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 -------------------------------------------------------------- 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.