The following are pre-publication drafts of articles from the
Morbidity and Mortality Weekly Report dated August 4, 1995. Late-breaking articles, and final editorial revisions are not included;
therefore, these articles should be considered preliminary, and not
to be released to the public. --CDC
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Acute Hepatitis and Renal Failure Following Ingestion of Raw Carp
Gallbladders -- Maryland and Pennsylvania, 1991 and 1994
     In some cultures, eating gallbladders from certain species of
snakes, birds, or fish is believed to improve health. A syndrome of
acute hepatitis and renal failure following the ingestion of raw
carp gallbladders has been described previously among persons
living in Asia (1-4). This report summarizes two cases of this
syndrome that occurred in residents of Pennsylvania who had eaten
the raw bile and gallbladders of carp caught in Maryland.
     Patient 1. On July 11, 1991, a 59-year-old man who had
immigrated from Korea ate the uncooked gallbladder of a carp he had
caught in Maryland from a tributary of the Susquehanna River. Six
hours after eating the gallbladder, he developed diarrhea and
abdominal pain. On July 14, he was admitted to a hospital with mild
jaundice and persistent nausea and vomiting. Laboratory testing
revealed elevated levels of serum creatinine (10 mg/dL [normal:
0.7-1.5 mg/dL]), total bilirubin (3.5 mg/dL [normal: 0.1-1.2
mg/dL]), and transaminases (aspartate aminotransferase [AST] 171
U/L [normal: less than 54 U/L] and alanine aminotransferase [ALT]
1043 U/L [normal: less than 52 U/L]). Renal ultrasound detected no
evidence of hydronephrosis. Despite transient progression of his
renal failure, the patient did not require dialysis. He was
discharged from the hospital after 6 days with normal urine output,
a serum creatinine of 4 mg/dL and normal liver function.
     Patient 2. On October 30, 1994, a 41-year-old man who had
immigrated from Cambodia ate the raw gallbladders from three carp
he had caught at a reservoir near Cowonigo, Maryland. Two hours
after eating the gallbladders, he developed transient right upper
quadrant abdominal pain, nausea, vomiting, and diarrhea. On
November 3, he consulted his physician because of recurrent nausea,
abdominal pain, and decreased urinary output. Laboratory findings
were consistent with acute hepatitis (AST 1032 U/L, ALT 2028 U/L,
and total bilirubin 4.8 mg/dL) and acute renal failure (serum
creatinine 6.0 mg/dL). Abdominal ultrasound revealed normal-sized
kidneys; there was no evidence of urinary or biliary tract
obstruction. The patient was hospitalized for hemodialysis when, 5
days after his exposure, his serum creatinine increased to 12.6
mg/dL. The patient's renal and hepatic function gradually improved,
and he was discharged on November 16 with a serum creatinine of 8
mg/dL and markedly improved liver function.
Reported by: SJ Goldstein, MD, RM Raja, MD, M Kramer, MD, W Hirsch,
MD, Div of Nephrology, Albert Einstein Medical Center,
Philadelphia, Pennsylvania. EB May, PhD, Div of Fisheries, Maryland
Dept of Natural Resources, Oxford. Foodborne and Diarrheal Diseases
Br, Div of Bacterial and Mycotic Diseases, National Center for
Infectious Diseases, CDC.
Editorial Note: Despite the widespread use of basic public health
food safety and hygiene measures, clinicians and public health
practitioners have encountered an increasing diversity of foodborne
illnesses. Factors contributing to this trend include changes in
the technology of food production, greater importation of food from
other countries, and a diversification of food preparation and
eating habits.
     Although acute hepatitis and renal failure following ingestion
of raw carp gallbladders have not been reported previously in
persons in the United States, such cases have been recognized in
persons in Taiwan (1,2), Hong Kong (3), and South Korea (4).
Clinical manifestations of this syndrome include acute
gastrointestinal symptoms followed several days later by jaundice
and oliguria. Histologic studies of kidney and liver tissue
specimens from patients demonstrate acute tubular necrosis and
focal hepatitis (4). Although the bile component(s) responsible for
this syndrome have not been characterized fully (5), cyprinol, a
C27 alcohol found in the bile of cyprinid fish, may have a direct
toxic affect on the kidneys (1). No specific treatment has been
identified; renal and hepatic impairment generally resolve within
3 weeks with supportive care.
     Five species of fish belonging to the order Cypriniformes have
been associated with bile-induced hepatitis and renal failure (4).
Two of these species are found in the United States: the common
carp (Cyprinus carpio), which is abundant and widely distributed in
North America, and the grass carp (Ctenopharyngodon idellus), which
has been introduced in many areas in the eastern United States (J.
Sheferland, Chesapeake Bay Field Station, U.S. Fish and Wildlife
Service, personal communication, 1995). Because they can be caught
without limit, carp are an inexpensive food source used extensively
by some populations.
     The syndrome of bile-induced hepatitis and renal failure
described in this report, in addition to previous reports of
foodborne illnesses (e.g., trichinosis [6] and mushroom poisoning
[7]), suggest that clinicians should be aware of eating habits and
food exposures that may pose a risk for their patients. The cases
described in this report also underscore the importance of
obtaining careful food histories from patients, including those
whose illness may not initially appear to be food-related.
References
1. Chen WY, Yen TS, Cheng JT, Hsieh BS, Hsu HC. Acute renal failure
due to ingestion of raw bile of Grass Carp (Ctenopharyngodon
idellus). J Formosan Med Assoc 1976;75:149-57.
2. Lim PS, Lin JL, Hu SA, Huang CC. Acute renal failure due to
ingestion of the gallbladder of grass carp: report of 3 cases with
review of the literature. Renal Failure 1993;15:639-44.
3. Chan DWS, Yeung CK, Chan MK. Acute renal failure after eating
raw fish gall bladder. BMJ 1985;290:897.
4. Park SK, Kim DG, Kang SK, et al. Toxic acute renal failure and
hepatitis after ingestion of raw carp bile. Nephron 1990;56:188-93.
5. Yip LL, Chow CL, Yung KH, Chiu KW. Toxic material from the
gallbladder of the grass carp (Ctenopharyngodon idellus). Toxicon
1981;19:567-9.
6. CDC. Trichinella spiralis infection--United States, 1990. MMWR
1991;40:57-60.
7. CDC. Mushroom poisoning among Laotian refugees--1981. MMWR
1982;31:287-8.

Chancroid Detected by Polymerase Chain Reaction -- Jackson,
Mississippi, 1994-1995
     Chancroid is a sexually transmitted disease (STD) caused by
infection with Haemophilus ducreyi and is characterized by genital
ulceration. Chancroid is underreported in the United States (1),
reflecting, in part, difficulties in diagnosis because of clinical
similarities between chancroid and other ulcerative STDs. In
addition, laboratory confirmation by culture is 53%-84% sensitive
and often is unavailable in clinical settings (2). In September
1994, clinicians at the District V STD clinic of the Mississippi
State Department of Health (MSDH) in Jackson reported examining
patients with genital ulcers characteristic of chancroid but lacked
capacity to confirm the diagnosis. To determine the cause of the
ulcers, MSDH, in conjunction with CDC, conducted an investigation
of all patients with genital ulcers examined at the Jackson STD
clinic during October 20, 1994-February 1, 1995. This report
summarizes the findings of the investigation.
     Swab specimens were obtained from the genital ulcers of all
patients examined at the Jackson STD clinic. Specimens were tested
at an independent laboratory using a research prototype multiplex
polymerase chain reaction (PCR) assay that can amplify and
subsequently detect DNA from H. ducreyi, Treponema pallidum, and
herpes simplex virus (HSV) from a single swab specimen (3). All
positive PCR results were confirmed by additional PCR research
assays that amplify and detect different gene sequences. Serologic
testing included standard human immunodeficiency virus (HIV)
testing at the Mississippi State Public Health Laboratory.
     During October 20, 1994-February 1, 1995, a total of 81
patients with genital ulcers were examined at the clinic. Of these,
66 (82%) were male. The median age was 33 years (range: 16 years-81
years). Of the 81 patients, 41 (51%) had H. ducreyi infection
confirmed by PCR. For 33 patients, DNA sequences from H. ducreyi
only were identified; for seven, DNA sequences from H. ducreyi and
one other organism were identified; and for one, DNA sequences from
H. ducreyi and two other organisms were identified (Table 1, page
573). For 12 (15%) patients, no etiology was identified. Of 79
patients tested for HIV antibody, eight (10%) were positive.
     Because this investigation confirmed a high prevalence of
chancroid among persons with genital ulcers, MSDH now recommends
presumptive treatment for both syphilis and chancroid for all
patients in Jackson with nonherpetic genital ulcers and for their
sex partners. In March 1995, MSDH initiated statewide surveillance
for genital ulcers by requesting 25 public clinics and emergency
departments to record information about every patient with a
genital ulcer. In addition, a case-control study is under way in
Jackson to assess risk factors for chancroid, syphilis, and genital
herpes. MSDH plans to examine risk and health-seeking behaviors of
persons with genital ulcers and to provide additional
HIV-prevention services to these persons.
Reported by: RM Webb, MD, R Hotchkiss, MD, Div of Community Health
Svcs, M Currier, MD, State Epidemiologist, Mississippi State Dept
of Health; D Grillo, MD, P Byers, MD, D Jones, V Grant, District V
Health Dept, Jackson. JB Weiss, PhD, KA Orle, MS, Roche Molecular
Systems, Alameda, California. Epidemiology and Surveillance Br,
Behavioral Research and Intervention Br, and Program Development
and Support Br, Div of Sexually Transmitted Disease Prevention,
National Center for Prevention Svcs; Treponemal Pathogenesis and
Immunology Br, Div of Sexually Transmitted Diseases Laboratory
Research, National Center for Infectious Diseases, CDC.
Editorial Note: In the United States, H. ducreyi accounts for a
small proportion of genital ulcers. Although the number of reported
cases of chancroid has decreased every year since 1987, cases are
still reported from some large urban areas. In 1994, a total of 773
cases of chancroid were reported to CDC, including 357 from New
York City, 201 from New Orleans, 38 from Houston, and 36 from
Chicago (CDC, unpublished data, 1995). The investigation in
Jackson, Mississippi, suggests that a substantially greater number
of cases of chancroid occur than are reported. Based on sensitive
PCR testing, approximately half the cases of genital ulcers were
found to involve chancroid. Because chancroid is difficult to
diagnose by clinical and traditional laboratory means, it probably
is underdiagnosed and undertreated in many set-tings (1).
     Identification of chancroid is particularly important because
it is the STD most strongly associated with an increased risk for
HIV transmission (4,5). Without proper treatment, ulcers require
longer periods to heal, thereby prolonging for patients their
susceptibility to or risk for HIV transmission or acquisition.
     Chancroid should be considered in the differential diagnosis
of genital ulcers. Clinicians who suspect chancroid should confirm
the diagnosis by culture. Assistance can be obtained from state and
territorial public health laboratories or STD programs, which also
can contact CDC's Division of Sexually Transmitted Diseases
Laboratory Research, National Center for Infectious Diseases (fax
[404] 639-3976), or Epidemiology and Surveillance Branch, Division
of Sexually Transmitted Disease Prevention, National Center for
Prevention Services (fax [404] 639-8610). In communities in which
the prevalence of chancroid is high, patients with genital ulcers
should be treated presumptively for both chancroid and syphilis, as
recommended in the 1993 Sexually Transmitted Diseases Treatment
Guidelines (6).
     Syphilis and genital herpes, the two most common ulcerative
STDs in the United States, also have been associated with an
increased risk for HIV infection (7). In Jackson, a high proportion
of all patients with genital ulcers tested positive for HIV
antibodies. This finding underscores the need for health-care
personnel in other areas to evaluate the occurrence of HIV
infection among patients with genital ulcers and to target
HIV-prevention services toward persons and populations with or at
risk for ulcerative STDs.
References
1. Schulte JM, Martich FA, Schmid GP. Chancroid in the United
States, 1981-1990: evidence for underreporting of cases. MMWR
1992;41(no. SS-3):57-61.
2. Morse SA. Chancroid and Haemophilus ducreyi. Clin Microbiol Rev
1989;2:137-57.
3. Orle KA, Martin DH, Gates CA, Johnson SR, Morse SA, Weiss JB.
Multiplex PCR detection of Haemophilus ducreyi, Treponema pallidum,
and herpes simplex viruses types -1 and -2, from genital ulcers
[Abstract no. C-437]. In: Abstracts of the 94th general meeting of
the American Society for Microbiology. Washington, DC: American
Society for Microbiology, 1994.
4. Jessamine PG, Plummer FA, Achola JON, et al. Human
immunodeficiency virus, genital ulcers, and the male foreskin:
synergism in HIV-1 transmission. Scand J Infect Dis
1990;69(suppl):181-6.
5. Telzak EE, Chiasson MA, Bevier PJ, Stoneburner RL, Castro KG,
Jaffe HW. HIV-1 seroconversion in patients with and without genital
ulcer disease. Ann Intern Med 1993;119:1181-6.
6. CDC. 1993 Sexually transmitted diseases treatment guidelines.
MMWR 1993;42(no. RR-14).
7. Wasserheit JN. Epidemiological synergy: interrelationships
between human immunodeficiency virus infection and other sexually
transmitted diseases. Sex Transm Dis 1992;19:61-77.

Notice to Readers
Update: Recommendations to Prevent Hepatitis B Virus Transmission
-- United States
     In October 1994, the Advisory Committee on Immunization
Practices (ACIP) approved recommendations expanding the vaccination
strategy to eliminate hepatitis B virus (HBV) transmission in the
United States. These recommendations include:
     1. Vaccination of all unvaccinated children aged less than 11
years who are Pacific Islanders or who reside in households of
first-generation immigrants from countries where HBV is of high or
intermediate endemicity.
     2. Vaccination of all 11-12-year-old children who have not
previously received hepatitis B vaccine.
Reported by: Epidemiology and Surveillance Div, National
Immunization Program; Hepatitis Br, Div of Viral and Rickettsial
Diseases, National Center for Infectious Diseases, CDC.
Editorial Note: In November 1991, the ACIP recommended that
hepatitis B vaccine be integrated into infant vaccination schedules
(1). However, high rates of HBV infection continue to occur among
children aged 0-10 years who are Alaskan Natives, Pacific
Islanders, and infants of first-generation immigrant mothers from
areas where HBV infection is of high or intermediate endemicity.
Among children in these populations, the prevalence of chronic HBV
infection ranges from 2%-5%, and infection rates average 2% per
year (2,3). These infections occur in children born to women who
are hepatitis B surface antigen-negative and account for a large
proportion of the chronic HBV infections that occur each year in
the United States. Of the estimated 1 million Asian and Pacific
Islander children aged 2-10 years in the United States, less than
10% have received hepatitis B vaccine. Special efforts should be
made to ensure hepatitis B vaccination of these populations because
of their high risk for chronic HBV infection and death from
HBV-related chronic liver disease.
     Routine infant hepatitis B vaccination is the most effective
means to prevent HBV transmission in the United States. The effect
of routine infant vaccination on acute disease incidence may not be
apparent for 20-30 years because currently most infections occur
among young adults. Vaccination of previously unvaccinated children
at age 11-12 years should result in a more rapid decline in the
incidence of HBV infection. However, adolescent hepatitis B
vaccination should not supplant vaccination of infants, because
routine infant hepatitis B vaccination would eventually eliminate
the need for adolescent and adult vaccination.
     Vaccination recommendations are most effective when they
become integrated into routine health care. Although preventive
health services and vaccination visits for adolescents are not well
established in the United States, hepatitis B vaccination of this
age group has been successful in settings including schools and
clinical practices (4,5). The ACIP has recommended that hepatitis
B vaccination of adolescents be done as part of a routine
adolescent vaccination visit at age 11-12 years. This visit should
be used to ensure that all adolescents have received three doses of
hepatitis B vaccine, two doses of measles-mumps-rubella vaccine, a
booster dose of tetanus and diphtheria toxoids, and to assess
whether adolescents are immune to varicella. The establishment of
an adolescent vaccination visit provides the opportunity to deliver
preventive health-care services to this underserved population.
References
1. Mahoney FJ, Lawrence M, Scott K, Le Q, Lambert S, Farley T.
Continuing risk for hepatitis B virus transmission among Southeast
Asian infants in Louisiana. Pediatrics (in press).
2. Hurie MB, Mast EE, Davis JP. Horizontal transmission of
hepatitis B virus infection to United States-born children of Hmong
refugees. Pediatrics 1992;89:269-73.
3. CDC. Hepatitis B virus: a comprehensive strategy for eliminating
transmission in the United States through universal childhood
vaccination--recommendations of the Immunization Practices Advisory
Committee (ACIP). MMWR 1991;40(no. RR-13).
4. CDC. Hepatitis B vaccination of adolescents--California,
Louisiana, and Oregon, 1992-1994. MMWR 1994;43:605-9.
5. Kollar LM, Rosenthal SL, Biro FM. Hepatitis B vaccine series
compliance in adolescents. Pediatr Infect Dis J 1994;13:1006-8.

Notice to Readers
Availability of Applications for Public Health Leadership Institute
     The CDC/University of California Public Health Leadership
Institute (PHLI) is a 1-year scholars' program that includes an
intensive on-site week, scheduled for March 18-23, 1996. The PHLI
is conducted under a cooperative agreement between CDC's Public
Health Practice Program Office and the University of California at
Los Angeles. The fifth year of the PHLI will begin on October 30,
1995, with an orientation for scholars at the American Public
Health Association annual meeting in San Diego.
     Senior state, local, and international health officials,
including deputy directors nominated by state health directors, are
eligible. Applications must be submitted by August 31, 1995.
Selected scholars will be notified by September 25, 1995.
Additional information and applications are available from the
Director, PHLI, telephone (510) 649-1599.