Software Vault: The Diamond Collection/The Diamond Collection (Software Vault)(Digital Impact).ISO/cdr17/hicn801.zip/HICN801.TXT

Text File | 1995-01-31 | 36KB | 823 lines

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Date: Mon, 02 Jan 95 22:25:26 MST
From: [e-mail] (HICNet Medical News)
To: hicnews
Subject: [MMWR] Hantavirus Pulmonary Syndrome
Message-ID: <[e-mail]>

             Hantavirus Pulmonary Syndrome -- Virginia, 1993

     Hantavirus pulmonary syndrome (HPS) was first recognized in June
1993
as a result of the investigation of a cluster of fatal cases of adult
respiratory distress syndrome (ARDS) in the southwestern United States
(1).
During that month, a 61-year-old man was admitted to a hospital in
southern
Pennsylvania with ARDS; recent testing of all available specimens from
this
patient has confirmed the diagnosis of HPS. This report summarizes the
case
investigation.
     When hospitalized on June 28, 1993, the man reported a 4-day
history
of fever, chills, headache, myalgia, nausea, vomiting, and diarrhea.
After
admission, he became hypotensive and increasingly short of breath and
was
transferred to a tertiary-care medical center. Laboratory findings
included
leukocytosis (white blood cell count 25,300/mm3), hemoconcentration
(hemoglobin of 20.0 g/L), thrombocytopenia (platelet count
65,000/mm3), and
elevated blood urea nitrogen, creatinine (peak value 6.8 ug/dL),
prothrombin time, activated partial thromboplastin time, aspartate
aminotransferase (peak value 8500 U/L), lactic dehydrogenase, and
lipase
levels. A chest radiograph indicated bilateral diffuse infiltrates.
During
his prolonged hospital course, he required respiratory and circulatory
support and hemodialysis. He was discharged on July 22, 1993.
     An enzyme-linked immunosorbent assay with heterologous antigens
performed on serum samples obtained on July 2 and July 20 were highly
suspect for hantavirus antibodies. Subsequent retesting of these
samples,
as well as of an additional sample obtained in September 1994, with
Sin
Nombre virus (SNV) antigens confirmed the diagnosis of HPS.
     In April 1993, the patient had started hiking on the Appalachian
Trail
northbound from Georgia through North Carolina, Tennessee, Virginia,
and
West Virginia. From May 13 through June 20, he hiked primarily along
the
Appalachian Trail in Virginia and reported evidence of mice, including
excreta and rodent traps in shelters and bunkhouses.
     To further characterize the prevalence of hantavirus in local
rodent
populations, the offices of Epidemiology and Environmental Health of
the
Virginia Department of Health, local health departments, the National
Park
Service, and CDC are conducting rodent trapping.

Reported by: BH Hamory, MD, C Zwillich, MD, T Bollard, MD, JO Ballard,
MD,
The Milton S Hershey Medical Center, Hershey; M Connor, DO,
Chambersberg
Hospital, Chambersberg; P Lurie, MD, M Moll, MD, J Rankin, DVM, State
Epidemiologist, Pennsylvania Dept of Health. C Smith, MD, New River
Health
District, Radford; S Jenkins, VMD, E Barrett, DMD, GB Miller, Jr, MD,
State
Epidemiologist, Virginia Dept of Health. W Frampton, DVM, S Lanser
MPH, CR
Nichols, MPA, State Epidemiologist, Utah Dept of Health. DT King,
Harpers
Ferry, West Virginia; A Kingsbury, MS, Washington, DC, National Park
Service, US Dept of the Interior. Special Pathogens Br, Div of Viral
and
Rickettsial Diseases, National Center for Infectious Diseases, CDC.

Editorial Note: This report describes the first known case of HPS in
the
mid-Atlantic states. The patient's infection probably was acquired
along
the Appalachian Trail in Virginia, an area within the range of
habitation
of the primary rodent reservoir of SNV, Peromyscus maniculatus (deer
mouse). The prodromal illness and respiratory failure are consistent
with
HPS (2); the renal involvement characteristic of Eurasian hemorrhagic
fever
with renal syndrome (HFRS) has not been typical of HPS. Moderate
elevations
( greater than 2.5 ug/dL) in serum creatinine have occurred in only
10% of
fatal cases of HPS; prominent renal involvement, such as that which
occurred in this patient, has been documented only in two cases from
the
southeastern United States, both of which are believed to have been
associated with hantaviruses other than SNV (provisionally named Black
Creek Canal virus and Bayou virus) (3,4). Thus, the marked liver
transaminase elevation in this patient has not been a prominent
feature in
other cases of HPS, although the prominent liver dysfunction has
occurred
with HFRS (5,6). However, because both renal and hepatic dysfunction
can
be caused by antecedent hypotension and other factors, additional case
investigation is ongoing to clarify the relevance of these findings.
     Since June 1993, when HPS was first recognized in the United
States,
98 cases have been identified in 21 states. The mean age of case-
patients
has been 35.1 years (range: 12-69 years), and the case-fatality rate
is
52%; 52 (54%) cases have occurred in males. The earliest
retrospectively
identified case, inferred by a history of a compatible illness and
elevated
IgG titers detected for SNV, occurred in a 38-year-old man in Utah in
1959.
     The findings in this report extend the geographic area for risk
of
human infection with hantaviruses in the contiguous United States and
emphasize the continued importance of minimizing exposure to rodents
and
their excreta. Persons engaged in outdoor activities such as camping
or
hiking should take precautions to reduce contact with rodents (7).
National
surveillance for HPS continues to characterize the spectrum of
clinical
illness associated with SNV and identify additional pathogenic
hantaviruses
and rodent hosts. Suspected cases of HPS should be reported through
local
and state health departments for evaluation and investigation.

References
1. CDC. Outbreak of acute illness--southwestern United States, 1993.
MMWR
1993;42:421-4.
2. Duchin JS, Koster FT, Peters CJ, et al. Hantavirus pulmonary
syndrome:
a clinical description of 17 patients with a newly recognized disease.
N
Engl J Med 1994;330:949-55.
3. CDC. Newly identified hantavirus--Florida, 1994. MMWR
1994;43:99,105.
4. CDC. Hantavirus pulmonary syndrome--northeastern United States,
1994.
MMWR 1994;43:548-9,555-6.
5. Chan YC, Wong TW, Yap EH, et al. Haemorrhagic fever with renal
syndrome
involving the liver. Med J Aust 1987;147:248-9.
6. Elisaf M, Stefanaki S, Repanti M, Korakis H, Tsianos E, Siamopoulos
KC.
Liver involvement in hemorrhagic fever with renal syndrome. J Clin
Gastroenterology 1993;17:33-7.
7. CDC. Hantavirus infection--southwestern United States: interim
recommendations for risk reduction. MMWR 1993;42(no. RR-11).



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Date: Mon, 02 Jan 95 22:26:21 MST
From: [e-mail] (HICNet Medical News)
To: hicnews
Subject: [MMWR] Alcohol Involvement in Fatal Traffic Accidents
Message-ID: <[e-mail]>

             Alcohol Involvement in Fatal Motor-Vehicle Crashes --
                        United States, 1992-1993

     The following figure compares alcohol involvement in fatal
motor-vehicle crashes for 1992 and 1993 in the United States. A fatal
crash
is considered alcohol-related by the National Highway Traffic Safety
Administration (NHTSA) if either a driver or nonoccupant (e.g.,
pedestrian)
had a blood alcohol concentration (BAC) of greater than or equal to
0.01
g/dL in a police-reported traffic crash. Because BACs are not
available for
all persons in fatal crashes, NHTSA estimates the number of alcohol-
related
traffic fatalities based on a discriminant analysis (1) of information
from
all crashes for which driver or nonoccupant BAC data are available.
     The number of alcohol-involved fatalities decreased from 1992 to
1993
for most age groups. For BACs of 0.01 g/dL-0.09 g/dL, the overall
decrease
in alcohol-involved fatalities was 4%; at greater than or equal to
0.10
g/dL, the legal limit of intoxication in most states, the number of
crash
fatalities decreased 2%. The increase in fatalities for the
nonalcohol-involved crashes probably resulted from a variety of
factors,
including an increase in the number and changes in the type of vehicle
miles traveled (2).

References
1. Klein TM. A method of estimating posterior BAC distributions for
persons
involved in fatal traffic accidents: final report. Washington, DC: US
Department of Transportation, National Highway Traffic Safety
Administration, 1986; report no. DOT-HS-807-094.
2. Wagenaar AC, Streff FM. Macroeconomic conditions and alcohol-
impaired
driving. J Stud Alcohol 1989;50:217-25.



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Date: Mon, 02 Jan 95 22:27:30 MST
From: [e-mail] (HICNet Medical News)
To: hicnews
Subject: [MMWR 9 Dec 94] Acute Pulmonary Hemorrage Among Infants
Message-ID: <[e-mail]>

          Acute Pulmonary Hemorrhage/Hemosiderosis Among Infants --
              Cleveland, January 1993-November 1994

     Hemosiderosis is an uncommon childhood disease characterized by
spontaneous pulmonary hemorrhage often associated with iron deficiency
anemia. During January 1993-November 1994, eight cases of acute
pulmonary
hemorrhage/hemosiderosis were diagnosed among infants at a children's
referral hospital in Cleveland. In comparison, during 1983-1993, a
total
of three cases of pulmonary hemosiderosis were diagnosed among infants
and children at this hospital. This report summarizes the preliminary
results of the ongoing epidemiologic, clinical, and laboratory
investigations by pediatric pulmonologists in Cleveland, the Ohio
Department of Health, the City of Cleveland Department of Public
Health,
the Cuyahoga County Board of Health, and CDC.
     In 1993, cases were diagnosed in January (one case) and October
(one); in 1994, cases were diagnosed in March (one), June (one), July
(two), September (one), and November (one). For each of the eight
infants
(mean age: 10.3 weeks; range: 4 weeks-16 weeks), onset of hemoptysis
was
associated with pallor and an abrupt cessation in crying; fever was
not
reported for any of the infants. Other reported symptoms on admission
included limpness, lethargy, and grunting. At the time of initial
evaluation at the hospital, seven infants required admission to the
pediatric intensive-care unit because of hemoptysis and respiratory
distress.
     All eight infants were black, and seven were male. The median age
of their mothers was 20 years (range: 15-29 years). Seven of the
pregnancies and deliveries occurred without complications; one infant
born at 27 weeks' gestation and weighing 2 lbs, 2 oz (950 g) had
complications of severe prematurity. All infants lived within a 6-mile
radius of the hospital. No infants were breast fed; before admission,
all
were fed cow's-milk-based formula.
     Laboratory findings on admission included a normal white blood
cell
count (median=13.8 cells/mm3) and features consistent with a
normocytic,
normochromic anemia characteristic of acute blood loss with a mean
hematocrit of 27.1% (normal: 36.0%-47.0%) and a mean hemoglobin of 9.1
g/dL (normal: 10.0-15.0 g/dL). Red blood cell morphology was
suggestive
of a microangiopathic process: microscopic examination indicated that
five of the eight infants had mild to moderate (1+ to 2+) hemolysis
characterized by the presence of microcytes, burr cells, spherocytes,
and
bizarre fragments. Based on guaiac testing, occult blood was present
in
the stool of three infants. Results of coagulation studies included
normal prothrombin and partial thromboplastin time for all infants.
Chest
radiographs of all infants showed diffuse, bilateral infiltrates
consistent with pulmonary hemorrhage. In six infants, the mean serum
magnesium level was 2.1 mg/dL (normal: 1.4-1.9 mg/dL).
     Cultures of blood, urine, and bronchoalveolar lavage from seven
infants were negative for bacterial, mycotic, and viral pathogens.
Cultures of bronchoalveolar lavage from one infant grew Bacillus sp.
Hemosiderin-laden macrophages--indicating continued pulmonary
hemorrhage-
-were detected in each of the seven infants who underwent bronchoscopy
more than 2 weeks after the acute hemorrhage. No other source of
bleeding
(i.e., gastrointestinal or nasopharyngeal) was identified during
endoscopic evaluation. Immunoglobulin G levels to cow's milk proteins
were above normal (>20 U/mL) in five of seven infants.
     Five infants required mechanical ventilation for an average of 5
days. All infants survived the first hospitalization and were
discharged
in stable condition without evidence of hemoptysis after a median
length
of stay of 10 days (range: 2-35 days). In five infants, acute
hemoptysis
necessitating readmission recurred within 1 day to 6 months of
discharge.
One death--attributed to severe hypoxic encephalopathy secondary to
recurring pulmonary hemorrhage--occurred in a 9-week-old full-term
infant.
     Local surveillance measures and active case finding have not
identified additional cases in the Cleveland area. A case-control
study
is under way to determine risk factors for acute pulmonary hemorrhage
among infants.

Reported by: DG Dearborn, MD, MD Infeld, MD, P Smith, DO, C Judge, MD,
Rainbow Babies and Childrens Hospital; TE Horgan, MPH, T Allan, MPH,
Cuyahoga County Board of Health; JA Zimomra, MPA, Cleveland Dept of
Public Health, Cleveland; BK Mortensen, PhD, SA Burkett, MA, K
Winpisinger-Slay, MS, S Wagner, MPH, Ohio Dept of Health. Div of
Environmental Hazards and Health Effects, Div of Birth Defects and
Developmental Disabilities, and Div of Environmental Health Laboratory
Sciences, National Center for Environmental Health, CDC.

Editorial Note: The eight cases of acute pulmonary
hemorrhage/hemosiderosis described in this report exceed the number
expected at this hospital during a 2-year period. Massive acute
pulmonary
hemorrhage occurs rarely in infants; it usually is attributed to
cardiac
or vascular malformations, infectious processes, immune vasculitides,
trauma, or known milk protein allergies. Cases for which the etiology
is
undetermined, such as these eight reported from Cleveland,
traditionally
have been classified as idiopathic pulmonary hemosiderosis (IPH) and
account for less than 5% of all cases of pulmonary hemorrhage during
infancy.
     The pathologic mechanism for IPH in children is unknown. Recent
histomorphologic techniques suggest that the initial histopathologic
damage occurs at the alveolar epithelial surface (1). IPH has been
associated with circulating antibodies to cow's milk protein; however,
this association has not been consistently reproduced (1,2). In
addition,
some reports have described familial occurrences of pulmonary
hemosiderosis, suggesting a possible genetic vulnerability to a
toxicant
(3,4).
     To identify additional cases of acute pulmonary
hemorrhage/hemosiderosis, CDC has established the following
provisional
surveillance case definition: hemoptysis in an infant aged less than 1
year not attributed to cardiac or vascular malformations, infectious
processes, or trauma. A case report form is available from CDC.
Physicians should report possible cases through state health
departments
to CDC's Air Pollution and Respiratory Health Branch, Division of
Environmental Hazards and Health Effects, National Center for
Environmental Health; Internet: [e-mail]; telephone
(404)
488-7320; or fax [phone].

References
1. Levy J, Wilmott R. Pulmonary hemosiderosis. In: Hilman BC, ed.
Pediatric respiratory disease: diagnosis and treatment. Philadelphia:
WB
Saunders, 1993:543-9.
2. Heiner DC, Sears JW, Kniker WT. Multiple precipitins to cow's milk
in
chronic respiratory disease. Am J Dis Child 1962;103:634-54.
3. Breckenridge RL, Ross JS. Idiopathic pulmonary hemosiderosis: a
report
of familial occurrence. Chest 1979;75:636-9.
4. Beckerman RC, Taussig LM, Pinnas JL. Familial idiopathic pulmonary
hemosiderosis. Am J Dis Child 1979;133:609-11.



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Date: Mon, 02 Jan 95 22:28:33 MST
From: [e-mail] (HICNet Medical News)
To: hicnews
Subject: [MMWR] Injury Construction Workers Installing Frame Walls
Message-ID: <[e-mail]>

         Injuries Among Construction Workers During the Raising
            of Wood-Framed Walls -- Colorado and California

     In Colorado, traumatic spinal cord injuries that produce
documentable motor, sensory, bowel, and/or bladder impairments must be
reported to the state or local health department. Persons with such
injuries are interviewed by staff of the Colorado Department of Public
Health and Environment (CDPHE) Spinal Cord Injury Early Notification
System (ENS)*; injuries that occur in workplaces are investigated by
staff of the CDPHE Sentinel Event Notification System for Occupational
Risk (SENSOR) program**. This report describes the investigation of a
construction-related spinal cord injury reported to the CDPHE SENSOR
program on February 8, 1993, and summarizes information about a
similar
case in California.
     On February 1, 1993, the construction worker sustained a spinal
cord
injury--which resulted in permanent paraplegia--while attempting to
raise
a preconstructed wood-framed wall of a single-family house. A crew of
three workers was using a standard procedure that consisted of laying
the
wall on the ground and "walking it up" to a vertical orientation. The
wall was approximately 18 feet wide and 25 feet high at the center
peak.
During the procedure, two workers were positioned at the outer edges
of
the wall and one in the center. As the workers were raising the wall,
they realized it was too heavy for them to control, possibly because
it
had become wet from snow that had accumulated on it during the
previous
evening. While the crew was attempting to lower the wall back to a
horizontal orientation, the weight of the wall shifted; the crew lost
control of the wall, and it fell to the ground. The worker in the
center
could not escape the falling wall and was trapped under it, sustaining
a fracture dislocation of the seventh thoracic vertebra and spinal
cord
injury.
     During the investigation of this injury, Colorado SENSOR staff
determined that the building technique used in this incident is common
in the construction industry and that many companies employ similar
practices for raising prefabricated walls. Colorado SENSOR staff
learned
of a similar incident that had occurred in California and resulted in
a
permanently disabling spinal cord injury. In that incident, an
unspecified number of workers were raising a 19 x 17-1/2-foot rain-
soaked
wood-framed wall with an attached chimney chase. As the workers
attempted
to lift the wall, the base slipped forward, causing the wall to fall
back
toward the workers. Although most of the workers were able to clear
the
area before the wall collapsed, three were pinned beneath the wall as
it
fell. One of the three sustained fracture dislocations of the T12 and
L1
vertebrae, spinal cord injury, and subsequent permanent paralysis.

Reported by: K Gerhart, MS, Craig Hospital, Englewood; M Heinzman, R
Johnson, M Cook, MS, RE Hoffman, MD, State Epidemiologist, Colorado
Dept
of Public Health and Environment. F Reinisch, MPH, AM Osorio, MD, GW
Rutherford, III, MD, State Epidemiologist, California State Dept of

·
(continued next message)


 @FROM   :[e-mail]
· (Continued from last message)
Health Svcs. Div of Safety Research, and Div of Surveillance, Hazard
Evaluations, and Field Studies, National Institute for Occupational
Safety and Health, CDC.

Editorial Note: The estimated annual incidence of acute traumatic
spinal
cord injury in the United States ranges from 28 to 50 injuries per
million persons (1)***. During 1988 (the most recent year for which
national published data are available), the estimated prevalence of
spinal cord injuries that resulted in paraplegia and quadriplegia was
approximately 177,000 (2). Most injuries (61%) occurred in persons
aged
16-30 years (3). During 1988, the estimated total cost of spinal cord
injuries in the United States was $5.6 billion: $3.4 billion in direct
costs (i.e., hospitalization and other medical care, home
modifications,
equipment, and pharmaceuticals) and $2.2 billion in indirect costs
(i.e.,
the value of productivity lost to society) (2).
     During January 1989-December 1992, the average annual rate for
spinal cord injury in Colorado ranged from 34 to 43 cases per 1
million
population (mean: 37) (4). Of the 506 spinal cord injury cases
reported
in Colorado during this period, 51 (10%) occurred on the job (4),
including 14 (27%) among workers in the construction industry.
     The California Occupational Safety and Health Standards Board has
promulgated regulations for the raising of wood-framed walls at
construction sites. The regulation requires that temporary restraints
(e.g., cleats on the foundation or floor, or straps on the wall bottom
plate) be used when raising wood-framed walls measuring 10 or more
feet
to prevent inadvertent sliding or uplift of the bottom plate; anchor
bolts cannot be used to brace such walls. Compliance with the
procedures
outlined in this standard--if it had been in effect--may have
prevented
the incidents in both California and Colorado.
     Securing the base of a wall being raised manually is an important
measure for reducing some risks associated with raising wood-framed
walls. Other measures include 1) establishing industry guidelines that
classify size categories of walls according to linear feet of wood in
the
wall, specify the personnel or equipment required for raising each
category of wall, and provide an upper limit beyond which cranes or
boom
trucks must be used to raise the wall; 2) using pulley systems or
hydraulic jacks to raise walls; 3) developing a bracing system to
arrest
the fall of a wall; and 4) establishing and enforcing company and
industry policies that prohibit raising of wet wood-framed walls
unless
additional employees or other raising techniques are used.
     To further characterize incidents similar to those described in
this
report and to assist in developing prevention measures, information
about
other injuries that have resulted from raising wood-framed walls in
construction operations should be reported to Acting Chief, Injury
Surveillance Section, Surveillance and Field Investigation Branch,
Division of Safety Research, National Institute for Occupational
Safety
and Health; telephone [phone].

References
1. Kraus JF. Epidemiological aspects of acute spinal cord injury: a
review of incidence, prevalence, causes, and outcome. In: Becker DP,
Povlishock JT, eds. Central nervous system trauma status report, 1985.
Bethesda, Maryland: US Department of Health and Human Services, Public
Health Service, National Institutes of Health, National Institute of
Neurological and Communicative Disorders and Stroke, 1985:313-22.
2. Berkowitz M, Harvey C, Greene CG, Wilson SE. The economic
consequences
of traumatic spinal cord injury. New York: Demos Publications, 1992:1.
3. Stover SL, Fine PR, eds. Spinal cord injury: the facts and figures.
Birmingham, Alabama: University of Alabama at Birmingham, 1986.
4. Colorado Department of Public Health and Environment. 1992 Annual
report of the Spinal Cord Injury Early Notification System. Denver:
Colorado Department of Transportation Printing Office, 1993.

* Colorado is one of 21 states with spinal cord injury registries.
Colorado's registry, the ENS, begun in January 1986, is a
collaborative
project between the Rocky Mountain Regional Spinal Injury System and
the
CDPHE and is funded through a National Institute on Disability,
Rehabilitation, and Research grant and a cooperative agreement with
CDC.
** During 1987-1992, CDC funded SENSOR projects in 10 states to
develop
state-based capacity for recognizing, reporting, investigating, and
preventing selected occupational disorders. These 10 states and four
additional states received renewed SENSOR funding in 1992.
*** The range in estimated incidence rates reflects differences in
case
definitions. Some studies, for example, include hospital admissions
only,
which exclude acute fatal injuries.



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Date: Mon, 02 Jan 95 22:29:55 MST
From: [e-mail] (HICNet Medical News)
To: hicnews
Subject: [MMWR] Progress Towards Elimination of Neonatal Tetanus
Message-ID: <[e-mail]>

   Progress Toward the Global Elimination of Neonatal Tetanus, 1989-
1993

     Neonatal tetanus (NT) is a leading cause of neonatal mortality in
many parts of the world. During the 1980s, NT accounted for half of
all
neonatal deaths and one fourth of all infant mortality in some
countries
(1). In addition, in 1993, an estimated 515,000 neonatal deaths were
caused by NT* (2) for a global mortality rate of 4.1 per 1000 live
births. In 1989, the World Health Organization (WHO) adopted a
resolution
to eliminate NT worldwide (3), and in 1990, the World Summit for
Children
issued a declaration for global elimination of NT by the end of 1995
(4).
In 1993, WHO's goal was defined as the elimination of NT as a public
health problem by reducing its incidence to less than one case per
1000
live births for each health district (2) (baseline: in 1988, a total
of
32,454 NT cases were reported to WHO and an estimated 787,000 NT
deaths
occurred; the global NT mortality rate was 6.5 cases per 1000 live
births
[5])**. To achieve and maintain NT elimination, 80% or more of infants
need to be protected at birth through vaccination of their mothers
with
at least two doses of tetanus toxoid (TT2+) or through clean delivery
and
cord-care practices (2). In addition, effective surveillance systems
must
be developed to detect NT cases and enable timely investigation of
them.
This report, which is based on data from WHO, presents reported
coverage
with TT2+ in developing countries*** only and reported number of NT
cases
and estimated number of NT deaths in all countries, and summarizes
progress toward the global elimination of NT during 1989-1993 (WHO,
unpublished data, 1994).

     Global. From 1989 to 1993, vaccination coverage with TT2+ among
pregnant women increased from 27% to 45% (Figure 1). During the same
period, the number of NT cases reported to WHO decreased from 29,494
in
1989 to 14,232 in 1993. However, only 2%-5% of all NT cases were
reported
(2). Of the estimated 515,000 deaths worldwide, approximately 80%
occurred in 12 countries (Table 1). Most deaths (34.2%) occurred in
the
Southeast Asian Region (Table 2). Overall, an estimated 724,300 deaths
attributable to NT were prevented**** in 1993 by vaccination with
tetanus
toxoid. Of the 156 countries reporting NT incidence to WHO in 1993, a
total of 79 (51%) reported zero cases. In 1993, a total of 66% of live
births occurred in areas with NT surveillance, compared with 39% in
1985
and 73% in 1989.

     African Region. Coverage with TT2+ increased from 25% in 1989 to
40%
in 1993. In 1993, a total of 3461 cases (24% of the global total) were
reported, compared with 7299 cases in 1989. Of the 47 countries in the
region, 36 (77%) reported NT incidence to WHO for 1993; of these, four
reported zero cases.

     Region of the Americas. From 1989 through 1993, TT2+ coverage
increased from 29% to 40% in the Region of the Americas, where major
efforts were undertaken to vaccinate women of childbearing age in
high-risk areas. Reported cases decreased from 1430 in 1989 to 708 (5%
of the global total) in 1993; Brazil reported 216 cases (31% of the
regional total for 1993). Of the 47 countries in the region, 40 (85%)
reported NT incidence to WHO for 1993; of these, 25 reported zero
cases.

     Eastern Mediterranean Region. Coverage with TT2+ increased from
31%
in 1989 to 50% in 1993. The number of reported cases decreased from
6314
in 1989 to 3350 (24% of the global total) in 1993. Of the 23 countries
in the region, 21 (91%) reported NT incidence to WHO for 1993; of
these,
10 reported zero cases.

     European Region. In 1993, TT2+ coverage levels of 16% were
reported
in the European Region, where only Turkey routinely reports tetanus
toxoid coverage to WHO. During 1989-1992, 63-67 cases were reported
annually. In 1993, a total of 48 NT cases were reported in the region--
46
from Turkey. Of the 50 countries in the region, 30 (60%) reported NT
incidence to WHO for 1993; of these, 27 reported zero cases.

     Southeast Asian Region. In 1993, TT2+ coverage was reported to be
74%. The number of reported cases decreased from 14,102 (48% of the
global total) in 1989 to 5809 (40% of the global total) in 1993. Three
countries accounted for 97% of all NT cases reported in the region:
India
(4339 [75%] cases), Bangladesh (720 [12%]), and Indonesia (566 [10%]).
Of the 11 countries in the region, 10 (91%) reported NT incidence to
WHO
for 1993; of these, two reported zero cases.

     Western Pacific Region. In 1993, TT2+ coverage was 13% in the
Western Pacific Region (including China, which began administering
tetanus toxoid in selected areas in 1992). The number of cases
reported
to WHO increased from 282 in 1989 to 856 (6% of the global total) in
1993. Two countries reported 79% of the total cases for the region:
Vietnam (333 cases) and the Philippines (343 cases). Of the 35
countries
in the region, 18 (51%) reported NT incidence to WHO for 1993; of
these,
11 reported zero cases.

Reported by: Expanded Program on Immunization, Global Program for
Vaccines and Immunization, World Health Organization, Geneva.
International Health Program Office; National Immunization Program,
CDC.

Editorial Note: NT results from the effect of a neurotoxin elaborated
by
the anaerobic organism Clostridium tetani (6). Infection occurs when
the
umbilical cord becomes contaminated as a result of unclean childbirth
or
cord-care practices. Access to clean birth practices is ultimately the
long-term goal for prevention; however, most infants in developing
countries continue to be born at home under unsanitary conditions.
Although global tetanus toxoid coverage levels nearly doubled to 45%
during 1989-1993 in countries that administer the vaccine, reported
coverage levels are underestimated because annual estimates do not
include doses administered during previous years. In addition, many
women
do not maintain vaccination records, making verification of
vaccination
status difficult (7). WHO now recommends that women receive and
maintain
life-long vaccination records and that tetanus toxoid coverage be
monitored nationally by determining the proportion of children
protected
at birth when they seek their first diphtheria and tetanus toxoids and
pertussis vaccine dose.
     The findings in this report are subject to at least two
limitations.
First, because NT cases are grossly underreported, NT incidence is
underestimated. Second, the numbers of NT deaths and prevented deaths
are
based on projections from national data (which often are estimated) or
data extrapolated from other countries.
     As of August 1, 1994, the estimated NT case rate was less than
one
per 1000 live births nationwide (i.e., not by district) in 83
countries.
In addition, in 57 countries, the estimated rate of NT was one to five
cases per 1000 nationwide, while in 25 countries the estimated rate
was
higher than five cases per 1000. Although progress has been made
toward
eliminating NT as a public health problem, present resources and
commitments must be increased and activities greatly accelerated if
the
1995 goal is to be achieved by all countries (8). In 1993, the Global
Advisory Group of WHO's Expanded Program on Immunization identified
four
constraints to NT elimination (2): 1) insufficient funds to purchase
tetanus toxoid in selected high-risk countries; 2) lack of adequate
health-care infrastructure in many countries, resulting in limited
tetanus toxoid vaccination activities and poor access to clean birth
practices; 3) civil unrest in some high-risk countries; and 4) high
levels of NT underreporting.
     To reach the global elimination goal for NT, efforts must be
accelerated, especially in the 12 countries from which 80% of NT cases
were reported in 1993 and in countries where the incidence rate is
higher
than five per 1000 live births. Each country must identify areas where
the incidence rate is higher than one per 1000 live births, coverage
levels are low, or there is limited access to clean deliveries or
trained
birth attendants. These high-risk areas must be targeted for
intensified
vaccination efforts, including the use of mass vaccination campaigns.
In
addition, surveillance activities in all areas must be strengthened.
Finally, because NT is not a communicable disease, and C. tetani
cannot
be eradicated from the environment, ensuring long-term elimination of
NT
will require the development of adequate health-care delivery systems
to
reach those at greatest risk--infants of poor women residing in rural
areas in developing countries.

References
1. World Health Organization. Neonatal tetanus elimination. Tokyo:
World
Health Organization, Expanded Program on Immunization, Global Advisory
Group, October 16-20, 1989; publication no. WHO/EPI/GAG/89/WP.9.
2. Global Advisory Group, Expanded Program on Immunization, World
Health
Organization. Achieving the major disease control goals. Wkly
Epidemiol
Rec 1994;69:29-31,34-5.
3. World Health Assembly. Expanded Program on Immunization. Geneva:
World
Health Organization, May 19, 1989. (Resolution WHA42.32).
4. World Health Organization. Revised plan of action for neonatal
tetanus
elimination. Geneva: World Health Organization, Expanded Program on
Immunization, 1993; publication no. WHO/EPI/GEN/93.13.
5. World Health Organization. The global elimination of neonatal
tetanus:
progress to date. Bull World Health Organ 1994;72:155-64.
6. Galazka AM. Tetanus: the immunologic basis for immunization.
Geneva:
World Health Organization, Expanded Program on Immunization, 1993;
publication no. WHO/EPI/GEN/93.13.
7. Deming MS. Monitoring tetanus toxoid immunization coverage. Geneva:
World Health Organization, Expanded Program on Immunization, 1990;
document no. EPI/NNT/90/WP.3/Rev1.
8. World Health Organization. Global programme for vaccines and
immunization: proceedings of the Meeting of the Scientific Advisory
Group
of Experts. Geneva: World Health Organization, October 17-19, 1994.

* Estimates of NT deaths are derived from national mortality data, NT
mortality rates from NT surveys, or in the absence of surveys, by
assuming that rates are similar for countries with similar
socioeconomic
conditions and from tetanus toxoid coverage levels.
** Because the case-fatality rate for NT is high (100% in some
countries), WHO estimates only the number of deaths for NT, not number
of cases.
*** Countries are categorized as developing based on criteria
developed
by the United Nations and used by WHO for analytic purposes only.
**** The number of NT deaths prevented was calculated for each country
using the number of live births, NT mortality rate, and tetanus toxoid
coverage and efficacy.



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