Severe Pulmonary Disease Associated with Electronic-Cigarette-Product Use - Interim Guidance.

On September 6, 2019, this report was posted as an MMWR Early Release on the MMWR website (https://www.cdc.gov/mmwr). As of August 27, 2019, 215 possible cases of severe pulmonary disease associated with the use of electronic cigarette (e-cigarette) products (e.g., devices, liquids, refill pods, and cartridges) had been reported to CDC by 25 state health departments. E-cigarettes are devices that produce an aerosol by heating a liquid containing various chemicals, including nicotine, flavorings, and other additives (e.g., propellants, solvents, and oils). Users inhale the aerosol, including any additives, into their lungs. Aerosols produced by e-cigarettes can contain harmful or potentially harmful substances, including heavy metals such as lead, volatile organic compounds, ultrafine particles, cancer-causing chemicals, or other agents such as chemicals used for cleaning the device (1). E-cigarettes also can be used to deliver tetrahydrocannabinol (THC), the principal psychoactive component of cannabis, or other drugs; for example, "dabbing" involves superheating substances that contain high concentrations of THC and other plant compounds (e.g., cannabidiol) with the intent of inhaling the aerosol. E-cigarette users could potentially add other substances to the devices. This report summarizes available information and provides interim case definitions and guidance for reporting possible cases of severe pulmonary disease. The guidance in this report reflects data available as of September 6, 2019; guidance will be updated as additional information becomes available.

Notes from the Field: Cardiac Dysrhythmias After Loperamide Abuse - New York, 2008-2016.

Loperamide is an over-the-counter antidiarrheal with opioid-receptor agonist properties. Recommended over-the-counter doses (range = 2-8 mg daily) do not produce opioid effects in the central nervous system because of poor oral bioavailability and P-glycoprotein efflux* of the medication (1); recent reports suggest that large doses (50-300 mg) of loperamide produce euphoria, central nervous system depression, and cardiotoxicity (2-4). Abuse of loperamide for its euphoric effect or for self-treatment of opioid withdrawal is increasing (5). Cases of loperamide abuse reported to the Upstate New York Poison Center and New York City Poison Control Center were analyzed for demographic, exposure, clinical, and laboratory characteristics. Cases of intentional loperamide abuse reported to the National Poison Database System (NPDS) also were analyzed for demographic, dose, formulation, and outcome information.

Notes from the field: calls to poison centers for exposures to electronic cigarettes--United States, September 2010-February 2014.

Electronic nicotine delivery devices such as electronic cigarettes (e-cigarettes) are battery-powered devices that deliver nicotine, flavorings (e.g., fruit, mint, and chocolate), and other chemicals via an inhaled aerosol. E-cigarettes that are marketed without a therapeutic claim by the product manufacturer are currently not regulated by the Food and Drug Administration (FDA). In many states, there are no restrictions on the sale of e-cigarettes to minors. Although e-cigarette use is increasing among U.S. adolescents and adults, its overall impact on public health remains unclear. One area of concern is the potential of e-cigarettes to cause acute nicotine toxicity. To assess the frequency of exposures to e-cigarettes and characterize the reported adverse health effects associated with e-cigarettes, CDC analyzed data on calls to U.S. poison centers (PCs) about human exposures to e-cigarettes (exposure calls) for the period September 2010 (when new, unique codes were added specifically for capturing e-cigarette calls) through February 2014. To provide a comparison to a conventional product with known toxicity, the number and characteristics of e-cigarette exposure calls were compared with those of conventional tobacco cigarette exposure calls.

Clinical, laboratory, diagnostic, and histopathologic features of diethylene glycol poisoning--Panama, 2006.

STUDY OBJECTIVE: Diethylene glycol is a toxic industrial solvent responsible for more than 13 mass poisonings since 1937. Little is known about the clinical spectrum, progression, and neurotoxic potential of diethylene glycol-associated disease because of its high mortality and the absence of detailed information in published mass poisoning reports. This incident includes the largest proportion of cases with neurotoxic signs and symptoms. We characterize the features of a diethylene glycol mass poisoning resulting from a contaminated cough syrup distributed in Panama during 2006. METHODS: This was a retrospective chart review and descriptive analysis in a tertiary level, urban health care facility. A case was a person admitted to the Social Security Metropolitan Hospital in Panama City between June 1 and October 22, 2006, with unexplained acute kidney injury and a serum creatinine level of greater than or equal to 2 mg/dL, or unexplained chronic renal failure exacerbation (>2-fold increase in baseline serum creatinine level) and history of implicated cough syrup exposure. Main outcomes and measures were demographic, clinical, laboratory, diagnostic, histopathologic, and mortality data with descriptive statistics. RESULTS: Forty-six patients met inclusion criteria. Twenty-four (52%) were female patients; median age was 67 years (range 25 to 91 years). Patients were admitted with acute kidney injury or a chronic renal failure exacerbation (median serum creatinine level 10.0 mg/dL) a median of 5 days after symptom onset. Forty patients (87%; 95% confidence interval [CI] 74% to 95%) had neurologic signs, including limb (n=31; 77%; 95% CI 62% to 89%) or facial motor weakness (n=27; 68%; 95% CI 51% to 81%). Electrodiagnostics in 21 patients with objective weakness demonstrated a severe sensorimotor peripheral neuropathy (n=19; 90%; 95% CI 70% to 99%). In 14 patients without initial neurologic findings, elevated cerebrospinal fluid protein concentrations without pleocytosis were observed: almost all developed overt neurologic illness (n=13; 93%; 95% CI 66% to 100%). Despite use of intensive care and hemodialysis therapies, 27 (59%) died a median of 19 days (range 2 to 50 days) after presentation. CONCLUSION: A high proportion of patients with diethylene glycol poisoning developed progressive neurologic signs and symptoms in addition to acute kidney injury. Facial or limb weakness with unexplained acute kidney injury should prompt clinicians to consider diethylene glycol poisoning. Elevated cerebrospinal fluid protein concentrations without pleocytosis among diethylene glycol-exposed persons with acute kidney injury may be a predictor for progressive neurologic illness.

Passive multistate surveillance for neutropenia after use of cocaine or heroin possibly contaminated with levamisole.

STUDY OBJECTIVE: To characterize the demographic, clinical, and epidemiologic features of levamisole-associated neutropenia in cocaine or heroin users. METHODS: State health departments were recruited for participation when the Centers for Disease Control and Prevention (CDC) was notified of potential cases by a clinician, a health department official, or a poison center between October 15, 2009, and May 31, 2010. A case was defined as a person with an absolute neutrophil count less than 1,000 cells/µL (or a WBC count <2,000 cells/µL) and a self-reported history or laboratory confirmation of cocaine or heroin use. Health department officials abstracted data from medical charts, attempted a patient interview, and submitted data to CDC for descriptive analysis. RESULTS: Of the 46 potential cases reported from 6 states, half met eligibility criteria and had medical chart abstractions completed (n=23; 50%). Of these, close to half of the patients were interviewed (n=10; 43%). The average age was 44.4 years; just over half were men (n=12; 52%). The majority of patients presented to emergency departments (n=19; 83%). More than half presented with infectious illnesses (n=12; 52%), and nearly half reported active skin lesions (n=10; 44%). The majority of interview respondents used cocaine greater than 2 to 3 times a week (n=9; 90%), used cocaine more than 2 years (n=6; 60%), and preferred crack cocaine (n=6; 60%). All were unaware of exposure to levamisole through cocaine and of levamisole's inherent toxicity (n=10; 100%). CONCLUSION: Physicians should suspect levamisole exposure in patients using illicit drugs, cocaine in particular, who present with unexplained neutropenia. Most patients reported chronic cocaine use and were unaware of levamisole exposure. Cocaine use is more prevalent among men; however, our results identified a higher-than-expected proportion of female users with neutropenia, suggesting women may be at higher risk. Emergency physicians and practitioners are uniquely positioned to recognize these patients early during their hospital course, elucidate a history of cocaine or other drug exposure, and optimize the likelihood of confirming exposure by arranging for appropriate drug testing.

Multidrug-resistant typhoid fever with neurologic findings on the Malawi-Mozambique border.

BACKGROUND: Salmonella enterica serovar Typhi causes an estimated 22 million cases of typhoid fever and 216 000 deaths annually worldwide. We investigated an outbreak of unexplained febrile illnesses with neurologic findings, determined to be typhoid fever, along the Malawi-Mozambique border. METHODS: The investigation included active surveillance, interviews, examinations of ill and convalescent persons, medical chart reviews, and laboratory testing. Classification as a suspected case required fever and ≥1 other finding (eg, headache or abdominal pain); a probable case required fever and a positive rapid immunoglobulin M antibody test for typhoid (TUBEX TF); a confirmed case required isolation of Salmonella Typhi from blood or stool. Isolates underwent antimicrobial susceptibility testing and subtyping by pulsed-field gel electrophoresis (PFGE). RESULTS: We identified 303 cases from 18 villages with onset during March-November 2009; 214 were suspected, 43 were probable, and 46 were confirmed cases. Forty patients presented with focal neurologic abnormalities, including a constellation of upper motor neuron signs (n = 19), ataxia (n = 22), and parkinsonism (n = 8). Eleven patients died. All 42 isolates tested were resistant to ampicillin, chloramphenicol, and trimethoprim-sulfamethoxazole; 4 were also resistant to nalidixic acid. Thirty-five of 42 isolates were indistinguishable by PFGE. CONCLUSIONS: The unusual neurologic manifestations posed a diagnostic challenge that was resolved through rapid typhoid antibody testing in the field and subsequent blood culture confirmation in the Malawi national reference laboratory. Extending laboratory diagnostic capacity, including blood culture, to populations at risk for typhoid fever in Africa will improve outbreak detection, response, and clinical treatment.

Drugs and Drug Classes Involved in Overdose Deaths Among Females, United States: 1999-2017.

Background: Drug overdose deaths among U.S. women have risen steadily from 1999 to 2017, especially among certain ages. Various studies report involvement of drugs and drug classes in overdose deaths. Less is known, however, regarding the combinations that are most often indicated on death certificates, particularly among females. Analyzing mutually, exclusive drug/drug class combinations listed on death certificates of females are the objective of this study. Materials and Methods: Mortality data for U.S. female residents were obtained from the 1999 to 2017 National Vital Statistics System (n = 260,782). Analyses included deaths with an underlying cause of death based on International Classification of Diseases, 10th Revision (ICD-10) codes for drug overdoses. The drug/drug class involved included individual 4-digit ICD-10 codes in the range T36.0-T50.9, including poisoning deaths due to all drugs, excluding alcohol. Years from 1999 to 2017 were grouped in six 3-year categories with the most recent year (2017) left separate for analysis. All drug overdose deaths were analyzed in mutually exclusive categories. Results: From 1999 to 2017, the top-listed drug/drug class overall and by year grouping was solely "other and unspecified drugs, medicaments and biological substances"; however, that listing dropped from 25.8% from the 1999 to 2001 period to 14.1% in 2017. Overall, the next most frequent single drug/drug class mentions were "natural and semisynthetic opioids" (20,951; 8.0%) and "cocaine" (10,882; 4.2%). Two of the top five drug/drug class combinations included benzodiazepines ("natural and semisynthetic opioids"/"benzodiazepines" and "methadone"/"benzodiazepines"). Conclusions: Analyzing trends in drugs and drug classes involved in female drug overdose deaths is a critical foundation for developing gender-responsive public health interventions. Reducing high-risk drug use by improving prescribing practices, preventing drug use initiation, and addressing use of multiple drugs can help prevent overdose deaths.

Organizational and command aspects for coordinating the public health response to an outbreak of acute renal failure, Republic of Panama, 2006.

The Ministry of Health of Panama (MINSA) received several reports of ill persons who had clinical presentations of acute renal insufficiency or failure during September and October 2006. On 01 October 2006, the MINSA formally asked the Pan-American Health Organization (PAHO) and the US Centers for Disease Control and Prevention (CDC) to assist with the investigation. Additional agencies involved in the response included the US Food and Drug Administration (FDA), the Gorgas Institute for Health Studies (GIHS), and the Social Security Health System (SSHS) of Panama. Through a joint effort, the MINSA, CDC, FDA, GIHS, SSHS, and PAHO were able to characterize the illness, identify the etiological agent, identify the population-at-risk, and launch an unprecedented media and social mobilization effort to prevent additional cases.International outbreak responses may require familiarity with basic emergency management principles beyond technical or scientific considerations. The management, logistical capabilities, team interaction, and efficiency of outbreak investigations can be enhanced substantially by having staff already familiar with common operational frameworks for incident responses. This report describes the inter-agency coordination and organizational structure implemented during an international response to identify the cause of an outbreak of acute renal failure in Panama.

Characteristics and correlates of U.S. clinicians prescribing buprenorphine for opioid use disorder treatment using expanded authorities during the COVID-19 pandemic.

BACKGROUND: To determine how clinicians with a DATA waiver to prescribe buprenorphine for opioid use disorder (OUD) adapted during the COVID-19 pandemic to emergency authorities, including use of telehealth to prescribe buprenorphine, the challenges faced by clinicians, and strategies employed by them to manage patients with OUD. METHODS: From June 23, 2020 to August 19, 2020, we conducted an electronic survey of U.S. DATA-waivered clinicians. Descriptive statistics and multivariable logistic regression were used for analysis. RESULTS: Among 10,238 respondents, 68 % were physicians, 25 % nursing-related providers, and 6% physician assistants; 28 % reported never prescribing or not prescribing in the 12 months prior to the survey. Among the 72 % of clinicians who reported past 12-month buprenorphine prescribing (i.e. active practitioners during the pandemic) 30 % reported their practice setting closed to in-person visits during COVID-19; 33 % reported remote prescribing to new patients without an in-person examination. The strongest predictors of remote buprenorphine prescribing to new patients were prescribing buprenorphine to larger numbers of patients in an average month in the past year and closure of the practice setting during the pandemic; previous experience with remote prescribing to established patients prior to COVID-19 also was a significant predictor. Among clinicians prescribing to new patients without an in-person examination, 5.5 % reported difficulties with buprenorphine induction, most commonly withdrawal symptoms. CONCLUSIONS: Telehealth practices and prescribing to new patients without an in-person examination were adopted by DATA-waivered clinicians during the first six months of COVID-19. Permanent adoption of these authorities may enable expanded access to buprenorphine treatment.

Medication-associated diethylene glycol mass poisoning: a review and discussion on the origin of contamination.

Diethylene glycol (DEG), an extremely toxic chemical, has been implicated as the etiologic agent in at least 12 medication-associated mass poisonings over the last 70 years. Why DEG mass poisonings occur remains unclear. Most reports do not contain detailed reports of trace-back investigations into the etiology. The authors, therefore, conducted a systematic literature review on potential etiologies of these mass poisonings. The current available evidence suggests that substitution of DEG or DEG-containing compounds for pharmaceutical ingredients results from: (1) deception as to the true nature of certain ingredients by persons at some point in the pharmaceutical manufacturing process, and (2) failure to adhere to standardized quality control procedures in manufacturing pharmaceutical products intended for consumers. We discuss existing guidelines and new recommendations for prevention of these incidents.

Severe illness associated with reported use of synthetic cannabinoids: a public health investigation (Mississippi, 2015).

STUDY OBJECTIVES: In April 2015, a multistate outbreak of illness linked to synthetic cannabinoid (SC) use was unprecedented in magnitude and severity. We identified Mississippi cases in near-real time, collected information on cases to characterize the outbreak, and identified the causative SC. METHODS: A case was defined as any patient of a Mississippi healthcare facility who was suspected of SC use and presenting with ≥2 of the following symptoms: sweating, severe agitation, or psychosis during April 2-May 3, 2015. Clinicians reported cases to the Mississippi Poison Control Center (MPCC). We used MPCC data to identify cases at the University of Mississippi Medical Center (UMMC) to characterize in further detail, including demographics and clinical findings. Biologic samples were tested for known and unknown SCs by liquid chromatography quadrupole time-of-flight mass spectrometry (LC-QTOF/MS). RESULTS: Clinicians reported 721 cases (11 deaths) statewide; 119 (17%) were UMMC patients with detailed data for further analysis. Twelve (10%) were admitted to an intensive care unit and 2 (2%) died. Aggression (32%), hypertension (33%), and tachycardia (42%) were common. SCs were identified in serum from 39/56 patients (70%); 33/39 patients (85%) tested positive for MAB-CHMINACA (N-(1-amino-3,3-dimethyl-1-oxobutan-2-yl)-1-(cyclohexylmethyl)-1H-indazole-3-carboxamide) or its metabolites. Compared to all patients tested for SCs, those positive for MAB-CHMINACA were more likely to have altered mental status on examination (OR = 3.3, p = .05). CONCLUSION: SC use can cause severe health effects. MAB-CHMINACA was the most commonly detected SC in this outbreak. As new SCs are created, new strategies to optimize surveillance and patient care are needed to address this evolving public health threat.

Outbreak of acute renal failure in Panama in 2006: a case-control study.

OBJECTIVE: In September 2006, a Panamanian physician reported an unusual number of patients with unexplained acute renal failure frequently accompanied by severe neurological dysfunction. Twelve (57%) of 21 patients had died of the illness. This paper describes the investigation into the cause of the illness and the source of the outbreak. METHODS: Case-control and laboratory investigations were implemented. Case patients (with acute renal failure of unknown etiology and serum creatinine > 2 mg/dl) were individually matched to hospitalized controls for age (+/- 5 years), sex and admission date (< 2 days before the case patient). Questionnaire and biological data were collected. The main outcome measure was the odds of ingesting prescription cough syrup in cases and controls. FINDINGS: Forty-two case patients and 140 control patients participated. The median age of cases was 68 years (range: 25-91 years); 64% were male. After controlling for pre-existing hypertension and renal disease and the use of angiotensin-converting enzyme inhibitors, a significant association was found between ingestion of prescription cough syrup and illness onset (adjusted odds ratio: 31.0, 95% confidence interval: 6.93-138). Laboratory analyses confirmed the presence of diethylene glycol (DEG) in biological samples from case patients, 8% DEG contamination in cough syrup samples and 22% contamination in the glycerin used to prepare the cough syrup. CONCLUSION: The source of the outbreak was DEG-contaminated cough syrup. This investigation led to the recall of approximately 60 000 bottles of contaminated cough syrup, widespread screening of potentially exposed consumers and treatment of over 100 affected patients.

Public health investigation after the discovery of ricin in a South Carolina postal facility.

OBJECTIVES: In October 2003, a package containing ricin and a note threatening to poison water supplies was discovered in a South Carolina postal facility, becoming the first potential chemical terrorism event involving ricin in the United States. We examined the comprehensive public health investigation that followed and discuss the lessons learned from it. METHODS: An investigation consisting primarily of environmental sampling for ricin contamination, performance of health assessments on affected personnel, and local, regional, and national surveillance for ricin-associated illness. RESULTS: Laboratory analysis of 75 environmental sampling specimens revealed no ricin contamination. Health assessments of 36 affected employees were completed. Local surveillance initially identified 3 suspected cases, and national surveillance identified 399 outliers during the 2-week period after the incident. No confirmed cases of ricin-associated illness were identified. CONCLUSIONS: A multifaceted and multidisciplinary approach is required for an effective public health response to a chemical threat such as ricin. The results of all of the described activities were used to determine that the facility was safe to reopen and that no public health threat existed.

Identification and quantification of diethylene glycol in pharmaceuticals implicated in poisoning epidemics: an historical laboratory perspective.

Over the last several decades, mass poisonings of diethylene glycol (DEG), usually ingested as an unintended component of pharmaceutical preparations, have occurred. In order to promptly halt the rise in deaths due to ingestion of these pharmaceuticals, laboratory analysis has often been employed to identify and quantify the etiologic agent after the medications have been tentatively implicated. Over the past 15 years, the Centers for Disease Control and Prevention has been involved in identifying DEG in implicated pharmaceutical products during three poisoning epidemics that occurred in Nigeria (1990), Haiti (1995), and, most recently, in Panama (2006). In each case, the timeliness of the identification was paramount in reducing the mortality involved in these mass poisonings. Using state-of-the-art analytical technology, we were able to provide initial identification of DEG within 24 h of receiving samples for each epidemic, allowing a timely public health response. However, over the past 15 years, the analytical instrumentation available and the laboratory responses undertaken have changed. In addition, the type of information and the degree of confirmation of results requested during each epidemic varied based upon the number of individuals involved and the political tenor involved with the outbreak. We describe our historical approach to identifying and quantifying DEG during each of these outbreaks. Furthermore, the reoccurrence of outbreaks has prompted us to establish standard technology to use in potential future outbreaks to allow an even more timely response. This methodology includes the development of biomarkers of DEG exposure, which would be extremely useful in instances where pharmaceuticals are not clearly implicated.

Bongkrekic Acid-a Review of a Lesser-Known Mitochondrial Toxin.

INTRODUCTION: Bongkrekic acid (BA) has a unique mechanism of toxicity among the mitochondrial toxins: it inhibits adenine nucleotide translocase (ANT) rather than the electron transport chain. Bongkrekic acid is produced by the bacterium Burkholderia gladioli pathovar cocovenenans (B. cocovenenans) which has been implicated in outbreaks of food-borne illness involving coconut- and corn-based products in Indonesia and China. Our objective was to summarize what is known about the epidemiology, exposure sources, toxicokinetics, pathophysiology, clinical presentation, and diagnosis and treatment of human BA poisoning. METHODS: We searched MEDLINE (1946 to present), EMBASE (1947 to present), SCOPUS, The Indonesia Publication Index ( http://id.portalgaruda.org/ ), ToxNet, book chapters, Google searches, Pro-MED alerts, and references from previously published journal articles. We identified a total of 109 references which were reviewed. Of those, 29 (26 %) had relevant information and were included. Bongkrekic acid is a heat-stable, highly unsaturated tricarboxylic fatty acid with a molecular weight of 486 kDa. Outbreaks have been reported from Indonesia, China, and more recently in Mozambique. Very little is known about the toxicokinetics of BA. Bongkrekic acid produces its toxic effects by inhibiting mitochondrial (ANT). ANT can also alter cellular apoptosis. Signs and symptoms in humans are similar to the clinical findings from other mitochondrial poisons, but they vary in severity and time course. Management of patients is symptomatic and supportive. CONCLUSIONS: Bongkrekic acid is a mitochondrial ANT toxin and is reported primarily in outbreaks of food-borne poisoning involving coconut and corn. It should be considered in outbreaks of food-borne illness when signs and symptoms manifest involving the liver, brain, and kidneys and when coconut- or corn-based foods are implicated.

Association of acute toxic encephalopathy with litchi consumption in an outbreak in Muzaffarpur, India, 2014: a case-control study.

BACKGROUND: Outbreaks of unexplained illness frequently remain under-investigated. In India, outbreaks of an acute neurological illness with high mortality among children occur annually in Muzaffarpur, the country's largest litchi cultivation region. In 2014, we aimed to investigate the cause and risk factors for this illness. METHODS: In this hospital-based surveillance and nested age-matched case-control study, we did laboratory investigations to assess potential infectious and non-infectious causes of this acute neurological illness. Cases were children aged 15 years or younger who were admitted to two hospitals in Muzaffarpur with new-onset seizures or altered sensorium. Age-matched controls were residents of Muzaffarpur who were admitted to the same two hospitals for a non-neurologic illness within seven days of the date of admission of the case. Clinical specimens (blood, cerebrospinal fluid, and urine) and environmental specimens (litchis) were tested for evidence of infectious pathogens, pesticides, toxic metals, and other non-infectious causes, including presence of hypoglycin A or methylenecyclopropylglycine (MCPG), naturally-occurring fruit-based toxins that cause hypoglycaemia and metabolic derangement. Matched and unmatched (controlling for age) bivariate analyses were done and risk factors for illness were expressed as matched odds ratios and odds ratios (unmatched analyses). FINDINGS: Between May 26, and July 17, 2014, 390 patients meeting the case definition were admitted to the two referral hospitals in Muzaffarpur, of whom 122 (31%) died. On admission, 204 (62%) of 327 had blood glucose concentration of 70 mg/dL or less. 104 cases were compared with 104 age-matched hospital controls. Litchi consumption (matched odds ratio [mOR] 9·6 [95% CI 3·6 - 24]) and absence of an evening meal (2·2 [1·2-4·3]) in the 24 h preceding illness onset were associated with illness. The absence of an evening meal significantly modified the effect of eating litchis on illness (odds ratio [OR] 7·8 [95% CI 3·3-18·8], without evening meal; OR 3·6 [1·1-11·1] with an evening meal). Tests for infectious agents and pesticides were negative. Metabolites of hypoglycin A, MCPG, or both were detected in 48 [66%] of 73 urine specimens from case-patients and none from 15 controls; 72 (90%) of 80 case-patient specimens had abnormal plasma acylcarnitine profiles, consistent with severe disruption of fatty acid metabolism. In 36 litchi arils tested from Muzaffarpur, hypoglycin A concentrations ranged from 12·4 µg/g to 152·0 µg/g and MCPG ranged from 44·9 µg/g to 220·0 µg/g. INTERPRETATION: Our investigation suggests an outbreak of acute encephalopathy in Muzaffarpur associated with both hypoglycin A and MCPG toxicity. To prevent illness and reduce mortality in the region, we recommended minimising litchi consumption, ensuring receipt of an evening meal and implementing rapid glucose correction for suspected illness. A comprehensive investigative approach in Muzaffarpur led to timely public health recommendations, underscoring the importance of using systematic methods in other unexplained illness outbreaks. FUNDING: US Centers for Disease Control and Prevention.

Case definitions for chemical poisoning.

When human illness results from an unintentional or intentional release of a toxin (chemicals produced by metabolism in an organism [e.g., ricin]) or a toxicant (natural or synthetic chemicals not metabolically produced by an organism [e.g., nerve agents]) into the environment, uniform reporting is necessary to direct appropriate resources, assess the extent of morbidity and mortality, track poisoned persons, and monitor response to intervention. In this report, CDC presents case definitions to facilitate uniform reporting among local, state, and federal public health agencies of illness resulting from a chemical release. The report also explains the rationale for the structure of the case definitions, the audience for whom it is intended, the setting in which the case definitions might be used, and reasons each chemical presented in the report was selected. Clinical knowledge and diagnostic tools (e.g., biologic laboratory tests) for detecting chemical poisoning are likely to improve over time. CDC will create new case definitions and revise existing definitions to meet the needs related to emerging threats and to enhance case definition sensitivity and specificity, when possible, with developing clinical information.

Recognition of illness associated with covert chemical releases.

Public health threats from intentional releases of chemicals into the environment (ie, chemical terrorism) are an increasing concern in the United States. Recent situations of deliberate contamination of food and beverages with chemicals highlight the need for health care providers and public health officials to be alert for adult and pediatric patients in their communities who have signs and symptoms consistent with chemical exposures. In an effort to increase knowledge of surveillance and preparedness for illness related to potential chemical releases, we provide guidance to health care providers and public health personnel for recognizing illnesses or patterns of illnesses that might be associated with the intentional, covert release of chemical agents. In this article, we will discuss 5 examples of outbreaks of illnesses after a covert chemical release, obstacles to recognition of these illnesses, clues (ie, epidemiological patterns and syndromic presentations) that might enhance the recognition of illnesses from a covert chemical release, and public health strategies to enhance the rapid identification of a chemical terrorism event.

Strategies for recognizing acute chemical-associated foodborne illness.

The U.S. food supply is vulnerable to contamination with chemicals and toxins. Public health officials and clinicians may misdiagnose patients with acute chemical-associated foodborne illness (CAFI) due to unfamiliarity with chemical illness, increased familiarity with infectious foodborne illness, nonspecific presentation of most foodborne chemical poisoning, lack of readily available analytic methodologies to detect chemicals, and lack of education on how to develop a differential diagnosis for CAFI. This article will review the unique features of CAFI in the acute setting, address important questions to help differentiate CAFI from other foodborne illness, discuss laboratory features of CAFI, and provide health officials and clinicians with a clinical symptom-based approach to assist with proper identification and differentiation of acute CAFI.