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Tuesday, September 14, 2010

EQUINE INFECTIOUS ANEMIA - UK (02): ENGLAND, FRANCE, OIE

********************************************************

A ProMED-mail post



ProMED-mail is a program of the

International Society for Infectious Diseases





In this update:

[1] Equine infectious anemia, UK - Devon

[2} Equine infectious anemia, UK - Northumberland

[3] Equine infectious anemia, France



******

[1] Equine infectious anemia, UK - Devon

Date: 14 Sep 2010

Source: OIE WAHID (World Animal Health Information Database) Disease

Information 2010; 23(37) [edited]







Equine infectious anaemia, United Kingdom

-----------------------------------------

Information received on 13 Sep 2010 from Dr Nigel Gibbens, Chief

Veterinary Officer, Department for Environment, Food and Rural

Affairs, Department for Environment, Food and Rural Affairs, London,

United Kingdom



Summary

Report type: Immediate notification

Start date 08 Sep 2010

Date of 1st confirmation of the event 11 Sep 2010

Report date 13 Sep 2010

Date submitted to OIE 13 Sep 2010

Reason for notification: Reoccurrence of a listed disease

Date of previous occurrence 30 Apr 2010

Manifestation of disease: Clinical disease

Causal agent: Equine infectious anaemia virus

Nature of diagnosis: Laboratory (advanced)

This event pertains to a defined zone within the country



New outbreaks

Outbreak 1 (IDHR 2010/14) Highampton, Beaworth, Devon, England

Date of start of the outbreak 08 Sep 2010

Outbreak status: Continuing (or date resolved not provided)

Epidemiological unit: Farm

Species Equidae

Susceptible 3

Cases 1

Deaths O

Destroyed 1

Slaughtered O

Affected Population: The affected horse is a 6-year-old gelding

housed at a private farm. The horse was anemic with raised

temperature and ventral edema. 2 other horses are also present on the

premises, but show no clinical signs.



Epidemiology - Source of the outbreak(s) or origin of infection -

Unknown or inconclusive



Epidemiological comments: The EIA positive horse has been on the farm

since summer 2008 when it was imported into the United Kingdom. The

suspected case was reported by the private veterinarian due to

clinical illness and severe anemia. The horse was also found to be

positive for piroplasmosis. None of the other horses showed any

clinical signs. A full epidemiology inquiry is being carried out.



The infected horse was sampled on 9 Sep 2010. The horse was humanely

destroyed on 11 Sep 2010. The premises including any remaining horses

have been placed under restrictions and the horses have been sampled.



Control measures - Measures applied: Quarantine; Movement control

inside the country; Disinfection of infected

premises/establishment(s); Dipping / Spraying; Modified stamping out;

No vaccination; No treatment of affected animals



Measures to be applied - Screening.



Diagnostic test results

Laboratory name and type: Veterinary Laboratories Agency (VLA),

Weybridge (National laboratory)

Species Equidae

Test Coggin's test

Test date 11 Sep 2010

Result Positive



Future Reporting

The event is continuing. Weekly follow-up reports will be submitted.



--

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*****

[2} Equine infectious anemia, UK - Northumberland

Date: 7 Sep 2010

Source: OIE WAHID (World Animal Health Information Database) Disease

Information 2010; 23(37) [edited]







Equine infectious anaemia, United Kingdom

-----------------------------------------

Information received on 07 Sep 2010 from Dr Nigel Gibbens, Chief

Veterinary Officer, Department for Environment, Food and Rural

Affairs, Department for Environment, Food and Rural Affairs, London,

United Kingdom



Summary

Report type: Immediate notification

Start date 01 Sep 2010

Date of 1st confirmation of the event 06 Sep 2010

Report date 07 Sep 2010

Date submitted to OIE 07 Sep 2010

Reason for notification: Reoccurrence of a listed disease

Date of previous occurrence 30 Apr 2010

Manifestation of disease: Sub-clinical infection

Causal agent: Equine infectious anaemia virus

Nature of diagnosis: Laboratory (advanced)

This event pertains to a defined zone within the country

Related reports



Immediate notification (07 Sep 2010)

Follow-up report No. 1 (10 Sep 2010)



New outbreaks

Outbreak 1 Ashington, Northumberland, England

Date of start of the outbreak 01 Sep 2010

Outbreak status: Continuing (or date resolved not provided)

Epidemiological unit: Farm

Species: Equidae

Susceptible 17

Cases 1

Deaths O

Destroyed 1

Slaughtered O

Affected Population There were 17 non-thoroughbred horses on the

premises, including 6 imported from the Netherlands. One of the

imported horses tested positive for EIA and was humanely destroyed in

the afternoon of 7 Sep 2010. The remaining 16 horses are housed in

stable boxes and one in a loose yard. None are at grass.



Epidemiology - Source of the outbreak(s) or origin of infection.

Introduction of new live animals

Legal movement of animals



Epidemiological comments: The horses were introduced to the United

Kingdom as legal imports on 15 Aug 2010. They were subjected to a

documentary, identity and physical checks as part of routine

post-import testing. These checks disclosed documentary

irregularities and as a result of this the horses were sampled for

EIA on 1 Sep 2010. One horse was confirmed as positive for EIA by

AGID (Coggin's) test and the premises and all horses on it have been

placed under restriction. The remaining 5 imported horses were

confirmed negative by AGID. All horses on the premises are being

sampled and tested today (7 Sept 2010). The veterinary epidemiology

inquiry is on-going.



Control measures - Measures applied: Quarantine; Movement control

inside the country; Disinfection of infected

premises/establishment(s); No vaccination; No treatment of affected

animals



Measures to be applied - Screening



Laboratory name and type: Veterinary Laboratories Agency, Weybridge

(National laboratory)

Species Equidae

Test Coggin's test

Test date 06 Sep 2010

Result Positive



Future Reporting: The event is continuing. Weekly follow-up reports

will be submitted.



--

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********

[3] Equine infectious anemia, France

Date: 14 Sep 2010

Source: OIE WAHID (World Animal Health Information Database) Disease

Information 2010; 23(37) [edited]







Equine infectious anaemia, France

---------------------------------

Information received on 14 Sep 2010 from Dr Jean Luc Angot, Directeur

General Adjoint, Direction Generale de l'Alimentation, Ministere de

l'Agriculture et de la Peche, Paris, France



Summary

Report type: Immediate notification

Start date 07 Sep 2010

Date of 1st confirmation of the event 07 Sep 2010

Report date 14 Sep 2010

Date submitted to OIE 14 Sep 2010

Reason for notification:Reoccurrence of a listed disease

Date of previous occurrence December 2009

Manifestation of disease: Sub-clinical infection

Causal agent:Equine infectious anemia virus

Nature of diagnosis: Laboratory (advanced)

This event pertains to a defined zone within the country



New outbreaks

Outbreak 1 Steenvoorde, Nord

Date of start of the outbreak 07 Sep 2010

Outbreak status: Continuing (or date resolved not provided)

Epidemiological unit: Farm

Affected animals

Species: Equidae

Susceptible 40

Cases 3

Deaths O

Destroyed 0

Slaughtered O

Affected Population The affected farm is a farm producing mare's milk

for human consumption. The infected animals have been isolated and

will be euthanized in the following days. Control measures have been

imposed on the farm, including movement control and testing of all

horses in the holding.



Epidemiology - Source of the outbreak(s) or origin of infection;

Introduction of new live animals; Legal movement of animals



Epidemiological comments: The 3 infected horses were introduced in

France from Romania in April 2008.



No clinical signs were observed and affected animals were detected as

part of an epidemiological investigation targeting horses at risk of

equine infectious anemia (horses imported into France from Romania

since 1 Jan 2007).



Control measures - Measures applied; Movement control inside the

country; No vaccination; No treatment of affected animals



Measures to be applied - Control of arthropods; Quarantine;

Screening; Disinfection of infected premises/establishment(s);

Modified stamping out.



Laboratory name and type: ANSES (National Food Security Agency),

Dozule (National laboratory)

Species Equidae

Test Coggin's test

Test date 07 Sep 2010

Result Positive



Future Reporting

The event is continuing. Weekly follow-up reports will be submitted.



--

Communicated by:

ProMED-mail





[The full epidemiologic report for the outbreak in Devon will be of

great interest because of the previous outbreak of EIA reported

earlier this month in Northumberland. It and subsequent follow-up

reports will be of continuing interest as it is unclear whether there

is any connection to Romanian origin horses, either directly or via

the Netherlands.



The same question applies to the French outbreak, as there are

documented cases of EIA being exported to Germany and the UK from

Romania this year. Given the harsh report of the European Commission,

Food and Veterinary Office (FVO) -- see Equine infectious anemia -

Romania: control deficiencies 20100914.3313 -- after their mission to

Romania, one would have to presume that Romanian horses are somehow

involved. Good shoe leather epidemiology in terms of traceback of

exposed horses and movement of horses through different European

countries is of the utmost importance at this time because equine

infectious anemia is a very unforgiving disease, best dealt with by

humane euthanasia of infected animals because of their potential to

spread the disease to other nearby horses. - Mod.PC]



[see also:

Equine infectious anemia - Romania: control deficiencies 20100914.3313

Equine infectious anemia - UK: England, Devon 20100912.3298

Equine infectious anemia - Netherlands: (GE) RFI 20100909.3250

Equine infectious anemia - Germany (03): (HE) ex Romania 20100908.3232

Equine infectious anemia - Germany (02): (HE) OIE 20100904.3180

Equine infectious anemia: resources available 20100415.1226

Equine infectious anemia - UK ex Romania via Belgium: RFI 20100209.0439

Equine infectious anemia - Belgium: (WV) OIE 20100203.0371

Equine infectious anemia: UK ex Romania 20100121.0235]

...................sb/pc/ejp/lm



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thereon, are not guaranteed. The reader assumes all risks in

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and its associated service providers shall not be held

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EASTERN EQUINE ENCEPHALITIS - USA (29): (MICHIGAN)

**************************************************

A ProMED-mail post



ProMED-mail is a program of the

International Society for Infectious Diseases





Date: Mon 13 Sep 2010

Source: The Oakland Press, Associated Press (AP) report [edited]







Health officials are reminding people to be vigilant about taking

steps to prevent the spread of eastern equine encephalitis in

Michigan.



The Kalamazoo Gazette reports there have been recent reports of 7

more dead horses from the disease. They include 2 in Calhoun County

and 1 each in Allegan, Kalamazoo, Jackson, Eaton, and Shiawassee

counties.



Lab testing in recent months has confirmed 42 Michigan horses with

the mosquito borne disease. Another 77 have been diagnosed with

clinical signs.



The disease is rare but can be deadly among humans. Last month

[August 2010], Michigan health officials reported that lab tests

confirmed that 3 people contracted the disease.



Health officials say people should take steps to avoid being bitten

by mosquitoes and horses should be vaccinated.



--

Communicated by:

ProMED-mail





[The state of Michigan in the Great Lakes Region of the US can be

located on the HealthMap/ProMED-mail interactive map at

.

The counties mentioned are located in southern Michigan and can be

seen on the map at

.



Eastern equine encephalitis (EEE) is preventable. In horses, it

requires at least 2 initial vaccinations and then boosters every 6

months in areas likely to have active disease. The protective titer

of the EEE vaccine wanes quicker than other equine encephalitis

titers.



Mosquito repellents made for horses can be used on the animals in

accordance with the label directions.



Human beings should dress accordingly, wearing long sleeves, avoiding

dusk and dawn exposure when mosquitoes may be more active, and using

insect repellant with DEET. Elimination of mosquito breeding sites is

critical to reducing the mosquito population. Small puddles, such as

those inside of an old tire, or a constant puddle in the garden or

flower bed, or even unclean water buckets for pets or horses can

serve as breeding grounds for mosquitoes.



The disease is generally preventable in human beings and in pets. - Mod.TG]



[see also:

Eastern equine encephalitis - USA (28): (MI, FL) 20100907.3202

Eastern equine encephalitis - USA (26): (MI, FL) equine, human 20100901.3115

Eastern equine encephalitis - USA (24): (NY, MI) equine, cervid 20100827.3045

Eastern equine encephalitis - USA (23): (MI) 20100824.2975

Eastern equine encephalitis - USA (19): (MI) equine, human susp. 20100817.2850

Eastern equine encephalitis - USA (16): (MI) 20100814.2790

Eastern equine encephalitis - USA (10): (MA, MI) 20100728.2529]

...................................sb/tg/mj/lm



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thereon, are not guaranteed. The reader assumes all risks in

using information posted or archived by ProMED-mail. ISID

and its associated service providers shall not be held

responsible for errors or omissions or held liable for any

damages incurred as a result of use or reliance upon posted

or archived material.

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Dead Animal Flesh in Your Heart?

Other uses for dead animal parts besides food; http://www.maverickbio.com/biological-medical-device-materials.php?Heart-Valve-Materials-1

Sunday, September 12, 2010

PRION DISEASE UPDATE 2010 (08) / New Strain Found

******************************

A ProMED-mail post



ProMED-mail is a program of the

International Society for Infectious Diseases





[With the continuing decline of the number of cases in the human population

of variant Creutzfeldt-Jakob disease -- abbreviated previously as vCJD or

CJD (new var.) in ProMED-mail -- it has been decided to broaden the scope

of the occasional ProMED-mail updates to include other prion-related

diseases. In addition to vCJD, data on other forms of CJD: sporadic,

iatrogenic, familial, and GSS (Gerstmann-Straussler-Scheinker disease) are

included also since they may have some relevance to the incidence and

etiology of vCJD. - Mod.CP]



In this update:

[1] UK: National CJD Surveillance Unit -- monthly statistics as of Mon 6

Sep 2010 -- no new vCJD cases

[2] France: Institut de Veille Sanitaire -- monthly statistics as of Wed 1

Sep 2010 -- no new vCJD cases

[3] USA - National Prion Disease Pathology Surveillance Center -- Sat 31

Aug 2010

[4] New sporadic prion disease



******

[1] UK: National CJD Surveillance Unit -- monthly statistics as of Mon 6

Sep 2010 -- no new vCJD cases

Date: Mon 6 Sep 2010

Source: UK National CJD Surveillance Unit, monthly statistics [edited]







The number of deaths due to definite or probable vCJD cases remains 169. A

total of 4 definite/probable patients are still alive so that the total

number of definite or probable vCJD cases is still 173. So far, 2

fatalities have been recorded in 2010.



Although 3 new deaths due to vCJD were recorded in 2009 and 2 deaths so far

in 2010, the overall picture is still consistent with the view that the

vCJD outbreak in the UK is in decline, albeit now with a pronounced tail.

The 1st cases were observed in 1995, and the peak number of deaths was 28

in the year 2000, followed by 20 in 2001, 17 in 2002, 18 in 2003, 9 in

2004, 5 in 2005, 5 in 2006, 5 in 2007, one in 2008, 3 in 2009, and now 2 so

far in 2010.



Totals for all types of CJD cases in the UK so far in the year 2010

-------------------------------------------------------------------

During the 1st 8 months of 2010, there have been 95 referrals, 29 fatal

cases of sporadic CJD, 2 fatal cases of vCJD, 2 cases of iatrogenic CJD,

and single cases of familial CJD and GSS.



--

communicated by:

ProMED-mail





******

[2] France: Institut de Veille Sanitaire -- monthly statistics as of 1 Sep

2010 -- no new vCJD cases

Date: Wed 1 Sep 2010

Source: IVS - Maladie de Creutzfeldt-Jakob et maladies apparentees [in

French, trans. & summ. Mod.CP, edited]







During the 1st 8 months of 2010, there were 1090 referrals, 47 confirmed

cases of sporadic CJD, one case of familial CJD, and no cases of iatrogenic

CJD or vCJD.



A total of 25 cases of confirmed or probable vCJD have now been recorded in

France since records began in 1992. There was 1 case in 1996, 1 in 2000, 1

in 2001, 3 in 2002, 2 in 2004, 6 in 2005, 6 in 2006, 3 in 2007, 2 in 2009,

and none so far in 2010.



The 25 confirmed cases comprise 13 females and 12 males. All 25 are now

deceased. Their median age is 37 (between 19 and 58). 7 were resident in

the Ile-de-France and 18 in the provinces. All the identified cases have

been Met-Met homozygotes. No risk factor has been identified. One of the 25

had made frequent visits to the United Kingdom.



--

communicated by:

ProMED-mail





******

[3] USA - NPDPSC 31 Aug 2010 -- no indigenous vCJD cases

Date: Sat 31 Aug 2010

Source: US National Prion Disease Pathology Surveillance Center [edited]







During the 8 month period 1 Jan 2010 to 31 Aug 2010, there were 204

referrals, 124 of whom were classified as prion disease, comprising 85

cases of sporadic CJD, 20 of familial CJD, and no cases of iatrogenic CJD

or vCJD.



Since 1996 when records began there have been 3702 referrals, of which 2177

were classified as prion disease, comprising 1834 cases of sporadic CJD,

315 of familial CJD, 4 of iatrogenic CJD, and 3 of vCJD. The 3 cases of

VCJD, 2 were considered to have been contracted in in the United Kingdom

and one Saudi Arabia. The prion disease category includes 21 (19 in 2010)

cases with type determination pending in which vCJD has been excluded.



[There is a striking difference in the frequency of familial (genetic) CJD

in the three countries. In the UK familial CJD accounts for about 5 per

cent of all cases of CJD, in France it is about 2.4 to 5 per cent, whereas

in the USA it is 16 per cent. The relevant demographic and/or genetic

factors merit investigation. - Mod.CP]



--

communicated by:

ProMED-mail





******

[4] New sporadic prion disease

Date: Fri 13 Aug 2010

Source: Science Daily [edited]







New sporadic prion protein disease:

variably protease-sensitive prionopathy shares genotype characteristics

with Creutzfeldt-Jakob

-----------------------------------------------------------------------

A new sporadic prion protein disease has been discovered. Variably

protease-sensitive prionopathy (VPSPr), as it has been named, is the 2nd

type of complete sporadic disease to be identified since Creutzfeldt-Jakob

disease (CJD) was reported in the 1920s. The landmark finding from the

National Prion Disease Pathology Surveillance Center at Case Western

Reserve University is published in the August [2010] issue of Annals of

Neurology [see abstract below].



Normally, the human prion protein gene comes in 3 types due to its

capability to encode prion proteins that contain only the amino acid

methionine, commonly identified as M, both methionine and valine, commonly

identified as V, or only for the amino acid valine at position 129.

Therefore, when it comes to the prion protein gene unaffected people can be

identified as 129MM, 129MV or 129VV. Sporadic CJD (sCJD), which is the most

common human prion disease, can affect patients who have any one of the 3

types of the prion protein gene.



In 2008, Pierluigi Gambetti and Wen-Quan Zou, with collaborators, reported

the discovery of this novel disease, which affected patients who exhibit

only one of the 3 types of the prion protein gene. In this follow-up study,

they discovered that all 3 genetic groups can be affected also by this

novel disease which now joins sCJD in displaying this feature. However,

VPSPr is associated with an abnormal prion protein that exhibits

characteristics very different from those of sCJD, as well as other prion

diseases, suggesting that it may be caused by a different mechanism,

perhaps more akin to other neurodegenerative diseases, such as Alzheimer's

disease. This finding may exemplify, for the 1st time, the possibility that

the prion protein affects the brain with different mechanisms.



While examining cases received at the National Prion Disease Pathology

Surveillance Center where he is the director, Dr Gambetti observed that a

subset of cases had clinical and pathological features quite different from

those of all known types of human prion diseases. Further, after being

tested for prion proteins via the Western blot [technique] -- the gold

standard of prion disease diagnosis -- the cases were negative. Dr Gambetti

then collaborated with Dr Zou, associate director at the center, to solve

the riddle of a disease that exhibited some features of a prion disease in

histopathological examination but was negative using the standard Western

blot test.



Dr Zou's lab performed a full characterization of the disease and

discovered that the VPSPr-associated abnormal prion protein formed a

ladder-like electrophoretic profile on Western blotting. "When I obtained

the 1st Western blot result of these cases with a different antibody

against prions, I was surprised that these cases consistently exhibited

this particular profile; one that I had never seen in my more than 10 years

of work on human prion diseases," Dr Zou, assistant professor of pathology

at Case Western Reserve School of Medicine, recalls. This ladder-like

profile is quite distinctive and very different from the profile of common

prion diseases. "Discovery of this unique type of prion provides solid

evidence that this novel disease may possess a pathogenesis that is

different from that of the major prion diseases currently known," Dr Zou adds.



Despite extensive research, a relatively large group of neurodegenerative

diseases associated with dementia remain undefined. Before being discovered

and characterized, VPSPr was one of the undefined dementing diseases. The

discovery of VPSPr is chipping away at that group. In the 2 years since its

discovery, more than 30 cases have been reported.



"If, as the current evidence indicates, the VPSPr mechanism of affecting

the brain is different from that of other sporadic prion diseases, such as

sCJD, the discovery of VPSPr would also provide the 1st example that the

prion protein may spontaneously damage the brain with different

mechanisms," concludes Dr Gambetti, professor of pathology at Case Western

Reserve School of Medicine. "This might apply to other dementing illnesses

as well, and has implications for the strategies that need to be followed

to attain a cure."



Drs Gambetti and Zou, along with their extensive research team, plan to

further characterize the abnormal prion protein associated with VPSPr as

well as other important features of the protein, such as the disease's

propensity for transmission upon inoculation and its replication in test

tubes. These features in VPSPr will be compared with those of sCJD to

obtain a complete picture of how the abnormal prion protein attacks the

brain in these 2 diseases.



--

communicated by:

ProMED-mail rapporteur Mary Marshall



[The following is the reference for the paper discussed above followed by

the authors' abstract:

Zou WQ, Puoti G, Xiao X, Yuan J, Qing L, Cali I, et al. Variably

protease-sensitive prionopathy: A new sporadic disease of the prion

protein. Ann Neurol. 2010 Aug;68(2):162-72.

().



Department of Pathology, National Prion Disease Pathology Surveillance

Center, Case Western Reserve University, Cleveland, Ohio.



Abstract

--------

Objective: The objective of the study is to report 2 new genotypic forms of

protease-sensitive prionopathy (PSPr), a novel prion disease described in

2008, in 11 subjects all homozygous for valine at codon 129 of the prion

protein (PrP) gene (129VV). The 2 new PSPr forms affect individuals who are

either homozygous for methionine (129MM) or heterozygous for

methionine/valine (129MV).

Methods: A total of 15 affected subjects with 129MM, 129MV, and 129VV

underwent comparative evaluation at the National Prion Disease Pathology

Surveillance Center for clinical, histopathologic, immunohistochemical,

genotypical, and PrP characteristics.

Results: Disease duration (between 22 and 45 months) was significantly

different in the 129VV and 129MV subjects. Most other phenotypic features

along with the PrP electrophoretic profile were similar but distinguishable

in the 3 129 genotypes. A major difference laid in the sensitivity to

protease digestion of the disease-associated PrP, which was high in 129VV

but much lower, or altogether lacking, in 129MV and 129MM. This difference

prompted the substitution of the original designation with "variably

protease- sensitive prionopathy" (VPSPr). None of the subjects had

mutations in the PrP gene coding region.

Interpretation: Because all 3 129 genotypes are involved, and are

associated with distinguishable phenotypes, VPSPr becomes the 2nd sporadic

prion protein disease with this feature after Creutzfeldt-Jakob disease,

originally reported in 1920. However, the characteristics of the abnormal

prion protein suggest that VPSPr is different from typical prion diseases,

and perhaps more akin to subtypes of Gerstmann-Straussler-Scheinker disease.



VPSPr is not linked to eating infected meat. However, like CJD, the new

condition happens sporadically. It was 1st identified because of the

fast-advancing form of dementia seen in those affected. They were also

unable to speak or move. But tests for CJD proved negative. Further

molecular examination as described above has shown VPSPr was a prion

disease, but one which looked very different to those already known. - Mod.CP]



[see also:

Prion disease update 2010 (07) 20100809.2720

Prion disease update 2010 (06) 20100706.2248

Prion disease update 2010 (05) 20100507.1488

Prion disease update 2010 (04) 20100405.1091

Prion disease update 2010 (03) 20100304.0709

Prion disease update 2010 (02) 20100205.0386

Prion disease update 2010 20100107.0076

2009

---

Prion disease update 2009 (10) 20091103.3784

vCJD - Italy: susp. 20091024.3671

Prion disease update 2009 (09) 20091005.3461

Prion disease update 2009 (08) 20090908.3170

Prion disease update 2009 (07) 20090806.2783

Prion disease update 2009 (06) 20090706.2433

Prion disease update 2009 (05) 20090602.2054

Prion disease update 2009 (04) 20090406.1337

vCJD, 5th death - Spain (Cantabria) 20090307.0953

Prion disease update 2009 (03) 20090305.0918

Prion disease update 2009 (02) 20090202.0463

Prion disease update 2009 (01) 20090108.0076

2008

---

Prion disease update 2008 (14): new vCJD wave imminent? 20081218.3980

Prion disease update 2008 (13) 20081201.3780

Prion disease update 2008 (12) 20081103.345

Prion disease update 2008 (11) 20081006.3159

vCJD, mother & son - Spain: (Leon) 20080926.3051

Prion disease update 2008 (10) 20080902.2742

vCJD - Spain: susp. 20080410.1311

Prion disease update 2008 (05) 20080408.1285

Prion disease update 2008 (01): correction 20080104.0046

Prion disease update 2008 (01) 20080102.0014

2007

---

Prion disease update 2007 (08) 20071205.3923

Prion disease update 2007 (07) 20071105.3602

Prion disease update 2007 (06) 20071003.3269

Prion disease update 2007 (05) 20070901.2879

Prion disease update 2007 (04) 20070806.2560

Prion disease update 2007 (03) 20070702.2112

Prion disease update 2007 (02) 20070604.1812

Prion disease update 2007 20070514.1542

CJD (new var.) update 2007 (05) 20070403.1130

CJD (new var.) update 2007 (04) 20070305.0780

CJD (new var.) update 2007 (03) 20070205.0455

CJD (new var.) update 2007 (02): South Korea, susp 20070115.0199

2006

---

CJD (new var.), blood transfusion risk 20061208.3468

CJD, transmission risk - Canada (ON) 20061207.3457

CJD (new var.) update 2006 (12) 20061205.3431

CJD (new var.) update 2006 (11) 20061106.3190

CJD (new var.) update 2006 (10) 20061002.2820

CJD (new var.) - Netherlands: 2nd case 20060623.1741

CJD (new var.) - UK: 3rd transfusion-related case 20060209.0432

CJD (new var.) update 2006 (02) 20060206.0386

CJD (new var.) update 2006 20060111.0101

2005

---

CJD (new var.) update 2005 (12) 20051209.3547

CJD (new var.) update 2005 (11) 20051108.3270

CJD (new var.) update 2005 (10) 20051006.2916

CJD (new var.) update 2005 (02) 20050211.0467

CJD (new var.) - UK: update 2005 (01) 20050111.0095]



...................cp/ejp/sh







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ProMED-mail makes every effort to verify the reports that

are posted, but the accuracy and completeness of the

information, and of any statements or opinions based

thereon, are not guaranteed. The reader assumes all risks in

using information posted or archived by ProMED-mail. ISID

and its associated service providers shall not be held

responsible for errors or omissions or held liable for any

damages incurred as a result of use or reliance upon posted

or archived material.

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Friday, September 10, 2010

BOVINE TUBERCULOSIS, BOVINE - USA (07): (MICHIGAN)

**************************************************

A ProMED-mail post



ProMED-mail is a program of the

International Society for Infectious Diseases





Date: Tue 7 Sep 2010

Source: Up North Live [edited]







Second bovine TB case detected in Emmet County

----------------------------------------------

The Michigan Department of Agriculture (MDA) is holding an meeting for

Emmet County cow producers, after the United States Department of

Agriculture (USDA) classified a farm as being infected with bovine

tuberculosis (TB). Previous routine bovine TB surveillance testing

conducted by the MDA found a bovine TB positive herd in Emmet County in

March 2010. During the depopulation of the herd, a breeding bull was found

to be infected. During MDA's outbreak investigation of the herd it was

discovered the bull was leased to another producer in Emmet County.



On 13 Aug 2010, the United States Department of Agriculture (USDA)

classified the farm as being infected with bovine TB. This is the 2nd

infected herd in Northern Lower Michigan's Modified Accredited Advanced

Zone (MAAZ). The meeting for Emmet County producers is scheduled for Thu 16

Sep 2010 from 7:00 p.m. to 9:00 p.m. at the West Traverse Township Hall at

8001 M-119 in Harbor Springs. At this meeting, Dr James Averill (MDA's

bovine TB project coordinator) will discuss herd investigation, impact to

producers and the community, and answer questions.



"We have tested or scheduled all the cattle herds within a 10 mile [16 km]

radius circle around the positive herd that was identified last March

[2010], and they have been negative so far," said Dr Averill. "The trace

investigation is almost complete and only this herd was found to be exposed

to a lesioned animal. With this additional herd designation, the status of

the MAAZ is a concern as 4 positive cattle herds in a year may cause a drop

in our status. We've tested 67 farms in the special surveillance circle test."



On 4 Jan 2010, MDA, in coordination with USDA, expanded the MAAZ to include

Antrim, Charlevoix, Cheboygan, Crawford, Emmet, and Otsego counties. The

goal is to return bovine TB Free status to the entire state and testing is

an effective way to prevent bovine TB from spreading to other herds. MDA is

working to move a majority of the MAAZ to TB Free status while maintaining

MAAZ status for the above listed counties along with Presque Isle County.



"With the continued presence of bovine TB in the wild white-tailed deer

population in Northern Lower Michigan, Emmet County herd producers need to

utilize wildlife risk mitigation systems to protect their investments,"

said Averill. "As a reminder, producers should use such tools as disease

control permits, fencing, and sound livestock management practices to

reduce the risk of disease."



While infection can occur by nose-to-nose direct contact, infection is much

more likely to occur through indirect transmission through contaminated

feed. Beef and dairy farmers can decrease the risk of exposing their cattle

to bovine TB by limiting cattle-to-deer contact and protecting cattle feed

from deer.



This Emmet County herd is the 4th TB affected herd identified in Michigan

in 2010 -- a beef herd in Alcona County, and another in Alpena County are

in the Modified Accredited Zone (MAZ) where the disease is most prevalent.

The current bovine TB eradication effort began in 1998, and all of

Michigan's one million cattle were tested by the end of 2003. Testing

continues in the state for movement from one farm to another. Since 1998,

MDA and USDA have detected 50 cattle herds and 4 privately owned cervid

operations. These premises either have been depopulated or the herds were

quarantined and placed under a test-and-remove program.



--

communicated by:

ProMED-mail





[ProMED-mail post 20100325.0948 contains comments from Dr James Averill the

MDA bovine TB coordinator:



"If we test all the cattle herds within a 10-mile radius circle around the

positive herd, and they are negative, the status of the MAAZ will not be

impacted, as there would have to be at least 3 positive cattle herds in the

zone in a year, for the status to drop," said Dr James Averill, MDA's

bovine TB project coordinator.



Sadly these addition infected herds could affect the Modified Accredited

Advance Zone's status and may drop the status to Modified Accredited, which

would mean the entire state is in the same zone. A drop in status could

mean more testing for the state, and more testing for producers wishing to

move their animals. A map of the split state status may be found at

.



For more detailed information on bovine tuberculosis readers are encouraged

to see the moderator's comments on ProMED-mail post 20100325.0948.



The interactive HealthMap/ProMED map for Michigan is available at

- Mod.TG]



[see also:

Bovine tuberculosis, bovine - USA (06): (OH)20100715.2362

Bovine tuberculosis, bovine - USA (05): (CO) 20100614.1989

Bovine tuberculosis, bovine - USA (04): (KY) 20100528.1768

Bovine tuberculosis, cervid - USA: (MI) 20100418.1265

Bovine tuberculosis, bovine - USA (03): (NE) 20100409.1144

Bovine tuberculosis, bovine - USA (02): (MI) 20100325.0948

Bovine tuberculosis, bovine - USA: (SD) 20100107.0065

2009

---

Bovine tuberculosis - USA (12): (MN), cervid 20091222.4315

Bovine tuberculosis - USA (11): (IN) cervid 20090804.2742

Bovine tuberculosis - USA (10): (IN) cervid, bovine 20090714.2508

Bovine tuberculosis - USA (09): (IN) cervid, bovine 20090711.2480

Bovine tuberculosis - USA (08): (IN) cervid, bovine 20090628.2343

Bovine tuberculosis - USA (07): (MN) cervid 20090625.2307

Bovine tuberculosis - USA (06) (NE) (02) 20090620.2270

Bovine tuberculosis - USA (05): (NE) 20090613.2198

Bovine tuberculosis - USA (04): (TX) conf. 20090613.2195

Bovine tuberculosis - USA (03): (NE) cattle, elk 20090603.2060

Bovine tuberculosis - USA (02): (ND) 20090514.1811

Bovine tuberculosis - USA: (TX), susp 20090423.1536

Tuberculosis, captive wildlife - USA: (NE) 20090414.1423]



.................sb/tg/mj/sh







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information, and of any statements or opinions based

thereon, are not guaranteed. The reader assumes all risks in

using information posted or archived by ProMED-mail. ISID

and its associated service providers shall not be held

responsible for errors or omissions or held liable for any

damages incurred as a result of use or reliance upon posted

or archived material.

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Tuesday, August 31, 2010

USDA' Offical Admits: Protectionist "Food Safety" Policies Trump Public Health


With all the food recalls in the news lately, the big question on everyones mind is "WHY isn't the USDA doing more to test for contaminated foods prior to the products being offered to the public for sale?" And " WHY doesnt the USDA impose stricter regulations or require a vigious testing system?" Not suprisingly, most people arent even aware of the fact that the USDA does not even have the power of recall! It is up to the producers and processors to volunteer that info to the public. Due to the self-regulatory nature of these industries, you can see why they would be hesitant to report or recall any of their products as "unsafe," - nothing causes sales (and profits) to drop quicker than a product recall. When they do recall, it is usually done because they have no choice, ..people start to sicken and/or die and independant investigations begin.  In these cases, it is "report yourselves" or eventually be found out by the feds. The awful truth came out awhile back when a top USDA  Official spilled the beans in a public forum, and you can read all about his startling revelations here, in the link below,...regarding another case of a bad-meat recall that happened last year;
http://exposingfdanusda.blogspot.com/2010/05/usda-offical-tells-truth-for-change.html

After you have read the article in the link, be sure to read the latest update from Pro-Med (below) on the recent Cargill / BJs ground beef recall, and be sure to note the large, embolded text in red and you will find an example of USDA protecting distributors.

* And a note on the modern trend of "growing" beef. Since when do we "grow" beef?  In my day, you RAISED meat animals and grew crops. Why the switch? Think "PR" or "SPIN"

E. COLI VTEC NON-O157 - USA (07): O26, GROUND BEEF, ALERT, RECALL


*****************************************************************

A ProMED-mail post



ProMED-mail is a program of the

International Society for Infectious Diseases

Date: Sat 28 Aug 2010

Source: CNN [edited]

Cargill Meat Solutions Corp. has recalled about 8500 pounds of ground

beef that may be contaminated with E. coli, the U.S. Department of

Agriculture announced Sat 28 Aug 2010. The move came after 3 people,

2 in Maine and 1 in New York, were identified as becoming ill from a

strain of _E. coli_, the government said.

None of the 3 required hospitalization, said Cargill Inc. spokesman

Mike Martin.

The USDA says it believes certain BJ's Wholesale Club stores in

Connecticut, Maine, Maryland, Massachusetts, New Hampshire, New

Jersey, New York and Virginia received the products. The recalled

ground beef was shipped on 11 Jun 2010 to distribution centers, where

it was repackaged into consumer-size packages and sold under different

retail brand names. The USDA did not identify the brands.

The recalled beef bears the USDA establishment number "EST. 9400," a

product code of "W69032" and a "use/freeze by" date of 1 Jul 2010.

The USDA's Food Safety and Inspection Services, which said it became

aware of the problem on 5 Aug 2010, "determined that there is an

association between the ground beef products subject to recall and the

cluster of illnesses in the states of Maine and New York."

Saturday's statement identified the strain as _E. coli_ 026, which can

cause bloody diarrhea, dehydration and, in severe cases, kidney failure.

The government "strongly encourages consumers to check their freezers

and immediately discard any product subject to this recall."

The government lists the recall as Class 1, meaning "there is a

reasonable probability that the use of the product will cause serious,

adverse health consequences or death."
--
Communicated by:

ProMED-mail Rapporteur Brent Barrett

This outbreak once again underscores the relevance of non-O157 strains

of verotoxin-producing _E. coli_. Other _E. coli_ serogroups that have

been associated with VTEC (verotoxin-producing _E. coli_) disease

include motile ones such as O26:H11 and O104:H21 and non-motile ones

such as O111:NM (or H-). Such non-O157 isolates can be obtained from

sheep and cattle and, although they cause as many as 30 percent of

outbreaks of VTEC (1), appear to be somewhat less (or at least more

variably) virulent in a variety of in vivo and in vitro assays (2-4).

In analyzing the genetic and phenotypic profiles of non-O157 groups,

it has been found that they belong to their own lineages and have

unique profiles of virulence traits different from O157 (5). The

serogroups appearing to be most prominent are O26, O111, O128, and

O103 (6), the former serotype being the implicated strain in this

outbreak.

If a laboratory is using sorbitol-MacConkey (sMAC) plates to identify

VTEC by virtue of O157's inability to ferment sorbitol, the non-O157

strains will be missed. In a 3-year pediatric study from the

University of Washington, USA (7), 1851 stool samples were processed

for sorbitol fermentation as well as toxin production by EIA (enzyme

immunoassay), and 28 strains of O157 were found along with O103 (4

strains), O118 (2 strains), O111 (2 strains), and 3 other strains.

Clinically, the O157 infections had a higher frequency of bloody

stools, fecal leukocytes, and abdominal pain with shorter symptom

duration. Five (18 percent) of O157 infections developed HUS; none of

the non-O157 strains did. Since toxin assay did not identify all O157

strains found on sMAC plates, the investigators did not advocate

performing toxin assay alone. Non-O157 can produce hemolytic-uremic

syndrome, as demonstrated by a cluster of O121 cases associated with a

lake in Connecticut, USA (8).

Since toxin assays are not uniformly performed in many areas, and most

cases do not produce HUS, it is likely that cases due to non-O157

strains are being missed. How frequent this phenomenon will become

over time is unclear.

Because of the higher risk of morbidity and mortality in VTEC

infections treated with antimicrobials (9), antimicrobials should not

used for known acute cases.

References

----------

1. Hussain HS, Omaye ST: Introduction to the food safety concerns of

verotoxin-producing _Escherichia coli_. Exp Biol Med 2003; 228(4):

331-2; available at.

2. Blanco J, Blanco M, Blanco JE, et al: Verotoxin-producing

_Escherichia coli_ in Spain: prevalence, serotypes, and virulence

genes of O157:H7 and non-O157 VTEC in ruminants, raw beef products,

and humans. Exp Biol Med 2003; 228: 345-51; available at.

3. Law D, Kelly J: Use of heme and hemoglobin by _Escherichia coli_

O157 and other Shiga-toxin-producing _E. coli_ serogroups. Infect

Immun 1995; 63(20): 700-2; available at.

4. Tzipori S, Wachsmuth KI, Smithers J, Jackson C: Studies in

gnotobiotic piglets on non-O157:H7 _Escherichia coli_ serotypes

isolated from patients with hemorrhagic colitis. Gastroenterology

1988; 94(3): 590-7; abstract available at.

5. Schmidt H, Geitz C, Tarr PI, et al: Non-O157:H7 pathogenic

Shiga-toxin producing _Escherichia coli_: phenotypic and genetic

profiling of virulence traits and evidence for clonality. J Infect Dis

1999; 179(1): 115-23; available at.

6. Bettelheim KA: Role of non-O157 VTEC. Symp Ser Soc Appl Microbiol

2000; (29): 38S-50S; abstract available at.

7. Klein EJ, Stapp JR, Calusen CR, et al: Shiga toxin-producing

_Escherichia coli_ in children with diarrhea: a prospective

point-of-care study. J Pediatr 2002; 141(2): 172-7; available at.

8. McCarthy TA, Barrett NL, Hadler JL, et al: Hemolytic-uremic

syndrome and _Escherichia coli_ O121 at a lake in Connecticut, 1999.

Pediatrics 2001; 108(4): E59; available at.

9. Iijima K, Kamioka I, Nozu K: Management of diarrhea-associated

hemolytic uremic syndrome in children. Clin Exp Nephrol 2008; 12(1):

16-9; abstract available at

- Mod.LL]


[see also:

E. coli VTEC non-O157 - USA (06): O145, lettuce 20100528.1777

E. coli VTEC non-O157 - USA (05): O145, lettuce 20100525.1738

E. coli VTEC non-O157 - USA (04): O145, lettuce 20100517.1618

E. coli VTEC non-O157 - USA (03): O145, lettuce, recall 20100507.1483

E. coli VTEC non-O157 - USA (02): (OH, MI, NY) O145 20100505.1460

E. coli VTEC non-O157 - USA: (MI, OH) 20100427.1358

2008

----

E. coli VTEC non-O157, restaurant - USA (04): (OK), O111 20081201.3779

E. coli VTEC non-O157, restaurant - USA: (OK), O111 20080902.2748

E. coli VTEC non-O157, past. ice cream, 2007 - Belgium: Antwerp 20080218.0655

2007

----

E. coli VTEC non-O157, beef sausage - Denmark 20070602.1784

E. coli VTEC non-O157, 2000-2005 - USA (CT) 20070118.0240

2006

----

E. coli VTEC non-O157, lettuce - USA (UT)(02): background 20060905.2523

E. coli VTEC non-O157, lettuce - USA (UT) 20060904.2521

E. coli VTEC non-O157 - Norway (03) 20060416.1133

E. coli VTEC non-O157 - Norway 20060329.0947

E. coli VTEC non-O157, minced beef - Norway 20060304.0680

2005

----

E. coli O145, fatal - Slovenia 20050916.2739

2003

----

E. coli, VTEC non-O157 - UK (Scotland): correction 20030828.2166

E. coli, VTEC non-O157 - UK (Scotland) 20030825.2144

2001

----

E. coli O26 - South Korea 20010509.0896

1999

----

E. coli O111, diarrhea - USA (Texas) 19990707.1134

1997

----

E. coli, non-0157 - Belgium 19970610.1215]

...................ll/ejp/dk

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ProMED-mail makes every effort to verify the reports that

are posted, but the accuracy and completeness of the

information, and of any statements or opinions based

thereon, are not guaranteed. The reader assumes all risks in

using information posted or archived by ProMED-mail. ISID

and its associated service providers shall not be held

responsible for errors or omissions or held liable for any

damages incurred as a result of use or reliance upon posted

or archived material.

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