MMWR Weekly
Volume 57, No. 39
October 3, 2008  

HIV Prevalence Estimates
– United States, 2006

THE CASE:  A 17-year-old male was found in cardiac arrest following a blow to the chest. The patient immediately dropped to the ground and was unresponsive after being elbowed by a teammate who ran into him. Cardiopulmonary resuscitation (CPR) was initiated by his coach after no pulses were palpated, and the patient was taken to the ED. The paramedics arrived 5 minutes later and, as noted on the rhythm strip, found the patient to be in ventricular fibrillation. One 200 joule countershock was administered, converting the ventricular fibrillation to a normal sinus rhythm, and the patient was noted to regain consciousness.

Upon arrival at the ED, the patient reports only mild anterior chest wall pain and denies any substernal chest pain, shortness of breath, palpitations, weakness, or confusion. He states that he has never before fainted. The patient and his mother deny any significant past medical or family history, including any arrhythmias, unexplained sudden deaths, or cardiac structural diseases. He denies having a lower exercise tolerance than his teammates and also denies any smoking, drinking, use of medications, illicit substance abuse, or doping practices.

On physical examination, the primary survey of his airway, breathing, and circulation is unremarkable. The patient has a blood pressure of 130/71 mm Hg and a heart rate of 106 bpm, with a normal rhythm. The respirations are 28-30 breaths/min. The initial oxygen saturation is 83% while the patient is breathing room air, but it corrects to 98% on a non-rebreather mask and, subsequently, to 99% on 2 L nasal cannula. His mentation is intact and he remains alert, with a Glasgow Coma Scale rating of 15. The skin examination reveals mild ecchymosis just anterior to his sternum. The lungs are clear to auscultation bilaterally, and the cardiac examination reveals a regular rate, with normal S1 and S2 heart sounds and no clicks, gallops, rubs, or murmurs. The abdominal and neurologic examinations are unremarkable. The musculoskeletal exam shows the patient’s wingspan to be 95-100% of his height.

The patient is placed on a cardiac monitor upon arrival to the ED. A 12-lead electrocardiogram (ECG) is obtained that reveals sinus tachycardia at a rate of 110 bpm, with mild right-axis deviation. The QRS complex, QT interval, ST/T waves, and P waves are all noted to be normal (see Figure 2). A portable, upright chest radiograph shows somewhat underaerated lungs but no signs of fractures, widening of the mediastinum, cardiomegaly, or hemopneumothorax (see Figure 3). A complete blood count (CBC) is normal, except for a mildly elevated white blood cell (WBC) count of 13.6 ×10³/µL (13.6 ×10⁹/L). A metabolic panel is normal, including normal potassium and magnesium findings. The initial troponin I is 0.04 ng/mL (0.04 µg/L; normal range, 0.02-0.04 ng/mL; indeterminate 0.05-0.30 ng/mL). A urine drug screen is negative. Computed tomography (CT) scanning of the chest (see Figure 4) is remarkable only for mild pulmonary and periportal edema. The patient is admitted to the pediatric intensive care unit (PICU) for continuous cardiac monitoring and cardiology consultation. An echocardiogram is ordered in the ED, to be done in the PICU.

Commotio cordis (which is Latin for “disturbance of the heart”) is, in essence, a concussion of the heart. Initially described as early as 1857, it is defined as an instantaneous cardiac arrest produced by a witnessed, nonpenetrating blow to the chest, in the absence of preexisting heart disease or identifiable morphologic injury to the sternum, ribs, chest wall, or heart. Commotio cordis is a diagnosis of exclusion in that other causes, such as substance abuse, myocardial infarction, electrolyte abnormality, prolonged QT syndrome, and hypertrophic obstructive cardiomyopathy (HOCM), must first be ruled out with examinations such as urine drug screens, serial assessment of cardiac biomarkers and EKGs, electrolyte level testing, and echocardiography.^[1,2]

THE DISCUSSION:  Although reported as the second most common cause of sudden cardiac arrest in young athletes (behind HOCM), commotio cordis is underreported and underrecognized.^[2] The United States Commotio Cordis Registry (USCCR), in Minneapolis, Minnesota, reported that as of September 2001, only 180 cases had been documented. Up to 62% of these cases involved engagement in organized, competitive sports, with two-thirds of the patients being younger than 16 years of age and 80% being male. The oldest reported case was that of a 20-year-old man struck in the chest by a baseball, and the youngest case was that of a 7-week-old crying infant struck in the chest by his frustrated father. Eighty-one percent of cases involved a blunt, precordial blow from a projectile object propelled against a stationary chest wall, resulting in a relatively localized area of contact. It is notable that those who are most susceptible to commotio cordis are young athletic males. This is probably the result of the fact that there is less protection of the heart by subcutaneous fat, muscle bulk, and fully ossified ribs, all of which become more common in adulthood.^[2,3] A review of the USCCR data revealed that a vast majority of the 180 reported cases were caused by a blow to the chest from an object used during an organized youth sporting event. A baseball accounted for 53 of the cases, with a softball and a hockey puck following, at 14 and 10 cases, respectively. Other documented sporting cases have been caused by blows delivered by body parts, such as an elbow, knee, foot, or fist hitting the anterior chest wall (5-6 cases of each). Finally, daily activities, including parent-child discipline (5 cases), and even a fall from monkey bars (1 case), can lead to commotio cordis. Regardless of the mechanism, impacts resulting in commotio cordis are typically of low energy and velocity.^[1,4] The victim may collapse immediately after the blow, but in up to 50% of cases, there is a short delay between the times of impact and collapse.

In 1930, George Schlomka was the first to describe the factors that can lead to arrhythmia after a moderate precordial impact. He believed that the force, location, and type of object causing the impact determined the type of injury and the subsequent risk of arrhythmia.^[2] The force transmitted to the heart is directly related to the hardness of the striking object. Madia et al reported that the threshold speed of impact at which a standard baseball can cause ventricular fibrillation is between 25 and 30mph. When the speed is over 50mph, however, the likelihood of ventricular fibrillation actually decreases, although the possibility of myocardial contusion becomes greater. Furthermore, the authors stated that the impact must be directly over the cardiac silhouette near or just to the left of the sternum in order to instigate ventricular fibrillation. Impact on the center of the cardiac silhouette induced ventricular fibrillation in 30% of reported cases, compared with 13% and 4% at the left ventricular base and apex, respectively.^[4]

The utilization of a standard baseball leads to the incidence rate as above, but if the core of the ball is softer, then the rate for ventricular fibrillation drops. A study published by Link et al reported that changes to the cores of baseballs to make them softer led to a decrease in the rate of ventricular fibrillation with commotio cordis from 70% to 19%. As such, the use of safety baseballs with rubber cores of different degrees of hardness has been advocated in order to reduce the risk of such traumatic injury in young athletes.^[3,5]

Not all impacts to the anterior chest will lead to the ventricular fibrillation observed in commotio cordis. The impact must be delivered 10-30 milliseconds before the peak of the T wave in the cardiac cycle (see Figure 5) in order to induce ventricular fibrillation. Induction is likely secondary to the activation of potassium-carrying ion channels via mechanoelectric coupling. The activation of these ion channels generates an inward current, thus locally augmenting repolarization and resulting in premature ventricular depolarization and the initiation of unstable ventricular arrhythmias. If impact occurs during other portions of the cardiac cycle, different conduction disturbances, such as heart block, bundle branch block, or transient ST segment elevation, may be induced.^[2,4,5]

Regardless of etiology, if a young athlete goes into sudden cardiac arrest, CPR should be implemented immediately. Of sports-related cases of commotio cordis documented in the USCCR, 15% of patients survived. In cases in which CPR was instituted within 3 minutes of the impact, 68% of patients survived; however, if CPR was delayed by more than 3 minutes, only 3% of patients survived. Animal studies have shown that CPR instituted within the first 3 minutes of injury can increase survival rate by up to 25%. Concomitantly, early utilization of an automatic external defibrillator (AED) device has been proven to increase survival rates. With an AED recognizing ventricular fibrillation at a sensitivity of 98% and a specificity of 100%, defibrillation within the first 3 minutes can increase the survival rate by an additional 50% or more in animal models, yielding a survival rate of 46% at 4 minutes, and 25% at 6 minutes. The USCCR has recommended that all athletic venues should have an accessible AED. Preventative measures for commotio cordis include parental education, softer baseballs, and protective padding of an athlete’s precordium.^[1,4] Secondary prevention may involve avoidance of certain sports until the age of 18 years or older.

While the patient in this case was in the PICU, he was placed on continuous cardiac monitoring for 24 hours, and no incident of arrhythmia was noted. An echocardiogram was obtained that revealed a normal left ventricular systolic ejection fraction, with no structural abnormalities, valvular disease, or hypertrophy. A repeat 12-lead ECG showed no changes from the previous one, and subsequently, the serial troponins were measured at 0.25 and 0.04 ng/mL. A pediatric cardiologist consultation was unrevealing. The patient was transferred to the pediatric floor the next day, and he was discharged 2 days after initial admission, with no signs of post-arrest sequelae. The patient’s final diagnosis, in conjunction with the ED’s suspected admitting diagnosis, was commotio cordis.

References

1. Maron BJ, Gohman TE, Kyle SB, Estes NA 3rd, Link MS. Clinical profile and spectrum of commotio cordis. JAMA. 2002;287:1142-1146. Abstract
2. McCrory P. Commotio Cordis. Br J Sports Med. 2002;36:236-237. Abstract
3. Valani R, Mikrogianakis A, Goldman RD. Cardiac concussion (commotio cordis). CJEM. 2004;6:428-30. Abstract
4. Madias C, Maron BJ, Alsheikh-Ali AA, Estes Iii NA, Link MS. Commotio cordis. Indian Pacing Electrophysiol J. 2007;7:235-245. Abstract
5. Link M, Maron BJ, Wang PJ, et al. Reduced risk of sudden death from chest wall blows (commotio cordis) with safety baseballs. Pediatrics. 2002;109:873-77. Abstract

AP, 9/30/08 (http://www.chicagotribune.com/news/politics/sns-ap-med-cold-medicines,0,3666994.story)

A top government health official rejected the idea of an immediate ban on cough and cold medicines for young children, saying it might cause unintended harm.

Food and Drug Administration officials at a public hearing Thursday said they need to gather more data on whether over-the-counter remedies are safe and effective for children ages 2-6.

The FDA is also worried that a ban — as sought by leading pediatricians’ groups — might only drive parents to give adult medicines to their youngsters.

“That is a concern for us,” said Dr. John Jenkins, who heads the FDA’s Office of New Drugs. “We do not want to do something that we think will have a positive impact, only to have an unintended negative. That could be an even worse situation.”
With a new cold season coming, pediatricians are urging the government to demand a recall of over-the-counter cough and cold medicines for children younger than 6. The effectiveness of the medicines in children was never scientifically established, critics say, and problems with the drugs send thousands of kids to the emergency room every year.

“When a treatment is ineffective, its risks — unless zero — always exceed its benefits,” Dr. Michael Shannon of Children’s Hospital in Boston told the FDA panel.

The FDA this year warned against giving OTC cold medicines to children younger than 2. At that time, officials said they expected to decide by spring on recommendations for youngsters up to 11. Now the agency is seeking more advice from doctors, industry and consumers — and officials are not giving a timetable for a decision.

U.S. families spend at least $286 million a year on such cough and cold remedies for children, according to the Nielsen Co. market research firm. In any given week the medicines are used by an estimated 10 percent of all children, with the biggest exposure among 2- to 5-year-olds, a recent Boston University report found.

But colds usually clear up on their own after a few days. Many doctors say rest and plenty of fluids are what it takes to get over a cold.

The industry says OTC medicines have been used for decades in treating kids’ colds and are safe for those older than 2. Nonetheless, manufacturers are planning to carry out new studies involving the most common ingredients in the medications. The companies voluntarily stopped selling cough and cold medicines for babies and toddlers last fall.

FDA advisers said that was not enough and recommended that the drugs not be used for children younger than 6. An expert panel said children older than 2 could keep taking the medications while studies are undertaken to settle scientific questions about safety and effectiveness.

It turns out that when the FDA set standards for cough and cold medicines some 30 years ago, no separate studies were done for kids.

Cough and cold medicines send about 7,000 children to hospital emergency rooms each year with symptoms ranging from hives and drowsiness to unsteady walking. Low doses of a medicine are not likely to cause a problem; the main risk comes from unintentional overdoses.

The same ingredients usually are found in different products. For example, giving a child a cough syrup and a decongestant could inadvertently lead to an overdose.

The Consumer Healthcare Products Association, which represents the manufacturers, says preventable errors are the problem, not the safety of the ingredients in the medicines. The industry is starting an educational campaign aimed at parents, doctors and day care providers on the importance of following directions and storing medicines in places where kids cannot get at them.

“The data clearly show a majority of adverse events are direct result of misuse of our products,” said Linda Suydam, who heads the industry group.

Baltimore health commissioner Dr. Joshua Sharfstein sought to reassure FDA officials worried about unintended consequences if the government moves to restrict the medications and parents start dispensing adult drugs to their preschoolers. Sharfstein said the state of Maryland saw an immediate benefit after OTC cough and cold remedies for tots were removed from store shelves last fall. Calls to poison control about problems with the medicines involving children younger than 2 dropped by 40 percent, from 99 to 60, in the first six months of this year when compared with 2007. Calls involving children 2 to 6 also dropped, but by much less.

“The feared increases in poisonings simply did not happen,” said Sharfstein. “In fact, the opposite occurred.”

Treatment Guide.  “Hazardous Materials Exposure Guide:  A step-by-step Medical Response Guide”   Minnesota Dpt of Health.  2008.
http://health.state.mn.us/divs/phl/labep/hazmat/hazmatguide.PDF

MMWR, Oct.  2008: 

MMWR, Oct. 2008

MMWR, Oct.  2008:

Source:  MMWR, October, 2008

Source:  MMWR, Oct, 2008

Surveillance for Lyme Disease
United States, 1992–2006

MMWR Volume 57, No. SS-10
October 3, 2008  

ABSTRACT 

Problem/Condition: Lyme disease is a multisystem disease that occurs in North America, Europe, and Asia. In the United States, the etiologic agent is Borrelia burgdorferi sensu stricto, a spirochete transmitted to humans by infected Ixodes scapularis and I. pacificus ticks. The majority of patients with Lyme disease develop a characteristic rash, erythema migrans (EM), accompanied by symptoms of fever, malaise, fatigue, headache, myalgia, or arthralgia. Other manifestations of infection can include arthritis, carditis, and neurologic deficits. Lyme disease can be treated successfully with standard antibiotic regimens.

Reporting Period: 1992–2006.

Description of System: U.S. health departments report cases of Lyme disease voluntarily to CDC as part of the National Notifiable Disease Surveillance System. Variables collected include patient age, sex, race, county and state of residence, date of illness onset, and reported signs and symptoms.

Results: During 1992–2006, a total of 248,074 cases of Lyme disease were reported to CDC by health departments in the 50 states, the District of Columbia, and U.S. territories; the annual count increased 101%, from 9,908 cases in 1992 to 19,931 cases in 2006. During this 15-year period, 93% of cases were reported from 10 states (Connecticut, Delaware, Massachusetts, Maryland, Minnesota, New Jersey, New York, Pennsylvania, Rhode Island, and Wisconsin). Incidence was highest among children aged 5–14 years, and 53% of all reported cases occurred among males. More than 65% of patients with EM had illness onset in June and July, compared with 37% of patients with arthritis.

Interpretation: Lyme disease is the most commonly reported vectorborne illness in the United States. The geographic distribution of cases is highly focused, with the majority of reported cases occurring in the northeastern and north-central states. During 1992–2006, the number of reported cases more than doubled. A disproportionate increasing trend was observed in children and in young males compared with other demographic groups.

Public Health Action: The results presented in this report underscore the continued emergence of Lyme disease and the need for tick avoidance and early treatment interventions. Public health practitioners can use the data presented in this report to target prevention campaigns to populations with increasing incidence (i.e., children and young males).

Introduction

Lyme disease was first described in 1977 following investigation of a cluster of arthritis cases among children living near Lyme, Connecticut (1). Further study indicated that arthritis was a late manifestation of a multisystem, tick-transmitted disease. In 1981, a bacterial spirochete, Borrelia burgdorferi, was identified in Ixodes scapularis (2) and later demonstrated to be the etiologic agent of Lyme disease (3,4).

B. burgdorferi occurs naturally in reservoir hosts, including mice, squirrels, shrews, and other small vertebrates (5). Ixodes scapularis and I. pacificus (also referred to as blacklegged or deer ticks) become infected with B. burgdorferi while feeding on the blood of natural reservoir hosts. During subsequent blood meals, the ticks can transmit infection among reservoir hosts or to incidental hosts, including humans. Although deer are not infected with B. burgdorferi, they play a role in transporting ticks and maintaining tick populations.

In humans, infection with B. burgdorferi can result in dermatologic, musculoskeletal, neurologic, or cardiac abnormalities (6–8). In approximately 70%–80% of cases, patients develop a characteristic rash, erythema migrans (EM), within 30 days of infection with B. burgdorferi. EM is a red expanding rash, with or without central clearing, which often is accompanied by symptoms of fatigue, fever, headache, mild stiff neck, arthralgia, or myalgia. Within days or weeks, untreated infection can spread to other parts of the body, causing more serious neurologic conditions (e.g., meningitis, radiculopathy, and facial palsy) or cardiac abnormalities (e.g., carditis with atrioventricular heart block). Over a period of months or years, untreated infection can lead to mono- or oligoarticular arthritis, peripheral neuropathy, or encephalopathy.

Lyme disease is diagnosed on the basis of physician-observed clinical manifestations and a history of probable exposure to infected ticks (8). Laboratory tests are neither suggested nor required to confirm diagnosis for patients with recent onset (2–3 weeks) of a characteristic EM rash (9). However, positive results of recommended two-tiered serologic testing (10) can provide confirmation of infection in patients with musculo-skeletal, neurologic, or cardiac symptoms. Testing methods that have not been adequately validated can be misleading (11) and are not recommended (12).

The majority of infections can be cured with use of recommended antimicrobials. Patients with physician-diagnosed EM can be treated with oral doxycycline, amoxicillin, or cefuroxime axetil (7,8). Patients with other manifestations of Lyme disease are treated with either oral or intravenous antimicrobials (e.g., ceftriaxone), depending on the specific clinical condition.

Measures to prevent Lyme disease and other tickborne infections include avoiding tick-infested areas when possible, using insect repellents containing 20%–30% DEET (N,N-diethyl-m-toluamide) on exposed skin and clothing, and performing daily self-examination for ticks (13). Tick abundance can be reduced around private homes and in recreational areas by removing brush and leaf litter, creating a buffer zone of wood chips or gravel between forests and lawn, applying acaricides, and excluding deer (13,14). Tickborne illness can be mitigated by prompt and proper tick removal and by recognizing and seeking treatment for early signs of illness (8,15,16). A single dose of doxycycline should be considered for prophylaxis of Lyme disease in persons aged >8 years who have been bitten by a nymph or adult I. scapularis or I. pacificus tick in an area in which at least 20% of ticks are thought to be infected with B. burgdorferi (8). The tick must have been attached for >36 hours and prophylactic antibiotic administered within 72 hours of tick removal (8).

With the cooperation of state and local health departments, CDC initiated surveillance for Lyme disease in 1980; the first summary of 226 cases was published in 1981 (17). Before 1991, Lyme disease surveillance case definitions and reporting practices varied among states and between states and CDC. Standardized surveillance and reporting for Lyme disease began in 1991 after the Council of State and Territorial Epidemiologists (CSTE) designated Lyme disease as a nationally notifiable disease and published a standardized surveillance case definition* (18). This report describes the characteristics and distribution of Lyme disease cases reported in the United States during 1992–2006, providing 15-year trends and the frequency of reported symptoms. In addition, it details differences between cases reported from within and outside of the 10 states (Connecticut, Delaware, Maryland, Massachusetts, Minnesota, New Jersey, New York, Pennsylvania, Rhode Island, and Wisconsin) in which Lyme disease is highly endemic^† (19). These results underscore the continued emergence of Lyme disease and provide a basis for targeting prevention campaigns to populations with increasing incidence.

Methods 

Surveillance Case Definitions

During 1991–1996, a case of Lyme disease was defined for national surveillance purposes as 1) physician-diagnosed EM of >5 cm in diameter or 2) at least one objective late manifestation (i.e. musculoskeletal, cardiovascular, or neurologic) with laboratory confirmation of infection with B. burgdorferi (18). Laboratory confirmation required 1) isolation of B. burgdorferi from clinical specimens, 2) demonstration of diagnostic levels of immunoglobulin M (IgM) and immunoglobulin G (IgG) antibodies to B. burgdorferi in serum or cerebrospinal fluid (CSF), or 3) significant change in IgM or IgG antibody response in paired serum samples. In 1997, CSTE and CDC implemented a revised surveillance case definition on the basis of the availability of improved serologic testing (20). Clinical criteria were not changed; however, laboratory confirmation was modified to require 1) isolation of B. burgdorferi from a clinical specimen or 2) demonstration of diagnostic levels of IgM or IgG antibodies to B. burgdorferi in serum or CSF. A two-test approach (a sensitive enzyme immunoassay or immunofluorescence antibody assay followed by Western blot) was recommended but not required (10).

Data Sources

U.S. state and territorial health departments report cases of Lyme disease voluntarily to CDC as part of the National Notifiable Disease Surveillance System (NNDSS). Provisional data are transmitted to CDC weekly using the National Electronic Telecommunications System for Surveillance, and final data are published annually in CDC’s Summary of Notifiable Diseases (available at http://www.cdc.gov/mmwr). State or local health departments are responsible for ensuring that cases reported to CDC meet the case definition.

This report is based on data for all Lyme disease cases reported to CDC for 1992–2006.^§ During this 15-year period, state health officials used various methods to ascertain cases, including provider-initiated passive surveillance, laboratory-based surveillance, and enhanced or active surveillance. Basic demographic data (e.g., age, sex, race, and county of residence) were available for >90% of reported cases; however, information specific to Lyme disease (e.g., county of exposure, symptoms and signs, antibiotic treatment, and laboratory results) was incomplete. For example, only 61% of case reports contained data for reported signs and symptoms.

Annual U.S.-, state-, county-, sex-, and age group–specific incidence rates per 100,000 population were calculated using U.S. Census Bureau population estimates for July 1 for each year of the reporting period (1992–2006). Analyses of symptom data were restricted to case reports for which at least one symptom was coded as “yes” (n = 150,829 records). Characteristics of cases reported from the 10 HP2010 reference states were compared with cases reported from all other (non-HP2010) states and territories.

ResultsU.S. Case Counts and Rates

During 1992–2006, a total of 248,074 Lyme disease cases were reported to CDC. Although annual counts fluctuated by as much as 57% from year to year, the overall trend indicates a steady increase in the number of reported cases (Figure 1). During the 15-year study period, the number of cases reported increased 101%, from 9,908 cases in 1992 to 19,931 cases in 2006.

State Rates

The 15-year mean annual rate for all states ranged from <0.01 cases per 100,000 population in Montana and Colorado to 73.6 cases per 100,000 population in Connecticut (median: 0.5 cases) (Table 1). The 10 HP2010 reference states accounted for 229,782 cases, representing 92.6% of overall cases and at least 88% of cases reported in any single year. Reported annual rates for seven HP2010 reference states (Maryland, Massachusetts, Minnesota, New Jersey, New York, Pennsylvania, and Wisconsin) were relatively stable during 1992–2006. Annual rates were more variable in three states (Connecticut, Delaware, and Rhode Island), in part because of changes in surveillance practices. In Connecticut, annual rates per 100,000 population increased from 53.7 cases in 1992 to 133.9 cases in 2002; in 2003, the rate decreased to 40.3 cases. In Delaware, the number of cases increased from 339 in 2004 to 646 in 2005, boosting the annual rate per 100,000 population from 40.9 to 76.7 cases. The annual rate per 100,000 population reported in Rhode Island increased from 27.5 cases in 1992 to 68.5 cases in 2003, then declined to 23.1 cases in 2004 and 3.6 cases in 2005; 28.9 cases were reported in 2006.

County Rates

County of residence was provided for 243,430 (98.1%) cases. The mean number of counties reporting at least one case of Lyme disease was 714 (range: 625–796). In all years, the percentage of counties reporting at least one case was >75 in six states (Connecticut, Delaware, Massachusetts, Maryland, New Jersey, and Rhode Island). In contrast, during 1992–2006, the percentage of counties reporting at least one case increased from 33% to 74% in Minnesota, from 79% to 97% in Pennsylvania, and from 76% to 97% in Wisconsin. In New York, the percentage of counties reporting at least one case ranged from 61% to 85%, with no obvious increasing or decreasing temporal trend.

The 15-year average county-specific rate for counties reporting at least one case during 1992–2006 ranged from <0.01 cases per 100,000 population in Honolulu County, Hawaii, to 595.1 cases per 100,000 population in Nantucket County, Massachusetts (median: 0.7 cases per 100,000 population) (Figure 2). Counties with the highest average county-specific rate for three 5-year periods during the 15-year reporting period (1992–1996, 1997–2001, and 2002–2006) are presented (Table 2). Five counties ranked among the top 10 incidence counties for each 5-year period: Windham County, Connecticut; Nantucket County, Massachusetts; Hunterdon County, New Jersey; Dutchess County, New York; and Putnam County, New York. The only counties outside the northeast to rank among the top 10 counties for any 5-year period were Washburn County and Burnett County, Wisconsin. Because of marked differences in population size across counties, a high rate does not necessarily indicate a substantial number of reported cases.

Selected Demographics

Information regarding age was available for 241,931 (97.5%) reported cases. Reported ages ranged from <1--106 years and were bimodal in distribution (Figure 3). Average annual rates peaked among children aged 5–9 years (8.6 cases per 100,000 population) and adults aged 55–59 years (7.8 cases per 100,000 population). The lowest rate was reported among adults aged 20–24 years (3.0 cases per 100,000 population).

Information about sex was available for 243,564 (99.1%) reported cases. Of these, 129,349 (53.1%) occurred among males, yielding an average annual rate per 100,000 population of 6.3 cases for males and 5.4 cases for females. During 1992–2006, rates increased disproportionately among males compared with females (Figure 4). This trend was most pronounced among persons aged 5–19 years; rates per 100,000 population in this age group increased 194% in males, from 3.5 cases in 1992 to 10.3 cases in 2006, and 114% in females, from 2.9 cases in 1992 to 6.2 cases in 2006.

Information regarding race was available for 166,194 (70.0%) reported cases. Of these, 156,346 (94.1%) patients were identified as white, 2,765 (1.7%) as black, 1,299 (0.8 %) as Asian/Pacific Islander, and 452 (0.3%) as American Indian/Alaska Native.

Age and sex of persons with Lyme disease differed among the 10 HP2010 reference states compared with other states. In the reference states, the modal age was 7 years, and males accounted for 120,369 (53.4%) reported cases. In the remaining states, the modal age was 44 years, and males accounted for 8,890 (49.4%) cases.

Seasonality

Month of disease onset was available for 188,340 (75.9%) reported cases (Figure 5). Although cases occurred in all months of the year; the majority (48,413 [25.7%]) of patients had onset in June, July (56,507 [30.0%]), or August (22,867 [12.1%]), the 3 months in which ticks actively seek mammalian hosts and human outdoor activity is greatest. In the HP2010 reference states, 99,762 (56.5%) cases had onset during June or July, compared with 5,518 (44.2%) among non-HP2010 reference states. Among 150,829 cases with reported clinical features, seasonal variation was most pronounced for cases with EM (Figure 6). Approximately 67% of patients with EM had onset in June and July, compared with 37% of those with arthritis.

Clinical Features

Information on clinical features of illness was available for 150,829 (60.8%) cases. Among these, EM was reported for 104,387 (69.2%) cases, arthritis characterized by brief attacks of joint swelling for 48,272 (32.0%) cases, neurologic symptoms (facial palsy or cranial neuritis, radiculoneuropathy, lymphocytic meningitis, encephalitis, or encephalomyelitis) for 18,157 (12.0%) cases, and second- or third-degree atrioventricular block for 1,222 (0.8%) cases. More than one clinical manifestation was reported for 19,321 (12.8%) cases. Data on clinical features of cases from all states was representative of data on clinical features of cases from the HP2010 reference states. By comparison, among 7,745 cases reported from non-HP2010 states, EM was reported less frequently (4,887 cases [63.0%]), and musculoskeletal, neurologic, and cardiac manifestations were reported more frequently (3,285 cases [42.4%], 1,442 cases [18.6%], and 100 cases [1.3%], respectively).

Temporal trends in national data indicate that the overall frequency of reported clinical features were generally stable over time (Figure 7). However, the frequency of reported symptoms was highly variable across the youngest age categories (Figure 8) and among HP2010 reference states (Table 3).

Discussion

During 1992–2006, the annual number of Lyme disease cases reported to CDC increased considerably, while remaining highly focused in northeastern and north-central states. Multiple reasons might explain this increase, including a true increase in the number of infections, enhanced surveillance, increased awareness among health-care professionals and the public, misdiagnosis, and reporting errors (21–23). In six HP2010 reference states (Connecticut, Delaware, Massachusetts, Maryland, New Jersey, and Rhode Island) in which the majority of counties regularly reported cases, a true increase in transmission might have resulted from greater tick densities and encroachment of human development into rural and suburban areas. In other HP2010 reference states, particularly Minnesota, Pennsylvania, and Wisconsin, the number of counties reporting cases increased appreciably, suggesting an additional role for geographic expansion of reservoir mammals and vector ticks into new areas. In certain states, especially those in the southeastern United States, Lyme disease surveillance is complicated by the occurrence of southern tick-associated rash illness, a condition that can resemble early Lyme disease but is not caused by B. burgdorferi (24–26).

Overall, features of reported cases changed little over time. Peak rates were reported among children, males, and whites in each year throughout the 15-year period. However, rates increased disproportionately among young males compared with young females; the reasons for this difference are not known. The proportion of cases with EM and arthritis, the most commonly reported symptoms, has been relatively stable since 1993. However, across age categories, the frequency of reported symptoms varied widely among persons aged <20 years, with the lowest percentage of EM (58.2%) and the highest percentage of arthritis (38.7%) reported for children aged 10--14 years. These findings provide a basis for targeting prevention campaigns to populations with increasing incidence.

The findings in this report highlight both the benefits of infectious disease surveillance and the opportunity for improvement. Detailed analysis of reported cases enables public health authorities to define the demographics and distribution of disease and to survey trends. However, growing case counts and the implementation of electronic laboratory reporting have created a substantial reporting burden on certain state and local health departments as they attempt to verify compliance with the surveillance case definition (27,28). This burden has caused certain states to curtail or modify portions of their surveillance system, resulting in fluctuations in case tallies. In 2007, CSTE revised the national surveillance case definition for Lyme disease with the twin goals of reducing the burden of reporting while potentially enhancing the system’s ability to capture a broader range of clinical manifestations. The revised case definition, which was implemented in January 2008, specifies required laboratory evidence in more detail than previous iterations and allows reporting of confirmed and, for the first time, probable cases of Lyme disease to CDC (29).

Limitations

The findings in this report are subject to at least three limitations. First, an unknown portion of all Lyme disease cases are reported; cases probably are underreported in areas in which the disease is endemic and overreported in areas in which the disease is not endemic. Misdiagnosis and overreporting from areas in which the disease is not endemic might explain the demographic differences noted between cases reported from HP2010 and non-HP2010 reference states. Second, variation in reporting practices and adherence to the surveillance case definition occurs among states, in part because states invest unequally in infrastructure for Lyme disease surveillance. As a result, Lyme disease–specific variables for cases reported by certain states are incomplete, unavailable, or not transmitted to CDC. Finally, cases are reported on the basis of the patient’s state of residence rather than on the state in which the exposure occurred. Therefore, Lyme disease in a traveler returning from an area in which the disease is highly endemic cannot be construed as evidence of local transmission.

Conclusion

The number of reported cases of Lyme disease continues to increase, underscoring the need for targeted prevention strategies, early disease recognition and treatment, and a sustainable surveillance system. During the 15-year study period, incidence increased disproportionately among children, particularly males. Geographic expansion was apparent in Minnesota, Pennsylvania, and Wisconsin. Differences in the features of cases reported from HP2010 reference states and all other states suggest either aberrant reporting or fundamental differences in the epidemiology of Lyme disease in areas in which the disease is not endemic. The percentage of cases for which signs of disseminated infection were reported did not decrease during the reporting period, underscoring the need for continued education about early disease recognition and treatment. Despite the limitations of national surveillance data, these findings are useful in defining demographics, distribution, and trends in Lyme disease cases. Intensive surveillance methodologies, such as active population-based surveillance and the use of nonhuman data (e.g., serologic testing of dogs and surveillance for vectors), could be used to augment these data and provide a better understanding of this emerging infectious disease.

Acknowledgments

The data provided in this report were collected and reported by state, territorial, and local health departments, health-care providers, and laboratories.

References

1. Steere AC, Malawista SE, Snydman DR, et al. Lyme arthritis: an epidemic of oligoarticular arthritis in children and adults in three Connecticut communities. Arthritis Rheum 1977;20:7–17.
2. Burgdorfer W, Barbour AG, Hayes SF, Benach JL, Grunwaldt E, Davis JP. Lyme disease—a tick-borne spirochetosis? Science 1982;216:1317–9.
3. Benach JL, Bosler EM, Hanrahan JP, et al. Spirochetes isolated from the blood of two patients with Lyme disease. N Engl J Med 1983;308:740–2.
4. Steere AC, Grodzicki RL, Kornblatt AN, et al. The spirochetal etiology of Lyme disease. N Engl J Med 1983;308:733–40.
5. Dennis DT, Piesman, JF. Overview of tick-borne infections in humans. In: Goodman JL, Dennis DT, Sonenshine DE, eds. Tick-borne infections of humans.Washington, DC: ASM Press; 2005.
6. Shapiro ED, Gerber MA. Lyme disease. Clin Infect Dis 2000;31:533–42.
7. Steere AC, Coburn J, Glickstein L. The emergence of Lyme disease. J Clin Invest 2004;113:1093–101.
8. Wormser GP, Dattwyler RJ, Shapiro ED, et al. The clinical assessment, treatment, and prevention of Lyme disease, human granulocytic anaplasmosis, and babesiosis: clinical practice guidelines by the Infectious Diseases Society of America. Clin Infect Dis 2006;43:1089–134.
9. American College of Physicians. Guidelines for laboratory evaluation in the diagnosis of Lyme disease. Ann Intern Med 1997;127:1106–8.
10. CDC. Recommendations for test performance and interpretation from the Second National Conference on Serologic Diagnosis of Lyme Disease. MMWR 1995;44:590–1.
11. Klempner MS, Schmid CH, Hu L, et al. Intralaboratory reliability of serologic and urine testing for Lyme disease. Am J Med 2001;110:217–9.
12. CDC. Notice to readers: caution regarding testing for Lyme disease. MMWR 2005;54:125.
13. Piesman J, Eisen L. Prevention of tick-borne diseases. Annu Rev Entomol 2008;53:323–43.
14. Ginsberg HS, Butler M, Zhioua E. Effect of deer exclusion by fencing on abundance of Amblyomma americanum (Acari: Ixodidae) on Fire Island, New York, USA. J Vector Ecol 2002;27:215–21.
15. des Vignes F, Piesman J, Heffernan R, Schulze TL, Stafford KC III, Fish D. Effect of tick removal on transmission of Borrelia burgdorferi and Ehrlichia phagocytophila by Ixodes scapularis nymphs. J Infect Dis 2001;183:773–8.
16. Piesman J, Dolan MC. Protection against Lyme disease spirochete transmission provided by prompt removal of nymphal Ixodes scapularis (Acari: Ixodidae). J Med Entomol 2002;39:509–12.
17. CDC. Lyme disease—United States, 1980. MMWR 1981;30:489–92, 497.
18. CDC. Case definitions for public health surveillance. MMWR 1990;39(No. RR-13).
19. US Department of Health and Human Services. Healthy people 2010 (conference ed, in 2 vols). Washington, DC: US Department of Health and Human Services; 2000. Available at http://www.health.gov/healthypeople.
20. CDC. Case definitions for infectious conditions under public health surveillance. MMWR 1997;46(No. RR-10).
21. Meek JI, Roberts CL, Smith EV Jr, Cartter ML. Underreporting of Lyme disease by Connecticut physicians, 1992. J Public Health Manag Pract 1996;2:61–5.
22. Rose CD, Fawcett PT, Gibney KM, Doughty RA. The overdiagnosis of Lyme disease in children residing in an endemic area. Clin Pediatr (Phila) 1994;33:663–8.
23. Steere AC, Taylor E, McHugh GL, Logigian EL. The overdiagnosis of Lyme disease. JAMA 1993;269:1812–6.
24. Campbell GL, Paul WS, Schriefer ME, Craven RB, Robbins KE, Dennis DT. Epidemiologic and diagnostic studies of patients with suspected early Lyme disease, Missouri, 1990–1993. J Infect Dis 1995;172:470–80.
25. Wormser GP, Masters E, Liveris D, et al. Microbiologic evaluation of patients from Missouri with erythema migrans. Clin Infect Dis 2005;40:423–8.
26. Wormser GP, Masters E, Nowakowski J, et al. Prospective clinical evaluation of patients from Missouri and New York with erythema migrans–like skin lesions. Clin Infect Dis 2005;41:958–65.
27. CDC. Effect of electronic laboratory reporting on the burden of Lyme disease surveillance—New Jersey, 2001–2006. MMWR 2008;57:42–5.
28. Kudish K, Sleavin W, Hathcock L. Lyme disease trends: Delaware, 2000–2004. Del Med J 2007;79:51–8.
29. Council of State and Territorial Epidemiologists. Position statement 07-ID-11: revised national surveillance case definition for Lyme disease. Atlanta, GA: Council of State and Territorial Epidemiologists; 2007. Available at http://www.cste.org/ps/2007ps/2007psfinal/id/07-id-11.pdf.

* The Lyme disease surveillance case definition was developed to standardize national public health surveillance and reporting of Lyme disease cases; it is not meant to be used as absolute criteria for clinical diagnosis.

Medical News Today, 10/2/08 (http://www.medicalnewstoday.com/articles/123817.php)

Teleflex Medical, a leading global supplier of disposable products for critical care and surgical applications, has received clearance from the FDA to market the Hudson RCI Neb-U-Mask®, a respiratory device that allows for the concurrent delivery of aerosolized medication and a high concentration of medical gases to treat acute asthma exacerbations.

Asthma is a chronic inflammatory disease of the airways. According to the National Asthma Education and Prevention Program, asthma affects more than 22 million people in the United States, and is one of the most chronic childhood diseases. It is estimated that asthma accounts for approximately 1 in every 250 deaths worldwide. Many of the deaths are preventable. Despite current available therapy with the use of bronchodilators and corticoids, alleviation of obstruction may not occur rapidly enough to prevent ventilatory failure and endotracheal intubation.

During an acute asthma attack, a patient may be given oxygen or heliox in combination with pharmacologic therapies. The challenge of this treatment approach is the lack of a device that allows for the simultaneous delivery of medical gases and aerosolized medication. In a study published in the Annals of Emergency Medicine in 2002, low oxygen saturation has been correlated inversely with the rate of hospitalization1, which puts caregivers in a difficult situation when faced with the choice of medication delivery over an interruption of high levels of oxygen therapy.

The Neb-U-Mask addresses this unmet clinical need by allowing the concurrent delivery of aerosolized medications and high concentrations of oxygen or heliox. The system is composed of an innovative wye design, featuring a nebulizer connection and MDI adaptor, a non-rebreathing mask with a 750ml gas reservoir bag, and color coded tubing. This patented design promotes positive patient outcomes by avoiding therapy interruption. The nebulizer connection features a valved port, which maintains a closed system when a nebulizer is not in use. This closed system design allows for delivery of high levels of oxygen or heliox gas mixtures.

“We are pleased to add the Neb-U-Mask to our extensive line of asthma management solutions,” said Whitney Reynolds, director of respiratory care marketing. “At Teleflex Medical our ultimate goal is to provide products and education programs to help patients with asthma live a normal, healthy, and productive life. But knowing that acute asthma attacks are prevalent, we must provide caregivers the tools they need to achieve positive patient outcomes.”

The system is available for sale today in both adult and pediatric versions. The system is conveniently packaged with a Micro Mist® nebulizer, allowing for a “grab and go” response in an emergency situation.

About Teleflex Medical

Headquartered in Research Triangle Park, North Carolina, Teleflex Medical is a leading global provider of medical products and solutions designed to help healthcare providers improve outcomes, reduce infection and improve patient and provider safety. A business segment of Teleflex Incorporated (NYSE: TFX), the company produces disposable medical products for critical care and surgical applications, surgical instruments and devices, cardiac devices and other specialty products for device manufacturers. The Teleflex Medical family of brands includes the trusted names of Hudson RCI®, Arrow®, Beere® Deknatel®, Gibeck®, KMedic®, Pilling®, Pleur-Evac®, Rüsch®, Sheridan®, SMD™, SSI™, Taut®, TFX OEM® and Weck®. http://www.teleflexmedical.com

Medical News Today, 10/2/08 (http://www.medicalnewstoday.com/articles/123778.php)

Janssen-Cilag Ltd today announced the launch of its new carbapenem antibiotic, Doribax™, for the treatment of complicated intra abdominal infections, as well as nosocomial pneumonia and ventilator associated pneumonia in adult patients. Doripenem is a broad-spectrum, I.V. antibiotic with activity against a wide range of Gram-positive and Gram-negative pathogens and was developed to meet a rapidly growing need for new antibiotics as hospital bacteria become increasingly resistant to existing antibiotic therapies.

Bacterial resistance against a wide range of antibiotics is on the increase in almost all European countries.1 Potentially life threatening infections caused by Gram-negative bacteria, such as Pseudomonas aeruginosa, are a particular problem as there are relatively limited antibiotic options available. Patients who acquire an infection in hospital are seven times more likely to die in hospital than uninfected patients2 and they currently cost the NHS an estimated £930 million per year.3

Dr David Livermore, Director of the Health Protection Agency’s Antibiotic Resistance Monitoring & Reference Laboratory (ARMRL) commented, ‘Carbapenems are powerful weapons against severe hospital infections and the development of new antibiotics in this class is critical to the fight against resistance – along with good infection control and appropriate use of all antibiotics, old and new.’

Doripenem belongs to a class of antibacterial agents called carbapenems, which are important for treating serious infections, and is active against both Gram-positive and Gram-negative bacteria. In a clinical trial in patients with ventilator associated pneumonia, doripenem was associated with a five day reduction in total length of hospital stay (p=0.01) and a three day reduction in mechanical ventilation (p=0.03) when compared to imipenem.4

Dr Robert Masterton, Consultant Microbiologist, at Crosshouse Hospital, Kilmarnock, said ‘In an era when no new classes of antibiotics active against difficult to treat Gram-negative pathogens are available, doripenem is a development within an existing group of antibiotics – the carbapenems – which presents clinicians with potential useful advantages over the existing drugs of this type. These benefits promise to deliver real patient benefits, particularly in severe sepsis, which are to be welcomed and so will help maintain our armoury of weapons against such pathogens.’

Doripenem is the first product from Janssen-Cilag’s antibiotic pipeline to be launched and represents a significant commitment to the investment in and development of novel antibiotics.

Dr Peter Barnes, Medical Director for Janssen-Cilag commented; ‘Healthcare professionals have highlighted a critical need for the development of new antibiotics. The development of novel antibiotics, such as doripenem, will help to tackle the growing problem of microbial resistance.’

References

1. European Antimicrobial Resistance Surveillance System, EARSS Annual Report 2005, October 2006.

2. Department of Public Health & Policy, London School of Hygiene & Tropical Medicine, Research Briefing: Hospital acquired infections.

3. Plowman R et al. The rate and cost of hospital acquired infections occurring in patients admitted to selected specialties of a district general hospital in England and the national burden imposed. Journal of hospital infection. 2001; 47:198-209

4. Merchant S et al. Hospital resource utilization with Doripenem versus Imipenem in the treatment of ventilator-associated pneumonia. Clinical Therapeutics. 2008; 30(4): 717-733.

5. Doribax Summary of Product Characteristics (2008)

- Doripenem is licensed in the UK for the treatment of serious hospital acquired infections including nosocomial and ventilator associated pneumonia, complicated urinary tract infections and complicated intra abdominal infections.5

- The recommended dose for doripenem is 500 mg administered every 8 hours by IV infusion over 1 hour, or as a 4 hour infusion for more serious infections.

- In clinical trials doripenem was generally well tolerated.