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Persons using assistive technology might not be able to fully access information in this file. For assistance, please send e-mail to: mmwrq@cdc.gov. Type 508 Accommodation and the title of the report in the subject line of e-mail. Summary of Notifiable Diseases --- United States, 2006Please note: Errata have been published for this article. To view the errata, please click here and here.
Prepared by
PrefaceThe Summary of Notifiable Diseases --- United States, 2006 contains the official statistics, in tabular and graphic form, for the reported occurrence of nationally notifiable infectious diseases in the United States for 2006. Unless otherwise noted, the data are final totals for 2006 reported as of June 30, 2007. These statistics are collected and compiled from reports sent by state and territorial health departments 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.cdc.gov/mmwr/summary.html. This site also includes publications from previous years. The Highlights section presents noteworthy epidemiologic and prevention information for 2006 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 during 2006.* The tables provide the number of cases reported to CDC for 2006 as well as the distribution of cases by month, geographic location, and the patient's demographic characteristics (age, sex, race, and ethnicity). Part 2 contains graphs and maps that depict summary data for certain notifiable infectious diseases described in tabular form in Part 1. Part 3 contains tables that list the number of cases of notifiable diseases reported to CDC since 1975. This section also includes a table enumerating deaths associated with specified notifiable diseases reported to CDC's National Center for Health Statistics (NCHS) during 2002--2004. 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 about the current report and descriptions of how information is or could be used are invited. Comments should be sent to Public Health Surveillance Team --- NNDSS, Division of Integrated Surveillance Systems and Services, National Center for Public Health Informatics at soib@cdc.gov. BackgroundThe infectious diseases designated as notifiable at the national level during 2006 are listed on page 5. 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.cdc.gov/epo/dphsi/nndsshis.htm. In 1961, CDC assumed responsibility for the collection and publication of data on nationally notifiable diseases. NNDSS is neither a single surveillance system nor a method of reporting. Certain NNDSS data are reported to CDC through separate surveillance information systems and through different reporting mechanisms; however, these data are aggregated and compiled for publication purposes. Notifiable disease reporting at the local level protects the public's health by ensuring the proper identification and follow-up of cases. Public health workers ensure that persons who are already ill receive appropriate treatment; trace contacts who need vaccines, treatment, quarantine, or education; investigate and halt outbreaks; eliminate environmental hazards; and close premises where spread has occurred. Surveillance of notifiable conditions helps public health authorities to monitor the impact 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, detect changes in health-care practices, develop and implement public health programs and interventions, and contribute data to monitor global trends. 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 and territorial health departments and CDC collaborate in determining which diseases should be nationally notifiable. CSTE, with input from CDC, makes recommendations annually for additions and deletions. Although disease reporting is mandated by legislation or regulation at the state and local levels, state reporting to CDC is voluntary. Reporting completeness of notifiable diseases is highly variable and related to the condition or disease being reported (1). The list of diseases considered notifiable varies by state and year. Current and historic national public health surveillance case definitions used for classifying and enumerating cases consistently across reporting jurisdictions are available at http://www.cdc.gov/epo/dphsi/nndsshis.htm. Revised International Health RegulationsIn May 2005, the World Health Assembly adopted revised International Health regulations (IHR) (2) that went into effect in the United States on July 18, 2007. This international legal instrument governs the role of the World Health Organization (WHO) and its member countries, including the United States, in identifying, responding to and sharing information about Public Health Emergencies of International Concern (PHEIC). A PHEIC is an extraordinary event that 1) constitutes a public health risk to other countries through international spread of disease, and 2) potentially requires a coordinated international response. The IHR are designed to prevent and protect against the international spread of diseases while minimizing the effect on world travel and trade. Countries that have adopted these rules have a much broader responsibility to detect, respond to, and report public health emergencies that potentially require a coordinated international response in addition to taking preventive measures. The IHR will help countries work together to identify, respond to, and share information about public health emergencies of international concern. The revised IHR represent a conceptual shift from a predefined disease list to a framework of reporting and responding to events on the basis of an assessment of public health criteria, including seriousness, unexpectedness, and international travel and trade implications. PHEIC are events that fall within those criteria (further defined in a decision algorithm in Annex 2 of the revised IHR). Four conditions always constitute a PHEIC and do not require the use of the IHR decision instrument in Annex 2: Severe Acute Respiratory Syndrome (SARS), smallpox, poliomyelitis caused by wild-type poliovirus, and human influenza caused by a new subtype. Any other event requires the use of the decision algorithm in Annex 2 of the IHR to determine if it is a potential PHEIC. Examples of events that require the use of the decision instrument include, but are not limited to, cholera, pneumonic plague, yellow fever, West Nile fever, viral hemorrhagic fevers, and meningococcal disease. Other biologic, chemical, or radiologic events might fit the decision algorithm and also must be reportable to WHO. All WHO member states are required to notify WHO of a potential PHEIC. WHO makes the final determination about the existence of a PHEIC. Health-care providers in the United States are required to report diseases, conditions, or outbreaks as determined by local, state, or territorial law and regulation, and as outlined in each state's list of reportable conditions. All health-care providers should work with their local, state, and territorial health agencies to identify and report events that might constitute a potential PHEIC occurring in their location. U.S. State and Territorial Departments of Health have agreed to report information about a potential PHEIC to the most relevant federal agency responsible for the event. In the case of human disease, the U.S. State or Territorial Departments of Health will notify CDC rapidly through existing formal and informal reporting mechanisms (3). CDC will further analyze the event based on the decision algorithm in Annex 2 of the IHR and notify the U.S. Department of Health and Human Services (DHHS) Secretary's Operations Center (SOC), as appropriate. DHHS has the lead role in carrying out the IHR, in cooperation with multiple federal departments and agencies. The HHS SOC is the central body for the United States responsible for reporting potential events to the 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 the 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:
Additonal information concerning IHR is available at http://www.who.int/csr/ihr/en, http://www.globalhealth.gov/ihr/index.html, http://www.cdc.gov/cogh/ihregulations.htm, and http://www.cste.org/PS/2007ps/2007psfinal/ID/07-ID-06.pdf. At its annual meeting in June 2007, the Council of State and Territorial Epidemiologists (CSTE) approved a position statement to support the implementation of the 2005 IHR in the United States (3). CSTE also approved a position statement in support of the 2005 IHR adding initial detections of novel influenza A virus infections to the list of nationally notifiable diseases reportable to NNDSS, beginning in January 2007 (4).
* No cases of diphtheria, neuroinvasive or nonneuroinvasive western equine encephalitis virus disease, paralytic poliomyelitis, severe acute respiratory syndrome--associated coronavirus (SARS-CoV), smallpox, yellow fever, or varicella deaths were reported in the United States in 2006; these conditions do not appear in the tables in Part 1. For certain other nationally notifiable diseases, incidence data were reported to CDC but are not included in the tables or graphs of this Summary. Data on chronic hepatitis B and hepatitis C virus infection (past or present) are not included because they are undergoing data quality review. CDC is upgrading its national surveillance data management system for human immunodeficiency virus (HIV) and acquired immunodeficiency syndrome (AIDS). During this transition, CDC is not updating AIDS or HIV infection surveillance data. Therefore, no updates are provided for HIV and AIDS data in this Summary. Infectious Diseases
Designated as Notifiable at the National Level During 2006
|
| Acquired immunodeficiency syndrome (AIDS)† | Lyme disease |
| Anthrax | Malaria |
| Botulism | Measles |
| foodborne | Meningococcal disease, invasive§ |
| infant | Mumps |
| other (wound and unspecified) | Pertussis |
| Brucellosis | Plague |
| Chancroid | Poliomyelitis, paralytic |
| Chlamydia trachomatis, genital infection | Psittacosis |
| Cholera | Q fever |
| Coccidioidomycosis | Rabies |
| Cryptosporidiosis | animal |
| Cyclosporiasis | human |
| Diphtheria | Rocky Mountain spotted fever |
| Domestic arboviral diseases, neuroinvasive and nonneuroinvasive | Rubella |
| California serogroup virus disease | Rubella, congenital syndrome |
| eastern equine encephalitis virus disease | Salmonellosis |
| Powassan virus disease | Severe acute respiratory syndrome--associated coronavirus (SARS-CoV) disease |
| St. Louis encephalitis virus disease | Shiga toxin-producing Escherichia coli (STEC)¶ |
| West Nile virus disease | Shigellosis |
| western equine encephalitis virus disease | Smallpox |
| Ehrlichiosis | Streptococcal disease, invasive, group A |
| human granulocytic | Streptococcal toxic-shock syndrome |
| human monocytic | Streptococcus pneumoniae, invasive disease |
| human, other or unspecified agent | age <5 years |
| Giardiasis | Streptococcus pneumoniae, invasive disease, drug-resistant |
| Gonorrhea | all ages |
| Haemophilus influenzae, invasive disease | Syphilis |
| Hansen disease (leprosy) | Syphilis, congenital |
| Hantavirus pulmonary syndrome | Tetanus |
| Hemolytic uremic syndrome, postdiarrheal | Toxic-shock syndrome (other than streptococcal) |
| Hepatitis A, acute | Trichinellosis |
| Hepatitis B, acute | Tuberculosis |
| Hepatitis B, chronic | Tularemia |
| Hepatitis B virus, perinatal infection | Typhoid fever |
| Hepatitis C, acute | Vancomycin-intermediate Staphylococcus aureus infection (VISA) |
| Hepatitis C virus infection (past or present)§ | Vancomycin-resistant Staphylococcus aureus infection (VRSA) |
| Human immunodeficiency virus (HIV) infection | Varicella infection (morbidity) |
| adult (age >13 yrs) | Varicella (mortality) |
| pediatric (age <13 yrs) | Yellow fever |
| Influenza-associated pediatric mortality | |
| Legionellosis§ | |
| Listeriosis |
† The 2005 CSTE position statement approving changes to the AIDS case definition for adults and adolescents aged >13 years is pending final review and publication in MMWR.
§ In accord with position statements approved by CSTE in 2005, the national surveillance case definitions for hepatitis C virus infection (past or present), legionellosis, and meningococcal disease were revised.
¶ Beginning in 2006, STEC replaced the Enterohemorrhagic Escherichia coli infection category that was previously nationally notifiable.
Provisional data concerning the reported occurrence of nationally notifiable infectious diseases are published weekly in MMWR. After each reporting year, staff in state and territorial 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. 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 compiled and published in the Summary.
Data in the Summary are derived primarily from reports transmitted to CDC from health departments in the 50 states, five territories (American Samoa, the Commonwealth of the Northern Mariana Islands, Guam, Puerto Rico, and the U.S. Virgin Islands), 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, 2006, through the week ending December 30, 2006. More information regarding infectious notifiable diseases, including case definitions, is available at http://www.cdc.gov/epo/dphsi/phs.htm. Policies for reporting notifiable disease cases can vary by disease or reporting jurisdiction. The case-status categories used to determine which cases reported to NNDSS are published, by disease or condition, and are listed in the print criteria column of the 2006 NNDSS event code list (available at http://www.cdc.gov/epo/dphsi/phs/files/NNDSSeventcodelistJanuary2007.pdf).
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.
Coordinating Center for Health Information and Service
National Center for Health Statistics (NCHS)
Office of Vital and Health Statistics Systems (deaths from selected
notifiable diseases)
Coordinating Center for Infectious Diseases
National Center for HIV/AIDS, Viral Hepatitis, STD, and TB Prevention
(NCHHSTP)
Division of HIV/AIDS Prevention (AIDS and HIV infection)
Division of STD Prevention (chancroid; Chlamydia trachomatis,
genital infection; gonorrhea; and syphilis)
Division of Tuberculosis Elimination (tuberculosis)
National Center for Immunization and Respiratory Diseases
Influenza Division (influenza-associated pediatric mortality)
Division of Viral Diseases (poliomyelitis, varicella deaths, and
SARS-CoV)
National Center for Zoonotic, Vector-Borne, and Enteric Diseases
Division of Vector-Borne Infectious Diseases (arboviral diseases)
Division of Viral and Rickettsial Diseases (animal rabies)
Population estimates for the states are from the NCHS bridged-race estimates of the July 1, 2000--July 1, 2005 U.S. resident population from the vintage 2005 postcensal series by year, county, age, sex, race, and Hispanic origin, prepared under a collaborative arrangement with the U.S. Census Bureau. This data set was released on August 16, 2005, and is available at http://www.cdc.gov/nchs/about/major/dvs/popbridge/popbridge.htm. Populations for territories are 2005 estimates from the U.S. Census Bureau International Data Base Data Access--Display Mode, available at http://www.census.gov/ipc/www/idb/summaries.html. The choice of population denominators for incidence reported in MMWR is based on 1) the availability of census population data at the time of preparation for publication and 2) the desire for consistent use of the same population data to compute incidence reported by different CDC programs. Incidence in the Summary is calculated as the number of reported cases for each disease or condition divided by either the U.S. resident population for the specified demographic population or the total U.S. residential population, multiplied by 100,000. When a nationally notifiable disease is associated with a specific age restriction, the same age restriction is applied to the population in the denominator of the incidence calculation. In addition, population data from states in which the disease or condition was not notifiable or was not available were excluded from incidence calculations. Unless otherwise stated, disease totals for the United States do not include data for American Samoa, Guam, Puerto Rico, the Commonwealth of the Northern Mariana Islands, or the U.S. Virgin Islands.
Incidence data in the Summary are presented by the date of report to CDC as determined by the MMWR week and year assigned by the state or territorial health department, except for the domestic arboviral diseases, which are presented by date of diagnosis. Data are reported by the state in which the patient resided at the time of diagnosis. For certain nationally notifiable infectious diseases, surveillance data are reported independently to different CDC programs. Thus, surveillance data reported by other CDC programs might vary from data reported in the Summary because of differences in 1) the date used to aggregate data (e.g., date of report or date of disease occurrence), 2) the timing of reports, 3) the source of the data, 4) surveillance case definitions, and 5) policies regarding case jurisdiction (i.e., which state should report the case to CDC).
Data reported in the Summary are useful for analyzing disease trends and determining relative disease burdens. However, reporting practices affect how these data should be interpreted. Disease reporting is likely incomplete, and completeness might vary depending on the disease. 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 interests, resources, and priorities of state and local officials responsible for disease control and public health surveillance. Finally, factors such as changes in methods for public health surveillance, introduction of new diagnostic tests, or discovery of new disease entities can cause changes in disease reporting that are independent of the true incidence of disease.
Public health surveillance data are published for selected racial/ethnic populations because these variables can be risk markers for certain notifiable diseases. Race and ethnicity data also can be used to highlight populations for focused prevention efforts. 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 uniformly for all diseases. For example, certain disease programs collect data on race and ethnicity using one or two variables, based on the 1977 standards for collecting such data issued by the Office of Management and the Budget (OMB). However, beginning in 2003, certain CDC programs, such as the tuberculosis program, implemented OMB's 1997 revised standards for collecting such data; these programs collect data on multiple races per person using multiple race variables. In addition, although the recommended standard for classifying a person's race or ethnicity is based on self-reporting, this procedure might not always be followed.
Before 1990, data were reported to CDC as cumulative counts rather than individual case reports. In 1990, states began electronically capturing and reporting individual case reports (without personal identifiers) to CDC using the National Electronic Telecommunication System for Surveillance (NETSS). In 2001, CDC launched the National Electronic Disease Surveillance System (NEDSS), now a component of the Public Health Information Network (http://www.cdc.gov/phin), 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 level. One of the objectives of NEDSS is to improve the accuracy, completeness, and timeliness of disease reporting at the local, state, and national level (5). CDC has developed the NEDSS Base System (NBS), a public health surveillance information system that can be used by states that do not wish to develop their own NEDSS-based systems. NBS can capture data that already are in electronic form (e.g., electronic laboratory results, which are needed for case confirmation) rather than requiring that these data be entered manually as in the NETSS application. In 2006, NBS was used by 16 states to transmit nationally notifiable infectious diseases to CDC. Additional information concerning NEDSS is available at http://www.cdc.gov/NEDSS.
5. National Electronic Disease Surveillance System Working Group. National Electronic Disease Surveillance System (NEDSS): a standards-based approach to connect public health and clinical medicine. J Public Health Manag Pract 2001;7:43--50.
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).
In February 2006, the first naturally-occurring case of inhalation anthrax in the United States since 1976 occurred in a New York City resident. His exposure to Bacillus anthracis spores was determined to be the result of making traditional African drums using hard-dried animal hides that were contaminated with spores (1). The patient recovered with treatment (2). A subsequent, unrelated, fatal case of inhalation anthrax occurred in July 2006 in Scotland; exposure was suspected to result from the playing of traditional African drums. In both cases, the animal hides were suspected to originate from west Africa. These events demonstrate a previously unrecognized risk for serious illness and death from inhalation anthrax resulting from the making and playing of animal-skin drums.
Naturally occurring anthrax epizootics in animal populations continue to be reported in the United States annually. In 2006, epizootics were reported in four states, affecting livestock in Minnesota, North Dakota, and South Dakota and livestock and wildlife in Texas.
During 2006, for the second consecutive year, West Nile virus (WNV) activity was detected in all 48 contiguous states; in one state (Washington), human cases were reported for the first time (1). Cases of WNV disease in humans were reported from 731 counties in 43 states and the District of Columbia. Of these cases, 35% were West Nile neuroinvasive disease (WNND), 61% were uncomplicated fever, and 4% were clinically unspecified. Of the cases with WNND, 12% were fatal. The number of WNND cases reported was the highest since 2003; approximately 10% of these cases were from Idaho, which previously had reported very few cases. Since WNV was first recognized in the United States in 1999, a median of 1,229 (mean:1,238; range:19--2,946) WNND cases have been reported annually.
Botulism is a severe paralytic illness caused by the toxins of Clostridium botulinum. Exposure to toxin can occur by ingestion (foodborne botulism) or by in situ production from C. botulinum colonization of a wound (wound botulism) or the gastrointestinal tract (infant botulism and adult intestinal colonization of botulism) (1). In addition to the National Notifiable Diseases Surveillance System, CDC maintains intensive surveillance for cases of botulism in the United States. In 2006, cases were attributed to foodborne botulism, wound botulism, and infant botulism.
In 2006, two cattle herds in one state were reported by the U.S. Department of Agriculture (USDA) to be affected by brucellosis. USDA has designated 48 states and three territories as being free of cattle brucellosis, with one state regaining and another state losing Brucellosis Class Free state status (1). Brucella abortus remains enzootic in elk and bison in the greater Yellowstone National Park area, and Brucella suis is enzootic in feral swine in the southeast. Hunters exposed to these animals might be at increased risk for infection. Human cases can occur among immigrants and travelers returning from countries with endemic brucellosis and are associated with consumption of unpasteurized milk or soft cheeses. Pathogenic Brucella species are considered category B biologic threat agents because of a high potential for aerosol transmission (2). For the same reason, biosafety level 3 practices, containment, and equipment are recommended for laboratory manipulation of isolates (3).
Cases of cholera continue to be rare in the United States. The number of cases reported in 2006 was slightly higher than the average number of cases per year reported during 2001--2005 (4.6) (1). Foreign travel continues to be the primary source of illness for cholera in the United States. Cholera remains a global threat to health, particularly in areas with poor access to improved water and sanitation, such as sub-Saharan Africa (2). All patients with domestic exposure had consumed seafood (3). Crabs harvested from the U.S. Gulf Coast continue to be a common source of cholera, especially during warmer months, when environmental conditions favor the growth and survival of Vibrio species in marine water.
In 2006, the number of cryptosporidiosis cases continued to increase. This follows a dramatic increase in the number of cases in 2005. The reasons for this increase are unclear but might reflect changes in jurisdictional reporting patterns; increased testing for Cryptosporidium following the introduction of nitazoxanide, the first licensed treatment for the disease (1); or a real increase in infection and disease caused by Cryptosporidium. This drug introduction might have affected clinical practice by increasing the likelihood of health-care providers requesting Cryptosporidium testing, leading to an increase in subsequent case reports.
Although cryptosporidiosis is widespread geographically in the United States, a higher incidence is reported by northern states (2). However, this observation is difficult to interpret because of differences in cryptosporidiosis surveillance systems and reporting among states.
As in previous years, cryptosporidiosis case reports were clearly influenced by cryptosporidiosis outbreaks. Although cryptosporidiosis affects persons in all age groups, the number of reported cases was highest among children aged 1--9 years. A tenfold increase in transmission of cryptosporidiosis occurred during summer through early fall compared with winter, coinciding with increased use of recreational water by younger children, which is a known risk factor for cryptosporidiosis. Transmission through recreational water is facilitated by the substantial number of Cryptosporidium oocysts that can be shed by a single person; the extended periods of time that oocysts can be shed (3); the low infectious dose (4); the resistance of Cryptosporidium oocysts to chlorine (5); and the prevalence of improper pool maintenance (i.e., insufficient disinfection, filtration, and recirculation of water), particularly of children's wading pools (6).
Human monocytic ehrlichiosis and human granulocytic ehrlichiosis (now known as human [granulocytic] anaplasmosis) are emerging tick-borne diseases that became nationally notifiable in 1999. Because identification and reporting of these diseases remain incomplete, areas shown in the maps on pages 49--50 of this summary might not be definitive predictors for overall distribution or regional prevalence. Increases in numbers of reported cases of human rickettsial infections might result from several factors, including but not limited to increases in vector tick populations, increases in human-tick contact as a result of encroachment into tick habitat through suburban/rural recreational activities and housing construction; changes in case definitions, case report forms, and laboratory tests; and increased use of active surveillance methods to supplement previously passive surveillance methods as a result of increased resource availability and perception of high case density in newly surveyed areas.
The pathogen responsible for human granulocytic ehrlichiosis, genus Ehrlichia, has been reclassified and now belongs to the genus Anaplasma. Diseases resulting from infection with Ehrlichia chaffeensis, Anaplasma phagocytophilum (formerly Ehrlichia phagocytophila), and other pathogens (comprising Ehrlichia ewingii and undifferentiated species) have been referred to respectively by the acronyms "HME," "HGE," and "Ehrlichiosis (unspecified or other agent)." The case definitions for these diseases have been modified by a resolution adopted at the June 2007 meeting of the Council of State and Territorial Epidemiologists; the new category names and the new case definitions became effective January 1, 2008 (1).
In 2006, rates of gonorrhea in the United States increased for the second consecutive year (1). Increases in gonorrhea rates in eight western states during 2000--2005 have been described previously (2). Increases in quinolone-resistant Neisseria gonorrhoeae in 2006 led to changes in national guidelines that now limit the recommended treatment of gonorrhea to a single class of drugs, the cephalosporins (3). The combination of increases in gonorrhea morbidity with increases in resistance and decreased treatment options have increased the need for better understanding of the epidemiology of gonorrhea.
Before the introduction of effective vaccines, Haemophilus influenzae type b (Hib) was the leading cause of bacterial meningitis and other invasive bacterial disease among children aged <5 years. Incidence of invasive Hib disease began to decline dramatically in the late 1980s, coincident with licensure of conjugate Hib vaccines; incidence has declined >99% compared with the prevaccine era (1). During 2006, approximately 8% of all cases of invasive Haemophilus influenzae (Hi) disease reported among children aged <5 years were attributed to Hib, reflecting successful delivery of highly effective conjugate Hib vaccines to children beginning at age 2 months (2). Nevertheless, for approximately 50% of reported cases, serotype information was either unknown or missing, and some of these also might be Hib cases. Accurate laboratory information is essential to correctly identify the serotype of the causative Hi isolate and to assess progress toward elimination of Hib invasive disease (3).
The number of cases of Hansen disease (HD) reported in the United States peaked at 361 in 1985 and has declined since 1988. In 2006, cases were reported from 20 states and two territories. HD is not highly transmissible; cases appear to be related predominantly to immigration. HD outpatient clinics operated under the guidance and direction of the U.S. Department of Health and Human Services, Health Resources and Services Administration exist in Phoenix, Arizona; Los Angeles, Martinez, and San Diego, California; Miami, Florida; Chicago, Illinois; Baton Rouge, Louisiana; Boston, Massachusetts; New York City, New York; San Juan, Puerto Rico; Austin, Dallas, Harlingen, Houston, and San Antonio, Texas; and Seattle, Washington. Services provided to HD patients include diagnosis, treatment, follow-up of patients and contacts, disability prevention and monitoring, education, and a referral system for HD health-care services. Approximately 6,500 person in the United States are living with HD. Additional information regarding access to clinical care is available at http://www.hrsa.gov/hansens.
Hemolytic uremic syndrome (HUS) is characterized by the triad of hemolytic anemia, thrombocytopenia, and renal insufficiency. The most common etiology of HUS in the United States is infection with Shiga toxin-producing Escherichia coli, principally E. coli O157:H7 (1). Approximately 8% of persons infected with E. coli O157:H7 progress to HUS (2). During 2006, the majority of reported cases occurred among children aged <5 years.
An early and severe influenza season during 2003--2004 was associated with deaths in children in multiple states, prompting CDC to request that all state, territorial, and local health departments report laboratory confirmed influenza-associated pediatric deaths in children aged <18 years (1,2). During the 2003--04 influenza season, 153 pediatric influenza-associated deaths were reported to CDC by 40 state health departments (3). In June 2004, the Council of State and Territorial Epidemiologists added influenza-associated pediatric mortality to the list of conditions reportable to the National Notifiable Diseases Surveillance System (NNDSS) (4). Cumulative year-to-date incidence data are published each week in MMWR Table I for low-incidence nationally notifiable diseases.
During 2006, a total of 43 influenza-associated pediatric deaths were reported to CDC. The median age at death was 4 years (range: 28 days--17 years): seven children (16%) were aged <6 months; 12 (28%) were aged 6--23 months; five (12%) were aged 24--59 months; and 19 (44%) were aged >5 years. In 2006, approximately half of all influenza-associated pediatric deaths occurred in the inpatient setting; a slight increase occurred in the number of children who died in the emergency room or outside the hospital compared with 2005 (22 and 17, respectively). Twenty (47%) children had one or more underlying or chronic condition, and 21 (53%) were previously healthy. The more common chronic conditions reported included moderate to severe developmental delay (n = 8), neuromuscular disorders (n = 5), chronic pulmonary disease (n = 5), seizure disorder (n = 4), and asthma (n = 4). Bacterial coinfections were confirmed in seven children. Pathogens cultured were Staphylococcus aureus, sensitivity not done; Staphylococcus aureus, methicillin-sensitive; Streptococcus viridans; Group A Streptococcus; Pseudomonas aeruginosa, and one infection with an unidentified gram-negative bacteria. Of the six (14%) children who received >1 dose of influenza vaccine before the onset of illness during the 2005--06 season, only three were fully vaccinated. The current recommendations of the Advisory Committee on Immunization Practices highlight the importance of administering 2 doses of influenza vaccine for previously unvaccinated children aged 6 months--<9years (5). Continued surveillance of severe influenza-related mortality is important to monitor the impact of influenza and the possible effects of interventions in children.
During 2005--2006, nationwide legionellosis case counts increased for the second year in a row. In 2005, in collaboration with CDC, the Council for State and Territorial Epidemiologists adopted a position statement to improve reporting of travel-associated legionellosis (1); this might have resulted in an increase in case reporting. Nearly all regions of the United States, with the exception of the West North Central area, reported more cases in 2006 than in 2005. Other possible explanations for the increase include an actual increase in disease incidence or increased use of Legionella diagnostic tests.
Listeriosis is a rare but severe infection caused by Listeria monocytogenes that has been a nationally notifiable disease since 2000. Listeriosis is primarily foodborne and occurs most frequently among persons who are older, pregnant, or immunocompromised. During 2005, the majority of reported cases occurred among persons aged >65 years.
Molecular subtyping of L. monocytogenes isolates and sharing of that information through PulseNet has enhanced the ability of public health officials to detect and investigate outbreaks. Recent outbreaks have been linked to ready-to-eat deli meat (1) and unpasteurized cheese (2). During 2006, the incidence of listeriosis in FoodNet active surveillance sites was 0.3 cases per 100,000 population, representing a decrease of 34% compared with 1996--1998; however, incidence remained higher than at its lowest point in 2002 (3).
All clinical isolates should be submitted to state public health laboratories for pulsed-field gel electrophoresis (PFGE) pattern determination, and all persons with listeriosis should be interviewed by a public health official or health-care provider using a standard Listeria case form (available at http://www.cdc.gov/nationalsurveillance/ListeriaCaseReportFormOMB0920-0004.pdf). Rapid analysis of surveillance data will allow identification of possible food sources of outbreaks.
In 2006, the Council of State and Territorial Epidemiologists (CSTE) approved a modified case classification for measles, simultaneously with those for rubella and congenital rubella syndrome (1). Because measles is no longer endemic in the United States, its future epidemiology in the U.S. will reflect its global epidemiology. The modification of the case classification clearly identifies the origin of each case and will help define the impact of imported cases on the epidemiology of measles in the United States.
As in recent years, 95% of confirmed measles cases reported during 2006 were import-associated. Of these, 31 cases were internationally imported, 20 resulted from exposure to persons with imported infections, and in one case, virologic evidence indicated an imported source. The sources for the remaining three cases were classified as unknown because no link to importation was detected. Nearly half of all cases occurred among adults aged 20--39 years, and 20% occurred in adults aged >40 years. Four outbreaks occurred during 2006 (size range: 3--18 cases), all from imported sources. Three imported cases occurred in each of two outbreaks, with no secondary transmission. In another outbreak; one imported case and two secondary cases occurred in an immigrant community. In the fourth outbreak, 18 cases occurred among persons aged 25--46 years, most of whom had unknown vaccination histories. The primary exposure setting for this outbreak was a large office building and nearby businesses. Five case-patients were foreign born, including the index case-patient, who had arrived in the United States 9 days before onset of symptoms.
Measles can be prevented by adhering to recommendations for vaccination, including guidelines for travelers (2,3). Although the elimination of endemic measles in the United States has been achieved, and population immunity remains high (4), an outbreak can occur when measles is introduced into a susceptible group, often at significant cost to control (5).
Neisseria meningitidis is a leading cause of bacterial meningitis and sepsis in the United States. Rates of meningococcal disease are highest among infants, with a second peak at age 18 years (1). The proportion of cases caused by each serogroup of N. meningitidis varies by age group. Among adolescents aged 11--19 years, 75% of cases are caused by serogroups contained in the tetravalent (A,C,Y,W-135) meningococcal conjugate vaccine ([MCV4] Menactra® (Sanofi Pasteur, Swiftwater, Pennsylvania). The majority of cases in infants are caused by serogroup B, for which no vaccine is licensed in the United States.
MCV4 is licensed for persons aged 2--55 years. In 2007, CDC's Advisory Committee on Immunization Practices revised recommendations for routine use of MCV4 to include children aged 11--12 years at the preadolescent vaccination visit and adolescents aged 13--18 years at the earliest opportunity (2). MCV4 also is recommended for college freshmen living in dormitories and other populations aged 2--55 years at increased risk for meningococcal disease (1). Further reductions in meningococcal disease could be achieved with the development of an effective serogroup B vaccine.
Since vaccine licensure in 1967, the number of cases of mumps in the United States has declined steadily. Since 2001, an average of 265 mumps cases (range: 231--293 cases) has been reported each year (1). However, in 2006, the largest mumps outbreak in >20 years occurred, with >5,000 cases reported (1--3). The outbreak began in Iowa in December 2005, peaked in April 2006, and declined to lower levels of reporting during summer 2006 (3). The majority of cases occurred during March--May, 2006 (3). The outbreak was primarily focal in geographic distribution; 84% of cases were reported by six contiguous midwestern states (Illinois, Iowa, Kansas, Nebraska, South Dakota, and Wisconsin) (3). In contrast to the childhood age range traditionally associated with mumps disease, young adults aged 18--24 years were the age group most highly affected (1--3). In 2006, a total of 63% of reported cases occurred in females; previously, no gender differences in case rates had been reported (3).
In response to the outbreak, the Advisory Committee on Immunization Practices (ACIP) updated criteria for mumps immunity and mumps vaccination recommendations (4). Acceptable presumptive evidence of immunity to mumps includes one of the following: 1) documentation of adequate vaccination, 2) laboratory evidence of immunity, 3) birth before 1957, or 4) documentation of physician-diagnosed mumps. Documentation of adequate vaccination now requires 2 doses of a live mumps virus vaccine for school-aged children (grades K--12) and adults at high risk (i.e., persons who work in health-care facilities, international travelers, and students at post--high school educational institutions). Health-care workers born before 1957 without other evidence of immunity should now consider 1 dose of live mumps vaccine. During an outbreak, a second dose of live mumps vaccine should be considered for children aged 1--4 years and adults at low risk if affected by the outbreak; health-care workers born before 1957 without other evidence of immunity should strongly consider 2 doses of live mumps vaccine.
In 2006, incidence of reported pertussis decreased to 5.35 cases per 100,000 population after peaking during 2004--2005 at 8.9 per 100,000. Infants aged <6 months, who are too young to be fully vaccinated, had the highest reported rate of pertussis (84.21 per 100,000 population), but adolescents aged 10--19 years and adults aged >20 years contributed the greatest number of reported cases. Adolescents and adults might be a source of transmission of pertussis to young infants who are at higher risk for severe disease and death and are recommended to be vaccinated with tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis vaccine (Tdap) (1,2). In 2006, coverage with Tdap in adolescents aged 13--17 years was 10.8%, compared with 49.4% coverage with tetanus and diphtheria toxoids vaccine (Td) (3). The decrease in reported pertussis incidence in 2006 is unlikely to be related to use of Tdap and is more likely related to the cyclical nature of disease.
The number of human plague cases reported in 2006 was the greatest number since 1994 and was fourfold higher than the average for the preceding 5 years. Six cases were classified as primary septicemic plague, approximately twice the usual frequency of this disease manifestation. Nearly half of the cases reported in 2006 were from New Mexico (n = 8); two of these cases were fatal. Although factors governing the occurrence of plague are incompletely understood, the disease appears to fluctuate naturally in response to climactic factors.
In 2006, the Council of State and Territorial Epidemiologists (CSTE) recommended revision of the surveillance case definition for paralytic poliomyelitis to include nonparalytic poliovirus infection and the addition of non-paralytic poliovirus infection to the list of nationally notifiable diseases reported through the National Notifiable Diseases Surveillance System (1). These changes resulted from the identification in 2005 of a type 1 vaccine-derived poliovirus (VDPV) infection among unvaccinated Minnesota Amish children who were not paralyzed (2). Public health officials should remain alert that paralytic poliomyelitis or poliovirus infections might occur in high-risk (i.e., unvaccinated or undervaccinated) populations and should report any detected poliovirus infections attributed to either wild or vaccine-derived polioviruses and any paralytic poliomyelitis cases.
Psittacosis is an avian zoonosis with a spectrum of disease that ranges from a mild influenza-like illness to severe pneumonia with multiorgan involvement. Case reports of psittacosis in 2006 increased slightly compared with the previous four years. Further information regarding diagnosis, treatment, and prevention of psittacosis is available at http://www.avma.org/pubhlth/psittacosis.asp.
During 2006, the majority (92%) of animal rabies cases were reported in wild animal species. Overall an 8.2% increase in rabies cases was reported in animals compared with 2005 (1). In the United States five animal species are recognized as reservoir species for various rabies virus variants over defined geographic regions: raccoons (eastern United States), bats (various species, all U.S. states except Hawaii), skunks (North Central United States, South Central United States, and California), foxes (Alaska, Arizona, and Texas), and mongoose (Puerto Rico). During 2006, bats became the second most reported species with rabies.
Reported cases of rabies in domestic animals remain low in part because of high vaccination rates. Dog-to-dog transmission has not been reported in 2 years, making the United States free of the canine rabies virus variant in 2006. As in the past decade, cats were the most commonly reported domestic animal with rabies during 2006.
Vaccination programs to control rabies in wild carnivores were ongoing through the distribution of baits containing an oral rabies vaccine in the Eastern United States and Texas. Oral rabies vaccination programs in Texas are being maintained as a barrier to prevent the reintroduction of canine rabies from Mexico. Oral rabies vaccination programs are also being conducted in the Eastern United States to attempt to stop the westward spread of the raccoon rabies virus variant. Active surveillance conducted by the U. S. Department of Agriculture (USDA) to monitor oral rabies vaccination programs were further enhanced by the deployment of the Direct Rapid Immunohistochemical Test (DRIT) which USDA began implementing in the last half of 2005 after receiving training on its use at CDC. This test is used for screening the large number of samples collected by USDA in the field, reducing the burden on state laboratories and allowing for faster processing of surveillance samples (2).
Three cases of human rabies were identified during 2006: one in a male aged 16 years from Texas, one in a female aged 10 years from Indiana, and one in a male aged 11 years from California. The cases in Texas and Indiana were attributable to bat-associated rabies virus variants; free-tailed bat and sliver-haired bat respectively. The case in California was associated with a canine variant from the Philippines. The patient had recently immigrated from the Philippines where an exposure to a dog was noted approximately 2 years before onset of rabies (2).
During 2006, as in previous years, the majority of reported cases occurred among persons aged <5 years. Since 1993, the most frequently reported isolates have been Salmonella enterica serotype Typhimurium and S. enterica serotype Enteritidis (1). The epidemiology of Salmonella has been changing over the past decade. Salmonella serotype Typhimurium has decreased in incidence, while incidence of serotypes Newport, Mississippi, and Javiana have increased. Specific control programs might have led to the reduction of serotype Enteritidis infections, which have been associated with the consumption of internally contaminated eggs. Rates of antibiotic resistance among several serotypes have been increasing; a substantial proportion of serotypes Typhimurium and Newport isolates are resistant to multiple drugs (2).
The epidemiology of Salmonella infections is based on serotype characterization; in 2005, the Council of State and Territorial Epidemiologists adopted a position statement for serotype-specific reporting of laboratory-confirmed salmonellosis cases (3). However, reporting through the National Notifiable Diseases Surveillance System (NNDSS) does not include serotype; serotypes for Salmonella isolates are reported through the Public Health Laboratory Information System (PHLIS). The National Electronic Disease Surveillance System (NEDSS) or compatible systems eventually will replace PHLIS; users of NEDSS or compatible systems should report serotype in NEDSS.
Escherichia coli O157:H7 has been nationally notifiable since 1994 (1). National surveillance for all Shiga toxin-producing E. coli (STEC), under the name enterohemorrhagic E. coli (EHEC), began in 2001. As of January 1, 2006, the nationally notifiable diseases case definition designation changed from EHEC to STEC, and serotype-specific reporting was implemented (2). Because diagnosis solely on the basis of detection of Shiga toxin does not sufficiently protect the public's health, characterizing STEC isolates by serotype and pulsed-field gel electrophoresis (PFGE) patterns is critical to detect, investigate, and control outbreaks. Screening of stool specimens by clinical diagnostic laboratories for Shiga toxin by enzyme immunoassay, subsequent bacterial culture using sorbitol MacConkey agar (SMAC), and forwarding enrichment broths from Shiga toxin-positive specimens that do not yield STEC O157 to state or local public health laboratories are important for public health surveillance of STEC infections (3).
Healthy cattle, which harbor the organism as part of the bowel flora, are the main animal reservoir of STEC. The majority of reported outbreaks are caused by contaminated food or water. The substantial decline in cases reported during 2002--2003 coincided with industry and regulatory control activities and with a decrease in the contamination of ground beef (4). However, during 2005--2006, incidence of human STEC infections increased. Reasons for the increases are not known. Three large multistate outbreaks of E. coli O157 infections during fall 2006 caused by contaminated spinach and lettuce suggest that produce that is consumed raw is an important source of STEC infection (5,6).
During 1978--2003, the number of shigellosis cases reported to CDC consistently exceeded 17,000. The approximately 14,000 cases of shigellosis reported to CDC in 2004 represented an all-time low. This number increased to approximately 16,000 in 2005 and decreased slightly in 2006. Shigella sonnei infections continue to account for >75% of shigellosis in the United States (1). Certain cases of shigellosis are acquired during international travel (2,3). In addition to spread from one person to another, shigellae can be transmitted through contaminated foods, sexual contact, and water used for drinking or recreational purposes (1). Resistance to ampicillin and trimethoprim-sulfamethoxazole among S. sonnei strains in the United States remains common (4).
In 1994, the Council of State and Territorial Epidemiologists (CSTE) adopted a position statement making drug-resistant Streptococcus pneumoniae (DRSP) invasive disease a nationally notifiable disease (1). In 2000, in anticipation of the routine introduction of the 7-valent pneumococcal conjugate vaccine (PCV7) (2), CSTE made invasive pneumococcal disease (IPD) among children aged <5 years nationally notifiable (3). Consequently, the National Notifiable Diseases Surveillance System (NNDSS) had two event codes for reporting IPD that were not mutually exclusive: DRSP among persons of all ages and IPD among children aged <5 years.
To avoid submissions of duplicate reports, CSTE modified the case classification of DRSP and IPD in 2006. Under the modified case definition, which became effective in January 2007, cases with isolates causing IPD from children aged <5 years for whom antibacterial susceptibilities are available and determined to be DRSP should be reported only as DRSP, and cases with isolates causing IPD from children aged <5 years who are susceptible or for which susceptibilities are not available should be reported only as IPD in children aged <5 years (4). Only susceptible IPD episodes among children aged <5 years are reported in this Summary. In 2006, for the first time after several years of increasing case counts, the number of cases of pneumococcal disease in both reportable categories declined. The initial increases in reported cases likely represented improvements in surveillance and possibly duplicate reporting of DRSP and IPD cases during the first few years after the adoption of the 2000 position statement. Other data sources have demonstrated substantial declines in the incidence of IPD and DRSP among children and adults after introduction of PCV7 (5,6).
Although PCV7 has been recommended for use in children since 2000, recommendations for use of the 23-valent pneumococcal polysaccharide vaccine for adults aged >65 years and for older children and adults with underlying illnesses were updated in 1997 (7). Cases of susceptible IPD among persons aged >5 years are not nationally notifiable.
States are encouraged to evaluate their own pneumococcal disease surveillance programs (8). CSTE also has recommended that technology for pneumococcal serotyping using polymerase chain reaction (PCR) (9) should be shared with state public health laboratories to improve surveillance for vaccine- and nonvaccine-preventable IPD among children aged <5 years (4). PCR is used by the majority of state public health laboratories to detect a variety of infectious diseases; therefore, this technology should allow most, if not all, state health departments to enhance surveillance for vaccine-preventable IPD. With better data, public health officials will be able to assess the burden of vaccine-preventable IPD and to evaluate current PCV7 immunization programs.
In 2006, primary and secondary (P&S) syphilis cases reported to CDC increased for the sixth consecutive year (1). During 2005--2006, the number of P&S syphilis cases reported to CDC increased 11.8%. Overall increases in rates during 2001--2006 were observed primarily among men (2). However, after decreasing during 2001--2004, the rate of primary and secondary syphilis among women increased, from 0.8 cases per 100,000 population in 2004 to 1.0 cases per 100,000 population in 2006. During 2005--2006, P&S syphilis increased among persons of all races and ethnicities.
In 2005, CDC requested that all state health departments report the sex of partners of persons with syphilis. In 2006, of all P&S syphilis cases reported from the 30 areas (29 states and Washington, D.C.) for which complete data were available, 64% occurred among men who have sex with men (3).
Although the majority of cases of syphilis in the United States occur among men who have sex with men, recent increases in the number of cases reported among women suggest that heterosexually transmitted syphilis might be an emerging problem. In collaboration with partners throughout the United States, CDC updated the Syphilis Elimination Plan for 2005--2010 and is now working to implement it (4). Collaboration with multiple organizations, public health professionals, the private medical community, and other partners is essential for the successful elimination of syphilis in the United States.
In 2006, incidence of reported tetanus and case fatality continued to be low. No neonatal cases were reported. The majority of cases occurred among persons aged 25--59 years and those aged >60 years. Mortality from tetanus was associated with diabetes, intravenous drug use, and advanced age, especially in the setting of unknown vaccination status.
Despite recommendations that travelers to countries in which typhoid fever is endemic should be vaccinated with either of two effective vaccines available in the United States, approximately three fourths of all cases occur among persons who reported international travel during the preceding month and were not immunized. Persons visiting South Asia appear to be at particular risk, even during short visits (1). Salmonella Typhi strains with decreased susceptibility to ciprofloxacin are increasingly frequent in that region and might require treatment with alternative antimicrobial agents (2,3). Although the number of S. Typhi infections is decreasing, the number of illnesses attributed to S. Paratyphi A infection is increasing. In a cross-sectional laboratory-based surveillance study conducted by CDC, 80% of patients with paratyphoid fever acquired their infections in South Asia, and 75% were infected with nalidixic acid-resistant strains. A vaccine for paratyphoid fever is needed (4).
Since implementation of the varicella vaccine program in 1995, varicella morbidity and mortality have declined substantially. During 1995--2006, the number of cases declined 85%, the number of hospitalizations declined 85%, and the number of deaths declined 82% (1). In 2006, the Advisory Committee on Immunization Practices (ACIP) updated recommendations for varicella vaccination to include a second dose for children and catch-up vaccination for persons without evidence of immunity (2). With this new recommendation, case-based and outbreak surveillance for varicella will become increasingly important. In 2006, a total of 33 states and the District of Columbia reported varicella data through the National Notifiable Diseases Surveillance System (NNDSS): 23 (70%) sites reported case-based data and 10 (30%) reported aggregate data. An additional 12 states conducted either statewide or sentinel case-based varicella surveillance but did not report these data through NNDSS. Although varicella was not a notifiable disease in Indiana in 2006, a total of 910 cases were reported.
General
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AIDS
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Botulism
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Brucellosis
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Chancroid
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Chlamydia trachomatis, Genital Infection
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Cholera
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Coccidioidomycosis
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Cryptosporidiosis
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CDC. Diagnostic procedures for stool specimens. Atlanta, GA: US Department of Health and Human Services, CDC; 2007. Available at http://www.dpd.cdc.gov/dpdx/HTML/DiagnosticProcedures.htm.
Cyclosporiasis
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. Available at http://newton.nap.edu/catalog/11745.html#toc.
Herwaldt BL. Cyclospora cayetanensis: a review, focusing on the outbreaks of cyclosporiasis in the 1990s. Clin Infect Dis 2000;31:1040--57.
Diphtheria
Dewinter LM, Bernard KA, Romney MG. Human clinical isolates of Corynebacterium diphtheriae and Corynebacterium ulcerans collected in Canada from 1999 to 2003 but not fitting reporting criteria for cases of diphtheria. Clin Microbiol 2005;43:3447--9.
Domestic Arboviral Diseases, Neuroinvasive and Nonneuroinvasive
CDC. West Nile virus activity---United States, January 1--December 1, 2005. MMWR 2005;54:1253--6.
Hayes EB, Komar N, Nasci RS, et al. Epidemiology and transmission dynamics of West Nile virus disease. Emerg Infect Dis 2005;11:1167--73.
Ehrlichiosis (Human Granulocytic and Human Monocytic)
Dumler JS, Madigan JE, Pusterla N, and Bakken JS. Ehrlichioses in humans: epidemiology, clinical presentation, diagnosis, and treatment. Clin Iinfect Dis 2007;45:45--51.
Demma LJ, Holman RC, McQuiston JH, Krebs JW, Swerdlow DL. Epidemiology of human ehrlichiosis and anaplasmosis in the United States, 2001--2002. Am J Trop Med Hyg 2005;73:400--09.
Paddock CD, Childs JE. Ehrlichia chaffeensis: a prototypical emerging pathogen [Review]. J Clin Microbiol 2003;16:37--64.
Giardiasis
Stuart JM, Orr HJ, Warburton FG, et al. Risk factors for sporadic giardiasis: a case-control study in southwestern England. Emerg Infect Dis 2003;9:229--33.
CDC. Diagnostic procedures for stool specimens. Atlanta, GA: US Department of Health and Human Services, CDC; 2007. Available at http://www.dpd.cdc.gov/dpdx/HTML/DiagnosticProcedures.htm.
Gonorrhea
CDC. Sexually transmitted diseases treatment guidelines, 2006. MMWR 2006;55(No. RR-11).
CDC. Sexually transmitted diseases surveillance 2006 supplement: Gonococcal Isolate Surveillance Project (GISP) annual report 2006. Atlanta, GA: US Department of Health and Human Services, CDC. In press.
Haemophilus influenzae, Invasive Disease
Fry AM, Lurie P, Gidley M, Schmink S, Lingappa J, Rosenstein NE. Haemophilus influenzae type b (Hib) disease among Amish children in Pennsylvania: reasons for persistent disease. Pediatrics 2001;108:1--6.
Dworkin MS, Park L, Borchardt SM. The changing epidemiology of invasive Haemophilus influenzae disease, especially in persons >65 years old. Clin Infect Dis 2007;44:810--6.
McVernon J, Trotter CL, Slack MPE, et al. Trends in type b infections in adults in England and Wales: surveillance study. BMJ 2004;329:655--8.
Flannery B, Heffernan RT, Harrison LH, et al. Changes in invasive pneumococcal disease among HIV-infected adults living in the era of childhood pneumococcal immunization. Ann Intern Med 2006;144:1--9.
Hansen Disease (Leprosy)
Britton WJ, Lockwood NJ. Leprosy. Lancet 2004;363:1209--19.
Hartzell JD, Zapor M, Peng S, Straight T. Leprosy: a case series and review. South Med J 2004;97:1252--6.
Hastings R, ed. Leprosy. 2nd ed. New York, NY: Churchill Livingstone; 1994.
Joyce MP, Scollard DM. Leprosy (Hansen's disease). In: Rakel RE, Bope ET, eds. Conn's current therapy 2004: latest approved methods of treatment for the practicing physician. 56th ed. Philadelphia, PA: Saunders; 2004:100--5.
Ooi WW, Moschella SL. Update on leprosy in immigrants in the United States: status in the year 2000. Clin Infect Dis 2001;32:930--7.
Bruce S, Schroeder TL, Ellner K, Rubin H, Williams T, Wolf JE Jr. Armadillo exposure and Hansen's disease: an epidemiologic survey in southern Texas. J Am Acad Dermatol 2000;43(2 Pt1):223--8.
Hantavirus Pulmonary Syndrome
CDC. Hantavirus pulmonary syndrome---five states, 2006. MMWR 2006;55:627--9.
Hemolytic Uremic Syndrome, Postdiarrheal
Banatvala N, Griffin PM, Greene KED, et al. The United States Prospective Hemolytic Uremic Syndrome Study; microbiologic, serologic, clinical, and epidemiologic findings. J Infect Dis 2001;183:1063--70.
Mahon BE, Griffin PM, Mead PS, Tauxe RV. Hemolytic uremic syndrome surveillance to monitor trends in infection with Escherichia coli O157:H7 and other Shiga toxin-producing E. coli [Letter]. Emerg Infect Dis 1997;3:409--12.
Hepatitis A
Armstrong GL, Bell BP. Hepatitis A virus infections in the United States: model-based estimates and implications for childhood immunization. Pediatrics 2002;109:839--45.
Bell BP, Kruszon-Moran D, Shapiro CN, Lambert SB, McQuillan GM, Margolis HS. Hepatitis A virus infection in the United States: serologic results from the Third National Health and Nutrition Examination Survey. Vaccine 2005;23:5798--806.
Wasley A, Samandari T, Bell BP. Incidence of hepatitis A in the United States in the era of vaccination. JAMA 2005;294:194--201.
Wasley A, Fiore A, Bell BP. Hepatitis A in the era of vaccination. Epidemiol Rev 2006;28:101--11.
Hepatitis B
Armstrong GL, Mast EE, Wojczynski M, Margolis HS. Childhood hepatitis B virus infections in the United States before hepatitis B immunization. Pediatrics 2001;108:1123--8.
Shepard CW, Simard EP, Finelli L, Fiore A, Bell BP. Hepatitis B virus infection: epidemiology and vaccination. Epidemiol Rev 2006;28:112--25.
Goldstein ST, Alter MJ, Williams IT, et al. Incidence and risk factors for acute hepatitis B in the United States, 1982--1998: implications for vaccination programs. J Infect Dis 2002;185:713--9.
McQuillan GM, Coleman PJ, Kruszon-Moran D, Moyer LA, Lambert SB, Margolis HS. Prevalence of hepatitis B virus infection in the United States: The National Health and Nutrition Examination Surveys, 1976 through 1994. Am J Public Health 1999;89:14--8.
Hepatitis C
Armstrong GL, Wasley A, Simard EP, McQuillan GM, Kuhnert WL, Alter MJ. The prevalence of hepatitis C virus infection in the United States, 1999 through 2002. Ann Intern Med 2006;144:705--14.
Armstrong GA, Alter MJ, McQuillan GM, Margolis HS. The past incidence of hepatitis C virus infection: implications for the future burden of chronic liver disease in the United States. Hepatology 2000;31:777--82.
Shepard CW, Finelli L, Alter MJ. The global epidemiology of hepatitis C. Lancet Infect Dis 2005;5:558--67.
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.
Council of State and Territorial Epidemiologists. Influenza-associated pediatric mortality 2004. Position statement 04-ID-04. Available at http://www.cste.org/position%20statements/searchbyyear2004.asp.
Guarner J, Paddock CD, Shieh WJ, et al. Histopathologic and immunohistochemical features of fatal influenza virus infection in children during the 2003--2004 season. Clin Infect Dis 2006:43;132--40.
Legionellosis
Cowgill KD, Lucas CE, Benson RF, et al. Recurrence of legionnaires disease at a hotel in the United States Virgin Islands over a 20-year period. Clin Infect Dis 2005;40:1205--7.
Fields BS, Benson RF, Besser RE. Legionella and kegionnaires' disease: 25 years of investigation. Clin Microbiol Rev 2002;15:506--26.
European Working Group on Legionella Infections. European guidelines for control and prevention of travel associated legionnaires' disease. London, UK: United Kingdom Health Protection Agency; 2005.
Joseph CA. Legionnaires' disease in Europe 2000--2002. Epidemiol Infect 2004;132:417--24.
Marston BJ, Lipman HB, Breiman RF. Surveillance for legionnaires' disease: risk factors for morbidity and mortality. Arch Intern Med 1994;154:2417--22.
Listeriosis
Gottlieb SL, Newbern EC, Griffin PM, et al. Multistate outbreak of listeriosis linked to turkey deli meat and subsequent changes in US regulatory policy. Clin Infect Dis 2006;42:29--36.
Mead PS, Dunne EF, Graves L, et al. Nationwide outbreak of listeriosis due to contaminated meat. Epidemiol Infect 2006;134:744--51.
Mead PS, Slutsker L, Dietz V, et al. Food-related illness and death in the United States. Emerg Infect Dis 1998;5:607--25.
Slutsker L, Schuchat A. Listeriosis in humans. In: Ryser ET Marth EH, eds. Listeria, listeriosis, and food safety. 2nd ed. New York, NY: Marcel Dekker, Inc.; Little, Brown and Company; 1999:75--95.
Tappero J, Schuchat A, Deaver K, Mascola L, Wenger J, for the Listeriosis Study Group. Reduction in the incidence of human listeriosis in the United States: effectiveness of prevention efforts. JAMA 1995;273:1118--22.
Lyme Disease
Stafford KC III. Tick management handbook: an integrated guide for homeowners, pest control operators, and public health officials for the prevention of tick-associated disease. New Haven, CT: Connecticut Agricultural Experiment Station; 2004. Available at http://www.cdc.gov/ncidod/dvbid/lyme/resources/handbook.pdf.
Hayes EB, Piesman J. How can we prevent Lyme disease? N Engl J Med 2003;348:2424--30.
Aguero-Rosenfeld ME, Wang G, Schwartz I, Wormser GP. Diagnosis of Lyme borreliosis. Clin Microbiol Rev 2005;18:484--509.
Medical Letter. Treatment of Lyme disease. Med Lett Drugs Ther 2005;47:41--3.
CDC. Caution regarding testing for Lyme disease. MMWR 2005;54:125.
Malaria
Baird JK. Effectiveness of antimalarial drugs. N Engl J Med 2005;352:1565--77.
Chen LH, Keystone JS. New strategies for the prevention of malaria in travelers. Infect Dis Clin N Amer 2005;19:185--210.
Guinovart C, Navia MM, Tanner M, et al. Malaria: burden of disease. Curr Mol Med 2006;6:137--40.
Leder K, Black J, O'Brien D, et al. Malaria in travelers: a review of the GeoSentinel Surveillance Network. Clin Infect Dis 2004;39:1104--12.
Measles
Papania M, Hinman A, Katz S, Orenstein W, McCauley M, eds. Progress toward measles elimination---absence of measles as an endemic disease in the United States. J Infect Dis 2004;189(Suppl 1):S1--257.
Rota PA, Liffick SL, Rota JS, et al. Molecular epidemiology of measles viruses in the United States, 1997--2001. Emerg Infect Dis 2002;8:902--8.
De Serres G, Gay NJ, Farrington CP. Epidemiology of transmissible diseases after elimination. Am J Epidemiol 2000;151:1039--48.
Meningococcal Disease
Rosenstein NE, Perkins BA, Stephens DS, et al. Meningococcal disease. N Engl J Med 2001;344:1378--88.
Rosenstein NE, Perkins BA, Stephens DS, et al. The changing epidemiology of meningococcal disease in the United States, 1992--1996. J Infect Dis 1999;180:1894--901.
Mumps
CDC. Mumps epidemic---Iowa, 2006. MMWR 2006;55:366--8.
CDC. Update: mumps activity---United States, January 1--October 7, 2006. MMWR 2006;55:1152--3.
Harling R, White JM, Ramsay ME, et al. The effectiveness of the mumps component of the MMR vaccine: a case control study. Vaccine 2005;23:4070--4.
Schaffzin JK, Pollock L, Schulte C, et al. Effectiveness of previous mumps vaccination during a summer camp outbreak. Pediatrics 2007;120:e862--8.
Pertussis
Bisgard KM, Rhodes P, Connelly BL, et al. Pertussis vaccine effectiveness among children 6 to 59 months of age in the United States, 1998--2001. Pediatrics 2005;116:e285--94.
Bisgard KM, Pascual FB, Ehresmann KR, et al. Infant pertussis: who was the source? Pediatr Infect Dis J 2004;23:985--9.
CDC. Pertussis---United States, 2001--2003. MMWR 2005;54:1283--6.
Lee GM, Lebaron C, Murphy TV, Lett S, Schauer S, Lieu TA. Pertussis in adolescents and adults: should we vaccinate? Pediatrics 2005;115:1675--84.
Plague
CDC. Imported plague---New York City, 2002. MMWR 2003;53:725--8.
Enscore RE, Biggerstaff BJ, Brown TL, et al. Modeling relationships between climate and the frequency of human plague cases in the southwestern United States, 1960--1997. Am J Trop Med Hyg 2002;66:186--96.
Inglesby TV, Dennis DT, Henderson DA, et al. Plague as a biological weapon: medical and public health management. Working Group on Civilian Biodefense [Review]. JAMA 2000;283:2281--90.
Dennis DT, Gage KL, Gratz N, Poland JD, Tikhomirov E. Plague manual: epidemiology, distribution, surveillance and control. Geneva, Switzerland: World Health Organization; 1999.
Poliomyelitis
Alexander LN, Seward JF, Santibanez TA, et al. Vaccine policy changes and epidemiology of polio in the United States. JAMA 2004;292:1696--702.
Q Fever
McQuiston JH, Holman RC, McCall CL, Childs JE, Swerdlow DL, Thompson HA. National surveillance and the epidemiology of Q fever in the United States, 1978--2004. Am J Trop Med Hyg 2006;75:36--40.
Mcquiston JH, Nargund VN, Miller JD, Priestly R, Shaw EI, Thompson HA. Prevalence of antibodies to Coxiella burnetii among veterinary school dairy herds in the United States, 2003. Vector Borne Zoonotic Dis 2005;5:90--1.
Raoult D, Tissot-Dupont H, Foucault C, et al. Q fever 1985--1998. Clinical and epidemiologic features of 1,383 infections [Review]. Medicine 2000;79:109--25.
Bernard KW, Parham GL, Winkler WG, Helmick CG. Q fever control measures: recommendations for research facilities using sheep. Infect Control 1982;3:461--5.
Rabies, Animal and Human
Blanton JD, Hanlon CA, Ruprrecht CE. Rabies surveillance in the United States during 2006. J Am Vet Med Assoc 2007;231:540--56.
Rocky Mountain spotted fever
Chapman AS, Murphy SM, Demma LJ, et al. Rocky Mountain spotted fever in the United States, 1997--2002. Vector Borne Zoonotic Dis 2006;6:170--8.
Demma LJ, Traeger MS, Nicholson WL, et al. Rocky Mountain spotted fever from an unexpected tick reservoir in Arizona. N Engl J Med 2005;353:587--94.
Thorner AR, Walker DH, Petri WA. Rocky Mountain spotted fever [Review]. Clin Infect Dis 1998;27:1353--60.
Rubella
Reef S, Cochi S, eds. The evidence for the elimination of rubella and congenital rubella syndrome in the United States: a public health achievement. Clin Infect Dis 2006;43(Suppl 3):S123--68.
Salmonellosis
Braden CR. Salmonella enterica serotype Enteritidis and eggs: a national epidemic in the United States. Clin Infect Dis 2006;43:512--7.
Olsen SJ, Bishop R, Brenner FW, et al. The changing epidemiology of Salmonella: trends in serotypes isolated from humans in the United States, 1987--1997. J Infect Dis 2001;183:756--61.
Voetsch AC, Van Gilder TJ, Angulo FJ, et al. FoodNet estimate of burden of illness caused by nontyphoidal Salmonella infections in the United States. Clin Infect Dis 2004;38(Suppl 3):S127--34.
Shiga Toxin-Producing Enterohemorrhagic Escherichia coli
Bender JB, Hedberg CW, Besser JM, et al. Surveillance for Escherichia coli O157:H7 infections in Minnesota by molecular subtyping. N Engl J Med 1997;337:388--94.
Brooks JT, Sowers EG, Wells JB, et al. Non-O157 Shiga toxin-producing Escherichia coli infections in the United States, 1983--2002. J Infect Dis 2005;192:1422--9.
Crump JA, Sulka AC, Langer AJ, et al. An outbreak of Escherichia coli O157:H7 among visitors to a dairy farm. N Engl J Med 2002;347:555--60.
Griffin PM, Mead PS, Sivapalasingam S. Escherichia coli O157:H7 and other enterohemorrhagic E. coli. In: Blaser MJ, Smith PD, Ravdin JI, Greenberg HB, Guerrant RL, eds. Infections of the gastrointestinal tract. Philadelphia, PA: Lippincott Williams & Wilkins; 2002:627--42.
Mead PS, Griffin PM. Escherichia coli O157:H7. Lancet 1998;352:1207--12.
Shigellosis
Shane A, Crump J, Tucker N, Painter J, Mintz E. Sharing Shigella: risk factors and costs of a multi-community outbreak of shigellosis. Arch Pediatr Adolesc Med 2003;157:601--3.
Gupta A, Polyak CS, Bishop RD, Sobel J, Mintz ED. Laboratory-confirmed shigellosis in the United States, 1989--2002: epidemiologic trends and patterns. Clin Infect Dis 2004;38:1372--7.
Sivapalasingam S, Nelson JM, Joyce K, Hoekstra M, Angulo FJ, Mintz ED. A high prevalence of antimicrobial resistance among Shigella isolates in the United States, 1999--2002. Antimicrob Agents Chemother 2006;50:49--54.
Streptococcal Disease, Invasive, Group A
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.
CDC. Active Bacterial Core Surveillance report. Emerging Infections Program Network. Group A Streptococcus, 2005. Atlanta, GA: US Department of Health and Human Services, CDC; 2007. Available at http://www.cdc.gov/ncidod/dbmd/abcs/survreports/gas05.pdf.
Jordan HT, Richards CL, Burton DC, Thigpen MC, Van Beneden CA. Group A streptococcal disease in long-term care facilities: descriptive epidemiology and potential control measures. Clin Infect Dis 2007;45:742--52.
CDC. Investigating clusters of group A streptococcal disease. Atlanta, GA: US Department of Health and Human Services, CDC; 2005. Available at http://www.cdc.gov/strepAcalculator.
The Prevention of Invasive Group A Streptococcal Infections Workshop participants. Prevention of invasive group A streptococcal disease among household contacts of case patients and among postpartum and postsurgical patients: recommendations from the Centers for Disease Control and Prevention. Clin Infect Dis 2002;35:950--9.
Streptococcal Toxic-Shock Syndrome
Bisno AL. Brito MO. Collins CM. Molecular basis of group A streptococcal virulence. Lancet Infect Dis 2003;3: 191--200.
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.
Stevens DL. Streptococcal toxic shock syndrome associated with necrotizing fasciitis. Annu Rev Med 2000;51: 271--88.
The Prevention of Invasive Group A Streptococcal Infections Workshop participants. Prevention of invasive group A streptococcal disease among household contacts of case patients and among postpartum and postsurgical patients: recommendations from the Centers for Disease Control and Prevention. Clin Infect Dis 2002;35:950--9.
Streptococcus pneumoniae, Invasive, Drug-Resistant
Clinical and Laboratory Standards Institute. Performance standards for antimicrobial susceptibility testing: 15th informational supplement [No. M100-S15]. Wayne, PA: National Committee for Clinical Laboratory Standards; 2005.
Flannery B, Schrag S, Bennett NM, et al. Impact of childhood vaccination on racial disparities in invasive Streptococcus pneumoniae infections. JAMA 2004;291:2197--203.
Kyaw MH, Lynfield R, Schaffner W, et al. Effect of introduction of the pneumococcal conjugate vaccine on drug-resistant Streptococcus pneumoniae. N Engl J Med 2006;354:1455--63.
Poehling KA, Talbot TR, Griffin MR, et al. Invasive pneumococcal disease among infants before and after introduction of pneumococcal conjugate vaccine. JAMA 2006;295:1668--74.
Ray GT, Whitney CG, Fireman BH, Ciuryla V, Black SB. Cost-effectiveness of pneumococcal conjugate vaccine: evidence from the first 5 years of use in the United States incorporating herd effects. Pediatr Infect Dis J 2006;25:494--501.
Syphilis, Congenital
CDC. Congenital syphilis---United States, 2002. MMWR 2004;53:716--9.
Syphilis, Primary and Secondary
CDC. The national plan to eliminate syphilis from the United States. Atlanta, GA: US Department of Health and Human Services, CDC; 1999.
CDC. The national plan to eliminate syphilis from the United States. Atlanta, GA: US Department of Health and Human Services, CDC; 2006.
CDC Sexually transmitted disease surveillance supplement 2006; syphilis surveillance report. Atlanta, GA: US Department of Health and Human Services, CDC. In press.
Tetanus
CDC. Tetanus---Puerto Rico, 2002. MMWR 2002;51:613--5.
McQuillan GM, Kruszon-Moran D, Deforest A, Chu SY, Wharton M. Serologic immunity to diphtheria and tetanus in the United States. Ann Intern Med 2002;136:660--6.
McQuillan GM, Kruszon-Moran D, Deforest A, Chu SY, Wharton M. Serologic immunity to diphtheria and tetanus in the United States. Ann Intern Med 2002;136:660--6.
Trichinellosis
CDC. Trichinellosis associated with bear meat---New York and Tennessee, 2003. MMWR 2004;53:606--10.
Moorhead A, Grunenwald PE, Dietz VJ, Schantz PM. Trichinellosis in the United States, 1991--1996: declining but not gone. Am J Trop Med Hyg 1999;60:66--9.
Tuberculosis
CDC. Reported tuberculosis in the United States, 2003. Atlanta, GA: US Department of Health and Human Services, CDC; 2004. Available at http://www.cdc.gov/tb/default.htm.
CDC. Trends in tuberculosis---United States, 2004. MMWR 2005;54:245--9.
Saraiya M, Cookson ST, Tribble P, et al. Tuberculosis screening among foreign-born persons applying for permanent US residence. Am J Public Health 2002;92:826--9.
Talbot EA, Moore M, McCray E, Binkin NJ. Tuberculosis among foreign-born persons in the United States, 1993--1998. JAMA 2000;284:2894--900.
Tularemia
CDC. Outbreak of tularemia among commercially distributed prairie dogs, 2002. MMWR 2002;51:688, 699.
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.
Feldman KA, Enscore RE, Lathrop SL, et al. Outbreak of primary pneumonic tularemia on Martha's Vineyard. N Engl J Med 2001;345:1219--26.
Petersen JM, Schriefer ME. Tularemia: emergence/ re-emergence. Vet Res 2005;36:455--67.
Typhoid Fever
Crump J, Barrett TJ, Nelson JT, Angulo FJ. Reevaluating fluoroquinolone breakpoints for Salmonella enterica serotype Typhi and for non-Typhi Salmonellae. Clin Infect Dis 2003;37:75--81.
Kubota K, Barrett TJ, Hunter S et al. Analysis of Salmonella serotype Typhi pulsed-field gel electrophoresis patterns associated with international travel. J Clin Micro 2005;43:1205--9.
Olsen SJ, Bleasdale SC, Magnano AR, et al. Outbreaks of typhoid fever in the United States, 1960--1999. Epidemiol Infect 2003;130:13--21.
Reller M, Olsen S, Kressel A. Sexual transmission of typhoid fever: a multi-state outbreak among men who have sex with men. Clin Infect Dis 2003;37:141--4.
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
Seward JF, Zhang JX, Maupin TJ, Mascola L, Jumaan AO. Contagiousness of varicella in vaccinated cases: a household contact study. JAMA 2004;292:704-8.
CDC. Public health response to varicella outbreaks---United States, 2003--2004. MMWR 2006;55:993--5.
CDC. Varicella surveillance practices, United States, 2004. MMWR 2006;55:1126--9.
Vancomycin-Intermediate Staphylococcus aureus Infection (VISA)/Vancomycin-Resistant Staphylococcus aureus Infection (VRSA)
Fridkin SK, Hageman J, McDougal LK, et al. Vancomycin-Intermediate Staphylococcus aureus Epidemiology Study Group. Epidemiological and microbiological characterization of infections caused by Staphylococcus aureus with reduced susceptibility to vancomycin, United States, 1997--2001. Clin Infect Dis 2003;36:429--39.
Chang S, Sievert DM, Hageman JC, et al. Vancomycin-Resistant Staphylococcus aureus Investigative Team. Infection with vancomycin-resistant Staphylococcus aureus containing the vanA resistance gene. N Engl J Med 2003;348:1342--7.
Whitener CJ, Park SY, Browne FA, et al. Vancomycin-resistant Staphylococcus aureus in the absence of vancomycin exposure. Clin Infect Dis 2004;38:1049--55.
Weigel LM, Clewell DB, Gill SR, et al. Genetic analysis of a high-level vancomycin-resistant isolate of Staphylococcus aureus. Science 2003;302:1569--71.
McDonald LC, Hageman JC. Vancomycin intermediate and resistant Staphylococcus aureus: what the nephrologist needs to know. Nephrol News Issues 2004;8:63--4, 66--7, 71--2.
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