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Man is infected either by eating food contaminated with ova pain breast treatment purchase ibuprofen line, or by direct contact with infected dogs unifour pain treatment center lenoir nc order ibuprofen online pills. It contains germ inating parasitic par ticles called “hydatid sand” containing 400 pain buttocks treatment buy discount ibuprofen on-line,000 scoleces/ml low back pain treatment kerala discount ibuprofen 400 mg overnight delivery. Patients often have eosinophilia and may have positive serologic tests for hydatid disease. Tr e a t m e n t Tr e a t m e n t i s s u r g i c a l r e m o v a l o f t h e i n t a c t c y s t. Ev e r y e ort must be made to avoid rupturing these cysts during removal, or else the scoleces may contaminate the adjacent tissues with possible recur rence of multiple cysts or allergic reaction. The cortical opening need only be 3/4 the cyst diameter but no less e-surg. Placing 10%formalin soaked cottonoids on the cavity for a few minutes is 61 (p 3750) controversial 22. Some of the more common ones or those of particular relevance to neurosurgery include: 1. Usually 3–10 mm in diameter and are frequently located in the basal gan glia (due to spread by small perforating vessels) 2. Management: a) optimal management has not been defined b) trials with alternative antifungals. In one survivor, surgical drainage of a brain abscess was performed in addition to treatm ent w ith a 6-w eek course of am photericin B, rifam picin, and ch loram phenicol. New [24] Centers for Disease Control (Morbidity and Mortal Yo r k 1 9 8 5 ity Weekly Report). Magnetic in a Patient Who Received a Cadaveric Dura Mater 22 Re so n a n ce Im a gin g a n d Co m p u t e r ize d To m o gr a p h y Graft. Precautions En cep h alitis: Nat ion al In st it u the of Allergy an d In fec in Handling Tissues, Fluids and Other Contaminated tious Diseases Collaborative Antiviral Study. Multifocal Co n se cu t ive Se r ie s o f 2 3 0 Ne u r o p a t h o lo gica lly Ve r i Le u ko e n ce p h a lit is Ca u s e d b y Va r ic e lla Zo s t e r Vir u s fied Cases. Diagnosis of cella zoster virus vasculopathies: diverse clinical Cr e u t zfeld t Ja kob Dise a se b y Me a su r e m e n t of S1 0 0 manifestations, laboratory features, pathogenesis, Protein in Serum: Prospective Case-Control Study. Fatal Fam Ab n or m a l Pr ot ein s in t h e Ce r eb r osp in a l Flu id of ilial Insomnia: A Second Kindred with Mutation of Patients with Creutzfeldt-Jakob Disease. Fatal Fami Protein in Cerebrospinal Fluid as a Marker for Trans lial Insomnia, a Prion Disease with a Mutation at missible Spongiform Encephaloptahies. Fatal familial and Reliability of Periodic Sharp Wave Complexes in insomnia: Clinical and pathologic study of five new Cr e u t zfeld t Ja kob Dise a se. Single photon Re lat e d Tr a n sm issib le Sp o n gifo r m En ce p h a lo p a emission computed tomography in the identifica thies. Investigation 197:943–960 of Variant Creutzfeldt-Jakob Disease and Other [15] Klitzman R. Transmis in Fixation of Autopsy Brain Tissue to Reduce Risk of sion of Creutzfeldt-Jakob Disease via a Corneal In adverten t Tran sm ission of Creutzfeldt-Jakob Dis Tr a n s p la n t. Iatrogenic ous system infections in immunocompromised Cr e u t zfeld t Ja kob Dise ase a t t h e Mille n n iu m. Fam ilial Creutzfeldt-Jakob Disease 1984; 310:1001–1007 (Codon 200 Mutation) With Supranuclear Palsy. Neurocysticercosis: A 1996; 347:921–925 new classification based on active and inactive [21] Du y P, Wolf J, Collins G, et al. Ca n d id a ce r eb r o sp in a l flu id 22 tion of the Cysticercosis Enzyme-Linked Immunoe shunt infection. Report of two new cases and lectrotransfer Blot in Patients with review of the literature. New York: Chur Co m p u t e d To m o gr a p h y, Ult r a so u n d, a n d Nu cle a r cill Livingstone; 2002:498–510 Magnetic Resonance. Short hydrocephalus secondary to cryptococcal meningi Co u r se o f Alb e n d a zo le Th e r a p y fo r Ne u r o cys t ice r co this by use of shunting. Extraparenchym al n eurocysticercosis: report of meningitis and uncontrollable intracranial hyper five cases and review of management. Surgical Treatment of Hydatid Cysts of the Central Nervous System in e-surg. It circu lates w ith in th e su barach n oid sp ace, bet w ee n th e arach n oid an d th e p ial membranes. A s m a ll a m o u n t m a y a lso b e p r o d u ce d b y t h e e p e n d ym a l lining of the ventricles. Rosenmuller’s fossa: located just inferior to cavernous sinus, may be exposed by drilling o anterior clinoids to allow access to ophthalmic artery aneurysms 8. Then either: a) rhinorrhea: through middle ear > eustachian tube > nasopharynx b) otorrhea: via perforated tympanic membrane > external auditory canal 23. Including: post-transsphenoidal surgery and post skull base surgery b) posttraumatic (more common): 67–77%of cases 2. It is rep or t e d t o occu r p ost -op in u p 13 to 30%of cases of skull-base surgery. Unlike traumatic leaks, these tend to be intermittent, the sense of smell is usually preserved, 14 and pneumocephalus is uncommon. May b e d u e t o ar ach n oid gran u lat ion s e r od in g in t o air sin u s com p ar t m e n t 23. Meningitis may promote inflammatory changes at the site of the leak, with a resultant cessation of the leak. However, this often proves to be a temporary resolution, providing a false sense of security. Pneum ococcal m eningitis is the m ost com m on pathogen (83%of cases18), m ortality is lower than in pneum ococcal m eningitis w ithout underlying fistula (< 10%vs. Very sensitive &specific b) collect fluid and obtain quantitative glucose (urine glucose detection strips are too sensitive, and may be positive even with excess mucus). An old, but unreliable, sign d) reservoir sign: a gush of fluid that occurs with a certain head position. Some of the studied radiopharmaceuticals are no longer available b) intrathecal (visible) dye studies: some success with indigo carmine or fluorescein (p. Mayneed provocative maneu vers (coronal scans prone (brow up) or in position of leak, intrathecal saline infusion (requires Har 26 vard pum p) ). Th e r e w a s n o d i erence in the incidence or morbidity of 27 meningitis between treated and untreated patients. Fu r t h e r m o r e, t h e r isk o f sele ct in g r e sist a n t 9 strains appears real and is therefore usually avoided. If a fron t al cran iotom y is be in g p er for m e d, an in t r ad u r al ap p r oa ch sh ou ld b e u se d sin ce p r ob le m s m ay ar ise in d isse ct in g t h e d u ra o of the floor of the frontal fossa, wherein the dura almost always tears and then it is di cult to know if an identified tear is the cause of the leak or if it is iatrogenic. If th e fistu la site is u n id en tified p reop eratively, u se a bifron tal bone flap. Gen eral t ech n iq ues of intradural approach: Clo s e b o n e d e fe ct s w it h fa t, m u s cle, ca r t ila ge, o r b o n. Clo s e d u r a l d e fe ct w it h fa s cia la t a, t e m p o r a lis m u s cle fa s cia, o r p e r icr a n iu m. If t h e leak is u n id en t ified p re-op an d in t ra-op, t h e n p ack bot h cr ibrifor m p lates an d sp h en oid sinus (incise dura over tuberculum sellae, drill through bone to reach sphenoid sinus, remove muco sa or pack it inferiorly, pack with fat). If u sed, p lace t h e d rip ch am ber at t h e level of sh ou ld er for 3–5 days (for precautions, see above). Le a k s i n t o s p h e n o i d s i n u s (i n c l u d i n g p o s t t r a n s s p h e n o i d a l s u r g e r y l e a k) 1. Clin ic a l Th e syn d r o m e o f sp o n t a n e o u s in t r a cr a n ia l h yp o t e n sio n is ch a ra ct e r ize d b y t h e fo llow in g in t h e absence of antecedent trauma or dural puncture: 1. Oth er causes of dural injur y are degen erative disc disease, osteophytes an d bony 34 spurs. Th e o r t h o st a t ic h e a d a ch e is b e lie ve d t o b e ca u s e d b y t h e d e sce n t o f t h e b r a in, ca u s in g s t r a in 33,37,47 on intracranial structures sensitive to pain. Associa t e d 39 with low lying cerebellar tonsils occurred,seen in 36%ofpatients, e acement of peri chiasm atic and prepontine cisterns, bow ing of the optic chiasm, flattening of pons, and 33,36,37,48 ventricular collapse 23 Enhancement of the pachymeninges, sparing the leptomeninges, is common from dilation 33,46,48 of subdural blood vessels Engorgement of veins. Can also see venous distension sign as transverse sinus becomes 49 dilated and convex Pituitary hyperem ia 34,50 Subdural fluid collections seen in 50%of patients. Ca n b e h yg r o m a s ve r s u s h e m a t o m a s, with hygromas being twice as frequent as hematomas. Contrast remains for 24 hours, hence it can aide in detection of intermittent leaks.
These are often of little tissues pain treatment osteoarthritis 400mg ibuprofen fast delivery, and the appropriate cleaning or benefit in household settings as disposal of contaminated objects nerve pain treatment for shingles buy cheapest ibuprofen. Outbreak measures In countries such as Australia where In communities with appropriate modern polio has been eradicated a single case sewerage systems pain treatment center of greater washington purchase ibuprofen 400 mg amex, faeces and urine from of polio is considered a public health infected patients can be disposed of emergency and the Department of directly into sewers without preliminary Human Services must be notified disinfection chiropractic treatment for shingles pain cheap ibuprofen amex. The Department required for all other potentially investigates to: contaminated items. Antibiotic treatment may delay or ocular and nasal secretions from infected attenuate antibody formation so birds. Rare person to Infectious agent least two weeks after the acute person transmission has occurred. Culture of the organism is generally not Infected birds may shed the agent Identification performed because of danger to intermittently for a prolonged period. Shedding may be precipitated by stress the onset of psittacosis is usually abrupt Birds on the birds such as cold, crowding or with fever, prominent headache, Birds suspected of being infected should shipping. The incubation period is four days to four Older adults and pregnant women may the illness usually lasts for seven to ten weeks, commonly ten days. Most cases are sporadic but outbreaks Control measures Complications include encephalitis, of infection may occur rarely within Preventive measures endocarditis, myocarditis and individual households or through contact Educate the public about the danger of thrombophlebitis. Relapses may occur, with affected pet shops or poultry household or occupational exposure to especially when there has been processing plants. This Humans which birds have frequent contact such is especially common for psittacine birds Infection is generally diagnosed by as cages and bird feeders. Cats, setting of clinically-compatible illness is Appropriate surveillance of commercial dogs, goats or sheep may be infected but significant. Prophylactic use of tetracyclines can suppress, but not eliminate, infection in flocks and may complicate investigations. Further information Psittacosis is bacterial disease of both Sick birds may have eye or nasal • Your local doctor wild and domestic birds that can affect discharge or ruffled feathers, and may • Better Health Channel, people. Stop wild birds getting • Victorian Department of Human close to your pet bird’s cage as they can What are the symptoms in Services, 1300 651 160 spread disease. Psittacosis in humans may cause a flu I think I may be infected what like illness or pneumonia. Birds do not have to be sick to or cold conditions and do not buy birds spread the disease. The risk of getting the Clean cages, food and water bowls daily disease is greater when the birds are and use litter which creates dust such as under stress, for example just after being newspaper. You may unknowingly come into Use a 1:100 diluted solution of household contact with infected birds while feeding bleach to disinfect any ill bird’s cage, wild birds, cleaning feeding stations or bowl etc. The cannot be disinfected and rinse all spread of psittacosis from person to disinfected items before replacing them. Do not allow birds to get close to your face and wash hands thoroughly after contact with birds. The onset of Q fever infection is usually Coxiellae-contaminated dust or aerosols. Transient mild rashes IgA class antibody to phase I antigen is contaminated by placental tissues, are an occasional feature. It also testing between acute and convalescent infected animal has been suggested as a occurs in others handling fomites such sera collected at least 14 days apart. Contaminated clothing should be restricted to immunised ascertain the most likely source of may also be a source. Control of case higher frequency of exposure to high risk Acute cases of Q fever generally require Non-immune staff should be excluded environments, rather than differential treatment with doxycycline or from the worksite until vaccinated. Consultation with an infectious diseases There is a risk of severe local reactions to physician should be sought. Vaccination Control of environment induces lifelong immunity in most If a clear source is identified, disinfection vaccinees. High rates of rabies are reported consultation with the chief veterinary specific prodrome of fever, headache, from the Philippines, Thailand and officer. Rabies periods of excitation and agitation fluorescent antibody of a clinical is a very rare infection of travellers to leading to delirium, confusion, specimen such as neural tissue endemic areas outside of Australia. The criterion for a suspect rabies case is progressive encephalitis with a past history of exposure in a rabies endemic area. Ongoing serological Transmission from person to person is is also reportable to the World Health testing and virus studies suggest that this theoretically possible but it has only ever Organization. It can also occur Susceptibility and resistance Rabies is a disease primarily of animals. Infected dogs remain the highest risk the most frequent way that humans developed the disease. It is also transmit the virus to other animals, continue to be the main hosts in most recommended for travellers who will be although they may transmit the disease African, Asian and Latin American spending prolonged periods. Contact such countries in the world where the animal data on rabies infected countries – see as patting bats or exposure to urine and population is free of rabies. Where possible, without Control of contacts placing other persons at risk of exposure, Other individuals exposed to the source the bat should be kept and the animal are identified and offered post Department of Human Services exposure prophylaxis. Contacts that have consulted about arranging testing of the open wound or mucous membrane bat for virus carriage. Rabies and Australian bat lyssavirus exposure information sheet Pre-exposure prophylaxis Post-exposure treatment for If the exposure is connected to an Pre-exposure vaccination should be persons bitten or scratched Australian bat, where possible without recommended to those people whose the decision to offer post-exposure placing other persons at risk of exposure, occupation or recreational activities prophylaxis to a potentially exposed the bat should be kept so that the place them at increased risk of being person should be made in consultation Department of Human Services can bitten or scratched by a bat. Pre-exposure vaccination administration into the anterolateral aspect of the thigh is also acceptable. Rickettsiae (and Reservoir Method of diagnosis their associated diseases) of particular Humans are incidental hosts and are not In endemic areas the clinical picture is importance in Australia are R. An exception is There is great variation in the severity of isolation of the rickettsia after inoculation louse-borne typhus illness produced by each organism. Humans are the principal papule forming at the site of the bite although these need to be interpreted reservoir for louse-borne typhus and the where the infection was introduced. This with caution because of cross-reactivity human body louse (pediculosis humanus usually becomes necrotic and forms a between strains. The disease is not directly transmitted adenitis in the lymph glands draining the the variation in incubation may be in from person to person. Disease occurrence is often febrile illness and probably two or three features are continuous fever, cough and associated with the modification of days after the temperature returns to signs of bronchitis or pneumonia, natural habitats by humans such as normal. People are at risk of infection for photophobia, conjunctivitis, generalised when a forest is felled and replaced by a as long as they remain in infected areas. Queensland but its geographic 180 the blue book: Guidelines forthe control of infectious diseases Control measures Outbreak measures Preventive measures Except in the case of an epidemic of There is no vaccine available. People who louse borne typhus, no outbreak enter infected areas can be protected by measures are necessary. Control of contacts Consider active case finding if other people were exposed to the same setting as the case such as a camping holiday or military exercise. It is spread by School exclusion: readmit the day after area or by fungal culture. Direct transmission occurs through Infected hairs become brittle and the highly contagious M. Infection can occur from direct or indirect contact with skin Period of communicability • tinea pedis is commonly known as and scalp lesions of infected persons or the fungus persists on contaminated ‘athlete’s foot’. Adults are affected more often susceptible to tinea capitis (Microsporum the hands or feet. It is aggravated by friction treatment of choice for resistant and excessive perspiration in axillary and infection, for example T. Feet should be kept dry as An injury to the nail predisposes to tinea possible and exposed to air by wearing unguium infection. Control of contacts Shower areas should be frequently Investigate household contacts, pets and hosed and rapidly drained. Control of case Control depends on the cause: Outbreak measures Children and parents should be educated • for tinea corporis infected children about modes of spread, prevention and should be excluded from schools and the necessity of maintaining a high swimming pools until at least 24 hours standard of personal hygiene. In case of following the commencement of epidemics, consider examination of all appropriate treatment. Ringworm of the foot (commonly known Further information Ringworm is a fungal infection that can as tinea or athlete’s foot) the • Your local doctor affect any part of the body. The incubation period lasts from one to Exclude infected persons from three weeks. It is usually dry and • Do not share clothing or personal scaly or moist and crusted, but it may linen.
Electroencephalogr Clin tion with a double coil: the importance of coil orientation midwest pain treatment center fremont ohio ibuprofen 400mg otc. Magnetic and electrical Activation of the epileptic focus by transcranial magnetic transcranial brain stimulation: physiological mechanisms stimulation of the human brain key pain management treatment center purchase ibuprofen visa. Corticomotor threshold is reduced in Activation of epileptic foci by transcranial magnetic stimula early sporadic amyotrophic lateral sclerosis pain tmj treatment generic ibuprofen 600 mg visa. Muscle Nerve tion: effects on secretion of prolactin and luteinizing hor 1997;20:1137–1141 regional pain treatment center order ibuprofen online from canada. A new method for reproducible coil positioning in vealed by transcutaneous magnetic stimulation of the brain. J transcranial magnetic stimulation for mapping the human Physiol 1967;191:673–690. Electroencephalogr Clin cal study of the corticospinal projections in amyotrophic lat Neurophysiol 1991;81:63–70. Muscle Nerve of cortical motor function as revealed by stereotactic trans 2000;23:1044–1050. Motor cortex plasticity during constraint brachial plexus injury: segmental demyelination and axonal induced movement therapy in stroke patients. The glu invasive differentiation of motor cortical representation of tamate antagonist riluzole suppresses intracortical facilita hand muscles by mapping of optimal current directions. J Phys evidence of hearing loss in humans due to transcranial mag iol 1993;460:201–219. Measurement of the electric arrest and counting errors with rapid-rate transcranial mag field induced into inhomogeneous volume conductors by netic stimulation. Lumbosacral nerve root evoked by transcranial magnetic stimulation during the ac stimulation comparing electrical with surface magnetic coil quisition of new fine motor skills. Lancet 1996;348: Does a C3–C4 propriospinal system transmit corticospinal 233–237. Ann Neurol facilitation of muscle responses to cortical stimulation by 1995;38:910–915. Pennisi G, Rapisarda G, Bella R, Calabrese V, Maertens de brain stimulation study with focal magnetic pulses. Stroke tion for detection of preclinical cervical spondylotic myelop 1999;30:2666–2670. Motor recovery following stroke: a transcranial mag Oxford: Clarendon Press; 1993. Ugawa Y, Uesaka Y, Terao Y, Suzuki M, Sakai K, Hanajima R, Changes in the balance between motor cortical excitation Kanazawa I. Clinical utility of magnetic corticospinal tract and inhibition in focal, task specific dystonia. The course of cortico-hypoglossal projections in tical reorganization in patients with facial palsy. Quantifica the International Workshop on the Safety of Repetitive tion of upper motor neuron loss in amyotrophic lateral scle Transcranial Magnetic Stimulation, June 5–7, 1996. Motor cortex ment of postexcitatory inhibition in patients with focal dys excitability in patients with focal epilepsy. Low-frequency re of the late excitatory potential in the hand following mag petitive transcranial magnetic stimulation of the motor cor netic stimulation of the motor cortex. Can J nerve stimulation in assessment of phrenic nerve conduction Neurol Sci 1998;25:48–54. Facilitation of human first magnetic stimulation: its current role in epilepsy research. Muscle Nerve 1998;21: cortical and cervical magnetic stimulation with recording of 1033–1039. It is an overview of the most important endocrine diseases, it helps to learn the correct endocrine diagnostics and offers an effective treatment of endocrine diseases. I wish it would be a principal aid in basic medicine study for students of medicine, but also a concise endocrinology guide for physicians who exert a medical practice. Peabody from the year 1927: “The essence of the practice of medicine is that it is an intensely personal matterthe treatment of a disease may be entirely impersonal; the care of a patient must be entirely personal. The significance of the intimate personal relationship between physician and patient cannot be too strongly emphasized, for in an extraordinarily large number of cases both diagnosis and treatment are directly dependent on it One of the essential qualities of the clinician is interest in humanity, for the secret of the care of the patient is in caring for the patient”, is timely until now and should serve as additional guidance. Hypothalamus deficiency syndrome – Hypopituitarism – 13 Hypothalamic hypopituitarism Kallmann s syndrome 13 Frohlich syndrome 13 Prader-Willi syndrome 13 Laurence-Moon-Biedl syndrome 13 Anorexia nervosa 13 Diabetes insipidus centralis 13 B Diseases of the pituitary – Classification 14 B. The system is based on a number of glands, which secrete hormones into internal medium to act on target tissues. Hormones first interact with specific high-affinity receptors in the cells, or on the cells of target tissues. Receptor activation then initiates a cascade of linked biochemical reactions within the cells, that produce the specific response. Hormones represent chemical messengers diverse molecular structures (proteins, peptides, steroids) are released from endocrine glands coordinate the activities of many different cells. Endocrine diseases – heterogeneous group – wide range of manifestations affecting many other organs. Hormones – active molecules Hormones are biologically high active drugs of the body which control the metabolic activity all different tissues and organs in the body. They play an important role in development and growth of the body, they control the reproduction mechanisms, they help how to adapt on everyday life-stress and how to survive. Hormones can be classified according to chemical composition, solubility properties, the location of receptors, or the nature of the signal used to mediate their action within the cell. Endocrine pathology Pathology arising within the gland is called a primary disease. Adrenal gland: (two glands, left and right adrenal gland): Adrenal cortex: aldosterone, cortisol /steroids/, androgens, esterogens /steroids/. Adrenal medulla: epinephrine (adrenaline), norepinephrine (noradrenaline), opamine /catecholamines/. Anterior pituitary (adenohypophysis) hormone secretion is controlled by substances produced in hypothalamus and released into portal blood circulation. Anterior pituitary hormones = trophins are controlled by hypothalamic releasing/ or inhibiting hormones. Hormone release (in the hypothalamus and pituitary) is regulated by numerous stimuli of nervous metabolic, physical hormonal origin, in particular feedback control by hormones produced by the target glands (thyroid, adrenal cortex and gonads). Philadelphia: Churchill Livingstone/Elsevier Health Sciences Division, 2006, xvi, 1381 p. Disorders of the hypothalamus and pituitary may present as endocrine or neurologic dysfunction. The pituitary plays a central role in several major endocrine axes, so that investigation and treatment involves several other glands. The presence of hypothalamic tumours may initiate the early onset of normal mechanisms of pubertal maturation, with excessive skeletal growth but a reduced ultimate height. The initial defect can be congenital, which can be associated with a reduced sense of smell – anosmia. Dominant clinical signs are obesity in childhood, associated with underdeveloped infantile genitalia as a consequence of gonadotrophin deficiency. The reduction in genital size is not real, as a penile shaft is buried in the suprapubic fat pad and is normal in size. The testes are also normal in size for a prepubertal boy = Pseudo dystrophia adiposogenitalis. Laurence-Moon-Biedl syndrome is a central hypogonadism associated with retinitis pigmentosa, polydactylia and congenital heart defects. Disorder presents as anorexia, severe weight loss, amenorrhea, behavioral changes hyperactivity and preoccupation with food. Treatment: estrogens replacement is indicated, continued preoccupation with food and persistent dieting behaviour. Metoclopramide, domperidone) Dopamine-depleting drugs * Reserpine * alpha Methyldopa * Oestrogens * Oral contraceptive pills Pathological Common * Disconnection hypeprolactinemia.
The scientists’ presence seemed to pain treatment center of the bluegrass ibuprofen 400mg overnight delivery have a disconcerting effect on the work ers at the Nebraska plant ohio valley pain treatment center order ibuprofen mastercard. You put these 6 laser treatment for dogs back pain discount ibuprofen 400mg without prescription,000 pounds into a boil tank and you blew it over by steam all at one time into the batch cooker pain treatment center hartford hospital purchase 400mg ibuprofen otc. And then we had to clean up, pick up that 6,000 pounds and put it in barrels and disinfect the area. But I am living proof that you can have scrapie brain sprayed all over you, in your eyes, in your mouth, your ears, and you can get in among it and you can clean it up with shovels, put it in barrels, bring it back around and do it all over again and, after five and a half years, only have a couple of twitches here and there. By May of 1996, one had died of a perforated gut, and another had gone down with a vague disease that the scientists were unable to identify, but none had shown signs of spon giform brain disease. He took an infected ham ster brain, mixed it with soil, and packed the mixture into pots that he buried in his back yard. Three years later he dug up the package and discovered that “between 2 and 3 log units of the input infectivity of nearly 5 log units sur vived this exposure, with little leaching of virus into deeper soil layers. These results have implications for environmental contamination by scrapie and sim ilar agents, including those of bovine spongiform encephalopathy and Creutzfeldt-Jakob Disease. A sample containing “input infectivity of 5 log units” was enough to kill 100,000 hamsters, and after burial for three years, it still retained enough infectivity to kill between 100 and 1,000. Gajdusek’s experiment helped explain how the infectious agent could persist in soil and defeat even Iceland’s severe scrapie eradication campaign. Gajdusek undertook another experiment, in collaboration with Paul Brown and other researchers, which showed that the scrapie agent could even sur vive for an hour at 360 degrees centigrade (680 degrees fahrenheit)—a tem perature adequate to melt lead and to reduce a good-sized slab of meat to fine ash. I can think of few better techniques for distributing it far and wide over the countryside. What they should be doing is burying the bodies of the cattle in lime on the farms where the dis ease occurred. If the scrapie analogy holds, the soil surface on those farms will be heavily contaminated anyway, and there would be no danger of con taminating men and vehicles when transporting the carcasses away. Although this sterilization procedure is effective for conventional pathogens, neither chem ical inactivates the agents of spongiform encephalopathy, and one of the electrodes subsequently transmitted spongiform encephalopathy to a chim panzee 18 months after implantation in the cerebral cortex. There was no way of proving whether they had gotten their disease through occupational exposure, but it seemed a good possibility. Aside from medical accidents, however, Creutzfeldt-Jakob Disease seemed generally difficult to transmit. Kuru, the other known human spongiform encephalopathy, had spread fairly rapidly within a specific tribe, multiplying into a devastating epidemic within a contained geographic region. The first cases were observed in Germany in the 1920s, but the disease did not receive much attention until Gajdusek started taking it seriously in the 1960s, and it has never been made a reportable disease, so statistical estimates of its frequency can only be roughly charted. Under Gajdusek’s leadership, though, surveillance began in a number of countries around the world, and the data that filtered back showed a fairly consistent pattern. It occurred in England, where scrapie was endemic, and it occurred at similar rates of incidence in New Zealand, where scrapie had never been reported. Its worldwide distribution resembled the pattern Bent Proteins 117 you might expect from a rare genetic disorder or sporadic mutation, and some characteristics of the disease supported this conclusion. A theory that promised to explain this paradox came from Stanley Prusiner, a neurologist at the University of California School of Medicine at San Fran cisco. He had a background in biochemistry research, and was fascinated when he started reading about the spongiform diseases. Those who tried to unravel the chemistry of the disease hadn’t taken a very careful approach. Marsh and Kimberlin had dis covered that hamsters could incubate the disease even more rapidly than mice and that their brains accumulated higher levels of the disease agent than other experimental host animals. By using hamsters instead of mice and by modi fying the testing procedure, Prusiner was able to complete experiments in 60 days that previously would have taken a full year. He spun samples in centrifuges and treated them with enzymes trying to break down other brain tissues while leaving the infectious agent intact. Further studies showed that it was a “glyco protein”—a protein with sugars attached to the amino acid chain. These discoveries slotted in neatly with research in England by a young Indian scientist named Harash Narang. Using an electron microscope, Narang had found rod-shaped particles in sections of scrapie-infected brain tissue and shown that the particles could be stained by substances that selectively bind to sugars. He called them “tubulofilamentous particles,” and they looked at first like good candidates to be the long-sought scrapie virus. Gajdusek guessed that Narang was looking at a con tamination accident, but when other scientists found that they could repro duce his result, the mood turned excited. Gajdusek wrote a personal letter to Narang’s employers at the British Public Health Service Laboratories, congrat ulating them on the discovery of what Narang called a “nemavirus. Prusiner studied Narang’s particles and concluded that they were composed largely, if not entirely, of the protein he had been observing in his experiments. The same protein was also found in another type of deposit that appeared in some, but not all, spongiform-infected brains— “amyloid plaques. Amyloid plaques looked like little waxy buildups in the brain, and for a long time they had been considered accumulations of waste material formed as byproducts of aging or some unknown disease process. Solutions of the protein tended to cluster together and to crystallize into rod like structures resembling Narang’s particles. Prusiner proposed a new theory— that both the particles and amyloid plaques were crystallized formations of a protein that, by itself, might constitute the disease agent. If this were the case, Prusiner suggested scrapping the term “slow virus” and replacing it with a new term coined to capture the concept of a protein that behaved infectiously like a virus. Prions, he said in a 1982 article in Science magazine, were “proteinaceous infectious particles which are resistant to inactivation by most procedures that modify nucleic acids. The prion is known to be capable of initiating the produc tion of new prions, at least in certain mammalian cells. The evi dence gathered so far, however, indicates the prion has no nucleic acid at all. He had found some evidence to support the theory, but it was circumstantial, highly speculative evidence. And as he himself acknowledged, his theory ran so contrary to existing scientific knowledge that it could rightly be considered a “heresy” against “the principle that genetic information invariably flows from nucleic acids to proteins,” a principle so entrenched that it “has been called the central dogma of molecular biology. The prion remains a mystery in more ways than one—perhaps the most controversial being why the gov ernment gave $4 million to a scientist whose work is disputed by virtually every other researcher in his field save his immediate collaborators. They charged Prusiner with egotism, hogging the scientific spotlight, and medical McCarthyism aimed at suppressing research by his com petitors. One of Prusiner’s former post-doctoral research assistants accused him of flacking the word “prion” to the press: “He rammed that word down the throats of everybody in that laboratory and in the world. If we coin a new term for it, and go out and tell people of the potential link to Alzheimer’s, we’re going to draw people’s attention to this. But I talked to the press Of the slow virus mess And invented a name to confound it! Rohwer reexamined previous research into the infectious agent and disagreed with researchers’ conclusions regarding its size and seem ing indestructibility. Kimberlin opposed the prion theory based on his work showing that there were dozens of different strains of the disease agent. According to Kimberlin, the existence of strains showed that the disease agent contained genetic information—a “genome” made of nucleic acid. And Stan Prusiner, bless his heart, never even tried—which is wise, because you can’t do it. In New York, scientists at the Institute for Basic Research in Developmental Disabilities also formed a united front. Wisniewski and Patricia Mertz had identified string-like structures in scrapie brains—somewhat more elabo rate shapes than Narang’s rod-shaped structures—which they called “scrapie associated fibrils. He engaged molecular biologists to help him clone the gene that makes the scrapie protein. They succeeded, and to Prusiner’s surprise, discovered that the PrP gene was found in normal hamsters as well as sick ones.
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