SWITZERLAND: BEAU SOLEIL school.

http://www.beausoleil.ch/DownloadCenter/medical.pdf

Useful  paediatric questionnaire.by SWISS SCHOOL: BEAU SOLEIL @ 200,000 Francs/year.

AUSTRALIA: LEGIONELLOSIS

LEGIONELLOSIS - AUSTRALIA: (VICTORIA) FATAL, COOLING TOWER SUSPECTED
******************************

**************************************
A ProMED-mail post
<http://www.promedmail.org>
ProMED-mail is a program of the
International Society for Infectious Diseases
<http://www.isid.org>

Date: Thu 24 Jan 2013
Source: ABC News [edited]
<http://www.abc.net.au/news/2013-01-24/legionnaires-outbreak-claims-a-life/4482478>


A man is dead, and 4 others have been treated in hospital after a
Legionnaires' disease outbreak in Footscray, in Melbourne's west.

A man aged in his 50s who had other significant medical conditions
died early today [24 Jan 2013] at Western Hospital. Three other people
have been discharged after recovering from the flu-like illness, while
another remains in hospital.

Health Department officials are testing and disinfecting about 2 dozen
air-conditioning cooling towers in Footscray.

Legionnaires' disease is acquired through breathing in very fine
droplets of water that contain the bacteria, such as spray drifts
which are vented off from cooling towers. The acting chief health
officer, Dr Michael Ackland, says all the patients spent time in an
area within a 2-km radius of central Footscray. Dr Ackland says
thorough decontamination and cleaning of infected towers should
eliminate the disease, and there is no longer any risk to the public.
"There should be no risk to people travelling in the Footscray area
now, as all the cooling towers are now being disinfected, cleaned and
rendered safe," he said.

But he says anyone in the area who has been unwell and has flu-like
symptoms should go to their doctor. "Legionnaires' disease can take 10
days to manifest itself after an exposure," he said. "So if indeed any
of the cooling towers that we are examining are ultimately found to be
the cause of this problem, then, yes, people may well come forward as
new cases." Dr Ackland says the cases were individually reported
between 8 Dec 2012 and yesterday [23 Jan 2013], when the common link
to the Footscray area was confirmed.

A 56-year-old St Albans man, a 93-year-old Yarraville woman, and a
69-year-old Footscray man have been treated in hospital and
discharged. A 75-year-old West Footscray woman is still in hospital.

- --
Communicated by:
Alexandra Volosinas
<alexandra.volosinas@gmail.com>

[The following is extracted from moderator ML's comments in
ProMED-mail post Legionellosis - Australia: (VI) cooling tower susp
20121204.1436695:

Legionellosis is an infectious disease caused usually by inhalation of
aerosols containing _Legionella_ species. Legionnaires' disease is the
acute pneumonic form of legionellosis; more than 70 percent of cases
of legionnaires' disease are due to _L. pneumophila_ serogroup 1,
except in Australia and New Zealand, where _L. pneumophila_ serogroup
1 has accounted for only 45.7 percent of cases of community-acquired
legionellosis, and _Legionella longbeachae_ has accounted for 30.4
percent of cases (Yu VL, et al: Distribution of _Legionella_ species
and serogroups isolated by culture in patients with sporadic
community-acquired legionellosis: An international collaborative
survey. J Infect Dis. 2002; 186(1): 127-8. Available at
<http://www.legionella.org/lp_distribution.pdf>). Legionnaires'
disease due to _L. longbeachae_ has been associated with the use of
potting soil and gardening.

The news report above does not say how the diagnosis of legionnaires'
disease was made or what species of _Legionella_ was implicated in the
5 cases, but presumably it is _L. pneumophila_, a water-borne
pathogen, since a cooling tower is being tested as a possible source.

A diagnosis of even a single case of legionnaires' disease implies the
presence of an environmental source to which other susceptible
individuals are likely to have been exposed. It is, therefore, a
public health imperative to find that source to prevent further cases.
The effect of wind speed and direction on _Legionella_-contaminated
plumes from cooling towers may influence the distribution of cases.

Genotyping of patient and environmental isolates has become a helpful
tool to establish transmission pathways. The predominance of one
genotype of _Legionella_ isolated from patient specimens would suggest
transmission from a common source. Because _Legionella_ may be found
in environmental samples without linkage to any cases of
legionellosis, the actual causative infectious reservoir can be
confirmed by matching the genotype of clinical and environmental
isolates (see <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC86783/> and
<http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2730281/>).

However, this is difficult in legionellosis outbreaks, because,
frequently, the diagnosis of legionnaires' disease is made only on the
basis of urinary _L. pneumophila_ serogroup 1 antigen testing or
serology, rather than isolation of the organism from cultures of
respiratory tract specimens. Consequently, clinical isolates are often
not available for genotyping.

Footscray, with a population of 13 203 (2011), is a suburb 5 km (3.1
miles) west of Melbourne, Victoria, Australia

KIKUCHI-FUJIMOTO DISEASE

• Xavier Bosch^1* and Antonio Guilabert²

• * Corresponding author: Xavier Bosch xbosch@teleline.es

Author Affiliations

¹ Department of Internal Medicine, Hospital Clinic, University of Barcelona, Spain
² Department of Dermat

For all author emails, please log on.

Orphan

The electronic version of http://www.OJRD.com/content/1/1/18

Received:	11 May 2006
Accepted:	23 May 2006
Published:	23 May 2006

Abstract

Kikuchi-Fujimoto disease (KFD) is a benign and self-limited disorder, characterized by regional cervical lymphadenopathy with tenderness, usually accompanied with mild fever and night sweats. Less frequent symptoms include weight loss, nausea, vomiting, sore throat. Kikuchi-Fujimoto disease is an extremely rare disease known to have a worldwide distribution with higher prevalence among Japanese and other Asiatic individuals. The clinical, histopathological and immunohistochemical features appear to point to a viral etiology, a hypothesis that still has not been proven. KFD is generally diagnosed on the basis of an excisional biopsy of affected lymph nodes. Its recognition is crucial especially because this disease can be mistaken for systemic lupus erythematosus, malignant lymphoma or even, though rarely, for adenocarcinoma. Clinicians' and pathologists' awareness of this disorder may help prevent misdiagnsois and inappropriate treatment. The diagnosis of KFD merits active consideration in any nodal biopsy showing fragmentation, necrosis and karyorrhexis, especially in young individuals presenting with posterior cervical lymphadenopathy. Treatment is symptomatic (analgesics-antipyretics, non-steroidal anti-inflammatory drugs and, rarely, corticosteroids). Spontaneous recovery occurs in 1 to 4 months. Patients with Kikuchi-Fujimoto disease should be followed-up for several years to survey the possibility of the development of systemic lupus erythematosus.

Disease name and synonyms

Kikuchi-Fujimoto disease

Kikuchi's disease

Histiocytic necrotizing lymphadenitis

Definition

Kikuchi-Fujimoto disease (KFD) is an enigmatic, benign and self-limited syndrome characterized by regional lymphadenopathy with tenderness, predominantly in the cervical region, usually accompanied by mild fever and night sweats.

Initially described in Japan, KFD was first reported in 1972 almost simultaneously by Kikuchi [1] and by Fujimoto et al. [2] as a lymphadenitis with focal proliferation of reticular cells accompanied by numerous histiocytes and extensive nuclear debris [3].

Epidemiology

Kikuchi-Fujimoto disease is an extremely rare disease known to have a worldwide distribution with a higher prevalence among Japanese and other Asiatic individuals [4]. Only isolated cases are reported in Europe. Affected patients are most often young adults under the age of 30 years; the disease is seldom reported in children. A female preponderance of cases has been underlined in the literature (female to male ratio 4:1). Recent reports seem to indicate that the female preponderance was overemphasized in the past and that the actual ratio is closer to 1:1 [4,5].

Etiology and pathogenesis

There is much speculation about the etiology of KFD. A viral or autoimmune cause has been suggested. The role of Epstein-Barr virus, as well as other viruses (HHV6, HHV8, parvovirus B19) in the pathogenesis of KFD remains controversial and not convincingly demonstrated [4]. A viral infection is, nonetheless, possible by virtue of clinical manifestations, as described by Unger et al. [6] that include upper respiratory prodrome, atypical lymphocytosis and lack of response to antibiotic therapy, and certain histopathologic features (i.e., T-cells as revealed by immunological marker studies). KFD has also been recorded in HIV- and HTLV-1-positive patients [7].

On the other hand, electron microscopic studies have identified tubular reticular structures in the cytoplasm of stimulated lymphocytes and histiocytes in patients with KFD [3]. Since these structures have also been noted within endothelial cells and lymphocytes of patients with systemic lupus erythematosus (SLE) and other autoimmune disorders, some authors hypothesized that KFD may reflect a self-limited autoimmune condition induced by virus-infected transformed lymphocytes [8]. It is possible that KFD may represent an exuberant T-cell mediated immune response in a genetically susceptible individual to a variety of non-specific stimuli [4].

Although the mechanism of cell death involved in KFD has not been extensively studied, Ohshima et al. have shown that apoptotic cell death may play a role in the pathogenesis of the disease [9]. According to these authors, proliferating CD8 positive T-cells may act as "killers" and "victims" in the apoptotic process via Fas- and perforine- pathways.

Clinical manifestations

The onset of KFD is acute or subacute, evolving over a period of two to three weeks. Cervical lymphadenopathy is almost always present consisting of tender lymph nodes that involve mainly the posterior cervical triangle. Lymph node size has been found to range from 0.5 to 4 cm, but it may reach 5 to 6 cm and rarely larger than 6 cm. Generalized lymphadenopathy can occur [5,10] but is very rare. In addition to lymphadenopathy, 30 to 50% of patients with KFD may have fever, usually of low-grade, associated with upper respiratory symptoms. Less frequent symptoms include weight loss, nausea, vomiting, sore throat and night sweats [11,12]. Leukopenia can be found in up to 50% of the cases. Atypical lymphocytes in the peripheral blood have also been observed. Involvement of extranodal sites in KFD is uncommon but skin, eye and bone marrow affection, and liver dysfunction have been reported [4]. KFD has also been reported as a cause of prolonged fever of unknown origin [13]. Although the disease has been linked to SLE, as well as to other autoimmune conditions [4,14], the real strength of such associations remains to be clarified. There have been anecdotal reports of unusual features of KFD including carcinoma [15], diffuse large B-cell lymphoma [16] and hemophagocytic syndrome [17]. There are occasional reports describing cases of extranodal skin involvement or, even more rarely, of fatal multicentric disease.

Diagnosis

Kikuchi-Fujimoto disease is generally diagnosed on the basis of an excisional biopsy of affected lymph nodes. No specific diagnostic laboratory tests are available. The results of a wide range of laboratory studies are usually normal. Nevertheless, some patients have anemia, slight elevation of the erythrocyte sedimentation rate and even leukopenia. Of note, one third of patients present atypical peripheral blood lymphocytes [5]. Characteristic histopathologic findings of KFD include irregular paracortical areas of coagulative necrosis with abundant karyorrhectic debris, which can distort the nodal architecture, and large number of different types of histiocytes at the margin of the necrotic areas. The karyorrhectic foci are formed by different cellular types, predominantly histiocytes and plasmacytoid monocytes but also immunoblasts and small and large lymphocytes. Neutrophils are characteristically absent and plasma cells are either absent or scarce. Importantly, atypia in the reactive immunoblastic component is not uncommon and can be mistaken for lymphoma [18]. The immunophenotype of KFD typically consists of a predominance of T-cells, with very few B-cells. There is an abundance of CD8+ T-cells over CD4+. The histiocytes express histiocyte-associated antigens such as lysozyme, myeloperoxidase (MPO) and CD68.

Finally, striking plasmacytoid monocytes are also positive for CD68 but not for MPO [4].

Differential diagnosis

Although KFD is considered very uncommon, this disorder must be included in the differential diagnosis of 'lymph node enlargement' since its course and treatment differ dramatically from those of lymphoma, tuberculosis and SLE. The histological differential diagnosis of KFD mainly includes reactive lesions as lymphadenitis associated with SLE or herpes simplex, non-Hodgkin's lymphoma, plasmacytoid T-cell leukemia, Kawasaki's disease, myeloid tumor and even metastasic adenocarcinoma [4].

The differentiation of KFD from SLE can sometimes be problematic because both can show similar clinical and histological features. Furthermore, KFD has been reported in association with SLE. In this case, before making the diagnosis of KFD, laboratory tests including C3, C4, anti-Sm, and LE cells are needed to rule out SLE.

The diagnosis of KFD is generally not difficult, although early lesions lacking overt necrosis can be misdiagnosed as malignant lymphoma, due to the presence of abundant immunoblasts [7]. Features of KFD that may help prevent its misdiagnosis as malignant lymphoma include incomplete architectural effacement with patent sinuses, presence of numerous reactive histiocytes, relatively low mitotic rates, absence of Reed-Sternberg cells.

The recognition of KFD is necessary because one can avoid laborious investigation for infectious and lymphoproliferative diseases.

Clinical course and management

Kikuchi-Fujimoto disease is typically self-limited within one to four months. A low but possible recurrence rate of 3 to 4% has been reported [3]. In some few patients, SLE may occur some years later. No risk to other family members is felt to be associated with KFD [7]. Symptomatic measures aimed to relief the distressing local and systemic complains should be employed. Analgesics-antipyretics and nonsteroidal anti-inflammatory drugs may be used to alleviate lymph node tenderness and fever. The use of corticosteroids has been recommended in severe extranodal or generalized KFD but is of uncertain efficacy. Surgical consultation may be indicated for a diagnostic excisional lymph node biopsy. Patients with KFD require a systematic survey and regular follow-up for several years to rule out the development of SLE. The cervical lymphadenopathy runs a benign course and appears to resolve spontaneously 1 to 6 months after definite diagnosis.

References

1. Kikuchi M: Lymphadenitis showing focal reticulum cell hyperplasia with nuclear debris and phagocytes: a clinicopathological study.
   Acta Hematol Jpn 1972, 35:379-380.
   
2. Fujimoto Y, Kozima Y, Yamaguchi K: Cervical subacute necrotizing lymphadenitis: a new clinicopathologic entity.
   Naika 1972, 20:920-927.
   
3. Dorfman RF: Histiocytic necrotizing lymphadenitis of Kikuchi and Fujimoto.
   Arch Pathol Lab Med 1987, 111:1026-1029. PubMed Abstract
   
4. Bosch X, Guilabert A, Miquel R, Campo E: Enigmatic Kikuchi-Fujimoto disease: a comprehensive review.
   Am J Clin Pathol 2004, 122:141-152. PubMed Abstract | Publisher Full Text
   
5. Lin HC, Su CY, Huang CC, Hwang CF, Chien CY: Kikuchi's disease. A review and analysis of 61 cases.
   Otoralyngol Head Neck Surg 2003, 128:650-653. Publisher Full Text
   
6. Unger PD, Rappaport KM, Strauchen JA: Necrotizing lymphadenitis (Kikuchi's disease). Report of four cases of an unusual pseudo-lymphomatous lesion and immunologic marker studies.
   Arch Pathol LabMed 1987, 111:1031-1034.
   
7. Pileri AS, Pileri A, Yasukawa K, Kuo TS, Sullivan K: The Karma of Kiluchi's disease.
   Clin Immunol 2005, 114:27-29. PubMed Abstract | Publisher Full Text
   
8. Imamura M, Ueno H, Matsuura A, Kamiya H, Suzuki T, Kikuchi K, Onoe T: An ultrastructural study of subacute necrotizing lymphadenitis.
   Am J Pathol 1982, 107:292-299. PubMed Abstract
   
9. Ohshima K, Shimazaki K, Kume T, Suzumiya J, Kanda M, Kikuchi M: Perforin and Fas pathways of cytotoxic T-cells in histiocytic necrotizing lymphadenitis.
   Histopathology 1998, 33:471-478. PubMed Abstract | Publisher Full Text
   
10. Kuo T: Kikuchi's disease (histiocytic necrotizing lymphadenitis). A clinicopathologic study of 79 cases with an analysis of histologic subtypes, immunohistology, and DNA ploidy.
    Am J Surg Pathol 1995, 19:798-809. PubMed Abstract
    
11. Yen A, Fearneyhough P, Raimer SS, Hudnall SD: EBV-associated Kikuchi's histiocytic necrotizing lymphadenitis with cutaneous manifestations.
    J Am Acad Dermatol 1997, 36:342-346. PubMed Abstract | Publisher Full Text
    
12. Bosch X, Guilabert A: Kikuchi-Fujimoto disease.
    Med Clin (Barc) 2004, 123:471-476. PubMed Abstract | Publisher Full Text
    
13. Kapadia Y, Robinson BA, Angus HB: Kikuchi's disease presenting as fever of unknown origin.
    Lancet 1989, 2:1519-1520. PubMed Abstract | Publisher Full Text
    
14. Martinez-Vazquez C, Hughes G, Bordon J, Alonso-Alonso J, Anibarro-Garcia A, Redondo-Martinez E, Touza-Rey F: Histiocytic necrotizing lymphadenitis, Kikuchi-Fujimoto's disease, associated with systemic lupus erythemotosus.
    QJM 1997, 90:531-533. PubMed Abstract | Publisher Full Text
    
15. Radhi JivI, Skinnider L, McFadden A: Kikuchi's lymphadenitis and carcinoma of the stomach.
    J Clin Pathol 1997, 50:530-531. PubMed Abstract | PubMed Central Full Text
    
16. Yoshino T, Mannami T, Ichimura K, Takenaka K, Nose S, Yamadori I, Akagi T: Two cases of histiocytic necrotizing lymphadenitis (Kikuchi-Fujimoto's disease) following diffuse large B-cell lymphoma.
    Hum Pathol 2000, 31:1328-1331. PubMed Abstract | Publisher Full Text
    
17. Kelly J, Kelleher K, Khan MK: A case of haemophagocytic syndrome and Kikuchi-Fujimoto disease occurring concurrently in a 17-year-old-female.
    Int J Clin Pract 2000, 54:547-559. PubMed Abstract
    
18. Tsang WYW, Chan JKC, Ng CS: Kikuchi's lymphadenitis. A morphologic analysis of 75 cases with special reference to unusual features.
    Am J Surg Pathol 1994, 18:219-231. PubMed Abstract

ANTIBIOTIC RESISTANCE

From UK DAILY MAIL

 

Thursday, Jan 24 2013 3PM  14°F 6PM 13°F 5-Day Forecast

Antibiotic resistance is now as serious a threat as terrorism and could trigger an 'apocalyptic scenario', warns UK's top doctor

• Dame Sally Davies said people may die from routine infections after surgery within 20 years
• This is due to a lack of effective antibiotics
• Says situation so serious that the issue should be added to Government's list of civil emergencies

By Anna Hodgekiss
PUBLISHED: 12:35 GMT, 24 January 2013 | UPDATED: 12:42 GMT, 24 January 2013

• Comments (85)
• Share

Growing numbers of drug-resistant diseases could trigger an ‘apocalyptic scenario’ comparable to a catastrophic terrorist attack, Britain’s chief medical officer warned yesterday. 
Dame Sally Davies said there was risk that within 20 years people going for simple operations would die of routine infections because we may ‘run out of antibiotics’ that work.
She told MPs the threat from infections that are resistant to antibiotics was so serious that the issue should be added to the Government’s national risk register of civil emergencies.

There is a risk that within 20 years, people going for simple operations may die of routine infections due to a lack of effective antibiotics

The register was established in 2008 to advise the public and businesses on national emergencies that Britain could face in the next five years.

The highest priority risks on the latest register include a deadly flu outbreak and catastrophic terrorist attacks.

 

More...

• Man flu really DOES exist: The way men's brains are wired means their symptoms really are worse
• Homeopathy is 'rubbish' and shouldn't be available on the NHS, says Britain's top doctor

Speaking to MPs on the Commons science and technology committee, Davies said she would ask the Cabinet Office to add antibiotic resistance to the national risk register in the light of an annual report on infectious disease she will publish in March.
A Department of Health spokesperson told MailOnline the publication would coincide with a government strategy to promote more responsible use of antibiotics among doctors.
She said: 'We are broadly concerned about antibiotic resistance and we are going to be publishing a strategy in March with guidance on this.'
Hospital superbugs such as MRSA are some of the best known antibiotic-resistant diseases, but MPs were warned about infections such as gonorrhea and TB that affect the general population. 
Some antibiotics have already been lost to resistance.

Some antibiotics have already been lost to resistance, for example penicillin is no longer effective for some wound infections

Penicillin is no longer effective for staphylococcal wound infections, ampicillin (a form of penicillin) is no longer used for infections of the urinary tract and ciprofloxacin (a synthetic antibiotic) is now useless in treating gonorrhoea. Many more are under threat.
New antibiotics are hard to find and to licence, the Health Protection Agency has warned.
From the 1940s to the 1990s the answer was to develop new antibiotics, but this development has slowed.
New antibiotics are less profitable than treatments for chronic diseases, and much of the pharmaceutical industry now concentrates on other areas of medicine.
Dame Sally told the Commons Science and Technology Committee: ‘We need to get our act together in this country.’
She said: 'There are few public health issues of potentially greater importance for society than antibiotic resistance. It means we are at increasing risk  of developing infections that cannot be treated – but resistance can be managed.
'Antibiotics are losing their effectiveness at a rate that is both alarming and irreversible – similar to global warming.
'I urge patients and prescribers to think about the drugs they are requesting and dispensing.
'Bacteria are adapting and finding ways to survive the effects of antibiotics, ultimately becoming resistant so they no longer work. And the more you use an antibiotic, the more bacteria become resistant to it.'
Changes in modern medicine have exacerbated the problem by making patients more susceptible to infections.
For example, cancer treatments weaken the immune system, and the use of catheters increases the chances of bugs entering the bloodstream.
David Heymann, Chairman of the HPA said: 'Antimicrobial resistance is a global problem and it requires an international solution to tackle it. sistance and suggests ways that could help to form a basis for action to address them.
'Bacteria will always evolve to become resistant and this is a natural part of the cycle of evolution but by reducing the pressures that cause resistance we can help to preserve the antibiotics that we do have and no-one can underestimate how important this is.
'Tackling this problem is going to require effort from individuals, organisations and nations alike. But by working together we can help to combat this problem.'

Read more: http://www.dailymail.co.uk/health/article-2267567/Antibiotic-resistance-terrorism-trigger-apocalyptic-scenario-warns-UKs-doctor.html#ixzz2IuNydLnZ
Follow us: @MailOnline on Twitter | DailyMail on Facebook

"MGUS" now = MULTIPLE MYELOMA

http://bloodjournal.hematologylibrary.org/content/113/22/5412.full

From BLOOD

Monoclonal gammopathy of undetermined significance (MGUS) consistently precedes multiple myeloma: a prospective study

1. Ola Landgren1,2,
2. Robert A. Kyle3,4,
3. Ruth M. Pfeiffer1,
4. Jerry A. Katzmann3,4,
5. Neil E. Caporaso1,
6. Richard B. Hayes1,
7. Angela Dispenzieri3,4,
8. Shaji Kumar3,
9. Raynell J. Clark4,
10. Dalsu Baris1,
11. Robert Hoover1, and
12. S. Vincent Rajkumar3

+ Author Affiliations

1. ¹Division of Cancer Epidemiology and Genetics, and
2. ²Center for Cancer Research, Medical Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD;
3. ³Division of Hematology and Internal Medicine, and
4. ⁴Division of Clinical Biochemistry & Immunology and Laboratory Medicine & Pathology, Mayo Clinic, Rochester, MN

 

Next Section

Abstract

Monoclonal gammopathy of undetermined significance (MGUS) is a premalignant plasma-cell proliferative disorder associated with a life-long risk of progression to multiple myeloma (MM). It is not known whether MM is always preceded by a premalignant asymptomatic MGUS stage. Among 77 469 healthy adults enrolled in the nationwide population-based prospective Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial, we identified 71 subjects who developed MM during the course of the study in whom serially collected (up to 6) prediagnostic serum samples obtained 2 to 9.8 years prior to MM diagnosis were available. Using assays for monoclonal (M)–proteins (electrophoresis/immunofixation) and kappa-lambda free light chains (FLCs), we determined longitudinally the prevalence of MGUS and characterized patterns of monoclonal immunoglobulin abnormalities prior to MM diagnosis. MGUS was present in 100.0% (87.2%-100.0%), 98.3% (90.8%-100.0%), 97.9% (88.9%-100.0%), 94.6% (81.8%-99.3%), 100.0% (86.3%-100.0%), 93.3% (68.1%-99.8%), and 82.4% (56.6%-96.2%) at 2, 3, 4, 5, 6, 7, and 8+ years prior to MM diagnosis, respectively. In approximately half the study population, the M-protein concentration and involved FLC-ratio levels showed a yearly increase prior to MM diagnosis. In the present study, an asymptomatic MGUS stage consistently preceded MM. Novel molecular markers are needed to better predict progression to MM in patients with MGUS.

Previous SectionNext Section

Introduction

Multiple myeloma (MM) is a clonal plasma-cell proliferative disorder with a median survival of approximately 4 years.¹ Almost 19 900 new MM cases and 10 700 MM deaths are expected in the United States during 2008.² Monoclonal gammopathy of undetermined significance (MGUS) is one of the most common premalignant disorders in Western countries, with a prevalence of 3.2% in the white general population 50 years of age or older.³ It is an asymptomatic condition characterized by the presence of a monoclonal immunoglobulin (M-protein) in the absence of any clinical signs or symptoms of MM or other lymphoproliferative malignancies.^4,5

Long-term follow-up studies of MGUS patients show an excess risk of developing MM.⁶ However, a key gap in our understanding is whether MM is always preceded by MGUS, or if MM typically arises de novo. This knowledge is critically important in understanding the pathogenesis of MM and to develop preventive strategies. We hypothesize that a premalignant plasma-cell proliferative stage characterized by asymptomatic M-protein production, clinically defined as MGUS, is present in all patients with MM years prior to the development of the malignancy. The confirmation of this hypothesis would emphasize the need to focus on identifying risk factors for MGUS and to improve our knowledge on underlying mechanisms of transformation from MGUS to MM, with the aim to define better predictive markers of progression and to develop chemopreventive approaches.

Thus far, it has been impossible to determine whether a protracted premalignant phase MGUS precedes MM in all patients. Taking advantage of the large nationwide US PLCO (Prostate, Lung, Colorectal, and Ovarian) Cancer Screening Trial,⁷ we used a unique study design to conduct the first prospective study to address this question. Among 77 469 persons in the screened arm who were cancer-free at baseline, we identified 71 subjects who developed MM during the course of the study in whom serially collected prediagnostic serum samples obtained at least 2 years (up to 9.8 years) prior to MM diagnosis were available. Using multiple prediagnostic blood samples (up to 6 samples) obtained annually in the same subject, we applied serum protein electrophoresis, immunofixation, and kappa-lambda free light chain (FLC) assays to define the prevalence of MGUS prior to the diagnosis of MM, and characterized longitudinally patterns of M-protein abnormalities prior to MM diagnosis.

SWISS HIRSLANDEN HOSPITALS WORLD'S BEST

http://www.remgro.com/english/about/company_history.asp

SWISS HIRSLANDEN Hospital GROUP part of MEDICLINIC which is part of the South African REMGRO LIMITED

Preferred by those who want doctors who are not pressed for TIME and where patients can be ADMITTED ,without government limitation,.for DIAGNOSIS and not evicted from Hospital to obey Government orders.

NEW TICK-BORN INFECTION BORRELIA MIYAMOTOI IMPORTED INTO USA.

   

Published Date: 2013-01-18 19:54:42
Subject: PRO/AH/EDR> Tick-borne borreliosis - USA: (South. New Engl., NY) B. miyamotoi
Archive Number: 20130118.1504740
TICK-BORNE BORRELIOSIS - USA: (SOUTHERN NEW ENGLAND, NEW YORK) BORRELIA MIYAMOTOI
*********************************************************************************
A ProMED-mail post
http://www.promedmail.org
ProMED-mail is a program of the
International Society for Infectious Diseases
http://www.isid.org

Date: Wed 16 Jan 2013

Source: New Haven Register [edited]

http://nhregister.com/articles/2013/01/16/news/doc50f72407958c0516150206.txt

A new tick-borne infection, similar to Lyme disease, has been found in humans in this region [Connecticut, Massachusetts, Rhode Island, New York] for the 1st time, according to researchers at the Yale schools of Public Health and Medicine. And while its unfamiliarity may result in some misdiagnosis -- the disease, carried by deer ticks, has yet to be given a name -- the good news is that the same treatment used for Lyme disease will cure this infection as well.

NO BULL'S EYE RASH
RELAPSING FEVER

The report, whose primary author is Dr Peter Krause, senior research scientist at the School of Public Health, is published in the 17 Jan 2013 issue of the New England Journal of Medicine. So far 18 patients in southern New England and New York State have been found to have the infection, caused by a bacterium, _Borrelia miyamotoi_, according to a release. It was first found in ticks in 1995 in Japan, then in deer ticks in Connecticut in 2001, Krause said. "The 1st time it was discovered in humans was 2011," when 46 cases of this disease were reported in central Russia, he said.



The discovery is unusual because usually new tick-borne diseases are found when people get sick and then are traced to the insect. "This is the 1st time we have found an infectious organism carried by ticks before we have recognized the disease in humans," said Durland Fish, professor of epidemiology at the School of Public Health and the study's senior author, in the release. "We usually discover new diseases during an epidemic and then try to figure out what is causing it."



While the number of cases so far is small, Krause said there are 30 000 reported cases of Lyme disease in this country each year, and that infection "is probably 7 times as common" as the new disease, which would make more than 4000 cases. But scientists believe the actual number of Lyme disease infections each year is 10 times as high as the reported number.



Symptoms are similar to Lyme -- fever, headache, muscle ache, and fatigue -- but 10 percent of the Russian patients also had relapses of their fever. "They had fever; it was there a few days ... anywhere between a week and a month later they came down with fever again," Krause said. "Some people have had as many as 10 relapses over the course of a year." The Americans discovered with the infection "were treated for suspected Lyme disease so they didn't have relapsing fever ... I think it's likely that some people will have relapsing fever from this," Krause said.



One way to diagnose the new disease is by the 2-part Lyme screening test. "Unfortunately, these patients with _B. miyamotoi_ [infection]... some of them tested positive to that 1st screening test ... but when we did the 2nd test ... that test was negative," Krause said. That result points to the new infection, he said.

"I think we could expect looking ahead that we will find a lot more of these cases," Krause said.

[Byline: Ed Stannard]
Communicated by:

ProMED-mail



[The above news report refers to a recent publication: Krause PJ, Narasimhan S, Wormser GP, et al. Human _Borrelia miyamotoi_ Infection in the United States. N Engl J Med 2013; 368:291-293. In this study, antibody against _Borrelia miyamotoi_ GlpQ protein (an antigen that is nonreactive to _Borrelia burgdorferi_ antibody) was assayed in archived serum samples obtained from 875 patients who were living in areas where Lyme disease is endemic (southern New England and New York State) between 1990 and 2010. 18 of these patients who had been evaluated for Lyme disease had serologic evidence of _B. miyamotoi_ infection; 3 of the 18 patients had serologic evidence of recent _Borrelia miyamotoi_ infection and were not immunocompromised. 5 of the 18 were co-infected, 4 of whom had concomitant Lyme disease based on a typical erythema migrans skin lesion and 1 had concomitant babesiosis.



In the same issue of the New England Journal of Medicine, there is the related article: Gugliotta JL, Goethert HK, Victor P. Berardi VP, Telford SR. Meningoencephalitis from _Borrelia miyamotoi_ in an Immunocompromised Patient. N Engl J Med 2013; 368:240-245. This article describes an immunocompromised elderly patient with a history of tick-exposure who developed progressive dementia and lymphocytic pleocytosis on cerebrospinal fluid (CSF) exam. Spirochetes were visualized in the CSF that differed qualitatively from _Borrelia burgdorferi sensu lato_, the cause of Lyme disease, with respect to their morphologic characteristics and behavior in vitro. PCR assay with the use of primers specific for the _B. miyamotoi_ genogroup and subsequent sequencing and phylogenetic analysis of the 16S rRNA and flagellin genes confirmed that the patient's CSF specimens contained a borrelia within the American clade of the _B. miyamotoi_-like spirochetes. The patient developed of a Jarisch-Herxheimer reaction after receiving antibiotic therapy with ceftriaxone, as do some patients with Lyme disease or relapsing fever. The patient experienced a clinical and microbiologic response to antibiotic treatment; the post-treatment CSF sample was negative for _B. miyamotoi_ on PCR assay.



Lyme disease, also called Lyme borreliosis, is a multisystemic disorder caused by spirochetes belonging to the _Borrelia burgdorferi sensu lato_ complex, a genetically diverse group of spirochetes (http://ijs.sgmjournals.org/content/42/3/378.full.pdf). At least three species of the B. burgdorferi sensu lato complex (_B. afzelii_, _B. garinii_, and _B. burgdorferi sensu stricto_) are known to cause Lyme disease in humans, although _B. burgdorferi sensu stricto_ is the only pathogenic species to cause Lyme disease in North America. It also occurs in Europe, but is less prevalent in most regions than _B. garinii_ or _B. afzelii_, the two major European pathogenic genospecies. Vectors of _B. burgdorferi sensu lato_ complex are hard-bodied _Ixodes_ ticks, and various small and medium-sized mammals and ground-feeding bird species are reservoir-competent hosts. Individual ticks can be infected with more than one genospecies of _B. burgdorferi sensu lato_ complex.



The relapsing-fever group of borrelia, which includes _B. miyamotoi_, is genetically diverse and causes a disease characterized by a high temperature that cyclically remits. _Borrelia hermsii_ is the most frequent cause of tick-borne relapsing fever in the USA. This spirochete is transmitted to humans by the soft tick _Ornithodoros hermsi_, which unlike hard ticks, transmit spirochetes through a brief (less than 30 minutes' duration) and painless nocturnal bite. Humans typically are exposed to these ticks during an overnight stay in rodent-infested dwellings at elevations greater than 2000 feet. In the USA, a majority of the reported cases are from California and Washington. Louse-borne relapsing fever, an illness similar to the tick-borne disease, is caused by _Borrelia recurrentis_, which is transmitted from human to human by the body louse and is spread under conditions of crowding and poor personal hygiene. It remains endemic in parts of central and east Africa and the South American Andes, but has occasionally been imported into the USA.



In the USA, _B. miyamotoi_ has been detected in _Ixodes scapularis_, in Russia and Japan in _Ixodes persulcatus_ (Fukunaga M, Takahashi Y, Tsuruta Y, et al. Genetic and phenotypic analysis of Borrelia miyamotoi sp. nov., isolated from the ixodid tick Ixodes persulcatus, the vector for Lyme disease in Japan. Int J Syst Bacteriol 1995;45:804-810), and in western Europe, _Ixodes ricinus_, the same tick species that spread _B. burgdorferi sensu lato_ complex, the causative agents of Lyme disease.



As described in patients in the USA by Krause et al in the New England Journal of Medicine article above, _B. miyamotoi_ has also caused in patients in Russia an acute febrile illness with fever as high as 39.5 degrees C (103.1 degrees F) and usually does not cause the bull's eye shaped rash that characterizes Lyme disease (Platonov AE, Karan LS, Nadezhda M. Kolyasnikova NM, et al. Humans Infected with Relapsing Fever Spirochete Borrelia miyamotoi, Russia. Emerg Infect Dis 2011;17. Available at:

http://wwwnc.cdc.gov/eid/pdfs/10-1474-ahead_of_print.pdf). In the Gugliotta et al New England Journal of Medicine article referred to above, _B. miyamoto_ apparently has caused progressive dementia without fever in an immunocompromised patient. These recent articles point out that _B. miyamotoi_ may be the cause of an acute febrile illness or meningoencephalitis associated with dementia in regions where _Ixodes_ ticks are endemic.

OBIT:Dr.T.PARRY JONES OBE

From UK DAILY MAIL

Inventor of the first electronic breathalyser which helped catch millions of drink drivers worldwide has died at the age of 77

• Dr Tom Parry Jones has died at his home in Anglesey, north Wales, aged 77
• Invented the breathalyser in 1974, manufactured it and sold it across globe
• Was given an OBE for his contribution to the improvement of road safety

By James Rush
PUBLISHED: 03:57 GMT, 15 January 2013 | UPDATED: 11:02 GMT, 15 January 2013

The inventor of the world's first electronic breathalyser machine has died at the age of 77.
Dr Tom Parry Jones revolutionised road safety after he came up with the invention which has caught millions of drink drivers worldwide.
The scientist invented the electronic device in 1974 and went on to manufacture and sell it to police forces across the world.

Read more: http://www.dailymail.co.uk/news/article-2262572/Dr-Tom-Parry-Jones-Inventor-electronic-breathalyser-helped-catch-millions-drink-drivers-worldwide-died-age-77.html#ixzz2I2fnrm5x
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CANADA:FreshPoint Inc. lettuce: E.coli (0157)

E. COLI EHEC - CANADA (03): (NOVA SCOTIA, NEW BRUNSWICK, ONTARIO)
O157, LETTUCE
******************************

*************************************************
A ProMED-mail post
<http://www.promedmail.org>
ProMED-mail is a program of the
International Society for Infectious Diseases
<http://www.isid.org>

Date: Sat 12 Jan 2013
Source: Canadian Broadcasting Corp [edited]
<http://www.cbc.ca/news/canada/nova-scotia/story/2013/01/11/nb-ecoli-lettuce-kfc-taco-bell-nova-scoita.html>


The source of a potentially deadly strain of _E. coli_ [O157] in Nova
Scotia, New Brunswick and Ontario was likely lettuce served at
KFC/Taco Bell outlets, health officials say. All suspect lettuce has
been recalled, they said Friday afternoon, 11 Jan 2013.

"The evidence from our collaborative investigation leads us to believe
that the common food source was distributed to this fast-food
restaurant chain," said Dr. Frank Atherton, Nova Scotia's deputy chief
medical officer of health. "Lettuce has a limited shelf life, and we
have not seen a new case in more than a week. This tells us it is
highly unlikely the food item remains in the food chain. As an added
precaution, the Canadian Food Inspection Agency is issuing a recall of
the lettuce products."

He added that the fault did not lie with the restaurants, but with
FreshPoint, the company that supplied the lettuce. No new cases of _E.
coli_ O157 are expected, officials said.

Nova Scotia has had 10 confirmed cases of _E. coli_ O157 in the past
couple of weeks. At least 5 are linked to the outbreak. New Brunswick
has also had 6 confirmed cases, while Ontario has had 5. All of the
patients have been treated and are recovering, Atherton said.

Dr. Eilish Cleary, New Brunswick's chief medical officer, said it was
hard to pin down the particular outlet. The lettuce was distributed to
other fast-food chains, but the cases were all linked to Taco
Bell/KFC. "When we looked at the food history of our patients, they
had eaten at several locations, so we were unable to pinpoint exactly
which ones they were exposed at," she said.

Sabir Sami, president of KFC/Taco Bell parent company Yum Restaurants,
said his company takes the developments seriously. "We're obviously
concerned, as this lettuce provided to us by FreshPoint has been
distributed to many area restaurants in Canada, including ours," he
said in a news release. "We have removed all the affected lettuce from
our restaurants in Canada and want to reassure our customers that our
food is perfectly safe to eat. The health and safety of our customers
is our top priority."

- --
Communicated by:
Stephen Rankin
<skrankin.sr@gmail.com>

LONDON: ON-LINE GP advice

https://www.jbc-doctor.com/about/doctors
John BELL & CROYDEN

Founded in 1798
Pharmacists to Her Majesty Queen Elizabeth II
50-54 Wigmore Street, London

Meet our doctors

All DrThom doctors work together as a team from our London office.All our doctors are trained to provide online care across the spectrum of services that we offer, so you may receive care from any member of team at different times.
Each online clinic also has a nominated doctor whose role is to monitor the care provided through that clinic- you can see a picture of that doctor on each online clinic homepage.

	Dr Thom Van Every MB ChB BSc MRCOG MBA Position: Medical Director I got my medical training at the University of Birmingham Medical School. After gaining an MBA from London Business School, I worked at Chelsea & Westminster Hospital in London as a Senior House Officer. There, I spotted patient’s inconvenience when getting sexual health treatment and initiated the online doctor service. I am a member of the Royal College of Obstetricians and Gynaecologists and have done voluntary work in Cambodia, Madagascar and Sao Tome e Principe. As a passionate swimmer, I swim year-round in the cold waters of Tooting Lido.
	Dr Tom Brett MBBS FRACGP Position: Lead General Practitioner I moved to Australia a year after graduating from St Thomas's Hospital Medical School in 1992. During my stay in Australia, I attained fellowship of the Royal Australian College of General Practitioners and a Certificate in Sexual Health and HIV prescribing. I worked as the director of the Brisbane North Division of General Practice and was chairman of the GP committee of the Australian Herpes Management forum prior to coming back to London in 2006.
	Dr Tatjana Street Staatsexamen (Munich) MRCGP DFFP Position: General Practitioner I Completed my medical training in Germany in 1996, I worked in various UK hospitals for three years before I began my GP training. I was granted my GP qualification in 2002. Since then, I have worked as an NHS GP in London and Cambridge. Currently, I work part time in a London NHS GP practice and my expertise lies in sexual health.

MYELOMA FOUNDATION: 1-3 BUTADIENE:

New Study Provides Clues to What Causes Myeloma

By Brian G.M. Durie, MD on January 10, 2013 12:03 PM | No Comments | No TrackBacks

Six months ago, cancer was added to the list of illnesses covered by the $3.4 billion World Trade Center fund. Now, as reported on December 19th in the New York Times, the New York City Health Department has completed a study that compares cancer rates among 9/11 responders with overall cancer rates for New York State. Myeloma is at the top of the list of cancers occurring at a statistically higher rate in 9/11 responders. Myeloma is occurring at a 3-fold increased rate: the rate being +185% versus the average for New York State. Thyroid cancer was at +102% and prostate cancer at +43%. All others were not statistically increased in this study.

The findings are controversial in part because it is very early to be assessing the ultimate risks--and therefore much too soon to be drawing conclusions for most cancers, the occurrence of which will increase over time. However, the early increase in myeloma cases is quite remarkable and suggests a particular susceptibility to the exposures at 9/11 sites.

The specific chemical identified by the Zadroga Act reviewers (6 months ago) was 1-3 butadiene, a chemical linked to rubbers and other  fumes present at the 9/11 sites.  The chemical 1-3 butadiene is metabolized in the body via an epoxy mechanism. A study which I published in 2009 (Leukemia article on DNA SNP) showed that myeloma patients are more likely to have a defect in this epoxy metabolism, and, therefore, are potentially more susceptible to the toxic effects.

So it seems that a story is coming together linking exposure, susceptibility, and early onset of myeloma in the 9/11 setting. More studies and follow-ups are needed, but these findings are plausible and satisfy elements of what are called the "Bradford Hill Criteria," used to link toxic exposures and the development of cancer such as myeloma. There is already "proof of principle" that several toxic chemicals can cause myeloma, including pesticides, solvents, and chemicals such as 1-3 butadiene.

TORONTO: Mt.SINAI CEO job $500-600,000/yr plus perks.

People Joseph Mapa plans to leave Mount Sinai Hospital TORONTO – Earlier this month, Mount Sinai Hospital President and CEO Joseph Mapa (pictured) issued the following statement: I wanted you to know that earlier today our Board Chair, Lawrence Bloomberg, informed our Mount Sinai Hospital Board of Directors of my decision to step down as President and CEO, 18 months from now, by January, 2013. This timeframe is intended to ensure continuity of leadership and is consistent with the ongoing discussions I have had with our Board Chair about the future of the Hospital and my personal goals. For the past 11 years, I have been proud to serve as your President and CEO. Together we have accomplished so much for our Hospital, our patients, and our community. Mount Sinai is in a very strong position, poised for a great future with an exceptionally talented team of staff, volunteers, physicians, scientists and Board. I consider it a privilege to be a part of this team. From a personal perspective I believe the time is right. I have been given a unique opportunity to serve within the Dean's Office and as the Executive-in-Residence at the University of Toronto Scarborough upon completion of my tenure here. In this role, I will help build a leading edge framework for health studies and contribute to a long-term vision for this campus. Many of you know that I have always been drawn to the academic world and I am looking forward to furthering my deep commitment to the healthcare sector. Over the next 18 months I will work closely with our Board, our Senior Management and Clinical Leadership Teams to push forward our important agenda and to ensure a smooth transition. I will keep you informed as the Board implements a formal search for my successor. For now, there is much work to be done. I remain focused on our collective mission and working with all of you to ensure that the Hospital continues on a dynamic trajectory. Yours very truly, Joseph Mapa President and Chief Executive Joseph Mapa joined Mount Sinai Hospital in 1977 and is a graduate of the Department of Health Administration, Faculty of Medicine, University of Toronto. He also holds an MBA from the Joseph I. Rotman School of Management, University of Toronto, and has achieved Fellowships in both the Canadian College of Health Service Executives and the American College of Healthcare Executives. A strong proponent of the special role of a teaching hospital, Mapa has co-authored three books on health care and is an Assistant Professor in the Department of Health Administration, Faculty of Medicine, University of Toronto. (WEB COMMENT.  Next CEO should be at least bilingual,(Eng/French),have high level Secondary education with Northern European & Cleveland/Harvard/Mayo post-grad Hospital experience. Meetings with Millionaire donors & Politicians are an important part of the job. Public speaking training essential.  Ideally MD,MPH,MBA,LLB (with specialty in Health Law)

DER SPIEGEL: VIRTUAL AUTOPSIES

Forensics Revolution Virtual Autopsies Provide New Insights into Death

By Frank Thadeusz

Universität Zürich Institut für Rechtsmedizin

It used to be that the cause of death could only be determined by cutting a corpse open. But a new, virtual procedure developed by Swiss researchers is providing new insights into dead bodies. It could help identify previously undiscovered murders.

A couple is sitting at the breakfast table, when the wife suddenly complains about a severe headache. She jumps up, screams and collapses. But only when she stops breathing at around noon does her husband call an ambulance.

ANZEIGE

For the investigating criminologists, this case of unbelievable heartlessness raised one question above all: What could the man have done to his wife? Their surprising conclusion was that he did nothing, and that he was only guilty of a shocking lack of interest in his partner. Forensic scientists with the Institute of Forensic Medicine at the University of Zurich in Switzerland diagnosed blood in the cerebrospinal fluid as well as a small aneurysm that had burst in the woman's head, which indicated that she had died of natural causes.
In another case, the Zurich police searched for the weapon with which a woman had been murdered. The forensic pathologists discovered tiny metal particles in the chin region. That find eventually led the police to the corpus delicti: a kitchen knife.
To solve both cases, it wasn't enough for the forensic scientists to simply cut open the sternum of the dead woman, in accordance with the standard procedure used when conducting a classic internal autopsy. To examine the circumstance of death, they didn't perform an autopsy on the body. Rather, they reviewed three-dimensional images of the dead women they had stored on their computer.
The method, in which forensic scientists combine images from powerful computed tomography (CT) and magnetic resonance imaging (MRI) together with surface scans of corpses is called "virtual autopsy."
More Efficient Autopsies
With the help of these combined imaging techniques, experts are now capable of gaining revealing and fascinating insights into the interiors of dead bodies. Most of all, they are finding fractures and hemorrhages that were not discovered during conventional autopsies.
Experts rave about the new method which is, at the very least, expected to complement classic autopsy. The idea is that after imaging a body, radiologists can draw abnormalities they encounter on the screen to the attention of forensic scientists.
"This enables forensic scientists to plan their autopsies much more efficiently," says Dominic Wichmann, a specialist in internal medicine at the University Hospital in Hamburg's Eppendorf district. In a study recently published in the journal Annals of Internal Medicine, Wichmann praises the benefits of virtual autopsies. Likewise, specialists with the United States Federal Bureau of Investigation (FBI) have been traveling to Switzerland lately to marvel at the computer-aided autopsies being performed at the University of Zurich.
Forensic scientist Michael Thali refers to the suite of devices he developed as "Virtobot." The idea for virtual autopsy began with the murder of a woman and the question of whether the killer had beaten her to death with a hammer or a bicycle wrench.
When he first tried to solve the mystery with the help of a computer, Thali and his staff were still housed in a cold barrack-like building on the campus of the University of Bern. "We were freezing in the winter, with only the computers putting off heat," says radiologist Steffen Ross, a member of the team for many years now.
A 'Revolution'
It was only the move to the University of Zurich and a bequest from a wealthy ophthalmologist that led to the project's breakthrough. But it was poorly received in the professional world at first. "Initially we were decried as the enfant terrible of forensics," says Thali. Older champions of the autopsy room would often tersely refer to the idea of virtual autopsy as "crap," Thali recalls.
But a younger generation of forensic scientists, who have since taken over at most institutions, are much more open to the new technology. Michael Tsokos, the chief forensic scientist at Berlin's Charité Hospital, recently ordered a pared-down version of the Virtobot. "We use a version that a poor city-state like Berlin can afford," says Tsokos.
He characterizes the new possibilities of post mortem imaging a "revolution for forensic medicine," on a par with the discovery of the genetic fingerprint and hair analysis. "If (former German politician) Uwe Barschel or (singer) Kurt Cobain had been pushed into CT scan machines, their deaths wouldn't raise so many questions today," says Tsokos.
In addition to Charité, three out of a total of 35 forensic medicine institutes at German universities can now conduct virtual autopsies. But even in Berlin, scans are made of only a fraction of dead bodies due to a lack of technicians trained to use the equipment. Tsokos and his colleagues likewise felt clueless at first. The manufacturer hadn't provided anything resembling a manual on how to store, archive and interpret the data that had been obtained.
The complexity of the new procedure means that the once prominent role of the forensic scientist as the maestro of the autopsy table could fade. In Thali's laboratory in Zurich, he wouldn't even be able to operate his suite of machines without radiologists and engineers as equal partners at his side.
Dwindling Number of Autopsies
Furthermore, virtual autopsies could also lead to changes in ordinary autopsies. Nowadays most family doctors decide whether or not a person died of natural causes. But this practice has fallen into disrepute in Germany. Forensic scientist Tsokos suspects that about half of all homicides are currently being overlooked. He attributes this to doctors who simply have not mastered this part of their profession, or who do not treat it with sufficient seriousness.
Employees at the Institute of Forensic Medicine of the Hannover Medical School (MHH) in northern Germany agree with Tsokos's critical assessment. In an essay recently published in the German criminology journal Archiv für Kriminologie, the MHH experts write "that the post-mortem in more than 10 percent of cases is performed incompletely or not in accordance with legal requirements." They conclude: "The inspection of corpses currently does not satisfy the intended quality standards, especially not with regard to legal certainty."
In contrast to forensic medicine institutes, autopsies are hardly performed at all in hospitals anymore. Whereas a forensic autopsy is ordered by the public prosecutor's office in suspected murder cases, a pathologist can only perform a clinical autopsy with the permission of the family of the deceased.
There has been a drastic decline in this clinical form of autopsy in Germany in the last few decades. Only about 3 percent of all corpses of the recently deceased are opened up to inspect the internal organs. By comparison, 10 times as many cases end up in a pathology department in Austria.

The main reason is that relatives are often determined not to allow the body of their deceased family member be cut open, says specialist Wichmann of the Hamburg university hospital. The bereaved are far less queasy about virtual autopsy. To their delight, the Swiss pioneers have also discovered that the new autopsy method makes it less likely that they will be confronted with excessively bloody experiences, such as in the case of a mountain climber who had fallen to his death in the Swiss Alps. The diagnosis reached by Thali's team included a shattered neurocranium, a fractured lumbar spine and a broken lower leg -- all done on a computer screen.
Other examinations, even those performed virtually, can still be messy. A dead body that remained undetected in an apartment for weeks and has begun to decompose still isn't easy to look at, even in the form of a 3-D image on a computer screen.

Translated from the German by Christopher Sultan