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Syphilis - Continued

3. Judson FN. Fear of AIDS and gonorrhea rates in homosexual men. Lancet 1983;II: 159-60.

4. CDC. Declining rates of rectal and pharyngeal gonorrhea among males-New York City. MMWR 1984;33:295-7.

5. Rathbun KC. Congenital syphilis. Sex Transm Dis 1983;10:93-9.

6. Mascola L, Pelosi R, Blount JH, Binkin NJ, Alexander CE, Cates W Jr. Congenital syphilis—why is it still occurring? JAMA (in press).

7. Ingall D, Musher D. Syphilis. In: Remington JS, Klein JO, eds. Infectious diseases of the fetus and newborn infant. Philadelphia: WB Saunders, 1983:335-74.

Investigating Problems with Respirators

From July 1, 1983, through June 30, 1984, the National Institute for Occupational Safety and Health (NIOSH) received 35 reports of problems with respirators (Table 4). Investigations of each report revealed that 21 (60%) of the problems involved self-contained breathing apparatus; nine of these were classified as causing or likely to cause immediate death or illness of or injury to the user. A report of one investigation follows.

On July 15, 1983, a manufacturer of compressed-gas cylinders notified NIOSH of reported cracks in some of its cylinders. These cylinders were used in various breathing apparatus that had been approved by NIOSH and the Mine Safety and Health Administration (MSHA), U.S. Department of Labor, in their joint program for respirator approval. Company officials indicated that one of the cracked cylinders had ruptured; at least one other cracked cylinder was later reported to have ruptured. Since all defective cylinders were discovered in storage or during maintenance, no adverse effects occurred to workers; however, the defects were classified as potentially life-threatening.

Several respirators, previously approved by NIOSH, incorporated the potentially defective cylinders produced by the company. All manufacturers of these respirators were contacted, and although each stocked this company's cylinders, only two had sold units containing cylinders with serial numbers specified by the company. Approximately 7,000 cylinders were potentially defective, and about 2,000 of these were estimated to be in the hands of users. On July 21, 1983, NIOSH issued a Warning to Users, describing the problem, identifying the serial numbers, and recommending that the potentially defective cylinders be emptied and not used. The U.S. Department of Transportation (DOT), which regulates the interstate shipment of compressed-gas cylinders, then issued a notice to recall the cylinders. After further ruptures occurred, DOT, in February 1984, reduced the allowable pressure for these cylinders from 4,500 to 4,000 pounds per square inch. NIOSH issued a Notice to Users on February 29, 1984, advising owners of more than 75,000 cylinders manufactured by this company

TABLE 4. Problems associated with respirators and reported to NIOSH 1983-June 30, 1984

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Number reported

4

2

1

2

14

12

35

July 1,

"Potentially life-threatening.

*For example: short life, high breathing resistance, facepiece irritation, chemical damage, failure to filter dust from breathing zone.

9 For example: improper seals, pinholes and tears, dents in threads, overfilled cartridge.

Respirators - Continued

of this requirement for reduced pressure and of the reduced service time that results from the required reduction in pressure. No further ruptures have occurred in cylinders with reduced pressure, and as cracked cylinders are found during the ongoing schedule of physical examinations, they are removed from service.

Reported by Certification Br, Div of Safety Research, National Institute for Occupational Safety and Health, CDC.

Editorial Note: The joint NIOSH/MSHA program for approving respirators is mandated by the Mine Safety and Health Amendments Act of 1977. It is conducted in accordance with requirements published in the Code of Federal Regulations, Title 30, Part 11. The Occupational Safety and Health Administration and several other federal regulatory agencies require the use of NIOSH/MSHA-approved respirators wherever such devices are needed to protect workers.

NIOSH receives reports of problems identified in approved respirators from respirator users and from investigations carried out by manufacturers. Problems include deficiencies in the design and performance of respirators and difficulties with their use. NIOSH classifies reported problems according to their potential for causing adverse health effects. Problems classified "A" have resulted in or are likely to result in immediate death or illness of or injury to the user. Those classified "B" may result in future illness of the user. Those classified "C" will probably lead to a worker either rejecting or refusing to wear a respirator. Problems classified "D" have no apparent immediate or future effect on the health and safety of the user. NIOSH notifies the respirator manufacturer of the reported problems and requests an investigation and corrective action, if needed. This information is also used in research to improve the design and performance of respirators. NIOSH may request that defective respirators be recalled, retrofitted, or replaced. Sale of the respirator as a NIOSH/MSHA-approved apparatus may also be stopped. When necessary, users of respirators are alerted to deficiencies or difficulties that could affect their health and safety. If the manufacturer cannot identify and notify purchasers of the defective respirators, NIOSH issues a warning to more than 9,000 users of respirators and other interested persons.

Users of NIOSH/MSHA-approved respirators who find defects in or notice inadequate performance of approved respirators are asked to report these findings to: Respirator Problem Coordinator, Certification Branch, Division of Safety Research, NIOSH, 944 Chestnut Ridge Road, Morgantown, West Virginia 26505; phone: (304) 291-4595 or FTS 923-4595.

*Any device designed to provide the wearer with respiratory protection against inhalation of a hazardous atmosphere.

Experimental Infection of Chimpanzees with
Lymphadenopathy-Associated Virus

Evidence from two investigations indicates that the retrovirus etiologically linked to acquired immunodeficiency syndrome (AIDS) may infect chimpanzees (Pan troglodytes). In the first study, investigators from CDC and Emory University's Yerkes Regional Primate Research Center, Atlanta, Georgia, inoculated two chimpanzees with lymphadenopathy-associated virus (LAV) (1), one of two prototype retrovirus isolates etiologically associated with AIDS (2). Both animals were virologically and serologically negative before inoculation; both were injected simultaneously with concentrated virus and autologous lymphocytes that had been infected in vitro with LAV. Both animals were immunostimulated concomitantly by inoculation of diphtheria-tetanus toxoid and pneumococcal vaccine. One animal received human lymphocytes as an additional immunostimulant.

Six days after inoculation, a retrovirus identified as LAV by reverse transcriptase assay, direct immunofluorescence, p25 competitive radioimmunoprecipitation, and electron micros

LAV - Continued

copy was identified from peripheral lymphocytes of both animals. The virus was isolated from both animals from six consecutive lymphocyte specimens obtained every 2-4 weeks. The most recent specimens were obtained more than 4 months after inoculation. Antibody to the major core protein (p25) of LAV was first detected 3 months after inoculation and was again present at 4 months. In both animals, five consecutive postinoculation T1/T8 ratio determinations have shown an apparent downward trend, although values are significantly below normal in only one. No clinical illness has been detected in the animals, and physical examinations have remained normal.

In the second study, investigators at the National Institutes of Health (NIH) and Southwest Foundation for Biomedical Research have found evidence of transmission of HTLV-III to two chimpanzees receiving human plasma from an individual with the lymphadenopathy syndrome. Evidence for infection includes anti-HTLV-III seroconversion, depression of T/T ratios, and, in one animal, the development of severe, prolonged lymphadenopathy coincident with seroconversion.

Reported by H McClure, DVM, B Swenson, DVM, F King, PhD, Yerkes Regional Primate Research Center, Emory University, Atlanta, Georgia; J-C Chermann, PhD, F Barre-Sinousi, PhD, L Montagnier, MD, Institut Pasteur, Paris, France; J Eichberg, Southwest Foundation for Biomedical Research, San Antonio, Texas; C Saxinger, R Gallo, National Cancer Institute; H Alter, H Masur, A Macher, Clinical Center, C Lane, A Fauci, National Institute of Allergy and Infectious Diseases, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland; Div of Viral Diseases, Div of Host Factors, Center for Infectious Diseases, CDC.

Editorial Note: Primate transmission experiments have been under way at CDC and NIH for some time. LAV and HTLV-III, as well as human AIDS tissue, have been inoculated into several species of primates, including marmosets, rhesus monkeys, and chimpanzees. Except for some lymphocyte changes (3), no disease or infection has been previously reported. The studies reported here indicate that LAV/HTLV-III can be transmitted to chimpanzees both by inoculating virus isolates and human plasma. In some instances, immunologic abnormalities and prolonged lymphadenopathy have followed inoculation, but opportunistic infections or tumors characteristic of AIDS have not developed. Transmission of HTLV-III from lymphocyte-poor human plasma is consistent with reports of AIDS among recipients of plasma or anti-hemophilic concentrates made from pooled plasma (4,5).

The virus isolated from the LAV-inoculated chimpanzees was morphologically and immunologically identical to LAV. Virus particles were morphologically distinct from the Type D retrovirus etiologically implicated in "simian AIDS," a transmissible syndrome of macaques (6,7).

Long-term follow-up of the LAV and HTLV-Ill-infected chimpanzees, as well as other primates, is continuing. Careful examination of the interaction between infection and host response in primates could clarify the pathogenesis of AIDS in humans.

References

1. Barre-Sinoussi F, Chermann JC, Rey F, et al. Isolation of a T-lymphotropic retrovirus from a patient at risk for acquired immune deficiency syndrome (AIDS). Science 1983;220:868-71.

2. Gallo RC, Salahuddin SZ, Popovic M, et al. Frequent detection and isolation of cytopathic retroviruses (HTLV-III) from patients with AIDS and at risk for AIDS. Science 1984;224:500-3.

3. Gajdusek DC, Amyx HL, Gibbs CJ, et al. Transmission experiments with human T-lymphotropic retroviruses and human AIDS tissue. Lancet 1984;1:1415-6.

4. Curran JW, Lawrence DN, Jaffe HW, et al. Acquired immunodeficiency syndrome (AIDS) associated with transfusions. N Engl J Med 1984;310:69-75.

5. Evatt BL, Ramsey RB, Lawrence DN, Zyla LD, Curran JW. Acquired immunodeficiency syndrome in hemophilia patients. Ann Int Med 1984;100:495-8.

6. Marx PA, Maul DH, Osborn KG, et al. Simian AIDS: isolation of a type D retrovirus and transmission of the disease. Science 1984;223:1083-6.

7. Letvin NL, Aldrich WR, King NW, et al. Experimental transmission of macaque AIDS by means of inoculation of macaque lymphoma tissue. Lancet 1983;ll:599-602.

International Conference on Acquired Immunodeficiency Syndrome

An International Conference on Acquired Immunodeficiency Syndrome (AIDS) will be held April 15-17, 1985, at the World Congress Center, Atlanta, Georgia, sponsored by CDC; the National Institutes of Health; the Food and Drug Administration; the Alcohol, Drug Abuse, and Mental Health Administration; the Health Resources and Services Administration; and the World Health Organization. The purpose of the meeting is to review strategies for the prevention and control of AIDS and to exchange information on screening and diagnostic tests for AIDS and on the epidemiology, virology, immunology, clinical manifestations, and treatment of AIDS. Seating will be available for 1,800 participants. An announcement of keynote speakers and a call for abstracts will be published later. To obtain further information and future announcements, contact:

AIDS Conference
Building 1, Room 2047
Centers for Disease Control
Atlanta, Georgia 30333.

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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August 10, 1984 / Vol. 33 / No. 31

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445 Acute Schistosomiasis with Transverse
Myelitis in American Students
Returning from Kenya

448 Work-Related Allergies in

Insect-Raising Facilities
Intenza

1983-1984 Season

3 1994

Acute Schistosomiasis with Transverse myelitis
in American Students Returning from Kenya

The University

of Micingan Public Health Library

In early May 1984, CDC received reports that 15 (83%) of 18 American students participating in a travel/study program in Kenya had acquired Schistosoma mansoni infections. Two of these students developed flaccid paraplegia. Although data are incomplete on all 18 students, no unusual attributes could be identified in these two students that might explain why their infections were associated with severe neurologic disease. General background information and the case histories of these students follow.

All 18 students arrived in Kenya on February 13, 1984. From March 5 to March 25, they shared housing in the Machakos district. To provide a place for bathing, the students dammed a small stream; two of the infected students recalled experiencing an itchy rash shortly after bathing at this site. Subsequently, the group separated, as the students took individual assignments in various regions of the country. Between April 26 and May 12, 14 of the 15 infected individuals became acutely ill with fever, diarrhea, malaise, and weight loss.

Student 1: This 21-year-old white male was in good health and had never traveled outside the United States. He was immunized against tetanus, typhoid, cholera, and yellow fever, and received an injection of immune globulin before arriving in Kenya. While in Kenya, he took weekly chloroquine and Fansidar® for malaria prophylaxis. In early April, he complained of fever, abdominal pain, and diarrhea without blood or mucus, all of which resolved without therapy. He became ill again on April 26, with fever, chills, sweats, anorexia, mild nonbloody diarrhea, and abdominal pain. There was no hematuria or cough. He was treated orally with chloroquine for a presumptive diagnosis of malaria. On April 28, he developed severe lumbar back pain without tenderness or radiation and had associated numbness, without weakness, in both feet. On May 1, he had difficulty recognizing the position of his feet and had extreme proximal lower extremity weakness. On May 2, he became ataxic and developed urinary retention. A diagnosis of transverse myelitis secondary to schistosomiasis was made when stool examinations showed ova of S. mansoni. The patient was treated with praziquantel and prednisone. He was transported to the United States on May 5.

On evaluation in the United States, the student had no rash, fever, lymphadenopathy, hepatosplenomegaly, or point tenderness on palpation of the spinal column. Neurologic examination revealed a flaccid paraplegia at and below the level of T-10. There was marked sensory loss, including loss of vibratory sensation. Superficial and deep tendon reflexes could not be elicited.

A white blood cell count revealed moderate eosinophilia. A myelogram showed no obstruction or mass, but a CAT scan showed the lumbar cord to be slightly enlarged, without focal abnormalities. Examination of cerebrospinal fluid (CSF) showed pleocytosis and elevated protein; however, eosinophilic pleocytosis was not present. Fecal examination showed 500 U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES/PUBLIC HEALTH SERVICE

US DEPOSITORY

AUG 28190

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