Infectious Disease Epidemiology - Objectives of hepatitis C ...

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  • The average incubation period for hepatitis A is 30 days, with a range of 15 to 50 days. Patients characteristically have abrupt onset of symptoms which can include fever, malaise, anorexia, nausea, abdominal discomfort, dark urine, and jaundice. The severity of clinical disease associated with HAV infection increases with increasing age; jaundice occurs among less than 10% of children younger than 6 years of age, 40%-50% of older children, and 70%-80% of adults. Complications of hepatitis A include fulminant hepatitis, in which the case fatality rate can be greater than 50% despite medical interventions such as liver transplantation; cholestatic hepatitis, with very high bilirubin levels that can persist for months; and relapsing hepatitis, in which exacerbations can occur weeks to months after apparent recovery. Chronic infection does not occur following HAV infection.
  • The diagnosis of acute HAV infection is confirmed during the acute or early convalescent phase of infection by the presence of IgM antibodies to HAV (IgM anti-HAV). IgM anti-HAV is generally present 5-10 days before the onset of symptoms and is no longer detectable in the vast majority of patients 6 months later. IgG anti-HAV, which also appears early in the course of infection, remains detectable for the lifetime of the individual and confers lifelong protection against infection. Commercial tests are available for the detection of IgM and total (IgM and IgG) anti-HAV in serum.
    In infected persons, HAV replicates in the liver, is excreted in bile, and is shed in the stool. Peak infectivity occurs during the 2-week period before onset of jaundice or elevation of liver enzymes, when the concentration of virus in stool is highest. The concentration of virus in stool declines after jaundice appears. Children and infants can shed HAV for longer periods than adults, up to several months after the onset of clinical illness. Chronic shedding of HAV in feces does not occur; however, shedding can occur in persons who have relapsing illness. Viremia occurs soon after infection and persists through the period of liver enzyme (alanine aminotransferase [ALT]) elevation.
    HAV RNA can be detected in the blood and stool of most persons during the acute phase of infection by using nucleic acid amplification methods, such as PCR, and nucleic acid sequencing has been used to determine the relatedness of HAV isolates. These methods, however, are available in only a limited number of research laboratories and are not used generally for diagnostic purposes.
  • Trends in acute viral hepatitis can be monitored through cases reported to surveillance systems using a standard case definition. The surveillance case definition for acute hepatitis A includes both clinical and laboratory criteria. The clinical criteria consist of an acute illness with discrete onset of symptoms AND presentation of jaundice OR elevated liver enzymes. The laboratory criterion is IgM anti-HAV positivity. In addition, the case definition can be met if the person meets the clinical criteria and had an epidemiological link with a person who has laboratory-confirmed hepatitis A (i.e., household or sex contact with an infected person during the 15-50 days before the onset of symptoms). All patients who meet this case definition should be reported to the local or state health department. Case reports of acute hepatitis A are then transmitted weekly by state health departments to CDC via the National Electronic Telecommunications System for Surveillance (NETSS).
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    Feces can contain up to 108 infectious virions per milliliter and are the primary source of HAV. Viremia occurs during the preclinical and clinical phases of illness, and HAV has been transmitted by transfusion (before screening of blood and blood products for HAV was initiated) and by injection drug use. Virus has also been found in saliva and urine during the incubation period in experimentally infected animals, but transmission by saliva or urine has not been reported to occur.
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    Transmission of HAV generally occurs when susceptible persons put anything in their mouths that has been contaminated with the feces of an infected person. Close personal contact is the most common mode of HAV transmission, as demonstrated by infections among household and sex contacts of persons with hepatitis A and among children in day-care center outbreaks. Contaminated food and water can also serve as vehicles of HAV transmission. HAV transmission can occur when an infected food handler directly handles uncooked or cooked foods. Outbreaks have also been reported in association with foods contaminated before wholesale distribution, such as fresh vegetables contaminated at the time of harvesting or processing. HAV transmission can occur as a result of blood exposures such as injecting drug use or blood transfusion because viremia can occur prior to the onset of illness in infected persons. Screening of blood products for HAV has essentially eliminated the already extremely low risk associated with transfusion.
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    Worldwide, four different patterns of HAV transmission can be defined on the basis of age-specific seroprevalence data. In general, these transmission patterns correlate with socioeconomic and hygienic conditions. In many developing countries where environmental sanitation is generally poor, nearly all children have evidence of prior HAV infection. In these highly endemic areas, outbreaks rarely occur, but the frequency of clinically recognized disease due to HAV infection varies. In some areas, disease rates might be high because of the pervasiveness of the virus in the environment. As hygienic conditions improve, transmission shifts to older age groups and the incidence of clinically evident disease increases. In most industrialized countries, low levels of endemic HAV transmission occur. Because most of the population is susceptible to HAV infection in these industrialized countries, clinically apparent disease is recognized and outbreaks occur. In a few countries, primarily in Scandinavia, hepatitis A outbreaks are uncommon, and nearly all HAV transmission occurs among illegal drug users and travelers to high or intermediate endemic areas.
  • From 1990 through 2000, the most frequently reported source of infection was personal contact (household or sex) with an infected person (14%). Two percent of cases involved a child or employee in day-care; 6% of cases were a contact of a child or employee in day-care; 5% of cases reported recent international travel; and 4% of cases reported being part of a recognized foodborne outbreak. Injection drug use was a reported risk factor in 6% of cases; men who have sex with men represented 10% of cases. Forty-six percent of reported hepatitis A cases could not identify a risk factor for their infection.
    Note: Risk factor percentages rounded to nearest percent
  • Good hygienic practices and adequate sanitation are important elements in the prevention of HAV infection, particularly in the developing world. However, hepatitis A vaccine is the key component in the overall strategy to prevent HAV infection in the United States. Immune globulin is also available for pre-exposure and post-exposure prophylaxis.
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    IG is a sterile preparation of concentrated antibodies made from pooled human plasma. IG provides protection against hepatitis A through passive transfer of antibody. IG is 80%‑90% effective in preventing clinical hepatitis A when administered before exposure or early in the incubation period after exposure. IG can be used for pre-exposure prophylaxis for travelers to areas of high or intermediate endemicity of hepatitis A, particularly when the planned departure is less than 2-4 weeks later. In this situation, immunity from vaccination might not have developed by the time of departure. Post-exposure prophylaxis with IG is effective if administered within 14 days of exposure. The primary routine indication for post-exposure prophylaxis is for household or other intimate contacts of persons with hepatitis A. In addition, post-exposure prophylaxis might be indicated when hepatitis A cases occur in some institutional settings (e.g., child day-care centers) and after some common source exposures (e.g., persons who ate food prepared by an infected food handler). Local and/or state health departments should be consulted regarding the use of IG for post-exposure prophylaxis in these settings.
  • The two inactivated vaccines licensed in the United States, HAVRIX® * (manufactured by GlaxoSmithKline) and VAQTA® * (manufactured by Merck & Co., Inc.), are highly immunogenic. Approximately 97%-100% of children, adolescents, and adults develop protective levels of antibody within 1 month after the first dose of vaccine; essentially 100% of vaccinees develop protective antibody with high geometric mean concentrations after completing the two-dose series. The vaccines are highly efficacious: In published studies, 94%-100% of children were protected against clinical hepatitis A after receiving the equivalent of one dose.
    *Use of trade names is for identification only and does not imply endorsement by the Public Health Service or the U.S. Department of Health and Human Services.
  • This slide depicts hepatitis A incidence from 1980 to 2002. In 1995, hepatitis A vaccine was licensed by the FDA and became available in the United States. In 1996, the ACIP published the first national recommendations for vaccine use in hepatitis A prevention. These recommendations were updated and extended in 1999. Hepatitis A incidence has been falling, beginning in 1998, to below recorded historical lows, even compared with national hepatitis surveillance that was first begun in the 1960s. The provisional 2002 rate of 2.9 per 100,000 represents a 67% decline from the previously recorded lowest rate of 8.9 cases per 100,000 in 1983.
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    The change in incidence from the baseline period to 2002 can be seen dramatically in this state and county map of the United States. During the baseline period of 1987-1997, there were many counties, particularly in the west, with rates averaging 20 or more cases per 100,000. By 2002, there were few counties with rates of 5 or more cases per 100,000.
  • Infectious Disease Epidemiology - Objectives of hepatitis C ...

    1. 1. Epidemiology of Infectious Diseases Catherine Diamond MD MPH UCI Infectious Diseases & Epidemiology Divisions (714) 456-7612 diamondc@uci.edu
    2. 2. Surveillance  Routine collection, analysis & reporting of data monitoring morbidity & mortality trends for public health purposes  Active: agency actively contacts hospitals/MDs on a regular basis to find cases  Passive: agency receives reports from hospitals/MDS  Sentinel systems: certain MDs or hospitals report designated cases in order to catch trends early
    3. 3. Trends  Secular trend: a change in the prevalence of infection over years, usually due to better living conditions, better hygiene & vaccination, e.g. decrease in TB in US  Seasonal trend: refers to changes in the prevalence of infection occurring over the year, e.g. influenza outbreaks. Changes of temperature, crowding, humidity may play a role
    4. 4. Endemic vs. Epidemic vs. Pandemic  Endemic infection-infection or disease that occurs regularly at low to moderate frequency  Epidemics occur when there are sudden increases in frequency in frequency above endemic levels  Pandemics are global epidemics, an epidemic occurring over a wide area & usually affecting a large portion of the population. The size of outbreaks is dependent on factors such as the ratio of susceptible to immune subjects, period of infectivity, population density etc
    5. 5. What is an Outbreak?  The occurrence of cases of an illness clearly in excess of expectancy  Usually compare current number of cases with the number over a comparable period sometime in the past an increase in the number of cases over past experience for a given population, time & place  Must take into account seasonal variations in disease incidence for diseases such as influenza
    6. 6. Three Common Conditions for the Occurrence of an Epidemic or Outbreak 1. The introduction a new pathogen, or the increased amount of or change in virulence of a known pathogen from an infected human, animal, bird or arthropod vector or from air, water, food, soil, drug or other environmental source 2. An adequate number of exposed & susceptible persons 3. An effective means of transmission between the source of the pathogen & the susceptible persons
    7. 7. Why Should We Study Outbreak Investigations?  Outbreaks are important public health events  Outbreaks are experiments of nature & allow the opportunity to learn more about the natural history of disease  Outbreaks represent breakdowns in public health  You might end up investigating an outbreak someday  Outbreaks are real life examples of practical applications of epidemiologic methods  Outbreaks are interesting
    8. 8. What Are the Steps in a Outbreak Investigation? 1. Verify the diagnosis 2. Confirm the existence of an outbreak 3. Identify & count cases (establish case definition) 4. Orient data in terms of time, place & person 5. Formulate & test hypotheses 6. Identify & implement control measures
    9. 9. Steps in an Outbreak Investigation  Different investigators may have slightly different lists of steps  The logistics of preparing for an outbreak investigation could be considered as one of the steps  The steps are not necessarily carried out exactly in the order listed
    10. 10. Step 1: Verify the Diagnosis  Is it an epidemic? Be certain it is real & not a false alarm ( pseudoepidemic)  In hospital setting, pseudoepidemics may be due to false positive diagnosis resulting from contamination e.g. environmental contamination of specimens during laboratory processing  In contrast, there may also be artifactual clustering of real cases, e.g. change in reporting due to change in diagnostic methods, new physician/clinic in town, changes in local/national awareness. HIV/AIDS examples
    11. 11. Step 2: Confirm the Existence of an Outbreak  Compare the magnitude of the current problem with baseline  Problems with determining baselines  Lack of data  Varying or no case definition  Incomplete reporting, lack of surveillance
    12. 12. Step 3: Identify & Count Cases  Case definition usually specifies a person with:  Some set of symptoms or signs or laboratory diagnosis  Occurring in some time period  In some specific setting  Remember spectrum of disease (you may want to include asymptomatic/subclinical cases since information about them may be crucial to investigation)
    13. 13. Secondary Cases  Consider whether you want to include secondary cases.  Secondary cases are persons who were infected as a result of exposure to a primary case  E.g. in a food borne outbreak of E coli 0157: H7 primary cases were infected by consumption of contaminated hamburger & secondary cases would be infected through exposure to a primary case (e.g. in a day care)  These secondary cases were not exposed to the source of the outbreak & their inclusion in the risk factor analysis would tend to bias toward the null  In many cases it is desirable to look for secondary cases & collect information on them but not include them in the primary analysis
    14. 14. Evolving Case Definitions  Patients may not have laboratory tests because the tests are expensive, difficult to obtain or clinically not necessary  Early on, investigators use a loose case definition which includes confirmed, probable & even possible cases  Later a tighter case definition may increase the ability to detect a true association  Ideally your case definition will include most if not all of the actual cases & very few or no false positive cases
    15. 15. Definite vs. Probable vs. Possible Cases  Definite case: laboratory confirmation  E.g. E coli 0157:H7 isolated from stool culture in a resident of the county with onset of symptoms during a specified time period  Probable case: typical clinical features without laboratory confirmation  Bloody diarrhea with same person, place & time restrictions  Possible case: fewer of the typical clinical features  Abdominal cramps & diarrhea with the same person, place & time restrictions
    16. 16. Identify Cases 1. Conduct a systematic search a. Cast a wide net regarding geography & population b. The original cases may or may not be representative of the true extent of the problem 2. Use multiple sources which may include a. Medical systems: hospitals, laboratories, physician's office, clinics b. Surveillance data c. Media/press announcements d. Special surveys e.g. if outbreak involved a defined population such as persons on a cruise ship you could survey that entire population
    17. 17. Step 4: Orient Data in Terms of Time, Place & Person  Characterize the cases in terms of time, place & person:  Time: draw epidemic curves  Place: construct spot maps  Person: compare groups
    18. 18. Time & Outbreaks: The Epidemic Curve  An epidemic curve is a graph of the distribution of cases according to time of onset. From the curve you can tell:  Where you are in the time course of an epidemic (e.g. beginning, middle, end)  From the pattern of the curve, you may be able to draw inferences about the mode of spread of the causative agent ( e.g. person- to-person, common source)
    19. 19. Common Source or Point Outbreaks  Common source or point outbreaks refer to the exposure of a susceptible population to a common source of a pathogen often at the same time, such as at a church picnic or neighborhood restaurant  These most frequently result in a short, sharp epidemic curve with cases clustered around single defined peak value. If the agent is transmissible to other by person to person contact then secondary peaks may occur
    20. 20. Common Source or Point Outbreaks  For a common source exposure, if you have identified the disease & know its usual incubation period (the time interval between exposure to an infectious agent & the appearance of the first signs or symptoms of disease) , you can estimate a probable time period of exposure & use that information to focus your investigation  The minimum incubation time should correspond to the interval between exposure & the first case  The average incubation period should correspond to the interval between exposure & the peak of the outbreak or the time occurrence of the median case
    21. 21. Types of Epidemic Curves  The commercial distribution of food through many states or a chain of stores has created a new form of common source epidemic in which the time & pattern of delivery, purchase & consumption in a local area define the nature of the epidemic  If exposure occurs over different times, the epidemic curve can spread out continuously
    22. 22. Figure 1. Outbreak-Associated Confirmed Cases of S. enteritidis Infection in Minnesota in September and October 1994, According to the Date of Onset. One hundred fifty cases were reported.
    23. 23. Propagative Epidemic Curves  Propagative or progressive epidemic curves result from epidemics involving the spread of a pathogen from one susceptible individual to another e.g. measles, influenza- frequently occur in propagative epidemics  Curve with some clusters of irregular peaks & somewhat spread out is consistent with person to person spread  Mixed epidemics involve both a single, common exposure to an infectious agent & secondary propagative spread to other individuals e.g. many food borne pathogens (Salmonella, Hepatitis A) & airborne organisms (TB)  Mixed type of curves such as a single large peak followed by successive smaller peaks may be seen when a common source outbreak occurs followed by secondary person to person spread
    24. 24. Place of Outbreak: Spot Maps  Demonstrate geographic extent of the problem  Demonstrate cluster or pattern illustrating where cases live, work or may have been exposed  Most famous example of a spot map is John Snow’s spot map of the distribution of cholera cases around the Broad Street pump
    25. 25. Distribution of Cholera Deaths in Golden Square Area of London August-September 1848
    26. 26. Characterize Cases  Characterize the cases completely & systematically by developing a questionnaire before the patients are contacted. Collect:  Identifying information: Name, address, telephone number  Demographic information: Age, sex, race, occupation  Clinical information: symptoms, date of onset, medical evaluation  Risk factor information: depends on the disease being investigated
    27. 27. Personal Characteristics & Outbreaks  The case group must be thoroughly described in terms of age, race, sex, occupation, diagnosis & other factors  Rates are then calculated to identify high risk groups  E.g. age, sex (HIV), occupation (HCW)
    28. 28. Step 5: Formulate & Test Hypotheses  Generate hypotheses to explain outbreak  Usually conduct a case control or cohort study  Consider evidence for causation
    29. 29. Cohort vs. Case Control Study Design  In cohort study, you have knowledge of entire population (e.g. can count how many individuals were exposed and how many were infected)  Can compare attack rate in the exposed and unexposed  Can calculate RR (incidence in exposed/incidence in unexposed)  But often only have information regarding some of the population and then need to use a case control design  Can compare proportion of cases and proportion of controls eating food item  Can calculate OR (AD/ BC)
    30. 30. Coccidiodomycosis Outbreak Following Northridge Earthquake  39% of cases vs. 17% of controls reported physically being in a dust cloud OR 3.0 (95% CI 1.6-54). Duration of time spent in dust cloud correlates with OR:  0 minutes OR 1.0  1-15 minutes OR 1.7  16-30 minutes OR 3.0  >30 minutes OR 5.2
    31. 31. Causation  Strength of the association. The stronger the association, the more likely it is real  Consistency with other studies. A consistent finding is more plausible  Exposure precedes disease  Dose-response effect (not mandatory but adds credibility)  Biologic plausibility  Removal of agent decreases or eliminates disease
    32. 32. Attack Rate  Attack rate is an incidence rate  Used when occurrence of disease among a population at risk increases greatly over short period of time, often related to a specific exposure  The disease rapidly follows the exposure during a fixed time period  Often used for food borne illness  Attack rate= ill X 100 during a time period (ill + well)
    33. 33. Secondary Attack Rate  Secondary attack rate yields an index of the spread of disease within a household or similar circumscribed unit  The secondary attack rate is used to measure infectivity: the capacity of the agent to enter & multiply in a susceptible host & thus produce infection or disease
    34. 34. Case Fatality Rate  Case fatality rate: the number of deaths caused by a disease among people who have the disease  An index of the deadliness of a particular disease  CFR= # of deaths due to disease X X 100 # of cases due to disease X
    35. 35. Step 6: Implementing Control & Prevention Measures  Eliminating or treating the source-e.g. removing an infected foodhandler from work & treating appropriately  Cohorting patients- a common approach in hospitals, childcare & other institutional setting  Preventing further exposures-e.g. as in the HIV/AIDS epidemic through educational efforts to change knowledge & behaviors  Protecting the population at risk- e.g. through vaccination  System changes. For example, changing the method by which meat inspection is conducted to decrease the risk of contamination with E coli 0157:H7
    36. 36. Use of Molecular Subtyping in Infectious Disease in Infectious Disease Outbreak  Molecular subtyping of patient & source outbreaks has become an increasingly important part of outbreak investigations  Many methods of subtyping including pulsed field gel electrophoresis (PFGE) & restriction fragment length polymorphism (RFLP)  Within a species of infectious agents, there are multiple strains with different genetic compositions. Subtyping techniques attempt to determine the degree of genetic relatedness of different isolates  Outbreaks are nearly always caused by a single strain of the causative organism & thus termed clonal  Subtyping of isolates can be used to determine whether the isolated involved are closely related & are therefore likely to be associated with a common source  The results of subtyping can be applied to the case definition  Subtyping is usually not immediately available & thus is not used in the initial case definition but may be incorporated in later analysis
    37. 37. Case Scenario  You are the county epidemiologist in a county on the Pennsylvania/Ohio border  Between November 13 & December 3, 26 cases of hepatitis are reported to your county health department  Although you just started working there, this seems like a lot to you! You decide to investigate…
    38. 38. Step 1: Verify the Diagnosis  How would you verify the diagnosis of Hepatitis A?
    39. 39. Step 1: Verify the Diagnosis  Review clinical & laboratory features of the cases to determine if they are consistent with the diagnosis of hepatitis A
    40. 40. HEPATITIS A CLINICAL FEATURES •Jaundice by <6 yrs <10% age group: 6-14 yrs 40%-50% >14 yrs 70%-80% •Rare complications: Fulminant hepatitis Cholestatic hepatitis Relapsing hepatitis •Incubation period: Average 30 days Range 15-50 days •Chronic sequelae: None
    41. 41. 0 1 2 3 4 5 6 7 8 9 10 11 12 13 Week Response Clinical illness ALT IgM IgG HAV in stool Infection Viremia EVENTS IN HEPATITIS A VIRUS INFECTION
    42. 42. Step 2: Confirm the Existence of an Outbreak  How would you confirm the existence of an outbreak?
    43. 43. Step 2: Confirm the Existence of an Outbreak  Compare the number of cases against historical numbers  Between November 13 & December 3, 26 cases of Hepatitis A were reported to the county health department compared with 1 case in the previous 4 months  FYI in Orange County in 2002, there were 91 reported cases of hepatitis A (3.1 cases per 100,000 population)
    44. 44. Step 3: Identify & Count Cases  What would be your case definition?  How would you identify cases?  Would you include secondary cases?
    45. 45. ACUTE HEPATITIS A CASE DEFINITION FOR SURVEILLANCE  Clinical criteria An acute illness with: • discrete onset of symptoms (e.g. fatigue, abdominal pain, loss of appetite, intermittent nausea, vomiting), & • jaundice or elevated serum aminotransferase levels  Laboratory criteria • IgM antibody to hepatitis A virus (anti-HAV) positive  Case Classification • Confirmed. A case that meets the clinical case definition & is laboratory confirmed or a case that meets the clinical case definition & occurs in a person who has an epidemiologic link with a person who has laboratory-confirmed hepatitis A (i.e., household or sexual contact with an infected person during the 15-50 days before the onset of symptoms)
    46. 46. Step 3: Identify & Count Cases  Case definition: defined as a person with discrete symptom onset between November 13 & December 4 in association with the presence of IgM antibody to HAV in your county
    47. 47. Step 3: Identify & Count Cases  Identify cases:  State health department requests counties to immediately report all HAV cases  The county contacts all county physicians, hospitals, laboratories & neighboring county & state health departments to rapidly report cases  Advertisements/media/signs  Secondary cases might bias toward the null; could collect early on but might not include in analysis
    48. 48. Step 4: Orient Data in Terms of Time, Place & Person  What would the epidemic curve look like?  What would a spot map look like?  Are there specific demographic or other characteristics of the cases?
    49. 49. Step 4: Orient Data in Terms of Time, Place & Person  A spot map would likely show more cases in the geographic area nearest the restaurant  Presumably cases would reflect the demographics of restaurant goers, patients with symptomatic hepatitis A & residents of the county  22 (51%) were male  Median age 34 years (range 5-66)  All were white  14 (33%) hospitalized  No travel, injection drug use or male- male sex
    50. 50. Step 5: Formulate & Test Hypotheses  What do you hypothesize is the cause of the outbreak?  How would you collect data to prove this hypothesis?  How would you analyze data to validate your hypothesis?
    51. 51. Step 5: Formulate & Test Hypotheses  Infected food product vs. infected employee  The CDC Viral Hepatitis Surveillance Program Questionnaire  Case control study  Genetic relatedness of hepatitis A sequence.
    52. 52. Food Item Case Control OR Green Onions 38/40 (95) 30/60 (50%) 12.7 (2.6-60.1) Diced Tomatoes 12/38 (31) 8/64 (13) 3.0 (1.1-8.4) With green onions 8/40 (20) 3/64 (5) 4.8 (1.1-22.4) Without green onions 5/39 (13) 5/64 (8) 1.9 (0.5-6.9) Honey Mustard Sauce 7/39 (18) 3/64 (5) 6.4 (1.3-31.8) With green onions 4/40 (10) 1/64 (2) 8.0 (0.9-71.6) Without green onions 3/38 (8) 2/64 (3) 2.9 (0.5-17.5)
    53. 53. CONCENTRATION OF HEPATITIS A VIRUS IN VARIOUS BODY FLUIDS Source: Viral Hepatitis and Liver Disease 1984;9-22 J Infect Dis 1989;160:887-890 Feces Serum Saliva Urine 100 102 104 106 108 1010 BodyFluids Infectious Doses per mL
    54. 54. • Close personal contact (e.g., household contact, sex contact, child day-care centers) • Contaminated food, water (e.g., infected food handlers) • Blood exposure (rare) (e.g., injection drug use, rarely by transfusion) • No risk factor identified for 40%-50% of cases HEPATITIS A VIRUS TRANSMISSION
    55. 55. Endemicity Diseas e Rate Peak Age of Infection Transmission Patterns Early childhood Late childhood/ young adults Young adults High Moderate Low Very low Low to high High Low Very low Adult s Person to person; outbreaks uncommon Person to person; food & waterborne outbreaks Person to person; food & waterborne outbreaks Travelers; outbreaks uncommon GLOBAL PATTERNS OF HEPATITIS A VIRUS TRANSMISSION
    56. 56. Unknown 46% Contact of day- care child/employee 6% Other Contact 8% Child/employee in day-care 2% Food- or waterborne outbreak 4% Injection drug use 6% Sexual or Household Contact 14% Men who have sex with men 10% International travel 5% RISK FACTORS ASSOCIATED WITH REPORTED HEPATITIS A, 1990-2000, UNITED STATES Source: NNDSS/VHSP
    57. 57. Cause of the HAV Epidemic  Green onions grown & processed in Mexico then shipped on ice to US restaurant where they are chopped and placed raw in giant vats of mild salsa  Possible contact with HAV-infected workers especially children working in the field during green onion harvesting/preparation  Possible contact with HAV-contaminated water during irrigation, rinsing, icing
    58. 58. Step 6 Implementing Control & Prevention Measures  What control measures would you implement?  How would you prevent future cases?
    59. 59. Step 6 Implementing Control & Prevention Measures  Control  Immunoglobulin  Close restaurant  Prevention  Vaccination  Public health announcements to avoid raw green onions  Agricultural quality control  Water quality for irrigation  Provide sanitary facilities for field workers  Child-care for field workers  Prevent HAV transmission
    60. 60. PREVENTING HEPATITIS A • Hygiene (e.g., hand washing) • Sanitation (e.g., clean water sources) • Hepatitis A vaccine (pre-exposure) • Immune globulin (pre- & post-exposure)
    61. 61.  Pre-exposure  travelers to intermediate & high HAV-endemic regions  Post-exposure (within 14 days) Routine  household & other intimate contacts Selected situations  institutions (e.g., day-care centers)  common source exposure (e.g., food prepared by infected food handler) HEPATITIS A PREVENTION IMMUNE GLOBULIN
    62. 62. • Highly immunogenic • 97%-100% of children, adolescents, & adults have protective levels of antibody within 1 month of receiving first dose; essentially 100% have protective levels after second dose • Highly efficacious • In published studies, 94%-100% of children protected against clinical hepatitis A after equivalent of one dose HEPATITIS A VACCINES
    63. 63. Hepatitis A Incidence, United States, 1980-2002* 0 4 8 12 16 1980 '85 1990 '95 2000 Year Cases/100,000 1999 ACIP recommendations 2002 rate* = 2.9 1996 ACIP recommendations 1995 vaccine licensure *2002 rate provisional
    64. 64. rate per 100,000 0-4 5-9 10-19 >=20 DC NYC 1987-97 average incidence 2002 incidence > = 20 10 - 19 5 - 9 0 - 4 Rate per 100,000 rate per 100,000 0-4 5-9 10-19 >=20 DC NYC Hepatitis A Incidence
    65. 65. Conclusion  Step 1: Verify the diagnosis  Step 2: Confirm the existence of an outbreak  Step 3: Identify & count cases  Step 4: Orient data in terms of time, place & person  Step 5: Formulate & test hypothesis  Step 6: Implementing control & prevention measures
    66. 66. Acknowledgements  Lisa Jackson, MD MPH University of Washington for lecture outline  HAV slides from CDC website www.cdc.gov  Dentinger et. al. An Outbreak of Hepatitis A Associated with Green Onions. J. Infect Dis 2001; 183: 1273-6.  CDC. Hepatitis A Outbreak Associated with Green Onions at a Restaurant- Monaca, PA, 2003. MMWR 2003; 52: 1155-1157.

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