of

providing postexposure follow-up testing is estimated

at $2 to $4 million; the cost for each person who

4 Issues and Answers
benefits from therapy is estimated at $200,000 (CDC,

unpublished data). 

Even in the absence of both available postexposure

prophylaxis and limited specific measures for disease

prevention, individual institutions should consider implementing policies and procedures for follow-up after

percutaneous or per mucosal exposure to anti-HCV

positive blood to address individual workers’ concerns

about their risk and outcome. Above all, institutions

should ensure education of health-care providers regarding the risk and prevention of blood borne infections in the occupational setting (24), including

hepatitis C, and such information should be routinely

updated to ensure accuracy.

Summary Recommendations

 1. No postexposure prophylaxis is available for

hepatitis C; immune globulin is not recommended.

 2. Institutions should provide to health-care workers

accurate and up-to-date information on the risk

and prevention of all blood borne pathogens,

including hepatitis C.

 3. Institutions should consider implementing policies

and procedures for follow-up of health-care

workers after percutaneous or per mucosal

exposure to anti-HCV positive blood. Such

policies might include baseline testing of the

source for anti-HCV and baseline and 6 month

follow-up testing of the person exposed for

anti-HCV and ALT activity. All anti-HCV results

reported as repeatedly reactive by EIA should be

confirmed by supplemental anti-HCV testing.

 4. There are currently no recommendations

regarding restriction of health-care workers with

hepatitis C. The risk of transmission from an

infected worker to a patient appears to be very

low. Furthermore, there are no serologic assays

that can determine infectivity nor are there data to

determine the threshold concentration of virus

required for transmission. As recommended for all

health-care workers, those who are anti-HCV

positive should follow strict aseptic technique and

standard (universal) precautions, including

appropriate use of hand washing, protective

barriers, and care in the use and disposal of

needles and other sharp instruments.

Selected References

 1. Alter MJ, Gerety RJ, Smallwood L, et al. Sporadic

non-A, non-B hepatitis: frequency and

epidemiology in an urban United States

population. J Infect Dis 1982;145:886-893.

 2. Alter MJ. Epidemiology of hepatitis C in the West.

Semin Liver Dis 1995;15:5-14.

 3. Polish LB, Tong MJ, Co RL, et al. Risk factors for

hepatitis C virus infection among health care

personnel in a community hospital. Am J Infect

Control 1993;21:196-200.

 4. Sartori M, La Terra G, Aglietta M, et al.

Transmission of hepatitis C via blood splash into

conjunctiva. Scand J Infect Dis 1993;25:270-271.

 5. Mitsui T, Iwano K, Masuko K, et al. Hepatitis C

virus infection in medical personnel after

needlestick accident. Hepatology

1992;16:1109-1114.

 6. Hernandez ME, Bruguera M, Puyuelo T, Barrera

JM, Sanchez Tapias JM, Rodes J. Risk of

needle-stick injuries in the transmission of

hepatitis C virus in hospital personnel. J Hepatol

1992;16:56-58.

 7. Zuckerman J, Clewley G, Griffiths P, Cockcroft A.

Prevalence of hepatitis C antibodies in clinical

health-care workers. Lancet 1994;343:1618-1620.

 8. Petrosilla N, Puro V, Ippolito G, and Italian Study

Group on Blood-borne Occupational Risk in

Dialysis. Prevalence of hepatitis C antibodies in

health-care workers. Lancet 1994;344:339-340.

 9. Lanphear BP, Linnemann CC, Cannon CG, et al.

Hepatitis C virus infection in health care workers:

risk of exposure and infection. Infect Control Hosp

Epidemiol 1994;15:745-750.

10. Louie M, Low DE, Feinman SV, et al. Prevalence of

bloodborne infective agents among people

admitted to a Canadian hospital. Can Med Assoc J

1992;146:1331-1334.

11. Kelen GD, Green GB, Purcell RH, et al. Hepatitis B

and hepatitis C in emergency department patients.

N Engl J Med 1992;326:1399-1404.

12. Bile K, Aden C, Norder H, et al. Important role of

hepatitis C virus infection as a cause of chronic

liver disease in Somalia. Scand J Infect Dis

1993;25:559-564.

13. Alter MJ, Coleman PJ, Alexander WJ, et al.

Importance of heterosexual activity in the

transmission of hepatitis B and non-A, non-B

hepatitis. JAMA 1989;262:1201-1205.

14. Tassopoulos NC, Hatzakis A, Vassilopoulou-Kada

H, et al. Hepatitis C virus is associated with

hospital epidemic of acute non-a, non-B hepatitis

[abstract]. Program and Abstracts of the 1990

International Symposium on Viral Hepatitis and

Liver Disease, Houston, 1990, p.155.

15. NSW Health Department. Investigation of

possible patient-to-patient transmission of

hepatitis C in a hospital. NSW Public Health

Bulletin 1994;5:47-51.

16. Esteban JI, Gomez J, Martell M, et al. Repeated

transmission of HCV from surgeon to patients

during cardiac surgery [abstract]. Hepatology

1995;22:347A.

Hepatitis Surveillance 5
17. Bukh J, Miller RH, Purcell RH. Genetic

heterogeneity of hepatitis C virus: quasispecies

and genotypes. Sem Liv Dis 1995;15:41-63.

18. Farci P, Alter HJ, Wong DC, et al. Prevention of

hepatitis C virus infection in chimpanzees after

antibody-mediated in vitro neutralization. Proc

Natl Acad Sci 1994;91:7792-7796.

19. Krawczynski K, Alter MJ, Tankersley DL, et al.

Effect of immune globulin on the prevention of

experimental hepatitis C virus infection. J Infect

Dis 1996, in press.

20. Ohto H, Terazawa S, Sasaki N, et al. Transmission

of hepatitis C virus from mothers to infants. N

Engl J Med 1994;330:744-750.

21. Lin HH, Kao JH, Hsu HY, et al. Possible role of

high-titer maternal viremia in perinatal

transmission of hepatitis C virus. J Infect Dis

1994;169:638-641.

22. Centers for Disease Control. Public Health Service

inter-agency guidelines for screening donors of

blood, plasma, organs, tissues, and semen for

evidence of hepatitis B and hepatitis C. MMWR

1991:40(RR-4):13-14.

23. Fried MW, Hoofnagle, JH. Therapy of hepatitis C.

Semin Liver Dis 1995;15:82-91.

24. Centers for Disease Control. Update: universal

precautions for prevention of transmission of

human immunodeficiency virus, hepatitis B virus,

and other bloodborne pathogens in health-care

settings. MMWR 1988;37:377-382,387-388.

Is the recent increase in the reported cases of hepatitis C / NANB a real increase?

Introduction

The numbers of hepatitis C and non-A, non-B

(NANB) hepatitis cases reported in the United States

have fluctuated dramatically in the last 5 years, particularly since tests for antibody to hepatitis C virus (antiHCV) were introduced in 1990. In addition, the

reported incidence of this disease has varied considerably between different surveillance systems (Table 1).

The incidence of hepatitis C reported to the National

Electronic Telecommunications System for Surveillance

(NETSS) declined moderately from 1985 to 1990, but

then increased by almost 130% from 1990 to 1992. The

incidence rate in 1994 was still 73% higher than its 1990

level. In contrast, the incidence of hepatitis C in the Sentinel Counties Study of Acute Viral Hepatitis (1), which

was initially 4-fold higher than the NETSS reported incidence, declined by 80% from 1989 through 1989. A

similar decline was also observed in cases reported to

the Viral Hepatitis Surveillance Program (VHSP). Possible reasons for these discrepancies include the widespread use of new diagnostic tests in laboratory-based

reporting. The increase in cases reported to NETSS

may have been the result of laboratory reports of

chronically infected patients, or anti-HCV positive patients identified through screening programs. To better

determine the reasons for these changes in nationwide

reporting, during July-August of 1995 the Hepatitis

Branch conducted a survey of a sample of county

health departments to determine their practices and

policies with regard to the reporting of hepatitis C and

NANB hepatitis cases.

Methods

Counties were selected as a stratified random sample of those counties that had reported at least one case

of hepatitis C/NANB in 1993. The selection list consisted of 790 such counties, and a 20% sample of 161

counties was selected. Stratification of the sample by

population size ensured that large counties would

have a high probability of selection. 

Each county health department was asked to complete a questionnaire that covered seven categories: reporting sources of data, case definitions, laboratory

reporting, follow-up for incomplete case reports, resources for surveillance, uses to which data were put,

and information on respondents. 

Results

The data presented here are based on a preliminary

analysis of the first 90 questionnaires that were returned. This represented an early response rate of 56%.

In a preliminary analysis comparing county health deYear NETSS*

Sentinel

Counties†

1985 1.81 8.29

1986 1.55 8.65

1987 1.23 6.83

1988 1.07 7.64

1989 1.02 9.06

1990 1.03 5.51

1991 1.42 3.41

1992 2.36 2.35

1993 1.86 1.83

1994 1.78 1.70

* National Electronic Telecommunications Systems for

* Surveillance

†

 Sentinel Counties Study of Acute Viral Hepatitis

Table 1. Reported Cases of Hepatitis C/non-A, non-B

Hepatitis per 100,000 Population in Two Surveillance

Systems, 1985-94

6 Issues and Answers
partments that had or had not responded, no

differences were found in population size or geographic location. Respondents included public health

nurses and epidemiologists. About half of the respondents had worked at the health department for more

than 10 years.

Respondents cited hospitals (34%) as the most common source of case reports prior to 1991; laboratories

were next (20%). From 1991 to the present, they cited

laboratories as the most common source of case reports

(53%); hospitals were second (30%). Physicians were

cited as the third most common reporting source in

each period. Blood banks and other sources were cited

with similar rankings in each period.

Nearly half of the health departments surveyed did

not apply published case definition criteria when reporting acute hepatitis C/NANB cases. Fifty-six percent of respondents said that a case would be reported

as hepatitis C/NANB on the basis of a physician’s diagnosis alone. Forty-nine percent said that they accepted

cases on the basis of laboratory reports alone. Discrete

dates of onset of symptoms were required by only 36%

of respondents, and exclusion of hepatitis A and B was

required by 40% of respondents. 

A large percentage of respondents said they followed up on incomplete case reports; however, 39% of

these respondents also stated that they would accept

and report a case on the basis of a laboratory report

alone. When asked how they obtained the information

required to provide an accurate diagnosis, 96% of respondents said they contacted the physician who made

the report. Sixty-eight percent did follow-up that included contacting the patient. Only 39% determined if

supplemental testing was done on specimens that were

reported positive for anti-HCV.

Among the 23% of respondents who did not do follow-up on incomplete case reports, 52% said other public health problems took priority, while 50% cited lack

of personnel. Thirty-six percent cited the lack of any effective intervention for hepatitis C/NANB patients as a

reason.

Eighty-five percent of respondents reported increases in the number of cases reported during the past

5 years, mostly owing to laboratory reporting of antiHCV positivity without evidence of acute disease.

Only 12% cited a true increase in the disease incidence

in their county or jurisdiction.

When asked to cite actions taken by the county

health department in response to reported cases of

hepatitis C/NANB, 77% of respondents said they provided counseling to patients. Thirty percent said they

published newsletters containing data on hepatitis

C/NANB.

We asked respondents to suggest ways that CDC

could improve reporting of hepatitis C/NANB. Most

pronounced was an expression of confusion regarding

what should be done with case reports of persons with

chronic hepatitis C/NANB. Many respondents felt that

CDC should publish a clearer, updated case definition.

Many also wanted guidelines from CDC for follow-up

of incomplete case reports. Respondents suggested that

CDC create educational programs targeting health-care

workers in an effort to increase the reporting of diseases to the county health departments.

Summary. Since testing for anti-HCV became

widely available, county health departments have increasingly relied on laboratories as sources of case reports for hepatitis C/NANB. This has resulted in an

artifactual increase in the reported incidence of hepatitis C because of the reporting of anti-HCV- positive

persons with no clinical or epidemiologic evidence of

acute disease. Physician-reported cases continue to be

a small proportion of all reported hepatitis C/NANB

cases. In addition, many county health departments

confirmed that they pass these laboratory test positive

results on to the state health departments without sufficient confirmation of acute disease. Primarily because

of lack of personnel and other diseases being seen as

higher priority, county health departments do not attempt to obtain additional information necessary to

confirm acute disease. 

Further analysis of the survey results is being conducted. Issues to be examined include the purpose of

surveillance of viral hepatitis; the importance of focusing on acute, symptomatic disease to determine true incidence; and the need for separate surveillance systems

to monitor patients with chronic infections and chronic

liver disease. Such surveillance efforts in the future will

depend on strict adherence to case definitions, and on

adequate resources to support them. The case

definition is shown on page 22 of this report.

References

1. Alter MJ, Mast, EE. The epidemiology of viral

hepatitis in the United States. Gastroenterology

Clinics of North America 1994;23:437-455. 

Hepatitis Surveillance 7

New Horizons

Evaluating the effectiveness of the programs to prevent

hepatitis B virus (HBV) transmission in the United States.

The Hepatitis Branch, in collaboration with the National Immunization Program, has drafted disease reduction goals for the prevention of hepatitis B virus

(HBV) transmission in the United States (Table 1).

These goals were developed with comments from statebased immunization staff and the Council of State and

Territorial Epidemiologists. Unlike other vaccine-preventable disease reduction targets, the targets for hepatitis B are not based on acute disease surveillance

reported through the National Notifiable Diseases Surveillance System (NNDSS). Because most HBV infections in children <10 years of age are asymptomatic,

evaluation based on NNDSS data will not reliably

measure the effectiveness of hepatitis B vaccination

programs, especially those directed at infants. Assessment of programs that target infants should primarily

be evaluated by vaccination coverage surveys. The utility of various data sources, including coverage surveys,

population-based serologic surveys, and surveillance

for acute disease for evaluating all of the components

of hepatitis B prevention programs, will vary depending on the age-group targeted by the program (Table

2). As the data obtained by evaluation tools improves,

additional disease reduction targets can be proposed,

Perinatal Program

1. Goals for the reduction of perinatal HBV

infections in the United States.

By 2000, reduce the estimated number of perinatal infections by 80%, from 9,500 to 1,900. 

Objectives for HBsAg screening of pregnant

women

By 1998 ensure that:

every state has a law requiring HBsAg screening of all pregnant women. 

every state has developed a method to evaluate

HBsAg screening of pregnant women.

By 2000 ensure that:

90% of pregnant women are screened for

HBsAg prior to delivery.

Objectives for the identification and tracking of

infants born to HBsAg positive women.

By 2000, ensure that 

90% of the estimated 20,000 births to HBsAgpositive pregnant women are identified each

year in the U.S.

90% of infants born to HBsAg-positive women

receive the first dose of hepatitis B vaccine and

hepatitis B immune globulin (HBIG) at birth.

90% of infants born to HBsAg-positive mothers receive the remaining 2 doses of hepatitis

B vaccine by 6-8 months of age. 

2. Goals for the prevention of HBV transmission

in households of HBsAg-positive pregnant

women.

by 1998, every state should establish a program to vaccinate household contacts of

HBsAg-positive pregnant women.

by 2000, >70% of household contacts are offered hepatitis B vaccine each year.

Infant Vaccination Program

1. Goals for hepatitis B vaccination of infants

By the year 1998, ensure that 90% or more of

2 year-old children have received hepatitis B

vaccine. 

Interim objectives for hepatitis B vaccination

coverage of 2 year-old children 

By 1998, ensure that all states have developed activities to ensure that children in ethnically defined populations where HBV

infection is of high or intermediate endemicity (i.e., Alaskan Natives, Asian/Pacific Islanders, infants born to first

generation immigrant/refugee women from

countries with a high/intermediate endemicity of HBV infection) are completely

vaccinated in the first 12 months of life.

Table 1. Disease Reduction Goals for Hepatitis B Vaccination Programs 

Hepatitis Surveillance 9
especially one for adolescent vaccination programs.

The following narrative provides perspective on the

relative importance of different data sources in evaluating each hepatitis B vaccination activity. 

Program to prevent perinatal HBV infection

In 1990, federal funding became available to support programs to prevent perinatal HBV transmission

in the United States. Considerable efforts have been

made on program implementation; however, measuring the effectiveness of perinatal program activities has

been challenging. 

Coverage surveys: To assess the effectiveness of current activities, disease reduction goals have been established to evaluate key programmatic elements

including; hepatitis B surface antigen (HBsAg) screening of pregnant women, immunoprophylaxis (hepatitis

B immune globulin (HBIG) and vaccine) at birth, and

completion of the vaccine series by 6-8 months of age

(Table 1). These goals have been established to ensure

that> 80% of perinatal HBV infections are prevented. 

In March 1995, the Hepatitis Branch, CDC, conducted a survey of hepatitis B program coordinators to

measure progress in reaching these goals. The results

of this survey revealed that 12 states had laws or regulations requiring HBsAg screening of pregnant women.

Overall, 52 program coordinators provided data on the

prevalence of HBsAg screening. For women who received services in the public sector, most projects (60%)

reported that >90% of pregnant women were screened;

however, 20% of the program managers did not know

what percentage of pregnant women were screened

(Table 3). For women who received services in the private sector, 28% of projects reported that >90% of pregnant women were screened and >50% of the projects

did not know what percentage of pregnant women

were screened. 

The birth of infants to HBsAg-positive women is the

critical surveillance event in the perinatal program and

reporting of these births is the major indicator of program effectiveness. To evaluate reporting, the Hepatitis

Branch has provided projects with estimates on the

number of births to HBsAg-positive women that occur

each year in the United States (Table 3). These figures

are based on natality data and the estimated prevalence of chronic HBV infection among pregnant

women by race and ethnicity. Specifically, the estimates are derived by using the following race/ethnicity- specific rates of HBsAg positivity: whites = 0.13%;

blacks = 0.5%; Hispanics = 0.12%; Asian, U.S.-born =

1.6%; Asian, foreign-born = 8.9%; other = 0.5%. Based

on natality data, an estimated 20,000 infants are born to

HBsAg-positive women each year in the United States. 

The prevalence figures used to calculate the number

of births to HBsAg-positive women are derived from

the National Health and Nutrition Examination Survey

(NHANES III). NHANES III is a population-based seroprevalence survey which includes approximately

21,000 people nationwide. NHANES III has a limited

capacity to provide estimates on the number of HBsAgpositive births in each state. There are several reasons

for this. NHANES has a limited sample size and the

prevalence of HBsAg among women of childbearing

age is low, thus, the confidence limits around the

NHANES estimates are wide. In addition, NHANES

cannot provide estimates on the prevalence of HBsAg

for foreign-born Asian women (there are too few in the

survey). These estimates are derived from the medical

literature (1-5). Finally, it is likely there is considerable

variability in the prevalence of HBsAg-positive women

by race and ethnicity in different parts of the country. 

Considering these limitations, CDC has calculated a

“lower confidence limit” on the number of HBsAgpositive births that are expected to occur in each state.

These calculations are derived using the standard error

of the NHANES data and state-specific natality data.

To evaluate reporting, projects can compare the total

number of HBsAg-positive births identified each year

to the number that are expected to occur based on

natality data. 

Table 3 shows that 7,500 HBsAg-positive births

were identified in 1993 and that most projects reported

approximately 20%-40% of the expected number of

HBsAg-positive births. The rates of immunoprophylaxis for these infants are consistent with the national

goals and provide a measure of the number of periData Source

Program/Age-group Coverage Surveys Serologic Surveys Disease Surveillance *

Prevention of Perinatal Infection +++ +/- +

Routine Infant Vaccination +++ +++ +/-

Risk Group Vaccination under VFC

Children of immigrant mothers + +++ +

Adolescents (i.e., STD clinics, drug treatment) +++ + +++

Vaccination of Adolescents at 11-12 years of age + + +++

*This level of utility would be achieved only with addition of a special category for perinatal infection and if infants are tested and

 infections reported.

Table 2. Relative Importance of Sources of Data for Determining the Effectiveness of Hepatitis B Vac cination.

10 New Horizons
Site

%Women

screened

Public sector

%Women

screened

Private sector

Expected

HBsAg+

birth

Lower 95%

CL on pos.

birth

HBsAg+

births

identified

Observed/

Expected

# infants

tracked

% of tracked

with first

dose at birth

% of tracked

complete at

6-8 months

Alabama >95 U 205 98 107 0.52 107 0.93 0.93

Alaska U 90-95 132 93 NA NA NA NA NA

American Samoa 90-95 U 132 114 79 0.60 79 1.00 0.51

Arizona <85 >95 192 105 30 0.16 0 NA NA

Arkansas >95 U 97 44 41 0.42 31 1.00 1.00

California >95 >95 5508 4365 1872 0.34 1884 1.00 0.89

CNMI 85-89 90-95 147 130 80 0.54 80 NA NA

Colorado <80 <80 171 103 57 0.33 57 0.97 0.64

Connecticut 90-95 90-95 171 102 92 0.54 85 0.74 0.51

Delaware 95 U 43 24 11 0.26 11 0.82 0.36

Florida 100 U 636 344 272 0.42 272 0.98 0.77

Georgia U U 447 246 95 0.21 95 0.75 0.52

Hawaii >95 >95 502 393 251 0.50 251 0.99 0.92

Idaho NA NA 33 15 NA NA NA NA NA

Illinois 90-95 90-95 852 537 25 0.03 14 1.00 0.86

Indiana <80 U 196 87 26 0.13 11 1.00 0.82

Iowa <80 U 102 56 18 0.18 18 1.00 0.56

Kansas U U 119 69 29 0.24 20 0.75 0.75

Kentucky 90-95 90-95 116 49 12 0.10 12 0.92 0.75

Louisiana >95 U 290 152 398 1.38 338 0.91 0.49

Maine U 80-89 33 15 12 0.36 12 1.00 1.00

Maryland >95 U 416 267 146 0.35 146 0.99 0.68

Massachusetts >95 U 415 285 208 0.50 208 0.89 0.57

Michigan 85-89 U 461 235 268 0.58 268 1.00 0.76

Minnesota U NA 292 197 213 0.73 213 1.00 0.78

Mississippi >95 U 165 80 105 0.64 103 1.00 0.87

Missouri 100 U 226 113 17 0.08 17 0.88 0.76

Montana NA NA 26 11 NA NA NA NA NA

Nebraska U U 61 31 4 0.07 4 0.75 1.00

Nevada <80 U 99 66 52 0.53 52 0.96 1.23

New Hampshire >95 >95 32 14 7 0.22 7 1.00 NA

New Jersey >95 U 619 419 1 0.00 1 1.00 1.00

New Mexico 90-95 U 72 37 35 0.49 35 NA NA

New York >95 >95 516 300 357 0.69 357 0.99 0.82

New York City >95 >95 1205 912 1149 0.95 1149 0.98 0.78

North Carolina 90-95 U 352 180 67 0.19 0 NA NA

North Dakota <80 <80 21 10 3 0.14 3 1.00 0.33

Ohio >95 U 443 213 135 0.30 109 1.00 0.87

Oklahoma <80 U 154 83 14 0.09 14 1.00 0.43

Oregon >95 U 160 104 84 0.53 84 0.99 0.46

Palau >95 U 35 NA 50 1.43 50 0.94 0.9

Pennsylvania <80 U 559 316 151 0.27 151 0.47 0.37

Puerto Rico NA NA 77 29 48 0.62 39 0.69 NA

Rhode Island >95 85-89 64 43 45 0.70 45 0.93 0.71

South Carolina 90-95 U 201 98 44 0.22 22 NA NA

South Dakota NA NA 26 11 NA NA NA NA NA

Tennessee U U 218 104 131 0.60 115 0.99 0.93

Texas <80 <80 1141 711 521 0.46 444 0.91 0.72

Utah 90-95 <80 109 65 28 0.26 28 1.00 0.89

Vermont >95 >95 15 6 0 0.00 NA NA NA

Virginia U U 460 293 67 0.15 67 0.99 0.72

Washington U U 433 309 200 0.46 203 0.99 0.29

Washington D.C 90-95 80-84 71 40 95 1.34 49 0.55 0.45

W. Virginia U U 40 15 3 0.08 3 0.67 0.67

Wisconsin 90-95 90-95 272 170 138 0.51 135 0.93 0.9

Wyoming NA NA 14 6 NA NA NA NA NA

U.S. 19155 12914 7627 0.40 7498 0.83 0.75

U = Unknown

NA = Not available

Table 3. Survey of hepatitis B program managers, March 1995, Vaccination and completion rates of inf ants

born to HBsAg+ women in 1993

Hepatitis Surveillance 11
natal HBV infections prevented with a high degree of

certainty. 

There are several reasons why projects did not identify the majority of HBsAg-positive births in the United

States including: 1) at the time of the survey, many program coordinators did not track pregnant women who

received services from private providers; 2) several

states were just implementing perinatal programs in

1993, and; 3) there may be considerable variation in the

prevalence of chronic HBV infection among different

ethnic groups by state. For example, a state with a

large number of births to foreign-born Asian women

from Japan (where the HBsAg prevalence is 2%) may

report a much lower number of HBsAg-positive births

than a state with a high percentage of births to women

from Southeast Asia (where HBsAg prevalence is 10%).

In addition, there may be variability in the prevalence

of HBsAg among women of other ethnic/racial groups

in different parts of the country. For example, a study

from New York state suggests that the prevalence of

HBsAg among white women in New York is 0.07% (approximately half the prevalence that has been observed

in NHANES) (6). 

Population-based serological surveys: NHANES

has been used to determine the prevalence of HBV infection in the U.S. In NHANES II (1976-1980), children

as young as 6 months of age were tested, while in

NHANES III (1989-1992) 6-year-olds were the youngest age-group tested. Because the prevalence of HBV infection is low among 1- to 2-year-old children and the

sample size of NHANES is limited, future NHANES

surveys will not provide a reliable measure of perinatal

program effectiveness. 

Surveillance for acute hepatitis B: Given the natural history of perinatal HBV infection, few symptomatic cases would be expected to be reported to

NNDSS. Over the past 10 years, approximately 300 children 5 years of age were reported annually; however,

only 10% of these cases were reported to the Viral

Hepatitis Surveillance Program (VHSP). The lack of

epidemiologic data makes it difficult to interpret disease trends in this age-group (see Table4).

However, surveillance for perinatal HBV infection

could become a part of the VHSP. Postvaccination testing of infants born to HBsAg-positive mothers provides “sentinel surveillance” for the effectiveness of the

program. Review of the immunization history of infants found to be HBsAg positive provides ongoing

quality control of the program with respect to “on time

vaccination”. CSTE has changed the case definition of

acute HBV infection to include perinatal HBV infections.

Routine infant vaccination

Vaccination coverage data combined with serologic

surveys will provide the best indicator of program

effectiveness.

Coverage surveys: Hepatitis B vaccination coverage

has been included in the National Immunization Survey conducted by the National Immunization Program. The dose-specific ratio of

diphtheria-tetanus-pertussis (DTP) to hepatitis B vaccine delivered can be determined for state immunization projects and selected immunization projects that

are IAP grantees. Provider-based assessments can provide hepatitis B vaccination coverage by practice type

and provider specialty. Infant hepatitis B vaccination

coverage data should be used to ensure high coverage

in ethnically defined populations with high rates of

early childhood HBV infection. 

 Age Group

< 5 yr 5-10 11-19

Year NNDSS* VHSP†§ VHSP/NNDSS NNDSS VHSP VHSP/NNDSS NNDSS VHSP VHSP/NNDSS

% % %

1983 312 90 29 147 78 53 2374 950 40

1984 228 69 30 141 56 40 2603 953 37

1985 273 61 22 149 45 30 2498 1100 44

1986 279 71 25 140 52 37 2552 1099 43

1987 435 47 11 181 57 32 2388 987 41

1988 353 48 14 144 54 38 1978 935 47

1989 322 56 17 151 71 47 2143 966 45

1990 316 30 10 141 30 21 1879 560 30

1991 220 23 11 130 27 21 1594 491 31

1992 228 26 11 106 24 23 1398 413 30

1993 133 12 9 114 24 27 983 377 38

* National Notifiable Diseases Surveillance System

†

 Viral Hepatitis Surveillance System

§ Meeting case definition

Table 4. Cases of hepatitis B in children and adolescents reported to CDC surveillance systems, 1983 -93

12 New Horizons
Population-based serological surveys: Because few

children with acute HBV infection develop

symptomatic disease, serologic surveillance provides

the best measure of program effectiveness in

preventing early childhood HBV infection. In

NHANES II, serologic testing of children 6 months to 5

years of age detected a low prevalence of HBV infection in blacks and whites (1.29% and 0.33%, respectively), but among Asian children born in the US, the

rate of infection was 6.3%. While the prevalence of

HBV infection may be too low to detect an important

difference in the prevalence of HBV infection among

blacks and whites, a reduction in the prevalence of

HBV infection among Asian children should be detected in NHANES IV. In addition, special serologic

surveys in populations with previously defined high

rates of early childhood HBV infection (i.e., Alaskan Eskimos, Pacific Islanders, Hawaiian school children) will

continue to confirm the long-term effectiveness of routine infant vaccination (7-10).

Surveillance for acute hepatitis B: Given the natural history of early childhood HBV infection, few symptomatic cases would be expected to be reported to

NNDSS. Over the past 10 years, fewer than 500 children <10 years of age have been reported annually.

Only 20% of these cases are reported to the VHSP, and

the lack of epidemiologic data makes it difficult to interpret disease trends in this age-group (Table4). Overall, it is strongly encouraged that all cases of hepatitis B

in children be reported using the VHSP case report

form. Only after more complete reporting occurs can

the utility of disease surveillance be ascertained for

monitoring disease reduction. 

Vaccination of children of immigrant mothers

Specific goals for “catch-up” vaccination of children

of immigrant mothers have not been established. However, serologic surveillance could be an effective means

to determine the effectiveness of vaccination in these

populations since they are not adequately represented

in surveys to determine general vaccination coverage. 

Coverage data: Special coverage surveys would be

required to monitor the level of catch-up immunization

in these populations and to estimate its effect on preventing early childhood HBV infections. 

Population-based serological surveys: Data from

NHANES II and NHANES III has shown that the

prevalence of HBV infection is at least six times greater

in US-born Asian women than in blacks or whites.

Thus, sequential monitoring of age-specific HBV infection rates in the appropriate ethnic/racial groups will

provide the best measure of the effectiveness of catchup hepatitis B vaccination. In addition, special studies

will be used to monitor catch-up vaccination efforts for

children living in Asian/Pacific Islander communities

(10). 

Surveillance for acute hepatitis B: Current reported cases of hepatitis B in children 10 years of age

do not reliably reflect the rate of HBV infection in this

age-group. All cases of hepatitis B in children should

be reported to NNDSS and VHSP. Once more complete

reporting occurs, the utility of disease surveillance for

monitoring disease reduction can be ascertained for

this age-group. However, the disproportionately high

rate of reported disease for Asian children can be used

as an indicator of the effectiveness of this catch-up immunization effort (Table 5).

Age-group (years)

<5 5-10 11-19

Race/ethnicity No. % No. % No. %

White, non-Hispanic 235 (47) 231 (47) 4981 (60)

Black, non-Hispanic 152 (30) 135 (28) 2309 (28)

Hispanic 27 ( 5) 40 ( 8) 553 ( 7)

Asian/Pacific Islander 85 (17) 75 (15) 250 ( 3)

American Indian/Alaska Native 5 ( 1) 9 ( 2) 126 ( 2)

Source of Infection (mutually exclusive groups)

Transfusion/blood product 18 ( 4) 17 ( 4) 72 (0.9)

Dialysis 2 (0.4) 0 6 (0.1)

Non-sexual contact of confirmed case 212 ( 46) 120 (27) 1141 ( 14)

Sexual contact/multiple partners 0 0 460 ( 6)

Homosexual contact 0 0 262 ( 3)

Injection drug use 0 0 885 ( 11)

Occupational exposure 0 0 131 ( 2)

Other percutaneous exposure 1 (0.2) 0 11 (0.1)

Unknown 224 ( 49) 315 (70) 5314 ( 64)

Table 5. Epidemiologic characteristics of cases of hepatitis B in children and adolescents reporte d to VHSP,

1983-93

Hepatitis Surveillance 13
Vaccination of adolescents

Specific disease reduction goals for the vaccination

of adolescents have not been established. However, because most HBV infections in this group are symptomatic, specific disease surveillance and vaccination

coverage will be the best means to monitor the effectiveness of adolescent hepatitis B vaccination.

Coverage data: At a meeting of hepatitis B program

coordinators in Atlanta, a tentative goal for vaccination

of adolescents was established. The group suggested

that 70% of 14 year old children (or whatever cohort is

measured) should have received 3 doses of hepatitis B

vaccine by the year 2000. Beginning in 1996, the National Health Interview Survey will provide vaccination coverage data on a national sample of adolescents.

This data will be extremely useful in measuring progress in achieving comprehensive vaccination coverage

in adolescents for a number of vaccine antigens including hepatitis B. 

Vaccination coverage data obtained in other settings

serving high risk adolescents (i.e., clinics for sexually

transmitted diseases, drug treatment centers) is needed

to determine the degree to which these groups have

been vaccinated against HBV. However, this surveillance method is not expected to reliably predict or

monitor disease reduction. 

Population-based serological surveys: Data from

NHANES II and NHANES III has shown that the agespecific prevalence of HBV infection increases significantly among teenagers. While it is not known the

degree to which adolescent vaccination will lower the

prevalence of HBV infection, it is not clear at this time

whether seroprevalence data will provide a useful indicator of disease reduction. 

Surveillance for acute hepatitis B: Surveillance for

acute hepatitis B is possibly the best means of monitoring the effectiveness of any aspect of adolescent immunization since a large proportion of HBV infections in

this age-group are symptomatic. In contrast to adults,

the male-to-female ratio in this age-group is almost

equal and suggests the greater importance of sexually

transmitted infections. While approximately 1,500

cases of hepatitis B in this age-group have been reported to the NNDSS annually over the past 10 years,

only 30% were reported to VHSP. It is strongly encouraged that all cases of hepatitis B in teenagers be reported using the VHSP case report form. Only after

more complete reporting occurs can the utility of disease surveillance be ascertained for monitoring disease

reduction. Since program implementation, hepatitis B

vaccination coverage has increased rapidly and was estimated to be 58% for 19-24 month old children in the

4th quarter of 1994.

References

1. Stevens CE, Toy PT, Tong MJ, et al. Perinatal

hepatitis B virus transmission in the United States.

Prevention by passive-active immunization.

JAMA 1985:253;1740-45.

 2. Friedman SM, De Silva LP, Fox HE, Bernard G.

Hepatitis B screening in a New York City obstetric

service. Am J Public Health 1988:78;308-10.

3. Klontz KC: A program to provide hepatitis B

immunoprophylaxis to infants born to HBsAgpositive Asian and Pacific Island women. West J

Med 1987:146;195-99.

4. Wong DC, Purcell RH, Rosen L: Prevalence of

antibody to hepatitis A and hepatitis B viruses in

selected populations in the South Pacific. Am J

Epidemiol 1979:110;227-36.

5. McQuillan GM, Townsend TR, Johannes CB et al.

Prevention of perinatal transmission of hepatitis B

virus: The sensitivity, specificity, and predictive

value of the recommended screening questions to

detect high-risk women in an obstetric population.

Am J Epidemiol 1987:126:484-491.

6. Ikeda RM, Birkhead GS, Flynn MK, Thompson SF,

Morse DL. Use of multiple reporting sources for

perinatal hepatitis B surveillance and follow-up.

Am J Epidemiol 1995:142;765-770.

 7. Wainwright, McMahon BJ, Bulkow LR, Parkinson

AJ, Harpster AP, Hadler SC. Duration of

Immunogenicity and Efficacy of Hepatitis B

Vaccine in a Yupik Eskimo

Population-Preliminary Results of an 8-Year

Study. Prevention of Viral Hepatitis. In Hollinger

FB. ed. Viral Hepatitis and Liver Disease.

Baltimore:Williams and Wilkins; 1991:762-765.

 8. Stevens CE, Toy PT, Taylor PE, Lee T, Yip HY.

Prospects for control of hepatitis B virus infection:

implications of childhood vaccination and long

term protection. Pediatrics (supplement)

90:1992;170-73.

 9. Mahoney FJ, Woodruff BA, Erben JJ, et al Effect of

hepatitis B vaccination program on the prevalence

of hepatitis B virus infection. JID 1993;167:203-7.

10. Mahoney FJ, Lawrence M, McFarland L, Scott C,

Le Q, Farley T. Continuing transmission of

hepatitis B virus infection among US-born

Southeast Asian children.

Pediatrics:1995;96:1113-1116.

14 New Horizons
Trends Based on Reporting to the National Notifiable

Diseases Surveillance System, 1993

From 1992 to 1993, the National Notifiable Diseases

Surveillance System (NNDSS) reported an overall reduction of 7% in the reported incidence rate for all

types of viral hepatitis combined (Table 1 and Figure

1), and the total case count was at its lowest level in 26

years. Although total cases of hepatitis A actually increased modestly, there were substantial decreases in

the total case counts for hepatitis B (down 17% from

1992) and hepatitis C / non-A, non-B (NANB) hepatitis

(down 20%). The increase in reported cases of hepatitis

C/NANB hepatitis for the years 1990 through 1992 appeared to be largely due to the reporting of anti-HCVpositive persons identified by routine screening who

did not have acute hepatitis. This increase was not observed in 1993. 

Types of Hepatitis

Hepatitis A Hepatitis B Non-A, Non-B Unspecified Total

Year No. Rate* No. Rate No. Rate No. Rate No. Rate

1966 32,859 16.77 1,497 0.79 † † § §34,356 17.56

1967 38,909 19.67 2,458 1.28 † † § §41,367 20.95

1968 45,893 22.96 4,829 2.49 † † § §

50,722 25.45

1969 48,416 23.98 5,909 3.02 † † § §54,325 27.00

1970 56,797 27.87 8,310 4.08 † † § §65,107 31.95

1971 59,606 28.90 9,556 4.74 † † § §

69,162 33.64

1972 54,074 25.97 9,402 4.52 † † § §63,476 30.49

1973 50,749 24.18 8,451 4.03 † † § §59,200 28.21

1974 40,358 19.54 10,631 5.15 † † 8,351 3.95 59,340 28.07

1975 35,855 16.82 13,121 6.30 † † 7,158 3.44 56,134 26.34

1976 33,288 15.51 14,973 7.14 † † 7,488 3.57 55,749 25.97

1977 31,153 14.40 16,831 7.78 † † 8,639 3.99 56,623 26.17

1978 29,500 13.53 15,016 6.89 † † 8,776 4.02 53,292 24.44

1979 30,407 13.82 15,452 7.02 † †10,524 4.79 56,393 25.62

1980 29,087 12.84 19,015 8.39 † †11,894 5.25 59,996 26.49

1981 25,802 11.25 21,152 9.22 † †10,975 4.79 57,929 25.26

1982 23,403 10.11 22,177 9.58 2,629 1.14 8,564 3.40 56,773 24.52

1983 21,532 9.20 24,318 10.39 3,470 1.48 7,149 3.05 56,469 24.12

1984 22,040 9.33 26,115 11.06 3,871 1.64 5,531 2.34 57,557 24.37

1985 23,257 10.04 26,654 11.51 4,192 1.81 5,530 2.39 59,633 25.76

1986 23,430 10.02 26,107 11.17 3,634 1.55 3,940 1.69 57,111 24.43

1987 25,280 10.39 25,916 10.65 2,999 1.23 3,102 1.27 57,297 23.54

1988 28,507 11.59 23,177 9.42 2,619 1.07 2,470 1.00 56,773 23.10

1989 35,821 14.43 23,419 9.43 2,529 1.02 2,306 0.93 64,075 25.81

1990 31,441 12.64 21,102 8.48 2,553 1.03 1,671 0.67 56,767 22.81

1991 24,378 9.67 18,003 7.14 3,582 1.42 1,260 0.50 47,223 18.73

1992 23,112 9.06 16,126 6.32 6,010 2.36 884 0.35 46,132 18.09

1993 24,238 9.39 13,361 5.18 4,786 1.86 627 0.24 43,012 16.68

* Rate per 100,000 population

†

 Not reported until 1982

§

 Not reported until 1974

Table 1. Reported Cases of Viral Hepatitis, by Type and Year, United States, 1966-93

Hepatitis Surveillance 15
Hepatitis A

The most recent peak in the incidence of hepatitis A occurred in

1989, when almost 36,000 cases

were reported to the NNDSS (Table 1). As in previous years when

epidemics of hepatitis A swept the

nation, the peak in 1989 was followed by rapid reductions in reported case levels. In 1993, the case

count began increasing again, up

5% over the 1992 level. Although

peaks in incidence of hepatitis A exhibited a 7- to 10-year recurrent pattern during 1954-1971, a

subsequent peak (albeit much

smaller) was not observed until

1989 (Figure 1). Data from outbreak

investigations conducted as early

as 1983 in Oregon (1) and from

1986 through 1987 in other areas of

the country indicated that injection drug users were involved in an increasing number of outbreaks (2,3). Although the number of hepatitis A cases associated with

injection drug use peaked in 1989, contact with another

hepatitis patient and day-care attendance continued to

be the most frequent risk factors reported. 

Trends in hepatitis A varied by region (Figure 2). In

the West, the incidence of hepatitis A reached a peak in

1989 and the increase observed nationwide during

1992-1993 has primarily been focused in this region.

The Southeast had a slight increase in incidence in

1993. In the Northeast, the incidence continued declining in 1993, and in the Midwest, hepatitis A incidence

reached a peak in 1992 and declined in 1993. 

 Analysis of risk factors from the Viral Hepatitis Surveillance Program (VHSP) suggests that cases resulting

from person-to-person contact reached their highest

levels for all regions in 1989. In that year, the western

states reported proportionately more cases attributable

to day-care-related exposures and foodborne outbreaks

than did other regions. In general, however, the regions did not differ substantially with respect to the

distribution of risk factors. 

Incidence rates for hepatitis A in 1993 were plotted

by county for the United States (Figure 3A). The West

Figure 1. Viral Hepatitis by Year, United States, 1952-93

For 1985 and 1986, excludes cases from New York; data not available

Source: MMWR

Figure 2. Reported cases of hepatitis A and B, by region, United States, 1975-93

16 Trends Based on Reporting to the National Notifiable Diseases Surveillance System, 1993
Figure 3A. Reported Cases of Hepatitis A per 100,000 Population, United States, 1993

Source: MMWR

Rate per 100,000 No cases 4.0 - < 8.0

8.0 - < 12.0 12.0 +

New York City

District of Columbia

Virgin Islands

Puerto Rico

Guam

American Samoa

Commonwealth

of the Northern

Mariana Islands

Hepatitis Surveillance 17
had the highest proportion of counties with moderate-to-high rates of

hepatitis A (8 to 12 or more cases

per 100,000 population). High rates

of hepatitis A were observed in a

moderate number of counties in

the Midwest (west north-central

and east north-central regions) and

a smaller number of counties in the

south Atlantic, east south-central,

and west south-central regions. In

the West the higher incidence rates

were closely correlated with demographic factors, e.g., counties with

10% or more of the population classified as American Indian had average rates 3.5 times higher than

counties with less than 10% of the

population so classified. Similarly,

counties with 15% or more of the

population classified as Hispanic had average rates 2.1

times higher than counties with less than 15% of the

population so classified (2). County-specific rates require care in interpretation since counties in the West

are much larger and not as numerous as counties in the

Midwest and East. Population density must also be

taken into account when comparing regional rates to

ensure that the total case numbers of the larger western

counties are not misinterpreted. 

During 1983-1993, trends in incidence rates of hepatitis A were similar for all age-groups (Figure4A). However, persons 40 years old and older had rates less than

half of those for younger persons. After peaking in

1989, the incidence of hepatitis A decreased among persons 15 years old and older, and then remained unchanged since 1990. For those less than 15 years of age,

a peak occurred in 1990, and has declined since then. 

Hepatitis B

Since 1985, the incidence rate of hepatitis B has declined by 55% (Figure 1) to a level close to that reported in 1975 (Figure 1 and Table 1). Some of the

increase in hepatitis B incidence during 1966-1985 was

attributable to improvements in serologic diagnosis,

and some of the decrease in incidence in recent years

may be due to changes in state reporting practices, i.e.,

the case definition published by CDC and the Council

of State and Territorial Epidemiologists in 1990 had not

been uniformly adopted by all states. As states have

adopted the CDC case definition, or changed the definition being used, large variations in reported cases of

hepatitis B have been observed from some states during the last 3 years (4,5). State offices were contacted after they reported changes in hepatitis B incidence of

over 200% from the previous year. Each office contacted confirmed that changes in their use of case definitions or changes in the reporting of confirmed vs

suspected cases accounted for the unusual increase or

decrease. 

Despite these artifacts, there has been a significant,

prolonged decline in the incidence of hepatitis B in the

United States. Thirty-eight states reported decreases,

averaging 27% over 1992-93; however, 14 states reported increases in the incidence of hepatitis B from

1992 to 1993, with an average percentage increase of

19%. Regionally, hepatitis B incidence has been higher

and has shown wider variations over time in the West

than in the other regions (Figure 2). Each of the four regions reported increases in incidence until the mid1980s. By 1993, the rate in each region had declined,

with the Southeast having the highest rate and the

Northeast the lowest. As shown in Figure 2, the incidence rates for all of the regions have become more

nearly equal.

County-specific incidence rates for hepatitis B demonstrate the sporadic distribution of cases in the United

States (Figure 3B). High rate counties can be found in

each region and with few exceptions in each state.

Comparison of county rates should take into account

population density as well as geographic size. 

Age-specific incidence rates for hepatitis B have declined since 1985 (Figure 4B). The highest rates by age

were among 15- to 24-year-olds until 1987, and among

25- to 39-year-olds from 1987 to the present. Although

rates have dropped by 50% for these two age-groups

since 1985, they have remained relatively stable for persons aged 40 and older during this period. In 1993,

rates among 0- to 14-year-olds dropped by less than

4%.

Figure 4A. Reported Cases of Hepatitis A, by Age, United States, 1983-93*

18 Trends Based on Reporting to the National Notifiable Diseases Surveillance System, 1993
Figure 3B. Reported Cases of Hepatitis B per 100,000 Population, United States, 1993

Source: MMWR

Rate per 100,000 No cases 4.0 - < 8.0

8.0 - < 12.0 12.0 +

Hepatitis Surveillance 19

New York City

District of Columbia

Virgin Islands

Puerto Rico

Guam

American Samoa

Commonwealth

of the Northern

Mariana Islands
Non-A, Non-B Hepatitis

In 1989, the NNDSS reported an incidence rate of

1.02 cases of NANB hepatitis per 100,000 population.

From 1990 through 1992, the NNDSS reported that the

incidence of NANB hepatitis more than doubled (Table

1). In 1993, the rate dropped by 21% to 1.86 cases per

100,000. This decline is consistent with trends observed

in the Sentinel Counties study, where the incidence

rate of reported NANB hepatitis has declined by 80%

since 1989. This discrepancy between the two surveillance systems can be attributed to an artifactual increase in the number of cases reported to NNDSS as a

result of persons being screened by blood banks and

others for antibody to the hepatitis C virus (anti-HCV).

In some states, laboratory reports of anti-HCV positivity in the absence of confirmation of acute clinical disease are accepted as case reports of NANB hepatitis,

leading to the artifactual changes in the reported incidence of this disease. Persons who may test positive for

anti-HCV include not only those with acute symptomatic hepatitis C, but also persons with past and

chronic HCV infections, and persons with no viral

hepatitis infections (false positives).

For all cases of suspected viral hepatitis, CDC recommends 1) using case definitions agreed upon by the

Council of State and Territorial Epidemiologists and

CDC, 2) diagnosing cases on the basis of both clinical

and serologic evidence, and 3) reporting only serologically confirmed cases to CDC, including hepatitis

C/NANB hepatitis diagnosed by exclusion of hepatitis

A and B. 

In April 1995, the NNDSS changed the category

heading for viral hepatitis in Table II of the MMWR to

reflect these reporting changes. Cases reported as hepatitis C or as hepatitis NANB are now combined in Table II as hepatitis C/NANB. Some patients with

hepatitis C may continue to present as NANB cases,

since an average of 20% of patients with acute hepatitis

C will not have developed anti-HCV (as determined by

the second-generation enzyme immunoassay by 5 to 6

weeks after onset of their hepatitis (6,7). In addition,

these tests may not detect any anti-HCV in approximately 10% of patients infected with HCV, or antiHCV testing may not have been performed. 

References

1. Shade CP, Komorwska D. Continuing outbreak of

hepatitis A linked with intravenous drug abuse in

Multnomah County. Public Health Rep 1988;

103:452-9.

2. Shapiro CN, Shaw FE, Mandel EJ, et al.

Epidemiology of hepatitis A in the United States.

In: Hollinger FB, Lemon SM, Margolis H, eds.

Viral hepatitis and liver disease. Baltimore:

Williams & Wilkins, 1991;71-6.

3. Centers for Disease Control and Prevention.

Hepatitis A among drug abusers. MMWR

1988;37:298-300,305.

4. Centers for Disease Control and Prevention. Case

definitions for public health surveillance. MMWR

1990;39(No. RR-13):17.

5. Centers for Disease Control and Prevention.

Summary of notifiable diseases, 1992. MMWR

1993;42(SS-3).

6. Alter MJ, Margolis HS, Krawczynski K, et al. The

natural history of community-acquired hepatitis C

in the United States. N Engl J Med

1992;327:1899-1905.

7. Alter MJ. The detection, transmission, and

outcome of hepatitis C virus infection. Infectious

Agents and Disease 1993;2:155-66.

 Figure 4B. Reported Cases of Hepatitis B, by Age, United States, 1983-93*

20 Trends Based on Reporting to the National Notifiable Diseases Surveillance System, 1993
Viral Hepatitis Surveillance Program, 1993

The total numbers of cases reported to the Viral

Hepatitis Surveillance Program (VHSP) are shown in

Table 1A. Approximately 36% of hepatitis A cases, 26%

of hepatitis B cases, and 18% of NANB hepatitis cases

reported to the NNDSS in 1993 were also reported to

the VHSP. These percentages reflect a substantial decline in reporting to the VHSP. Reporting to the VHSP

remains inconsistent among states, with increasing

numbers of states reporting fewer of their NNDSS

cases to the VHSP than in previous years (Table 1B). In

1987, six states reported to VHSP less than 15% of their

NNDSS cases; in 1993, this trend increased to 12 states.

The agreement between reporting to the NNDSS

and to the VHSP does not necessarily measure the completeness of reporting from a particular state, since not

all cases may be reported to the NNDSS and the two

systems have different reporting criteria. The increasing discrepancy between the two systems has resulted

in differences in the relative proportions of types of viral hepatitis reported. Before 1990, the proportions of

reported cases by type were similar between the two

surveillance systems. Since then, the proportion of

hepatitis cases reported as hepatitis A to the two systems have remained similar, but the proportion of

cases reported as hepatitis B have been discrepant: 24%

to 27% of the total VHSP cases were reported as hepatitis B, compared with 35% to 38% of total cases reported

to NNDSS. The VHSP also received reports on smaller

proportions of the total number of NANB hepatitis

cases (7% to 8% of total cases) than did NNDSS (up to

13% of total cases).

These differences in proportions of cases are partly

due to the fact that VHSP excludes cases that do not

meet the case definition (VHSP eliminated 15% of reported cases as noncases in 1993). In addition, because

of strict adherence to the case definition, VHSP classified a larger proportion of reported cases as nonspecific hepatitis: 15% of cases were classified as hepatitis

unspecified by the VHSP during 1993 compared with

1.5% of cases reported to NNDSS. Beginning with data

collected in 1995, hepatitis cases that have type unspecified are no longer requested or printed in the MMWR. 

 The VHSP excludes reported cases that do not meet

the case definition for acute viral hepatitis (see “Case

Definition” section, page 22 ), including cases that

seem to be due to chronic infections. Some responses to

the VHSP questionnaires are incomplete, and the information is insufficient to verify the case as an acute infection, or to confirm the serologic type of hepatitis,

even though partial testing may have been done. Cases

may also be reported too late to be included in the

analysis. The latest date for submitting case reports to

the VHSP for the calendar year is March 31 of the following year.

Year

1991 1992 1993

Reports submitted on Form CDC 53.1 Rev. 8-89 (new form) 18,064 16,433 13,563

Reports submitted on Form CDC 53.1 Rev. 8-84 (old form) 1,772 884 617

Reports submitted electronically as extended NETSS* records 810 961 1,427

Total cases reports submitted to VHSP 20,646 18,278 15,607

Total cases serologically confirmed 19,014 16,916 14,469

Total cases meeting case definition for acute hepatitis 17,094 15,362 13,199

Symptomatic hepatitis A 9,621 9,735 8,643

Symptomatic hepatitis B 5,771 4,411 3,526

Hepatitis A and B co-infection 237 151 174

Symptomatic non-A, non-B hepatitis 1,465 1,065 856

Total cases reported to NNDSS†

47,223 46,132 43,012

Hepatitis A 24,378 23,112 24,238

Hepatitis B 18,003 16,126 13,361

Hepatitis non-A, non-B 3,5822 6,010 4,786

Hepatitis, unspecified 1,260 884 627

* National Electronic Telecommunications System for Surveillance

†

 National Notifiable Diseases Surveillance System

Table 1A. Cases Reported to Viral Hepatitis Surveillance Program Compared with NNDSS, by Type of S ubmission, 1991-93

Hepatitis Surveillance 21
Case Definition

Epidemiologic data about reported cases of acute viral hepatitis are essential for defining the groups at risk

and for monitoring changes in such groups. Since new

disease acquisition is the event of interest, chronic infections should not be reported.

In 1990 the VHSP updated the case definition for

acute viral hepatitis to include IgM anti-HBc for improved diagnosis of acute hepatitis B, to clarify the reporting of NANB hepatitis, and to include delta

hepatitis as a separate diagnostic category. The clinical

criteria remain the same: an acute case must include an

illness with discrete date of onset, and jaundice or elevated serum aminotransferase levels greater than 2.5

times the upper limit of normal. The serologic criteria

used to distinguish the different types of hepatitis were

as follows: hepatitis A is defined as IgM anti-HAV-positive (regardless of HBsAg status); hepatitis B as IgM

anti-HBc-positive (if done) or HBsAg-positive and IgM

anti-HAV-negative (if done); and NANB hepatitis as

IgM anti-HAV-negative, and IgM anti-HBc-negative (if

done) or HBsAg-negative. Although by 1993 only 55%

of reported cases were tested for both hepatitis A and

B, 87% had sufficient serologic testing to designate a

specific type. Only those patients with a specific serologic diagnosis are included in the following analyses.

Cases are excluded if they do not satisfy the criteria

for acute viral hepatitis. Among serologically confirmed cases in 1993, 6% of hepatitis A cases, 13% of

hepatitis B cases, and 9% of NANB hepatitis cases were

excluded because they failed to meet the case criteria. Compared with hepatitis B patients who fulfilled the criteria for acute hepatitis, more persons

with hepatitis B who were asymptomatic or had no

date of onset were 14 years of age, were Asian/Pacific Islander, were dialysis patients, or had histories of blood transfusions or surgery. 

Except for age, NANB hepatitis patients not

meeting the case definition showed a similar pattern. Compared with NANB hepatitis patients who

fulfilled the criteria for acute hepatitis, more persons with NANB hepatitis who were asymptomatic or had no date of onset were 40 years of

age, were patients undergoing dialysis, or had histories of surgery. This pattern, as well as that for

hepatitis B, is consistent with that for the earlier

years. For both hepatitis B and NANB hepatitis,

these findings suggest that these persons may have

been routinely screened for HBsAg or for antibody

to the hepatitis C virus (anti-HCV), and found to

be positive without any evidence of acute illness. 

Hepatitis A and B coinfections were examined

in the 1993 data, and constituted approximately 1%

of cases meeting the case definition. These cases

displayed no specific clustering or associations

with geographic or demographic factors. For purposes of risk factor analysis, these cases were

counted twice, and included as hepatitis A cases

and hepatitis B cases.

75% - 100% 50% - 74% 25% - 49% 15% - 24% 0% - 14%

Alabama Colorado New York (excl NYC) Arizona Alaska

District of Columbia Indiana Rhode Island Georgia Arkansas

Delaware Maine Wyoming California

Florida Massachusetts Connecticut

Hawaii Michigan Idaho

Iowa Missouri Kansas

Illinois New Hampshire Kentucky

Louisiana Virginia Mississippi

Maryland Washington Montana

Minnesota Wisconsin New Jersey

North Carolina New Mexico

North Dakota New York City

Nebraska Oregon

Nevada South Carolina

Ohio South Dakota

Oklahoma Tennessee

Pennsylvania Texas

Utah

Vermont

West Virginia

Table 1B. Proportion of NNDSS-Reported Cases Reported to VHSP by States, 1993

22 Viral Hepatitis Surveillance Program, 1993
Use of Serologic Tests

for Diagnosis

Serologic testing for the diagnosis of hepatitis, beginning with

hepatitis B surface antigen

(HBsAg) in 1972, immunoglobulinM antibody to hepatitis A virus

(IgM anti-HAV) in 1981, and IgM

antibody to hepatitis B core antigen

(IgM anti-HBc) in 1984, has been

critical in distinguishing the types

of viral hepatitis. Serologic testing

for any marker using one or more

tests has increased from 60% in

1983 to 94% in 1993 (Figure 1). By

1993, only 6% of reported cases

were diagnosed on the basis of the

HBsAg test alone. However, there

has been a decline in the number of cases reported in

which testing for both hepatitis A and hepatitis B was

done. In 1989, 76% of physicians reported using tests

for both types (the highest percentage reached); this declined to 70% in 1990, 68% in 1991, 63% in 1992, and to

55% in 1993. At the same time, the number of cases reported in which testing only for hepatitis A was done

increased over this period, from 15% in 1989 to 28% in

1993. The reliance on testing for hepatitis A alone for

these cases may be related to the higher incidence of

hepatitis A in communitywide outbreaks since 1989. 

Demographic Characteristics

Among persons less than 15 years of age, hepatitis

A remained the most frequent of the types reported;

hepatitis B and NANB hepatitis were reported in small

numbers of persons in this age-group (Table 2). The

percentage of NANB hepatitis cases among patients 60

years old and older (8.8%) was the highest of the three

types. However, most persons who acquire any type of

viral hepatitis are between the ages of 20 and 39: approximately 45% of hepatitis A, 63% of hepatitis B, and

61% of NANB hepatitis are reported among persons in

this age span.

From 1992 to 1993, the number of hepatitis A cases

among patients 20-39 years of age decreased 10%; hepatitis B cases, 21%; and NANB hepatitis cases, 19%.

Demographic factors for all types showed patterns consistent with those of previous years (Table 2).

The male-to-female case ratios were similar to previous years: for hepatitis A, the male-to-female ratio

was 1.2:1; for hepatitis B, 1.5:1; and for NANB hepatitis, 1.4:1. 

Non-Hispanic whites accounted for the majority of

all types reported, including 57% of hepatitis A, 54% of

hepatitis B, and 65% of NANB hepatitis (Table 2). However, the proportion of each type of hepatitis reported

as non-Hispanic white declined. Non-Hispanic blacks

in 1993 continued to represent disproportionately

higher percentages of hepatitis B, accounting for 31%

of all hepatitis B cases. Among black patients with any

type of hepatitis, hepatitis A was the predominant type

in 1993, accounting for 55% of all cases. This represents

a shift from 1989, when 53% of all cases among blacks

were hepatitis B cases. Data from a large populationbased seroprevalence study confirm that the prevalence of HBV infection is more than four times higher

among blacks than among whites (1). The percentage

of blacks among NANB hepatitis patients increased

from 12% in 1989 to 22% in 1992, but decreased to 18%

in 1993. In 1989, Hispanic patients accounted for 9% of

reported hepatitis A cases. While this percentage increased to 12% by 1993, the absolute number of Hispanic cases declined, as was true for other

racial/ethnic groups. When the percentages of Hispanic cases were examined for both old reporting

forms and newly revised forms for the 1990 data, there

was no evidence that the coding of ethnicity separately

from race affected reporting of such cases. 

Analysis of Risk Factor Data

The analysis of epidemiologic data for 1993 took

into consideration the changes in both incidence and reporting practices. Reporting was analyzed by groups

of states to determine if significant biases existed in the

data when reports from all participating states were included for analysis. Criteria for good reporting states

(“core” states) included adequate serologic testing of

reported cases (at least 80% of reported cases tested for

IgM anti-HAV or HBsAg), and reporting to the VHSP

Figure 1. Serologic Tests to Diagnose Hepatitis, 1983-1993

Hepatitis Surveillance 23
of a high proportion of cases reported to NNDSS (at

least 50% of total cases reported to NNDSS also reported to VHSP). In addition, core states were further

subdivided into those with rates above the national average for each type, and those with rates below the national average, and comparisons were made between

these subgroups. Trends in these core states were then

compared to trends in the remaining states for evidence of consistency and potential bias. 

For hepatitis A, analysis of the core group of states

showed that trends were very similar between the core

states and all reporting states, and between the highrate and low-rate subgroups. In the trend analyses that

follow, hepatitis A risk factors were based on reported

cases from all reporting states, and trends were

analyzed by using absolute numbers of cases. For hepatitis B and C/NANB, a core group of 15 states were selected using the same reporting criteria and high levels

of serologic testing for HBV during 1983-1993. These

states accounted for approximately 30% of all cases of

hepatitis B reported to the VHSP in this period. 

For hepatitis B and C/NANB hepatitis, artifactual

changes in reporting levels resulted in significant differences between the trends for all VHSP states and the

trends in the core states, although there were no differences between high- and low-incidence states. For

hepatitis B and hepatitis C/NANB hepatitis, trends in

risk factors were analyzed by using absolute numbers

of cases from the core states only. 

Epidemiologic Characteristics

Table 3 presents crude frequencies of the potential

sources of infection reported by patients with viral

hepatitis. The same questionnaire was used for all patients with hepatitis, regardless of type. Although questions about selected risk factors associated primarily

with hepatitis A have not always been asked for

hepatitis B and NANB hepatitis, and vice versa, cases

reported in 1993 have shown an improvement in this

respect. Patients may also give a positive response to

more than one factor; therefore, the data listed in

Table3 are not mutually exclusive.

Hepatitis A

Personal contact with a hepatitis A patient continued to be the predominant source of infection among

persons with hepatitis A in 1993. The crude frequency

that this potential source was reported, 34%, was

Hepatitis A

N = 8,817

Hepatitis B

N = 3,714

Non-A, Non-B

Hepatitis

N = 856

Characteristic No. % No. % No. %

Age (Years)

<5 456 5.2 7 0.2 14 1.6

5-9 1,066 12.1 15 0.4 9 1.1

10-14 801 9.1 63 1.7 7 0.8

15-19 778 8.8 276 7.4 38 4.4

20-29 2,207 25.0 1,265 34.1 203 23.7

30-39 1,772 20.1 1,061 28.6 316 36.9

40-49 784 8.9 569 15.3 131 15.3

50-59 385 4.4 230 6.2 54 6.3

60+ 513 5.8 195 5.3 75 8.8

Unknown 55 0.6 33 0.9 9 1.1

Sex

Male 4,742 53.8 2,179 58.7 490 57.2

Female 3,917 44.4 1,478 39.8 349 40.8

Unknown 158 1.8 57 1.5 17 2.0

Race/Ethnicity

White, non-Hispanic 4,980 56.5 2,010 54.1 553 64.6

Black, non-Hispanic 1,579 17.9 1,140 30.7 155 18.1

Hispanic 1,072 12.2 202 5.4 57 6.7

American Indian or Alaskan Native 385 4.4 51 1.4 24 2.8

Asian or Pacific Islander 186 2.1 76 2.0 17 2.0

Unknown 615 7.0 235 6.3 50 5.8

Source: Viral Hepatitis Surveillance Program

Table 2. Distribution of Viral Hepatitis Types A, B, and Non-A, Non-B, by Age, Sex, and Ethic Grou p, United States, 1993.

24 Viral Hepatitis Surveillance Program, 1993
similar to the rates in previous years. Many persons reported two or more potential sources of infection. Of

those patients who were associated with day-care centers, 41% also reported personal contact with a hepatitis A patient, and 7% were part of a suspected

foodborne or waterborne outbreak. Of those reporting

contact with a hepatitis A patient, 6% also reported being part of a suspected foodborne or waterborne outbreak.

 Since hepatitis A has an average incubation period

of 30 days and is transmitted by the fecal-oral route,

the characteristics reported by persons with hepatitis A

as having occurred in the 6 weeks to 6 months prior to

illness (Table 3) are generally not applicable to transmission of this virus (2). Although homosexual men

are considered at increased risk of acquiring hepatitis

A (3), the frequency with which homosexual activity

was reported by persons with hepatitis A (3.6%) may

be understated, since only 46% of the patients were

asked the question in 1993. However, this percentage

has increased in recent years. The frequency with

which injection drug use was reported by patients with

hepatitis A may be more reliable than in the past, since

over 70% of patients with hepatitis A answered this

question in 1993. These improvements lend greater validity to these data than in previous years. 

Of patients reporting personal contact with a hepatitis A patient, 10% reported sexual, 45% reported household, and 45% reported other contact. Of those

reporting other than sexual or nonsexual household

contact, none had reported day-care-related exposures,

but 8% reported being a part of a suspected outbreak. 

To better define patterns of hepatitis A virus transmission, patients who reported more than one potential source of infection were assigned to only one group

on the basis of their most probable source. These mutually exclusive groups are shown in Table 4. Contact

with another person with hepatitis A was the risk factor most frequently cited. Association with a day-care

center and international travel were the two risk factors next in importance. 

The frequency with which the various risk factors

were reported was influenced by the age of the patient.

Contact with another person with hepatitis A was the

most frequently reported risk factor for all age-groups,

although the percentage of patients reporting this risk

factor decreased with increasing age. For persons less

than 15 years old, being a child in a day-care center

was the next most frequently reported risk factor. For

those aged 15-39, contact with a day-care child or employee was the next most important risk factor. Reporting of injection drug use as a risk factor for hepatitis A

Percentage of Patients

Characteristic

Hepatitis A

N = 8,817

Hepatitis B

N = 3,714

Non-A, Non-B

Hepatitis 

N = 856

Reported within 2-6 weeks of illness*

Child/employee in day-care center 6.8 1.6 1.7

Contact of day-care child/employee 10.9 4.7 5.0

Personal contact with hepatitis A patient 33.6 1.8 3.5

Suspected foodborne or waterborne outbreak 4.7 0.3 0.6

International travel 8.4 3.2 2.4

Reported within 6 weeks to 6 months of illness*

Blood transfusion 0.4 1.0 2.4

Injection Drug use 3.7 10.5 23.0

Medical/dental employment 2.9 3.5 4.0

Hemodialysis-associated 0.9 1.2 1.5

Personal contact with B/non-A, non-B patient+

3.8 17.7 13.2

Homosexual activity 3.6 6.9 3.5

Multiple sex partners 4.9 20.2 12.5

Dental work 11.1 15.5 16.8

Surgery 3.5 6.6 8.1

Acupuncture 0.5 0.5 0.5

Tattooing 1.8 4.3 5.7

Other percutaneous exposure 0.9 3.2 2.7

Known hepatitis B vaccine responder NA 0 NA

Ever received hepatitis B vaccine 3.4 NA 3.5

* Approximately 67% to 76% if hepatitis B patients, and 70% to 81% of NANB hepatitis patients answer ed these questions.

+

 Approximately 60% to 70% of hepatitis A patients answered the non-sexual questions; 46% answered th ese regarding sexual

 preferences of number of sex partners; therefore, reported frequencies for these risk factors may b e unreliable (see text).

Table 3. Crude Frequency of Potential Sources for Acquiring Viral Hepatitis and Other Characterist ics, 1993

Hepatitis Surveillance 25
dropped by 1993 to low levels (4%) for this age-group.

For persons over 40 years of age, international travel

and being a part of a suspected foodborne or waterborne outbreak were the next most frequent risk factors. 

International travel was reported in 6% of hepatitis

A cases in 1993. South and Central America were the locations visited most frequently (67% of travel-related

cases in 1993). Destinations in Asia and the South Pacific were visited next most often (10% of cases in

1993). The duration of stay was 1-3 days in 17% of

cases with international travel as a risk factor, 4-7 days

in 15%, and more than 7 days in 68%. Among patients

reporting short stays (1-3

days), over 90% reported

visits to South/Central

America. 

Race and ethnicity were

examined among hepatitis

A patients with international travel as a risk factor.

Hispanic patients accounted

for 47%, non-Hispanic

whites accounted for 43%,

and Asian/Pacific Islanders

for 8% of cases. Non-Hispanic blacks accounted for

less than 2% of travel-related cases in 1993. There

was an association between

race and location visited:

92% of Hispanic patients

with travel-related hepatitis

A visited South/Central

America, while 75% of nonHispanics did so. Among

Asian/Pacific Islander patients, 85% visited

Asian/South Pacific destinations, while 0% to 7% of

other races or ethnic groups visited these locations. 

Because the total number of hepatitis A cases reported has changed over the years, the absolute numbers of cases for each risk factor show more accurately

the trends over time for hepatitis A. The numbers of

cases associated with personal contact with another

hepatitis A patient during 1983-1993 have exhibited the

greatest variation (Figure 2), with an increase of over

100% occurring from 1983 to 1989, followed by a comparable decrease from 1989 to 1993. Day-care-related

cases increased more slowly during this period, but

Percentage of Patients By Age (years)

Epidemiologic Characteristics for Prior 6 weeks by

Mutually Exclusive Groups*

Total <1-14 15-39 40+

N = 8,817+ N = 2,323 N = 4,757 N = 1,682

Child/employee in day-care center 6.9 17.2 2.9 2.5

Contact of day-care child/employee 8.6 6.4 11.0 5.1

Personal contact with hepatitis A patient 22.0 29.0 21.8 12.8

Suspected food- or waterborne outbreak 2.2 1.2 2.1 3.9

International travel 6.3 8.2 5.2 6.5

Homosexual activity 4.9 0.2 6.9 3.9

Injection drug use 2.4 0.0 3.8 2.0

Unknown 46.7 37.8 46.3 63.3

Clinical characteristics

Jaundice 83.0 81.7 85.7 76.9

Hospitalized for hepatitis 18.8 10.6 19.5 29.1

Death as a result of hepatitis 1.7 0.2 2.0 3.2

* In decreasing order of exclusion.

+ Number includes age unknown.

Table 4. Epidemiologic and Clinical characteristics of Patients Reported with Hepatitis A, by Age Gr oup, United States,

1993

Figure 2. Trends in Selected Risk Factors for Patients Reported with Hepatitis A

by Mutually Exclusive Groups, United States, 1993

26 Viral Hepatitis Surveillance Program, 1993
peaked in 1989 also, followed by a drop of 47%. The

numbers of cases attributable to drug use increased

steadily between 1983 and 1989, and declined rapidly

to their present low level. Cases related to homosexual

activity remained at low levels from 1983 through

1987. By 1989, however, there was a 3.6-fold increase in

cases of hepatitis A among homosexual men, and outbreaks of hepatitis A in this population subgroup were

reported. Cases among homosexual men have remained at higher levels through 1993. Foreign travel

and foodborne outbreak-associated cases peaked in

1988 and declined overall since then.

 Jaundice characterized an average of 85% of the reported hepatitis A cases in 1993. Although this frequency was similar across age-groups, jaundice and

other symptoms are uncommon among young children

infected with hepatitis A virus. Thus, reported cases

substantially underestimate the infection burden

among the youngest age-group. The rate of hospitalization of patients with hepatitis A has remained steady

in 1993, and continues to increase with increasing age.

The case-fatality rate for hepatitis A patients also increased with age, and showed a slight increase with

time as well for those aged 15 and over in 1993.

Hepatitis B

Based on crude frequencies of reported risk factors,

contact with another hepatitis B patient, injection drug

use, and having multiple sex partners were the three

most frequently reported potential sources of infection

for hepatitis B patients in 1993 (Table 3). In 1993, having multiple sex partners was the most frequent potential source of infection reported. Homosexual

preference was reported by 7% of hepatitis B patients

during 1993. As with other types of hepatitis, several

possible sources of infection were often reported for

the same patient. 

Seventy-two percent of the persons with hepatitis B

were asked about potential risk factors commonly associated with hepatitis A that occurred within the 2 to 6

weeks prior to illness. Although these factors are generally not associated with the transmission of HBV because the incubation period is too short, health-care

workers interviewing patients with hepatitis are encouraged to obtain from each patient information on

all types of risk factors, both to detect newly emerging

problems (as occurred with injection drug use and

hepatitis A) and to ensure a complete exposure history

when cases are serologically classified. 

Events or conditions reported within the 6 months

prior to hepatitis B illness — such as history of dental

work, surgery, acupuncture, tattooing, or other percutaneous exposures — are not considered likely sources

of sporadic infection, but are primarily useful in identifying clusters of cases at the local level.

Of three patients reported with acute hepatitis B

and evidence of having responded to the hepatitis B

vaccine, all three were also reported to have coinfections with acute hepatitis A. After follow-up with the

reporting health department, none of these cases were

found to be true candidates for breakthrough infections.

Persons who reported multiple risk factors for hepatitis B were assigned to mutually exclusive groups (2,

4-6) (Table 5). As a percentage of all cases, being heterosexually active with multiple partners has replaced

injection drug use as the predominant risk factor for acquisition of hepatitis B. Personal contact with another

hepatitis B patient was the third most common risk

factor. Of personal contacts in 1993, 68% were sexual,

and 17% were nonsexual household contacts. The remaining 15% of personal contacts, classified as “other”,

are unclear as to specific sources because information

Percentage of Patients By Age (years)

Epidemiologic Characteristics for Prior 6 weeks by

Mutually Exclusive Groups*

Total <1-14 15-39 40+

N = 3,714+ N = 85 N = 2,602 N = 994

Injection drug use 10.5 0.0 12.3 6.8

Homosexual activity 9.4 0.0 10.6 6.7

Employed in medical/dental field 3.1 0.0 3.0 3.7

Hemodialysis 0.4 1.2 0.2 0.7

Personal contact with hepatitis B patient 8.3 25.9 8.3 6.6

Multiple sex partners 12.2 5.9 14.4 7.1

Blood transfusion 0.8 2.6 0.3 2.0

Unknown 55.3 64.4 50.9 66.4

Clinical characteristics

Jaundice 81.5 75.0 83.4 76.9

Hospitalized for hepatitis 28.2 21.0 25.5 36.0

Death as a result of hepatitis 1.4 0.0 1.1 2.1

* In decreasing order of exclusion.

+ Number includes age unknown.

Source: Viral Hepatitis Surveillance Program

Table 5. Epidemiologic and Clinical characteristics of Patients Reported with Hepatitis B, by Age Gro up, United States, 1993

Hepatitis Surveillance 27
was insufficient to determine how transmission occurred. Employment in the medical or dental field,

blood transfusions, and dialysis accounted for less than

5% of cases. For those patients employed in a medical,

dental or other field involving contact with human

blood, 23% reported frequent blood contact in 1993,

down from 36% in 1992. Transfusion as a source for

HBV has remained at a low level (0.8%) because of routine screening of blood donors for HBsAg and antiHBc, and because of donor selection and deferral

procedures. Screening for HBsAg has been mandatory

since 1972. Smaller improvements in preventing posttransfusion hepatitis B occurred in the mid-1980s, with

self-exclusion of high-risk donors related to the prevention of human immunodeficiency virus (HIV) infection

and later anti-HBc screening. Hepatitis B among children younger than 15 years old is associated primarily

with personal contact with another infected person.

The percentage for 1993, 26%, is somewhat higher than

the 22% reported in 1992. None of these patients reported injection drug use, while 6% reported multiple

sex partners in 1993 as their primary risk factor. The

percentages of persons reporting no known source of

infection in the youngest and oldest age-groups were

similar to those reported in 1992.

To ensure that possible biases owing to artifactual

decreases in reporting were minimized, the analysis of

trends in hepatitis B risk factors for 1983 to 1993 was restricted to the absolute numbers of cases reported in

the core states only. For these states during 1989-1993,

decreases occurred in the numbers of cases attributed

to injection drug use (an 83% decrease), personal contact with a hepatitis B patient (73% decrease), and multiple sexual partners (35% decrease).

The trends in risk factors associated with hepatitis B

in the core states, among men and women separately,

are shown in Figures 3 and 4. Among men, injection

drug use has shown the largest change from 1983 to

1993. After an increase of 116%

from 1983 to 1989, the numbers of

cases among men attributed to injection drug use decreased by

85% (Figure 3). Safer needle-using

practices, or changes in the types

of drugs used (injection to noninjection) are possible reasons for

this reduction. The numbers of

cases among men attributable to

personal contact with another

hepatitis B patient has been more

stable, showing a gradual decline

from 1989 to 1993. For these male

patients, 52% to 67% of contacts

were sexual, while 13% to 20%

were household contacts. Homosexual activity, the second most

commonly reported risk factor,

declined to its lowest level in

1993. Declines in the other reported risk factors —

health-care employment and blood transfusion — continued through 1993.

Risk factors for women with hepatitis B displayed

some of the same trends presented for men, with injection drug use as a risk factor increasing from 1983 to a

peak in 1989 (Figure 4), followed by a drop to pre-1983

levels. However, among women, contact with another

hepatitis B patient increased more dramatically than

among men and since 1990, was reported with a higher

frequency than injection drug use. As with men, the

majority of contacts associated with such cases have

been sexual, reaching 72% in 1993, while only 11%

have been household contacts.

The decrease in the percentage of female patients reporting medical and dental employment as a risk factor during 1983-1993 has been more pronounced than

that for men. This decline is most probably attributable

to immunization of health-care workers with hepatitis

B vaccine. The percentage of cases attributable to blood

transfusions has remained at low levels since 1988. The

same trends in both men and women have been observed in the Sentinel Counties study(19). 

Jaundice as a clinical characteristic of hepatitis B is a

common symptom in patients over 10 years of age (Table 5); 82% of all patients were reported with jaundice,

regardless of age. As with hepatitis A, jaundice and

other symptoms were notably less frequent for young

children, suggesting more extensive underrepresentation of this age-group among reported cases. Overall

hospitalization rates remained stable, showing little

change since 1988, but the rates of hospitalization for

patients 40 years old and older dropped slowly but

steadily, from 50% in 1985 to 36% in 1993. Death as a result of hepatitis B was reported in approximately 1% of

patients in 1993.

 Nationwide, the incidence of hepatitis B increased

by 67% from 1978 to 1985 and then declined to its lowFigure 3. Trends in Selected Risk Factors for Patients Reported with

Hepatitis B by Mutually Exclusive Groups, Males, Selected States, 1983-93

28 Viral Hepatitis Surveillance Program, 1993
est incidence since 1974. Since its

original licensing in 1981, hepatitis

B vaccine has been used in increasing quantities each year. However,

the role of the vaccine in the decline

of the incidence of hepatitis B varies

across risk groups. From 1985 to

1989, hepatitis B among homosexual men declined more rapidly than

among other risk groups, not because of vaccine use but because of

behavioral changes resulting from

awareness of acquired immunodeficiency syndrome (AIDS)(7). Hepatitis B also declined among

health-care workers during this period, who were the largest users of

hepatitis B vaccine. From 1989 to

1993, hepatitis B among injection

drug users declined by 46% despite

the low levels of vaccine usage in

this risk group. Hepatitis B among heterosexuals decreased during this period also, possibly due to wider

use of vaccine. 

Vaccination programs and vaccine usage have been

focused primarily on three risk groups: health-care

workers who are exposed to blood, staff and residents

of institutions for the developmentally disabled, and

staff and patients in hemodialysis units (9). For healthcare and public safety workers, the Department of Labor in 1991 issued regulations that require employers

to offer hepatitis B vaccine to persons at occupational

risk of infection. However, the ability to immunize the

groups that account for most of the HBV infections is

severely limited for several reasons: the failure both of

health-care providers and of the target populations to

recognize the specific groups at high risk for infection;

the difficulty in identifying persons with these highrisk behaviors before they become infected; and the difficulties in reaching these groups for the delivery of

vaccine and at the appropriate time for vaccination (7).

Adults in general, and groups such as injecting drug

users in particular, are extremely difficult to access for

delivery of vaccine (11). In addition, once persons begin the lifestyles associated with a high-risk group,

they may become infected before vaccine can be given.

Thus, the major obstacles to reducing the incidence of

HBV infection in the United States have been the difficulties in identifying persons before they become infected and vaccinating them promptly. To overcome

these problems, the Immunization Practices Advisory

Committee recommended in 1991 a program of routine

vaccination of all infants (9). In 1995 the same committee recommended the expansion of this program to

cover 1) vaccination of all unvaccinated children aged

<15 years who are Pacific Islanders or who reside in

households of first-generation immigrants from countries where HBV is of high or intermediate endemicity;

and 2) vaccination of all 11- to 12-year-old children

who have not previously received hepatitis B vaccine

(9). 

Hepatitis C/Non-A, Non-B Hepatitis

Based on the crude frequencies with which risk factors were reported, injection drug use was the risk factor most commonly reported by hepatitis C/NANB

patients (Table 3). Many of these persons also reported

more than one potential source of infection. Of those reporting contact with another person with hepatitis

C/NANB, 25% also reported injection drug use and 5%

reported employment in a medical or a dental field. Of

those reporting multiple sex partners, 35% also reported injection drug use.

The behaviors commonly associated with hepatitis

A that were reported by persons with hepatitis

C/NANB to have occurred within 6 weeks of illness

are generally not applicable to the transmission of

hepatitis C/NANB (Table 3). Since transmission of

NANB hepatitis by the fecal-oral route has not been

demonstrated in this country, reporting an association

with a foodborne or a waterborne outbreak represents

misclassification of the source. 

As with hepatitis B, potential exposures associated

with dental work, surgery, acupuncture, tattooing, and

other percutaneous procedures are not judged to be

probable sources of sporadic infection (12). Hepatitis

C/NANB patients with no known source of infection

reported these exposures at rates no different from

those of the general population. 

Based on assignment to mutually exclusive categories, persons with hepatitis C/NANB reported injection drug use most frequently, accounting for 23% of

cases during 1993 (Table 6). Blood transfusion accounted for 2% of cases, declining from 6% in 1990; contact with another infected person accounted for 5%,

Figure 4. Trends in Selected Risk Factors for Patients Reported with

Hepatitis B by Mutually Exclusive Groups, females, Selected States, 1983-93

Hepatitis Surveillance 29
and health-care employment for

4%. Of those patients reporting

health-care employment, the percentage reporting frequent (several

times weekly) blood contact

dropped over 1990 to 1993. Fiftyseven percent of patients employed in health-care reported

frequent blood contact in 1990. By

1993, the percentage dropped to

17%. Patients classified as having

multiple (2 or more) sex partners

as their most likely source of infection accounted for 7% of the patients with hepatitis C/NANB; in a

case-control study, this risk factor

was associated with acquiring disease (12). Overall, 58% of persons

reported no known source for their

infection. This percentage varied

by age, with 70% of persons

younger than 15 years old or 40 years old and older reporting no known source for their infection, compared

with 50% for persons 15-39 years of age. Among persons less than 15, 13.6% had a history of blood transfusion. 

 Among persons 15 to 39 years of age, injection drug

use was reported by 28% of all cases during 1993, unchanged from 1992 (Table 6). Ten percent reported multiple sex partners, 7% reported contact with another

infected person, 4% reported health-care employment,

and 1% reported blood transfusions. Of reported contacts with another infected person, an average of 59%

were sexual contacts, 16% were household nonsexual

contacts, and 25% were other (unspecified) types of

contact. In prior years, persons 40 years old and older

reported a history of blood transfusion most frequently

among their risk factors (in 1990, 16%), but this percentage declined substantially to 4% by 1993. Injection

drug use is now the most frequent risk factor for this

age-group (Table 6). 

Because total numbers of cases of hepatitis

C/NANB have declined, trends in the distribution of

risk factors are more accurately reflected by trends in

the absolute numbers of cases attributed to each factor.

In the core states, hepatitis C/NANB cases attributable

to drug use have declined rapidly since 1988, showing

a more than 62% decrease (Figure 5). A similar decrease of over 50% was seen in the Sentinel Counties

Study (14). 

The numbers of hepatitis C/NANB cases attributable to blood transfusions have decreased even more

dramatically, dropping by 94% from 1985 to 1993. The

significant decline in transfusion-associated cases,

Percentage of Patients By Age (years)

Epidemiologic Characteristics for Prior 6 weeks by

Mutually Exclusive Groups*

Total <1-14 15-39 40+

N = 856+ N = 30 N = 557 N = 260

Blood transfusion 2.3 13.6 0.9 4.3

Injection drug use 22.6 0.0 28.4 12.0

Employed in medical/dental field 3.9 0.0 3.8 4.6

Hemodialysis 0.7 0.0 0.2 1.9

Personal contact with hepatitis C/NANB patient 5.3 6.7 7.2 1.2

Multiple sex partners 7.4 0.0 9.9 3.1

Unknown 57.8 79.7 49.6 72.9

Clinical characteristics

Jaundice 66.9 75.0 69.6 60.1

Hospitalized for hepatitis 32.9 32.1 28.8 41.7

Death as a result of hepatitis 1.9 0.0 0.8 4.5

* In decreasing order of exclusion.

+ Number includes age unknown.

Source: Viral Hepatitis Surveillance Program

Table 6. Epidemiologic and Clinical characteristics of Patients Reported with Hepatitis C/Non-A, Non -B Hepatitis, by Age

Group, United States, 1993

Figure 5. Trends in Selected Risk Factors for Patients Reported with

Hepatitis C/NANB, by Mutually Exclusive Groups, Selected States, 1983-93

30 Viral Hepatitis Surveillance Program, 1993
which began in the mid- 1980s, resulted from a series

of events: changes in the blood donor population

caused by self-exclusion of high-risk donors, as part of

efforts to prevent HIV infection (15,16); the introduction of screening blood donors for alanine aminotranferase and anti-HBc as surrogate markers for hepatitis

C/NANB in 1986 and 1987; and use of first- and second-generation anti-HCV markers for screening donors in 1990 to the present. 

Jaundice was reported as a clinical symptom in 67%

of reported hepatitis C/NANB patients in 1993 (Table

6). Hospitalization and case-fatality rates were higher

in hepatitis C/NANB patients than in patients with

hepatitis A or B. Those 40 years old and older experienced the highest rates. 

The majority of NANB hepatitis cases in this country are caused by the hepatitis C virus (14); the remainder are probably due mostly to other bloodborne hepatitis agents. Outbreaks of hepatitis E, an enterically

transmitted form of hepatitis NANB, have been reported in rural Mexican villages (17), as well as in Asia

and North and West Africa (18), but no outbreaks have

been reported in this country (19). In the United States

and other countries where hepatitis E outbreaks have

not been documented to occur, rare hepatitis E cases

have been reported, primarily among travelers returning from HEV-endemic regions (20). No secondary

transmission to family members or other persons in association with these cases has been reported. In the

United States, hepatitis E cases have been reported

with no history of travel to HEV-endemic areas; however, the mode of HEV transmission for these cases has

not been determined.

Discussion

Viral hepatitis surveillance in 1993 revealed several

important changes from earlier years. First, total cases

reported to the VHSP declined more than 51% from

1990 to 1993, as a result of both real declines in the incidence of hepatitis A and B, and a number of states that

previously reported now submitting fewer or none of

their cases to the VHSP. Second, the use of serologic

tests to diagnose the specific type of hepatitis has declined, with fewer reported cases being diagnosed on

the basis of tests for both hepatitis A and B. Third,

analysis of trends in risk factors for the acquisition of

the different types of hepatitis indicated that injection

drug use has declined dramatically for hepatitis A, B,

and hepatitis C/NANB. Finally, more widespread use

of hepatitis B vaccine may be having an effect on the

number of hepatitis B cases acquired by heterosexual

activity. 

Underreporting and incomplete case ascertainment

are potential sources of inaccuracy and may lead to inaccurate conclusions from surveillance data, particularly in the relative frequencies of reported risk factors

(21). Since case ascertainment is dependent on the availability of sensitive and specific serologic tests, estimates of the frequency of disease types such as

hepatitis C/NANB, for which there are no markers of

acute disease, are likely to be the least reliable. The

analysis of VHSP data on biases in the reporting of

hepatitis B and hepatitis C/NANB showed that consistent reporting practices are critical for the accurate interpretation of surveillance data in this country. In

addition, national data are averaged over many regions with potentially large geographic differences in

risk factors and disease incidence. Therefore, the overall frequencies of various risk factors may not reflect

their importance in smaller geographic areas.

Despite the drawbacks associated with a passive

surveillance system, the data collected through the

VHSP are essential for monitoring trends in the

epidemiologic characteristics of the various types of viral hepatitis. These data are also valuable for monitoring the impact of prevention programs on disease in

various high-risk groups, such as those targeted to receive hepatitis B vaccine. The recently recommended

program for the universal immunization of infants for

hepatitis B was the direct result of the analysis of surveillance data, and provides evidence that contributors

to the VHSP have made a positive impact on public

health. 

Many dedicated public health practitioners, local

medical authorities, and public health communities

contribute to this surveillance system through their

timely diagnosis and reporting of hepatitis cases. We

are grateful for their continued participation and encourage them to continue to improve their use of serologic testing, their consistency in reporting, and the

quality of the information they provide.

References

1. McQuillan GM, Townsend TR, Fields HA, et al.

Seroepidemiology of hepatitis B virus infection in

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2. Francis DP, Maynard JE. The transmission and

outcome of hepatitis A, B, and non-A, non-B: a

review. Epidemiol Rev 1979;1:17-31.

3. Corey L, Holmes KK. Sexual transmission of

hepatitis A in homosexual men—incidence and

mechanism. N Engl J Med 1980;302:435-8.

 4. Dienstag JL, Ryan DM. Occupational exposure to

hepatitis B virus in hospital personnel: infection or

immunization? Am J Epidemiol 1982;115:26-39.

5. Hadler SC, Doto IL, Maynard JE, et al.

Occupational risk of hepatitis B infection in

hospital workers. J Infect Control 1985;6:24-31.

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6. Schreeder MT, Thompson SE, Hadler SC, et al.

Hepatitis B in homosexual men: prevalence of

infection and factors related to transmission. J

Infect Dis l982;146:7-15.

7. Alter MJ, Hadler SC, Margolis HS, et al. The

changing epidemiology of hepatitis B in the

United States. JAMA 1990;263:1218-22. 

8. Immunization Practices Advisory Committee.

Recommendations for protection against viral

hepatitis. MMWR 1985;34:313-24,329-35.

9. Immunization Practices Advisory Committee.

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eliminating transmission in the United States

through universal childhood vaccination. MMWR

1991;40:1-25.

10. Immunization Practices Advisory Committee.

Update: recommendations to prevent hepatitis B

virus transmission — United States. MMWR

1995;44:574-5.

11. Margolis HS, Alter MJ, Hadler SC. Hepatitis B:

evolving epidemiology and implications for

control. Semin Liver Dis 1991;11:84-92.

12. Alter MJ, Coleman PJ, Alexander WJ, et al.

Importance of heterosexual activity in the

transmission of hepatitis B and non-A, non-B

hepatitis. JAMA 1989;262:1201-5.

13. Alter MJ, Hadler SC, Judson FN, et al. Risk factors

for acute non-A, non-B hepatitis in the United

States and association with hepatitis C virus

infection. JAMA 1990;264:2231-5.

14. Alter MJ. The detection, transmission, and

outcome of hepatitis C virus infection. Infectious

Agents and Disease 1993;2:155-66.

15. Aach RD, Szmuness W, Mosley JW, et al. Serum

alanine aminotransferase of donors in relation to

the risk of non-A, non-B hepatitis in recipients. N

Engl J Med 1981;304:989-94.

16. Koziol DE, Holland PV, Alling DW, et al.

Antibody to hepatitis B core antigen as a

paradoxical marker for non-A, non-B hepatitis

agents in donated blood. Ann Intern Med

1986;104:488-95.

17. CDC. Enterically transmitted non-A, non-B

hepatitis—Mexico. MMWR 1987;36:597-602.

18. Bellabbes EH, Bourguermouh A, Benatallah A,

Illoul G. Epidemic non-A, non-B hepatitis in

Algeria: strong evidence for its spreading by

water. J Med Virol 1985;16:257-63.

19. Mast EJ, Alter MJ. Epidemiology of viral hepatitis:

an overview. Seminars in Virology 1993;4:273-83.

20. DeCock KM, Bradley DW, Sandford NG,

Govindarajan S, Maynard JE, Redeker AG.

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Pakistan. Ann Intern Med 1987;106:227-30.

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32 Viral Hepatitis Surveillance Program, 1993
Appendix (Form CDC 53.1 Rev. 8-89) 

State and Territorial Epidemiologists and

Laboratory Directors 

Key to all disease surveillance activities are the state and territorial epidemiologists and laboratory directors. The

epidemiologists and laboratory directors listed below were in the positions shown as of June 1995.

State/Territory Epidemiologist Laboratory Director 

Alabama John P. Lofgren, MD William J. Callan, PhD 

Alaska John P. Middaugh, MD Gregory V. Hayes 

Arizona Lawrence Sands, DO, MPH Barbara J. Erickson, PhD 

Arkansas Thomas C. McChesney, DVM Michael G. Foreman 

California Duc J. Vugia, MD, MPH Michael G. Volz, PhD 

Colorado Richard E. Hoffman, MD, MPH Ronald L. Cada, DrPH 

Connecticut James L. Hadler, MD, MPH Sanders F. Hawkins, PhD 

Delaware A. LeRoy Hathcock, PhD Mahadeo P. Verma, PhD 

District of Columbia Martin E. Levy, MD, MPH James B. Thomas, ScD 

Florida Richard S. Hopkins, MD, MSPH E. Charles Hartwig, ScD 

Georgia Kathleen E. Toomey, MD, MPH Elizabeth A. Franko, DrPH 

Hawaii Richard L. Vogt, MD Vernon K. Miyamoto, PhD 

Idaho Jesse F. Greenblatt, MD, MPH Richard H. Hudson, PhD 

Illinois Byron J. Francis, MD, MPH David F. Carpenter, PhD 

Indiana Edmundo M. Muniz, MD, PhD, Msc Barbara Wilder (Acting) 

lowa M. Patricia Quinlisk, MD, MPH W. J. Hausler, Jr, PhD 

Kansas Andrew R. Pelletier, MD Roger H. Carlson, PhD 

Kentucky Reginald Finger, MD, MPH Thomas E. Maxson, DrPH 

Louisiana Louise McFarland, DrPH Henry B. Bradford, Jr, PhD 

Maine Kathleen F. Gensheimer, MD, MPH Philip W. Haines, DrPH 

Maryland Diane M. Dwyer, MD J. Mehsen Joseph, PhD 

Massachusetts Alfred DeMaria, Jr, MD Ralph J. Timperi, MPH 

Michigan Kenneth R. Wilcox, Jr, MD, DrPH Robert Martin, DrPH 

Minnesota Michael T. Osterholm, PhD, MPH Pauline Bouchard, JD, MPH 

Mississippi Mary Currier, MD, MPH Joe O. Graves, PhD 

Missouri H. Denny Donnell, Jr, MD, MPH Eric C. Blank, DrPH 

Montana Todd D. Damrow, PhD, MPH Douglas O. Abbott, PhD 

Nebraska Thomas J. Safranek, MD John D. Blosser 

Nevada Randall L. Todd, DrPH Arthur F. DiSalvo, MD 

New Hampshire M. Geoffrey Smith, MD, MPH Veronica C. Malmberg, MSN 

New Jersey Kenneth C. Spitalny, MD Shahiedy I. Shahied, PhD 

New Mexico C. Mack Sewell, DrPH, MS Loris W. Hughes, PhD 

New York City Benjamin A. Mojica, MD, MPH Stanley Reimer 

New York State Dale L. Morse, MD, MS Lawrence S. Sturman, MD, PhD 

North Carolina J. Newton MacCormack, MD, MPH Samuel N. Merritt, DrPH 

North Dakota Larry A. Shireley, MS, MPH James D. Anders, MPH 

Ohio Thomas J. Halpin, MD, MPH Kathleen L. Meckstroth, DrPH 

Oklahoma Joe P. Mallonee, MPH (Acting) Garry L. McKee, PhD 

Oregon David Fleming, MD Michael R. Skeels, PhD, MPH 

Pennsylvania James T. Rankin, Jr, DVM, PhD, MPH Bruce Kieger, DrPH 

Rhode Island Barbara A. DeBuono, MD, MPH Walter Combs, PhD 

South Carolina James J. Gibson, MD, MPH Harold Dowda, PhD 

South Dakota Susan E Lance, DVM, MPH Richard S. Steece, PhD 

Tennessee Kerry Gateley, MD Michael W. Kimberly, DrPH 

Texas Diane M. Simpson, MD, PhD David L. Maserang, PhD 

Utah Craig R. Nichols, MPA Charles D. Brokopp, DrPH 

Vermont Robert O’Grady (Acting) Burton W. Wilke, Jr, PhD 

Virginia Grayson B. Miller, Jr, MD James L. Pearson, DrPH 

Washington Paul Stehr-Green, DrPH, MPH Jon M. Counts, DrPH 

West Virginia Loretta E. Haddy, MA, MS Frank W. Lambert, Jr, DrPH 

Wisconsin Jeffrey P. Davis, MD Ronald H. Laessig, PhD 

Wyoming Gayle L. Miller, DVM, MPH Carl H. Blank, DrPH 

American Samoa Julia L. Lyons, MD, MPH —

Federated States of Micronesia Vacant —

Guam Robert L. Haddock, DVM, MPH Jeff Benjamin (Acting) 

Marshall Islands Tony de Brum —

Northern Mariana Islands A. Mark Durand, MD, MPH —

Palau Jill McCready, MS, MPH —

Puerto Rico Carmen C. Deseda, MD Adolpho Firpo-Betancourt, MD 

Virgin Islands Donna M. Green, MD Norbert Mantor, PhD