Summary of Notifiable Diseases — United States, 2012

Please note: An erratum has been published for this article. To view the erratum, please click here.

Deborah A. Adams, Coordinator, Summary of Notifiable Diseases

Ruth Ann Jajosky, DMD

Umed Ajani, MBBS

Jeffrey Kriseman, PhD

Pearl Sharp

Diana H. Onweh

Alan W. Schley

Willie J. Anderson

Anna Grigoryan, MD

Aaron E. Aranas, MPH

Michael S. Wodajo

John P. Abellera, MPH

Division of Health Informatics and Surveillance ,

Office of Public Health Scientific Services, CDC

Preface

The Summary of Notifiable Diseases — United States, 2012 contains the official statistics, in tabular and graphic form, for the reported occurrence of nationally notifiable infectious diseases in the United States for 2012. Unless otherwise noted, the data are final totals for 2012 reported as of June 30, 2013. 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/mmwr_nd/index.html. This site also includes Summary publications from previous years.

The Highlights section presents noteworthy epidemiologic and prevention information for 2012 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 2012.* The tables provide the number of cases reported to CDC for 2012 and the distribution of cases by month, geographic location, and patients' demographic characteristics (e.g., age, sex, race, and ethnicity). Part 2 contains graphs and maps that depict summary data for selected 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 1981. This section also includes a table enumerating deaths associated with specified notifiable diseases reported to CDC's National Center for Health Statistics (NCHS) during 2004–2010. 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 the Data Operations Team at soib@cdc.gov.

Background

The infectious diseases designated as notifiable at the national level during 2012 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/lyme/. 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. Rather, it is a 'system of systems', which is coordinated at the national level across disease-specific programs in order to optimize data compilation, analysis, and dissemination of notifiable disease data.

Case notifications about nationally notifiable diseases are sent to CDC voluntarily without personal identifiers by state and selected local health departments. Data about nationally notifiable diseases are obtained through reportable disease surveillance. Health-care providers, hospitals, laboratories, and other public health reporters are required by legislation, regulation, or rules to report cases about reportable diseases and conditions to local, county, state, or territorial public health authorities. Case-reporting of reportable diseases 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 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 reportable varies by reporting jurisdiction and year. The list of notifiable diseases (the diseases or conditions that state and local health departments send to CDC) also might vary by year. Current and historic national public health surveillance case definitions used for classifying and enumerating cases consistently at the national level across reporting jurisdictions are available at http://wwwn.cdc.gov/nndss/script/casedefDefault.aspx.

Infectious Diseases Designated as Notifiable at the National Level During 2012*

Anthrax

Arboviral diseases, neuroinvasive and nonneuroinvasive

California serogroup viruses

Eastern equine encephalitis virus

Powassan virus

St. Louis encephalitis virus

West Nile virus

Western equine encephalitis virus

Babesiosis

Botulism

foodborne

infant

other (wound and unspecified)

Brucellosis

Chancroid

Chlamydia trachomatis infection

Cholera

toxigenic Vibrio cholerae 01 or 0139

Coccidioidomycosis

Cryptosporidiosis†

Cyclosporiasis

Dengue virus infections

Dengue fever

Dengue hemorrhagic fever

Dengue shock syndrome

Diphtheria

Ehrlichiosis/Anaplasmosis

Ehrlichia chaffeensis

Ehrlichia ewingii

Anaplasma phagocytophilum

Undetermined human ehrlichiosis/anaplasmosis

Giardiasis

Gonorrhea

Haemophilus influenzae, invasive disease

Hansen disease (leprosy)

Hantavirus pulmonary syndrome

Hemolytic uremic syndrome, post-diarrheal

Hepatitis, viral

Hepatitis A, acute†

Hepatitis B, acute†

Hepatitis B virus, perinatal infection

Hepatitis B, chronic†

Hepatitis C, acute†

Hepatitis C, past or present†

Human Immunodeficiency Virus (HIV) infection diagnosis§

Influenza-associated pediatric mortality

Invasive pneumococcal disease

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

Rubella

Rubella, congenital syndrome

Salmonellosis†

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

Shiga toxin-producing Escherichia coli (STEC)

Shigellosis†

Smallpox

Spotted fever rickettsiosis

Streptococcal toxic-shock syndrome

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†

any species of the family Vibrionaceae, other than toxigenic Vibrio cholerae 01 or 0139

Viral Hemorrhagic Fever

Crimean-Congo Hemorrhagic fever virus

Ebola virus

Lassa virus

Lujo virus

Marburg virus

New World Arenaviruses (Guanarito, Lujo, Machupo, Junin, and Sabia viruses)

Yellow fever

* This list reflects position statements approved in 2011 by the Council of State and Territorial Epidemiologists (CSTE) for national surveillance, which were implemented in January 2012. No additions or deletions of diseases or conditions were made to the list of nationally notifiable infectious diseases. National surveillance case definitions for these diseases and conditions are available at http://wwwn.cdc.gov/nndss/.

† The year 2012 reflects a modified surveillance case definition for this condition, per approved 2011 CSTE position statements.

§ AIDS has been reclassified as HIV stage III.

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 differ from 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 7, 2012 through the week ending December 29, 2012. More information regarding infectious notifiable diseases, including national surveillance case definitions, is available at http://wwwn.cdc.gov/nndss. 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 2012 NNDSS event code list (Exhibit).

The print criteria for NNDSS are as follows: for a report of a nationally notifiable disease to print in MMWR, the reporting state or territory must have designated the disease reportable in their state or territory for the year corresponding to the year of report to CDC. After the criterion is met, the disease-specific criteria listed in the Exhibit are applied. When the above-listed table indicates that all reports will be earmarked for printing, this means that cases designated with unknown or suspect case confirmation status will print just as probable and confirmed cases will print. Because CSTE position statements are not customarily finalized until July of each year, the NNDSS data for the newly added conditions are not usually available from all reporting jurisdictions until January of the year following the approval of the CSTE position statement.

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 Public Health Scientific Services

National Center for Health Statistics (NCHS)

Office of Vital and Health Statistics Systems (deaths from selected notifiable diseases)

Office of Infectious Diseases

National Center for HIV/AIDS, Viral Hepatitis, STD and TB Prevention

Division of HIV/AIDS Prevention (AIDS and HIV infection), Division of Viral Hepatitis, 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, initial detections of novel influenza A virus infections)
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)

NCHS postcensal estimates of the resident population of the United States for July 1, 2011–July 1, 2012, by year, county, single-year of age (range: 0 to ≥85 years), bridged-race, (white, black or African American, American Indian or Alaska Native, Asian or Pacific Islander), Hispanic origin (not Hispanic or Latino, Hispanic or Latino), and sex (Vintage 2011), prepared under a collaborative arrangement with the U.S. Census Bureau. Population estimates for states are available at http://www.cy118119.com/nchs/nvss/bridged_race/data_documentation.htm#vintage2011 as of June 13, 2013.

Population estimates for territories are 2012 estimates from the U.S. Census Bureau. 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 reportable or was not available are 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 jurisdiction of the person's "usual residence" at the time of disease onset (http://wwwn.cdc.gov/nndss/document/11-SI-04.pdf). 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 jurisdiction should submit the case notification to CDC).

Data reported in the Summary are useful for analyzing disease trends and determining relative disease numbers. 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 actual 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 caused by the transition from NETSS to the National Electronic Disease Surveillance System (NEDSS), which 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 as individual case reports. In 1990, using NETSS, states began electronically capturing and reporting individual cases 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. One of the objectives of NEDSS is to improve the accurracy, completeness, and timeliness of disease reporting at the local, atate, and national levels. A major feature of NEDSS 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. Certain public health surveillance information systems are NEDSS-compatible. In 2001, CDC initiated development of the first NEDSS-compatible system, which is referred to as the NEDSS Base System (NBS). The first state went into production with the NBS in 2003. Since the development of the NBS, states and vendors have developed several other NEDSS compatible systems.

A total of 57 health departments (50 state health departments, 2 city health departments [New York City and Washington DC] and 5 territorial health departments) send CDC notifiable disease data for inclusion in this report. As of October 2012, all 50 state health departments use NEDSS-compatible public health surveillance information systems: 32 (64%) use state- or vendor-developed systems and 18 (36%) use the CDC-developed NBS. In addition, New York City uses a vendor-developed system and Washington DC uses both the NBS and a vendor-developed system. Lastly, as of October 2012, all five territorial health departments were not using NEDSS–compatible systems. Additional information concerning NEDSS is available at http://wwwn.cdc.gov/nndss/script/nedss.aspx.

Method 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. Only data from reporting jurisdictions which made the nationally notifiable condition reportable are included in the tables of this report. This ensures the data displayed in this report are from population-based surveillance efforts, and are generally comparable across jurisdictions. When a nationally notifiable disease is not reportable in a reporting jurisdiction, an "N" indicator for "not reportable" is inserted in the table for the specified reporting jurisdiction and year. Determining which nationally notifiable infectious diseases are reportable in NNDSS reporting jurisdictions was decided by asking them to update previously analyzed results of the 2010 CSTE State Reportable Conditions Assessment (SRCA) individually, because the 2012 SRCA results were not available at the time this report was prepared. The 2010 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 >6 months in 2010 by clinicians, laboratories, hospitals, or "other" public health reporters, as mandated by law or regulation. Additional background information about the SRCA has been published previously (2).

Revised International Health Regulations

In May 2005, the World Health Assembly adopted revised International Health regulations (IHR) (3) 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. All WHO member states are required to notify WHO of a potential PHEIC. WHO makes the final determination about the existence of a PHEIC.

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. IHR will help countries work together to identify, respond to, and share information about PHEIC.

The revised IHR reflects 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. A PHEIC is an event that falls 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 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 reported to WHO.

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 (4). 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. 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 and http://www.cy118119.com/globalhealth/ihregulations.htm. At its annual meeting in June 2007, CSTE approved a position statement to support the implementation of IHR in the United States (4). 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 (5).

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. Jajosky R, Rey A, Park M, et al. Findings from the Council of State and Territorial Epidemiologists' 2008 assessment of state reportable and nationally notifiable conditions in the United States and considerations for the future. Public Health Manag Pract 2011;17:255–64.
3. World Health Organization. Third report of Committee A. Annex 2. Geneva, Switzerland: World Health Organization; 2005. Available at http://whqlibdoc.who.int/publications/2008/9789241580410_eng.pdf.
4. 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://c.ymcdn.com/sites/www.cste.org/resource/resmgr/PS/07-ID-06.pdf.
5. Council of State and Territorial Epidemiologists. Council of State and Territorial Epidemiologists position statement; 2007. National reporting for initial detections of novel influenza A viruses. Available at http://c.ymcdn.com/sites/www.cste.org/resource/resmgr/PS/07-ID-01.pdf.

Highlights for 2012

Below are summary highlights for certain national notifiable diseases. Highlights are intended to assist in the interpretation of major occurrences that affect disease incidence or surveillance trends (e.g., outbreaks, vaccine licensure, or policy changes).

Anthrax

Naturally occurring outbreaks of anthrax occur every year among U.S. wildlife and livestock populations. In 2012, anthrax outbreaks were reported in states that routinely experience such outbreaks including Texas, North Dakota, and Nevada; however, livestock outbreaks occurred in 2012 in Mississippi, Oregon, and Colorado, where anthrax outbreaks had not been reported in livestock for 20 years or more. These outbreaks were associated with potential cutaneous exposures in persons handling and disposing of affected livestock and collecting diagnostic specimens. Although no human infections resulted, these exposures reflect the importance of timely recognition of anthrax in susceptible animals and the use of appropriate protective measures to prevent human exposures.

Domestic Arboviral Disease, Neuroinvasive and Nonneuroinvasive

During 2012, a large multistate outbreak of West Nile virus (WNV) disease occurred, and more cases were reported nationally than in any year since 2003 (1). A total of 5,674 WNV disease cases were reported, including 2,873 cases of neuroinvasive disease (e.g., meningitis, encephalitis, and acute flaccid paralysis) and 286 deaths. WNV disease cases were reported from 48 states (including the first reported from Maine), the District of Columbia, and Puerto Rico. However, approximately half of the WNV neuroinvasive disease cases were reported from just four states: California, Illinois, Louisiana, and Texas. Despite an increased incidence of neuroinvasive disease in 2012, national surveillance data showed no evidence of changes in epidemiology or increased disease severity compared with the previous 8 years (2).

After WNV, the next most commonly reported cause of neuroinvasive arboviral disease was La Crosse virus, followed by Eastern equine encephalitis virus, Powassan virus, and St. Louis encephalitis virus. The 15 Eastern equine encephalitis disease cases were the largest reported since 2005, and included the first ever reported from Vermont. Eastern equine encephalitis virus disease, although rare, remained the most severe domestic arboviral disease, with a 33% case fatality rate.

1. CDC. West Nile virus disease and other arboviral diseases—United States, 2012. MMWR 2013;62:513–7.
2. Lindsey NP, Staples JE, Delorey MJ, Fischer M. Lack of evidence of increased West Nile virus disease severity in the United States in 2012. Am J Trop Med Hyg 2014;90:163–8.

Babesiosis

Babesiosis, a tickborne disease, is caused by protozoan parasites of the genus Babesia that infect red blood cells. Babesia infection can range from asymptomatic to life threatening. Clinical manifestations might include fever, chills, other nonspecific influenza-like symptoms, and hemolytic anemia. Babesia parasites usually are tickborne, but they also are transmissible via blood transfusion or congenitally (1). In recent years, reports of tickborne and transfusion-associated cases have increased in number and geographic distribution (1).

During 2012, a total of 911 unique cases were reported among residents of 14 of the 22 states where babesiosis surveillance was conducted; 871 (96%) cases were reported among residents of seven states (Connecticut, Massachusetts, Minnesota, New Jersey, New York, Rhode Island, and Wisconsin). The median age of patients was 62 years (range: age <1–98 years); 572 (63%) were male, 308 (34%) were female, and the sex was unknown for 31 (3%). Among the patients for whom data were available, 459 (72%) of 638 had symptom onset dates during June–August.

1. Herwaldt BL, Linden JV, Bosserman E, et al. Transfusion-associated babesiosis in the United States: a description of cases. Ann Intern Med 2011;155:509–19.

Botulism

Botulism is a severe paralytic illness caused by toxins produced by Clostridium botulinum. Exposure to toxin can occur by ingestion (foodborne botulism), in situ production from C. botulinum colonization of either a wound (wound botulism) or the gastrointestinal tract (infant botulism and adult intestinal colonization botulism), or overdose of botulinum toxin used for cosmetic or therapeutic purposes (1). Instances of reported botulism from all of these exposure routes were reported in 2012, with infant botulism remaining the most frequently observed transmission category. During 2012, two outbreaks (events with two or more cases) of foodborne botulism (four cases and eight cases) occurred in an Arizona prison. These cases were associated with consumption of pruno, an illicit alcoholic brew. Additionally, an outbreak (two cases) was associated with home-canned spaghetti and meat, and another (three cases) with home-canned beets.

All states maintain 24-hour telephone services for reporting of botulism and other public health emergencies. Health-care providers should report suspected botulism cases immediately to their state health departments. CDC maintains intensive surveillance for cases of botulism in the United States and provides consultation and antitoxin for suspected cases. State health departments can reach the CDC botulism duty officer on call 24 hours a day, 7 days a week, via the CDC Emergency Operations Center (telephone: 770–488–7100).

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

Brucellosis

The number of brucellosis cases reported in 2012 increased by 44%, from 79 cases in 2011 to 114 cases in 2012. Although cases reported from Arizona, California, Florida, Illinois, North Carolina, and Texas accounted for almost three quarters (73.7%) of the reported cases, the number of reported cases from Florida in 2012 was more than doubled that reported in 2011. Health-care providers and health departments are encouraged to continue reporting cases to CDC. In an effort to remind laboratories working with the Brucella spp. of exposure risks associated with specimen handling and manipulation, the Bacterial Special Pathogens Branch (BSPB) has recently updated laboratory exposure risk assessment and PEP guidelines (1), which are now available at http://www.cy118119.com/brucellosis/laboratories/risk-level.html.

Recommendations for safe laboratory practices when handling Brucella spp. can be found at http://www.cy118119.com/brucellosis/laboratories/safety.html. BSPB is available for assistance with evaluating risk occurring after laboratory exposures, and can be contacted via e-mail (bspb@cdc.gov), or by telephone (404–639–1711).

1. Traxler RM, Guerra MA, Morrow MG, et al. Review of brucellosis cases from laboratory exposures in the United States in 2008 to 2011 and improved strategies for disease prevention. J Clin Microbiol 2013;51:3132–6.

Chlamydia

In 2012, more than 1.4 million cases of Chlamydia trachomatis infections were reported; the largest number of cases ever reported to CDC for any condition (1). This case count corresponds to a rate of 456.7 cases per 100,000 population, an increase of only 0.7% compared with the rate in 2011, the smallest annual increase since nationwide reporting for chlamydia began. The rate among women aged 15–19 years decreased 5.6% from 3,485.2 cases per 100,000 females in 2011 to 3,291.5 cases per 100,000 women in 2012. Similarly, chlamydia rates for men aged 15–19 years decreased 5.1% from 816.3 cases per 100,000 males in 2011 to 774.8 cases per 100,000 males in 2012. This is the first time that chlamydia rates among persons aged 15–19 years have decreased since 2000. Because chlamydial infections are usually asymptomatic, reported case rates are affected by screening coverage. Decreases in reported cases might reflect reduced screening or changes in morbidity.

1. CDC. Sexually transmitted disease surveillance 2012. Atlanta, GA: US Department of Health and Human Services; 2014.

Cholera

Cholera continues to be rare in the United States and is most often acquired during travel in countries where toxigenic Vibrio cholerae O1 or O139 is circulating (1). Since epidemic cholera emerged in Haiti in October 2010, associated cases have been reported in the United States in travelers who have recently arrived from Hispaniola (2). Of the 17 cholera infections reported in the United States in 2012, a total of 16 were travel-associated; 12 patients had arrived recently from Hispaniola (nine from Haiti and three from the Dominican Republic) and four from other cholera-affected countries. Cholera remains a global threat to health, particularly in areas with poor access to improved water and sanitation, such as Haiti and sub-Saharan Africa (3,4).

1. Steinberg EB, Greene KD, Bopp CA, et al. Cholera in the United States, 1995–2000: trends at the end of the twentieth century. J Infect Dis 2001;184:799–802.
2. Newton AE, Heiman KE, Schmitz A, et al. Cholera in United States associated with epidemic in Hispaniola. Emerg Infect Dis 2011;17:2166–8.
3. Tappero JW, Tauxe RV. Lessons learned during public health response to cholera epidemic in Haiti and the Dominican Republic. Emerg Infect Dis 2011;17:2087–93.
4. Mintz ED, Guerrant RL. A lion in our village—the unconscionable tragedy of cholera in Africa. N Engl J Med 2009;360:1060–3.

Coccidioidomycosis

Coccidioidomycosis is a fungal infection caused by inhalation of airborne Coccidioides spp. spores that are present in the arid soil of California, other parts of the southwestern United States, and parts of Central and South America. After a substantial overall increase during 1998–2011 (1), the incidence of reported coccidioidomycosis decreased by approximately 22% during 2012. The decrease was similar in Arizona and California, the two states that report the most cases. Incidence decreased among all age groups, although rates remained highest among persons aged ≥60 years. Since 2009, the majority of cases have occurred among women in Arizona, whereas the majority of cases have occurred among men elsewhere in the United States.

The reasons for the recent decrease are not known but might be related to changes in the environment, changes in the at-risk population, or changes in testing practices. The majority of laboratories in endemic areas perform testing using an enzyme immunoassay, the specificity of which is controversial (2). Despite the decrease in reported cases in 2012, the morbidity of this disease in Arizona and California remains considerable (3). Coccidioidomycosis is currently the second most commonly reported infectious condition in Arizona (12,920) and the fifth in California (4,431). More than 25,000 coccidioidomycosis-associated hospitalizations occurred in California during 2000–2011, totaling more than $2 billion in hospital charges (4). 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 areas in which the disease is endemic.

1. CDC. Increase in reported coccidioidomycosis—United States, 1998–2011. MMWR 2013;62:217–21.
2. Kuberski T, Herrig J, Pappagianis D. False-positive IgM serology in coccidioidomycosis. J Clin Microbiol 2010;48:2047–9.
3. Hector RF, Rutherford GW, Tsang CA, et al. The public health impact of coccidioidomycosis in Arizona and California. Int J Environ Res Public Health 2011;8:1150–73.
4. Sondermeyer G, Lee L, Gilliss D, Tabnak F, Vugia D. Coccidioidomycosis-associated hospitalizations, California, USA, 2000–2011. Emerg Infect Dis 2013;19:1590–7.

Congenital Rubella Syndrome

Infection with rubella virus during pregnancy, generally during the first trimester, can result in congenital rubella syndrome (CRS) in the infant. The devastating manifestations of CRS can include deafness, cataracts, cardiac defects, mental retardation, and death (1). With the elimination of rubella from the United States, congenital rubella syndrome is rare in this country (2). However, rubella still circulates outside the Western hemisphere, especially in regions where rubella vaccination programs are not well developed (3). In 2012, three infants were born in the United States with CRS. All three mothers had been in Africa early during their pregnancies (4).

1. Plotkin SA, Reef SE. Rubella vaccine. In: Plotkin SA, Orenstein WA, Offit PA, eds. Vaccines. 5th ed. Philadelphia, PA: Elsevier, 2008:735–71.
2. CDC. Elimination of rubella and congenital rubella syndrome—United States, 1969–2004. MMWR 2005;54:279–82.
3. World Health Organization. Immunization surveillance, assessment and monitoring. Geneva, Switzerland: World Health Organization; 2014. Available at http://www.who.int/entity/immunization_monitoring/data/year_vaccine_introduction.xls.
4. CDC. Three cases of CRS in the post-elimination era, Alabama, Illinois, and Maryland, 2012. MMWR 2013;62:226–9.

Cryptosporidiosis

Cryptosporidiosis is a nationally notifiable gastrointestinal illness caused by the extremely chlorine-tolerant protozoa of the genus Cryptosporidium. Cryptosporidium is transmitted by the fecal-oral route with the ingestion of Cryptosporidium oocysts through the consumption of fecally contaminated food or water or through direct person-to-person or animal-to-person contact.

Although cryptosporidiosis affects persons in all age groups, cases are reported most frequently in children aged 1–4 years (1). A substantial increase in transmission of Cryptosporidium in children occurs during summer through early fall, coinciding with increased use of recreational water, which is a known risk factor for cryptosporidiosis. Cryptosporidium has emerged as the leading cause of reported recreational water-associated outbreaks (2). Transmission through recreational water is facilitated by the substantial number of Cryptosporidium oocysts that can be shed in a single bowel movement (3), the extended time that oocysts can be shed (4), the low infectious dose (5), and the extreme tolerance of Cryptosporidium oocysts to chlorine (6).

To reduce the number of cryptosporidiosis cases associated with recreational water, enhanced public health prevention measures are needed. In the United States, pool codes are reviewed and approved by state or local public health officials; no federal agency regulates the design, construction, and operation of public treated recreational water venues (e.g., pools). This lack of uniform national standards has been identified as a barrier to the prevention and control of outbreaks associated with treated recreational water. To provide support to state and local health departments, CDC is sponsoring development of the Model Aquatic Health Code (MAHC) (http://www.cy118119.com/mahc). MAHC is a collaborative effort between local, state, and federal public health agencies and the aquatics sector to develop a data-driven, knowledge-based resource for state and local jurisdictions reviewing and updating their existing pool codes to optimally prevent and control recreational water-associated illness, including cryptosporidiosis. The first official edition of MAHC will be available in the summer of 2014.

The systematic collection and molecular characterization of Cryptosporidium isolates would further the understanding of U.S. cryptosporidiosis epidemiology by revealing transmission patterns and potential risk factors (7). Such an effort would require phasing out the practice of preserving stool specimens with formalin, which decreases the ability to perform molecular amplification methods.

1. CDC. Cryptosporidiosis surveillance—United States, 2009–2010. MMWR 2012;61:(No. SS-5).
2. CDC. Surveillance for waterborne disease outbreaks and other health events associated with recreational water—United States, 2007–2008. MMWR 2011;60:(No. SS-12).
3. Goodgame RW, Genta RM, White AC, Chappell CL. Intensity of infection in AIDS-associated cryptosporidiosis. J Infect Dis 1993;167:704–9.
4. Jokipii L, Jokipii AM. Timing of symptoms and oocyst excretion in human cryptosporidiosis. N Engl J Med 1986;315:1643–7.
5. Chappell CL, Okhuysen PC, Langer-Curry R, et al. Cryptosporidium hominis: experimental challenge of healthy adults. Am J Trop Med Hyg 2006;75:851–7.
6. Shields JM, Hill VR, Arrowood MJ, Beach MJ. Inactivation of Cryptosporidium parvum under chlorinated recreational water conditions. J Water Health 2008;6:513–20.
7. Chalmers RM, Elwin K, Thomas AL, Guy EC, Mason B. Long-term Cryptosporidium typing reveals the aetiology and species-specific epidemiology of human cryptosporidiosis in England and Wales, 2000 to 2003. Euro Surveill 2009;14:2.

Cyclosporiasis

Approximately one third of the laboratory-confirmed cases of cyclosporiasis—and the only outbreak—that were reported in the United States in 2012 occurred in Texas. Overall, CDC received notification of 44 laboratory-confirmed cases in Texas residents during 2012, nine of which were classified as outbreak associated. The illnesses in the reported outbreak were associated with eating at a Mexican-style restaurant in Texas during June and July 2012. Because many of the food items served at the restaurant contained similar combinations of ingredients, no vehicle of infection could be definitively implicated.

Of the 35 confirmed cases in Texas residents that were not associated with this restaurant, 31 occurred in persons not known to have traveled outside of the United States or Canada during the 14 days before becoming ill; their illness onset dates ranged from mid-June to mid-September. Even after excluding the nine restaurant-associated cases, the number of cases reported in Texas during 2012 was substantially higher than the 14 cases reported in 2011. During 2012, although the Texas Department of State Health Services conducted an epidemiologic investigation of the non-restaurant–associated cases, no vehicles of infection could be implicated. Molecular subtyping tools, which would facilitate linking cases to each other and to particular food items or sources, are not yet available for Cyclospora cayetanensis (1,2).

1. Hall RL, Jones JL, Herwaldt BL. Surveillance for laboratory-confirmed sporadic cases of cyclosporiasis–United States, 1997–2008. MMWR 2011;60:(No. SS-2).
2. Herwaldt BL. The ongoing saga of US outbreaks of cyclosporiasis associated with imported fresh produce: what Cyclospora cayetanensis has taught us and what we have yet to learn. In: Institute of Medicine. Addressing foodborne threats to health: policies, practices, and global coordination. Washington, DC: The National Academies Press; 2006:85–115, 133–40.

Dengue

During 2012, Florida, California, and Illinois reported the largest number of dengue cases in the 50 United States. In late 2012, an epidemic began in Puerto Rico, resulting in more reported cases in this territory than during 2011, but fewer than during the large epidemic in 2010. Persons of all age groups (range: age 0–9 through >80) were affected by dengue in 2012. The majority of dengue cases reported in the United States in 2012 were travel-associated and from top travel destinations (Jamaica, Dominican Republic, Haiti, and Puerto Rico).

Diphtheria

During 2012, one probable, nonfatal case of diphtheria was reported to CDC representing the first since 2003. One man aged 28 years who was a resident of New York had a positive polymerase chain reaction test for diphtheria tox gene A and B. The patient was inadequately immunized and also had a history of AIDS. All close family members were culture negative.

Ehrlichiosis and Anaplasmosis

In 2012, the reported incidence of Ehrlichia chaffeensis (1,128 cases) and Anaplasma phagocytophilum (2,389) were within the range of the incidence of the previous 5 years. A total of 17 cases of Ehrlichia ewingii were reported, with Illinois, Kansas, and Virginia each reporting a case for the first time. Increased use of molecular methods might be responsible for differentiating more reported cases of E. ewingii from E. chaffeensis and A. phagocytophilum.

Giardiasis

Giardia is transmitted through the fecal-oral route with the ingestion of Giardia cysts through the consumption of fecally contaminated water or through person-to-person (or, to a lesser extent, animal-to-person) transmission. Giardiasis normally is characterized by diarrhea, abdominal cramps, bloating, weight loss, and malabsorption.

Although giardiasis is the most common enteric parasitic infection in the United States and no declines in incidence have occurred in recent years, knowledge of its epidemiology remains incomplete. Giardiasis symptomatology is variable, infected persons can shed Giardia for several weeks, and recent studies indicate a potential for chronic sequelae from giardiasis (1,2). New epidemiologic studies are needed to identify effective public health prevention measures.

The majority of data on giardiasis transmission come from outbreak investigations; however, the overwhelming majority of reported giardiasis cases are not linked to known outbreaks. During 2009–2010, <1% of reported giardiasis cases were associated with outbreaks (3). The relative contributions of person-to-person, animal-to-person, foodborne, and waterborne transmission to sporadic human giardiasis in the United States are not well understood.

Until recently, no reliable serologic assays for Giardia have been available, and no population studies of Giardia seroprevalence have been conducted. With recent laboratory advances (4), such studies might now be feasible and would contribute substantially to understanding the prevalence of giardiasis in the United States. Enhanced genotyping methods would increase knowledge of the molecular epidemiology of Giardia, including elucidating species-specific subassemblages (5). These tools, combined with traditional epidemiology and surveillance, would improve understanding of giardiasis risk factors, enable researchers to identify outbreaks by linking cases currently classified as sporadic infections, and provide risk factor information needed to inform prevention strategies.

1. Cantey PT, Roy S, Lee B, et al. Study of nonoutbreak giardiasis: novel findings and implications for research. Am J Med 2011;124:1175.e1–8.
2. Wensaas KA, Langeland N, Hanevik K, et al. Irritable bowel syndrome and chronic fatigue 3 years after acute giardiasis: historic cohort study. Gut 2012;61:214–9.
3. CDC. Giardiasis surveillance—United States, 2009–2010. MMWR 2012;61:(No. SS-5).
4. Priest JW, Moss DM, Visvesvara GS, et al. Multiplex assay detection of immunoglobulin G antibodies that recognize Giardia intestinalis and Cryptosporidium parvum antigens. Clin Vaccine Immunol 2010;17:
   1695–707.
5. Feng Y, Xiao L. Zoonotic potential and molecular epidemiology of Giardia species and giardiasis. Clin Microbiol Rev 2011;24:110–40.

Gonorrhea

After a 79% decline in the rate of reported gonorrhea during 1975–2009 and after reaching the lowest gonorrhea rate ever recorded in 2009, the national gonorrhea rate increased in 2012 for the third consecutive year. During 2009–2012, the national rate increased 9.6%. During 2011–2012, the rate increase was higher among men (8.3%) than women (0.6%), and in the West (19.4%) than Northeast (8.4%), Midwest (3.4%), or South (which decreased 1.4%). As in previous years, the highest rates were observed among persons aged 15–24 years, among blacks, and in the South. In 2012, the gonorrhea rate among blacks was 14.9 times the rate among whites (1).

Treatment for gonorrhea is complicated by antimicrobial resistance. Declining susceptibility to cephalosporins during 2006–2011 resulted in a change in the CDC treatment guidelines in 2012. The only CDC-recommended treatment regimen for gonorrhea is dual therapy with ceftriaxone and either azithromycin or doxycycline (2). In CDC's sentinel surveillance system, the Gonococcal Isolate Surveillance Project (GISP), the percentage of isolates with elevated ceftriaxone minimum inhibitory concentrations (MICs) decreased from 0.4% in 2011 to 0.3% in 2012, and the percentage of isolates with elevated cefixime MICs decreased from 1.4% in 2011 to 1.0% (1).

1. CDC. Sexually transmitted disease surveillance 2012. Atlanta, GA: US Department of Health and Human Services; 2014.
2. CDC. Update to CDC's sexually transmitted diseases treatment guidelines, 2010: oral cephalosporins no longer a recommended treatment for gonococcal infections. MMWR 2012;61:590–4.

Hansen Disease (leprosy)

The number of leprosy cases reported during 2011 and 2012 remained stable. More than half (69.5%) of all cases were reported from Hawaii (29.3%), California (15.8%), Florida (12.2%), and Texas (12.2%). The majority of cases (89%) reported location of acquisition of infection as unknown (73.2%) or as acquired outside of the United States (15.8%).

Hantavirus pulmonary syndrome

An outbreak of hantavirus infections in visitors to Yosemite National Park occurred during 2012, with 10 patients developing laboratory-confirmed hantavirus infection after overnight visits to the park during June and July. Eight patients had symptoms that met the case definition of Hantavirus pulmonary syndrome (HPS), and three patients died (1). The 10 confirmed patients came from three states: California (eight), Pennsylvania (one) and West Virginia (one). Further investigation found that nine patients had stayed in signature tent cabins at the Curry Village campground of the park; these structures have insulation between the canvas exterior and interior hard walls. Rodent infestations were detected in the insulation of these cabins, and all signature cabins were closed and dismantled. Efforts also were made to educate visitors and staff about HPS symptoms and prevention, and to preclude rodents from infesting existing structures at the park.

Also during 2012, a hiker who was camping in the Adirondak mountains of New York state developed HPS following an overnight stay in a three-sided shelter where rodent exposures were noted. Persons engaging in outdoor activities such as camping should be aware of the potential for exposure to rodents and hantavirus. Efforts should be made to eliminate rodents from overnight structures and to inspect structures carefully for potential rodent infestation. If a person develops symptoms of HPS within 8 weeks of the exposure, they should make their doctor aware of potential rodent exposures from outdoor activities so that hantavirus infection is considered.

Hantavirus infections, such as Punmala virus, that are not causing symptoms of HPS are not reportable. However, an imported case of hemorrhagic fever with renal syndrome (HFRS) occurred in a German visitor to Florida in 2012 (2). The patient had acute renal failure caused by Puumala virus infection, which was acquired in Germany. HFRS caused by Puumala virus is common in Germany and many other countries in Europe, with thousands of cases reported each year (3). HFRS should be considered as a cause of acute renal failure in visitors from areas where the disease is endemic in Europe.

1. CDC. Notes from the field: Hantavirus pulmonary syndrome in visitors to a national park—Yosemite Valley, California, 2012. MMWR 2012;60:952.
2. Knust B, Rollin PE. Twenty-year summary of surveillance for human hantavirus infections, United States. Emerg Infect Dis 2013;19:1934–7.
3. Heyman P, Ceianu CS, Christova I, et al. A five-year perspective on the situation of haemorrhagic fever with renal syndrome and status of the hantavirus reservoirs in Europe, 2005–2010. Euro Surveill 2011;16:3.

Hemolytic Uremic Syndrome

Hemolytic uremic syndrome (HUS) is characterized by the triad of hemolytic anemia, thrombocytopenia, and renal insufficiency. The most common etiology of postdiarrheal HUS in the United States is infection with Shiga toxin-producing Escherichia coli, principally E. coli O157:H7 (1,2). Approximately 6.3% of all persons were infected with E. coli O157:H7, but the condition progressed to HUS in 5% of children aged <5 years (3). During 2012, as has previously been reported, the majority of reported cases occurred among children aged 1–4 years.

1. 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.
2. Mody RK, Luna-Gierke RE, Jones TF, et al. Infections in pediatric postdiarrheal hemolytic uremic syndrome: factors associated with identifying shiga toxin-producing Escherichia coli. Arch Pediatr Adolesc Med 2012;166:902–9.
3. Gould LH, 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.

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. MMWR counts of deaths are by date of report in a calendar year and not by date of occurrence. A total of 52 influenza-associated pediatric deaths were reported to CDC during January 1–December 31, 2012. This compares with a mean of 73 deaths (range: 43–118) per year reported for seasonal influenza during 2005–2011. A total of 348 deaths were reported from April 15, 2009 to September 30, 2010, coinciding with the 2009 influenza A (H1N1) pandemic.

Of the 52 influenza-associated pediatric deaths reported to CDC during 2012, a total of 34 occurred during the 2011–12 influenza season and the remaining 18 occurred during the 2012–13 influenza season. Approximately 35 (67%) deaths were associated with influenza A viruses and 16 (31%) with influenza B viruses. One death was associated with an influenza virus for which the type was not determined. Of 35 influenza A viruses, subtype was determined for 22 (63%); 10 were 2009 influenza A (H1N1) (pH1N1) viruses and 12 were A(H3N2) viruses.

In 2012, the median age at the time of death was 6.9 years (range: 16 days–16.4 years). This is similar to that observed before the 2009 A (H1N1) pandemic during the years 2005–2008, January–April 2009, and 2011 (4–7.5 years), but lower than that seen when pH1N1 viruses circulated widely during May–December 2009 (9.3 years), and in 2010 (8.2 years). Seven children (13%) were aged <6 months, 12 (23%) were aged 6–59 months, and 33 (63%) were aged 5–17 years. The overall influenza-associated death rate for children aged <18 years during 2012 was 0.07 per 100,000 population. The rates by age group were 0.09 per 100,000 for children aged <5 years and 0.06 for children aged 5 to <18years (1).

Information on the location of death was available for all children. Twenty seven (52%) children died after being admitted to the hospital (25 were admitted to the intensive care unit), a total of 14 (27%) died in the emergency department, and 11 (21%) died outside the hospital. Information on underlying or chronic medical condition was reported for 51 (98%) children: 28 (55%) children had one or more underlying or chronic medical conditions placing them at increased risk for influenza-associated complications (2). The most common group of underlying conditions was neurologic disorders (e.g., moderate to severe developmental delay, seizure disorders, cerebral palsy, mitochondrial disorders, neuromuscular disorders, and neurologic conditions), reported for 15 of 51 children. Approximately ten of 51 children had cardiac disease or congenital heart disease, and 14 of 51 children had a chronic pulmonary condition (e.g., asthma, cystic fibrosis, or other chronic pulmonary disease). Of 29 children who had specimens collected for bacterial culture from normally sterile sites, eight (28%) had positive cultures. Staphylococcus aureus was detected in two of eight (25%) positive cultures; one was methicillin-sensitive and for the other, methicillin-sensitivity testing was not done. Two cultures (25%) were positive for Streptococcus pneumoniae and two (25%) were positive for Group A Streptococcus. Group B Streptococcus, Pseudomonas aeruginosa, and coagulase-negative staphylococcus were identified in one patient each with the exception of one child who had positive culture for two pathogens (MSSA and pseudomonas aeruginosa). All children aged ≥6 months were recommended to be vaccinated in 2012 (3). Of the 36 children aged ≥6 months for whom seasonal vaccination status was known, six (17%) were vaccinated against influenza, as recommended by the Advisory Committee on Immunization Practices (ACIP). Seven children were aged <6 months and ineligible for vaccination (2,4).

The number of influenza-associated pediatric deaths reported during 2012 was lower than that in 5 of the previous 7 years. Influenza seasons typically span 2 calendar years and can vary widely in terms of severity and timing of peak activity, thus affecting the number of deaths reported in a calendar year. The 2011–12 influenza season was unusually mild and the peak of activity occurred during mid-March (5). All 35 pediatric deaths associated with that season were reported in 2012 or later. The 2012–13 influenza season was more severe and began earlier, peaking in late December, 2012, but the majority of pediatric deaths associated with that season were reported in 2013 (6). Continued surveillance for influenza-associated mortality is important to monitor the effects of seasonal and novel influenza, factors contributing to severe influenza-associated disease, and the influence of interventions among children.

1. CDC. Bridged-race population estimates, data files, and documentation.Vintage 2012 post-censal estimates of the resident population of the United States (April 1, 2010, July 1, 2010–July 1, 2012), by year, county, single-year of age (0, 1, 2, 85 years and over), bridged race, Hispanic origin, and sex. Atlanta, GA: US Department of Health and Human Services, CDC; 2012. Available at http://www.cy118119.com/nchs/nvss/bridged_race/data_documentation.htm.
2. CDC. Prevention and control of influenza with vaccines: recommendations of the Advisory Committee on Immunization Practices (ACIP)—United States, 2012–13 influenza season. MMWR 2012;61:613–8.
3. CDC. Prevention and control of influenza with vaccines: recommendations of the Advisory Committee on Immunization Practices (ACIP), 2011. MMWR 2011;60:1128–32.
4. CDC. Recommended immunization schedules for persons aged 0 through 18 years—United States, 2012. MMWR 2012;61:147.
5. CDC. Update: influenza activity—United States, 2011–12 season and composition of the 2012–13 influenza vaccine. MMWR 2012;61:414–20.
6. CDC. Update: influenza activity—United States, 2012–13 season and composition of the 2013–14 influenza vaccine. MMWR 2012;62:473–9.

Listeriosis

Listeria monocytogenes infection (listeriosis) is rare but can cause severe invasive disease (e.g., bacteremia and meningitis). Listeriosis is predominately acquired through contaminated food and occurs most frequently among older adults, persons with certain immunocompromising conditions, and in pregnant women and their newborns. Pregnancy-associated listeriosis is usually a relatively mild illness for the woman, but can result in fetal loss or severe neonatal disease.

Since 2000, listeriosis has been nationally notifiable. During 2012, approximately 0.23 infections per 100,000 population were reported to NNDSS. Progress toward the 2020 national target of 0.20 infections per 100,000 population (1) is measured through the Foodborne Diseases Active Surveillance Network (FoodNet), which conducts active, population-based surveillance for listeriosis in 10 U.S. states. In 2012, FoodNet reported a preliminary annual incidence of Listeria monocytogenes of 0.25 infections per 100,000 population, similar to the rate reported to NNDSS (2).

The Listeria Initiative is an enhanced surveillance system designed to aid in the rapid investigation of listeriosis outbreaks by combining molecular subtyping results with epidemiologic data collected by state and local health departments (3). As part of the Listeria Initiative, CDC recommends that all clinical isolates of L. monocytogenes be forwarded routinely to a public health laboratory for pulsed-field gel electrophoresis (PFGE) subtyping, and that these PFGE subtyping results be submitted to PulseNet, the National Molecular Subtyping Network for Foodborne Disease Surveillance (4); clinical isolates should also be promptly sent to CDC for further characterization. Additionally, communicable disease programs are asked to interview all patients with listeriosis promptly using the standard Listeria Initiative questionnaire, which is available in English and Spanish at http://www.cy118119.com/listeria/surveillance.html.

The Listeria Initiative has aided in the timely identification and removal of contaminated food during several listeriosis investigations, including a multistate outbreak of 22 illnesses that was linked to imported ricotta salata (a semi-firm cheese) in 2012 (5).

1. US Department of Health and Human Services. Healthy People 2020 Objectives. Washington, DC: US Department of Health and Human Services; 2013. Available at http://www.healthypeople.gov/2020/topicsobjectives2020/objectiveslist.aspx?topicId=14.
2. CDC. Foodborne Diseases Active Surveillance Network. Atlanta, GA: US Department of Health and Human Services, CDC; 2012. Available at http://www.cy118119.com/features/dsfoodnet2012/reportcard.html.
3. CDC. The Listeria Initiative surveillance overview. Atlanta, GA: US Department of Health and Human Services, CDC; 2011. Available at http://www.cy118119.com/listeria/pdf/ListeriaInitiativeOverview_508.pdf.
4. CDC. PulseNet. Atlanta, GA: US Department of Health and Human Services, CDC; 2013. Available at http://www.cy118119.com/pulsenet/.
5. CDC. PulseNet Outbreaks. Atlanta, GA: US Department of Health and Human Services, CDC; 2012. Available at http://www.cy118119.com/listeria/outbreaks/cheese-09-12/index.html.

Lyme Disease

National surveillance for Lyme disease was implemented in the United States in 1991 using a case definition based on clinical and laboratory findings. The CSTE revised the case definition, effective 2008, to standardize laboratory criteria for confirmation and to allow reporting of probable cases.

During 2012, the number of confirmed and probable Lyme disease cases reported to CDC was similar to the number reported in 2010 and 2011, and substantially lower than the number reported in 2008 and 2009, however, the geographic distribution of cases increased nevertheless. In 2012, a total of 356 counties had a reported incidence of ≥10 confirmed cases per 100,000 persons, as compared with 324 counties in 2008.

Meningococcal Disease

Neisseria meningitidis is an important cause of bacterial meningitis and sepsis in the United States. The highest incidence of meningococcal disease occurs among infants aged <1 year, with a second peak occurring in adolescents and young adults (1,2). Among infants, disease incidence peaks within the first 6 months of life and most cases in this age group are caused by serogroup B (2). Rates of meningococcal disease are at historic lows in the United States, but meningococcal disease continues to cause significant morbidity and mortality in persons of all ages.

CDC's ACIP recommends routine use of quadrivalent (A, C, Y, W-135) meningococcal conjugate vaccine in adolescents and others at increased risk for meningococcal disease (1). In October 2010, a booster dose was recommended for adolescents at age 16 years (3). In 2012, coverage with at least 1 dose of meningococcal conjugate vaccine was 74.0% among adolescents aged 13–17 years in the United States; however, coverage ranged from 37.5% to 94.3%, by state (4).

1. CDC. Prevention and control of meningococcal disease: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR 2013;62:(No. RR-2).
2. Cohn AC, MacNeil JR, Harrison LH, 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.
3. CDC. Updated recommendations for use of meningococcal conjugate vaccines—Advisory Committee on Immunization Practices (ACIP), 2010. MMWR 2011;60:72–6.
4. CDC. National and state vaccination coverage among adolescents aged 13–17 years—United States, 2012. MMWR 2013;62:685–93.

Pertussis

Reported pertussis increased significantly between 2011 (incidence: 6.1 per 100,000 population) and 2012 (15.4 per 100,000 population). Several states experienced epidemic levels of disease, resulting in more U.S. pertussis case reports in 2012 (N = 48,277) than any year since 1955 (N = 62,786). Age-specific pertussis rates were highest among infants aged <1 year (126.7 per 100,000 population); adolescents aged 11–14 years contributed the second highest rates of disease nationally (59.2 per 100,000 population), followed closely by children aged 7–10 years (58.5 per 100,000).

Tetanus, diphtheria, and a cellular pertussis (Tdap) coverage among adolescents aged 13–17 years continues to improve (78.2% in 2011 to 84.6% in 2012); however, coverage among adults remains low (12.5% in 2011) (1–3). In February 2012, ACIP recommended that all adults aged ≥19 years not previously vaccinated with Tdap receive a single dose (3). In October 2012, the Tdap pregnancy recommendation was expanded to include vaccination during every pregnancy, regardless of a patient's Tdap history (4).

1. CDC. National and state vaccination coverage among adolescents aged 13–17 years—United States, 2011. MMWR 2012;61:671–7.
2. CDC. National and state vaccination coverage among adolescents aged 13–17 years—United States, 2012. MMWR 2013;62:685–93.
3. CDC. Noninfluenza vaccination coverage among adults—United States, 2011. MMWR 2013;62:66–72.
4. CDC. Updated recommendations for use of tetanus toxoid, reduced diphtheria toxoid and acellular pertussis (Tdap) vaccine in adults aged 65 years and older—Advisory Committee on Immunization Practices (ACIP), 2012. MMWR 2012;61:468–70.
5. CDC. Updated recommendations for use of tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis vaccine (Tdap) in pregnant women—Advisory Committee on Immunization Practices (ACIP), 2012. MMWR 2013;62:131–5.

Rabies

During 2012, one case of human rabies was reported in the United States. The case was reported from California after the patient died abroad and was diagnosed by the Swiss rabies center and confirmed at CDC as a rabies virus variant associated with the insectivorous Mexican free-tailed bat (Tadarida brasiliensis) (1). During 2012, the total number of animals submitted to state and local laboratories for rabies diagnosis increased 2.1%, compared with 2011. Among animals submitted, increases in the number of animals reported rabid were observed for the following species: bats (21.7%), cattle (76.9%), dogs (20.0%), horses/mules (6.8%), and sheep/goats (8.3%) (2). Decreases in the number of reported rabid cats (15.2%), foxes (20.4%), raccoons (1.4%), and skunks (5.4%) also were reported, compared with 2011 (2).

1. CDC. US-acquired human rabies with symptom onset and diagnosis abroad, 2012. MMWR 2012;61:777–81.
2. Dyer JL, Wallace R, Orciari L, et al. Rabies surveillance in the United States during 2012. J Am Vet Med Assoc 2013;243:805–15.

Salmonellosis

During 2012, a total of 17.4 laboratory-confirmed Salmonella infections per 100,000 population were reported; this is one and a half times the Healthy People 2020 objective of 11.4 infections per 100,000 population (1). Data from the Foodborne Diseases Active Surveillance Network (FoodNet), which conducts active surveillance for salmonellosis in 10 U.S. states, are used to measure progress toward Healthy People 2020 objectives. FoodNet reported a preliminary annual incidence of Salmonellosis in 2012 of 16.4 infections per 100,000 population, lower than the rate reported to NNDSS (2).

During 2012, as in previous years, the age groups with the highest number of reported cases of salmonellosis were children aged <5 years and adults aged ≥65 years. Salmonellosis is reported most frequently in late summer and early fall; in 2012, this seasonality was evident, with most reports in June, July, August, and September.

Accounting for underdiagnosis, Salmonella causes an estimated 1.2 million illnesses annually in the United States, approximately 1 million of which are transmitted by food consumed in the United States (3). Salmonella can contaminate a wide range of foods, and different serotypes tend to have different animal reservoirs and food sources, making control challenging.

During 2012, multistate outbreaks of Salmonella infections were linked to cantaloupe (serotypes Typhimurium and Newport); mangoes (serotype Branderup); ground beef (serotype Enteritidis); raw scraped ground tuna product (serotypes Bareilly and Nchanga); and peanut butter (serotype Bredeney) (4). An increasing number of outbreaks associated with contact with animals were also investigated, including outbreaks linked to live poultry (serotypes Infantis, Newport, Lille, Montevideo, and Hadar); small turtles (serotypes Sandiego, Pomona, and Poona) and hedgehogs (serotype Typhimurium); and dry dog food (serotype Infantis) (5).

In 2012, the national case definition for salmonellosis was updated to include a suspect category for reporting of cases of salmonellosis detected through the use of culture-independent diagnostic tests, which are increasingly being used by laboratories (6–8).

1. US Department of Health and Human Services. Healthy People 2020 objectives. Washington, DC: US Department of Health and Human Services; 2013. Available at http://www.healthypeople.gov/2020/topicsobjectives2020/objectiveslist.aspx?topicId=14.
2. CDC. Foodborne Diseases Active Surveillance Network. Atlanta, GA: US Department of Health and Human Services, CDC; 2013. Available at http://www.cy118119.com/foodnet/data/trends/tables/2012/table2a-b.html#table-2b.
3. Scallan E, Hoekstra RM, Angulo FJ, et al. Foodborne illness acquired in the United States–major pathogens. Emerg Infect Dis 2011;17:7–15.
4. CDC. Reports of selected Salmonella outbreak investigations. Atlanta, GA: US Department of Health and Human Services, CDC; 2013. Available at http://www.cy118119.com/salmonella/outbreaks.html.
5. CDC. Gastrointestinal (enteric) diseases from animals. Atlanta, GA: US Department of Health and Human Services, CDC; 2013. Available at www.cy118119.com/zoonotic/gi.
6. Council of State and Territorial Epidemiologists. Public health reporting and national notification for Salmonellosis. Position statement 11-ID-08. Atlanta, GA: Council of State and Territorial Epidemiologists; 2012. Available at http://c.ymcdn.com/sites/www.cste.org/resource/resmgr/PS/11-ID-08.pdf.
7. Cronquist AB, Mody RK, Atkinson R, et al. Impacts of culture-independent diagnostic practices on public health surveillance for bacterial enteric pathogens. Clin Infect Dis 2012;54(Suppl 5):S432–9.
8. Jones TF, Gerner-Smidt P. Nonculture diagnostic tests for enteric diseases. Emerg Infect Dis 2012;18:513–4.

Shigellosis

During 2012, the incidence of reported shigellosis in the United States was 4.9 infections per 100,000 population; Shigella infections have not declined over the past 10 years. During 2012, as in previous years, the age group with the highest number of reported cases was children aged <10 years. S. sonnei infections generally account for approximately 75% of reported shigellosis cases in the United States (1). Shigellosis does not demonstrate marked seasonality, likely reflecting the importance of person-to-person transmission.

Accounting for underdiagnosis, Shigella causes an estimated 494,000 illnesses annually in the United States, approximately 131,000 of which are transmitted by food consumed in the United States (1). Shigella is often spread from one person to another, including through sexual contact between men who have sex with men, and also can be transmitted by contaminated food or by contaminated water used for drinking or recreational purposes (3). Some cases are acquired during international travel (4,5). Day care-associated outbreaks are common and are often difficult to control (6).

During 2012, an outbreak of infections caused by Shigella sonnei with decreased susceptibility to azithromycin was reported in Los Angeles, California; this outbreak represents the first known transmission of Shigella sonnei with decreased susceptibility to azithromycin in the United States (7). Resistance to ampicillin and trimethoprim-sulfamethoxazole among S. sonnei strains in the United States remains common, and resistance to quinolones, including ciprofloxacin, is emerging and cause for concern (8).

In 2012, the national case definition for shigellosis was updated to include a "suspect" category for reporting of cases detected through the use of culture-independent diagnostic tests (9).

1. CDC. National Shigella surveillance annual summary, 2011. Atlanta, GA: US Department of Health and Human Services, CDC; 2013. Available at http://www.cy118119.com/ncezid/dfwed/pdfs/shigella-annual-report-2011-508c.pdf.
2. Scallan E, Hoekstra RM, Angulo FJ, et al. Foodborne illness acquired in the United States—major pathogens. Emerg Infect Dis 2011;17:7–15.
3. 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.
4. Ram PK, Crump JA, Gupta SK, Miller MA, Mintz ED. Review article: part II. Analysis of data gaps pertaining to Shigella infections in low and medium human development index countries, 1984–2005. Epidemiol Infect 2008;136:577–603.
5. Gupta SK, Strockbine N, Omondi M, et al. Short report: emergence of Shiga toxin 1 genes within Shigella dysenteriae Type 4 isolates from travelers returning from the island of Hispaniola. Am J Trop Med Hyg 2007;76:1163–5.
6. Arvelo W, Hinkle J, Nguyen TA, et al. Transmission risk factors and treatment of pediatric shigellosis during a large daycare center-associated outbreak of multidrug resistant Shigella sonnei. Pediatr Infect Dis J 2009;28:976–80.
7. CDC. Notes from the field: outbreak of infections caused by Shigella sonnei with decreased susceptibility to azithromycin—Los Angeles, CA, 2012. MMWR 2013;62:171.
8. CDC. National Antimicrobial Resistance Monitoring System for enteric bacteria (NARMS): Human isolates final report, 2011. Atlanta, GA: US Department of Health and Human Services, CDC; 2013. Available at http://www.cy118119.com/narms.
9. Council of State and Territorial Epidemiologists. Public health reporting and national notification for Shigellosis. Position statement 11-ID-19. Atlanta, GA: Council of State and Territorial Epidemiologists; 2012. Available at http://c.ymcdn.com/sites/www.cste.org/resource/resmgr/PS/11-ID-19.pdf.

Spotted Fever Rickettsiosis (Including RMSF)

During 2012, a total of 4,470 cases of spotted fever rickettsiosis (SFR) were reported, which was 60% more reported cases than during 2011 (2,802 cases) and the largest number of cases since reporting began. Case reports increased from 2011 to 2012 in every geographic region except the Pacific region, with the largest increases occurring in the East South Central (580 cases), South Atlantic (528 cases), and West South Central (377 cases). These recent changes in reported incidence suggest a widespread change in exposure to SFR during 2012 over a large portion of the United States, possibly because of increased tick vector activity. However, because tick population counts in the United States are not linked to this surveillance system, the reasons for this increase remain uncertain.

Shiga Toxin-Producing Escherichia coli

In 2012, the incidence in the United States of reported Shiga toxin-producing Escherichia coli (STEC) was 2.1 infections per 100,000 population. During 2012, as in previous years, the age group with the highest number of reported cases was children aged <5 years, although infections can occur in patients of all ages. During 2012, several multistate outbreaks of STEC infection were linked to foods, including organic spinach and spring mix blend (STEC O157:H7) and raw clover sprouts (STEC O26) (1).

Public health actions to monitor, prevent, and control STEC infections are taken on the basis of serogroup characterization. Development of postdiarrheal hemolytic uremic syndrome (HUS), a severe complication of STEC infection, is most strongly associated with STEC O157. Non-O157 STEC, a diverse group that varies in virulence, comprises more than 50 other serogroups. In the United States, STEC O157 is the most commonly reported serogroup causing human infection (2); however, increased use of assays for the detection of Shiga toxins in clinical laboratories in recent years has led to increased reporting of non-O157 STEC infection (3). STEC can produce Shiga toxin (Stx) 1, Stx 2, or both. In general, strains that produce certain types of Stx 2 are the most virulent (4). Accounting for underdiagnosis, an estimated >96,000 illnesses were caused by STEC O157, and approximately 168,000 illnesses were caused by non-O157 STEC occur each year (5).

Stool specimens from patients with community-acquired diarrhea submitted to clinical laboratories should be tested routinely both by culture for STEC O157 and by an assay that detects Shiga toxins (or the genes that encode them) (6). Detection of Shiga toxin alone is inadequate for clinical management and public health investigation; characterizing STEC isolates by serogroup and by pulsed-field gel electrophoresis pattern is important to detect, investigate, and control outbreaks.

1. CDC. Reports of selected E. coli outbreak investigations. Atlanta, GA: US Department of Health and Human Services, CDC; 2013. Available at http://www.cy118119.com/ecoli/outbreaks.html.
2. CDC. National Shiga toxin-producing Escherichia coli (STEC) Surveillance Annual Summary, 2011. Atlanta, Georgia: US Department of Health and Human Services, CDC; 2013. Available at http://www.cy118119.com/ncezid/dfwed/pdfs/national-stec-surv-summ-2011-508c.pdf.
3. Gould LH, Mody RK, Ong KL; Emerging Infections Program Foodnet Working Group. Increased recognition of non-O157 Shiga toxin-producing Escherichia coli infections in the United States during 2000–2010: epidemiologic features and comparison with E. coli O157 infections. Foodborne Pathog Dis 2013;10:453–60.
4. Mody RK, Griffin PM. Fecal shedding of Shiga toxin-producing Escherichia coli: what should be done to prevent secondary cases? Clin Infect Dis 2013;56:1141–4.
5. Scallan E, Hoekstra RM, Angulo FJ, et al. Foodborne illness acquired in the United States—major pathogens. Emerg Infect Dis 2011;17:7–15.
6. CDC. Recommendations for diagnosis of Shiga toxin-producing Escherichia coli infections by clinical laboratories, 2009. MMWR 2009;58:(No. RR-12).

Syphilis, Congenital

Trends in congenital syphilis (CS) usually follow trends in primary and secondary (P&S) syphilis among women, with a lag of 1–2 years. During 2005–2008, rates of female P&S and CS increased. From 2009 to 2012 the rates of female P&S and CS declined. In 2012, the CS rate of 7.8 cases per 100,000 live births was the lowest rate reported since the surveillance case definition for CS was revised in 1988. However, racial and ethnic disparities remain: rates of CS among blacks (29.6 cases per 100,000 live births) and among Hispanics (7.9 cases per 100,000 live births) were 14.1 and 3.8 higher times, respectively, the rate among whites (2.1 cases per 100,000 live births) (1).

1. CDC. Sexually transmitted disease surveillance 2012. Atlanta, GA: US Department of Health and Human Services, CDC; 2014.

Syphilis, Primary and Secondary

Rates of primary and secondary (P&S) syphilis increased from 4.5 cases per 100,000 population in 2011 to 5.0 cases per 100,000 population in 2012. Rates remained unchanged among women (0.9 cases per 100,000 population), but increased among men for the 12th consecutive year. Rates were highest in men aged 20–24 years and 25–29 years. The increase in cases during 2011–2012 (15%) was larger than in previous years (6% during 2008–2009, 10% during 2009–2010, and 8% during 2010–2011). During 2007–2011, rates among black men aged 20–24 years increased 75% from 54.9 to 96.2 cases per 100,000 population; the magnitude of this increase (41.3 cases per 100,000 population) was the greatest reported for any age, sex, or race/ethnicity group. (1) In 2012, rates among men remained highest among blacks aged 20–24 years and 25–29 years (96.7 cases and 89.2 cases per 100,000 population, respectively). (1) During 2007–2012, 33 states and areas reported sex-of-partner data for 70% or more cases of P&S syphilis each year; cases among men having sex with men (MSM) increased each year. In 2012, 75% of cases of all primary and secondary syphilis cases were among MSM.

1. CDC. Sexually transmitted disease surveillance 2012. Atlanta: U.S. Department of Health and Human Services, CDC; 2014.

Trichinellosis

The 12 cases in which a suspected or known source of infection was documented were attributed to the consumption of pork (n = six), bear (n = five), and wild boar (n = one). The pork exposures included domestic Berkshire (n = three), an unspecified type (n = two), and a foreign source (n = one). Of the persons who reported consuming bear meat, four admitted to either eating the meat rare or preparing it in a manner that was unlikely to thoroughly cook the meat (e.g., fried or with a countertop grill). For seven cases, no likely source of infection could be identified. The case reported in the Arizona resident occurred in late 2011 but was not reported until 2012.

Three small outbreaks were reported in 2012. The first was a three-person outbreak in a family for which no likely source of infection was identified because multiple undercooked pork and game meat meals were consumed during the incubation period. The second outbreak involved two persons who reported eating undercooked bear meat from Alaska. The third outbreak involved two persons who reported consuming undercooked pork chops at a restaurant and accounted for two of three domestic Berkshire pork-associated cases that might have come from free-range pigs. Although the U.S. demand for organic and free-range pork is increasing, the research regarding its safety relative to conventionally produced pork is limited and results are conflicting (1). Both organic/free-range and conventionally raised pork should be thoroughly cooked before consumption to prevent trichinellosis (2).

A confirmed diagnosis of trichinellosis is determined by a clinically compatible illness in a person with history of consumption of a likely meat source of infection and a positive laboratory test result that confirms infection with the parasite. In the majority of patients, trichinellosis is confirmed by serologic testing for Trichinella-specific antibodies. Specific antibodies typically are detectable between 3 and 5 weeks after infection, but might take as long as 60 days postinfection to develop (3). Multiple serum specimens should be drawn several weeks apart to demonstrate seroconversion in patients with clinically compatible illness and history of consumption of a likely meat source of infection whose initial specimen was negative. For patients without a clinically compatible illness and exposure to a likely meat source, the utility of serologic tests for Trichinella is limited because of the low predictive value of a positive result in such instances.

1. US Department of Agriculture. Food safety fact sheet: organic pork and food safety. West Lafayette, IN: US Department of Agriculture; 2011. Available at http://www.ars.usda.gov/SP2UserFiles/Place/36022000/Organic%20Pork%20Food%20Safety%20Fact%20Sheet.pdf.
2. CDC. Trichinellosis: prevention and control. July 19, 2013. Atlanta, GA: US Department of Health and Human Services, CDC; 2013. Available at http://www.cy118119.com/parasites/trichinellosis/prevent.html.
3. Morakote N, Sukhavat K, Khamboonruang C, et al. Persistence of IgG, IgM, and IgE antibodies in human trichinosis. Trop Med Parasitol 1992;43:167–9.

Typhoid Fever

Typhoid fever is rare in the United States, and approximately 75% of cases are associated with international travel (1). The risk for infection is highest for travelers visiting friends and relatives in countries where typhoid fever is endemic, perhaps because they are less likely than other travelers to seek pretravel vaccination and to observe strict safe water and food practices. The risk also is higher for travelers who visit the areas when it is most highly endemic, such as the Indian subcontinent, even for a short time (2). In 2011, CDC removed pretravel typhoid vaccination recommendations for 26 low-risk destinations; pretravel vaccination guidelines are available at www.cy118119.com/travel (3).

1. Lynch MF, Blanton EM, Bulens S, et al. Typhoid fever in the United States, 1999–2006. JAMA 2009;302:859–65.
2. 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.
3. Johnson KJ, Gallagher NM, Mintz ED, et al. From the CDC: new country-specific recommendations for pre-travel typhoid vaccination. J Travel Med 2011;18:430–3.

Varicella

In 2012, data on varicella cases were reported to CDC through the National Notifiable Diseases Surveillance System from 40 states, an increase from 39 states in 2011. A second dose of varicella vaccine was added to the vaccination schedule for children in 2006 (1); varicella incidence in the 31 states meeting criteria for adequate and consistent reporting (2) has declined 77.1% from 31.4 per 100,000 in 2006 to 7.2 per 100,000 in 2012.

Variables critical for monitoring the effect of the varicella vaccination program include age, vaccination status, disease severity (e.g., number of lesions), outcome of the case (e.g., hospitalized), and whether the case is associated with an outbreak. Among the cases reported from the 31 states with adequate and consistent reporting (2) through 2012, data on age, vaccination status, disease severity, outcome, and whether the case was outbreak-related were included for 92%, 45%, 22%, 28%, and 65% of the cases, respectively, compared with 82%, 44%, 14%, 30%, and 65% in 2011. Reporting improved for some variables but not others. States are encouraged to increase completeness of reporting of these and other demographic, clinical, and epidemiologic variables to allow for effective continued monitoring of the impact of the 2-dose varicella vaccine program and changing varicella epidemiology.

1. CDC. Prevention of varicella: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR 2007;56:(No. RR-4).
2. CDC. Evolution of varicella surveillance—selected states, 2000–2010. MMWR 2012;61:609–12.

Vibriosis

The incidence of reported vibriosis (infection caused by a species from the family Vibrionaceae other than toxigenic Vibrio cholerae O1 or O139) has increased over the past 15 years (1). Although vibriosis only became a nationally notifiable condition in 2007 (2), most states were reporting cases as early as 2000. In addition, the increase in reported cases nationally since 1996 is consistent with a similar increase in vibriosis cases reported by the 10 Foodborne Diseases Active Surveillance Network (FoodNet) sites (1). California and Florida report the largest numbers of cases annually. In 2012, an outbreak of V. parahemoyticus infections was associated with consumption of shellfish harvested from Oyster Bay Harbor, New York (3).

1. Newton A, Kendall M, Vugia DJ, et al. Increasing rates of vibriosis in the United States, 1996–2010: review of surveillance data from 2 systems. Clin Infect Dis 2012;54(Suppl 5):S391–5.
2. Council of State and Territorial Epidemiologists. National reporting for non-cholera Vibrio infections (vibriosis). Position statement 06-ID-05. Atlanta, GA: Council of State and Territorial Epidemiologists; 2006.
3. Martinez-Urtaza J, Baker-Austin C, Jones JL. Spread of pacific northwest Vibrio parahaemolyticus strain. N Engl J Med 2013;369:1573–4.

PART 1 Summaries of Notifiable Diseases in the United States, 2012

Abbreviations and Symbols Used in Tables

U Data not available.

N Not reportable (i.e., report of disease is not required in that jurisdiction).

— No reported cases.

Notes: Rates <0.01 after rounding are listed as 0.

Data in the MMWR Summary of Notifiable Diseases — United States, 2012 might differ from data in other CDC surveillance reports because of differences in the timing of reports, the source of the data, the use of different case definitions, and print criteria.

Selected Reading for 2012

General

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.

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

Atlas RM. Bioterriorism: from threat to reality. Annu Rev Microbiol 2002;56:167--85.

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.

Beltran VM, Harrison KM, Hall HI, Dean HD. Collection of social determinant of health measures in US national surveillance systems for HIV, viral hepatitis, STDs, and TB. Public Health Rep 2011 Sep--Oct;126 Suppl 3:41--53.

Boehmer TK, Patnaik JL, Burnite SJ, et al. Use of hospital discharge data to evaluate notifiable disease reporting to Colorado’s Electronic Disease Reporting System. Public Health Rep 2011 Jan--Feb;126:100--6.

Brookmeyer R, Stroup DF, eds. Monitoring the health of populations: statistical principles and methods for public health surveillance. New York, NY: Oxford University Press; 2004.

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. Available at http://www.cy118119.com/mmwr/preview/mmwrhtml/mm5714a4.htm?%0As_cid=mm5714a4_e.

CDC. Comparison of provisional with final notifiable disease case counts---National Notifiable Diseases Surveillance System, 2009. MMWR 2013;62;747--751. Available at http://www.cy118119.com/mmwr/preview/mmwrhtml/mm6236a4.htm?s_cid=mm6236a4_w.

CDC. Racial disparities in nationally notifiable diseases---United States, 2002. MMWR 2005;54:9--11. Available at http://www.cy118119.com/mmwr/preview/mmwrhtml/mm5401a4.htm.

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). Available at ftp://ftp.cdc.gov/pub/publications/mmwr/rr/rr4610.pdf.

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). Available at http://www.cy118119.com/mmwr/preview/mmwrhtml/rr5305a1.htm.

CDC. Framework for program evaluation in public health. MMWR 1999;48(No. RR-11). Available at http://www.cy118119.com/mmwr/PDF/RR/RR4811.pdf.

CDC. Historical perspectives: notifiable disease surveillance and notifiable disease statistics United States, June 1946 and June 1996. MMWR 1996;45:530--6. Available at http://www.cy118119.com/mmwr/preview/mmwrhtml/00042744.htm.

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

CDC. Manual for the surveillance of vaccine-preventable diseases 5th Edition. Atlanta, GA: US Department of Health and Human Services; CDC, 2012 Available at http://www.cy118119.com/vaccines/pubs/surv-manual/index.html.

CDC. NCHHSTP Atlas. US Department of Health and Human Services; CDC. Available at http://www.cy118119.com/nchhstp/atlas/.

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. Notice to Readers: Changes in presentation of data from the National Notifiable Diseases Surveillance System---January 13, 2006. MMWR 2006;55:13--14. Available at http://www.cy118119.com/mmwr//preview/mmwrhtml/mm5501a5.htm.

CDC. Public Health Information Network---improving early detection by using a standards-based approach to connecting public health and clinical medicine. MMWR 2004;53 (Suppl):199--202. Available at http://www.cy118119.com/mmwr/preview/mmwrhtml/su5301a36.htm.

CDC. Public Health Information Network: connecting public health. Atlanta, GA: US Department of Health and Human Services; CDC. Available at http://www.cy118119.com/phin/about/index.html.

CDC. Racial disparities in nationally notifiable diseases---United States, 2002. MMWR 2005 14;54:9--11. Available at http://www.cy118119.com/mmwr/preview/mmwrhtml/mm5401a4.htm.

CDC. Reporting race and ethnicity data---National Electronic Telecommunications System for Surveillance, 1994--1997. MMWR 1999;48:305--12. Available at http://www.cy118119.com/mmwr/preview/mmwrhtml/00056960.htm.

CDC. State Electronic Disease Surveillance Systems---United States, 2007 and 2010. MMWR 2011, 60;1421--23. Available at http://www.cy118119.com/mmwr/preview/mmwrhtml/mm6041a3.htm.

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

CDC. The cornerstone of public health practice: public health surveillance, 1961--2011. MMWR 2011: 60;15--21 Available at http://www.cy118119.com/mmwr/preview/mmwrhtml/su6004a4.htm?s_cid=su6004a4_w.

CDC. Updated guidelines for evaluating public health surveillance systems: recommendations from the Guidelines Working Group. MMWR 2001;50(No. RR-13). Available at http://www.cy118119.com/mmwr/preview/mmwrhtml/rr5013a1.htm.

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.

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

Cronquist AB, Mody RK, Atkinson R, et al. Impacts of culture-independent diagnostic practices on public health surveillance for bacterial enteric pathogens. Clin Infect Dis 2012;54 (Suppl 5):S432--9.

Dato V, Wagner MM, Fapohunda A. How outbreaks of infectious disease are detected: a review of surveillance systems and outbreaks. Public Health Rep 2004 Sep--Oct;119:464--71.

Doyle TJ, Ma H, Groseclose SL, Hopkins RS. PHSkb: a knowledgebase to support notifiable disease surveillance. BMC Med Inform Decis Mak 2005;5:27.

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.

Effler P, Ching-Lee M, Bogard A, et al. Statewide system of electronic notifiable disease reporting from clinical laboratories: comparing automated reporting with conventional methods. JAMA 1999;282:1845--50.

Frieden TR. A framework for public health action: the health impact pyramid. Am J Public Health 2010;100:590--95.

Freimuth V, Linnan HW, Potter P. Communicating the threat of emerging infections to the public. Emerg Infect Dis 2000;6:337--47.

German R. Sensitivity and predictive value positive measurements for public health surveillance systems. Epidemiology 2000;11:720--7.

Government Accountability Office. Emerging infectious diseases: review of state and federal disease surveillance efforts. Washington, DC: Government Accountability Office; 2004. GAO-04-877. Available at http://www.gao.gov/new.items/d04877.pdf.

Hardiman MC. World Health Organization Perspective on Implementation of International Health Regulations. Emerg Infect Dis 2012;18:1041--6.

Heyman DL, ed. Control of communicable diseases manual. 19th ed. Washington, DC: American Public Health Association; 2008.

Hopkins RS. Design and operation of state and local infectious disease surveillance systems. J Public Health Manag Practice 2005;11:184--90.

Jajosky RA, Groseclose SL. Evaluation of reporting timeliness of public health surveillance systems for infectious diseases. BMC Public Health 2004;4:29.

Jajosky R, Rey A, Park M, et al. Findings from the Council of State and Territorial Epidemiologists’ 2008 assessment of state reportable and nationally notifiable conditions in the United States and considerations for the future. J Public Health Manag Practice 2011;17:255--64.

Kleinman KP, Abrams AM. Assessing the utility of public health surveillance using specificity, sensitivity, and lives saved. Stat Med 2008;27:4057--68.

Koo D, Caldwell B. The role of providers and health plans in infectious disease surveillance. Eff Clin Pract 1999;2:247--52.

Krause G, Brodhun B, Altmann D, Claus H, Benzler J. Reliability of case definitions for public health surveillance assessed by round-robin test methodology. BMC Public Health 2006;6:129.

Lazarus R, Klompas M, Campion F, et al. Electronic support for public health: validated case finding and reporting for notifiable diseases using electronic medical data. J Am Med Inform Assoc 2009;16:18--24.

Lee LM, Teutsch SM, Thacker SB, St Louis ME, eds. Principles and practice of public health surveillance. 3rd ed. New York, NY: Oxford University Press; 2010:1--17.

Lin SS, Kelsey JL. Use of race and ethnicity in epidemiologic research: concepts, methodological issues, and suggestions for research. Epidemiol Rev 2000;22:187--202.

McNabb S, Chungong S, Ryan M, et al. Conceptual framework of public health surveillance and action and its application in health sector reform. BMC Public Health 2002;2:2.

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.

M’ikanatha NM, Lynfield R, Van Beneden CA, de Valk H. Infectious disease surveillance, 2nd edition. Malden, MA: Wiley; 2013.

Miller MA, Sentz J, Rabaa MA, et al. Global epidemiology of infections due to Shigella, Salmonella serotype Typhi, and enterotoxigenic Escherichia coli. Epidemiol Infect 2008;136:433--5.

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Overhage JM, Grannis S, McDonald CJ. A comparison of the completeness and timeliness of automated electronic laboratory reporting and spontaneous reporting of notifiable conditions. Am J Public Health 2008;98:344--50.

Panackal AA, M’ikanatha NM, Tsui FC, et al. Automatic electronic laboratory- based reporting of notifiable infectious diseases at a large health system. Emerg Infect Dis 2002;8:685--91.

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Quandelacy TM, Johns MC, Andraghetti R, et al. The role of disease surveillance in achieving IHR compliance by 2012. Biosecur Bioterror 2011 Dec; 9:408--12.

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Roush S, Murphy T. Historical comparisons of morbidity and mortality for vaccine-preventable diseases in the United States. JAMA 2007;298:2155--63.

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Vogt RL, Spittle R, Cronquist A, Patnaik JL. Evaluation of the timeliness and completeness of a web-based notifiable disease reporting system by a local health department. J Public Health Manag Pract 2006;12:540--4.

Anthrax

Blackburn JK, McNyset KM, Curtis A, Hugh-Jones ME. Modeling the geographic distribution of Bacillus anthracis, the causative agent of anthrax disease, for the contiguous United States using predictive ecological niche modeling. Am J Trop Med Hyg 2007;77:1103--10.

Hendricks KA, Wright ME, Shadomy SV, et al. Centers for Disease Control and Prevention (CDC) expert panel meetings on prevention and treatment of anthrax in adults. Emerg Infect Dis 2014:20.

Domestic Arboviral Disease, Neuroinvasive and Nonneuroinvasive

CDC. West Nile virus disease and other arboviral diseases---United States, 2012. MMWR 2013;62:513--7.

CDC. Fatal West Nile virus infection following probable transfusion-associated transmission---Colorado, 2012. MMWR 2013;64:622--4.

Gibney KB, Colborn J, Baty S, et al. Modifiable risk factors for West Nile virus infection during an outbreak---Arizona, 2010. Am J Trop Med Hyg 2012;86:895--901.

Lindsey NP, Staples JE, Delorey MJ, Fischer M. Lack of evidence of increased West Nile virus disease severity in the United States in 2012. Am J Trop Med Hyg 2014;90:163--8.

Lindsey NP, Staples JE, Lehman JA, Fischer M. Medical risk factors for severe West Nile virus disease, United States, 2008--2010. Am J Trop Med Hyg 2012;87:179--84.

Lindsey NP, Staples JE, Lehman JA, Fischer M. Surveillance for West Nile virus disease---United States, 1999--2008. MMWR 2010;59:(No. SS-2).

Petersen LR, Fischer M. Unpredictable and difficult to control: West Nile virus enters adolescence. N Engl J Med 2012;367:1281--4.

Reimann CA, Hayes EB, DiGuiseppi C, et al. Epidemiology of neuroinvasive arboviral disease in the United States, 1999--2007. Am J Trop Med Hyg 2008;79:974--79.

Weber I, Lindsey N, Bunko-Patterson A, et al. Completeness of West Nile virus testing among patients with meningitis and encephalitis during an outbreak in Arizona. Epidemiol Infect 2012;140:1632--36.

Babesiosis

CDC. Babesiosis surveillance---18 states, 2011. MMWR 2012;61:505--9.

Herwaldt BL, Linden JV, Bosserman E, et al. Transfusion-associated babesiosis in the United States: a description of cases. Ann Intern Med 2011;155:509--19.

Joseph JT, Purtill K, Wong SJ, et al. Vertical transmission of Babesia microti, United States. Emerg Infect Dis 2012;18:1318--21.

Menis M, Anderson SA, Izurieta HS, et al. Babesiosis among elderly Medicare beneficiaries, United States, 2006--2008. Emerg Infect Dis 2012;18:128--31.

Perez Acosta ME, Ender PT, Smith EM, Jahre JA. Babesia microti infection, eastern Pennsylvania, USA. Emerg Infect Dis 2013;19:1105--7.

Vannier E, Krause PJ. Human babesiosis. N Engl J Med 2012;366:2397--407.

Botulism

Arnon SS, Barzilay EJ. Clostridial infections: botulism and infants. In: Pickering LK, Baker CJ, Kimberlin DW, Long SS, eds. The Red Book: 2009 report of the Committee on Infectious Diseases. Elk Grove Village, NY: American Academy of Pediatrics; 2009:259--62.

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

CDC. Infant botulism---New York City, 2001--2002. MMWR 2003;52:21--4.

Fagan RP, McLaughlin JB, Castrodale LJ, et al. Endemic foodborne botulism among Alaska Native persons---Alaska, 1947--2007. Clin Infect Dis 2011;52:585--92.

Newkirk RW, Hedberg CW. Rapid detection of foodborne botulism outbreaks facilitated by epidemiological linking of cases: implications for food defense and public health response. Foodborne Pathog Dis 2012;9:150--5.

Shapiro RL, Hatheway C, Swerdlow DL. Botulism in the United States: a clinical and epidemiologic review. Ann Intern Med 1998;129:221--8.

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.

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

Sobel J, Tucker N, McLaughlin J, Maslanka S. Foodborne botulism in the United States, 1990--2000. Emerg Infect Dis 2004;10:1606--12.

Brucellosis

Ashford DA, di Pietra J, Lingappa J, et al. Adverse events in humans associated with accidental exposure to the livestock brucellosis vaccine RB51. Vaccine 2004;22:3435--9.

CDC. Brucellosis (Brucella melitensis, abortus, suis, and canis). Atlanta, GA: US Department of Health and Human Services; 2012.

CDC. Brucellosis. Atlanta, GA: US Department of Health and Human Services, CDC; 2010. Available at http://www.cy118119.com/nczved/divisions/dfbmd/diseases/brucellosis.

CDC. Brucellosis case definition. Atlanta, GA: US Department of Health and Human Services, CDC; 2010. http://wwwn.cdc.gov/nndss/script/casedef.aspx?CondYrID=625&DatePub=1/1/2010%2012:00:00%20AM.

CDC. Brucella suis infection associated with feral swine hunting---three states, 2007--2008. MMWR 2009;58:618--21.

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.

Chomel BB, DeBess EE, Mangiamele DM, et al. Changing trends in the epidemiology of human brucellosis in California from 1973 to 1992: a shift toward foodborne transmission. J Infect Dis 1994;170:1216--23.

Glynn MK, Lynn TV. Brucellosis. J Am Vet Med Assoc 2008;233:900--8.

Traxler RM, Lehman MW, Bosserman EA, Guerra MA, Smith TL. A literature review of laboratory-acquired brucellosis. J Clin Microbiol 2013;51:3055--62.

Yagupsky P, Baron EJ. Laboratory exposures to Brucellae and implications for bioterrorism. Emerg Infect Dis 2005;11:1180--5.

Chlamydia trachomatis infection

CDC. Sexually transmitted disease surveillance, 2012. Atlanta, GA: US Department of Health and Human Services; 2014.

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

Datta SP, Torrone E, Kyuszon-Moran D, et al. Chlamydia trachomatis trends in the United States among persons 14 to 19 years of age, 1999 to 2008. Sex Transm Dis 2012;39:92--6.

Satterwhite CL, Torrone E, Meites E, et al. Sexually transmitted infections among US women andmen: prevalence and incidence estimates, 2008. Sex Transm Dis 2013;40:187--93.

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--7.

Cholera

Besser RE, Feikin DR, Eberhart-Phillips JE, Mascola L, Griffin PM. Diagnosis and treatment of cholera in the United States. Are we prepared? JAMA 1994;272:1203--5.

Newton AE, Heiman KE, Schmitz A, et al. Cholera in United States associated with epidemic in Hispaniola. Emerg Infect Dis 2011;17:2166--8.

Siddique AK, Nair GB, Alam M, et al. El Tor cholera with severe disease: a new threat to Asia and beyond. Epidemiol Infect 2010;138:347--52.

Steinberg EB, Greene KD, Bopp CA, et al. Cholera in the United States, 1995--2000: trends at the end of the twentieth century. J Infect Dis 2001;184:799--802.

Tappero J, Tauxe RV. Lessons learned during public health response to cholera epidemic in Haiti and the Dominican Republic. Emerg Infect Dis 2011;17:2087--93.

World Health Organization. Cholera, 2012. Wkly Epidemiol Rec 2013;88:321--36.

Coccidioidomycosis

Chen S, Erhart L, Anderson S, et al. Coccidioidomycosis: knowledge, attitudes, and practices among healthcare providers---Arizona, 2007. Med Mycol 2011;49:649--56.

Huang JY, Bristow B, Shafir S, Sorvillo F. Coccidioidomycosis-associated deaths, United States, 1990--2008. Emerg Infect Dis 2012;18:1723--8.

Marsden-Haug N, Goldoft M, Ralston C, et al. Coccidioidomycosis acquired in Washington State. Clin Infect Dis 2012;56:847--50.

Cryptosporidiosis

CDC. Cryptosporidiosis surveillance---United States, 2009--2010. MMWR 2012;61:1--12.

CDC. Diagnostic procedures for stool specimens. Atlanta, GA: US Department of Health and Human Services, CDC; 2009. Available at http://www.dpd.cdc.gov/dpdx/HTML/DiagnosticProcedures.htm.

Hlavsa MC, Roberts VA, Anderson AR, et al. Surveillance for waterborne disease outbreaks and other health events associated with recreational water---United States, 2007--2008. MMWR 2011;60:1--32.

Roy SL, DeLong SM, Stenzel S, et al. Risk factors for sporadic cryptosporidiosis among immunocompetent persons in the United States from 1999 to 2001. J Clin Microbiol 2004;42:2944--51.

Yoder JS, Beach MJ. Cryptosporidium surveillance and risk factors in the United States. Exp Parasitol 2010;124:31--9.

Cyclosporiasis

Hall RL, Jones JL, Hurd S, et al. Population-based active surveillance for Cyclospora infection---United States, Foodborne Diseases Active Surveillance Network (FoodNet), 1997--2009. Clin Infect Dis 2012;54:S411--7.

Hall RL, Jones JL, Herwaldt BL. Surveillance for laboratory-confirmed sporadic cases of cyclosporiasis---United States, 1997--2008. MMWR 2011;60:(No. SS-2).

Herwaldt BL. The ongoing saga of U.S. outbreaks of cyclosporiasis associated with imported fresh produce: what Cyclospora cayetanensis has taught us and what we have yet to learn. In: Institute of Medicine. Addressing foodborne threats to health: policies, practices, and global coordination. Washington, DC: The National Academies Press; 2006:85--115, 133--40.

Herwaldt BL. Cyclospora cayetanensis: a review, focusing on the outbreaks of cyclosporiasis in the 1990s. Clin Infect Dis 2000;31:1040--57.

Ortega YR, Sanchez R. Update on Cyclospora cayetanensis, a food-borne and waterborne parasite. Clin Microbiol Rev 2010;23:218--34.

Ehrlichiosis and Anaplasmosis

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.

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

Dahlgren FS, Mandel EJ, Krebs JW, Massung RF, McQuiston JH. Increasing incidence of Ehrlichia chaffeensis and Anaplasma phagocytophilum in the United States, 2000--2007. Am J Trop Med Hyg 2011;85:124--31.

Dumler JS, Madigan JE, Pusterla N, Bakken JS. Ehrlichioses in humans: epidemiology, clinical presentation, diagnosis, and treatment. Clin Infect Dis 2007;45(Suppl 1):545--51.

Regan J, Matthias J, Green-Murphy A, et al. A confirmed Ehrlichia ewingii infection likely acquired through platelet transfusion. Clin Infect Dis 2013;56:E105--7.

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

Giardiasis

Brunkard JM, Ailes E, Roberts VA, et al. Surveillance for waterborne disease outbreaks associated with drinking water---United States, 2007--2008. MMWR 2011;60:(No. SS-12).

Cantey PT, Roy S, Lee B, et al. Study of nonoutbreak giardiasis: novel findings and implications for research. Am J Med 2011;124:1175.e1--8.

Clinical and Laboratory Standards Institute. Procedures for the recovery and identification of parasites from the intestinal tract; approved guideline. CLSI document M28--A2 Second Edition ed. Wayne, PA: Clinical and Laboratory Standards Institute; 2005.

Yoder JS, Gargano JY, Wallace RM, Beach MJ. Giardiasis surveillance---United States, 2009--2010. MMWR 2012;61:(No. SS-5).

Gonorrhea

CDC. Sexually transmitted disease surveillance, 2012. Atlanta, GA: US Department of Health and Human Services; 2014.

CDC. Update to CDC’s sexually transmitted diseases treatment guidelines, 2010: oral cephalosporins no longer a recommended treatment for gonococcal infections. MMWR 2012;61:590--4.

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

Torrone ES, Johnson RE, Tian LH, et al. Prevalence of Neisseria gonorrhoeae among persons 14 to 39 years of age, United States, 1999 to 2008. Sex Transm Dis 2013;40:202--5.

Hansen Disease (leprosy)

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

Bruce S, Schroeder TL, Ellner K, et al. Armadillo exposure and Hansen’s disease: an epidemiologic survey in southern Texas. J Am Acad Dermatol 2000;43:223--8.

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

Hastings R, editor. 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, et al. The continuing challenges of leprosy. Clin Microbiol Rev 2006;19:338--81.

Hantavirus pulmonary syndrome

CDC. Hantavirus pulmonary syndrome---United States: updated recommendations for risk reduction. MMWR 2002;51:(No. RR-9).

Khan AS, Khabbaz RF, Armstrong LR, et al. Hantavirus pulmonary syndrome---the first 100 US cases. J Infect Dis 1996;173:1297--303.

Knust B, Rollin PE. Twenty-year summary of surveillance for human hantavirus infections, United States. Emerg Infect Dis 2013:1934--7.

MacNeil A, Ksiazek TG, Rollin PE. Hantavirus pulmonary syndrome, United States, 1993--2009. Emerg Infect Dis 2011;17:1195--201.

MacNeil A, Nichol ST, Spiropoulou CF. Hantavirus pulmonary syndrome. Virus Res 2011;162:138--47.

Hepatitis

Klevens RM, Hu D, Jiles R, Holmberg SD. Evolving epidemiology of hepatitis C virus in the United States. Clin Infect Dis 2012;55:S3--9.

Moorman AC, Gordon SC, Rupp LB, et al. Baseline characteristics and mortality among people in care for chronic viral hepatitis: the chronic hepatitis cohort study. Clin Infect Dis 2013;56:40--50.

Holmberg SD. Emerging epidemic of hepatitis C in young nonurban injection drug users (IDU). Presented at: report on technical consultation. Hepatitis C virus infection in young persons who inject drugs. Washington, DC, February 26--27, 2013. Silver Spring, MD: US Department of Health and Human Services, FDA; 2013. Available at http://aids.gov/pdf/hcv-and-young-pwid-consultation-report.pdf.

US Food and Drug Administration. FDA approves rapid test for antibodies to hepatitis C virus. News and events Silver Springs, MD: US Department of Health and Human Services, FDA; 2013. Available at http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm217318.htm.

Hemoylitic Uremic Syndrome

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.

Mody RK, Luna-Gierke RE, Jones TF, et al. Infections in pediatric postdiarrheal hemolytic uremic syndrome: factors associated with identifying shiga toxin-producing Escherichia coli. Arch Pediatr Adolesc Med 2012;166:902--9.

Ong KL, Apostal M, Comstock N, et al. Strategies for surveillance of pediatric hemolytic uremic syndrome: Foodborne Diseases Active Surveillance Network (FoodNet), 2000--2007. Clin Infect Dis 2012;54(Suppl 5):S424--31.

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

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.

Blanton L, Peacock G, Cox CM, et al. Neurologic disorders among pediatric deaths associated with the 2009 pandemic influenza. Pediatrics 2012;130:390--6.

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 2011;60:1128--32.

Legionellosis

CDC. Legionellosis---United States, 2000--2009. MMWR 2011;60:1083--6.

CDC. Surveillance for waterborne disease outbreaks associated with drinking water and other nonrecreational water---United States, 2009--20010. MMWR 2013;62:714--20.

CDC. Surveillance for waterborne disease outbreaks and other health events associated with recreational water---United States, 2007--2008. MMWR 2011;60:1--32.

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

European Centre for Disease Prevention and Control. Legionnaires disease in Europe, 2011. Stockholm, Sweden: ECDC; 2013. Available at http://ecdc.europa.eu/en/publications/publications/legionnaires-disease-in-europe-2011.pdf.

European Working Group on Legionella Infections (EWGLI). EWGLI technical guidelines for the investigation, control, and prevention of travel associated Legionnaires’ disease. Stockholm, Sweden: ECDC; 2011. Available at http://ecdc.europa.eu/en/activities/surveillance/ELDSNet/Documents/EWGLI-Technical-Guidelines.pdf.

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

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.

Listeriosis

Cartwright EJ, Jackson KA, Johnson SD, et al. Listeriosis outbreaks and associated food vehicles, United States, 1998--2008. Emerg Infect Dis 2013;19:1--9.

CDC. Vital signs: Listeria illnesses, deaths, and outbreaks---United States, 2009--2011. MMWR 2013;62:448--52.

Gaul LK, Farag FH, Shim T, et al. Hospital-acquired listeriosis outbreak caused by contaminated diced celery---Texas, 2010. Clin Infect Dis 2013;56:20--6.

Jackson KA, Biggerstaff M, Tobin-D’Angelo M, et al. Multistate outbreak of Listeria monocytogenes associated with Mexican-style cheese made from pasteurized milk among pregnant, Hispanic women. J Food Prot 2011;74:949--53.

Jackson KA, Iwamoto M, Swerdlow DL. Pregnancy-associated listeriosis. Epidemiol Infect 2010;138:1503--9.

Laksanalamai P, Joseph LA, Silk BJ, et al. Genomic characterization of Listeria monocytogenes strains involved in a multistate listeriosis outbreak associated with cantaloupe in US. PLoS ONE 2012;7:e42448.

McCollum JT, Cronquist AB, Silk BJ, et al. Multistate outbreak of listeriosis associated with cantaloupe. N Engl J Med 2013;639:944--53.

Pouillot R, Hoelzer K, Jackson KA, et al. Relative risk of listeriosis in Foodborne Diseases Active Surveillance Network (FoodNet) sites according to age, pregnancy, and ethnicity. Clin Infect Dis 2012;54:S396--404.

Scallan E, Hoekstra RM, Angulo FJ, et al. Foodborne illness acquired in the United States---major pathogens. Emerg Infect Dis 2011;17:7--15.

Silk BJ, Date KA, Jackson KA, et al. Invasive listeriosis in the Foodborne Diseases Active Surveillance Network (FoodNet), 2004--2009: further targeted prevention needed for higher-risk groups. Clin Infect Dis 2012;54:S405--10.

Lyme disease

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

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

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.

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. http://www.ct.gov/caes/lib/caes/documents/publications/bulletins/b1010.pdf.

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--134.

Malaria

Abanyie FA, Agguin PM, Gutman J. State of malaria diagnostic testing at clinical laboratories in the United States, 2010: a nationwide survey. Malar J 2011;10:340.

Jensenius M, Han PV, Schlagenhauf P, et al. Acute and potentially life-threatening tropical diseases in western travelers---a GeoSentinel multicenter study, 1996--2011. Am J Trop Med 2013;88:397--404.

Krause G, Schoneberg I, Altmann D, Stark K. Chemoprophylaxis and malaria death rates. Emerg Infect Dis 2006;12:447--51.

Mali S, Kachur SP, Arguin PM. Malaria surveillance---United States, 2010. MMWR 2012;61:(No. SS-2).

Measles

CDC. Hospital-associated measles outbreak---Pennsylvania, March--April 2009. MMWR 2012;61:30--2.

Parker Fiebelkorn A, Uzicanin A. Measles (rubeola). In: The yellow book: CDC health information for international travel, 2012. New York, NY: Oxford University Press; 2012.

Meningococcal disease

CDC. Prevention and control of meningococcal disease: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR 2013;62:(No. RR-2).

Cohn AC, MacNeil JR, Harrison LH, 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.

Rosenstein NE, Perkins BA, Stephens DS, et al. Meningococcal disease. N Engl J Med 2001;334:1378--88.

Mumps

Barskey AE, Schulte C, Rosen JB, et al. Mumps outbreak in Orthodox Jewish communities in the United States. N Engl J Med 2012;367:1704--13.

Pertussis

CDC. Pertussis epidemic---Washington, 2012. MMWR 2012;61:517--22.

CDC. Updated recommendations for use of tetanus toxoid, reduced diphtheria toxoid and acellular pertussis (Tdap) vaccine in adults aged 65 years and older---Advisory Committee on Immunization Practices (ACIP), 2012. MMWR 2012;61:468--70.

CDC. Updated recommendations for use of tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis vaccine (Tdap) in pregnant women---Advisory Committee on Immunization Practices (ACIP), 2012. MMWR 2013;62:131--5.

Clark TA, Messonnier NE, Hadler SC. Pertussis control: time for something new? Trends Microbiol 2012;20:211--3.

Misegades LK, Winter K, Harriman K, et al. Association of childhood pertussis with receipt of 5 doses of pertussis vaccine by time since last vaccine dose, California, 2010. JAMA 2012;308:2126--32.

Plague

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

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

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

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.

Tourdjman M, Ibraheem M, Brett M, et al. Misidentification of Yersinia pestis by automated systems resulting in delayed diagnosis of human plague infections---Oregon and New Mexico, 2010--2011. Clin Infect Dis 2012;55:e58--60.

Polio

Alexander JP, Wallace G, Wassilak SG. Poliomyelitis. In: The yellow book: CDC health information for international travel, 2012. New York, NY: Oxford University Press; 2012.

Q Fever

Anderson A, Bijlmer H, Fournier PE, et al. Diagnosis and management of Q Fever---United States, 2013 recommendations from CDC and the Q Fever working group. MMWR 2013;62:1--28.

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

Kersh GJ, Fitzpatrick KA, Self JS, et al. Presence and persistence of Coxiella burnetii in the environments of goat farms associated with a Q fever outbreak. Appl Environ Microbiol 2013;79:1697--703.

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

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

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

Rabies

CDC. Compendium of animal rabies prevention and control, 2011: National Association of State Public Health Veterinarians, Inc. MMWR 2011;60:1--14.

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;59:1--9.

CDC. Human rabies prevention---United States, 2008: recommendation of the Advisory Committee on Immunization Practices (ACIP). MMWR 2008;57:1--28.

Salmonellosis

Chai SJ, White PL, Lathrop SL, et al. Salmonella enterica serotype Enteritidis: increasing incidence of domestically acquired infections. Clin Infect Dis 2012;54(Suppl 5):S488--97.

Cronquist AB, Mody RK, Atkinson R, et al. Impacts of culture-independent diagnostic practices on public health surveillance for bacterial enteric pathogens. Clin Infect Dis 2012;54(Suppl 5):S432--9.

Gaffga NH, Barton Behravesh C, Ettestad PJ, et al. Outbreak of salmonellosis linked to live poultry from a mail-order hatchery. N Engl J Med 2012;366:2065--73.

Guo C, Hoekstra RM, Schroeder CM, et al. Application of Bayesian techniques to model the burden of human salmonellosis attributable to US food commodities at the point of processing: adaptation of a Danish model. Foodborne Pathog Dis 2011;8:509--16.

Jackson BR, Griffin PM, Cole D, Walsh KA, Chai SJ. Outbreak-associated Salmonella enterica serotypes and food Commodities, United States, 1998--2008. Emerg Infect Dis 2013;19:1239--44.

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

Jones TF, Gerner-Smidt P. Nonculture diagnostic tests for enteric diseases. Emerg Infect Dis 2012;18:513--4.

Majowicz SE, Musto J, Scallan E, et al. The global burden of nontyphoidal Salmonella gastroenteritis. Clin Infect Dis 2010;50:882--9.

Medalla F, Hoekstra RM, Whichard JM, et al. Increase in resistance to ceftriaxone and nonsusceptibility to ciprofloxacin and decrease in multidrug resistance among Salmonella strains, United States, 1996--2009. Foodborne Pathog Dis 2013;10:302--9.

Mody RK, Meyer S, Trees E, et al. Outbreak of Salmonella enterica serotype I 4,5,12:i:- infections: the challenges of hypothesis generation and microwave cooking. Epidemiol Infect 2013;142:1--11.

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.

Painter JA, Hoekstra RM, Ayers T, et al. Attribution of foodborne illnesses, hospitalizations, and deaths to food commodities by using outbreak data, United States, 1998--2008. Emerg Infect Dis 2013;19:407--15.

Scallan E, Hoekstra RM, Angulo FJ, et al. Foodborne illness acquired in the United States---major pathogens. Emerg Infect Dis 2011;17:7--15.

Scallan E, Mahon BE, Hoekstra RM, Griffin PM. Estimates of illnesses, hospitalizations and deaths caused by major bacterial enteric pathogens in young children in the United States. Pediatr Infect Dis J 2013;32:217--21.

Sjolund-Karlsson M, Howie R, Krueger A, et al. CTX-M-producing non-Typhi Salmonella spp. isolated from humans, United States. Emerg Infect Dis 2011;17:97--9.

Shigellosis

CDC. Notes from the field: emergence of Shigella flexneri 2a resistant to ceftriaxone and ciprofloxacin---South Carolina, October 2010. MMWR 2010;59:1619.

CDC. Notes from the field: outbreak of infections caused by Shigella sonnei with decreased susceptibility to azithromycin---Los Angeles, California, 2012. MMWR 2013;62:171.

Garrett V, Bornschlegel K, Lange D, et al. A recurring outbreak of Shigella sonnei among traditionally observant Jewish children in New York City: the risks of daycare and household transmission. Epidemiol Infect 2006;134:1231--6.

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.

Folster JP, Pecic G, Bowen A, et al. Decreased susceptibility to ciprofloxacin among Shigella isolates in the United States, 2006 to 2009. Antimicrob Agents Chemother 2011;55:1758--60.

Haley CC, Ong KL, Hedberg K, et al. Risk factors for sporadic shigellosis, FoodNet 2005. Foodborne Pathog Dis 2010;7:741--7.

Howie RL, Folster JP, Bowen A, et al. Reduced azithromycin susceptibility in Shigella sonnei, United States. Microb Drug Resist 2010;16:245--8. Published online 2010 Jul 12.

Nygren B, Schilling K, Blanton E, et al. Foodborne outbreaks of shigellosis in the USA, 1998--2008. Epidemiol Infect 2012;141:1--9.

Scallan E, Mahon BE, Hoekstra RM, Griffin PM. Estimates of illnesses, hospitalizations and deaths caused by major bacterial enteric pathogens in young children in the United States. Pediatr Infect Dis J 2013;32:217--21.

Wallender EK, Ailes EC, Yoder JS, Roberts VA, Brunkard JM. Contributing factors to disease outbreaks associated with untreated groundwater. Ground Water 2013:10.1111/gwat.12121[Epub ahead of print].

Spotted Fever Rickettsiosis (Including Rocky Mountain Spotted Fever)

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

Dahlgren FS, Holman RC, Paddock CD, Callinan LS, McQuiston JH. Fatal Rocky Mountain spotted fever in the United States, 1999--2007. Am J Trop Med Hyg 2012;86:713--9.

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.

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.

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

Zientek J, Dahlgren FS, McQuiston JH, Regan J. Self-reported treatment practices by healthcare providers could lead to death from Rocky Mountain spotted fever. J Pediatr 2013;2014:416--8.

Shiga toxin-producing E. 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.

Cronquist AB, Mody RK, Atkinson R, et al. Impacts of culture-independent diagnostic practices on public health surveillance for bacterial enteric pathogens. Clin Infect Dis 2012;54(Suppl 5):S432--9.

Gould LH, Mody RK, Ong KL; Emerging Infections Program Foodnet Working Group. Increased recognition of non-O157 Shiga toxin-producing Escherichia coli infections in the United States during 2000--2010: epidemiologic features and comparison with E. coli O157 infections. Foodborne Pathog Dis 2013;10:453--60.

Hadler JL, Clogher P, Hurd S, et al. Ten-year trends and risk factors for non-O157 shiga toxin-producing Escherichia coli found through shiga toxin testing, Connecticut, 2000--2009. Clin Infect Dis 2011;53:269--76.

Hale CR, Scallan E, Cronquist AB, et al. Estimates of enteric illness attributable to contact with animals and their environments in the United States. Clin Infect Dis 2012;54(Suppl 5):S472--9.

Hedican EB, Medus C, Besser JM, 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.

Jones TF, Gerner-Smidt P. Nonculture diagnostic tests for enteric diseases. Emerg Infect Dis 2012r;18:513--4.

Lathrop S, Edge K, Bareta J, et al. Shiga toxin--producing Escherichia coli, New Mexico, USA. Emerg Infect Dis 2004--2007;15:1289.

McCollum JT, Williams NJ, Beam SW, et al. Multistate outbreak of Escherichia coli O157:H7 infections associated with in-store sampling of an aged raw-milk Gouda cheese, 2010. J Food Prot 2012;75:1759--65.

Mody RK, Luna-Gierke RE, Jones TF, et al. Infections in pediatric postdiarrheal hemolytic uremic syndrome: factors associated with identifying shiga toxin-producing Escherichia coli. Arch Pediatr Adolesc Med 2012;166:902--9.

Slayton RB, Turabelidze G, Bennett SD, et al. Outbreak of Shiga toxin-producing Escherichia coli (STEC) O157:H7 associated with romaine lettuce consumption, 2011. PLoS ONE 2013;8:e55300.

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

Streptococcal Toxic Shock Syndrome

CDC. Active bacterial core surveillance report, Emerging Infections Program Network, Group A Streptococcus, 2012. Atlanta, GA: US Department of Health and Human Services, CDC; 2012. Available at http://www.cy118119.com/abcs/reports-findings/survreports/gas12.pdf.

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

Dale JB, Fischetti VA, Carapatis JR, et al. Group A streptococcal vaccines: Paving a path for accelerated development. Vaccine 2013;31S:B216--22.

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.

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.

Syphilis, Primary and Secondary

CDC. Sexually transmitted disease surveillance, 2012. Atlanta, GA: US Department of Health and Human Services; 2014.

Su JR, Beltrami JF, Zaidi AA, Weinstock HS. Primary and secondary syphilis among black and Hispanic men who have sex with men: case report data from 27 states. Ann Intern Med 2011;155:145--51.

Trichinellosis

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 2009;22:127--45.

Hall RL, Lindsay A, Hammond C, et al. Outbreak of human trichinellosis in Northern California caused by Trichinella murrelli. Am J Trop Med Hyg 2012;87:297--302.

Kennedy ED, Hall RL, Montgomery SP, Pyburn DG, Jones JL. Trichinellosis surveillance---United States, 2002--2007. MMWR 2009;58:1--7.

Roy SL, Lopez AS, Schantz PM. Trichinellosis surveillance---United States, 1997--2001. MMWR 2003;52:1--8.

Tularemia

CDC. Tularemia---United States, 2001--2010. MMWR 2013;62:963--6.

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.

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 Tularemia. Vol. WHO/CDS/EPR/2007.7. Geneva, Switzerland: World Health Organization; 2007.

Weber IB, Turabelidze G, Patrick S, et al. Clinical recognition and management of tularemia in Missouri: a retrospective records review of 121 cases. Clin Infect Dis 2012;55:1283--90.

Typhoid Fever

Loharikar A, Newton A, Rowley P, et al. Typhoid fever outbreak associated with frozen mamey pulp imported from Guatemala to the western United States, 2010. Clin Infect Dis 2012;55:61--6.

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

Varicella

Bialek SR, Perella D, Zhang J, et al. Impact of a routine two-dose varicella vaccination program on varicella epidemiology. Pediatrics 2013;132:e1134--40.

CDC. Prevention of varicella: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR 2007;56:(No. RR-4).

CDC. Evolution of varicella surveillance---selected states, 2000--2010. MMWR 2012;61:609--12.

Lopez AS, Zhang J, Brown C, Bialek S. Varicella-related hospitalizations in the United States, 2000--2006: the 1-dose varicella vaccination era. Pediatrics 2011;127:238--45.

Marin M, Zhang JX, Seward JF. Near elimination of varicella deaths in the US after implementation of the vaccination program. Pediatrics 2011;128:214--20.

Vibriosis

CDC. Vibrio mimicus infection from consuming crayfish---Spokane, Washington. MMWR 2010;59:1374.

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 2008;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.

Newton A, Kendall M, Vugia DJ, Henao OL, Mahon BE. Increasing rates of vibriosis in the United States, 1996--2010: review of surveillance data from 2 systems. Clin Infect Dis 2012;54(Suppl 5):S391--5.

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 Fevers

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--81.

Ergonul O. Crimean-Congo Haemorrhagic Fever. Lancet 2006;6:203--14.

Fichet-Calvet E, Rogers DJ. Risk maps of Lassa fever in West Africa. PLoS Negl Trop Dis 2009;3:e388.

Rollin PE, Nichol ST, Zaki S, Ksiazek TG. Arenaviruses and filoviruses. In: Murray PR, Baron EJ, Landry ML, Jorgensen JH, Pfaller MA, eds. Manual of clinical microbiology, 9th edition. Washington, DC: ASM Press; 2007:1510--22.