Bioweapons Research: "YARU" The Rockefeller- funded Yale Facility

[Satyagraha]

This thread will focus on the Yale Arbovirus Research Unit (YARU), intially referenced in the following thread/quote:

What really happened in 1994?

What exactly is the "Yale Arbovirus Research Unit"

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Treatment of a Laboratory-Acquired Sabiá Virus Infection
http://content.nejm.org/cgi/content/full/333/5/294


Michele Barry, M.D., Mark Russi, M.D., M.P.H., Lori Armstrong, Ph.D., David Geller, M.D., Ph.D., Robert Tesh, M.D., Louise Dembry, M.D., Jean Paul Gonzalez, M.D., Ali S. Khan, M.D., and Clarence J. Peters, M.D.


Arenaviruses are a group of RNA viruses several of which have the potential to cause a deadly syndrome of hemorrhagic fever. In humans these viruses are usually transmitted by exposure to infected rodent excreta; occasional laboratory or nosocomial infections have been reported.1 Sabiá virus is an arenavirus that was first isolated in São Paulo, Brazil, in 1990 from an agricultural engineer who presented with a hemorrhagic fever syndrome and ultimately died. Necrosis of the liver was found at autopsy. The virus was subsequently characterized as a new member of the Tacaribe complex of the family Arenaviridae.2 A laboratory technician in Brazil who was involved in the characterization of the agent was also infected and had a severe nonfatal illness. Neither patient was treated with ribavirin.2

We now report a third case of Sabiá virus infection, which was successfully treated with ribavirin. We also discuss occupational exposure, the clinical course of the illness, and biosafety management in a university-hospital setting.

Case Report

Occupational Exposure

On August 8, 1994, a 46-year-old virologist working alone in a biosafety-level-3 laboratory used a high-speed centrifuge to clarify a harvest of infected Vero cells containing Sabiá virus. The centrifuge contained six 250-ml bottles in a rotor with an intact O-ring to seal the contents during centrifugation. Each screw-capped polycarbonate bottle contained approximately 200 ml of tissue-culture fluid. The centrifuge was run at 10,000 rpm for 10 minutes (10,200xg) at a temperature setting of 4°C. The virologist observed no indication of a problem during the centrifugation process. On opening the lid of the rotor to remove the centrifuge bottles, he noted that the outside of one bottle was wet and that fluid had leaked into the bottom of the rotor. No obvious break was identified at the time, and the virologist was wearing a surgical mask, a disposable solid-front gown, and gloves. He had no abrasions or scratches on his hands.

The virologist used a second pair of gloves during the decontamination of the rotor, but did not wear a positive air-purifying respirator, although it was available. He decontaminated the spillage by pouring a concentrated solution of sodium hypochlorite (5.25 percent) directly into the rotor bucket as well as inside and outside the bottle that had leaked. The combined bleach and liquid in the rotor were then absorbed with paper towels. After the incident, the virologist continued working alone in the laboratory for another three to four hours. All his protective garments as well as other contaminated material in the laboratory were autoclaved. Initially, he did not report the incident because he believed that no exposure to virus had occurred.

Case Presentation and Clinical Course

On August 16, 1994, the virologist noted myalgias, a mild headache, a stiff neck, and fever while driving home to New Haven, Connecticut, after a weekend visit to Boston. He treated himself with ibuprofen for two days before seeking medical care. On questioning, he described recrudescences of Plasmodium vivax infection that had never been treated with primaquine. He was concerned that this fever could represent a relapse of malaria. He initially did not recall any serious laboratory exposures. On physical examination he appeared mildly ill, with a temperature of 37.6°C (99.8°F), a pulse of 89 beats per minute, and a blood pressure of 130/80 mm Hg. The only remarkable features were mild conjunctival injection and shotty cervical nodes in the anterior chain. Laboratory studies performed that afternoon revealed a hematocrit of 42 percent, a white-cell count of 2600 per cubic millimeter, a platelet count of 138,000 per cubic millimeter, and an alanine aminotransferase level of 63 U per liter; urinalysis revealed moderate proteinuria (2+). After a smear proved negative for malaria, further review of possible infectious exposures led the patient to recall the August 8 laboratory incident with Sabiá virus.

The patient was immediately hospitalized and treated with intravenous ribavirin at a dosage used by the Centers for Disease Control and Prevention (CDC) for other arenavirus infections (a loading dose of 30 mg per kilogram of body weight, followed by a dose of 15 mg per kilogram every six hours for four days, and then by a dose of 7.5 mg per kilogram three times daily for six days). Pretreatment blood samples were sent for viral culture and examination by the polymerase chain reaction (PCR) for the presence of Sabiá virus RNA. PCR testing for Sabiá virus was reported to be positive on hospital day 2. The reverse-transcription PCR technique produces a fragment of 180 base pairs by using one primer specific for arenavirus in combination with one specific for Sabiá virus. Controls consisted of Sabiá virus RNA extracted from infected cell monolayers and normal human serum (Rico-Hesse R: personal communication).

Figure 1 shows the patient's temperature curve and laboratory values during hospitalization. No hemorrhagic manifestations were observed. His white-cell and platelet counts reached a nadir on hospital day 2: total white-cell count, 1300 per cubic millimeter; absolute neutrophil count, 650 per cubic millimeter; and platelet count, 98,000 per cubic millimeter. His serum alanine aminotransferase values peaked at 128 U per liter on day 10 of hospitalization. During treatment, his hematocrit dropped, and aminotransferase levels increased. He also reported a severe headache. The patient was sent home with a white-cell count of 3800 per cubic millimeter on August 29 after 10 days of intravenous ribavirin.


View larger version (10K):

Figure 1. Laboratory Findings in a Patient Infected with Sabiá Virus.

The patient was exposed to Sabiá virus on August 8, 1994, and became symptomatic on August 16. To convert values for total bilirubin to micromoles per liter, multiply by 17.1; to convert values for calcium to millimoles per liter, multiply by 0.25; and to convert values for phosphate to millimoles per liter, multiply by 0.3229.

Blood samples were collected daily from the patient before ribavirin therapy was begun and during the rest of his hospitalization. The serum samples were used to inoculate cultures of Vero E-6 cells maintained at 37°C, and the cultures were examined for the presence of Sabiá virus antigen 10 days after inoculation with the use of an indirect fluorescent-antibody technique with mouse ascitic fluids that were reactive to the Tacaribe group and specific for Machupo virus and a commercial fluorescein-labeled goat antimouse IgG antibody. Uninfected Vero cells served as controls. Cells inoculated with a serum sample obtained on admission to the hospital and before ribavirin therapy was begun were positive for viral antigen. IgM and IgG antibodies to Sabiá virus antigen (infected Vero cells) were subsequently detected by indirect fluorescent-antibody testing in a serum sample drawn during convalescence 35 days after the clinical onset of the illness. Serum samples obtained before this time were negative for Sabiá virus antibodies and served as negative controls. Attempts to isolate the virus from urine, semen, and blood were repeatedly negative after ribavirin therapy was begun.

Biosafety Management and Contact Surveillance

After PCR confirmation of infection with Sabiá virus, the patient was transferred to a negative-pressure isolation suite.3 The suite consisted of an anteroom with lower pressure than the surrounding hallway and two patient rooms with lower pressure than the anteroom. The patient remained in the same room throughout his hospital stay; the other patient room was used for the temporary storage of waste and for decontamination.

Once materials entered the negative-pressure isolation suite, they were considered to be contaminated. Items were double bagged and held in the adjacent negative-pressure storage room before being transported in an enclosed cart to the autoclave. Larger items were wiped with disinfectant before removal. Disposable items were bagged on removal from the room, autoclaved, and incinerated.

Throughout the patient's hospitalization universal precautions were used by all health care workers who came in contact with him or his specimens.4 Precautions were upgraded after PCR confirmation to include the use of fit-tested masks with high-efficiency particulate air filters, gowns, and gloves by all persons entering the patient's room and laboratory workers processing the patient's specimens. The number of health care workers who came in contact with the patient or his specimens was restricted.

Additional precautions were implemented in the laboratories to reduce the risk of potential exposure to aerosols from infected body fluids. All specimens were double bagged and carried by hand to the laboratories by the patient's physician. Chemistry specimens were processed in a negative-pressure room. Samples were spun in a sealed centrifuge, and serum was treated with Triton X-100 (10 µl of 10 percent Triton X-100 per milliliter of serum) to inactivate the virus. Hematologic specimens were processed in a Coulter counter that did not require removal of the top of the tube, and the effluents were treated with sodium hypochlorite and then autoclaved. The Coulter counter was also cleaned after use with several cycles of diluted bleach. Other laboratory tests were carried out within a biosafety cabinet.

All contacts of the patient were identified and stratified into risk groups. One hundred thirty-nine contacts were identified, consisting of workers providing patient care, hospital laboratory workers, colleagues, friends, and family members. No exposure had occurred that would have placed any contact at high risk of contracting the virus. However, all contacts were notified that a possible exposure to Sabiá virus had occurred, and they were enrolled in a medical-surveillance program. As part of the surveillance program, all contacts were interviewed, answered a questionnaire, and provided a blood sample for testing at the CDC; six weeks later, they completed a follow-up questionnaire and provided a second blood sample.

The contacts were also instructed to take their temperatures twice daily over the six-week period and to monitor for early symptoms of the disease. They were given a telephone number that was staffed 24 hours a day by physicians with expertise in occupational medicine and infectious diseases and who were familiar with the index case. No symptoms suggestive of Sabiá virus infection occurred in the group under surveillance during the six-week follow-up period; however, one subject had a viral syndrome with leukopenia and mild hepatitis just after the end of the six-week observation period. A serologic test (enzyme-linked immunosorbent assay) for arenavirus infection and PCR testing for Sabiá virus RNA were negative, and a serum sample obtained during convalescence was also negative for IgM and IgG antibodies to Sabiá virus antigen.

A protocol was generated with the emergency department for the triage and care of any secondary cases. The plans included restricting the number of health care workers who came in contact with people who might have been secondarily infected; immediately notifying the clinical laboratories, the hospital epidemiology department, the state health department, and the CDC of any additional suspected cases; isolating other potentially infected persons in a negative-pressure isolation suite; and having physicians familiar with the index patient clinically evaluate such persons.

Discussion

We describe the third confirmed case of Sabiá virus infection. The two previous cases were identified in Brazil.2 Four other arenaviruses (Lassa, Junin, Machupo, and Guanarito) have been associated with a hemorrhagic disease in humans.1 Each of these agents has a distinct geographic distribution, although they cause similar clinical manifestations and high mortality.1 Wild rodents serve as reservoirs for these arenaviruses; humans usually become infected by contact with contaminated rodent excreta. Little is known about the mode of transmission of Sabiá virus or its source in nature.

We believe that Sabiá virus was most likely transmitted to the investigator by aerosol, probably when the centrifugation rotor was opened and the leak was observed or during the decontamination process. [THIS WAS DEPICTED IN THE 1995 MOVIE OUTBREAK!!!! WAS THIS A PLANNED ATTACK TO SPREAD VIRUSES AND WAS DONE ON PURPOSE? WATCH THE MOVIE IT IS ALMOST LIKE IT WAS A PURPOSEFUL SABATOGE LIKE THE LIGHT BULB IN THE MOVIE "THE SOLDIER"!The 8-day incubation period in this case is consistent with that of other arenaviral illnesses (range, 6 to 21 days).1,3 We chose to treat the patient early with intravenous ribavirin, a guanosine analogue, since clinical studies have shown it to be effective in diminishing mortality in Lassa fever if given early in the course of illness.5 Clinically, our patient had an excellent response; he became afebrile and asymptomatic within 48 hours, in contrast to the other two patients with Sabiá virus infection, who had a prolonged course with hemorrhagic symptoms. His severe leukopenia and thrombocytopenia rapidly improved, and no further virus was detected in his blood by culture after treatment was initiated. The mild hemolysis was thought to be due to ribavirin therapy and is a well-described effect of the drug.6 The late peak in aminotransferase values, although not dramatic, was unusual, since it was asynchronous with the recovery from leukopenia and thrombocytopenia. It could have been caused by an adverse effect of the ribavirin not previously described, infection, or immunologic recovery from Sabiá virus. Hepatocellular damage and hepatitis have been described with Sabiá virus and other arenaviruses.1,2 The patient's late immunologic response, as reflected by the finding of IgG and IgM antibodies to Sabiá virus, may have been modified by treatment with ribavirin, or it may represent the natural response to Sabiá virus infection.

Since a number of nosocomial outbreaks have been described among hospital personnel attending acutely ill patients with arenavirus infections, a high level of precaution was instituted at our hospital, as recommended by the CDC.3 Although extensive experience in West Africa with Lassa fever has shown that universal precautions and nursing using barrier precautions generally prevent the transmission of Lassa virus in hospitals, we also instituted negative-pressure isolation, limited the number of hospital personnel caring for the patient, and required personnel potentially exposed to blood aerosols to wear respirators with high-efficiency particulate air filters.3,4 Clinical laboratory specimens were processed to minimize workers' exposure to aerosolized virus, and routine automated equipment for chemistry specimens was not used unless the specimen was first treated with Triton X-100. Contact surveillance with a follow-up of six weeks (well within the incubation period of arenaviral illnesses) identified no secondary cases.

Researchers need to recognize the risk of occupational exposure to Sabiá virus by aerosol. Ribavirin treatment may modify the clinical course of Sabiá virus infection. Although standard universal precautions may be adequate to prevent nosocomial spread, additional biosafety precautions should be considered when one is dealing with arenaviruses and other dangerous viruses whose mechanisms of transmission are unknown.


We are indebted to Ms. Carolyn Karbowski for assistance in the preparation of the manuscript, to Dr. Mark Cullen for his thoughtful comments, to Dr. Petrie Rainey for suggesting the Triton X-100 treatment, and to the Yale–New Haven Hospital house staff, laboratory workers, and nursing personnel for the professional care offered to this patient under unusual circumstances.


Source Information

From the Department of Internal Medicine (M.B., M.R., D.G., L.D.) and Yale Arbovirus Research Unit, Department of Epidemiology and Public Health (R.T.), Yale University School of Medicine, New Haven, Conn.; the Special Pathogens Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta (L.A., A.S.K., C.J.P.); and Institut Français de Recherche Scientifique pour le Développement en Coopération, Paris (J.P.G.).

Address reprint requests to Dr. Barry at the International Health Program, Yale University School of Medicine, 20 York St., New Haven, CT 06504.

References

Peters CJ, Johnson KM. Arenaviridae: lymphocytic choriomeningitis virus, Lassa virus, and other arenaviruses. In: Mandell GL, Bennett JE, Dolin R, eds. Mandell, Douglas and Bennett's principles and practice of infectious diseases. 4th ed. Vol. 2. New York: Churchill Livingstone, 1995:1572-9.  
Lisieux T, Coimbra TL, Nassar ES, et al. New arenavirus isolated in Brazil. Lancet 1994;343:391-392. [CrossRef][Medline]
Management of patients with suspected viral hemorrhagic fever. MMWR Morb Mortal Wkly Rep 1988;37:Suppl:1-15.
Fisher-Hoch SP, Price ME, Craven RB, et al. Safe intensive-care management of a severe case of Lassa fever with simple barrier nursing techniques. Lancet 1985;2:1227-1229. [Medline]
McCormick JB, King IJ, Webb PA, et al. Lassa fever: effective therapy with ribavirin. N Engl J Med 1986;314:20-26. [Abstract]
Canonico PG, Kastello MD, Spears CT, Brown JR, Jackson EA, Jenkins DE. Effects of ribavirin on red blood cells. Toxicol Appl Pharmacol 1984;74:155-162. [CrossRef][Medline]


This article has been cited by other articles:

Larson, R. A., Dai, D., Hosack, V. T., Tan, Y., Bolken, T. C., Hruby, D. E., Amberg, S. M. (2008). Identification of a Broad-Spectrum Arenavirus Entry Inhibitor. J. Virol. 82: 10768-10775 [Abstract] [Full Text]  
Kimman, T. G., Smit, E., Klein, M. R. (2008). Evidence-Based Biosafety: a Review of the Principles and Effectiveness of Microbiological Containment Measures. Clin. Microbiol. Rev. 21: 403-425 [Abstract] [Full Text]  
SBRANA, E., XIAO, S.-Y., GUZMAN, H., YE, M., TRAVASSOS DA ROSA, A. P. A., TESH, R. B. (2004). EFFICACY OF POST-EXPOSURE TREATMENT OF YELLOW FEVER WITH RIBAVIRIN IN A HAMSTER MODEL OF THE DISEASE. Am J Trop Med Hyg 71: 306-312 [Abstract] [Full Text]  
Gavin, P. J., Katz, B. Z. (2002). Intravenous Ribavirin Treatment for Severe Adenovirus Disease in Immunocompromised Children. Pediatrics 110: e9-9 [Abstract] [Full Text]  
Murphy, F. A., Johnson, K. M. (1995). An Exotic Viral Disease Acquired in a Laboratory. NEJM 333: 317-319 [Full Text]  

[Satyagraha]

From the "White House Initiative for Global Climate Change website:
http://clinton2.nara.gov/Initiatives/Climate/Video/shope-56.html

Nobel Laureates
Dr. Robert Shope
(Professor at University of Texas, Director of the Yale Arbovirus Research Unit for 24 years)

Robert Shope has devoted his career to the study of viruses carried by mosquitoes, ticks, and other biting insects. These viruses can cause life-threatening diseases in humans such as malaria, dengue and yellow fevers, and encephalitis. Since receiving hi s medical degree in 1954 from Cornell University, he has spent many years in Malaysia, Brazil, and other tropical sites studying these insect-borne diseases. He was a Professor of Epidemiology at Yale University's School of Medicine from 1975 to 1995, and served as the Director of the Yale Arbovirus Research Unit. During that period he was awarded many honors, including the Walter Reed Award from the American Society of Tropical Medicine and Hygiene. He is presently a Professor in the Departments of Path ology and Microbiology and Immunology at the University of Texas Medical Branch.

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Thank you, Mr. President. Health and the environment are closely linked. If there is a 6 °F warming, the heat alone in North American cities, such as Washington, D.C., will result in an excess of deaths, especially in elderly people who do not adapt well to severe warmth. We had an example in July of 1995 in Chicago, Illinois. There the temperature exceeded 90 °F night and day for a prolonged period, and there were 465 deaths recorded in Chicago related to the heat.

My own personal experience is with diseases transmitted by ticks, mosquitoes, and other biting insects. Let me talk about dengue virus. This causes a disease in people which typically gives them high fever, headache, muscle aches and pains, and sometimes a rash. There is a more severe form of dengue, dengue-hemorrhagic fever, in which the case mortality rate is about 10 percent. This virus is transmitted by a mosquito that lives in and around homes in warm climates. The mosquito is killed by a hard freeze ; therefore, it's northern limit is about Memphis, Tennessee, at the present time. In the last decade, we've seen a steady increase in the numbers of cases of dengue in tropical America, including Mexico. This disease is now literally on our southern border. I cannot tell you whether dengue epidemics will occur in the United States, but with climate change and warming, the mosquito will thrive further north.

These same factors apply to the vector of malaria, also a mosquito. Malaria is a disease that, worldwide, kills approximately 2 million people each year. It's a tropical disease, but recently has occurred in small outbreaks in the United States, in New Jersey, New York, and Texas, and with warming we can expect these outbreaks to continue and to enlarge.

The factors that I've talked about argue for controlling the environment while we still have time, and I will say that the best insurance is preparedness. There are many other diseases directly affected by rainfall and warming –– St. Louis encephalitis, t he tick-borne Lyme disease, and the newly recognized rodent-associated Hantavirus pulmonary syndrome, which broke out in 1993 in the southwestern part of the United States. Each nation in the world has its own set of diseases, some of which affect Americans abroad or can be transported and introduced into the United States. Therefore, the problem of climate change and health is of common interest among nations as are the solutions. Thank you.
 

[Satyagraha]

Sabia virus incident at Yale University.
Am Ind Hyg Assoc J.  1997; 58(1):51-3 (ISSN: 0002-8894)
Gandsman EJ; Aaslestad HG; Ouimet TC; Rupp WD
Office of Environmental Health and Safety, Yale University, New Haven, CT 06510, USA.
http://www.medscape.com/medline/abstract/9018837

An incident involving a human exposure to a newly isolated arenavirus, Sabia virus, in the Yale Arbovirus Research Unit occurred at Yale University on August 8, 1994. A senior-level visiting research scientist was exposed to Sabia virus while purifying the virus from a large volume of tissue culture fluid. The exposure resulted in development of a Sabia virus infection followed by recovery of the patient. The incident resulted in a comprehensive review by a Yale faculty committee and an external expert committee. As a result, a number of new practices and procedures were added to Yale's biosafety policy for investigating infectious agents in BL-3 facilities.

[Satyagraha]

Résumé de : ANSARI (MZ) & SHOPE (RE) - 1994 - Epidemiology of arboviral infections. Public Health Reviews, 22 (1-2), pp. 1-26.
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http://www.pasteur.fr/recherche/banques/CRORA/res6/re3266.htm

OBJECTIVE: To review the current state of knowledge regarding the epidemiology of arboviruses.

DATA SOURCES: Computerized literature searches, identification of papers through review of article bibliographies, and Yale Arbovirus Research Unit, USA.

STUDY SELECTION: Articles documenting research pertaining to the epidemiology of arboviruses with emphasis on factors that increase or decrease the spread of these infections. DATA EXTRACTION: The review articles were extracted independently by the authors.

DATA SYNTHESIS: Arboviral infections are a global health problem accounting for significant morbidity and mortality in human and animal populations. They belong to the families Togaviridae, Flaviviridae, Bunyaviridae, Reoviridae, and Rhabdoviridae, and are transmitted to humans and domestic animals by the bite of infected arthropods. Rodents and birds are significant vertebrate hosts, while humans are usually not involved in the maintenance and spread of most arboviruses. Ecologic changes and human behavior are important in the spread of these infections. Clinical features range from mild fevers to fatal encephalitis. Surveillance, immunization, and vector control are important methods of prevention.

CONCLUSION: It appears that the distribution and spread of arboviruses is greatly influenced by human behavior and ecologic changes in the environment. Awareness regarding these and other factors, such as travel history, history of bites of arthropods, concurrent epidemic pattern in the community, and knowledge of surveillance data are useful ways of identifying these infections. Future research may be directed toward methodical search for new arboviruses and their relation to human and animal disease.

[Satyagraha]

> Summer 2004 > In Memoriam
Virologist Robert E. Shope  
http://ysm.research.yale.edu/article.jsp?articleID=92
By Brendan Black

Esteemed virologist Robert Shope, professor emeritus in the Department of Epidemiology and Public Health at Yale School of Medicine, and professor of microbiology and immunology at the University of Texas Medical Branch (UTMB), died January 26 from complications of pulmonary fibrosis. He was 74 years old.

Born in Princeton, NJ, in 1929, Shope received a bachelor’s degree in zoology from Cornell University in 1951 and an M.D. in 1954 from Cornell Medical School. For 30 years Shope served as a faculty member at Yale University, gaining national prominence in the field of virology. He led several organizations including the Yale Arbovirus Research Unit and the American Society for Tropical Medicine and Hygiene.

Throughout his career, Shope researched thousands of viruses and arboviruses carried by insects and other arthropods and led investigations on a wide variety of diseases including Rift Valley fever, Lassa Fever, and yellow fever.

After retiring from Yale University in 1995, Shope served on the faculty at UTMB at Galveston as the co-director of the University’s Center for Biodefense Studies.

Shope is recalled by colleagues and friends as being an active and upbeat man who treated everyone the same regardless of age, education, or social status. UTMB has named a laboratory after him in honor of his contributions to the university and the scientific community.

[Satyagraha]

Can anyone crack this open? I get zip, zilch... but I doubt the info is gone.. just 'hard' to find...

World Reference Center and Arbovirus Diagnosis.
The Yale Arbovirus Research Unit serves as the arbovirus reference center for the world. ... Title : World Reference Center and Arbovirus Diagnosis. ... Subject Categories : MEDICINE AND MEDICAL RESEARCH;
stinet.dtic.mil/oai/oai?verb=getRecord&metadataPrefix=html&identifier=ADA092601 - [cache] - Ask

[Satyagraha]

Jean-Paul Gonzalez

Research Center for Emerging Viral Diseases
IRD UR 178
Center for Vaccine Development,
Institute of Science and Technology for Research and Development,
Mahidol University Salaya campus
Tel/Fax: (66) (0)2 441 0227
E-mail: frjpg@mahidol.ac.th

Present Position

Research Unit Director Emerging Diseases & Information Systems (UR178), IRD, France.
Co-Director of the Research Center for Emerging Viral Diseases (RCEVD)

Education

M.D., Docteur en Médecine Université de Bordeaux II, 1974
Ph.D., Faculty of Sciences, Clermont Ferrand University, 1984

Experiences

1979 Researcher , ORSTOM Laboratory, Pasteur Institute, Bangui

1981 Guest Researcher, Special Pathogen Branch, Centers for Diseases Control, Atlanta , USA

1984 Chief of Laboratory, Laboratory of arbovirus and virus of hemorragic viral fever, Pateur Institute, Bangui

1987 Chief of Service, Laboratory of experimental virology, Pateur Institute, Dakar, Senegal

1991 Professor Epidemiology and Public Health, Yale Arbovirus Research Unit, Ecole de Médecine Université, USA

1997-present
Visiting Professor of Microbiology, Research Center for Emerging Viral Disease, Center for Vaccine Development, Institute of Science and Technology for Research and Development, Mahidol University , Thailand

[Satyagraha]

http://www.jmedcbr.org/Editor%20Bios/Woodall.html

John P. Woodall, PhD
Brazil    

     

John (Jack) Woodall is a graduate of Cambridge University, UK, and received his PhD from London University, UK. 

His career began in Africa as Scientist in Her Majesty’s Overseas Research Service, at the East African Virus Research Institute, Entebbe, Uganda. 

Subsequently he joined The Rockefeller Foundation as director of its Belem Virus Laboratory in Brazil.  When the Foundation ended its association with its overseas virus laboratories, he became a Research Fellow at the Yale Arbovirus Research Unit in New Haven CT, and then head of the Arbovirus Laboratory, New York State Health Dept., Albany NY.  (Note: YARU initial startup funding by Rockefeller Foundation... they OWN YARU.)

Shortly after that he became a staff member of the U.S. Public Health Service and director of the Centers for Disease Control’s (CDC) San Juan Laboratories in Puerto Rico, which carried out research on dengue and schistosomiasis.  In 1981 he moved to the World Health Organization, Geneva, Switzerland, first in the Laboratory Unit, and then as Epidemiologist in the Division of Health Statistics (later Division of Health Situation & Trend Assessment). 

He was a member of the WHO Gulf Emergency Task Force in support of the UN Special Commission (UNSCOM) in Iraq, and Leader of the WHO delegation to the Third Review Conference on the Biological Weapons Convention, and to the Ad Hoc meetings of the Verex committee, both in Geneva. 

On retirement from WHO after 13 years, he returned to the Arbovirus Laboratory, New York State Health Dept., Albany, NY, as director. From 1998-2007 he has been visiting professor, Institute of Medical Biochemistry, and director, Nucleus for the Investigation of Emerging Infectious Diseases, at the Federal University of Rio de Janeiro, Brazil.  He retired from that post in 2007.

He was a co-founder of ProMED-mail, the online outbreak early warning system of the Program for Monitoring Emerging Diseases (ProMED) of the International Society for Infectious Diseases (ISID), and Web Site Editor and Council member (ex officio), American Society of Tropical Medicine & Hygiene. 

He is a member of the Biological Weapons Working Group of the Center for Arms Control and Non-Proliferation, Washington DC, and Board member, Sabin Vaccine Institute, Washington DC.  He has been editor of various publications for WHO, the Stockholm International Peace Research Institute & Sabin Vaccine Institute, is a reviewer for the Emerging Infectious Disease Journal, the Journal of the American Society of Tropical Medicine & Hygiene, and Virus Reviews & Research, and is presently a monthly columnist for The Scientist magazine.

His interests are arbovirus epidemiology, using the internet for rapid dissemination of disease outbreak information, and biodefense.

[Satyagraha]

Re: the Yale Lab incident with Sabia Virus
Excerpted from:
http://mrce.wustl.edu/docs/2008_BioSafetyCourseNotes/Lab%20Acquired%20Infections.pdf
(Note: i'll post the entire PDF in a separate thread; this contains only those pages relevant to the Yale lab.)

Biosafety Education
for the Research Scientist
Laboratory Acquired Infections
Joe Kanabrocki
Washington University in St. Louis
September 16, 2008

[trailhound]

Nice thread.

[Satyagraha]

Arenavirus Infection -- Connecticut, 1994
http://www.cdc.gov/mmwr/preview/mmwrhtml/00032515.htm

On August 20, 1994, the Connecticut Department of Public Health and Addiction Services received a report of a case of acute illness in a virologist suspected to be associated with Sabia virus, a newly described arenavirus. This report presents preliminary findings from the case investigation.

On August 19, 1994, the virologist presented to the Tropical Medicine Clinic at Yale-New Haven Hospital with a 4-day history of fever, malaise, backache, stiff neck, and myalgias that he attributed to a recurrence of a Plasmodium vivax infection. On evaluation at the clinic, his temperature was 99.8 F (37.6 C) on antipyretics, and he had a normal physical examination. Laboratory evaluation included a negative malaria smear, a total white blood cell count (WBC) of 2600 cells/mm3 (normal: 4000-10,000 cells/mm3), a platelet count of 138,000 cells/mm3 (normal: 150,000-350,000 cells/mm3), 2+ proteinuria, and alanine aminotransferase (ALT) of 6356 U/L (upper limit normal: 35 U/L).

A history of a possible laboratory exposure to Sabia virus was obtained, and the man was hospitalized for prompt treatment with intravenous ribavirin, an antiviral drug that is effective against other arenavirus infections such as Lassa fever (1).

On admission, the patient had a temperature of 103 F (39.4 C). Within 24 hours of hospitalization, his total WBC and platelet count had declined to a low of 1400 cells/mm3 and 92,000 cells/mm3, respectively. His ALT peaked at 128 U/L on the 9th day of hospitalization. No hemorrhagic manifestations of the infection were observed during hospitalization. A diagnosis of Sabia infection was confirmed on acute serum by amplification of a portion of the viral genome by polymerase chain reaction and by isolation of the virus from blood. The patient recovered and was discharged on August 26.

On August 8, the virologist was apparently exposed to an aerosol of Sabia virus when a centrifuge bottle developed a crack, and tissue culture supernatant containing the virus leaked into the high-speed centrifuge. At the time of the incident, the virologist was working alone in the biosafety level-3 laboratory (negative pressure with HEPA-filtered exhaust system). He cleaned the spilled material from the centrifuge while wearing a gown, surgical mask, and gloves.

Persons who came in contact with the patient or with his biological specimens in the hospital laboratories since onset of his illness were notified and enrolled in a surveillance program. None of these persons have had exposure to the patient that would suggest a high risk for secondary infection. As of August 31, none of the persons under surveillance have reported a febrile illness.

Reported by: M Barry, MD, F Bia, MD, M Cullen, MD, L Dembry, MD, S Fischer, MD, D Geller, MD, W Hierholzer, MD, P McPhedran, MD, P Rainey, MD, M Russi, MD, E Snyder, MD, E Wrone, MD, Yale Univ School of Medicine and Yale-New Haven Hospital; JP Gonzalez, MD, R Rico-Hesse, PhD, R Tesh, MD, R Ryder, MD, R Shope, MD, Yale Arbovirus Research Unit, Yale Univ; WP Quinn, MPH, New Haven Health Dept; PD Galbraith, DMD, ML Cartter, MD, JL Hadler, MD, State Epidemiologist, Connecticut Dept of Public Health and Addiction Svcs. A DeMaria, Jr, MD, State Epidemiologist, Massachusetts Dept of Public Health. Div of Field Epidemiology, Epidemiology Program Office; Special Pathogens Br, Div of Viral and Rickettsial Diseases, National Center for Infectious Diseases, CDC.

Editorial Note

Editorial Note: Sabia virus was isolated by scientists in Sau Paulo, Brazil, in 1990 and characterized by scientists in Belem, Brazil, and at the Yale Arbovirus Research Unit (2). Only two cases of Sabia virus infection (both in Brazil) have been reported (2). One was a naturally acquired infection in an agricultural engineer who was probably infected by exposure to an infected rodent (the natural reservoir of other known arenaviruses). The engineer died approximately 2 weeks after becoming ill. The second case was in a laboratory technician who was working with the virus. He had a severe illness characterized by 15 days of fever, chills, malaise, headache, generalized myalgia, sore throat, conjunctivitis, nausea, vomiting, diarrhea, epigastric pain, bleeding gums, and leukopenia. He recovered after hospitalization and treatment with intravenous fluids.

Little is known about the modes of transmission of the Sabia virus. Based on the pathogenesis of other arenaviruses, the Sabia virus is not believed to be infectious until the patient exhibits symptoms. Other arenaviruses can be transmitted by needle-stick but do not readily spread from person to person. Persons in casual contact with persons with arenavirus infection are not at risk for disease and do not require medical follow-up.


References

1. McCormick JB, King IJ, Webb PA, et al. Lassa fever: effective therapy with ribavirin. N Engl J Med 1986;314:20-6.

2. Coimbra TLM, Nassar ES, Burattini MN, et al. New arenavirus isolated in Brazil. Lancet 1994;343:391-2.

+------------------------------------------------------------------- ------+ |             | | Erratum: Vol. 43, No. 34 | |             | | SOURCE: MMWR 43(35);659 DATE: Sep 09, 1994 | |             | | In the article "Arenavirus Infection -- Connecticut, 1994" on | | page 635, the last sentence of the second paragraph should read | | "Laboratory evaluation included a negative malaria smear..., and | | alanine aminotransferase (ALT) of 63 U/L (upper limit normal: 35 | | U/L).       | |             | +------------------------------------------------------------------- ------+

**Questions or messages regarding errors in formatting should be addressed to mmwrq@cdc.gov.

[Satyagraha]

Monday, Sep. 05, 1994
A Deadly Virus Escapes
http://www.time.com/time/magazine/article/0,9171,981359,00.html
By MICHAEL D. LEMONICK;Alice Park/New York

The accident must have come as a horrifying shock, even for an experienced scientist. One minute, a sample was spinning in a high-speed centrifuge. Then, suddenly, the container cracked, and the sample -- tissue contaminated by a rare, potentially lethal virus -- spattered the inside of the centrifuge. Fortunately, the Yale University researcher working with the deadly germs was wearing a lab gown, latex gloves and a mask, as required under federal guidelines. He also knew the proper procedure for dealing with a deadly spill: rub every surface with bleach, sterilize all instruments that have been exposed, then wipe everything down again with alcohol. There was just one rule he failed to follow. Having decided the danger was over, he didn't bother to report the accident, and a few days later he left town to visit an old friend in Boston.

Bad move. Although he would not realize it for about a week, the scientist -- his name has not been officially released -- had been infected with the mysterious Brazilian Sabia virus. Soon after he got back to Yale, he was running a fever that reached 103F. An experimental antiviral drug eventually stopped the illness, but the man had exposed five people, including two children, before being confined to a hospital isolation ward, and another 75 or so health-care workers after that. All of them are under observation. While the patient slowly recovered last week, Yale officials had to decide whether he would be disciplined for breaking lab rules. They also suspended all research on live Sabia virus and called in the federal Centers for Disease Control to evaluate the setup and procedures at the Yale Arbovirus Research Unit, where the accident took place. Says Dr. Peter Galbraith of the Connecticut health department: "We are concerned that the incident was not reported immediately. But all our information at this point indicates it's a well-run lab."

Luckily, there was never much danger to the general public. The concerns will only intensify in the weeks ahead with the publication of the gripping book Hot Zone, about a deadly-virus crisis in Virginia in 1989 (see following stories). Sabia is almost certainly carried by rodents and is not contagious by casual contact (the afflicted scientist evidently got it from tiny bits of tissue that flew into his unprotected eyes or nose or both). The Yale lab, moreover, is classified as a level-3 biohazard facility, meaning, among other things, that it is kept at negative air pressure. Outside air can flow in through tiny cracks, but air flows out only via heavily filtered vents.

Even so, the accident has raised questions about whether such dangerous disease agents are being handled carefully enough. Sabia and several related viruses -- Junin, Machupo and Guanarito in South America and Lassa in Africa, all members of the arenavirus family -- are particularly frightening because they can kill in such a grisly way. Characteristic symptoms are high fever, uncontrolled bleeding in virtually every organ and finally shock. The liver turns yellow and decomposes. Blood can leak from literally every bodily orifice, including the eyes and the pores of the skin.

But while some other arenaviruses have been known to doctors for at least two decades, Sabia was never seen before 1990. In that year, a female agricultural engineer checked into a hospital in Sao Paulo, Brazil, with a high fever. Within days she was dead. Brazilian scientists tried to identify the infectious agent; one of their number fell ill and nearly died in the process. But they could determine only that it was a member of the arenavirus clan, so they sent a sample on to Yale for further identification.

It was the infected Yale researcher who originally helped show that this was a brand-new virus. That is still almost all scientists know about it. Says Dr. Robert Shope, director of the Yale virus lab: "We're reasoning by analogy to other arenaviruses that Sabia has a rodent reservoir. Once the reservoir and transmission are understood, it should be possible to take measures to control the infection. This is our ultimate aim."

That is also the aim for the scores of other viruses that the Yale lab and a select few others in the U.S. receive constantly from around the world. Says Shope: "About 100 of the viruses we have can infect people, and of those, 10% to 20% can kill." But even if scientists find ways to deal with all of those, there will always be more. New viruses are continually leaping from animal populations, where they have circulated harmlessly for years, into humans, and the problem has only become worse as people have moved into formerly uninhabited areas.

Yale officials said last week that they had never contemplated shutting down the research lab entirely. What they might have to consider, though, perhaps in consultation with the CDC, is treating Sabia virus as a so-called class 4 biohazard from now on, which means researchers will be able to handle it only inside a glove box or while wearing a space suit. Lassa and Guanarito are deemed class 4 already. The CDC might also do well to institute a rule that any unclassified infectious agent should be considered class 4 until proved otherwise.

Meanwhile, the first potential U.S. victims will be coming off Sabia watch next week; so far, nobody has shown any evidence of symptoms. They were lucky the Yale man was dealing with a virus that is not highly contagious. If researchers do not tighten some of their procedures, the next outbreak might not be so benign.

 Click to Print Find this article at:
http://www.time.com/time/magazine/article/0,9171,981359,00.html

[Satyagraha]

[author=Sane link=topic=134859.msg817120#msg817120 date=1253409959]

What really happened in 1994?
What exactly is the "Yale Arbovirus Research Unit"
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~

Treatment of a Laboratory-Acquired Sabiá Virus Infection
http://content.nejm.org/cgi/content/full/333/5/294

Michele Barry, M.D., Mark Russi, M.D., M.P.H., Lori Armstrong, Ph.D., David Geller, M.D., Ph.D., Robert Tesh, M.D., Louise Dembry, M.D., Jean Paul Gonzalez, M.D., Ali S. Khan, M.D., and Clarence J. Peters, M.D.

Arenaviruses are a group of RNA viruses several of which have the potential to cause a deadly syndrome of hemorrhagic fever. In humans these viruses are usually transmitted by exposure to infected rodent excreta; occasional laboratory or nosocomial infections have been reported.1 Sabiá virus is an arenavirus that was first isolated in São Paulo, Brazil, in 1990 from an agricultural engineer who presented with a hemorrhagic fever syndrome and ultimately died. Necrosis of the liver was found at autopsy. The virus was subsequently characterized as a new member of the Tacaribe complex of the family Arenaviridae.2 A laboratory technician in Brazil who was involved in the characterization of the agent was also infected and had a severe nonfatal illness. Neither patient was treated with ribavirin.2

We now report a third case of Sabiá virus infection, which was successfully treated with ribavirin. We also discuss occupational exposure, the clinical course of the illness, and biosafety management in a university-hospital setting.

Case Report
Occupational Exposure

On August 8, 1994, a 46-year-old virologist working alone in a biosafety-level-3 laboratory used a high-speed centrifuge to clarify a harvest of infected Vero cells containing Sabiá virus. The centrifuge contained six 250-ml bottles in a rotor with an intact O-ring to seal the contents during centrifugation. Each screw-capped polycarbonate bottle contained approximately 200 ml of tissue-culture fluid. The centrifuge was run at 10,000 rpm for 10 minutes (10,200xg) at a temperature setting of 4°C. The virologist observed no indication of a problem during the centrifugation process. On opening the lid of the rotor to remove the centrifuge bottles, he noted that the outside of one bottle was wet and that fluid had leaked into the bottom of the rotor. No obvious break was identified at the time, and the virologist was wearing a surgical mask, a disposable solid-front gown, and gloves. He had no abrasions or scratches on his hands.

The virologist used a second pair of gloves during the decontamination of the rotor, but did not wear a positive air-purifying respirator, although it was available. He decontaminated the spillage by pouring a concentrated solution of sodium hypochlorite (5.25 percent) directly into the rotor bucket as well as inside and outside the bottle that had leaked. The combined bleach and liquid in the rotor were then absorbed with paper towels. After the incident, the virologist continued working alone in the laboratory for another three to four hours. All his protective garments as well as other contaminated material in the laboratory were autoclaved. Initially, he did not report the incident because he believed that no exposure to virus had occurred.

Case Presentation and Clinical Course

On August 16, 1994, the virologist noted myalgias, a mild headache, a stiff neck, and fever while driving home to New Haven, Connecticut, after a weekend visit to Boston. He treated himself with ibuprofen for two days before seeking medical care. On questioning, he described recrudescences of Plasmodium vivax infection that had never been treated with primaquine. He was concerned that this fever could represent a relapse of malaria. He initially did not recall any serious laboratory exposures. On physical examination he appeared mildly ill, with a temperature of 37.6°C (99.8°F), a pulse of 89 beats per minute, and a blood pressure of 130/80 mm Hg. The only remarkable features were mild conjunctival injection and shotty cervical nodes in the anterior chain. Laboratory studies performed that afternoon revealed a hematocrit of 42 percent, a white-cell count of 2600 per cubic millimeter, a platelet count of 138,000 per cubic millimeter, and an alanine aminotransferase level of 63 U per liter; urinalysis revealed moderate proteinuria (2+). After a smear proved negative for malaria, further review of possible infectious exposures led the patient to recall the August 8 laboratory incident with Sabiá virus.

The patient was immediately hospitalized and treated with intravenous ribavirin at a dosage used by the Centers for Disease Control and Prevention (CDC) for other arenavirus infections (a loading dose of 30 mg per kilogram of body weight, followed by a dose of 15 mg per kilogram every six hours for four days, and then by a dose of 7.5 mg per kilogram three times daily for six days). Pretreatment blood samples were sent for viral culture and examination by the polymerase chain reaction (PCR) for the presence of Sabiá virus RNA. PCR testing for Sabiá virus was reported to be positive on hospital day 2. The reverse-transcription PCR technique produces a fragment of 180 base pairs by using one primer specific for arenavirus in combination with one specific for Sabiá virus. Controls consisted of Sabiá virus RNA extracted from infected cell monolayers and normal human serum (Rico-Hesse R: personal communication).

Figure 1 shows the patient's temperature curve and laboratory values during hospitalization. No hemorrhagic manifestations were observed. His white-cell and platelet counts reached a nadir on hospital day 2: total white-cell count, 1300 per cubic millimeter; absolute neutrophil count, 650 per cubic millimeter; and platelet count, 98,000 per cubic millimeter. His serum alanine aminotransferase values peaked at 128 U per liter on day 10 of hospitalization. During treatment, his hematocrit dropped, and aminotransferase levels increased. He also reported a severe headache. The patient was sent home with a white-cell count of 3800 per cubic millimeter on August 29 after 10 days of intravenous ribavirin.


Figure 1. Laboratory Findings in a Patient Infected with Sabiá Virus.

The patient was exposed to Sabiá virus on August 8, 1994, and became symptomatic on August 16. To convert values for total bilirubin to micromoles per liter, multiply by 17.1; to convert values for calcium to millimoles per liter, multiply by 0.25; and to convert values for phosphate to millimoles per liter, multiply by 0.3229.

Blood samples were collected daily from the patient before ribavirin therapy was begun and during the rest of his hospitalization. The serum samples were used to inoculate cultures of Vero E-6 cells maintained at 37°C, and the cultures were examined for the presence of Sabiá virus antigen 10 days after inoculation with the use of an indirect fluorescent-antibody technique with mouse ascitic fluids that were reactive to the Tacaribe group and specific for Machupo virus and a commercial fluorescein-labeled goat antimouse IgG antibody. Uninfected Vero cells served as controls. Cells inoculated with a serum sample obtained on admission to the hospital and before ribavirin therapy was begun were positive for viral antigen. IgM and IgG antibodies to Sabiá virus antigen (infected Vero cells) were subsequently detected by indirect fluorescent-antibody testing in a serum sample drawn during convalescence 35 days after the clinical onset of the illness. Serum samples obtained before this time were negative for Sabiá virus antibodies and served as negative controls. Attempts to isolate the virus from urine, semen, and blood were repeatedly negative after ribavirin therapy was begun.

Biosafety Management and Contact Surveillance

After PCR confirmation of infection with Sabiá virus, the patient was transferred to a negative-pressure isolation suite.3 The suite consisted of an anteroom with lower pressure than the surrounding hallway and two patient rooms with lower pressure than the anteroom. The patient remained in the same room throughout his hospital stay; the other patient room was used for the temporary storage of waste and for decontamination.

Once materials entered the negative-pressure isolation suite, they were considered to be contaminated. Items were double bagged and held in the adjacent negative-pressure storage room before being transported in an enclosed cart to the autoclave. Larger items were wiped with disinfectant before removal. Disposable items were bagged on removal from the room, autoclaved, and incinerated.

Throughout the patient's hospitalization universal precautions were used by all health care workers who came in contact with him or his specimens.4 Precautions were upgraded after PCR confirmation to include the use of fit-tested masks with high-efficiency particulate air filters, gowns, and gloves by all persons entering the patient's room and laboratory workers processing the patient's specimens. The number of health care workers who came in contact with the patient or his specimens was restricted.

Additional precautions were implemented in the laboratories to reduce the risk of potential exposure to aerosols from infected body fluids. All specimens were double bagged and carried by hand to the laboratories by the patient's physician. Chemistry specimens were processed in a negative-pressure room. Samples were spun in a sealed centrifuge, and serum was treated with Triton X-100 (10 µl of 10 percent Triton X-100 per milliliter of serum) to inactivate the virus. Hematologic specimens were processed in a Coulter counter that did not require removal of the top of the tube, and the effluents were treated with sodium hypochlorite and then autoclaved. The Coulter counter was also cleaned after use with several cycles of diluted bleach. Other laboratory tests were carried out within a biosafety cabinet.

All contacts of the patient were identified and stratified into risk groups. One hundred thirty-nine contacts were identified, consisting of workers providing patient care, hospital laboratory workers, colleagues, friends, and family members. No exposure had occurred that would have placed any contact at high risk of contracting the virus. However, all contacts were notified that a possible exposure to Sabiá virus had occurred, and they were enrolled in a medical-surveillance program. As part of the surveillance program, all contacts were interviewed, answered a questionnaire, and provided a blood sample for testing at the CDC; six weeks later, they completed a follow-up questionnaire and provided a second blood sample.

The contacts were also instructed to take their temperatures twice daily over the six-week period and to monitor for early symptoms of the disease. They were given a telephone number that was staffed 24 hours a day by physicians with expertise in occupational medicine and infectious diseases and who were familiar with the index case. No symptoms suggestive of Sabiá virus infection occurred in the group under surveillance during the six-week follow-up period; however, one subject had a viral syndrome with leukopenia and mild hepatitis just after the end of the six-week observation period. A serologic test (enzyme-linked immunosorbent assay) for arenavirus infection and PCR testing for Sabiá virus RNA were negative, and a serum sample obtained during convalescence was also negative for IgM and IgG antibodies to Sabiá virus antigen.

A protocol was generated with the emergency department for the triage and care of any secondary cases. The plans included restricting the number of health care workers who came in contact with people who might have been secondarily infected; immediately notifying the clinical laboratories, the hospital epidemiology department, the state health department, and the CDC of any additional suspected cases; isolating other potentially infected persons in a negative-pressure isolation suite; and having physicians familiar with the index patient clinically evaluate such persons.

Discussion

We describe the third confirmed case of Sabiá virus infection. The two previous cases were identified in Brazil.² Four other arenaviruses (Lassa, Junin, Machupo, and Guanarito) have been associated with a hemorrhagic disease in humans.¹ Each of these agents has a distinct geographic distribution, although they cause similar clinical manifestations and high mortality.¹ Wild rodents serve as reservoirs for these arenaviruses; humans usually become infected by contact with contaminated rodent excreta. Little is known about the mode of transmission of Sabiá virus or its source in nature.

We believe that Sabiá virus was most likely transmitted to the investigator by aerosol, probably when the centrifugation rotor was opened and the leak was observed or during the decontamination process.

[THIS WAS DEPICTED IN THE 1995 MOVIE OUTBREAK!!!! WAS THIS A PLANNED ATTACK TO SPREAD VIRUSES AND WAS DONE ON PURPOSE? WATCH THE MOVIE IT IS ALMOST LIKE IT WAS A PURPOSEFUL SABATOGE LIKE THE LIGHT BULB IN THE MOVIE "THE SOLDIER"!

The 8-day incubation period in this case is consistent with that of other arenaviral illnesses (range, 6 to 21 days).^1,3 We chose to treat the patient early with intravenous ribavirin, a guanosine analogue, since clinical studies have shown it to be effective in diminishing mortality in Lassa fever if given early in the course of illness.⁵ Clinically, our patient had an excellent response; he became afebrile and asymptomatic within 48 hours, in contrast to the other two patients with Sabiá virus infection, who had a prolonged course with hemorrhagic symptoms. His severe leukopenia and thrombocytopenia rapidly improved, and no further virus was detected in his blood by culture after treatment was initiated. The mild hemolysis was thought to be due to ribavirin therapy and is a well-described effect of the drug.⁶ The late peak in aminotransferase values, although not dramatic, was unusual, since it was asynchronous with the recovery from leukopenia and thrombocytopenia. It could have been caused by an adverse effect of the ribavirin not previously described, infection, or immunologic recovery from Sabiá virus. Hepatocellular damage and hepatitis have been described with Sabiá virus and other arenaviruses.^1,2 The patient's late immunologic response, as reflected by the finding of IgG and IgM antibodies to Sabiá virus, may have been modified by treatment with ribavirin, or it may represent the natural response to Sabiá virus infection.

Since a number of nosocomial outbreaks have been described among hospital personnel attending acutely ill patients with arenavirus infections, a high level of precaution was instituted at our hospital, as recommended by the CDC.³ Although extensive experience in West Africa with Lassa fever has shown that universal precautions and nursing using barrier precautions generally prevent the transmission of Lassa virus in hospitals, we also instituted negative-pressure isolation, limited the number of hospital personnel caring for the patient, and required personnel potentially exposed to blood aerosols to wear respirators with high-efficiency particulate air filters.^3,4 Clinical laboratory specimens were processed to minimize workers' exposure to aerosolized virus, and routine automated equipment for chemistry specimens was not used unless the specimen was first treated with Triton X-100. Contact surveillance with a follow-up of six weeks (well within the incubation period of arenaviral illnesses) identified no secondary cases.

Researchers need to recognize the risk of occupational exposure to Sabiá virus by aerosol. Ribavirin treatment may modify the clinical course of Sabiá virus infection. Although standard universal precautions may be adequate to prevent nosocomial spread, additional biosafety precautions should be considered when one is dealing with arenaviruses and other dangerous viruses whose mechanisms of transmission are unknown.

We are indebted to Ms. Carolyn Karbowski for assistance in the preparation of the manuscript, to Dr. Mark Cullen for his thoughtful comments, to Dr. Petrie Rainey for suggesting the Triton X-100 treatment, and to the Yale–New Haven Hospital house staff, laboratory workers, and nursing personnel for the professional care offered to this patient under unusual circumstances.


Source Information

From the Department of Internal Medicine (M.B., M.R., D.G., L.D.) and Yale Arbovirus Research Unit, Department of Epidemiology and Public Health (R.T.), Yale University School of Medicine, New Haven, Conn.; the Special Pathogens Branch, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta (L.A., A.S.K., C.J.P.); and Institut Français de Recherche Scientifique pour le Développement en Coopération, Paris (J.P.G.).

Address reprint requests to Dr. Barry at the International Health Program, Yale University School of Medicine, 20 York St., New Haven, CT 06504.

References

1. Peters CJ, Johnson KM. Arenaviridae: lymphocytic choriomeningitis virus, Lassa virus, and other arenaviruses. In: Mandell GL, Bennett JE, Dolin R, eds.
    Mandell, Douglas and Bennett's principles and practice of infectious diseases. 4th ed. Vol. 2. New York: Churchill Livingstone, 1995:1572-9.  

2. Lisieux T, Coimbra TL, Nassar ES, et al. New arenavirus isolated in Brazil. Lancet 1994;343:391-392. [CrossRef][Medline]
    Management of patients with suspected viral hemorrhagic fever. MMWR Morb Mortal Wkly Rep 1988;37:Suppl:1-15.

3. Fisher-Hoch SP, Price ME, Craven RB, et al. Safe intensive-care management of a severe case of Lassa fever with simple barrier
    nursing techniques. Lancet 1985;2:1227-1229. [Medline]

4. McCormick JB, King IJ, Webb PA, et al. Lassa fever: effective therapy with ribavirin. N Engl J Med 1986;314:20-26. [Abstract]

5. Canonico PG, Kastello MD, Spears CT, Brown JR, Jackson EA, Jenkins DE. Effects of ribavirin on red blood cells.
    Toxicol Appl Pharmacol 1984;74:155-162. [CrossRef][Medline]


This article has been cited by other articles:

1. Larson, R. A., Dai, D., Hosack, V. T., Tan, Y., Bolken, T. C., Hruby, D. E., Amberg, S. M. (2008). Identification of a Broad-Spectrum Arenavirus
    Entry Inhibitor. J. Virol. 82: 10768-10775 [Abstract] [Full Text]  

2. Kimman, T. G., Smit, E., Klein, M. R. (2008). Evidence-Based Biosafety: a Review of the Principles and Effectiveness of Microbiological
   Containment Measures. Clin. Microbiol. Rev. 21: 403-425 [Abstract] [Full Text]  

3. SBRANA, E., XIAO, S.-Y., GUZMAN, H., YE, M., TRAVASSOS DA ROSA, A. P. A., TESH, R. B. (2004). EFFICACY OF POST-EXPOSURE
   TREATMENT OF YELLOW FEVER WITH RIBAVIRIN IN A HAMSTER MODEL OF THE DISEASE. Am J Trop Med Hyg 71: 306-312 [Abstract] [Full Text]  

4. Gavin, P. J., Katz, B. Z. (2002). Intravenous Ribavirin Treatment for Severe Adenovirus Disease in Immunocompromised Children.
    Pediatrics 110: e9-9 [Abstract] [Full Text]  

5. Murphy, F. A., Johnson, K. M. (1995). An Exotic Viral Disease Acquired in a Laboratory. NEJM 333: 317-319 [Full Text]  

[Satyagraha]

Some comments on this guy:

Note that shortly after the lab worker got sick, this guy was able to turn a crisis into an opportunity!! Amazing guy... he was able to get two journal articles out on the subject of the lab technician who contracted Sabia virus in Gonzalez' lab.

In addition to the usual suspects in bioweapons research, (dengue fever, encephalitis)  there are a few types of Ebola, and lots of Hantavirus and other hemmoraghic fevers. There are also a number of articles on remote sensing the progression of disease through a population. A lot of these actually.
Then we have the eugenics-'biodiversity' books...

This guy is a paperclip transplant I think... just a guess but he's got a resume Dr. Mengele would have been proud of, and a rich collection of deadly virii to test on clumsy lab workers.

Jean-Paul Gonzalez


Present Position

Research Unit Director Emerging Diseases & Information Systems (UR178), IRD, France.
Co-Director of the Research Center for Emerging Viral Diseases (RCEVD)

Publications:
http://www.th.ird.fr/publications/publications_auteur_gonzalez.html


(This is excerpted from the full list, available at the source link:)
1995

•  Gonzalez, J. 1995. Ebola, une rivière tranquille au coeur de l'Afrique . Cahiers Santé . 5: 145-146

•  Gonzalez, J.P., A. Sanchez and R. Rico-Hesse. 1995. Venezuelan Molecular phylogeny of Guanarito virus, an emerging human arenavirus. Journal of the American Society of Tropical Medicine & Hygiene , 53, 1-6
•  Barry, M., Russi, M., Armstrong, L., Geller, D., Tesh, R., Denbry, L., Gonzalez, JP., Khan, A., Peters, CJ., (1995) Treatment of a laboratory-acquired Sabiá virus infection. New England Journal of Medicine , 333: 294-9

•  Cornet, JP, Zeller H., Ba K., Camicas JL, Gonzalez JP & Wilson ML. 1995, Contribution à l'étude des tiques ( Acarina: Ixodina )
    vectrices de la fièvre hémorragique de Crimée Congo au Sénégal 1: Analyse du parasitisme chez les petits rongeurs. Acarologia 36, 3: 15-21

1996

•  Gonzalez, J.P., Bowen M, Nicholl S. and Rico-Hesse R, 1996 Genetic characterization of Sabiá arenavirus an emerging human pathogen. (1996), Journal of General Virology ,221: 218-324

1997 (Nothing???)

1998

•  Gonzalez JP, Camicas JL, Cornet JP & Wilson ML, 1998, Biological and clinical responses of West African sheeep to Crimean-Congo haemorrhagic fever virus experimental infection. Research in Virology , 149, 445-55

•  Thiongane Y., Thonnon J., Zeller H., Lo M.M., Faty A., Diagne F., Gonzalez J.P., Akakpo J.A., Fontenille D. & Digoutte J.P., 1998. Données récentes de l'épidémiologie de la Fièvre de la Vallée du Rift (F.V.R.) au Sénégal. Dakar Médical , 1998, 96:1-6

1999

•  Faye O., Fontenille D, Thonnon J., Gonzalez, J.P. Cornet J.P. & Camicas J.L. 1999. Transmission expérimentale du virus de la fièvre hémorragique de Crimée-Congo par la tique Rhipicephalus evertsi evertsi ( Acarina : Ixodidae ). Bulletin de Société de Pathologie Exotique . 92, 3 ; 143-147

2000

•  Gonzalez JP, Nakoune E, Slenczka W, Vidal P & Morvan J. 2000. Ebola and Marburg virus antibody prevalence in selected populations of the central african republic . Microbes and Infection. 1; 1:6

•  Nitatpattana N., Chauvancy G, Dardaine J, Poblap T, Jumronsawat K, Tangkanapul W, Poonsuksombat D, Yoksan S & Gonzalez JP. 2000. Serological study of Hantavirus in the rodent population of Nakhon Pathom and Nakhon Ratchasima province of Thailand . South East Asian Journal of Tropical Medicine and Hygien , 31 ;2 :277-282

•  Nitatpattana N., Chauvancy G, Jumronsawat K, Poblap T, Yoksan S & Gonzalez JP 2000. Preliminary study on a potential circulation of Arenavirus in the rodent population of nakhon pathom province ( Thailand ) and their medical importance in an evolcutive environment. South East Asian Journal of Tropical Medicine and Hygien , 31 ;1 :62-5

2001

•  Hugot JP, Denys CH & Gonzalez JP 2001 Evolution of the Old World Arenaviridae and their Rodent Hosts : Generalized Host-Transfer or Association by Descent ? Infection, Genetics and Evolution , 1 : 22-25

•  Nitatpattana Narong, Timothy Henrich, Somnuek Palabodeewat, Waraluk Tangkanakul,Duangporn Poonsuksombat, Gilles Chauvancy, Philippe Barbazan, Sutee Yoksan, and Jean-Paul Gonzalez , 2001. Unveiling the risk of Hantavirus infection in Thailand  : are rodents a factor of disease emergencies ? Tropical Medicine & International Health, 6,12 :1-7

2002

•  Gonzalez JP, 2002 Arénavirus du nouveau monde : virus en évolution et maladies émergentes. Feuillets de Biologie , 43, 247 : 1-9

•  Barbazan P., Yoksan S. and Gonzalez JP., 2002. Dengue hemorrhagic fever epidemiology in Thailand : description and forecast of epidemics. Microbes and Infection , 4, 7: 699-705

2003

•  Gonzalez Jean Paul, 2003, SARS : at least and at last, are we learning from the worst ? Infection, Genetics and Evolution  ; 3 - 5 :1-3

•  Henrich T, Sombat Hutchaleelaha, Vitaya Jiwariyavej, Barbazan P, Narong Nitatpattana, Sutee Yoksan & Gonzalez JP. 2003 Geographic dynamics of viral encephalitis in Thailand, Microbes and Infection, 5(7):603-115

•  Parola Philippe, Cornet Jean-Paul, Sanogo Yibayiri Osée, Miller R. Scott, Huynh Van Thien, Gonzalez Jean-Paul, Raoult Didier, Telford Sam R. & Wongsrichanalai Chansuda, 2003. Detection of Ehrlichia spp. , Anaplasma spp., and other Eubacteria in Ticks from the Thai-Myanmar Border and Vietnam , Journal of Clinical Microbiology , 41 (4): 1600-1608

•  Parola P, Sanogo OY, Lerdthusnee K, Zeaiter Z, Chauvancy G, Gonzalez JP, Miller RS, Telford SR 3rd, Wongsrichanalai C, Raoult D. 2003. Identification of Rickettsia spp. and Bartonella spp . in from the Thai-Myanmar border. Annals of New York Academy of Sciences. 990 : 173-8

2004

•  Cornet JP, Kittayapong P & Gonzalez JP, 2004. Le risque de transmission d'arbovirus par les tiques en Thaïlande, Médecine Tropicale , 64 (1): 43-49

•  Leroy E. M., P. Telfer, P. Yaba, B. Kumulungui, P. Rouquet, P. Roques, J.-P. Gonzalez, T. G. Ksiazek, P. E. Rollin, and E. Nerrienet, 2004, A Serological Survey of Ebola Virus Infection in Central African Non-Human Primates. Journal of Infectious Disease . 190 : 1891-1895

2005

•  Allela L, Bourry O, Pouillot R, Délicat A, Yaba Ph, Kumulungui B, Rouquet P, Gonzalez JP, and Leroy E M., 2005 Ebola Virus Antibody in Dogs and Human Risk. Emerging Infectious Diseases ;Vol.11; 3: 385-390 - www.cdc.gov/eid

•  Gonzalez Jean-Paul, Vincent Herbreteau, Jacques Morvan & Eric Leroy 2005. Ebola virus circulation in Africa: A balance between clinical expression and epidemiological silence Bulletin de la société de pathologie exotique ; 98( 3):210-7

•  Herbreteau V., G. Salem, M. Souris, J-P. Hugot, and J-P. Gonzalez, 2005. Sizing up human health through remote sensing: uses and misuses Parassitologia , special issue 47: 63-79

•  Herbreteau V., J.P. Gonzalez, H. Andrianasolo, P. Kittayapong, J.P. Hugot. 2005 Mapping the potential distribution of Bandicota indica , vector of zoonoses in Thailand , by use of remote sensing and geographic information systems (a case of Nakhon Pathom province). NHJCU , 5:61-67

•  Leroy Eric, Brice Kumulungui, Xavier Pourrut, Pierre Rouquet, Philippe Yaba, André Délicat, Jaenusz Paweska, Sherif R Zaki, Pierre Rollin, Jean-Paul Gonzalez & Robert Swanepoel 2005. Fruits bats as a reservoir of Ebola virus. Nature. 2005 Dec 1;438(7068): 575-6

•  Pourrut X, Kumulungui B, Wittmann T, Moussavou G, Delicat A, Yaba P, Nkoghe D, Gonzalez JP, Leroy EM. 2005 The natural history of Ebola virus in Africa. Microbes and Infection ;7 (7-8):1005-14

•  Suputthamongkol Y, Nitatpattana N, Chayakulkeeree M, Palabodeewat S, Yoksan S, Gonzalez JP. 2005 Hantavirus infection in Thailand: first clinical case report. South East Asian Journal Tropical Medicine Public Health . 36(3):700-3

2006

•  Emonet S, Lemasson JJ, Gonzalez JP, de Lamballerie X, Charrel RN. 2006 Phylogeny and evolution of old world arenaviruses. Virology . 5;350(2):251-7

•  Grard G, Moureau G, Charrel RN, Lemasson JJ, Gonzalez JP, Gallian P, Gritsun TS, Holmes EC, Gould EA, de Lamballerie X. 2006. Genetic characterization of tick-borne flaviviruses: New insights into evolution, pathogenetic determinants and taxonomy. Virology. [Epub ahead of print]

•  Herbreteau Vincent, Florent Demoraes, W. Khaungaew, Jean-Paul Gonzalez , Pattamaporn Kittayapong, and Marc Souris - Use of geographic information system and remote sensing for assessing environment influence on leptospirosis incidence, Phrae province, Thailand, Annals of NYork Academy of Sciences 1081 ; 5p

•  Leroy E, Pourrut X, Gonzalez JP. 2006 [Bats, reservoir of the Ebola virus : the mystery is dissipated]. Medecine Science (Paris). 2005 Dec; 22 (1):78-80

•  Poblap Tawal, Narong Nitatpattana, Aree Chaimarin, Philippe Barbazan, Gilles Chauvancy, Sutee Yoksan & Jean-Paul Gonzalez . Virus Silent Transmission, Nakon Pathom Prov. Thailand 2001 Asian Society of Tropical Medicine and Hygiene. 37 ; 5 : 1-5

2007

•  Misse D, Yssel H, Trabattoni D, Oblet C, Lo Caputo S, Mazzotta F, Pene J, Gonzalez JP, Clerici M, Veas F. IL-22 participates in an innate anti-HIV-1 host-resistance network through acute-phase protein induction. J Immunol. 2007 Jan 1;178(1):407-15

Books and chapters published in collective books

2001- 2010 

•  Jean-Paul Gonzalez , 2004. Emerging Viral Diseases (A tribute to Professor Natth Bramapavarati). In Natth Bramapavarati : From Molecule to Community ; Yun Tsi Edit. Bangkok: 253-260

•  Salvato MS, Clegg JCS, Buchmeier M.J., Charrel RN, Gonzalez J-P, et al. 2005. Arenaviridae. In : Virus Taxonomy, VIIIth Report of the ICTV (CM Fauquet, MA Mayo, J Maniloff, U Desselberger, & LA Ball, eds), 725-733. Elsevier/Academic Press, London

•  Jean-François Guégan, // Jean-Paul Gonzalez & Jean-Pierre Hugot . 2005. Biodiversité : Science et Gouvernance Biodiversité et Santé des Populations : Perspectives pour le Futur.

•  Jean-Paul Gonzalez , Xavier Pourrut et Eric Leroy. Ebola virus C. Invasion, Establishment, and Spread in the Human Host : Case Studies In Wildlife and Emerging Zoonotic Diseases: JMackensie & JMills edits. CRC Press. Advances in Virology (In press)

•  Jean-Paul Gonzalez , Sébastien Emonet, Xavier de Lamballerie and Rémi Charrel . 2007. Arenaviruses. chapter 15. C. Invasion, Establishment, and Spread in the Human Host : Case Studies In Wildlife and Emerging Zoonotic Diseases: OpCit.

•  Jean-Paul Gonzalez et al. 2007. Of Bats, Forest, People and Health: Unveiling the Fundamentals of Bat Borne Viral Zoonoses Emergence PART I Synthetic analyses Chapter 6 In People, Health and Forests Carol J. Pierce Colfer and Eckhard Kleinau, eds. Press. Advances in Virology

•  Mondet Bernard, Seyler Thomas , Gonzalez Jean Paul. 2006. Dynamique des pathologies et évolution des risques sanitaires liés à l'urbanisation: exemple de la ville de Chennai. Ecologie Humaine edit.

•  P. Vidal, // & JPGonzalez . Chapter 42 Infectious Disease and the Arts. 2007. In Encyclopedia of infectious diseases, Edited by Michel Tibayrenc ISBN 0-471 Copyright © 2000 Wiley (Imprint), Inc. 142 pp 32

•  J.-P. Gonzalez , et al. 2007. Fundamentals, domains and diffusion of disease emergence: Tools and strategies for a new paradigm. In Encyclopedia of infectious diseases, Edited by Michel Tibayrenc ISBN 0-471 Copyright © 2000 Wiley (Imprint), Inc. (In Press) 32 pp

•  Marc Souris, Narong Nitapattana, Philippe Barbazan, Sutee Yoksan, Laurent Schnell & JP Gonzalez, 2002. Water Borne Diseases : Chao Praya River Basin Diseases Evolution in a Changing environment In Comprehensive Assessment of Water Management in Agriculture : A comparative study on river basin development and management. JF Molle et coll. Edit. IRD/IWMRI
   

     

[trailhound]

 

 Looks like the yale bioweapons program is carefully pitched as 'biodefence'

http://www.yalepharma.com/YalePharmaRs/Specialty/Biodefence/biodefence.html

[trailhound]

Interview with Robert Shope

http://www.liebertonline.com/doi/abs/10.1089/153036603765627460

[Satyagraha]

Great finds LD, thanks!

[TahoeBlue]

Interview with Robert Shope

http://www.liebertonline.com/doi/abs/10.1089/153036603765627460

Amazing find...



The network of intrigue that Anita referenced was that she was suspected of being part of SS Reichsfurhrer Himmler’s spy network in New York City. During this time, Dr. Erich Traub was also part of SS Reichsfurhrer Himmler’s spy network in New York. During WW I, Traub was a captain in the German army working as an expert in animal infectious diseases, particularly in horses. His veterinary corps led the germ warfare attacks on horses in the United States and Romania with a bacterium called glanders. He was also a member of the National Socialist Motorists Corps (NSKK) [11]
 
The NSKK (German: Nationalsozialistisches Kraftfahrerkorps) also known as the National Socialist Drivers Corps was paramilitary organization of the Nazi Party that officially existed from  1931-1945. In April of 1930, Adolf Hitler joined the NSKK as one of its first members. In 1945, NSKK was disbanded or went underground.  The group was declared a “condemned organization” at the Nuremberg Trials. This was due to the NSKK’s orgins in Heinrich Heydrick’s SA and its doctrine of Aryan superority required  of its members.
 
During the 1930’s and preceding WWII, Traub worked at the Rockefeller Institute of Princeton in New Jersey on viruses and bacterium. He was an active member of the Amerika Deutscher Volksbund, a German-American club also known as Camp Sigfried. Camp Sigried was the national headquarters of the American Nazi movement. On weekends, about forty thousand people throughout New York participated in mass Nazi rallies marching in lockstep divisions, carrying swastika flags, burning Jewish U.S. congressmen in effigy, and singing Nazi songs pledging their allegiance to the Third Reich as if they were in Nuremberg Nazi Germany.
 
Dr. Traub’s detailed debriefing from 1949 under Operation Paperclip of Himmler’s secret SS biological warfare research on Insel Riems, and his activities there and during the war and for the Soviets, laid the groundwork for Fort Detrick’s offshore germ warfare animal disease lab on USAD’s Plum Island. Dr. Traub was a founding father ...

I was then sent to Malaya...U.S.Army's medical Research Unit [MARU] ...
Bob [Robert] Traub was the commanding officer, and Ben Ellisberg and Patricia Webb, a physician who ran the Pediatric Fever Ward, were the people....

related: Personal recollections of the 1957 H2N2 flu pandemic --by JTCoyoté  

The Plum Island - Deitrick - Dr. Richard E. Shope - Dr Robert Shope (son) and Erich Traub - PaperClip Connection

A very interesting Obit... One of their own has fallen...  Connections to  H2N2  Plum Island : Robert E. Shope : Col. Robert Traub and her first husband, the well-known rickettsiologist, Bennett Elisberg

Obituary In Memoriam Patricia AnnWebb (1925–2005)

1957 - US Army Medical Research Unit in Kuala Lampur - Col. Robert Traub,  Robert E. Shope, C. E. Gordon Smith , Pat Webb, Ben Elisberg made one of the first isolations of the H2N2 Asian

They just "happen" to be there all together johnny on the spot, to "Discover" this "New" and "Novel" form of H1N1 which we call H2N2 before the epidemic started. I can't help but believe they released it.  Robert had worked at Deitrick (with his dad) and like his dad, was an expert in pig cholera (H1N1) and was also connected to Erich Traub and Plum Island.

Richard Shope is also associated with Project Whitecoat testing infectious diseases on servicemen starting in 1954.

So Dad sends his son "something" to distribute in far off Malasia that spreads to SE Asia, China.  Gordon Smith was basically and American Brit (like Pat Webb) and was of "The London School" and associated with the Wellcome Trust, which just happens to fund the 1958 Birth Cohort (why not 1956 or 57 or 59 or 60?). They were prepared and ready for something big. Also during this time period were the Nuclear above ground tests which forever changed the C14 content in humans.

Extinction of Human H1N1 Virus (1957)
Influenza A (H1N1) abruptly disappeared from humans in 1957 and was replaced by a new reassortant virus that combined genes from the H1N1 strain and an avian virus. This new influenza A (H2N2) strain contained three new segments from the avian source and maintained the other five segments from the H1N1 strain of 1918 lineage. 17

After this pandemic subtype emerged, human influenza A (H1N1) was not detected again until 1977.


THE LAYTON FAMILY OF THE PEOPLES TEMPLE: LUCIFIER’S SERVANTS
 
Tim Stoen along with Deborah Layton-Blakely had been central figures in stashing Peoples Temple assets in the millions in secret bank accounts by establishing two offshore dummy Panamanian corporations: Briget, S.A. and Asociacion Evangelica de las Americas, S.A.  [4]
 
Deborah Layton is one of the key central figures in the Peoples Temple CIA project. Deborah is the daughter of the southern aristocratic Dr. Laurence Laird Layton of the chemical warfare division of the U.S. Agricultural Department (USDA). Plum Island Animal Disease Center and the chemical warfare division of the USDA was the brainchild of (Operation Paperclip) Dr. Erich Traub straight out of Reichsfuhrer Heinrich Himmler’s secret SS biological warfare laboratory on the island of Insel Riems on the Baltic Sea. [5] Keep that in mind, Jonestown was also an agricultural experimental camp, and Dr. Layton and Layton family were some of its major covert funders.

[TahoeBlue]

Interview with Robert Shope
http://www.liebertonline.com/doi/abs/10.1089/153036603765627460  

"I was first attached to a unit that was operating at CAMP DIETRICK , now called Fort Dietrick, where I worked for about six months ON A CLASSIFIED OPERATION CALLED "WHITECOAT".

Whitecoat has since been declassified, and I can tell you that it involved INFECTING VOLLUNTEERS WITH Q FEVER organisms.

So what was/were Q-Fever organisms? eh?

http://en.wikipedia.org/wiki/Q_fever

Q fever is a disease caused by infection with Coxiella burnetii,[1] a bacterium that affects humans and other animals. This organism is uncommon but may be found in cattle, sheep, goats and other domestic mammals, including cats and dogs. The infection results from inhalation of endospores, and from contact with the milk, urine, feces, vaginal mucus, or semen of infected animals. Rarely, the disease is tick borne. [2] The incubation period is 9–40 days. A human being can be infected by a single bacterium.[3] The bacterium is an obligate intracellular pathogen.
...
The pathogen of Q fever was discovered in 1937, when Frank Macfarlane Burnet and Mavis Freeman isolated the bacterium from one of Derrick’s patients.[6] It was originally identified as a species of Rickettsia. H.R. Cox and Davis isolated it from ticks in Montana, USA in 1938.[7] It is a zoonotic disease whose most common animal reservoirs are cattle, sheep and goats. Coxiella burnetii is no longer regarded as closely related to Rickettsiae but as similar to Legionella and Francisella and is a proteobacterium.
...
During the course, the disease can progress to an atypical pneumonia, which can result in a life threatening acute respiratory distress syndrome (ARDS), whereby such symptoms usually occur during the first 4 to 5 days of infection.

Less often the Q fever causes (granulomatous) hepatitis which may be asymptomatic or becomes symptomatic with malaise, fever, liver enlargement (hepatomegaly) and pain in the right upper quadrant of the abdomen. Whereas transaminase values are often elevated, jaundice is uncommon. Retinal vasculitis is a rare manifestation of Q fever.[8]

The chronic form of Q fever is virtually identical to inflammation of the inner lining of the heart (endocarditis),[9] which can occur months or decades following the infection. It is usually fatal if untreated. However, with appropriate treatment the mortality falls to around 10%.
,...

Biological warfare
Q fever has been described as a possible biological weapon.[19]

The United States investigated Q fever as a potential biological warfare agent in the 1950s with eventual standardization as agent OU. At Fort Detrick and Dugway Proving Ground human trials were conducted on Whitecoat volunteers to determine the median infective dose (18 MICLD50/person i.h.) and course of infection. As a standardized biological it was manufactured in large quantities at Pine Bluff Arsenal, with 5,098 gallons in the arsenal in bulk at the time of demilitarization in 1970.

Q fever is a category "B" agent.[20] It can be contagious and is very stable in aerosols in a wide range of temperatures. Q fever microorganisms may survive on surfaces up to 60 days.

[TahoeBlue]

http://www.vri.cz/userfiles/file/hide/CNFI/Murphy_interview.pdf

VECTOR-BORNE AND ZOONOTIC DISEASES
Volume 8, Number 1, 2008

Interview with Frederick A. Murphy, Ph.D.
Professor of Pathology and McLaughlin Professor in Residence
University of Texas Medical Branch, Galveston


Frederick A. Murphy is Professor, Department of Pathology, University of Texas Medical Branch (UTMB) at Galveston. At UTMB he is also a member of the Institute for Human Infections and Immunity, the Galveston
National Laboratory, the Center for Biodefense and Emerging Diseases, and the McLaughlin Endowment Program. Previously, he served as Dean and Distinguished Professor, School of Veterinary Medicine, and Distinguished Professor, Department of Internal Medicine, School of Medicine, University of California Davis. Dr. Murphy received a BS and DVM from Cornell University and a PhD from the University of California, Davis. He served as Chief, Viral Pathology Branch, then Director of the Division of Viral and Rickettsial Diseases and later Director of the National Center for Infectious Diseases, Centers for Disease Control, Atlanta.

His honors include elected membership in the Institute of Medicine of the U.S. National Academies of Sciences, the Presidential Rank Award from the U.S. government, membership in the German Academy of Natural Sciences and the USSR Academy of Medical Sciences, the K.F. Meyer Gold Headed Cane, Doctor of Medicine and Surgery honoris causa, University of Turku, Finland, and Doctor of Science honoris causa, University of Guelph, Ontario, Canada.

Most recently he has served as a member of the US Department of Health and Human Services Secretary’s Council on Public Health Preparedness. He has been a member of the Institute of Medicine Committee on Microbial Threats, co-chair of the National Research Council Committee on Occupational Health and Safety in the Care and Use of Nonhuman Primates, member of the National Academies of Sciences Committee on Public Health, Agriculture, Basic Research, Counter-terrorism and Non-proliferation Activities in Russia, and member of the Institute of Medicine/National Academies of Sciences Committee on Transmissible Spongiform Encephalopathies.

...
What events and discoveries led to the identification of the Ebola and Marburg viruses and what was your role in those discoveries? Was that the main focus of your research at the time?


Marburg virus was discovered in Germany.

I am the only American left who worked on Marburg virus at the time of its discovery in 1967. Only three of us worked on the virus at CDC, Bob Kissling, Robbie Robinson, and myself— exposing so few virologists was the biosafety strategy of the time. In any case, it was a very exciting time. We borrowed a mobile laboratory (housed in an 18-wheeler) from the NIH and set it up in the CDC parking lot.

It had never been used before, so getting its systems to work was a challenge. Nevertheless, we did some good work on Marburg virus. That work became the motivation to build “hot labs” at the CDC.

By 1976, when my colleagues Karl Johnson, Patricia Webb, Jim Lange, and myself discovered Ebola virus, biocontainment was much better. The excitement surrounding this discovery was even greater than for Marburg
virus, mostly because of the case-fatality rate in Africa. The events surrounding the discovery of Ebola virus and the WHO team’s trip to Zaire are well described in Richard Preston’s book, “The Hot Zone.” I have no argument with his story.

At the time of the Ebola hemorrhagic fever outbreaks in Zaire and Sudan in 1976 I was running CDC’s Viral Pathology Branch. We took each disease episode and each new virus as they came. Discovery and characterization of
new viruses were part and parcel of the prevention and control activities of the CDC—the notion, “know thine enemy,” was well entrenched as a key part of the overall mission. I hope this notion is never lost.

One of my favorite criticisms of CDC folklore concerns the nature of the earliest work on a new virus or a new disease. The folklore is  that all early investigation is grounded in classical surveillance and epidemiologic outbreak investigation. Not so! Rather, the early work on new zoonotic diseases such as Ebola and Marburg hemorrhagic fevers and their etiologic
agents comes under the heading, “basic research”— that is, field-based and laboratorybased research. Those responsible for zoonotic disease prevention and control need to understand this.

http://www.amazon.com/Hot-Zone-Terrifying-True-Story/dp/0385479565

[TahoeBlue]

http://www.carnegiemnh.org/assets/science/library/archives/Traub/Guide-to-the-Correspondence-of-Dr-Traub.doc

The Papers of Robert S. Traub
Carnegie Museum of Natural History Archives
Processed by Eric Skinner, Summer 2001

Abstract:
The correspondence of Robert S. Traub deals primarily with Dr. Traub’s work with fleas, chiggers and medical entomology. The papers include Dr. Traub’s correspondence with other scientists, information on his collection of fleas, personnel matters and some personal letters. The collection includes 12 boxes of correspondence plus 9 boxes of unprocessed photographs and drawings, a total of 19.5 linear feet.

...

Biography:
Dr. Robert S. Traub, Colonel, U.S. Army (Retired) was born in Manhattan, New York on May 26, 1916. He earned degrees in biology and medical entomology from three of the premier universities in the United States: City College of New York (B.S., cum laude, 1938), Cornell University (M.S., 1939), and the University of Illinois (Ph.D., 1947). Over the course of his career, Dr. Traub became the world’s foremost authority on fleas and flea-borne diseases.

He was also involved in the chemoprophylaxis of chigger-borne rickettsiosis (scrub typhus, tsutsugamushi disease) following World War II.  Dr. Traub intentionally caught the disease through chigger bites to test a vaccine for typhus, which proved effective.

In addition, Dr. Traub was also an evolutionary theoretician, focusing on host-parasite zoogeography and co evolution. Dr. Traub’s research led to the development of a theory of how 2,200 species of fleas evolved, each along with their host species, over the course of 125 million years. Through this, Dr. Traub was able to provide support to the much debated theory of continental drift.

Dr. Traub was commissioned into the U.S. Army in 1943 and served in the China-Burma-India Theater of the war. His other military assignments included the U.S. Army Typhus Commission, U.S. Army Medical Research Units in Malaysia and Borneo, and the Commission on Hemorrhagic Fever in Korea.

From 1946 to 1955 he was Chief, Department of Entomology, Walter Reed Medical Center. He then served as Commanding Officer of the U.S. Army Medical Research Unit (Malaya). In 1959, Dr. Traub was appointed Chief, Entomological Research Branch, and Interim Chief, Preventive Medicine Branch, Army Medical Research and Development Command. Dr. Traub retired from the Army at the rank of Colonel in 1962.

He then became a professor in the department of microbiology in the University of Maryland School of Medicine. Following his retirement from the University of Maryland in 1983, Dr. Traub served as Honorary Curator of Siphonoptera at the U.S. National Museum of Natural History. He retired from this position in 1994.

Over the course of his career, Dr. Traub described over 150 new species and 30 new genera or sub-genera of fleas and 124 new species of chiggers. He also amassed a collection of fleas with over 70,000 specimens, second only to the collection at the British Natural History Museum in size. The bulk of his work centered on Southern Mexico, Northern Africa and Southeast Asia.

In 1948, Dr. Traub was a member of a research team which was nominated for a Nobel Prize for investigating scrub typhus. He was awarded the Harry Hoogstraal Medal For Outstanding Achievement in Medical Entomology in 1989 by the American Society of Tropical Medicine and Hygiene.
   
Over the course of his career, Dr. Traub authored, co-authored, or edited over 200 technical publications, at least 93 of which dealt with fleas. Books from the Traub collection which were cataloged into the Carnegie Museum of Natural History Library are identified by a memorial bookplate.
 
Dr. Traub died in Bethesda, Maryland on December 21, 1996.
...
The significant correspondents include Miriam Rothschild, Harry Hoogstraal, Abdu Farhang-Azad, N.G. Gratz, R.H. Green, W.L. Jellison, R.E. Lewis, Li Kuei-chen and Chin Tai-Hsiung, Frank J. Radovsky, Vernon J. Tipton and P.F.D. Van Peenen.
...
RO-RY: 1985-1973
...
Rothschild, Miriam 1986-: CBE, DSC, FRS, Peterborough, England: 1994-1986
Rothschild, Miriam: 1985-1983
Rothschild, Miriam: 1984-1985: 1985-1984
...
SE-SI: 1990-1975
...
Shope, Robert E.: Professor of Entomology, Yale Arbovirus Research Unit, Dept. of Epidemiology and Public Health, Yale University, New Haven, CT. 1983