Epidemic/Biological Hazard Update: July 2/2012 (Bird Flu, Measles, Radioactive Pet Bowls, Chikungunya, Dengue Fever, Cholera)

















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  1. Science 18 June 1971:
    Vol. 172 no. 3989 pp. 1265-1267
    DOI: 10.1126/science.172.3989.1265
    Production of Hemadsorption-Negative Areas by Serums Containing Australia Antigen

    David H. Carver,
    Dexter S. Y. SetoExposure of human Wi-38 cells to human serums containing Australia antigen, and presumably serum hepatitis virus, renders the cells refractory to infection by Newcastle disease virus as detected by the hemadsorption-negative plaque test for intrinsic interference. Induction of the Newcastle disease virus refractory state could be passed in cell culture with up to a 1 : 100,000 dilution of material obtained from cells “infected” with serums containing Australia antigen after filtration (0.45-µm pores) and heating to 60°C for 1 hour. Human antiserums to the Australia antigen prevented induction of the Newcastle disease virus refractory state.

    Newcastle disease, pseudo-pest or fowl, or pneumoencephalitis, is an acute, highly contagious, febrile disease of fowl (chickens, turkeys and pheasants). The course of the disease is of short duration. It is characterised by severe respiratory and nervous symptoms, including difficult breathing, depression and stupor, twitching of the head and neck, marked weakness, a twisted neck and perhaps paralysis. Egg production is interrupted for weeks.

    Erich Traub was a German veterinarian and scientist/virologist who specialized in foot-and-mouth disease, Rinderpest and Newcastle disease. Traub was a member of the National Socialist Motor Corps (NSKK), a Nazi motorist corps, from 1938–1942. He worked directly for Heinrich Himmler, head of the Schutzstaffel (SS), as the lab chief of the Nazi’s leading bio-weapons facility on Riems Island.

    Fort Terry on Plum Island was part of the U.S. biological warfare program in 1944-46, working on veterinary testing in connection with the weaponization of brucellosis. After the war, research on biological weapons continued at Pine Bluff in Arkansas and Fort Detrick, Maryland, while officially at least Plum Island was transferred to the U.S. Department of Agriculture. From 1949, Plum Island also conducted work on biological weapons against animals and livestock, such as foot-and-mouth disease, Rinderpest, Newcastle disease, African swine fever and plague and malaria in birds. Traub’s biological warfare work from the Second World War onward involved at least the first three of these.
    Archiv f/ir die gesamte Virusforsehung 42, 363–365 (1974)

    There have been reports of Newcastle’s disease showing up in an aviary in south Florida. Newcastle’s disease is a deadly virus that is extremely contagious and can be passed on from contact with any bodily secretions or contaminated food or water. It is advisable to always wash your hands after contact with birds outside your own flock, and especially with birds under quarantine. The symptoms of Newcastle’s disease vary between different strain, but can be any of the following signs:
    • Respiratory problems – gasping, coughing
    • Nervous issues – depression, lack of appetite, muscular tremors, drooping wings, twisting of the head and neck, circling, complete paralysis
    • swelling of the tissues around the eyes and neck
    • greenish, watery diarrhea
    • misshapen, rough or thin-shelled eggs or reduced egg production
    In acute cases, death can be sudden and in the beginning of an outbreak within a flock, the remaining birds don’t appear sick. In a flock with a strong immunity to the disease, the respiratory and digestive symptoms are generally mild, but progressive and are followed with a week of nervous symptoms, especially twisted heads.
    Newcastle’s disease is taken very seriously by state agencies, which in some cases, have slaughtered healthy birds simply based on their concern over the disease. It was once consider along with other major diseases to be used as a biological weapon by the US government, until those programs were shut down.

    Newcastle disease virus (NDV) – A type strain for avian paramyxoviruses. Members of this family have a single stranded, linear, RNA, with an elliptical symmetry. The total genome is roughly 16,000 nucleotides. Replication of the the virus takes place in the cytoplasm of the host cell.
    NDV is a contagious and fatal viral disease affecting most species of birds. Clinical signs are extremely variable depending on the strain of virus, species and age of bird, concurrent disease, and preexisting immunity. Four broad clinical syndromes are recognized by scientists. They are Viscerotropic velogenic, Neurotropic velogenic, Mesogenic, and Lentogenic. NDV is so virulent that many birds die without showing any clinical signs. A death rate of almost 100 percent can occur in unvaccinated poultry flocks. NDV can infect and cause death even in vaccinated poultry. Fortunately NDV has not infected domestic chicken flocks in the United States since the last outbreak was eradicated in 1974.
    NDV is spread primarily through direct contact between healthy birds and the bodily discharges of infected birds. The disease is transmitted through infected birds’ droppings and secretions from the nose, mouth, and eyes. NDV spreads rapidly among birds kept in confinement, such as commercially raised chickens.
    High concentrations of the NDV are found in birds’ bodily discharges; therefore, the disease can be spread easily by mechanical means. Virus-bearing material can be picked up on shoes and clothing and carried from an infected flock to a healthy one.
    NDV can survive for several weeks in a warm and humid environment on birds’ feathers, manure, and other materials. It can survive indefinitely in frozen material. However, the virus is destroyed rapidly by dehydration and by the ultraviolet rays in sunlight.
    Smuggled pet birds, especially Amazon parrots from Latin America, pose a great risk of introducing NDV into the US. Amazon parrots that are carriers of the disease but do not show symptoms are capable of shedding NDV for more than 400 days.

    Treatment: There is no known treatment for Newcastle Disease.

    9 by Springer-Verlag 1974
    Positive Reaction between Australia Antiflen
    and Anti-Human Liver Antibody
    Brief Report
    The “Stefan S. Nicolau” Institute of Virology,
    Bucharest, Romania
    Received July 1, 1974
    Soon after its discovery, Australia antigen (AuAg) was correlated with viral
    hepatitis B and considered to be a hepatitis associated antigen (1, 2, 3). The antigen
    has been detected in the blood of patients suffering from acute or chronic viral
    hepatitis or from other diseases having no connection with viral hepatitis, but in
    which a hepatic involvement could be proved.
    In viral hepatitis the liver cell is affected by lesions of various intensity, causing
    sometimes large zones of cellular lysis. As we have previously shown, the
    severity of the hepatic lesion is expressed in the patients’ blood by protein (4, 5)
    and nucleic acid (6) values significantly higher than the normal limits. Thus, it is
    demonstrated that in the case of morphofunctionM alteration of hcpatocytes the
    constituents of these cells are released into the blood flow.
    Investigations on the physico-ehemical properties of AuAg made us conclude
    that the behaviour of this antigen is rather that of a protein–such as high molecular
    weight macroglobulins–than that of a viral particle (7).
    Under these conditions it can be assumed that the “Australia antigen”
    occurring in sera from patients or clinically healthy persons, which interacts with
    serum antibodies or induces the appearance of such antibodies, might represent
    liver cell proteins. Of course, the possibility that AuAg should carry the virus or
    “infravirus” (8) of hepatitis adsorbed onto its surface should not be neglected.
    I-Ienee, AuAg would not be the etiological agent of infectious hepatitis, but it
    would indicate an injury of the liver cell by infection with an unidentified hepatotropic
    virus, or by another cause, independent of infectious hepatitis.
    In order to check this hypothesis, we imagined an experimental model relying
    on electroimmunodiffusion techniques. We used the following immune reactants:
    a) 7 sera with high AuAg titers from viral hepatitis patients;
    b) sera from normal subjects, containing neither AuAg nor homologous antibodies
    c) sera from rabbits immunized with cellular extract from human embryo liver,
    triturated in physiological saline and centrifuged to remove nuclei and to achieve
    The results of the interaction between these 3 preparations, subjected to
    electroimmunodiffusion, are given in Table 1. It can be seen that the anti-human
    liver immune serum gave positive reactions of various intensity with the sera
    from AuAg-positive patients. At the same time, it was found that rabbit sera also
    reacted with the sera from healthy subjects. These positive reactions were interpreted
    as being caused by blood traces present in the liver extract used for the
    immunization of rabbits that induced antibodies. To remove these species-specific
    antibodies, adsorption onto human red blood cells and desiccated human plasma
    was used. Under these conditions, rabbit sera reacted no longer with serum from
    healthy subjects, but still gave positive reactions with AuAg. It should be mentioned
    that each sample of immune rabbit serum adsorbed onto the aforementioned
    preparations was tested separately against AuAg from human sera and normal
    (AuAg-negative) human sera. The positive reactions would be due to the interaction
    between immune rabbit serum and liver protein, since the reactions became
    negative following immune adsorption of rabbit serum onto liver extract from
    healthy human embryo, as it results from Table 1.
    The positive reaction between immune anti-human liver sera and AuAg from
    human sera would suggest that positivity of the immune precipitation reactions
    employed in the diagnosis of hepatitis B could be due to the interaction between
    liver proteins released by injured hepatoeytes and the serum antibodies to these
    proteins that may become antigens. The fact that AuAg interacts with antihuman liver antibodies made us consider it to be a morphologically structured
    protein released by the human liver cell that underwent a lesion following viral
    infection, and not the virus responsible for hepatitis B.
    We thank Prof. Dr. P. Sirbu (Maternity Hospital “Giulesti”, Bucharest) for having
    so kindly supplied us with the human embryo liver tissue used for preparation of the
    specific antiserum.

    1 Secondary hepatotropic viruses
    The most important virus species with regard to their
    ability to cause concomitant inflammatory reactions
    of the liver are (1.) herpesviruses, (2.) rubella viruses,
    (3.) Coxsackie viruses, and (4.) paramyxoviruses

    1.4 Paramyxoviruses
    1.4.1 Measles hepatitis
    The measles virus, discovered in 1911, is a large
    (100_150 nm) paramyxovirus with a lipid envelope.
    Concomitant measles hepatitis occurs in 80% of all
    adults suffering from measles. It generally takes an anicteric,
    clinically bland course, and in most cases even
    goes unnoticed. Diagnosis is based on the elevation of
    transaminases and the detection of IgM antibodies.
    Cytologically, multinuclear giant cells are found in nasal
    secretion. The prognosis for measles hepatitis is good.
    Despite lifelong immunity, however, the measles virus is
    able to persist latently in cells, especially in lymphocytes
    (as in autoimmune hepatitis). (73, 75, 78)
    1.4.2 Parotitis hepatitis
    The parotitis virus, an RNA virus of the paramyxovirus
    group, can also cause mumps hepatitis with corresponding
    minimal histological and laboratory findings.
    1.4.3 Giant-cell hepatitis
    In 1991 in Canada, J. Phillips et al. determined the presence
    of paramyxoviruses in patients with an infaust
    course of giant-cell hepatitis: out of ten patients, only
    five survived with the help of liver transplantation. Paramyxovirus
    nucleocapsid protein, with a diameter of
    12_17 nm, was detected in the cytoplasm of the hepatocytes.
    (77) Until then, this paramyxovirus had been
    unknown. It can cause severe acute hepatitis, which
    might even be fatal. (74, 76, 79) (s. p. 425!)

    Measles outbreak kills 12 children in Pakistani tribal area
    Monday, 14 May 2012

    The U.N. children’s agency UNICEF said there had been 143 measles alerts this year in Pakistan’s seven-district, semi-autonomous tribal belt. (File photo)
    By AFP
    MIRANSHAH Pakistan
    A measles outbreak has killed 12 children in one of Pakistan’s lawless tribal districts and is spreading as fighting, power cuts and curfews cause a vaccine shortage, doctors said Monday.

    North Waziristan, a restive and deeply poor area bordering Afghanistan, is Pakistan’s most notorious Taliban and al-Qaeda stronghold, hit frequently by U.S. drone strikes targeting Islamist militants.

    “For the past three weeks we are daily receiving five to 10 children suffering from measles,” said doctor Mohammad Ali Shah, chief of the main hospital in Miranshah, the area’s biggest town.

    He would normally see only one or two deaths a year from the disease, he said.

    But another doctor, Mohammad Sadiq, said 12 children and a man had died from measles in the last three weeks, and that there were up to 70 confirmed cases in hospital.
    The U.N. children’s agency UNICEF said there had been 143 measles alerts this year in Pakistan’s seven-district, semi-autonomous tribal belt.

    The measles virus is highly contagious and can be fatal, but can easily be prevented by proper immunization.

    However Shah said: “We do not have proper storage for measles vaccination because of long power outages and curfews and most of our stock expires due to these reasons.”

    Poverty and poor transport facilities mean villagers in the rugged, mountainous areas cannot come to hospitals for treatment, he added, while military operations and unrest mean vaccination teams cannot reach them.

    “There is accumulation of significant number of unvaccinated children in different parts of this region which are revealing as outbreaks or alerts over time to time,” said Doctor Quamrul Hasan of the World Health Organization (WHO).

    WHO and local health officials are to carry out a supplementary campaign in the tribal areas aimed at vaccinating more than a million children aged under 10 by the end of June, he said.

    Polio vaccination campaigns in tribal areas have in the past suffered because of rumors — sometimes spread by radio stations or from mosque loudspeakers — they were a Western conspiracy to sterilize children to reduce the Muslim population.

    But UNICEF said work had been done to tackle misconceptions and there was less suspicion of the measles vaccine, administered by injection, than of the orally-administered polio dose.

    Nearly 140,000 people died of measles worldwide in 2010, according to the World Health Organization — 95 percent in low income countries with poor health infrastructure.

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