Streptococcus pneumoniae is the leading bacterial cause of community-acquired pneumonia hospitalizations and an important cause of bacteremia and meningitis, especially among young children and older adults (1,2). A 7-valent pneumococcal conjugate vaccine (PCV7) was licensed and the Advisory Committee on Immunization Practices formulated recommendations for its use in infants and children in February 2000 (2). Vaccination coverage rapidly increased during the second half of 2000, in part through funding by CDC's Vaccines for Children program. Subsequently, active population-and laboratory-based surveillance demonstrated substantial reductions in invasive pneumococcal disease (IPD) among children and adults (3). In addition, decreases in hospitalizations and ambulatory-care visits for all-cause pneumonia also were reported (4,5). To gauge whether the effects of PCV7 on reducing pneumonia continue, CDC is monitoring pneumonia hospitalizations by using data from the Nationwide Inpatient Sample. This report provides an update for 2005 and 2006, the most recent years for which information is available. In 2005 and 2006, the incidence rates for all-cause pneumonia hospitalizations among children aged <2 years were 9.1 per 1,000 and 8.1 per 1,000, respectively. In 2006, the rate for all-cause pneumonia among children aged <2 years was approximately 35% lower than during 1997-1999. Most of this decrease occurred soon after the vaccine was licensed in 2000, and the rates have remained relatively stable since then. The rate for all-cause pneumonia among children aged 2-4 years did not change after PCV7 licensure and has remained stable. Continued monitoring of pneumonia-related hospitalizations among children is needed to track the effects of pneumococcal immunization programs. The Nationwide Inpatient Sample contains data on inpatient stays from states that participate in the Healthcare Cost and Utilization Project, sponsored by the Agency for Healthcare Research and Quality. The project is a stratified probability sample of U.S. acute-care hospitals and the largest all-payer inpatient-care database available in the United States. In 2006, this database recorded information from approximately 8 million hospitalizations (approximately 20% of all U.S. hospitalizations) from 1,045 hospitals in 38 states. Data are weighted to generate national estimates while accounting for complex sampling design (6). For this analysis, all-cause pneumonia hospitalization was defined as a record in which International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) codes 480-486 (pneumonia) or 487.0 (influenza with pneumonia) were assigned as the primary diagnosis. Trends in hospitalizations for nonpneumonia acute respiratory illness (ARI) also were evaluated to assess the possibility that, after PCV7 introduction, practitioners were less likely to assign a pneumonia code for respiratory conditions in a vaccinated child and more likely to make other respiratory diagnoses. A nonpneumonia ARI hospitalization was defined as a record with any of the following ICD-9-CM codes assigned as the primary diagnosis: 381-383 (otitis media and mastoiditis), 460-466 (acute respiratory infections, including acute bronchitis, bronchiolitis, acute nasopharyngitis, sinusitis, pharyngitis, tonsillitis, laryngitis, tracheitis, and other acute upper respiratory infections), 487 (influenza, excluding 487.0), 490 (bronchitis), 491 (chronic bronchitis), or 493 (asthma).#
However, the updated analysis of national hospital discharge data suggests that reductions in all-cause pneumonia hospitalizations among U.S. children aged <2 years after routine PCV7 use have been sustained and that the benefits of PCV7 might extend beyond the documented changes in IPD (3) to hospitalizations for pneumonia. Moreover, rates of nonpneumonia ARI also declined after introduction of PCV7, indicating that the decreases in pneumonia hospitalizations likely were not the result of a shift in coding of respiratory hospitalizations to nonpneumonia ARI codes. In addition, the analysis suggests that the declines were unlikely to result from a reduction in total hospitalization rates. The transient increase in all-cause pneumonia rates from 2004 to 2005 might reflect increased circulation of respiratory viruses or other seasonal variation.
Although many nonpneumonia ARI diagnoses traditionally have not been considered manifestations of S. pneumoniae infection, recent data indicate that the pneumococcus might contribute to a wider range of childhood respiratory illness than previously thought. A randomized clinical trial performed in child care centers in Israel suggested that immunization with a 9-valent pneumococcal conjugate vaccine reduced reported episodes of upper respiratory infections, lower respiratory infections, and otitis media by 15%, 16%, and 17%, respectively (7). Furthermore, in a trial of 9-valent pneumococcal conjugate vaccine among South African children, vaccinated children had 45% fewer influenza A-associated pneumonia episodes than unvaccinated children, suggesting that S. pneumoniae might be a copathogen in illnesses diagnosed as influenza (8).
Although rates of IPD have decreased substantially among children aged 2-4 years after PCV7 introduction (3), a reduction in all-cause pneumonia hospitalizations was not observed in this age group. The reasons for this are unknown but might be associated with lower overall rates of pneumococcal infection in this age group. In addition, other etiologic agents are becoming more common causes of pneumonia in children aged >2 years (1). The findings in this report are subject to at least three limitations. First, identification of hospitalizations for pneumonia and nonpneumonia ARI was based on ICD-9-CM codes and might be subject to misclassification, despite internal quality control and validation for consistency within the Nationwide Inpatient Sample. Second, establishing the etiology of pneumonia is difficult. Nationwide Inpatient Sample data are deidentified before public release and chart reviews cannot be performed to confirm recorded diagnoses. Because most pneumococcal pneumonias are classified as pneumonias without further characterization, this report provides an estimate of the effect of PCV7 on all-cause pneumonia without regard to pneumococcal serotypes. Furthermore, serotyping is not part of routine diagnostic work-ups, and this information would not be recorded in medical charts. However, the decrease in nonpneumonia ARI hospitalizations among children aged <2 years suggests that the decreases in pneumonia hospitalizations were unlikely to result from a shift in coding of pneumonia to nonpneumonia ARI codes. Finally, factors other than shifts in coding could affect hospitalization rates. Reduced clinician concerns for severe pneumococcal disease among immunized children, for example, might lead to outpatient treatment rather than hospitalization. However, other data indicate that ambulatory-care visits for pneumonia among children aged <2 years also have decreased since introduction of PCV7 (5). In addition, the proportion of all hospitalizations that were attributable to pneumonia or nonpneumonia ARI decreased significantly, suggesting that the declines were unlikely to result from a secular reduction in overall hospitalization rate.
Despite the substantial morbidity associated with childhood pneumonia, no pneumonia-specific prospective populationbased surveillance system exists for monitoring trends in the incidence of pneumonia hospitalizations or pneumonia-related ambulatory-care visits in the United States. Monitoring childhood pneumonia is important for the evaluation of effects of current and future pneumococcal immunization programs. Increases in pneumococcal disease caused by serotypes not included in PCV7 could result in some increase in pneumonia, even though observed increases in non-PCV7 serotype IPD have been modest thus far (9). In addition, extended-valency pneumococcal conjugate vaccines are expected to be licensed by late 2009 to early 2010 and might further reduce pneumonia rates. Finally, vaccination of children against influenza, as recommended by the Advisory Committee on Immunization Practices, is increasing and also might reduce pneumonia hospitalization rates (10).  (2). Although only 1%-4% of those infected with LACV develop any symptoms, children aged <16 years are at highest risk for severe neurologic disease and possible long-term sequelae (2,3). The effects of LACV infection during pregnancy and the potential for intrauterine transmission and adverse birth or developmental outcomes are unknown. This report describes the first known case of LACV infection in a pregnant woman, with evidence of possible congenital infection with LACV in her infant, based on the presence of immunoglobulin M (IgM) antibodies in umbilical cord serum at delivery. The infant was born healthy with normal neurologic and cognitive functions and no LACV symptoms. Further investigation is needed to confirm the potential for intrauterine LACV transmission and to identify immediate and long-term health risks posed to infants. Because of the potential for congenital infection, pregnant women in areas where LACV is endemic should be advised to avoid mosquitoes; health-care providers should monitor for LACV infection and sequelae among infants born to women infected with LACV during pregnancy.
In August 2006, a previously healthy woman aged 43 years in week 21 of her pregnancy was admitted to a West Virginia hospital after experiencing severe headaches, photophobia, stiff neck, fever, weakness, confusion, and a red papular rash. The patient had reported a 3-month history of severe headaches, which were diagnosed initially as migraines and treated with morphine for pain. Two previous pregnancies had proceeded without complication, and each resulted in delivery of a healthy infant. The patient's medical history included anxiety, depression, and hypothyroidism, for which she received ongoing thyroid hormone replacement therapy.
After hospital admission, analysis of cerebrospinal fluid revealed an elevated white blood cell count (556 cells/mm 3 ), elevated protein (66 mg/dL), and normal glucose (55 mg/dL). A diagnostic panel for viral encephalitis was performed, and the patient's serum was determined positive for the presence of LACVspecific IgM and immunoglobulin G (IgG) antibodies by immunofluorescence assay and for IgM by capture enzyme-linked immunosorbent assay (ELISA) (Table ). The patient's serum was negative for IgM and IgG antibodies to the other three diseases in the diagnostic panel: eastern equine encephalitis, western equine encephalitis, and St. Louis encephalitis. A diagnosis of La Crosse encephalitis was made, and supportive therapy was initiated. During hospitalization, the patient experienced a low-grade fever and exhibited panleukocytosis (absolute neutrophil count: 12,800/L), which persisted after discharge despite resolution of clinical signs.
After reporting the case to the West Virginia Department of Health and Human Resources, active follow-up of the patient and her fetus was initiated in collaboration with the patient's primary-care providers and CDC. With her consent, the patient's medical and prenatal histories were reviewed. Because guidelines for evaluating pregnant women infected with LACV do not exist, interim guidelines for West Nile virus were used to direct maternal and infant follow-up (4). Specifically, collection of blood and tissue products at time of delivery was arranged with the patient's obstetrician. Umbilical cord serum and maternal serum were tested for LACV-specific antibodies by ELISA and serum-dilution plaque-reduction neutralization test (PRNT). Sera also were tested for neutralizing antibodies to the closely related Jamestown Canyon virus by PRNT to rule out potential cross-reactivity. Umbilical cord and placental tissue were tested for LACV RNA by reverse transcriptionpolymerase chain reaction (RT-PCR). Data were collected regarding the infant's health at delivery and through routine well-child visits during the first 6 months of life.
The patient had a normal, spontaneous, vaginal delivery of a healthy girl at approximately 40 weeks gestation. The child MMWR January 16, 2009 had normal birth weight (2,970 g), length (52 cm), and head circumference (33 cm). Apgar scores at 1 minute and 5 minutes postpartum were within normal limits (8 and 9, respectively). LACV-specific IgM antibodies were detected in umbilical cord serum, although no evidence of LACV RNA was detected in umbilical cord tissue or placental tissue by RT-PCR (Table ).
The mother declined collection of additional specimens of infant serum for confirmation of congenital LACV infection. Maternal serum collected at 11 weeks postpartum was positive for LACV IgG antibodies but negative for IgM. Except for intermittent nasal congestion associated with upper respiratory infections, the infant remained healthy and exhibited appropriate growth and development through the first 6 months of life. No neurologic abnormalities or decreased cognitive functions were observed. Editorial Note: This report summarizes the first case of symptomatic LACV infection identified during pregnancy. Congenital LACV infection of the fetus was suggested through identification of IgM antibodies in umbilical cord serum, although the newborn was asymptomatic and development was normal. Although unlikely to cross the placental barrier, LACV IgM antibodies detected in cord serum might have been attributable to transplacental leakage induced by uterine contractions that disrupt placental barriers during labor, which has been documented for anti-Toxoplasma IgM antibodies (5). Because specificity of standard laboratory techniques used to detect LACV IgM antibodies in cord serum or newborn serum is unknown, a follow-up evaluation of infant serum is necessary to confirm congenital infection. However, in this case, the mother declined collection of any additional specimens from her infant.
Certain infectious diseases have more severe clinical presentations in pregnant women (6). Symptomatic LACV infection is rare among adults; therefore, effects of pregnancy on the risk for or severity of illness are unknown. Because LACV-specific IgM can be present for as long as 9 months after infection (1), LACV might not have been responsible for the symptoms reported during this woman's pregnancy. However, the woman resided in an area where LACV is known to be endemic; during 2006, 16 (24%) of 67 LACV cases in the United States reported to CDC occurred in West Virginia, including three other cases from the same county as this patient.  Although antimicrobial treatment of pregnant women often is controversial because of limited information regarding efficacy and risk to the developing infant (7), certain in vitro evidence indicates that the antiviral agent ribavirin might be useful for treating LACV infection in nonpregnant patients (2). However, supportive treatment continues as the standard of care for managing all LACV patients (2).
Congenital infection with other arboviral diseases has been reviewed and documented previously (8). Although no human congenital infection with a bunyavirus of the California serogroup has been reported, congenital infection with other bunyaviruses of the Bunyamwera serogroup has been associated with macrocephaly. In addition, animal studies have determined that infection with LACV during pregnancy can cause teratogenic effects in domestic rabbits, Mongolian gerbils, and sheep (9,10).
Pregnant women in areas where LACV is endemic should take precautions to reduce risk for infection by avoiding mosquitoes, wearing protective clothing, and applying a mosquito repellent to skin and clothing. Additionally, health-care providers serving areas where LACV is endemic should consider LACV in the differential diagnosis of viral encephalitis. As a nationally notifiable disease, all probable and confirmed cases of LACV should be reported to the appropriate state and local public health authorities. When LACV infection is suspected in a pregnant woman or infant, appropriate serologic and virologic testing by a public health reference laboratory is recommended. Testing breast milk for the presence of LACV also might be reasonable to evaluate the potential for maternal-infant transmission and to determine the suitability for continued breastfeeding. Additional investigations are needed to confirm the potential for congenital infection with LACV and to identify immediate and long-term health risks LACV poses to infants.

# Updated Guidelines for the Use of Nucleic Acid Amplification Tests in the Diagnosis of Tuberculosis
Guidelines for the use of nucleic acid amplification (NAA) tests for the diagnosis of tuberculosis (TB) were published in 1996 (1) and updated in 2000 (2). Since then, NAA testing has become a routine procedure in many settings because NAA tests can reliably detect Mycobacterium tuberculosis bacteria in specimens 1 or more weeks earlier than culture (3). Earlier laboratory confirmation of TB can lead to earlier treatment initiation, improved patient outcomes, increased opportunities to interrupt transmission, and more effective public health interventions (4,5). Because of the increasing use of NAA tests and the potential impact on patient care and public health, in June 2008, CDC and the Association of Public Health Laboratories (APHL) convened a panel of clinicians, laboratorians, and TB control officials to assess existing guidelines (1,2) and make recommendations for using NAA tests for laboratory confirmation of TB. On the basis of the panel's report and consultations with the Advisory Council for the Elimination of TB (ACET),- CDC recommends that NAA testing be performed on at least one respiratory specimen from each patient with signs and symptoms of pulmonary TB for whom a diagnosis of TB is being considered but has not yet been established, and for whom the test result would alter case management or TB control activities, such as contact investigations. These guidelines update the previously published guidelines (1,2).

# Background
Conventional tests for laboratory confirmation of TB include acid-fast bacilli (AFB) smear microscopy, which can produce results in 24 hours, and culture, which requires 2-6 weeks to produce results (5,6). Although rapid and inexpensive, AFB smear microscopy is limited by its poor sensitivity (45%-80% with culture-confirmed pulmonary TB cases) and its poor positive predictive value (50%-80%) for TB in settings in which nontuberculous mycobacteria are commonly isolated (3,6,7).
NAA tests can provide results within 24-48 hours. The Amplified Mycobacterium tuberculosis Direct Test (MTD, Gen-Probe, San Diego, California) was approved by the Food and Drug Administration (FDA) in 1995 for use with AFB smear-positive respiratory specimens, and in a supplement application, an enhanced MTD test was approved in 1999 for use with AFB smear-negative respiratory specimens from patients suspected to have TB. In addition, the Amplicor Mycobacterium tuberculosis Test (Amplicor, Roche Diagnostics, Basel, Switzerland) was approved by FDA in 1996 for use with AFB smear-positive respiratory specimens from patients suspected to have TB. NAA tests for TB that have not been FDA-approved also have been used clinically (e.g., NAA tests based on analyte specific reagents, often called "home-brew" or "in-house" tests) (8,9).
Compared with AFB smear microscopy, the added value of NAA testing lies in its 1) greater positive predictive value (>95%) with AFB smear-positive specimens in settings in which nontuberculous mycobacteria are common and 2) ability to confirm rapidly the presence of M. tuberculosis in 50%-80% of AFB smear-negative, culture-positive specimens (3,(7)(8)(9). Compared with culture, NAA tests can detect the presence of M. tuberculosis bacteria in a specimen weeks earlier than culture for 80%-90% of patients suspected to have pulmonary TB whose TB is ultimately confirmed by culture (3,8,9). These advantages can impact patient care and TB control efforts, such as by avoiding unnecessary contact investigations or respiratory isolation for patients whose AFB smear-positive specimens do not contain M. tuberculosis.
Despite being commercially available for more than a decade (1), NAA tests for TB have not been widely used in the United States largely because of 1) an uncertainty as to whether NAA test results influence case-management decisions or TB control activities; 2) a lack of information on the overall costeffectiveness of NAA testing for TB; and 3) a lack of demand from clinicians and public health authorities. However, recent studies showed that 1) clinicians already rely on the NAA test result as the deciding factor for the initiation of therapy for 20%-50% of TB cases in settings where NAA testing is a routine practice (4,7) and 2) overall cost savings can be achieved by using NAA test results for prioritizing contact investigations, making decisions regarding respiratory isolation, or reducing nonindicated TB treatment (4,7).
In response to the increasing demand for NAA testing for TB and recognition of the importance of prompt laboratory results in TB diagnosis and control, ACET requested that APHL and CDC convene a panel to evaluate the available information (e.g., current practices, existing guidelines, and publications) and to propose new guidelines for the use of NAA tests for TB diagnosis. The panel met in June 2008 and included TB clinicians; TB control officials; laboratory directors or supervisors from small, medium, and large public health laboratories, hospital laboratories, and commercial laboratories; and representatives from the TB Regional Training and Medical Consultation Centers, ACET, APHL, and CDC. In brief, the panel recommended  that NAA testing become a standard practice in the United States to aid in the initial diagnosis of patients suspected to have TB, rather than just being a reasonable approach, as suggested in previously published guidelines (1,2). On the basis of the panel's report and consultations with ACET, CDC developed revised guidelines.

# Updated Recommendation
NAA testing should be performed on at least one respiratory specimen from each patient with signs and symptoms of pulmonary TB for whom a diagnosis of TB is being considered but has not yet been established, and for whom the test result would alter case management or TB control activities. The following testing and interpretation algorithm is proposed.  (8,9).

# Revised Testing and Interpretation Algorithm

# Cautions
Culture remains the gold standard for laboratory confirmation of TB and is required for isolating bacteria for drug-susceptibility testing and genotyping. In accordance with current recommendations (6), sufficient numbers and portions of specimens should always be reserved for culturing. Nonetheless, NAA testing should become standard practice for patients suspected to have TB, and all clinicians and public health TB programs should have access to NAA testing for TB to shorten the time needed to diagnose TB from 1-2 weeks to 1-2 days (3). More rapid laboratory results should lead to earlier treatment initiation, improved patient outcomes, and increased opportunities to interrupt transmission (4,5). Rapid laboratory confirmation of TB also can help reduce inappropriate use of fluoroquinolones as empiric monotherapy of pneumonias, a practice which is suspected to lead to development of fluoroquinolone-resistant M. tuberculosis and delays in initiating appropriate anti-TB therapy (10).
To maximize benefits of NAA testing, the interval from specimen collection to communication of the laboratory report to the treating clinician should be as brief as possible. NAA test results should be available within 48 hours of specimen collection. Laboratorians should treat an initial positive NAA test result as a critical test value, immediately report the result to the clinician and public health authorities, and be available for consultation regarding test interpretation and the possible need for additional testing.
Although NAA testing is recommended to aid in the initial diagnosis of persons suspected to have TB, the currently available NAA tests should not be ordered routinely when the clinical suspicion of TB is low, because the positive predictive value of the NAA test is <50% for such cases (8). Clinicians, laboratorians, and TB control officials should be aware of the appropriate uses of NAA tests.
Clinicians should interpret all laboratory results on the basis of the clinical situation. A single negative NAA test result should not be used as a definitive result to exclude TB, especially when the clinical suspicion of TB is moderate to high. Rather, the negative NAA test result should be used as additional information in making clinical decisions, to expedite testing for an alternative diagnosis, or to prevent unnecessary TB treatment. Consultation with a TB expert should be considered if the clinician is not experienced in the interpretation of NAA tests or the diagnosis and treatment of TB.
Although FDA-approved NAA tests for TB are eligible for Medicare or Medicaid reimbursement, the costs of adding NAA testing to the routine testing of respiratory specimens from patients suspected to have TB might be considerable (e.g., operating costs exceed $100 per MTD test) (8). However, NAA testing has the potential to provide overall cost savings to the treatment center and TB control program through reduced costs for isolation, reduced costs of contact investigations of persons who do not have TB, and increased opportunities to prevent transmission. Within the parameters of these guidelines, each TB control or treatment program should evaluate the overall costs and benefits of NAA testing in deciding the value and optimal use of the test in their setting.
Because the testing algorithm includes NAA testing of AFB smear-negative specimens, laboratories must use an FDA-approved test for such specimens or a test produced and validated in accordance with applicable FDA and Clinical Laboratory Improvement Amendments (CLIA) regulations.  However, the performance of in-house tests or FDA-approved tests used for nonapproved indications (off-label use) is variable (8,9), and insufficient information is available to provide recommendations on the use of such tests for the diagnosis of TB. Their use should be guided by the clinical context, and the results of such tests should be interpreted on the basis of performance in the local laboratory and in validation studies.
For procedural and economic reasons, NAA testing might be impractical in laboratories with a small volume of testing. Referral of samples for NAA testing to high-volume laboratories might be preferable to improve cost-efficiency, proficiency, and turnaround times. The New York and Florida Fast Track Programs are successful NAA testing services that could serve as models for a regional service (5).
Information is limited regarding NAA test performance for nonrespiratory specimens or specimens from patients under treatment (8). NAA results often remain positive after culture results become negative during therapy. Further research is needed before specific recommendations can be made on the use of NAA testing in the diagnosis of extrapulmonary TB and TB in children who cannot produce sputum; however, evidence exists for the utility of such testing in individual cases (8).
These guidelines do not address the use of molecular tests for detecting drug resistance, which is an urgent public health and diagnostic need. No molecular drug-susceptibility tests (DSTs) have been approved by FDA for use in the United States, although well-characterized molecular DSTs are commercially available in Europe and elsewhere.  Nonetheless, a proposed revision of the Diagnostic Standards and Classification of Tuberculosis in Adults and Children ( 6) is likely to support the use of molecular DSTs for AFB smear-positive sputum sediments from TB patients who are suspected to have drugresistant disease or who are from a region or population with a high prevalence of drug resistance.
- 0 2 - - - 0 2 - - - 0 2 - - Massachusetts - 0 5 - 1 - 0 1 - - - 0 2 - - New Hampshire - 0 2 - - - 0 2 - - - 0 5 - - Rhode Island  - 0 2 - - - 0 1 - - - 0 14 - - Vermont  - 0 1 - - - 0 1 - - - 0 1 - 1 Mid.
- - 0 1 - 1 - 0 3 - - W.N. Central - 4 16 - 8 1 2 7 1 1 - 2 9 - - Iowa - 1 7 - 4 - 0 2 - - - 0 2 - - Kansas - 0 3 - 1 - 0 3 - - - 0 1 - - Minnesota - 0 8 - - - 0 4 - - - 0 4 - - Missouri - 1 3 - - 1 1 4 1 1 - 1 7 - - Nebraska  - 0 5 - 2 - 0 2 - - - 0 4 - - North Dakota - 0 0 - - - 0 1 - - - 0 0 - - South Dakota - 0 1 - 1 - 0 0 - - - 0 1 - - S.
- 1 5 - 1 2 0 2 2 1 Colorado - 0 3 - - - 0 3 - 2 - 0 2 - - Idaho  - 0 3 - - - 0 2 - - - 0 1 - - Montana  - 0 1 - - - 0 1 - - - 0 1 - - Nevada  - 0 3 - - - 0 3 - - - 0 2 - - New Mexico  - 0 3 - - - 0 2 - 1 - 0 1 - - Utah - 0 2 - - 1 0 3 1 - - 0 2 - - Wyoming  - 0 1 - - - 0 1 - - - 0 0 - - Pacific 1 10 24 1 10 4 7 17 4 6 - 4 10 - 1 Alaska - 0 1 - - 1 0 2 1 - - 0 1 - - California 1 7 24 1 9 3 5 13 3 4 - 3 8 - 1 Hawaii - 0 2 - - - 0 1 - 1 - 0 1 - - Oregon  - 0 3 - 1 - 1 3 - 1 - 0 2 - - Washington - 1 5 - - - 1 4 - - - 0 3 - - American Samoa - 0 0 - - - 0 0 - - N 0 0 N N C.N.M.I. - - - - - - - - - - - - - - - Guam - 0 0 - - - 0 0 - - - 0 0 - - Puerto Rico - 0 2 - - - 0 5 - 1 - 0 1 - - U.S. Virgin Islands - 0 0 - - - 0 0 - - - 0 0 - - C.
- - 0 1 - 1 - 0 1 - - Idaho  - 0 2 - - - 0 1 - - - 0 1 - - Montana  - 0 1 - - - 0 0 - - - 0 1 - - Nevada  - 0 2 - - - 0 3 - - 1 0 1 1 1 New Mexico  - 0 2 - - - 0 1 - - - 0 1 - - Utah 1 0 1 1 - - 0 1 - - - 0 1 - 3 Wyoming  - 0 1 - - - 0 0 - - - 0 1 - - Pacific