Summary of Notifiable Diseases --- United States, 2009

Prepared by

Patsy A. Hall-Baker, Coordinator, Summary of Notifiable Diseases1

Samuel L. Groseclose, DVM, MPH, Acting Division Director1

Ruth Ann Jajosky, DMD1

Deborah A. Adams1

Pearl Sharp1

Willie J. Anderson1

John P. Abellera, MPH1

Aaron E. Aranas, MPH, MBA1

Michelle Mayes1

Michael S. Wodajo1

Diana H. Onweh1

Meeyoung Park2

Jennifer Ward 1

1Division of Notifiable Diseases and Healthcare Information (proposed), the Office of Surveillance, Epidemiology, and and Laboratory Services, CDC

2McKing Consulting Corporation

Preface

The Summary of Notifiable Diseases--- United States, 2009 contains the official statistics, in tabular and graphic form, for the reported occurrence of nationally notifiable infectious diseases in the United States for 2009. Unless otherwise noted, the data are final totals for 2009 reported as of June 30, 2010. These statistics are collected and compiled from reports sent by state health departments and territories to the National Notifiable Diseases Surveillance System (NNDSS), which is operated by CDC in collaboration with the Council of State and Territorial Epidemiologists (CSTE). The Summary is available at http://www.cy118119.com/mmwr/summary.html. This site also includes Summary publications from previous years.

The Highlights section presents noteworthy epidemiologic and prevention information for 2009 for selected diseases and additional information to aid in the interpretation of surveillance and disease-trend data. Part 1 contains tables showing incidence data for the nationally notifiable infectious diseases reported during 2009.* The tables provide the number of cases reported to CDC for 2009 and the distribution of cases by month, geographic location, and the patients' demographic characteristics (age, sex, race, and ethnicity). Part 2 contains graphs and maps that depict summary data for certain notifiable infectious diseases described in tabular form in Part 1. Part 3 contains tables that list the number of cases of notifiable diseases reported to CDC since 1978. This section also includes a table enumerating deaths associated with specified notifiable diseases reported to CDC's National Center for Health Statistics (NCHS) during 2002--2007. The Selected Reading section presents general and disease-specific references for notifiable infectious diseases. These references provide additional information on surveillance and epidemiologic concerns, diagnostic concerns, and disease-control activities.

Comments and suggestions from readers are welcome. To increase the usefulness of future editions, comments regarding the current report and descriptions of how information is or could be used are invited. Comments should be sent to Data Operations Team--NNDSS, Division of Notifiable Diseases and Healthcare Information (proposed), Public Health Surveillance Program Office at soib@cdc.gov.

Background

The infectious diseases designated as notifiable at the national level during 2009 are listed in this section. A notifiable disease is one for which regular, frequent, and timely information regarding individual cases is considered necessary for the prevention and control of the disease. A brief history of the reporting of nationally notifiable infectious diseases in the United States is available at http://www.cy118119.com/ncphi/disss/nndss/nndsshis.htm. In 1961, CDC assumed responsibility for the collection and publication of data on nationally notifiable diseases. NNDSS is neither a single surveillance system nor a method of reporting. Certain NNDSS data are reported to CDC through separate surveillance information systems and through different reporting mechanisms; however, these data are aggregated and compiled for publication purposes.

Notifiable disease reporting at the local level protects the public's health by ensuring the proper identification and follow-up of cases. Public health workers ensure that persons who are already ill receive appropriate treatment; trace contacts who need vaccines, treatment, quarantine, or education; investigate and halt outbreaks; eliminate environmental hazards; and close premises where spread has occurred. Surveillance of notifiable conditions helps public health authorities to monitor the effect of notifiable conditions, measure disease trends, assess the effectiveness of control and prevention measures, identify populations or geographic areas at high risk, allocate resources appropriately, formulate prevention strategies, and develop public health policies. Monitoring surveillance data enables public health authorities to detect sudden changes in disease occurrence and distribution, identify changes in agents and host factors, and detect changes in health-care practices.

The list of nationally notifiable infectious diseases is revised periodically. A disease might be added to the list as a new pathogen emerges, or a disease might be deleted as its incidence declines. Public health officials at state health departments and CDC collaborate in determining which diseases should be nationally notifiable. CSTE, with input from CDC, makes recommendations annually for additions and deletions. Although disease reporting is mandated by legislation or regulation at the state and local levels, state reporting to CDC is voluntary. Reporting completeness of notifiable diseases is highly variable and related to the condition or disease being reported (1). The list of diseases considered notifiable varies by state and year. Current and historic national public health surveillance case definitions used for classifying and enumerating cases consistently across reporting jurisdictions are available at http://www.cy118119.com/ncphi/disss/nndss/nndsshis.htm.

Infectious Diseases Designated as Notifiable at the National Level during 2009*

Anthrax

Arboviral diseases, neuroinvasive and nonneuroinvasive

California serogroup virus

Eastern equine encephalitis virus

Powassan virus

St. Louis encephalitis virus

West Nile virus

Western equine encephalitis virus

Botulism

foodborne

infant

other (wound and unspecified)

Brucellosis

Chancroid

Chlamydia trachomatis infections

Cholera

Coccidioidomycosis

Cryptosporidiosis†

Cyclosporiasis

Diphtheria

Ehrlichiosis/Anaplasmosis

Ehrlichia chaffeensis

Ehrlichia ewingii

Anaplasma phagocytophilum

Undetermined

Giardiasis

Gonorrhea

Haemophilus influenzae, invasive disease

Hansen disease (Leprosy)

Hantavirus pulmonary syndrome

Hemolytic uremic syndrome, post-diarrheal

Hepatitis, viral, acute

Hepatitis A, acute

Hepatitis B, acute

Hepatitis B virus, perinatal infection

Hepatitis C, acute

Hepatitis, viral, chronic

Chronic Hepatitis B

Hepatitis C virus infection (past or present)

Human Immunodeficiency Virus (HIV) diagnosis§

Influenza-associated pediatric mortality

Legionellosis

Listeriosis

Lyme disease

Malaria

Measles†

Meningococcal disease

Mumps

Novel influenza A virus infections

Pertussis

Plague

Poliomyelitis, paralytic

Poliovirus infection, nonparalytic

Psittacosis

Q fever†

Acute

Chronic

Rabies

Animal

Human

Rocky Mountain spotted fever

Rubella†

Rubella, congenital syndrome

Salmonellosis

Severe acute respiratory syndrome-associated coronavirus (SARS-CoV) disease

Shiga toxin-producing Escherichia coli (STEC)

Shigellosis

Smallpox

Streptococcal disease, invasive, Group A

Streptococcal toxic-shock syndrome

Streptococcus pneumoniae, drug resistant, all ages, invasive disease

Streptococcus pneumoniae, invasive disease non-drug resistant, in children aged <5 years

Syphilis

Syphilis, congenital

Tetanus

Toxic-shock syndrome (other than streptococcal)

Trichinellosis

Tuberculosis†

Tularemia

Typhoid fever

Vancomycin-intermediate Staphylococcus aureus (VISA) infection

Vancomycin-resistant Staphylococcus aureus (VRSA) infection

Varicella (morbidity)

Varicella (mortality)

Vibriosis

Yellow fever

Data Sources

Provisional data concerning the reported occurrence of nationally notifiable infectious diseases are published weekly in MMWR. After each reporting year, staff in state health departments finalize reports of cases for that year with local or county health departments and reconcile the data with reports previously sent to CDC throughout the year. These data are compiled in final form in the Summary.

Notifiable disease reports are the authoritative and archival counts of cases. They are approved by the appropriate chief epidemiologist from each submitting state or territory before being published in the Summary. Data published in MMWR Surveillance Summaries or other surveillance reports produced by CDC programs might not agree exactly with data reported in the annual Summary because of differences in the timing of reports, the source of the data, or surveillance methodology.

Data in the Summary were derived primarily from reports transmitted to CDC from health departments in the 50 states, five territories, New York City, and the District of Columbia. Data were reported for MMWR weeks 1--52, which correspond to the period for the week ending January 10, 2009, through the week ending January 2, 2010. More information regarding infectious notifiable diseases, including case definitions, is available at http://www.cy118119.com/ncphi/disss/nndss/nndsshis.htm. Policies for reporting notifiable disease cases can vary by disease or reporting jurisdiction. The case-status categories used to determine which cases reported to NNDSS are published by disease or condition and are listed in the print criteria column of the 2009 NNDSS event code list (Exhibit).

Final data for certain diseases are derived from the surveillance records of the CDC programs listed below. Requests for further information regarding these data should be directed to the appropriate program.

Office of Surveillance, Epidemiology and Laboratory Services

National Center for Health Statistics (NCHS)
Office of Vital and Health Statistics Systems (deaths from selected notifiable diseases)

Office of Infectious Diseases (Proposed)

National Center for HIV/AIDS, Viral Hepatitis, STD and TB Prevention
Division of HIV/AIDS Prevention (AIDS and HIV infection)
Division of STD Prevention (chancroid; Chlamydia trachomatis, genital infection; gonorrhea; and syphilis)
Division of Tuberculosis Elimination (tuberculosis)

National Center for Immunization and Respiratory Diseases
Influenza Division (influenza-associated pediatric mortality)
Division of Viral Diseases, (poliomyelitis, varicella [morbidity and mortality], and SARS-CoV)

National Center for Emerging and Zoonotic Infectious Diseases
Division of Vector-Borne Diseases (arboviral diseases)
Division of Viral and Rickettsial Diseases (animal rabies)

Population estimates for the states are from the NCHS bridged-race estimates of the July 1, 2000--July 1, 2008 U.S. resident population from the vintage 2008 postcensal series by year, county, age, sex, race, and Hispanic origin, prepared under a collaborative arrangement with the U.S. Census Bureau. This data set was released on September 2, 2009, and is available at http://www.cy118119.com/nchs/nvss/bridged_race.htm.

Populations for territories are 2008 estimates from the U.S. Census Bureau International Data Base, available at http://www.census.gov/ipc/www/idb/summaries.html. The choice of population denominators for incidence reported in MMWR is based on 1) the availability of census population data at the time of preparation for publication and 2) the desire for consistent use of the same population data to compute incidence reported by different CDC programs. Incidence in the Summary is calculated as the number of reported cases for each disease or condition divided by either the U.S. resident population for the specified demographic population or the total U.S. resident population, multiplied by 100,000. When a nationally notifiable disease is associated with a specific age restriction, the same age restriction is applied to the population in the denominator of the incidence calculation. In addition, population data from states in which the disease or condition was not notifiable or was not available were excluded from incidence calculations. Unless otherwise stated, disease totals for the United States do not include data for American Samoa, Guam, Puerto Rico, the Commonwealth of the Northern Mariana Islands, or the U.S. Virgin Islands.

Interpreting Data

Incidence data in the Summary are presented by the date of report to CDC as determined by the MMWR week and year assigned by the state or territorial health department, except for the domestic arboviral diseases, which are presented by date of diagnosis. Data are reported by the state in which the patient resided at the time of diagnosis. For certain nationally notifiable infectious diseases, surveillance data are reported independently to different CDC programs. For this reason, surveillance data reported by other CDC programs might vary from data reported in the Summary because of differences in 1) the date used to aggregate data (e.g., date of report or date of disease occurrence), 2) the timing of reports, 3) the source of the data, 4) surveillance case definitions, and 5) policies regarding case jurisdiction (i.e., which state should report the case to CDC).

Data reported in the Summary are useful for analyzing disease trends and determining relative disease burdens. However, reporting practices affect how these data should be interpreted. Disease reporting is likely incomplete, and completeness might vary depending on the disease and reporting state. The degree of completeness of data reporting might be influenced by the diagnostic facilities available, control measures in effect, public awareness of a specific disease, and the resources and priorities of state and local officials responsible for disease control and public health surveillance. Finally, factors such as changes in methods for public health surveillance, introduction of new diagnostic tests, or discovery of new disease entities can cause changes in disease reporting that are independent of the true incidence of disease.

Public health surveillance data are published for selected racial/ethnic populations because these variables can be risk markers for certain notifiable diseases. Race and ethnicity data also can be used to highlight populations for focused prevention programs. However, caution must be used when drawing conclusions from reported race and ethnicity data. Different racial/ethnic populations might have different patterns of access to health care, potentially resulting in data that are not representative of actual disease incidence among specific racial/ethnic populations. Surveillance data reported to NNDSS are in either individual case-specific form or summary form (i.e., aggregated data for a group of cases). Summary data often lack demographic information (e.g., race); therefore, the demographic-specific rates presented in the Summary might be underestimated.

In addition, not all race and ethnicity data are collected or reported uniformly for all diseases, the standards for race and ethnicity have changed over time, and the transition in implementation to the newest race and ethnicity standard has taken varying amounts of time for different CDC surveillance systems. For example, in 1990, the National Electronic Telecommunications System for Surveillance (NETSS) was established to facilitate data collection and submission of case-specific data to CDC's National Notifiable Diseases Surveillance System, except for selected diseases. In 1990, NETSS implemented the 1977 Office of Management and Budget (OMB) standard for race and ethnicity, in which race and ethnicity were collected in one variable. Other surveillance programs implemented two variables for collection of race and ethnicity data. The 1997 OMB race and ethnicity standard, which requires collection of multiple races per person using multiple race variables, should have been implemented by federal programs beginning January 1, 2003. In 2003, the CDC Tuberculosis and HIV/AIDS programs were able to update their surveillance information systems to implement 1997 OMB standards. In 2005 the Sexually Transmitted Diseases*Management Information System also was updated to implement the 1997 OMB standards. However other diseases reported to the NNDSS using NETSS were undergoing a major change in the manner in which data were collected and reported to CDC. This change is known as the transition from NETSS to the National Electronic Disease Surveillance System (NEDSS). NEDSS implemented the newer 1997 OMB standard for race and ethnicity. However, the transition from NETSS to NEDSS was slower than originally expected relative to reporting data to CDC using NEDSS; thus, some data are currently reported to CDC using NETSS formats, even if the data in the reporting jurisdictions are collected using NEDSS. Until the transition to NEDSS is complete, race and ethnicity data collected or reported to NETSS using different race and ethnicity standards will need to be converted to one standard. The data are now converted to the 1977 OMB standard originally implemented in NETSS.

Although the recommended standard for classifying a person's race or ethnicity is based on self-reporting, this procedure might not always be followed.

Transition in NNDSS Data Collection and Reporting

Before 1990, data were reported to CDC as cumulative counts rather than individual case reports. In 1990, using NETSS, states began electronically capturing and reporting individual case reports to CDC without personal identifiers. In 2001, CDC launched NEDSS, now a component of the Public Health Information Network, to promote the use of data and information system standards that advance the development of efficient, integrated, and interoperable surveillance information systems at the local, state, and federal levels. One of the objectives of NEDSS is to improve the accuracy, completeness, and timeliness of disease reporting at the local, state, and national levels. CDC has developed the NEDSS Base System (NBS), a public health surveillance information system adopted by 16 states; 31 states have their own NEDSS-compatible based system, and three are in the final stage of adopting their NEDSS-compatible system. A major feature of all NEDSS-compatible solutions, which includes NBS, is the ability to capture data already in electronic form (e.g., electronic laboratory results, which are needed for case confirmation) rather than enter these data manually as in NETSS. In 2009, 16 states used NBS to transmit nationally notifiable infectious diseases to CDC, 27 states used a NEDSS-compatible based system, and the remaining states and territorial jurisdictions continued to use NETSS or other applications. Additional information concerning NEDSS is available at http://www.cy118119.com/phin/activities/applications-services/nedss/index.html.

Methodology for Identifying which Nationally Notifiable Infectious Diseases are Reportable

States and jurisdictions are sovereign entities. Reportable conditions are determined by laws and regulations of each state and jurisdiction. It is possible that some conditions deemed nationally notifiable might not be reportable in certain states or jurisdictions. Determining which nationally notifiable infectious diseases are reportable in NNDSS reporting jurisdictions was determined by analyzing results of the 2009 CSTE State Reportable Conditions Assessment (SRCA). This assessment solicited information from each NNDSS reporting jurisdiction (all 50 U.S. states, the District of Columbia, New York City, and five U.S. territories) regarding which public health conditions were reportable for more than 6 months in 2009 by clinicians, laboratories, hospitals, or "other" public health reporters, as mandated by law or regulation. To assist in the implementation of SRCA, the NNDSS program provided technical assistance to the CSTE for the 2009 SRCA.

In 2007, SRCA became the first collaborative project of such technical magnitude ever conducted by CSTE and CDC. Previously, CDC and CSTE had gathered public health reporting requirements independently. The 2009 SRCA collected information regarding whether each reportable condition was 1) explicitly reportable (i.e., listed as a specific disease or as a category of diseases on reportable disease lists); 2) whether it was implicitly reportable (i.e., included in a general category of the reportable disease list, such as "rare diseases of public health importance"); or 3) not reportable. Only explicitly reportable conditions were considered reportable for the purpose of national public health surveillance and thus reflected in NNDSS. Moreover, to determine whether a condition included in SRCA was reportable across all public health reporter categories and for a specific nationally notifiable infectious disease (NNID) in a reporting jurisdiction, CDC developed and applied a condition algorithm and a results algorithm to run on the data collected in SRCA. Analyzed results of the 2009 SRCA were used to determine whether a NNID was not reportable in a reporting jurisdiction in 2009 and thus noted with an "N" indicator (for "not reportable") in the front tables of this report.

Unanalyzed results from the 2007, 2008, and 2009 SRCA are available using CSTE's web query tool at http://www.cste.org/dnn/programsandactivities/publichealthinformatics/statereportableconditionsqueryresults/tabid/261/default.aspx.

Revised International Health Regulations

In May 2005, the World Health Assembly adopted revised International Health regulations (IHR) (2) that went into effect in the United States on July 18, 2007. This international legal instrument governs the role of the World Health Organization (WHO) and its member countries, including the United States, in identifying, responding to, and sharing information about Public Health Emergencies of International Concern (PHEIC). A PHEIC is an extraordinary event that 1) constitutes a public health risk to other countries through international spread of disease, and 2) potentially requires a coordinated international response.

The IHR are designed to prevent and protect against the international spread of diseases while minimizing the effect on world travel and trade. Countries that have adopted these rules have a much broader responsibility to detect, respond to, and report public health emergencies that potentially require a coordinated international response in addition to taking preventive measures. The IHR will help countries work together to identify, respond to, and share information about PEHIC.

The revised IHR is a conceptual shift from a predefined disease list to a framework of reporting and responding to events on the basis of an assessment of public health criteria, including seriousness, unexpectedness, and international travel and trade implications. PHEIC are events that fall within those criteria (further defined in a decision algorithm in Annex 2 of the revised IHR). Four conditions always constitute a PHEIC and do not require the use of the IHR decision instrument in Annex 2: Severe Acute Respiratory Syndrome (SARS), smallpox, poliomyelitis caused by wild-type poliovirus, and human influenza caused by a new subtype. Any other event requires the use of the decision algorithm in Annex 2 of the IHR to determine if it is a potential PHEIC. Examples of events that require the use of the decision instrument include, but are not limited to, cholera, pneumonic plague, yellow fever, West Nile fever, viral hemorrhagic fevers, and meningococcal disease. Other biologic, chemical, or radiologic events might fit the decision algorithm and also must be reportable to WHO. All WHO member states are required to notify WHO of a potential PHEIC. WHO makes the final determination about the existence of a PHEIC.

Health-care providers in the United States are required to report diseases, conditions, or outbreaks as determined by local, state, or territorial law and regulation, and as outlined in each state's list of reportable conditions. All health-care providers should work with their local, state, and territorial health agencies to identify and report events that might constitute a potential PHEIC occurring in their location. U.S. State and Territorial Departments of Health have agreed to report information about a potential PHEIC to the most relevant federal agency responsible for the event. In the case of human disease, the U.S. State or Territorial Departments of Health will notify CDC rapidly through existing formal and informal reporting mechanisms (3). CDC will further analyze the event based on the decision algorithm in Annex 2 of the IHR and notify the U.S. Department of Health and Human Services (DHHS) Secretary's Operations Center (SOC), as appropriate.

DHHS has the lead role in carrying out the IHR, in cooperation with multiple federal departments and agencies. The DHHS SOC is the central body for the United States responsible for reporting potential events to WHO. The United States has 48 hours to assess the risk of the reported event. If authorities determine that a potential PHEIC exists, the WHO member country has 24 hours to report the event to WHO.

An IHR decision algorithm in Annex 2 has been developed to help countries determine whether an event should be reported. If any two of the following four questions can be answered in the affirmative, then a determination should be made that a potential PHEIC exists and WHO should be notified:

• Is the public health impact of the event serious?
• Is the event unusual or unexpected?
• Is there a significant risk of international spread?
• Is there a significant risk of international travel or trade restrictions?

Additional information concerning IHR is available at http://www.who.int/csr/ihr/en, http://www.globalhealth.gov/ihr/index.html, http://www.cy118119.com/globalhealth/ihregulations.htm, and http://www.cste.org/PS/2007ps/2007psfinal/ID/07-ID-06.pdf. At its annual meeting in June 2007, CSTE approved a position statement to support the implementation of IHR in the United States (3). CSTE also approved a position statement in support of the 2005 IHR adding initial detections of novel influenza A virus infections to the list of nationally notifiable diseases reportable to NNDSS, beginning in January 2007 (4).

1. Doyle TJ, Glynn MK, Groseclose LS. Completeness of notifiable infectious disease reporting in the United States: an analytical literature review. Am J Epidemiol 2002;155:866--74.
2. World Health Organization. Third report of Committee A. Annex 2. Geneva, Switzerland: World Health Organization; 2005. Available at http://www.who.int/gb/ebwha/pdf_files/WHA58/A58_55-en.pdf.
3. Council of State and Territorial Epidemiologists. Events that may constitute a public health emergency of international concern. Position statement 07-ID-06. Available at http://www.cste.org/PS/2007ps/2007psfinal/ID/07-ID-06.pdf.
4. Available at http://www.cste.org/PS/2007ps/2007psfinal/ID/07-ID-01.pdf.

Anthrax

In 2009, one confirmed case of gastrointestinal anthrax occurred in New Hampshire. The exposure was determined to be the result of participation in a drumming event where animal-hide drums were played. Although several drums were played at the event, two were found to be contaminated with the same Bacillus anthracis strain as infected the patient. The patient recovered with treatment; the case is the first related to animal-hide drum exposures that involved the gastrointestinal form of the disease (1). This event and previous unrelated cases of anthrax associated with contaminated animal-hide drums reported in 2006, 2007, and 2008 in the United States and the United Kingdom (2-5) reflect the low but potential risk for anthrax among persons who 1) make or use drums made of untreated animal hides from countries where anthrax is common in animals, and among persons who 2) are exposed to environments that are cross-contaminated by these activities.

Naturally occurring anthrax epizootics occur annually among U.S. wildlife and livestock populations; in 2009 such events were reported among wildlife and livestock in Texas, North and South Dakota, and Nevada.

1. CDC. Gastrointestinal anthrax after an animal-hide drumming event---New Hampshire and Massachusetts, 2009. MMWR 2010;59:872--7.
2. CDC. Cutaneous anthrax associated with drum making using goat hides from West Africa---Connecticut, 2007. MMWR 2008;57:628--31.
3. CDC. Inhalation anthrax associated with dried animal hides---Pennsylvania and New York City, 2006. MMWR 2006;55:280--2.
4. National Health Service Borders. Report on the management of an anthrax incident in the Scottish borders, July 2006 to May 2007. Melrose, UK: National Health Service Borders; 2007. Available at http://www.nhsborders.org.uk/uploads/18645/anthrax_report_131207.pdf.
5. Anaraki S, Addiman S, Nixon G, et al. Investigations and control measures following a case of inhalation anthrax in East London in a drum maker and drummer, October 2008. Euro Surveill 2008;13:19076.

Brucellosis

The number of reported brucellosis cases in the United States increased 46.3% in 2009 from the previous year; however, the 2009 case total remains consistent with reports from 2004 through 2007. The reason for the decline in 2008 is unknown. Overall, in 2009, the demographic characteristics of persons with brucellosis remained stable. For patients for whom ethnicity was identified, 61.5% were Hispanic. A majority of cases (55.6%) were reported from California, Florida, Georgia, Michigan, and Texas.

Substantial progress has been made to eradicate brucellosis from the U.S. domestic livestock population through the Cooperative State-Federal Brucellosis Eradication Program (1).By the end of July 2009, all 50 States, Puerto Rico, and the Virgin Islands were officially classified as Class Free for bovine brucellosis (Brucella abortus) (2). All States except Texas are classified as Stage III (Free) for swine brucellosis; Texas remains classified at Stage II. Brucella abortus remains enzootic in elk and bison in the greater Yellowstone National Park area, and Brucella suis is enzootic in feral swine in the Southeast.

Risk factors associated with brucellosis include the consumption of unpasteurized milk or soft cheeses. The risk for brucellosis from domestic dairy products is low. Unpasteurized dairy products from countries where brucellosis is endemic remain a source of the illness for immigrants and travelers. Hunters are at an elevated risk for contracting brucellosis from the carcass or meat of infected animals. In addition, exposure to Brucella spp. can occur accidentally in diagnostic and research laboratories because of their high potential for aerosol transmission (3). For the same reason, biosafety level 3 practices, containment, and equipment are recommended for laboratory manipulation of isolates (4). In the event of an exposure, post-exposure prophylaxis can effectively prevent illness (5). CDC provides recommendations for laboratory exposures and assistance with serologic monitoring of exposed laboratory workers at telephone 404-639-1711.

1. USDA APHIS. 2003. Brucellosis eradication: Uniform methods and rules, Effective October 1, 2003. APHIS 91-45-013. Available at http://www.aphis.usda.gov/animal_health/animal_diseases/brucellosis/downloads/umr_bovine_bruc.pdf.
2. Donch DA, Gertonson AA, Rhyan JH, Gilsdorf MJ. Status report---fiscal year 2009 cooperative state-federal Brucellosis Eradication Program. Washington, DC: US Department of Agriculture; 2010.
3. CDC. Bioterrorism agents/diseases, by category. Atlanta, GA: US Department of Health and Human Services, CDC; 2006. Available at: http://www.bt.cdc.gov/agent/agentlist-category.asp#adef.
4. CDC, National Institutes of Health. Biosafety in microbiological and biomedical laboratories (BMBL). 5th ed. Washington, DC: US Department of Health and Human Services, CDC, National Institutes of Health; 2007. Available at: http://www.cy118119.com/biosafety/publications/bmbl5/index.htm.
5. CDC. Laboratory-acquired brucellosis---Indiana and Minnesota, 2006. MMWR 2008;57:39--42.

Coccidioidomycosis

The incidence of coccidioiodomycosis increased in 2009, although this increase might be partially artifactual. In 2009, one of the major commercial laboratories in Arizona changed reporting practices to conform to the CSTE laboratory case definition, which was revised in 2007 to include cases with a single positive enzyme immunoassay result (1). As a result, the increase in 2009 case counts in Arizona might be attributed, at least in part, to an artifactual increase.

Approximately 60% of coccidioidomycosis cases in the United States occur in Arizona. The public health burden of this disease on Arizona is considerable, as described in a recent report, which explained the use of enhanced surveillance (2). Among this representative group of coccidioidomycosis case-patients, self-reported median duration of illness was 42 days, and 41% of case-patients were hospitalized for coccidioidomycosis; 74% of those employed and 59% of students were unable to attend school or work.

Physicians, particularly in areas where the disease is endemic, should continue to maintain a high suspicion for acute coccidioidomycosis, especially among patients with an influenza-like illness or pneumonia who live in or have visited disease-endemic areas.

1. Council of State and Territorial Epidemiologists. Revision of the surveillance case definition for Coccidioidomycosis. Position statement 07-ID-13. Atlanta, GA: Council of State and Territorial Epidemiologists; 2007. Available at http://www.cste.org/position%20statements/searchbyyear2007final.asp.
2. Tsang CA, Anderson SM, Imholte SB, Erhart LM, Chen S, Park BJ. Enhanced surveillance of coccidioidomycosis, Arizona, USA, 2007--2008. Emerg Infect Dis 2010;11:1738--44.

Cryptosporidiosis

In 2009, cryptosporidiosis incidence decreased for the second consecutive year. The decreases in incidence in 2008 and 2009 follow a >3-fold rise during 2005--2007. Whether the changes in cryptosporidiosis reporting reflect a true change in cryptosporidiosis incidence or reflect changing diagnosis, testing, and reporting patterns is unclear.

As in previous years, cryptosporidiosis case reports were influenced by outbreaks, particularly those associated with treated recreational water. Although cryptosporidiosis affects persons in all age groups, cases were most frequently reported in children aged 1--9 years. An almost tenfold increase in transmission of Cryptosporidium in these young children occurred during summer through early fall, coinciding with increased use of recreational water, which is a known risk factor for cryptosporidiosis. Good hygiene practices are essential to prevention, especially in high-risk settings. Persons should also avoid food and water that might be contaminated. Cryptosporidium oocysts can be detected routinely in treated recreational water (1). Contamination of, and the subsequent transmission through, recreational water is facilitated by the substantial number of Cryptosporidium oocysts that can be shed by a single person; the extended time that oocysts can be shed (2); the low infectious dose (3); and the chlorine tolerance of Cryptosporidium oocysts (4). The application of molecular epidemiology (i.e., genotyping and subtyping Cryptosporidium specimens) to clinical and environmental samples has demonstrated potential to expand our knowledge of Cryptosporidium epidemiology (5).

1. Shields JM, Gleim ER, Beach MJ. Prevalence of Cryptosporidium spp. and Giardia intestinalis in swimming pools, Atlanta, Georgia. Emerg Inf Dis 2008;14:948--50.
2. Chappell CL, Okhuysen PC, Sterling CR, DuPont HL. Cryptosporidium parvum: intensity of infection and oocyst excretion patterns in healthy volunteers. J Infect Dis 1996;173:232--6.
3. DuPont HL, Chappell CL, Sterling CR, Okhuysen PC, Rose JB, Jakubowski W. The infectivity of Cryptosporidium parvum in healthy volunteers. N Engl J Med 1995;332:855--9.
4. Shields JM, Hill VR, Arrowood MJ, Beach MJ. Inactivation of Cryptosporidium parvum under chlorinated recreational water conditions. J Water Health 2008;6:513--20.
5. Xiao L. Molecular epidemiology of cryptosporidiosis: an update. Exp Parasitol 2010;124:80--89

Ehrlichiosis and Anaplasmosis

Four categories of ehrlichiosis and anaplasmosis were reportable during 2009: 1) Ehrlichia chaffeensis, 2) Ehrlichia ewingii, 3) Anaplasma phagocytophilum, and 4) Human ehrlichiosis/anaplasmosis - undetermined.

During 2009, infections caused by E. chaffeensis were reported primarily from the lower Midwest and the Southeast, reflecting the historically known range of the primary tick vector species (Amblyomma americanum). Infection caused by A. phagocytophilum was reported primarily from the upper Midwest and coastal New England, reflecting both the range of the primary tick vector species (Ixodes scapularis) and preferred animal hosts for tick feeding. Missouri, Ohio, and South Carolina reported seven confirmed cases of E. ewingii infection. The category "Human ehrlichiosis/anaplasmosis - undetermined" includes cases for which a specific etiologic agent could not be identified using available serologic tests. The number of "Human ehrlichiosis/anaplasmosis - undetermined" cases reported from some northern states (1) reflects state-specific classifications based on indistinguishable antigenic cross-reactivity or situations in which physicians, confused regarding the likely causative agent, ordered single or inappropriate tests (e.g., ordering only ehrlichiosis tests in a region where anaplasmosis is expected to predominate).

During 2009, cases attributed to E. chaffeensis remained similar to numbers reported the previous year, whereas those attributed to A. phagocytophilum cases increased by 15% (1,009 to 1,161). The numbers of reported ehrlichiosis and anaplasmosis cases have increased more than twofold during the last decade. Increases in the numbers of reported cases might be the result of several factors, including ecological changes influencing vector tick populations and disease transmission, changes in diagnostic approaches that alter detection rates, or changes in surveillance and reporting. Changes in the case definition that became effective in January 2008 (2) also might have altered how cases were classified.

1. CDC. Anaplasmosis and ehrlichiosis--- Maine, 2008. MMWR 2009: 58(37):1033--6.
2. Council of State and Territorial Epidemiologists. Revision of the surveillance case definitions for ehrlichiosis. Position statement 07-ID-03. Atlanta, GA: Council of State and Territorial Epidemiologists; 2007. Available at http://www.cste.org/position%20statements/searchbyyear2007final.asp.

Gonorrhea

In 2009, the rate of gonorrhea was the lowest ever reported. During 2006--2009, decreases in gonorrhea rates were reported in all racial/ethnic groups and in all age groups. Although the gonorrhea rate among women has remained slightly higher than that among men, rates have decreased in both groups. Despite overall rate decreases, the rate for blacks in 2009 was 20.5 times higher than that for whites whereas the rates among American Indians/Alaska Natives and Hispanics were 4.2 and 2.2 times higher, respectively, than rates in whites (1).

1. CDC. Sexually transmitted disease surveillance, 2009. Atlanta, GA: U.S. Department of Health and Human Services.

Hansen Disease (Leprosy)

The number of cases of Hansen's disease (HD) reported in the United States peaked in 1985 and decreased until 2006. Since 2006 the annual number of reported cases has fluctuated between 73 and 109. Cases were reported from 20 states and one territory; 64.4% of cases were reported from California, Hawaii, and Texas. HD is not highly transmissible; cases appear to be related predominantly to immigration from areas in which the disease is endemic.  Information on access to clinical care is available at www.hrsa.gov/hansens.

Hantavirus Pulmonary Syndrome

Less than 7% of hantavirus pulmonary syndrome (HPS) cases in the United States have been in pediatric populations. Each year, 20--40 cases of HPS occur in the United States; cases in persons aged <17 years make up fewer than 7% of those cases, and cases in children aged <10 years are exceptionally rare. However, in 2009, six pediatric cases of HPS were identified (one case resulted in a fatality), including four cases in persons aged <10 years (1).

1. CDC. Hantavirus pulmonary syndrome in five pediatric patients---four states, 2009. MMWR 2009;58:1409--12.

Influenza-Associated Pediatric Mortality

In June 2004, the Council of State and Territorial Epidemiologists added influenza-associated pediatric mortality (i.e., among persons aged <18 years) to the list of conditions reportable to the National Notifiable Diseases Surveillance System. Cumulative year-to-date incidence is published each week in MMWR Table I for low-incidence nationally notifiable diseases.

The majority of pediatric deaths that occurred during the 2008--09 and 2009--10 influenza seasons, including those associated with the 2009 pandemic influenza A (H1N1) virus (2009 H1N1), were reported in 2009. The 2009 H1N1 virus was first detected in the United States in mid-April 2009 and became the predominant circulating influenza virus worldwide. From April 15 through the end of 2009, 96% of all subtyped influenza A viruses from the United States were 2009 H1N1. For this report, pediatric deaths associated with seasonal influenza viruses are analyzed separately from those associated with 2009 H1N1 infection. Influenza A viruses that were not subtyped are classified as seasonal influenza A viruses for deaths that occurred during January 1 -- April 14, 2009 and as 2009 H1N1 for deaths that occurred during April 15 -- December 31, 2009. Of the 358 influenza-associated pediatric deaths reported to CDC during 2009, a total of 290 (81%) were associated with the 2009 H1N1 virus and 68 (19%) were associated with seasonal influenza viruses. Of the 37 seasonal influenza A viruses, 11 (30%) were subtyped; 9 were seasonal A(H1N1) viruses and 2 were influenza A (H3N2) viruses. Twenty-six (70%) were influenza A viruses that were not subtyped and the remaining 31 were influenza B viruses.

The median age at the time of death in 2009 was higher for children presumed infected with 2009 H1N1 virus (9.3 years) than for those infected with seasonal influenza viruses (7.5 years). Both groups had a higher median age than was observed in the previous 3 years when the median age at death ranged from 4 years in 2006 to 7.4 years in 2007. The distributions of race, ethnicity, and sex were similar for children infected with the seasonal influenza viruses and children infected with the 2009 H1N1 virus. The proportion of children infected with seasonal influenza virus admitted to the hospital before death (73%) was similar to that among those infected with 2009 H1N1 virus (69%) but higher than that seen in the previous 3 years (range: 51%-- 62%). Children who died following infection with 2009 H1N1 virus were more likely to have at least one chronic condition placing them at increased risk for influenza-associated complications (67%) compared with children with seasonal influenza infection in 2009 (42%). During the previous 3 years, the percent of children with at least one chronic medical condition has ranged from 43% to 57%. Among children who had specimens collected for bacterial culture from sterile sites, no substantial difference was present in the proportion with bacterial coinfection for children with 2009 H1N1 (57%) and seasonal influenza infection (58%). For children with a bacterial coinfection, Staphylococcus aureus was identified in 12 of 18 (67%) children with seasonal influenza and 17 of 44 (39%) children with 2009 H1N1 infection. Of the S. aureus isolates identified among all deaths, 18 were methicillin-resistant, nine were methicillin-sensitive, and two did not have sensitivity testing performed. Coinfection with Streptococcus pneumoniae occurred in 2 of 18 (11%) children with seasonal influenza and 12 of 44 (27%) children with 2009 H1N1 infection.

Of 45 children aged ≥6 months who died with the seasonal influenza virus and for whom seasonal vaccination status was known, only seven (16%) were vaccinated against influenza as recommended by the Advisory Committee on Immunization Practices (ACIP) for 2009 (1). Of the 158 children aged ≥6 months who died with the 2009 A (H1N1) virus and for whom the vaccination status was known, 27 (17%) were vaccinated against seasonal influenza but only one (0.8%) received 2009 A(H1N1) vaccine according to ACIP recommendations.

Children who died with 2009 H1N1 were older and more likely to have an underlying condition that placed them at high risk for influenza complications than children who died with seasonal influenza. The proportion of children with bacterial co-infection was similar among those with seasonal influenza and 2009 H1N1. Continued surveillance of influenza-related mortality is important to monitor both the effects of seasonal and novel influenza and the effect of interventions in children.

1. CDC. Prevention and control of influenza: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR 2009: July 31, 2009 / 58(RR08);1-52.

Lyme disease

Lyme disease is caused in North America by Borrelia burgdorferi sensu stricto, a spirochete transmitted by certain species of Ixodes ticks. Manifestations of infection include erythema migrans, arthritis, carditis, and neurologic deficits. Effective January 2008, the national surveillance case definition was revised to include reporting of probable cases and to update laboratory criteria to reflect current testing practices. Between 2008 and 2009 there was a 3.6% increase in confirmed cases and 35.6% increase in probable cases. Much of the increase can be attributed to variability in surveillance practices, although evidence of true emergence exists in certain areas. Because of the burden on endemic states posed by Lyme disease surveillance, some states have modified surveillance protocols to better manage limited resources. States using modified methods, including case estimation, might report decreased case counts.

Measles

Measles was declared eliminated from the United States in 2000. Since then, elimination has been maintained through high population immunity (1). Nonetheless, because measles remains endemic in much of the world; importations continue to result in sporadic cases and outbreaks in the United States, which can be costly to control (2). In recent years, the majority of measles cases in 2009 (80%) were import associated (3). Measles was classified as internationally imported in 21 cases, 14 of which were in U.S. residents exposed while traveling abroad, and 7 of which were among international visitors. Source countries for imported measles cases in 2009 included: United Kingdom (8 ), India (6 ), China (2 ), Philippines (2 ), Vietnam (1 ), Italy (1 ), and Cape Verde (1 ).

Thirty-three states reported no measles cases in 2009; 11 states and the District of Columbia reported fewer than 3 cases, and 6 states reported a total of 8 outbreaks (defined as 3 or more epidemiologically linked cases). Outbreaks ranged from 3 to 15 cases (median: 4). Seven outbreaks (87%) had viral and/or epidemiologic evidence of imported source. Six outbreaks (75%) included case-patients who reported personal belief exemptions. Of the 45 unvaccinated U.S. residents with measles in 2009, 20 (44%) held personal or religious beliefs opposing vaccination, and 10 (22%) were among children aged 15 months to 5 years whose parents had chosen to delay their MMR vaccination.

1. Hutchins SS, Bellini W, Coronado V, et al. Population immunity to measles in the United States. J Infect Dis 2004:189(Suppl 1):S91--97.1.
2. Parker AA, Staggs W, Dayan G, et al. Implications of a 2005 measles outbreak in Indiana for sustained elimination of measles in the United States, N Engl J Med 2006; 355:447--55.
3. Council of State and Territorial Epidemiologists. Revision of measles, rubella, and congenital syndrome case classification as part of elimination goals in the United States. Position statement 2006-ID-16. Available at http://www.cste.org/position%20statements/searchbyyear2006.asap.

Mumps

The majority (90%) of mumps cases reported in the United States during 2009 were associated with a large outbreak focused in the Northeastern states (primarily New York and New Jersey) that began in New York in June 2009 (1). A total of 1,776 cases occurred through December 31, 2009. The outbreak primarily affected adolescent boys in the Orthodox Jewish communities. Fewer than 3% of the cases associated with this outbreak occurred among persons outside this community. Most cases (77%) were among males and 36% were among adolescents aged 13 to 17 years. Among the patients for whom vaccination status was reported, 88% had received at least 1 dose of mumps-containing vaccine, and 76% had received 2 doses. This was the largest mumps outbreak to occur in the United States since 2006 (2).

1. CDC. Mumps outbreak---New York, New Jersey, Quebec, 2009. MMWR 2009;58:1270--4.
2. Dayan G, Quinlisk P, et al. Recent resurgence of mumps in the United States. New Engl J Med 2008;358:1580--9.

Novel Influenza A

In 2007, the Council of State and Territorial Epidemiologists added novel influenza A virus infection to the list of conditions reportable to the National Notifiable Diseases Surveillance System. Novel influenza A virus infections are human infections with influenza A viruses that are different from currently circulating human influenza A (H1) and A (H3) viruses. These viruses include those that are subtyped as non-human in origin and those that cannot be subtyped with standard methods and reagents.

After recognition of the first cases of infection with 2009 pandemic influenza A (H1N1) virus in April 2009, CDC and state health departments initiated enhanced surveillance to identify additional cases of 2009 pandemic influenza A (H1N1) virus infection. From April 15 to July 24, 2009, state and territorial health departments were asked to submit a daily line list of individual confirmed and probable cases of 2009 pandemic influenza A (H1N1) virus infections to the Influenza Division at CDC. A total of 43,771 cases were reported from all 50 states, Washington DC, and four territories during that 14-week period.

In addition, four cases of human infection with novel influenza A viruses, unrelated to the 2009 pandemic influenza A (H1N1) virus strain, were reported from three states (two from Iowa, one from Kansas, and one from Minnesota). These four cases represented sporadic cases of human infection; two patients were infected with swine influenza A (H1N1) viruses, and the remaining two were infected with swine influenza A (H3N2) viruses. Transmission of swine influenza A viruses to humans usually occurs among persons in direct contact with pigs or in those who have visited places where pigs have been present (e.g. agricultural fairs, farms, and petting zoos). Three of the four patients had direct contact with pigs. No definite exposure to swine was identified in one case. These cases did not result in sustained human-to-human transmission or community outbreaks.

Surveillance for human infections with all novel influenza A viruses remains essential even with the sustained community transmission of the 2009 pandemic influenza A (H1N1) virus. The early identification and investigation of these cases is critical to evaluate the extent of outbreaks and possible human-to-human transmission.

Pertussis

Although the incidence of reported pertussis declined in the United States following the 2004 peak (8.9 per 100,000), overall incidence is increasing again (5.54 in 2009, 4.18 in 2008, and 3.53 in 2007). Infants aged <6 months, who are at greatest risk for severe disease and death, continued to have the highest reported rate of pertussis (126.9 per 100,000). However, adolescents (aged 10--19 years) and adults (aged >20 years) accounted for approximately half of reported cases in 2009, and the contribution of cases in persons aged 7-10 years has been increasing in recent years (13% in 2007, 23.5% of cases in 2008, 23% of cases in 2009). In 2005, a combined tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis vaccine (Tdap) was recommended for use among adolescents and adults (1,2). Tdap coverage continues to increase among persons aged 13--17 years (10.8% in 2006 to 55.6% in 2009) (3,4), and early data suggests a decline in reported pertussis incidence among adolescents following the introduction of Tdap (5). Continued monitoring of disease trends through national surveillance will be important to assess the direct effect of Tdap among target vaccine age groups and the indirect effects of vaccination on infants.

1. CDC. Preventing tetanus, diphtheria, and pertussis among adolescents; use of tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis vaccines: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR 2006;55(No. RR--3).
2. CDC. Preventing tetanus, diphtheria, and pertussis among adults: use of tetanus toxoid, reduced diphtheria toxoid and acellular pertussis vaccine: recommendations of the Advisory Committee on Immunization Practices (ACIP) and Recommendation of ACIP, supported by the Healthcare Infection Control Practices Advisory Committee (HICPAC), for use of Tdap among health-care personnel. MMWR 2006;55 (No. RR-17).
3. CDC. Vaccination coverage among adolescents aged 13--17 years---United States, 2006. MMWR 2007;56:885--8.
4. CDC. Vaccination coverage among adolescents aged 13--17 years---United States, 2009. MMWR 2010;59:1018--1023. Available at http://cdc.confex.com/cdc/nic2009/webprogram/Paper18157.html.

Poliomyelitis, Paralytic and Poliovirus Infections

Vaccine-Associated Paralytic Poliomyelitis (VAPP) is a rare adverse event that can occur following vaccination with live-attenuated oral poliovirus vaccine (OPV) (1). Inactivated poliovirus vaccine (IPV) does not cause VAPP. To reduce the risk of VAPP, the United States changed from an all OPV schedule to a sequential IPV/OPV schedule in 1997, and then to an all IPV schedule in 2000(2). Before the use of OPV was discontinued in 2000, approximately 8 cases of VAPP occurred in the United States each year (3). Since 2000, only two cases of VAPP have been reported in the United States, one in 2005 in a traveler to countries using OPV and a second, described below, who had common-variable immunodeficiency (CVID) (4).

In 2009, the Minnesota Department of Health reported VAPP in a U.S.-born resident with longstanding CVID. The case-patient, aged 44 years, had abrupt onset of limb and respiratory paralysis beginning in December 2008 and died in March 2009. A stool culture for enterovirus obtained in March 2009 tested positive for an enterovirus, which was later identified as type 2 vaccine-derived poliovirus. The number of genetic mutations in this virus suggested that it had been acquired by the case-patient in the mid 1990s, around the time that a household member was vaccinated with OPV (5).

1. CDC. Poliomyelitis prevention in the United States: introduction of a sequential vaccination schedule of inactivated poliovirus vaccine followed by oral poliovirus vaccine; recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR 1997;46(RR-3).
2. CDC. Poliomyelitis prevention in the United States: updated recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR 2000;49(RR-5).
3. Alexander LN, Seward JF, Santibanez TA, et al. Vaccine policy changes and epidemiology of poliomyelitis United States. JAMA 2004;292:1696--1701.
4. CDC. Imported vaccine-associated paralytic poliomyelitis United States, 2005. MMWR 2006:55:97--9.
5. DeVries, A, Harper, J, Murray, A. Neuroinvasive immunodeficiency-associated vaccine-derived polio Minnesota, 2008. Abstract #652 presented at the 47th Annual Meeting of IDSA, Philadelphia, PA, October 29-November 1, 2009.

Q Fever

During 2009, both acute and chronic Q fever infections were notifiable. Among the 113 cases reported in 2009, 93 were acute infection, and 20 were chronic Q fever. Cases remained distributed across the United States, in keeping with the consideration that Q fever is considered enzootic in ruminants (sheep, goats, and cattle) throughout the country.

During 2009, the number of cases of Q fever reported remained similar to those reported during the previous year. Although relatively few human cases are reported annually, Q fever is believed to be substantially underreported because of its nonspecific presentation and the subsequent failure of clinicians to suspect infection and request appropriate diagnostic tests.

Rabies

During 2009, four cases of human rabies were reported in the United States: an abortive infection in Texas, an imported case from India in Virginia, and two indigenous cases attributed to bat rabies virus variants in Indiana and Michigan. The Texas abortive rabies case marks the first documented human rabies case in which clinical and serologic findings were indicative of rabies and no alternate etiology for the illness was determined despite an extensive investigation. The patient experienced a shorter clinical course, less severe neurologic abnormalities, less stimulation of the immune system, and recovered without extensive medical intervention (1).

During June 2009, evidence on the number of doses of rabies vaccine required for postexposure prophylaxis (PEP) was presented to the Advisory Committee on Immunization Practices, and a change in the PEP guidelines was approved.

The new guidelines recommended that immunocompetent persons not previously vaccinated against rabies should receive human rabies immune globulin (20 IU/kg; day 0) and 4 doses of rabies vaccine (1mL IM; days 0, 3, 7, and 14). Persons who are immunocompromised should continue to receive the 5-dose PEP protocol with serologic testing to confirm adequate response to the vaccine (2).

During 2009, the majority (92%) of 6,694 rabid animals reported in the United States were wildlife. Overall, a 2% decrease was reported compared with 2008. Cats remain the most commonly reported rabid domestic animal (59% of rabid domestic animals). Reports of rabid domestic animals remain low in part because of increased vaccination rates and the continued elimination of dog-to-dog rabies transmission. Canine rabies remains a serious concern in many developing countries and public health education should target travelers and health-care providers with messages regarding rabies prevention measures and the potential risk of rabies exposure in countries where the disease is endemic in domestic animals (3).

1. CDC. Presumptive abortive human rabies---Texas, 2009. MMWR. 2010; 59: 185--190.
2. CDC. Use of a reduced (4-dose) vaccine schedule for postexposure prophylaxis to prevent human rabies: recommendations of the Advisory Committee on Immunization Practices. MMWR 2010; 59(No.R:R-2)
3. Blanton JD, Palmer D, Rupprecht CE. Rabies surveillance in the United States during 2009. J Am Vet Med Assoc. 2010; 237: (in press).

Rocky Mountain Spotted Fever

During 2009, RMSF cases decreased 29% from those reported in 2008. Cases reported in 2009 were distributed across the United States, reflecting the endemic status of Rocky Mountain spotted fever (RMSF) and the widespread ranges of the primary tick vectors (primarily Dermacentor variabilis and Dermacentor andersoni) responsible for transmission. RMSF cases associated with transmission by Rhipicephalus sanguineus, first reported in 2004 (1), continued to be reported from Arizona during 2009.

Although RMSF case reports increased more than 400% from 2000 through 2008 (495 to 2,563), case reporting in 2009 represented a decline of nearly 750 cases. This decrease might be the result of several factors, including ecological changes influencing vector tick populations and disease transmission, changes in diagnostic approaches that alter detection rates, or changes in surveillance and reporting. Because serologic tests commonly used to diagnose RMSF exhibit cross-reactivity between spotted fever rickettsial pathogens, some cases reported as RMSF during 2009 might actually have been caused by other spotted fever rickettsial infections.

1. L Demma, Traeger M, Nicholson W, et al. Rocky Mountain spotted fever from an unexpected tick vector in Arizona. New Engl J Med 2005;353:587--94.

Rubella, Congenital Rubella Syndrome

Rubella virus infection usually results in mild disease, but if contracted during pregnancy can result in vertical transmission to the fetus, leading to a constellation of congenital birth defects known as congenital rubella syndrome (CRS). Although rubella is no longer endemic in the United States, it remains common in many parts of the world. The U.S. strategy for ensuring maintenance of rubella and CRS elimination includes (1) maintaining high vaccination rates among children; (2) ensuring vaccination among all women of childbearing age; (3) continuing surveillance of both rubella and CRS; and (4) responding rapidly to any outbreaks of rubella (1).

The CRS case definition requires the presence of compatible congenital anomalies and laboratory evidence of rubella infection in the first year of infancy. Birth defects most often associated with CRS include cataracts, heart defects, and deafness. For a CRS case to be classified as an international importation, the mother must have acquired rubella virus infection outside the United States, or, in the absence of documented rubella virus infection, the mother must have been out of the United States for a period covering 21 days before and 24 weeks after conception. Laboratory confirmation of CRS in infants requires either rubella virus isolation, rubella virus detection by real-time polymerase chain reaction (RT-PCR), detection of serum rubella IgM, or serum IgG levels that persist longer than expected from passive transfer of maternal IgG (i.e., rubella titer that does not drop at the expected rate of a twofold dilution per month) (1).

Two CRS cases were reported in the United States in 2009. Both infants were born during 2008 and officially reported to CDC after investigations of the cases were completed in 2009. The first case was in an infant born to a U.S. resident with a travel history to India and China during time of conception and early in her first trimester of pregnancy. The infant, with a syndrome clinically compatible with CRS, tested positive at birth for infection with rubella genotype 2B virus. The source of infection for the second CRS case reported in 2009 is unknown. This infant was born to a U.S. resident who reported no international travel during her pregnancy. The case was diagnosed by PCR testing at a commercial laboratory; however, specimens were not available for confirmation and genotyping at CDC. Neither an epidemiologic nor virologic link to an importation could be established (CDC, unpublished data).

1. Reef SE, Cochi SL. The evidence for the elimination of rubella and congenital rubella syndrome in the United States: a public health achievement. Clin Infect Dis 2006;43 (Suppl 3):S123?5.

Syphilis, Primary and Secondary

In 2009, rates of primary and secondary syphilis increased for the eighth consecutive year, reaching the highest rate reported since 1995. Although increases have occurred mostly among men, in 2009 62% of cases from 44 states and the District of Columbia occurred in men who have sex with men. Increases also were observed among women during 2004--2008, mostly in the south. The overall rate in women declined slightly in 2009. In 2009, the primary and secondary syphilis rate among blacks was 9 times the rate among whites. During 2005--2009, syphilis rates increased 167% among black men aged 15-19 years and 212% among black men aged 20--24 years, the greatest increase observed in any age, sex, or racial/ethnic group. Among black women aged 15--24 years, rates more than doubled during 2005--2009 (1).

1. CDC. Sexually transmitted disease surveillance, 2009. Atlanta, GA: U.S. Department of Health and Human Services.

Trichinellosis

Of the 13 trichinellosis cases reported in 2009, five were associated with a shared meal that included a dish prepared with Trichinella-infected raw bear meat. One case-patient reported travelling to Southeast Asia and consuming raw pig's blood before the onset of illness. The implicated meat sources of five cases were pork (2), wild boar (2), and bear (1). Two cases of another disease were mistakenly reported as trichinellosis.

At least one outbreak associated with raw bear meat has been reported during 8 of the past 10 years (1-3). These results highlight the continued need for public health prevention messages aimed at persons who eat wild game meat, particularly bear, and for prevention messages targeted to cultural groups whose food choices might put them at a higher risk for Trichinella infection.

Proper cooking of meat dishes will prevent trichinellosis. Meat products, including sausages, ground meat, and other cuts of meat, should be cooked to internal temperatures of at least 160oF (4). Some species of Trichinella are resistant to freezing, so freezing might not be an effective prevention method.

1. CDC. Summary of Notifiable Diseases --- United States, 2008. MMWR 2010;57(No. 54).
2. Kennedy ED, Hall RL, Montgomery SP, Pyburn DG, Jones JL. Trichinellosis surveillance---United States, 2002--2007. In: Surveillance Summaries, December 4, 2009. MMWR 2009;58 (No. SS-9).
3. Roy SL, Lopez AS, Schantz PM. Trichinellosis surveillance---United States, 1997--2001. In: Surveillance Summaries, July 25, 2003. MMWR 2003;52(No. SS-6). Available at http://www.fsis.usda.gov/factsheets/meat_preparation_fact_sheets/index.asp.

Varicella

In 1981, varicella was removed from the National Notifiable Diseases list. Because of high disease burden and lack of established national surveillance for varicella when the one-dose varicella vaccination program was implemented in 1995, active surveillance sites were created to monitor the effect of the varicella vaccination program. Data from the active surveillance sites have indicated a greater than 90% decline in cases during 1995--2005 (1).

In 2002, the Council of State and Territorial Epidemiologists recommended that states move to case-based reporting for varicella by 2005. In 2003, varicella was added back to the national notifiable diseases list. As of 2009, 36 states were conducting case-based reporting for varicella. National data on varicella incidence reported through the National Notifiable Diseases Surveillance Sytem (NNDSS) are consistent with data reported through the active surveillance sites and document a decline in cases even as the number of states reporting has increased. During 2006--2009, the number of varicella cases reported through NNDSS decreased by 58% whereas the number of states and territories reporting increased from 31 to 36.

As varicella incidence has decreased, monitoring of cases has become more feasible nationwide and thus, NNDSS will be able to replace the active surveillance sites as the primary national source of surveillance data for varicella. Further declines in varicella disease burden are expected with implementation in 2006 of the universal recommendation for two doses of varicella vaccine for children (2). Therefore, all states should be advised of the importance of conducting varicella case-based reporting.

1. Guris D, Jumaan AO, Mascola L, et al. Changing varicella epidemiology in active surveillance sites---United States, 1995--2005. J Infect Dis 2008;197 Suppl 2:S71--5.
2. CDC. Prevention of varicella: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR 2007;56(RR-4). Available at: http://www.cy118119.com/mmwr/PDF/rr/rr5604.pdf.

Selected Reading for 2009

General

CDC. Automated detection and reporting of notifiable diseases using electronic medical records versus passive surveillance---Massachusetts, June 2006--July 2007. MMWR 2008;57:373--6.

CDC. Racial disparities in nationally notifiable diseases---United States, 2002. MMWR 2005;54:9--11.

CDC. Progress in improving state and local disease surveillance---United States, 2000--2005. MMWR 2005;54:822--5.

CDC. Case definitions for infectious conditions under public health surveillance. MMWR 1997;46(No. RR-10). Additional information available at http://www.cy118119.com/epo/dphsi/casedef/index.htm.

CDC. Demographic differences in notifiable infectious disease morbidity---United States, 1992--1994. MMWR 1997;46:637--41.

CDC. Framework for evaluating public health surveillance systems for early detection of outbreaks; recommendations from the CDC working group. MMWR 2004;53(No. RR-5).

CDC. Framework for program evaluation in public health. MMWR 1999;48(No. RR-11).

CDC. Historical perspectives: notifiable disease surveillance and notifiable disease statistics---United States, June 1946 and June 1996. MMWR 1996;45:530--6.

CDC. Manual of procedures for the reporting of nationally notifiable diseases to CDC. Atlanta, GA: US Department of Health and Human Services, Public Health Service, CDC; 1995.

CDC. Manual for the surveillance of vaccine-preventable diseases. 3rd ed. Atlanta, GA: US Department of Health and Human Services, Public Health Service, CDC; 2002. Available at http://www.cy118119.com/nip/ publications/surv-manual.

CDC. National Electronic Disease Surveillance System (NEDSS): a standards-based approach to connect public health and clinical medicine. J Public Health Manag Practice 2001;7:43--50.

CDC. Public Health Information Network (PHIN): overview. Atlanta, GA: US Department of Health and Human Services, CDC; 2006. Available at http://www.cy118119.com/phin/overview.html.

CDC. Reporting race and ethnicity data---National Electronic Telecommunications System for Surveillance, 1994--1997. MMWR 1999;48:305--12.

CDC. Sexually transmitted disease surveillance, 2009. Atlanta, GA: US Department of Health and Human Services, CDC; 2009. Available at http://www.cy118119.com/std/stats.

CDC. Sexually transmitted diseases treatment guidelines, 2010. MMWR 2010;59(No. RR-12).

CDC. Ten leading nationally notifiable infectious diseases---United States, 1995. MMWR 1996;45:883--4.

CDC. Updated guidelines for evaluating public health surveillance systems: recommendations from the Guidelines Working Group. MMWR 2001;50(No. RR-13).

CDC. Use of race and ethnicity in public health surveillance: summary of the CDC/ATSDR workshop. MMWR 1993;42(No. RR-10).

CDC. Potential effects of electronic laboratory reporting on improving timeliness of infectious disease notification --- Florida, 2002--2006. MMWR 2008;57:1325--8.

Adekoya N. Nationally notifable disease surveillance (NNDSS) and the Healthy People 2010 objectives. The eJournal of the South Carolina Medical Association 2005;101:e68--72. Available at http://www.scmanet.org/Downloads/e-Journal/SCMA_eJournal_March05.pdf.

Armstrong KE, McNabb S, Ferland LD, et al. Capacity of public health suveillance to comply with revised international health regulations, USA. Emerg Infect Dis 2010;5:804--8.

Baker MG, Fidler DP. Global public health surveillance under new international health regulations. Emerg Infect Dis 2006;12:1058--65.

Bayer R, Fairchild AL. Public health: surveillance and privacy. Science 2000;290:1898--9.

Chang M-H, Glynn MK, Groseclose SL. Endemic, notifiable bioterrorism-related diseases, United States, 1992--1999. Emerg Infect Dis 2003;9:556--64.

Chin JE, ed. Control of communicable diseases manual. 17th ed. Washington, DC: American Public Health Association; 2000.

Doyle TJ, Glynn MK, Groseclose SL. Completeness of notifiable infectious disease reporting in the United States: an analytical literature review. Am J Epidemiol 2002;155:866--74.

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Martin SM, Bean NH. Data management issues for emerging diseases and new tools for managing surveillance and laboratory data. Emerg Infect Dis 1995;1:124--8.

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McNabb S, Surdo A, Redmond A, et al. Applying a new conceptual framework to evaluate tuberculosis surveillance and action performance and measure the costs, Hillsborough County, Florida, 2002. Ann Epidemiol 2004;14:640--5.

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Thacker SB, Choi K, Brachman PS. The surveillance of infectious diseases. JAMA 1983;249:1181--5.

Anthrax

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Botulism

Barzilay, EJ. Botulism and Intestinal Botulism. In: DL Heymann, ed. Control of communicable diseases manual, Washington, DC: American Public Health Association Press; 2008.

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Sobel J. Botulism. Clin Infect Dis 2005;41:1167--73.

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Shapiro RL, Hatheway C, Becher J, Swerdlow DL. Botulism surveillance and emergency response: a public health strategy for a global challenge. JAMA 1997;278:433--5.

Brucellosis

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CDC. Public health consequences of a false-positive laboratory test result for Brucella---Florida, Georgia, and Michigan, 2005. MMWR 2008;57:603--5.

CDC. Laboratory-acquired brucellosis---Indiana and Minnesota, 2006. MMWR 2008;57:39--42.

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Chancroid

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Mertz KJ, Weiss JB, Webb RM, et al. An investigation of genital ulcers in Jackson, Mississippi, with use of a multiplex polymerase chain reaction assay: high prevalence of chancroid and human immunodeficiency virus infection. J Infect Dis 1998;178:1060--6.

Mertz KJ, Trees D, Levine WC, et al. Etiology of genital ulcers and prevalence of human immunodeficiency virus coinfection in 10 US cities. The Genital Ulcer Disease Surveillance Group. J Infect Dis 1998;178:1795

Chlamydia trachomatis infection

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Datta SP, Sternberg, M, Johnson RE, et al. Gonorrhea and chlamydia in the United States among persons 14 to 39 years of age, 1999 to 2002. Ann Intern Med 2007;147:89--96.

Satterwhite CL, Joesoef MR, Datta SD, Weinstock H. Estimates of Chlamydia trachomatis infections among men: United States. Sexually Transm Dis 2007;35:S3--7.

Satterwhite CL, Tian LH, Braxton J, Weinstock H. Chlamydia prevalence among women and men entering the National Job Training Program: United States, 2003--2007. Sex Transm Dis 2010; 37: 63--67.

Cholera

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Coccidioidomycosis

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Cryptosporidiosis

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Cyclosporiasis

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Diphtheria

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Ehrlichiosis and Anaplasmosis

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CDC. Diagnosis and management of tickborne rickettsial diseases: Rocky Mountain spotted fever, ehrlichioses, and anaplasmosis----United States. MMWR 2006;55(No. RR-4).

Demma LJ, Holman RC, McQuiston JH, Krebs JW, Swerdlow DL. Epidemiology of human ehrlichiosis and anaplasmosis in the United States, 2001---2002. Am J Trop Med Hyg 2005;73:400--9.

Giardiasis

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Yoder JS, Harral C, Beach MJ. Giardiasis surveillance---United States, 2006--2008. In: Surveillance Summaries, June 11, 2010. MMWR 2010;59(No. SS-6):15--25.

Yoder JS, Roberts V, Craun GF, et al. Surveillance for waterborne disease and outbreaks associated with drinking water and water not intended for drinking --- United States, 2005--2006. In: Surveillance Summaries, September 12, 2008. MMWR 2008;57 (No. SS-9):39--69.

Stuart JM, Orr HJ, Warburton FG, et al. Risk factors for sporadic giardiasis: a case-control study in southwestern England. Emerg Infect Dis 2003;9:229--33.

CDC. Diagnostic procedures for stool specimens. Atlanta, GA: US Department of Health and Human Services, CDC; 2007. Available at http://www.dpd.cdc.gov/dpdx/HTML/DiagnosticProcedures.htm.

Gonorrhea

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CDC. Sexually transmitted diseases treatment guidelines, 2010. MMWR 2010;59(No. RR-12).

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Datta SD, Sternberg M, Johnson RE, et al. Gonorrhea and chlamydia in the United States among persons 14 to 39 years of age, 1999 to 2002. Ann Int Med 2007;147:89--96.

Haemophilus influenzae, Invasive Disease

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Fry AM, Lurie P, Gidley M, Schmink S, Lingappa J, Rosenstein NE. Haemophilus influenzae type b (Hib) disease among Amish children in Pennsylvania: reasons for persistent disease. Pediatrics 2001;108:1--6.

Dworkin MS, Park L, Borchardt SM. The changing epidemiology of invasive Haemophilus influenzae Disease, especially in persons >65 Years Old. Clin Infect Dis 2007;44:810--6.

Schuchat A, Messonnier NR. From pandemic suspect to the postvaccine era: the Haemophilus influenzae story. Clin Infect Dis 2007;44:817--9.

Bender JM, Cox CM, Mottice S, et al. Invasive Haemophilus influenzae disease in Utah children: An 11-year population-based study in the era of conjugate vaccine. Clin Infect Dis 2010;50:e41--6.

Hansen Disease (Leprosy)

Britton WJ, Lockwood NJ. Leprosy. Lancet 2004;363:1209--19.

Bruce S, Schroeder TL, Ellner K, Rubin H, Williams T, Wolf JE Jr. Armadillo exposure and Hansen’s disease: an epidemiologic survey in southern Texas. J Am Acad Dermatol 2000;43(2 Pt1):223--8.

Hartzell JD, Zapor M, Peng S, Straight T. Leprosy: a case series and review. South Med J 2004;97:1252--6.

Hastings R, ed. Leprosy. 2nd ed. New York, NY: Churchill Livingstone; 1994.

Joyce MP, Scollard DM. Leprosy (Hansen’s disease). In: Rakel RE, Bope ET, eds. Conn’s current therapy 2004: latest approved methods of treatment for the practicing physician. 56th ed. Philadelphia, PA: Saunders; 2004:100--5.

Ooi WW, Moschella SL. Update on leprosy in immigrants in the United States: status in the year 2000. Clin Infect Dis 2001;32:930--7.

Scollard DM, Adams LB, Gillis TP, Krahenbuhl JL, Truman RW, Williams DL. The continuing challenges of leprosy. Clinical Microbiology Reviews, 2006;19(2):338--81.

Hantavirus pulmonary syndrome

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Hjelle B. Hantviruses and hantavirus cardiopulmonary syndrome in the Americas. In: Saluzzo J-F, Dodet B, eds. Factors in the emergence and control of rodent-borne viral diseases: Elsevier 1999;55--62.

Khan AS, Khabbaz RF, Armstrong LR, et al. Hantavirus pulmonary syndrome---the first 100 US cases. J Infect Dis 1996;173:1297--1303.

Levine JR, Fritz CL, Novak MG. Occupational risk of exposure to rodent-borne hantavirus at US forest service facilities in California. Am J Trop Med Hyg 2008;78:352--7.

Hemolytic Uremic Syndrome, Postdiarrheal

Banatvala N, Griffin PM, Greene KD, et al. The United States prospective hemolytic uremic syndrome study: microbiologic, serologic, clinical, and epidemiologic findings. J Infect Dis 2001;183:1063--70.

Gould L, Demma L, Jones TF, et al. Hemolytic uremic syndrome and death in persons with Escherichia coli O157:H7 infection, Foodborne Diseases Active Surveillance Network Sites, 2000--2006. Clin Infect Dis 2009;49:1480--5.

Tarr PI, Gordon CA Chandler WL. Shiga-toxin-producing Escherichia coli and haemolytic uraemic syndrome. Lancet 2005;365:1073--86.

Hepatitis B

Institute of Medicine 2010. Hepatitis and liver cancer: A national strategy for prevention and control of hepatitis B and C. Washington, DC: The National Academics Press.

Wasley A, Kruszon-Moran D, Kuhnert W, et al.. The prevalence of hepatitis B virus infection in the United States in the era of vaccination. J Infect Dis 2010;202:192--201.

Hepatitis B and C

Institute of Medicine 2010. Hepatitis and liver Cancer: A national strategy for prevention and control of hepatitis B and C. Washington, DC: The National Academics Press.

Influenza-Associated Pediatric Mortality

Bhat N, Wright JG, Broder KR, et al. Influenza-associated deaths among children in the United States, 2003--2004. N Engl J Med 2005;352:2559--67.

CDC. Update: Influenza-associated deaths reported among children aged <18 years---United States, 2003--04 influenza season. MMWR 2004;52:1254--5.

CDC. Update: influenza-associated deaths reported among children aged <18 years---United States, 2003--04 influenza Season. MMWR 2004;52:1286--8.

CDC. Mid-year addition of influenza-associated pediatric mortality to the list of nationally notifiable diseases, 2004. MMWR 2004;53:951--2.

CDC. Prevention and control of influenza: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR 2009;58(No. RR-08).

Council of State and Territorial Epidemiologists. Influenza-associated pediatric mortality, 2004. Atlanta, GA: Council of State and Territorial Epidemiologists; 2004. Available at http://www.cste.org/PositionStatementsResolutions2.htm.

Council of State and Territorial Epidemiologists. Position statement 04-ID-04: influenza-associated pediatric mortality 2004. Atlanta, GA: Council of State and Territorial Epidemiologists; 2004. Available at http://www.cste.org/ps/2004pdf/04-ID-04-final.pdf.

Guarner J, Paddock CD, Shieh WJ, et al. Histopathologic and immunohistochemical features of fatal influenza virus infection in children during the 2003--04 season. Clin Infect Dis 2006:43;132--4.

Finelli L, Fiore A, Dhara R, et al. Influenza-associated pediatric mortality in the United States: increase of Staphylococcus aureus coinfection Pediatrics 2008;122:805--11.

Legionellosis

CDC. Surveillance for travel-associated Legionnaires’ disease---United States, 2005--2006. MMWR 2007;56:1261--3.

Fields BS, Benson RF, Besser RE. Legionella and Legionnaires’ disease: 25 years of investigation. Clin Microbiol Rev 2002;15:506--26.

European Working Group on Legionella Infections. European guidelines for control and prevention of travel associated Legionnaires’ disease. London, UK: United Kingdom Health Protection Agency; 2005.

Joseph CA. Legionnaires’ disease in Europe 2000--2002. Epidemiol Infect 2004;132:417--24.

Marston BJ, Lipman HB, Breiman RF. Surveillance for Legionnaires’ disease: risk factors for morbidity and mortality. Arch Intern Med 1994;154:2417--22.

Neil K, Berkelman R. Increasing incidence of legionellosis in the United States: changing epidemiological trends. Clin Infect Dis 2008;47:591--9.

CDC. Increasing incidence of legionellosis in the United States, 2000--2009. MMWR (in press).

Listeriosis

Gottlieb SL, Newbern EC, Griffin PM, et al. Multistate outbreak of listeriosis linked to turkey deli meat and subsequent changes in US regulatory policy. Clin Infect Dis 2006;42:29--36.

Mead PS, Dunne EF, Graves L, et al. Nationwide outbreak of listeriosis due to contaminated meat. Epidemiol Infect 2006;134:744--51.

Mead PS, Slutsker L, Dietz V, et al. Food-related illness and death in the United States. Emerg Infect Dis 1998;5:607--25.

Slutsker L, Schuchat A. Listeriosis in humans. In: Ryser ET Marth EH, eds. Listeria, listeriosis, and food safety. 2nd ed. New York, NY: Marcel Dekker, Inc.; Little, Brown and Company; 1999:75--95.

Voetsch AC, Angulo FJ, Jones TF, et al. Reduction in the incidence of invasive listeriosis in Foodborne Diseases Active Surveillance Network Sites, 1996--2003. Clin Infect Dis 2007;44:513--20.

Lyme disease

Stafford, KC III. Tick management handbook: an integrated guide for homeowners, pest control operators, and public health officials for the prevention of tick-associated disease. New Haven, CT: Connecticut Agricultural Experiment Station; 2004. Available at http://www.cy118119.com/ncidod/dvbid/lyme/resources/handbook.pdf.

Connally NP, Durante AJ, Yousey-Hindes KM, et al. Peridomestic Lyme disease prevention: results of a population-based case-control study. Am J. Prev Med 2009;37:201--6.

Hayes EG, Piesman J. How can we prevent Lyme disease? N Engl J Med 2003;348:2424--30.

Bacon RM, Kugeler KJ, Mead PS. Surveillance for Lyme disease---United States, 1992--2006. In: Surveillance Summaries, October 3, 2008. MMWR 2008;57(No. SS-10)1--9.

CDC. Caution regarding testing for Lyme disease. MMWR 2005;54:125.

Wormser GP, Dattwyler RJ, Shapiro ED, et al. The clinical assessment, treatment, and prevention of Lyme disease, human granulocytic, anaplasmosis, and babesiosis: clinical practice guidelines by the Infectious Disease Society of America. Clin Infect Dis 2006;43:1089--1134.

Malaria

Baird JK. Effectiveness of antimalarial drugs. N Engl J Med 2005;352:1565--77.

Chen LH, Keystone JS. New strategies for the prevention of malaria in travelers. Infect Dis Clin N Amer 2005;19:185--210.

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Leder K, Black J, O’Brien D, et al. Malaria in travelers: a review of the GeoSentinel Surveillance Network. Clin Infect Dis 2004;39:1104--12.

Mali S, Steele S, Slutsker L, Arguin P. Malaria surveillance---United States, 2007. In: CDC Surveillance Summaries, April 17, 2009. MMWR 2009;58(No. SS-2);1--16.

Measles

CDC. Measles--- United States, January--July 2008. MMWR 2008;57:893--6.

Sugerman DE, Barskey, AE. Measles Outbreak in a highly vaccinated population, San Diego 2008: role of the intentionally unvaccinated. Pediatrics 2010; 125:747--755..

Papania M, Hinman A, Katz S, Orenstein W, McCauley M, eds. Progress toward measles elimination---absence of measles as an endemic disease in the United States. J Infect Dis 2004;189(Suppl 1):S1--257.

CDC. National, state, and local area vaccination coverage among children aged 19-35 months---United States, 2006. MMWR 2007;56:880--5.

Rota PA, Liffick SL, Rota JS, et al. Molecular epidemiology of measles viruses in the United States, 1997--2001. Emerg Infect Dis 2002;8:902--8.

CDC. Outbreak of measles---San Diego, California, January--February 2008. MMWR 2008;57:203--6.

Meningococcal Disease

CDC. Prevention and control of meningococcal disease: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR 2005;54(No. RR-7).

Rosenstein NE, Perkins BA, Stephens DS, et al. Meningococcal disease. N Engl J Med 2001;344:1378--88.

Cohn, AC, MacNeil, J, Harrison, et al. Changes in Neisseria meningitidis disease epidemiology in the United States, 1998--2007: implications for prevention of meningococcal disease. Clin Infect Dis 2010:50:184--91.

Mumps

CDC. Mumps outbreak---New York, New Jersey, Quebec, 2009. MMWR 2009;58:1270--4.

Barskey AE, Glasser JW, LeBaron CW. Mumps resurgence in the United States: a historical perspective on unexpected elements. Vaccine 2009; 27:6186--95.

CDC. Updated recommendations of the Advisory Committee on Immunization Practices (ACIP) for the control and elimination of mumps. MMWR 2006; 55:629--30.

Dayan G, Quinlisk P, et al. Recent resurgence of mumps in the United States. New Engl J Med 2008; 358:1580--9.

Anderson LJ, Seward JF. Mumps epidemiology and immunity: the anatomy of a modern epidemic. Pediatr Infect Dis J. 2008;27(Suppl 10):S75--9.

Bitsko RH, Cortese MM, Dayan GH, et al. Detection of RNA of mumps virus during an outbreak in a population with high level of measles, mumps, and rubella vaccine coverage. J Clin Microbiol 2008;46:1101--3.

Marin M, Quinlisk P, Shimabukuro T, et al. Mumps vaccination coverage and vaccine effectiveness in a large outbreak among college students---Iowa, 2006. Vaccine 2008;26:3601--7.

CDC. Updated recommendations for isolation of persons with mumps. MMWR 2008;57:1103--5.

Novel influenza A virus

Olsen CW. The emergence of novel swine influenza viruses in North America. Virus Res 2002;85:199--210.

Dowdle, WR. Influenza pandemic periodicity, virus recycling, and the art of risk assessment. Emerg Infect Dis 2006;12:34--9.

National Pork Board. Influenza: pigs, people and public health. Des Moines, IA: National Pork Board;2004. Available at: http://www.porkboard.org/PorkScience/Documents/PUBLICHEALTH%20influenza.pdf.

Shinde V. Triple-reassortant swine influenza A (H1) in humans in the United States, 2005--2009. N Engl J Med 2009; 360:2616--25

Jain S. Hospitalized patients with 2009 H1N1 influenza in the United States, April--June 2009. N Engl J Med 2009;361:1935--44

Novel Swine-Origin Influenza A (H1N1) Virus Investigation Team. Emergence of a novel swine-origin influenza A (H1N1) virus in humans. N Engl J Med 2009;360:2605--15

Pertussis

Bisgard KM, Rhodes P, Connelly BL, et al. Pertussis vaccine effectiveness among children 6 to 59 months of age in the United States, 1998--2001. Pediatrics 2005;116:e285--94.

Bisgard KM, Pascual FB, Ehresmann KR, et al. Infant pertussis: who was the source? Pediatr Infect Dis J 2004;23:985--9.

CDC. Preventing tetanus, diphtheria, and pertussis among adolescents; use of tetanus toxoid, reduced diphtheria toxoid and acellular pertussis vaccines: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR 2006;55(No. RR-3).

CDC. Recommended antimicrobial agents for the treatment and postexposure prophylaxis of pertussis: 2005 CDC guidelines. MMWR 2005;54(No. RR-14).

CDC. Pertussis---United States, 2001--2003. MMWR 2005;54:1283--6.

Lee GM, Lebaron C, Murphy TV, Lett S, Schauer S, Lieu TA. Pertussis in adolescents and adults: should we vaccinate? Pediatrics 2005;115:1675--84.

CDC. Preventing tetanus, diphtheria, and pertussis among adults: use of tetanus toxoid, reduced diphtheria toxoid and acellular pertussis vaccine (Tdap): recommendations of the Advisory Committee on Immunization Practices (ACIP) and recommendation of ACIP, supported by the Healthcare Infection Control Practices Advisory Committee (HICPAC), for use of Tdap among health-care personnel. MMWR 2006;55(No. RR-17).

Plague

CDC. Human plague---four states, 2006. MMWR 2006; 55:940--3.

Gould LH, Pape J, Ettestadt P et al. Dog-associated risk factors for human plague. Zoonoses and Public Health 2008;55:448--54.

Enscore RE, Biggerstaff BJ, Brown TL, et al. Modeling relationships between climate and the frequency of human plague cases in the southwestern United States, 1960--1997. Am J. Trop Med Hyg 2002;66:186--96.

Inglesby TV, Dennis DT, Henderson DA, et al. Plague as a biological weapon: medical and public health management. Working Group on Civilian Defense. JAMA 2000;283:2281--90.

Dennis DT, Gage KL, Gratz N. Poland JD, Tikhomirov E. Plague manual: epidemiology, distribution, surveillance, and control. Geneva, Switzerland. World Health Organization: 1999.

Poliomyelitis

CDC. Poliovirus infections in four unvaccinated children---Minnesota, August--October 2005. MMWR 2005; 54:1053--5.

Alexander LN, Seward JF, Santibanez TA, et al. Vaccine policy changes and epidemiology of polio in the United States. JAMA 2004;292:1696--702.

CDC. Progress toward interruption of wild poliovirus transmission---worldwide, January 2006--May 2007. MMWR 2007;56:682--5.

CDC. Laboratory surveillance for wild and vaccine-derived polioviruses---worldwide, January 2006--June 2007. MMWR 2007;56:965--9.

CDC. Update on vaccine-derived polioviruses---worldwide, January 2006--August 2007. MMWR 2007;56:996--1001.

CDC. Progress towards interruption of wild poliovirus transmission---worldwide, January 2006--May 2007. MMWR 2008;57:489--94.

Psittacosis

Mitchell SL, Wolff BJ, Thacker WL, et al. Genotyping of Chlamydophila psitttaci by real time PCR and high resolution melt analysis. J Clin Microbiol 2008;47:175--81.

Q Fever

Angelakis E, Raoult D. Q fever. Vet Micro 2010;140:2---309.

Tissot-Dupont D, Raoult D. Q fever. Infect Dis Clin North Am 2008;22:505--14.

Parker N, Barralet J, Bell A. Q fever. The Lancet 2006;367[9511]:679--88.

McQuiston JH, Holman RC, McCall CL, Childs JE, Swerdlow DL, Thompson HA. National surveillance and the epidemiology of Q fever in the United States, 1978--2004. Am J Trop Med Hyg 2006;75:36--40.

Raoult D, Tissot-Dupont H, Foucault C, et al. Q fever 1985--1998. Clinical and epidemiologic features of 1,383 infections [Review]. Medicine 2000:79:109--25.

Rabies

CDC. Compendium of animal rabies prevention and control, 2008: National Association of State and Territorial Public Health Veterinarians, Inc. MMWR 2008; 57(RR-2).

CDC. Use of a reduced (4-dose) vaccine schedule for postexposure prophylaxis to prevent human rabies: recommendations of the Advisory Committee on Immunization Practices. MMWR 2010; 59:(No.RR-2).

CDC. Human rabies prevention---United States, 2008: recommendation of the Advisory Committee on Immunization Practices (ACIP). MMWR 2008;57(No. RR-3).

Rocky Mountain Spotted Fever

Openshaw JJ, Swerdlow DL, Krebs JW, et al. Rocky Mountain spotted fever in the United States, 2000--2007: interpreting contemporary increases in incidence. Am J Trop Med Hyg 2010;83:174--82.

Adjemian JZ, Krebs J, Mandel E, McQuiston, J. Spatial clustering by disease severity among reported Rocky Mountain spotted fever cases in the United States, 2001--2005. Am J Trop Med Hyg 2009;80:72--7.

Walker D. Rickettsiae and rickettsial infections: the current state of knowledge. Clin Infect Dis 2007:45 (Suppl 1):539--44.

CDC. Diagnosis and management of tickborne rickettsial diseases: Rocky Mountain spotted fever, ehrlichioses, and anaplasmosis---United States. MMWR 2006;55(No. RR-4).

Chapman AS, Murphy SM, Demma LJ, et al. Rocky Mountain spotted fever in the United States, 1997--2002. Vector-borne Zoonotic Dis 2006;6:170--8.

Demma LJ, Traeger MS, Nicholson WL, et al. Rocky Mountain spotted fever from an unexpected tick reservoir in Arizona. N Engl J Med 2005;353:587--94.

Rubella, Congenital Rubella Syndrome

CDC. Control and prevention of rubella: evaluation and management of suspected outbreaks, rubella in pregnant women, and surveillance for congenital rubella syndrome. MMWR 2001;50(No. RR-12).

Reef S, Cochi S, eds. The evidence for the elimination of rubella and congenital rubella syndrome in the United States: a public health achievement. Clin Infect Dis 2006;43(Suppl 3):S123--68.

CDC. Achievements in public health: elimination of rubella and congenital rubella syndrome---United States, 1969--2004. MMWR 2005;54:279--82.

Salmonellosis

Braden CR. Salmonella enterica serotype Enteritidis and eggs: a national epidemic in the United States. Clin Infect Dis 2006;43:512--7.

Jones TF, Ingram LA, Cieslak PR, et al. Salmonellosis outcomes differ substantially by serotype. J Infect Dis 2008;198:109--14.

Olsen SJ, Bishop R, Brenner FW, et al. The changing epidemiology of Salmonella: trends in serotypes isolated from humans in the United States, 1987--1997. J Infect Dis 2001;183:756--61.

Voetsch AC, Van Gilder TJ, Angulo FJ, et al. FoodNet estimate of burden of illness caused by nontyphoidal Salmonella infections in the United States. Clin Infect Dis 2004;38(Suppl 3):S127--34.

SARS

CDC. Severe Acute Respiratory Syndrome. Available at http://www.cy118119.com/ncidod/sars.

World Health Organization. Severe Acute Respiratory Syndrome. Available at http://www.who.int/topics/sars/en.

Council of State and Territorial Epidemiologists. 2009 Position statement-09-ID-11: National Surveillance for Severe Acute Respiratory Syndrome. Available at http://www/cste.org/ps2009/09-ID-11.pdf.

Shiga toxin-producing Escherichia coli

Brooks JT, Sowers EG, Wells JB, et al. Non-O157 Shiga toxin-producing Escherichia coli infections in the United States, 1983--2002. J Infect Dis 2005;192:1422--9.

Crump JA, Sulka AC, Langer AJ, et al. An outbreak of Escherichia coli O157:H7 among visitors to a dairy farm. N Engl J Med 2002;347:555--60.

Griffin PM, Mead PS, Sivapalasingam S. Escherichia coli O157:H7 and other enterohemorrhagic E. coli. In: Blaser MJ, Smith PD, Ravdin JI, Greenberg HB, Guerrant RL, eds. Infections of the gastrointestinal tract. Philadelphia, PA: Lippincott Williams & Wilkins; 2002:627--42

Hedican EB, Medus C, Besser JM, Juni BA, et al. Characteristics of O157 versus non-O157 shiga toxin-producing Escherichia coli infections in Minnesota, 2000--2006. Clin Infect Dis 2009;49:358--64.

Mead PS, Griffin PM. Escherichia coli O157:H7. Lancet 1998;352:1207--12.

Tarr PI, Gordon CA Chandler WL. Shiga-toxin-producing Escherichia coli and haemolytic uraemic syndrome. Lancet 2005;365:1073--86.

Shigellosis

Shane A, Crump J, Tucker N, Painter J, Mintz E. Sharing Shigella: risk factors and costs of a multi-community outbreak of shigellosis. Arch Pediatr Adolesc Med 2003;157:601--3.

CDC. Outbreaks of multidrug-resistant Shigella sonnei gastroenteritis associated with day care centers---Kansas, Kentucky, and Missouri, 2005. MMWR 2006;55:1068--71.

Gupta A, Polyak CS, Bishop RD, Sobel J, Mintz ED. Laboratory-confirmed shigellosis in the United States, 1989--2002: epidemiologic trends and patterns. Clin Infect Dis 2004;38:1372--7.

Sivapalasingam S, Nelson JM, Joyce K, Hoekstra M, Angulo FJ, Mintz ED. A high prevalence of antimicrobial resistance among Shigella isolates in the United States, 1999--2002. Antimicrob Agents Chemother 2006;50:49--54.

Arvelo W, Hinkle CJ, Nguyen TA, et al. Transmission risk factors and treatment of pediatric shigellosis during a large daycare center-associated outbreak of multidrug resistant Shigella sonnei: Implications for the management of shigellosis outbreaks among children. Pediatr Infect Dis J 2009;976--80.

Streptococcal Toxic-Shock Syndrome

CDC. Active bacterial core surveillance report. 2010. Emerging Infections Program Network. Group A Streptococcus, 2009-Provisional. Atlanta, GA: US Department of Health and Human Services, CDC; 2010. Available at http://www.cy118119.com/abcs/reports-findings/survreports/gas09.pdf.

Martin JM, Green M. Group A Streptococcus. Seminars in pediatric infectious diseases 2006;17:140--8.

CDC. Investigating clusters of group A Streptococcal disease. Atlanta, GA: US Department of Health and Human Services, CDC:2009. Available at www.cy118119.com/strepAcaluculator.

The prevention of invasive group A streptococcal infections workshop participants. Prevention of invasive group A streptococcal disease among household contacts of case patients among postpartum and postsurgical patients: recommendations from the Centers for Disease Control and Prevention. Clin Infect Dis 2002;35:950--9.

O’Loughlin RE, Roberson A, Cieslak PR, et al. The epidemiology of invasive group A streptococcal infections and potential vaccine implications, United States, 2000---2004. Clin Infect Dis 2007;45:853--62.

Streptococcus pneumoniae, Invasive, Drug-Resistant

Clinical and Laboratory Standards Institute. Performance Standards for Antimicrobial Susceptibility Testing; Eighteenth Informational Supplement. CLSI Document M100-S18. Wayne, PA: Clinical and Laboratory Standards Institute; 2009.

Hsu HE, Shutt KA, Moore MR, et al. Effect of pneumococcal conjugate vaccine on pneumococcal meningitis. N Engl J Med 2009;360:244-56.

Ray GT, Pelton SI, Klugman KP, Strutton DR, Moore MR. Cost-effectiveness of pneumococcal conjugate vaccine: an update after 7 years of use in the United States. Vaccine 2009;27:6483--94.

Weinstein MP, Klugman KP, Jones RN. Rationale for revised penicillin susceptibility breakpoints versus Streptococcus pneumoniae: coping with antimicrobial susceptibility in an era of resistance. Clin Infect Dis 2009;48:1596--600.

CDC. Licensure of a 13-valent pneumococcal conjugate vaccine (PCV13) and recommendations for use among children: Advisory Committee on Immunization Practices (ACIP), 2010. MMWR. 2010;59:258--61.

CDC. Invasive pneumococcal disease in young children before licensure of 13-valent pneumococcal conjugate vaccine--- United States, 2007.MMWR. 2010;59:253--7.

Cohen AL, Harrison LH, Farley MM, et al. Prevention of invasive pneumococcal disease among HIV-infected adults in the era of childhood pneumococcal immunization. AIDS 2010;24:2253--62.

Hanquet G, Perrocheau A, Kissling E, et al. Surveillance of invasive pneumococcal disease in 30 EU countries: Towards a European system? Vaccine 2010;28:3920--8.

Pilishvili T, Lexau C, Farley MM, et al. Sustained reductions in invasive pneumococcal disease in the era of conjugate vaccine. J Infect Dis 2010;201:32--41.

Weatherholtz R, Millar EV, Moulton LH, et al. Invasive pneumococcal disease a decade after pneumococcal conjugate vaccine use in an American Indian population at high risk for disease. Clin Infect Dis 2010;50:1238--46.

Wenger JD, Zulz T, Bruden D, et al. Invasive pneumococcal disease in Alaskan children: impact of the seven-valent pneumococcal conjugate vaccine and the role of water supply. Pediatr Infect Dis J 2010:251--6.

Syphilis, Primary and Secondary

Centers for Disease Control and Prevention. Together we can. The National Plan to Eliminate Syphilis from the United States. Atlanta, GA: US Department of Health and Human Services, May 2006.

Heffelfinger JD, Swint EB, Berman SB, Weinstock HS. Trends in primary and secondary syphilis among men who have sex with men in the United States. Am J Public Health 2007;97:1076--83.

CDC. Sexually transmitted disease surveillance, 2009. Atlanta, GA: US Department of Health and Human Services. CDC.

CDC. Primary and secondary syphilis--- Jefferson County, Alabama, 2002--2007. MMWR 2009;58:463--7.

Tetanus

Pascual FB, McGinley EL, Zanardi LR, Cortese MM, Murphy TV. Tetanus surveillance---United States, 1998--2000. In: CDC Surveillance Summaries, June 20, 2003. MMWR 2003;52(No. SS-3).

CDC. Tetanus---Puerto Rico, 2002. MMWR 2002;51:613--5.

McQuillan GM, Kruszon-Moran D, Deforest A, Chu SY, Wharton M. Serologic immunity to diphtheria and tetanus in the United States. Ann Intern Med 2002;136:660--6.

Trichinellosis

CDC. Trichinellosis associated with bear meat---New York and Tennessee, 2003. MMWR 2004;53:606--10.

Roy SL, Lopez AS, Schantz PM. Trichinellosis surveillance---United States, 1997--2001. In: CDC Surveillance Summaries, July 25, 2003. MMWR 2003;52(No. SS-6).

Gamble HR, Bessonov AS, Cuperlovic K, et al. International Commission on Trichinellosis: recommendations on methods for the control of Trichinella in domestic and wild animals intended for human consumption. Vet Parasitol 2000;93:393--408.

Gottstein B, Pozio E, Nockler K. Epidemiology, diagnosis, treatment, and control of trichinellosis. Clin Microbiol Rev. Jan 2009;22:127--45.

Kennedy ED, Hall RL, Montgomery SP, Pyburn DG, Jones JL. Trichinellosis surveillance---United States, 2002--2007. In: Surveillance Summaries, December 4, 2009. MMWR 2009;58(No. SS-9).

Tuberculosis

CDC. Reported tuberculosis in the United States, 2003. Atlanta, GA: US Department of Health and Human Services, CDC; 2004. Available at http://www.cy118119.com/nchstp/tb.

CDC. Trends in tuberculosis---United States, 2004. MMWR 2005;54:245--9.

Saraiya M, Cookson ST, Tribble P, et al. Tuberculosis screening among foreign-born persons applying for permanent US residence. Am J Public Health 2002;92:826--9.

Talbot EA, Moore M, McCray E, Binkin NJ. Tuberculosis among foreign-born persons in the United States, 1993--1998. JAMA 2000;284:2894--900.

Tularemia

CDC. Tularemia---United States, 1990--2000. MMWR 2002;51:182--4.

Dennis DT, Inglesby TV, Henderson, DA, et al. Tularemia as a biological weapon: medical and public health management. JAMA 2001;285:2763--73.

CDC. Tularemia---Missouri, 2000--2007. MMWR 2009;58:744--8.

Kugeler KJ, Mead PS, Janusz AM, et al. Molecular epidemiology of Francisella tularensis in the United States. Clin Infect Dis 2009;48: 863--70.

Tarnvik A. WHO Guidelines on Tularaemia. Vol. WHO/CDS/EPR/2007.7. Geneva, Switzerland: World Health Organization; 2007

Typhoid Fever

Gupta S, Medalla F, Omondi MW, et al. Laboratory-based surveillance for paratyphoid fever in the United States: travel and antimicrobial resistance. Clin Infect Dis; 2008;46:1656-63.

Kubota K, Barrett TJ, Hunter S et al. Analysis of Salmonella serotype Typhi pulsed-field gel electrophoresis patterns associated with international travel. J Clin Micro 2005;43:1205--9.

Olsen SJ, Bleasdale SC, Magnano AR, et al. Outbreaks of typhoid fever in the United States, 1960--1999. Epidemiol Infect 2003;130:13--21.

Steinberg EB, Bishop RB, Dempsey AF, et al. Typhoid fever in travelers: who should be targeted for prevention? Clin Infect Dis 2004;39:186--91.

Lynch MF, Blanton EM, Bulens S, et al. Typhoid fever in the United States, 1999--2006. JAMA 2009;302:898--9

Varicella

CDC. Prevention of varicella: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR 2007;56(RR-4). Available at: http://www.cy118119.com/mmwr/PDF/rr/rr5604.pdf.

Marin M, Meissner HC, Seward JF. Varicella prevention in the United States: a review of successes and challenges. Pediatrics 2008;122:e744-e51.

Guris D, Jumaan AO, Mascola L, et al. Changing varicella epidemiology in active surveillance sites---United States, 1995--2005. J Infect Dis 2008;197 Suppl 2:S71--5.

Vibriosis

Daniels NA, MacKinnon L, Bishop R, et al. Vibrio parahaemolyticus infections in the United States, 1973-1998. J Infect Dis 2000;181:1661--6.

Dechet A, Yu PA, Koram N, Painter J. Nonfoodborne vibrio infections: an important cause of morbidity and mortality in the United States, 1997--2006. Clin Infect Dis;46:970--6.

McLaughlin JB, DePaola A, Bopp CA, et al. Outbreak of Vibrio parahaemolyticus gastroenteritis associated with Alaskan oysters. N Engl J Med 2005;353:1463--70.

Shapiro RL, Altekruse S, Hutwagner L, et al. The role of Gulf Coast oysters in warmer months in Vibrio vulnificus infections in the United States, 1998--1996. J Infect Dis 1998;178:752--9.

Viral hemorrhagic fever

Rollin PE, Nichol ST, Zaki S, Ksiazek TG. Arenaviruses and filoviruses. In: Manual of Clinical Microbiology, 9th ed 2007; ASM Press, Washington, 1510--22.

Fichet-Calvet E, Rogers DJ. Risk maps of Lassa fever in West Africa. PLoS Neglected Tropical Diseases 2009; 3(3):e388.

Ergonul O. Crimean-Congo Haemorrhagic Fever. Lancet Infectious Diseases 2006; 6(4):203--14.

Amorosa V, MacNeil A, McConnell R, et al. Imported Lassa fever, Pennsylvania, USA, 2010. Emerg Infect Dis. 2010;16:1598--600.

CDC. Imported case of Marburg Hemorrhagic fever---Colorado, 2008. MMWR 2009; 58:1377--1381.