Local Transmission of FREE

MMWR. 2002;51:931-923

Malaria transmission in the United States was largely eliminated during the mid-20th century; however, sporadic cases of locally acquired mosquito-transmitted malaria continue to occur. Since 1997, four separate probable mosquito-transmitted malaria outbreaks have been reported to CDC, including one from Virginia.^1-3 This report describes the investigation of two cases of Plasmodium vivax malaria that occurred in northern Virginia in August 2002, and underscores the need for clinicians to consider the possibility of malaria in patients with fever of unknown origin.

Case 1. On August 23, 2002, a person aged 19 years from northern Virginia sought medical care at a family health clinic with a 4-day history of fatigue, fever, and chills. The patient also complained of muscle aches and sinus pain. A sinus infection was diagnosed, and the patient was prescribed azithromycin and desloratadine. Four days later, the patient returned to the clinic with additional symptoms, dizziness, and nausea. On physical examination, the patient had a temperature of 103.5°F (39.7°C) and tachycardia. Laboratory results revealed pancytopenia (platelet count: 61,000/µL [normal: 130,000-400,000/µL], hemoglobin: 10 g/dL [normal: 11.5-16.0 g/dL], and white blood cell count: 3,300/µL [normal: 4,000-11,000/µL]). The patient's therapy was changed to oral levofloxacin. Malaria parasites were identified subsequently on a routine complete blood count smear taken 4 days after the initial clinic visit. The patient was contacted and administered chloroquine. A review of the initial malaria smear by a local university hospital confirmed the diagnosis of P. vivax malaria. The patient completed a 3-day course of chloroquine therapy and after a normal glucose-6-phosphate dehydrogenase (G6PD) test result was placed on primaquine for 14 days. The patient had complete resolution of symptoms.

Case 2. On August 25, a person aged 15 years from northern Virginia was taken to a local emergency department for treatment of 2 weeks of headaches and 4 days of fever, nausea, vomiting, malaise, and nose bleeds. On physical examination, the patient had a temperature of 105.0°F (40.6°C), tachycardia, splenomegaly, and jaundice. Laboratory values revealed pancytopenia (platelet count: 48,000/µL, hemoglobin: 11.6 g/dL, and white blood cell count: 3,200/µL). A malaria smear revealed Plasmodium sp. parasites reported initially as nonfalciparum. The patient was admitted to the hospital and administered quinine and clindamycin. The smear was confirmed subsequently as P. vivax by the Virginia Department of Health. The patient's physician contacted CDC for treatment recommendations on August 28 because the patient had tinnitus, requiring discontinuation of the quinine. The patient completed a 3-day course of chloroquine therapy and was discharged with complete resolution of symptoms on August 31. After a normal G6PD test result, the patient was placed on primaquine for 14 days.

The two patients had no risk factors for malaria, including international travel, blood transfusion, organ transplantation, or needle sharing. The patients lived approximately 0.5 miles apart; however, the 19-year-old patient reported numerous visits to friends who lived directly across the street from the 15-year-old patient. Residents in the neighborhood surrounding the patients' homes were asked about recent febrile illnesses. Medical records from two hospitals serving residents in the patients' neighborhood also were reviewed, and charts of patients with a diagnosis of fever of unknown origin were obtained. None of the patients' neighbors had unexplained febrile illnesses. Of 224 hospital records available for review, 21 documented fever with no underlying cause. One of the 21 patients had persistent symptoms; however, a malaria smear did not reveal malaria parasites. No further cases of locally acquired malaria have been reported in northern Virginia.

Washington Dulles International Airport is located <10 miles from the patients' homes. The airport receives nonstop international flights from countries in which P. vivax malaria is endemic. Ill travelers are sent to one of the hospitals included in the investigation's case-detection activities. Physicians at two Army bases located nearby were contacted and reported no known cases of malaria or fever of unknown origin in troops returning from areas in which malaria is endemic.

The patients' homes were visited. One home had several unscreened or poorly screened windows; the other had well-screened windows and a porch. Within the vicinity of both homes was a wooded area with a creek and ponds. As a part of ongoing West Nile virus (WNV) surveillance activities, trapping for anopheline mosquitoes within 10 miles of the patients' homes yielded Anopheles quadrimaculatus and An. punctipennis. Of approximately 870 anopheline mosquitoes tested, five pools (four to six mosquitoes per pool) captured within 2-6 miles of the patients' homes tested positive for P. vivax-210 circumsporozoite protein by using a field test (VecTest™ [Medical Analysis Systems, Inc., Camarillo, California]) on September 25 and 27 and October 1, 6, and 11. No mosquito pool has tested positive repeatedly in confirmatory testing by using polymerase chain reaction (PCR); however, efforts to confirm the positive VecTest™ mosquito pools are ongoing.

A Pastor, MD, Loudoun Healthcare Dept of Infectious Diseases; J Neely, Clarke Environmental Mosquito Management; D Goodfriend, MD, Loudoun County Dept of Health, Leesburg; J Marr, MD, S Jenkins, VMD, D Woolard, PhD, D Pettit, PhD, D Gaines, PhD, D Sockwell, MSPH, Virginia Dept of Health. C Garvey, MD, C Jordan, C Lacey, Montgomery County Health Svcs, Rockville; T DuVernoy, DVM, Maryland Dept of Health and Mental Hygiene. D Roberts, PhD, L Robert, PhD, P Santos, Div of Tropical Public Health, Uniformed Svcs, Univ of the Health Sciences, Bethesda, Maryland. R Wirtz, PhD, J MacArthur, MD, Div of Parasitic Diseases; M O'Brien, Div of Applied Public Health Training, Epidemiology Program Office; L Causer, MBBS, EIS Officer, CDC.

Despite malaria eradication certification in the United States in 1970,^4,5 10 outbreaks involving 17 cases of probable locally acquired mosquito-borne malaria transmission have occurred since 1992.¹ The two cases from northern Virginia represent the first cases of probable mosquito-borne malaria transmission in the United States since 1999^1,2 and the second reported outbreak in Virginia.³ These outbreaks share common features: (1) an initial case without known risk factors for malaria, (2) probable proximity to a person with malaria parasitemia, (3) presence of competent mosquito vectors, and (4) environmental conditions conducive to the maturation of the parasite in the mosquito.

Approximately 1,000-1,500 cases of malaria in the United States are reported annually to CDC.⁶ The majority are diagnosed in travelers from countries in which malaria is endemic. The source of infection in the two northern Virginia residents was probably the bite of an infective mosquito that had acquired the parasite by biting a malaria-infected person in the general vicinity. Several Anopheles sp. mosquitoes native to the United States are competent malaria vectors. The An. quadrimaculatus and An. punctipennis mosquitoes captured near the patients' homes have been implicated in previous cases of locally acquired malaria.^2,3 Numerous pools of these vectors were tested by using VecTest™. Although this test is used commonly in international settings,⁷ this is the first time the test has been used in an investigation of mosquito-borne malaria in the United States. The identification of five malaria-positive pools among approximately 870 tested mosquitoes is unexpectedly high and has not been observed previously during an investigation of a malaria outbreak in the United States. Rapid screening tests such as the VecTest™ were not available previously. However, because VecTest™ is a new tool for the investigation of local mosquito-borne malaria in the United States, its validity in this setting is unknown, and results need to be confirmed by using PCR. Efforts are under way to develop testing algorithms for screening mosquito pools by using VecTest™ and confirming results with PCR.

This investigation underscores the need for clinicians to consider the possibility of malaria in patients with fever of unknown origin. Although a thorough travel history and risk-factor assessment should be a part of the evaluation of febrile patients, the possibility of malaria in patients without international travel, blood transfusion, organ transplantation, or needle sharing should be considered. Rapid diagnosis and treatment with effective antimalarial drugs are the basis of patient case management and will reduce the chances that an infected host will transmit the parasite. The same precautions recommended for minimizing exposure to WNV should be followed for reducing exposure to malaria-infected Anopheles sp. mosquitoes, including wearing long-sleeved shirts and long trousers, using insect repellent containing N,N-diethyl-toluamide (DEET), and avoiding outdoor activities during the late evening. Prompt reporting of patients with malaria to local public health authorities assists in activating control measures for these isolated cases of mosquito-borne malaria.

This report is based on data contributed by L Frank, R Helfrich, Montgomery County Health Svcs, Rockville; C Lesser, Maryland Dept of Agriculture; D Blythe, MD, Maryland Dept of Health and Mental Hygiene.

References: 7 available

MMWR. 2002;51:897-899

2 tables omitted

Iron deficiency, the most common nutritional deficiency worldwide, has negative effects on work capacity and on motor and mental development in infants, children, and adolescents, and maternal iron deficiency anemia might cause low birthweight and preterm delivery.^1-3 Although iron deficiency is more common in developing countries, a significant prevalence was observed in the United States during the early 1990s among certain populations, such as toddlers and females of childbearing age.⁴ One of the national health objectives for 2010 is to reduce iron deficiency in these vulnerable populations by 3-4 percentage points (objective no. 19-12).⁵ CDC has published recommendations to prevent iron deficiency in the United States.⁶ To characterize the iron status of persons in the United States, CDC calculated the prevalence of iron deficiency and iron deficiency anemia by applying a multiple-indicator model to data from the 1999-2000 National Health and Nutrition Examination Survey (NHANES 1999-2000). These values were compared with those observed in the third National Health and Nutrition Examination Survey (NHANES III [1988-1994]) using the same multiple-indicator model. This report summarizes the results of this analysis, which indicate that iron deficiency remains 2-5 percentage points above the 2010 national health objectives. To prevent iron deficiency, vulnerable populations should be encouraged to eat iron-rich foods and breast-feed or use iron-fortified formula for infants.

Both NHANES surveys sampled the U.S. civilian, noninstitutionalized population and collected data through household interviews and physical examinations. In both surveys, blood was collected by venipuncture from all persons aged ≥1 year. Four biochemical measures of iron status were included in the analysis: hemoglobin, serum ferritin, transferrin saturation, and free erythrocyte protoporphyrin. Hemoglobin was measured in mobile examination centers in both surveys as part of a complete blood count by using an automated electronic counter: Coulter S-Plus Jr in NHANES III and Coulter MAXM in NHANES 1999-2000 (Coulter Electronics, Hialeah, Florida). In both surveys, the remaining three iron indicators were measured at CDC by using the same assay methods and comparable quality-control materials. Serum ferritin was measured with the Bio-Rad QuantImune Ferritin IRMA™ (Bio-Rad Laboratories, Hercules, California); transferrin saturation was calculated from serum iron and total iron-binding capacity, which were measured by a modification of the automated AAII-25 colorimetric method; and free erythrocyte protoporphyrin was measured by a modification of the Sassa method.⁷ Because abnormal values for these iron status indicators might be caused by inflammatory conditions rather than by poor iron status,⁸ a serum indicator of inflammation (C-reactive protein) also was used. This indicator was measured on participants aged ≥3 years by latex-enhanced nephelometry at the University of Washington.⁷

The definition of iron deficiency was an abnormal value for at least two of the following three indicators: serum ferritin, transferrin saturation, and free erythrocyte protoporphyrin. Persons with iron deficiency and a low hemoglobin value were considered to have iron deficiency anemia.⁴ The same threshold values to define abnormality for the four iron indicators were applied to both surveys. These thresholds were derived from NHANES III.⁴

The estimated prevalence of iron deficiency was greatest among toddlers aged 1-2 years (7%) and adolescent and adult females aged 12-49 years (9%-16%). The prevalence of iron deficiency was approximately two times higher among non-Hispanic black and Mexican-American females (19%-22%) than among non-Hispanic white females (10%). Excluding persons aged ≥3 years with elevated C-reactive protein levels (>1 mg/dL) from the analysis did not change prevalence estimates.

The prevalence of iron deficiency was similar in NHANES III and NHANES 1999-2000 in most age and sex groups. Exceptions included males aged 12-69 years and women aged 50-69 years; in these groups, the prevalence was substantially higher in NHANES 1999-2000 than in NHANES III as determined by a t-test.

The prevalence of iron deficiency anemia was examined for the populations in which iron deficiency was most common in NHANES 1999-2000. In these groups, the prevalence was <5%, which is similar to that observed in NHANES III.

AC Looker, PhD, Div of Health Examination Statistics, National Center for Health Statistics; ME Cogswell, DrPH, Div of Nutrition and Physical Activity, National Center for Chronic Disease Prevention and Health Promotion; EW Gunter, MT(ASCP), Div of Laboratory Sciences, National Center for Environmental Health, CDC.

Data from NHANES 1999-2000 indicate that iron deficiency anemia is uncommon in the United States, but iron deficiency remains above the 2010 objectives of 5%, 1%, and 7% for toddlers, preschool children, and females aged 12-49 years, respectively.⁵ Among minority females aged 12-49 years, the prevalence of iron deficiency was approximately three times greater than the 2010 national health objectives. Multiple factors, including dietary intake, parity, and socioeconomic status,^4,6 might explain the continued prevalence of iron deficiency in these groups. These factors were not included in this assessment of iron status.

The findings in this report are subject to at least two limitations. First, because abnormal values for iron status indicators might reflect inflammation rather than poor iron status,⁸ confounding by inflammation might have affected results in some age groups. The confounding could not be addressed in toddlers because data on inflammation in this age group were not available. The confounding might have been only partially addressed in middle-aged and older adults because C-reactive protein is less sensitive for detecting chronic inflammatory conditions common in older persons than it is in detecting inflammation from acute infections.⁹ Second, insufficient sample size also might have limited the ability to detect trends in iron deficiency over time. Data from the Pediatric Nutrition Surveillance System (PNSS) indicated that anemia continued to decline among toddlers in low-income households during the 1990s.¹⁰ Anemia is not always caused by iron deficiency, but the PNSS data suggest progress in improving iron status among children. However, the prevalence of iron deficiency did not differ substantially between the two NHANES surveys among toddlers, adolescents, or females aged 12-49 years, possibly because of limited study power resulting from the smaller sample size in NHANES 1999-2000. For example, power calculations revealed that a sample size of approximately 1,300 would be needed in each survey to demonstrate that the difference in prevalence among females aged 16-19 years (11% versus 16%) was statistically significant. Thus, additional years of data will be needed to ascertain whether progress has been made in achieving the 2010 national health objectives for reducing iron deficiency in vulnerable populations.

Many of the adverse consequences of iron deficiency are associated with its most severe form, iron deficiency anemia.^1,3 However, iron deficiency without anemia has been linked to negative impacts on cognitive development in children and adolescents.² Continued monitoring of iron status of the U.S. population is warranted because the prevalence of iron deficiency in vulnerable populations exceeds the 2010 national health objectives.

References: 10 available

MMWR. 2002;51:902

Staphylococcus aureus is one of the most common causes of hospital- and community-acquired infections.^1- 2 Since the recognition of vancomycin-resistant enterococci in 1988, the emergence of vancomycin-resistant S. aureus (VRSA) (minimum inhibitory concentration [MIC] ≥32 µg/mL³) has been anticipated. The transfer of the genetic element containing the vanA vancomycin resistance gene from Enterococcus faecalis to S. aureus was demonstrated in the laboratory in 1992⁴; the first clinical infection with VRSA was reported in July 2002.⁵ This report describes the second documented clinical isolate of VRSA from a patient.

On September 20, the patient was admitted to a hospital in Pennsylvania and evaluated for a chronic foot ulcer and possible osteomyelitis. A culture of the ulcer grew S. aureus. This isolate was tested for antimicrobial susceptibility by disk diffusion; a vancomycin-agar screen plate (brain heart infusion agar containing 6 µg/mL vancomycin) also was inoculated. Growth on the vancomycin screen plate and a 12 mm zone of inhibition around the vancomycin disk suggested that the isolate had decreased susceptibility to vancomycin. Further testing by Etest® confirmed that the isolate was resistant to vancomycin (MIC = 64 µg/mL). Following notification of the Pennsylvania Department of Health (PDH), the isolate was forwarded to CDC, where it was confirmed to be VRSA (vancomycin MIC = 32 µg/mL by broth microdilution testing). The isolate contained both the mecA and vanA genes mediating oxacillin and vancomycin resistance, respectively. The isolate was susceptible to chloramphenicol, linezolid, minocycline, quinupristin-dalfopristin, rifampin, and trimethoprim-sulfamethoxazole.

The patient has been discharged from the hospital and is responding to antimicrobial treatment. The patient is receiving home-health care. PDH and CDC are assisting health-care providers investigating this case of VRSA. The goals of this investigation include assessment of infection-control practices in the hospital and home setting and the possibility of transmission of the organism to other patients, health-care providers, and family or social contacts. Previous investigations of VRSA and vancomycin-intermediate S. aureus in the home setting demonstrated no transmission among family or home health-care contacts.^5- 6

The presence of vanA in this VRSA suggests that the resistance determinate was acquired from a vancomycin-resistant enterococcus. Development of this VRSA appears to be unrelated to the previous VRSA identified in Michigan.⁵ However, because both were probably the result of conjugation events, additional VRSA infections are likely to occur. Therefore, clinical microbiology laboratories must ensure that they are using susceptibility testing methods that will detect VRSA and that they are saving potential VRSA for confirmatory testing. In addition, more systematic surveillance for VRSA will enhance the ability of the public health system and the health-care system to rapidly address this resistant pathogen.

The public health response to this VRSA occurrence is ongoing. Using proper infection-control practices and good antimicrobial agent management will help limit the emergence and spread of antimicrobial-resistant microorganisms, including VRSA. CDC recommends contact precautions when caring for patients with these infections, including placing the patient in a private room, wearing gloves and a gown during patient contact, washing hands after contact with the patient and infectious body tissues or fluids, and not sharing patient-care items with other patients. CDC guidelines for preventing spread of VRSA are available at http://www.cdc.gov/ncidod/hip/10_20.pdf.

The isolation of S. aureus with confirmed or "presumptive" vancomycin resistance should be saved and reported through state and local health departments to CDC's Division of Healthcare Quality Promotion, National Center for Infectious Diseases, telephone 800-893-0485.

D Miller, V Urdaneta, MD, A Weltman, MD, Pennsylvania Dept of Health. Office of the Director, Div of Healthcare Quality Promotion, National Center for Infectious Diseases; S Park, EIS Officer, CDC.