Low Birth Weight - Continued

The overall proportion of LBW infants born in Asia has slightly decreased, but in Middle South Asia, where the problem is most acute, there is no evidence of change. Rates in this region remain between 20% and 50%. The marked change in Western South Asia is largely due to new data relating to countries, notably Turkey, for which no information was found previously. The most notable changes in Eastern South Asia are in Singapore (a marked decrease) and Thailand. The estimate for the latter country is based on government data for all institutional births (which comprise 36% of all births). The propotion of LBW infants in East Asia remains very low.

In Latin America, there is evidence of improvement in many countries, with rates in the south approaching those of developed countries. Data from countries whose governments publish national rates-Cuba, Panama, Uruguay, and Venezuela-all show a downward trend.

In Europe as a whole, the incidence of LBW has decreased from 7.7% to 6.5%, although this may be partly an artifact resulting from the availability of better information from Italy.

TABLE 1. Estimated number of births of all live infants and of low-birth-weight infants, by region, 1982, and estimated proportion of low-birth-weight infants, 1979 and 1982 Low-birth-weight infants

of error.

*Decimals are only shown for continents, since estimates for subregions are subject to a greater margin

§Previous estimate for Middle America corrected.

Sources:

United Nations, Department of International Economic and Social Affairs. Demographic indicators of countries: estimates and projects as assessed in 1980. New York, 1982.

Low Birth Weight - Continued

Some improvements are noted in Western and Northern Europe, but very little change took place in countries where the rates were already below 5% in 1979, nor is there any evidence of significant changes in Eastern Europe.

There are slight improvements in the rates for both Canada and the United States. Reported by WHO Weekly Epidemiological Record 1984:59;205-12.

Reference

1. World Health Organization. World Health Statistics Quarterly. 1980;33:197-224.

Notice to Readers

Availability of NIOSH Manual of Analytical Methods, Third Edition

The National Institute for Occupational Safety and Health (NIOSH) has announced that volumes 1 and 2 of the NIOSH Manual of Analytical Methods, Third Edition, are now available; a third volume is planned for 1985. This manual is the primary source of analytical methods cited in Criteria Documents, Current Intelligence Bulletins, and reports produced by NIOSH of health-hazard evaluations, industry-wide studies, and control-technology assessments.

The manual was first published in 1974 in loose-leaf form and contained 39 methods for analyzing 130 substances found in air and biologic samples; the 1974 manual was reprinted four times. From 1974 through 1979, the joint NIOSH/Occupational Safety and Health Administration (OSHA) Standards Completion Program established performance criteria and validated over 300 existing and new analytical methods (1,2). The seven-volume Second Edition was published during 1977-1981 (3). The Second Edition included methods contained in the First Edition, the new methods validated by the joint NIOSH/OSHA Program, and additional methods developed by NIOSH. Its 3,700 pages include 510 analytical methods for monitoring chemical exposures in the workplace. An estimated 6,000 copies are now in use.

NIOSH began work on the Third Edition in 1983. The major goals were to incorporate new data and analytic technology evaluated by NIOSH or used by NIOSH or contracting laboratories and to reduce the size of the manual by using a more concise format.

More than 60 chemists and industrial hygienists participated in the revision. Analytical methods were included for substances that: (1) are found frequently in field samples sent to NIOSH for analysis; (2) are referred to in NIOSH Criteria Documents or OSHA regulations; and (3) have a "high toxicity/exposure index," as determined from the known toxicity of the substance and the number of workers potentially exposed to it (4).

Discussion of each method begins with a summary, followed by a list of the reagents and equipment needed, special safety precautions, and instructions for taking and handling samples. Three indexes are included for cross reference: (1) method numbers used in the Third Edition; (2) method numbers used in the Second Edition; and (3) names and synonyms of the substance. A section on applicability helps users of the manual choose the most appropriate methods for their purposes. Chapters on the development and evaluation of methods, quality assurance, air sampling techniques, and biologic samples are included to expand on the protocols used by NIOSH to develop and apply the methods.

The NIOSH Manual of Analytical Methods, Third Edition, is available from the U.S. Government Printing Office, Washington, D.C. 20402, under a subscription service that includes the basic manual and all annual supplements through 1987. The manual is also available from the Superintendent of Documents for $31.00 (U.S. orders) or $38.75 (outside the United States). Questions and suggestions for improving the manual should be sent to: Manual Coordinator, NIOSH, Division of Physical Sciences and Engineering, Mail Stop R-2, 4676 Columbia Parkway, Cincinnati, Ohio 45226; telephone: (513) 684-4323.

Reported by Div of Physical Sciences and Engineering, National Institute for Occupational Safety and Health, CDC.

References

1. National Institute for Occupational Safety and Health. Documentation of the NIOSH validation tests. DHEW publication no. (NIOSH) 77-185, 1977.

2. National Institute for Occupational Safety and Health. Development and validation of methods for sampling and analysis of workplace toxic substances. DHHS publication no. (NIOSH) 80-133, 1980. 3. National Institute for Occupational Safety and Health Manual of analytical methods, 2nd ed. DHEW publication no. (NIOSH) 77-157-A (V.1), 77-157-B (V.2), 77-157-C (V.3), 78-175 (V.4), 79-141 (V.5); and DHHS publication no. (NIOSH) 80-125 (V.6) and 82-100 (V.7).

4. National Institute for Occupational Safety and Health. A model for the identification of high risk occupational groups using RTECS and NOHS data. DHHS publication no. (NIOSH) 83-117, 1983.

The Morbidity and Mortality Weekly Report is prepared by the Centers for Disease Control, Atlanta, Georgia, and available on a paid subscription basis from the Superintendent of Documents, U.S. Goverment Printing Office, Washington, D.C. 20402, (202) 783-3238.

The data in this report are provisional, based on weekly reports to CDC by state health departments. The reporting week concludes at close of business on Friday; compiled data on a national basis are officially released to the public on the succeeding Friday.

The editor welcomes accounts of interesting cases, outbreaks, environmental hazards, or other public health problems of current interest to health officials. Such reports and any other matters pertaining to editorial or other textual considerations should be addressed to: ATTN: Editor, Morbidity and Mortality Weekly Report, Centers for Disease Control, Atlanta, Georgia 30333.

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CENTERS FOR DISEASE CONTROL

August 24, 1984/ Vol. 33 / No. 33

MMWR

MORBIDITY AND MORTALITY WEEKLY REPORT

The first case of human rabies occurring in the United States since March 1983 was diagnosed July 27, 1984, in Houston, Texas. The patient, a 12-year-old Laotian refugee, had no known history of exposure to a rabid animal and had not traveled outside Texas since arriving in the United States in 1980.

The patient was in good health until July 11, when she complained of a headache. Over the next 4 days, she developed a sore throat, fever, fatigue, difficulty swallowing, and, finally, leg weakness. She was admitted to a community hospital in Houston on July 15. Initial evaluation disclosed a fever of 40 C (104 F), pharyngitis, retropharyngeal air, and a pneumomediastinum. The heart rate fluctuated between 100 beats/minute at rest to 280/minute when the patient was moved. She was treated for presumptive sepsis with antibiotics and corticosteroids. The following day, she was transferred to a university hospital because of the extreme lability of her heart rate and blood pressure. Provisional admitting diagnosis was Guillain-Barré syndrome. The patient was alert and oriented. There were no symptoms or signs except inability to swallow saliva and generalized weakness, more pronounced in the lower extemities; sensory examination was normal. Lumbar puncture revealed normal opening pressure, cell count, and protein. The patient was intubated because of profuse oral secretions, but rapidly became ventilator-dependent. On July 20, increased agitation was noted. Over the next 3 days, periods of decreased alertness and inability to follow commands developed. On July 24, her pupils became dilated and nonreactive to light. A brain biopsy was performed on July 27 after herpes simplex virus was recovered from a throat culture and a temporal focus of seizure activity developed on a repeat EEG. Histopathology revealed eosinophylic intracytoplasmic inclusions; electron microscopy revealed rhabdovirus, and the diagnosis of rabies was confirmed by fluorescent antibody testing. Experimental therapy with ribavirin was initiated. The patient died August 8, 27 days after onset of illness.

Sera and cerebrospinal fluid (CSF) were tested at CDC for rabies neutralizing antibodies using the rapid fluorescent focus inhibition test. On July 21, day 11 of illness, serum titer was lower than 1:5; on July 28, day 18, it had risen to 1:280. Appearance of neutralizing antibody in the serum may have been delayed because of the administration of corticosteroids early in the illness. CSF revealed a 1:11 titer on July 25. Rabies virus was isolated from a second

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES/PUBLIC HEALTH SERVICE

Human Rabies - Continued

brain biopsy obtained on July 31. Monoclonal antibody studies of the isolate have shown it to be a classic rabies virus, but it does not resemble two of the most common rabies virus substrains isolated in Texas from the Mexican free-tailed bat or from Texas skunks.

A total of 142 individuals (123 medical and paramedical personnel and 19 friends and family) with some degree of contact with the patient received postexposure prophylaxis. Reported by D Swanson, MD, R Feigin, MD, L Tanney, MD, M Feingold, MD, D Anderson, MD, C Baker, MD, L Jefferson, MD, V Knight, MD, J Laurent, MD, J Parke, MD, D Seavy, I Solis MD, Texas Children's Hospital, W Hill, MD, X Jones, R Wende, MD, Sam Houston Community Hospital, J Haughton, MD, J Baird, MPH, M Lugo-Faria, MD, G Reeve, PhD, M Wilson, MD, D Harrison, City of Houston Dept of Public Health, T Betz, MD, C Alexander, MD, Texas Dept of Health; Div of Viral Diseases, Center for Infectious Diseases, CDC.

Editorial Note: No more than five cases per year of human rabies have been reported in the United States since 1960. Despite its rarity, rabies should be considered in the differential diagnosis of progressive neurologic diseases, even in the absence of furious behavior, classic hydrophobia, or history of exposure.

In the present case, the pathogenesis of the retropharyngeal and mediastinal emphysema is unknown. The patient had many features of the less common paralytic form of rabies, in which hyperactivity is absent and paralysis dominates the clinical picture (1). The paralysis may ascend, as in the present case, mimicking Guillain-Barré syndrome. This presentation occurs in approximately 20% of human rabies cases, and appears more often after exposure to rabid bats and possibly after postexposure therapy with nerve-tissue vaccines available in some countries outside the United States.

The patient had no history of exposure to an animal known or suspected to be rabid before or after arrival in the United States. The possibility of acquisition outside the United States is remote. Although an exposure can be identified in most cases of rabies, no exposure has been identified in eight (19%) of the 43 cases occurring in the United States from 1960 through the present (2). Incubation periods of less than 1 year are found in 99% of cases; the longest well-documented incubation period was 701 days (3).

The large number of persons receiving postexposure prophylaxis because of contact with the patient demonstrates that tremendous costs may be incurred as a result of undiagnosed cases. The cost of a single postexposure regimen of five doses of human diploid cell rabies vaccine and 20 IU/kg of human rabies immune globulin is approximately $400 for the biologics alone. Postexposure therapy is indicated in certain circumstances after contact with a human rabies case. Although never reported, the theoretic possibility of human-to-human bite transmission exists, as does that of nonbite transmission by contamination of scratches, abrasions, or open wounds with potentially infectious material, such as saliva, urine, or brain tissue. Transmission between humans has only been documented in four persons who received corneal transplants from donors who died of undiagnosed rabies encephalitis. Once rabies is suspected, adherence to contact isolation procedures (4) can markedly reduce the need for postexposure therapy in health-care workers. Each potential exposure to human rabies should be carefully evaluated to minimize unnecessary rabies prophylaxis (5). References

1. Chopra JS, Banerjee AK, Murthy JMK, Pal SR. Paralytic rabies. A clinico-pathological study. Brain 1980;103:789-802.

2. Anderson LJ, Nicholson KG, Tauxe RV, Winkler WG. Human rabies in the United States 1960-1979: epidemiology, diagnosis, and prevention. Ann Intern Med 1984;100:728-35.

3. CDC. Human rabies death-West Virginia. MMWR 1965;14:195.

4. Garner JS, Simmons BP. Guideline for isolation precautions in hospitals. Infect Control 1983;4: 245-325.

5. ACIP. Rabies prevention-United States, 1984. MMWR 1984;33:393-408.