CDC info Enterovirus... upper resp. Aug 2014 auto-immune /suspicion

Non-Polio Enterovirus Enterovirus D68 in the United States, 2014

Share What We Know In 2014, the United States experienced a nationwide outbreak of enterovirus D68 (EV-D68) associated with severe respiratory illness. From mid-August 2014 to January 15, 2015, CDC or state public health laboratories confirmed a total of 1,153 people in 49 states and the District of Columbia with respiratory illness caused by EV-D68.
Almost all of the confirmed cases were among children, many whom had asthma or a history of wheezing. Additionally, there were likely millions of mild EV-D68 infections for which people did not seek medical treatment and/or get tested. CDC received about 2,600 specimens for enterovirus lab testing during 2014, which is substantially more than usual. About 36% of those tested positive for EV-D68. About 33% tested positive for an enterovirus or rhinovirus other than EV-D68.

EV-D68 was detected in specimens from 14 patients who died and had samples submitted for testing. State and local officials have the authority to determine and release information about the cause of these deaths. CDC's Role CDC worked with state and local health departments and clinical and state laboratories to enhance their capacity to identify and investigate outbreaks, perform diagnostic and molecular typing tests to detect enteroviruses, and enhance surveillance for enteroviruses to monitor seasonal activity.
CDC developed, and started using on October 14, 2014, a new, faster lab test for detecting EV-D68, allowing CDC to test and report results within a few days of receiving specimens. CDC’s lab test is a “real-time” reverse transcription polymerase chain reaction, or rRT-PCR, and it identifies all strains of EV-D68 that circulated during summer and fall 2014. It has fewer and shorter steps than the test that CDC and some states were using previously during this EV-D68 outbreak. CDC has made the protocols publicly available on its EV-D68 for Health Care Professionals web page and is exploring options for providing test kits to state public health labs.
CDC obtained one complete genomic sequence and six nearly complete genomic sequences from viruses representing the three known strains of EV-D68 that are causing infection at this time. Comparison of these sequences to sequences from previous years shows they are genetically related to strains of EV-D68 that were detected in previous years in the United States, Europe, and Asia. CDC has submitted the sequences to GenBank to make them available to the scientific community for further testing and analysis. CDC provided information to healthcare professionals, policymakers, general public, and partners in numerous formats, including Morbidity and Mortality Weekly Reports (MMWRs), health alerts, websites, social media, podcasts, infographics, and presentations.

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How do you catch it? (Web MD)

The bad news is that enteroviruses, which are thought to cause between 10 million and 15 million infections in the U.S. each year, are pretty hardy, says Stephen Morse, PhD. He's an infectious disease expert at Columbia’s Mailman School of Public Health, in New York City.

The “entero-“ part of their name means the viruses can survive stomach acid and infect the gut, as opposed to their cousins, the rhinoviruses, which can’t.

He says these germs can live on surfaces for hours and maybe as long as a day, depending on the temperature and humidity.

“It is a pretty tough virus,” he says.

The virus can be found in saliva, nasal mucus, or sputum, according to the CDC.

Touching a contaminated surface and then rubbing your nose or eyes is the usual way someone catches it. You can also get it from close person-to-person contact.

Protect yourself with good hand-washing habits. Tell kids to cover their mouth with a tissue when they cough. If no tissue is handy, teach them to cough into the crook of their elbow or upper sleeve instead of their hand.

Common disinfectants and detergents will kill enteroviruses, Morse says, so clean frequently touched surfaces like doorknobs and toys according to manufacturers’ directions.

In an article published in the Jan. 9 issue of the Morbidity and Mortality Weekly Report, the CDC said a test of the cerebrospinal fluid (which bathes the brain) in 71 patients with limb weakness showed they didn't have EV-D68 or any other pathogen. But when the CDC tested upper respiratory tract samples in a group of patients, EV-D68 was found in some of them.

Every year, children get limb-weakening neurologic illnesses caused by, among other things, viral infections, environmental toxins, genetic disorders, and Guillain-Barré syndrome, according to the CDC. In many cases, the cause is never identified.

SOURCES:News release, CDC.Mary Anne Jackson, MD, division director of infectious disease, Children’s Mercy Hospital, Kansas City, MO.Andi Shane, MD, medical director, hospital epidemiology;  associate director of pediatric infectious disease, Children’s Healthcare of Atlanta.Roya Samuels, MD, pediatrician, Steven & Alexandra Cohen Children’s Medical Center, New Hyde Park, NY.Stephen Morse, PhD, professor of epidemiology, Mailman School of Public Health, Columbia University, New York.William Schaffner, MD, infectious disease specialist, Vanderbilt University, Nashville, TN.

© 2014 WebMD, LLC. All rights reserved.

Sero-negative Spondylo-arthropathies

Aetiology

Definitions

Ankylosing Spondylitis

Reiters Disease

Psoriatic Arthropathy

Enteropathic Arthropathy

Sarcoidosis

Polymyalga Rheumatica

SLE

Scleroderma

Rheumatic Fever

Pigmented Villo-nodular Synovitis

Aetiology

HLA B27 found in 4 - 8% of the normal population and is a marker for a specific haptotype of the Class 1 antigens of the major histocompatability complex of antigens
Up to 20% of HLA B27 patients develop spondylo-arthropathy after exposure to shigella or other environmental agents
HLA B27 is passed on to 50% of the offspring
Randomly selected individuals with HLA B27 may have only a 2 - 10% chance of developing disease whereas the risk for HLA B27 positive relatives of HLA B27 patients with spondylitis is 25 - 50%
The link between HLA B27 and spondylo-arthropathies remains unknown but it may be that;
HLA B27 acts as a receptor site for infective agents
It may be a marker for immune response gene that determines susceptibility to environmental triggers
HLA B27 may induce tolerance to foreign antigens with which it cross reacts
HLA B27 also increased neutrophil motility (? significance)
HLA B27 is associated with;
Ankylosing Spondylitis 95%
Reiters 60 - 70%
Psoriatic Arthropathy 20% (60% if sacroiliitis)
JCA, (Pauciarticular Type II) 20% (50% if sacroiliitis)
Enteropathic Arthritis 5% (50 - 70% if sacroiliitis)

Definitions

Enthesopathies

Inflammation with cellular infiltration by lymphocytes plasma cells and PMN is associated with erosion and eburnation of sub-ligamentous bone

Syndesmophyte

Ossification within the annulus fibrosus leading to thin vertical radio dense areas. Predominantly in anterior and lateral aspects of the spine

Dagger Sign

Single dense central line on frontal radiographs related to ossification of supra spinous and inter spinous ligaments

Spondylodiscitis

Loss of inter vertebral disk height and extensive new bone formation resembling infection without clinical or laboratory evidence to support the diagnosis

Ankylosing Spondylitis

Definition

Chronic inflammatory condition of the spine and sacro-iliac joints characterised by osseous proliferation and associated with HLA B27
Bilateral and asymmetric involvement predominate PIP, DIP & MCP joints may be involved. Osteoporosis, erosions and deformity are less marked than in RA
Osseous proliferation may be exuberant

Incidence

Affects 1 per 1,000 people in Western Europe
Prevalence ~ 1% whites
Low incidence in black Americans and Negro's
Classic Ank Spond ® Male : Female 3 or 4:1
May be the incidence is equal but female form less likely to have progressive spinal deformity.
Onset usually aged 15 - 25 years ( less than 40 years)

Aetiology

Genetic predisposition HLA B27 but only a relatively small percentage of people with HLA B27 go on to have Ankylosing Spondylitis
Virtually all patients with Ank Spond have HLA B27.
50% of first degree relatives of spondylitic patients also HLA B27 and of this group 20% ® spondylitis
Trigger ?, similar to Reiters, ulcerative colitis, ? lymphatic drainage to SI and spinal region important.
? Environmental trigger

Pathology

Primary process is enthesopathy, inflammation at fibro-osseous junctions of syndesmotic joints (inter vertebral discs, sacroiliac ligaments, symphysis pubis, manubrium sterni and bony insertions of ligaments and tendons; entheses)
Three stages of the disease

Inflammatory reaction with round cell infiltrate, granulation tissue and bony erosion

Replacement of granulation tissue with fibrous tissue

Ossification of fibrous tissue ® ankylosis

Also see synovitis of diarthrodial joints
Fibroplasia ® cartilaginous metaplasia ® chondro-ossification and bony ankylosis which is typical of Ank Spond (and psoriasis) but rare in RA
SI joints, facet joints ® joint destruction, costo-vertebral joints also frequently involved ® reduced respiratory excursion

Clinical Features

Many remain undiagnosed
Insidious onset ® back-ache and stiffness
May have referred pain similar to sciatica
In woman diagnosis often delayed, progressive disease is less common and there is likely to be more peripheral joint involvement and less spinal involvement
Pain and swelling of other joints and at the point of tendon insertions (enthesopic features)
10% start as an asymmetrical poly arthritis
Morning stiffness with improvement following exercise
20% have a peripheral arthropathy ® up to 35% eventually
Loss of spinal mobility (extension first) with flattening of lumbar lordosis

Wright / Schober

Mark two points one 10cm above and one 5cm below the level of the iliac crests and flex ® should lengthern 5cm

Wall test ® heels, buttock and scapulae all should be able to touch but if decreased extension unable to do this
Chest expansion should be at least 5cm and is often markedly reduced in this disease due to costo-chondral arthrosis (not a reliable sign in the elderly or in those with COAD)
Ocular inflammation occurs in ~ 1/3 of patients (uveitis ~20% and conjunctivitis in 25%)
Aortic valve disease rarely a clinical problem present in ~ 3% and pericarditis and myocarditis may also be a feature
Occasionally pulmonary fibrosis
Associated with weight loss, fatigue, low grade fever
Spinal fractures (? stress #) often ® pseudarthrosis at the disco-vertebral junction. Epidural haematomas seen in ~ 20%
Cervical spine #'s heal well in halo
If neurological involvement 46% chance of being fixed and 29% mortality
Risk of massive epidural haemorrhage may ® ascending paralysis

Investigations

Rh factor is negative
ESR increased during active phase
HLA B27 present in 95% of cases (present in 5 - 10% normals)
95% of whites with Ank Spond have HLA B27 but only 60% of blacks
ALP & CPK increased

X-Rays

Erosions / fuzziness of the SI joints often the earliest feature ® bony ankylosis
Vertebral squaring due to flattening of the normal anterior convexity secondary to inflammation at point of annulus insertion ® ossification across the inter-vertebral discs ® bamboo spine
Peripheral joints erosive arthritis and ankylosis
Protrusio Acetabulae may be a feature
Three types of disco-vertebral lesions

Central intra osseous discal displacement (Schmorls' node)

Enthesopathy, peripheral lesion

Both peripheral and central

Diagnostic Criteria

Low back pain of more than 3/12 duration

Pain & stiffness in the thorax

Limited chest expansion

Limited lumbar motion

Past or present iritis

Radiological sacroiliitis

Radiological syndesmophytes

Need 4 of the five clinical criteria or the radiological criteria plus one other

Differential Diagnosis

Other sero-negative spondylo-arthropathies ® vertebral and SI joint disease (Reiters, psoriatic arthritis, ulcerative colitis & Crohns disease, Whipples disease, Behcets syndrome) all show some familial aggregation and are associated with HLA B27

Forestiers Disease

(Ankylosing Hyperostosis) Common disorder predominantly in older men ® widespread ossification of ligaments and tendon insertions (ALL in the cervical spine and in the lumbar spine ® pronounced but asymmetrical inter vertebral spur formation and bridging) Not an inflammatory disease and spinal pain and stiffness seldom severe. SI joints are not eroded and ESR normal. Associated with obesity and diabetes

Treatment

Anti inflammatory medication
Analgesics
Physiotherapy etc to preserve movement and prevent deformity
Rest and immobilisation contraindicated as ® increased osteoporosis and ankylosis
Significant hip involvement ® THR (often left with limited ROM)
Spinal osteotomy (lumbar or cervical) to "improve outlook on life"

Prognosis

Age of onset is the most important factor in determining prognosis and outcome

Reiters Disease (Reactive arthropathy)

Definition

Sero negative arthritis that follows urethritis, cervicitis or dysentery
Triad; (described by H. Reiter (1916)
Poly arthritis, urethritis and iritis / conjunctivitis

Incidence

Male : Female ratio 5:1
Probably the commonest type of large joint poly arthritis in young men
Usually males aged 15 - 40 years, rare in women, children & the elderly
Familial aggregation
Arthritis appears 2 - 6 weeks after initiating infection ®acute onset with asymmetric poly or oligo arthritis

Aetiology

Sero negative arthritis that follows urethritis, cervicitis or dysentery

Associated organisms

Lymphogranuloma venereum
Chlamydia trachomatis
Campylobacter
Shigella
Salmonella
Yersinia enterocolitica
Clostridia difficile

Asymmetrical changes are typical
Lack of osteoporosis and exuberant periostitis as in psoriatic arthropathy and Ank Spond
Also used to describe reactive arthritis associated with non-specific urogenital (urethritis, cystitis, prostatitis, cervicitis, balanitis) or bowel infection

Pathology

Organisms found in the joint (intracellular) ® triggers of local rather than systemic immune response

Clinically

Normal progression Urethritis ® Uveitis ® Arthritis
Urethritis not necessarily sexually transmitted and may occur in children

Skeletal

Affects particularly the large joints (knee and ankle)
Severe swelling of entire fingers and toes may be associated (sausage digits)
Involvement of DIP joints of toes think of Reiters or psoriasis
Backache and stiffness secondary to sacroiliitis and spondylitis common
3% of patients with Reiters syndrome will develop Ank Spond

Entheses

Tenosynovitis and plantar fasceitis common (enthesopathy)

Eyes

Unilateral or bilateral non infectious conjunctivitis occurs in ~ 40% and more disabling involvement includes iritis (~ 5%), uveitis, episcleritis and corneal ulceration

Integument

May have buccal ulcers and skin lesions
Balanitis Circinata (small shallow painless ulcers on the glans and urethral meatus)
Keratoderma Blenorrhagica (hyperkeratotic skin lesions, predominantly on the soles of the feet occurs in 10%)
Amyloidosis and pleurisy may develop
80% have symptoms for many years

Investigations

HLA B27 positive in 60 - 70% of cases
ESR may be high during the active phase
Cultures (urine, stool)

X-Rays

Initially normal ® erosive arthropathy eventually
Sacroiliitis in 25% of patients but more asymmetric than in Ank Spond
Vertebral changes similar to Ank Spond
Periosteal changes in ischial tuberosity, greater trochanter or site of insertion of Achilles tendon

Differential Diagnosis

Gouty arthritis
Other enteropathic arthritis
Gonococcal arthritis ® septic arthritis or reactive sterile arthritis

Treatment

General treatment for active bowel or urinary infection (Tetracyclines for urethritis)
Rest, splintage, anti-inflammatories
Local or oral steroids
Resistant cases not responding to NSAIDs may try methotrexate or azathiaprine
Generally today use tetracycline for 6 - 8 weeks to decrease the incidence and severity of recurrent attacks (especially if Chlamydia cultured in the urine)

Prognosis

Minority ® spontaneous remission and no recurrent episodes
Majority ® recurrent episodes of arthritis with the episodes lasting less than 6 months usually
Smaller minority ® continuous unremitting course

Psoriatic Arthropathy

Incidence

About 7% of patients with psoriasis ® evidence of inflammatory arthritis
? More common in men and tends to run in families
Usually over 30 years of age and skin disease usually precedes joint disease

Aetiology

~ 4% of chronic poly-arthritis pts ® have psoriasis but not all of these have psoriatic arthritis

Pathology

Similar to RA but
Less cellular infiltrate and more fibrosis
Pannus mainly on the surface and not eroding underneath cartilage
More bony proliferation and often ankylosis

Clinically

Characteristically involves distal joints of the hands and feet with 95% of patients having peripheral joint involvement
Usually pauci-articular asymmetric arthritis
25% have poly articular arthritis indistinguishable from RA
Bone and cartilage destruction may be unusually severe (Arthritis Mutilans)
Nail changes evident in 10% of psoriatics but 80% of those with arthritis ( oil droplet
discoloration, subungal hyperkeratosis and onycholysis)
5% have exclusively spinal involvement
10% arthritis preceeds psoriasis
Large joints may be involved
Tendon involvement may ® fixed deformities
40% develop spondylitis and 25% develop sacroiliitis and or Ank Spond
Ocular inflammation (iritis, conjunctivitis, episcleritis and keratoconjunctivitis sicca ) in 30%

Clinical forms

70% Asymmetric oligoarticular disease involving 2-3 joints, involvement of distal joints of hands and feet
15% Systemic poly arthritis similar to RA but Rh factor negative
10% Predominantly distal IP joint involvement
5% Arthritis Mutilans

Investigations

Rheumatoid factor negative
May have increased ESR
Mild normochromic normocytic anaemia
HLA B27 present in 20 - 60% of patients (especially those with overt sacroiliitis)
X-Rays Destruction of DIP and or PIP joints with erosions® pencil in cup deformities
Fluffy periostitis of long bones
Changes in large joints similar to rheumatoid
SI joint involvement fairly common, bilateral more than unilateral
Spinal involvement similar to Ank Spond

Treatment

Control skin disorder with topical preparations
Splintage to prevent or limit deformity
NSAIDs ® relief of joint symptoms
Intra-articular steroid injections no more than 3/year/joint and not for multiple joints
Gold ® improvement in more than 50% of patients
Immuno-suppressives for resistant cases eg methotrexate in 3 divided doses, 2.5mg increasing to a maximum of 15mg per week
Surgery: arthrodesis of distal joints may improve function
Care at surgery due to staph skin carriage ® infection risk

Enteropathic Arthropathy

Arthritis usually follows onset of colitis by at least 6 months to several years. Uncommonly onset may coincide
HLA B27 found in 70% of patients with spondylitis

Incidence

Synovitis seen in

11% patients with Ulcerative colitis
21% patients with Crohns

Aetiology

Associated with

Crohns
Ulcerative colitis
Bacillic dysentery
Whipples disease
Behcets disease

Clinically

Usually mono-articular affecting larger joints (knees and ankles) and resolves without residual defect

Treatment

Best treatment is control of the bowel disease
Give NSAIDs in short courses due to side effects
In ulcerative colitis procto-colectomy ® cure joint problems
In Crohns arthritis may appear before the bowel symptoms and surgery often not effective possibly due to the difficulty identifying the extent of the disease at the time of surgery.

Behcets' Syndrome

Definition

Muco-cutaneous ulceration of oral cavity and genitalia
Unknown aetiology

Clinically

Characterised by uveitis, corneal ulceration, erythema nodosum, cutaneous pustules, peripheral arthropathy
Arthritis is usually destructive and usually self limiting
Knees most commonly affected
SI joints sometimes involved

Whipples' Disease

Definition

Rare systemic disease which may affect any organ system

Incidence

Affects predominantly middle aged males

Aetiology

Evidence supports infectious aetiology
Strong association with Ank Spond

Pathology

Infiltration of involved tissue with large glycoprotein laden macrophages with small rod shaped bacilli is diagnostic of the condition

Clinically

Greater than 70% have an associated peripheral arthropathy

Treatment

Responds to antibiotics

Sarcoidosis

Definition

Granulomatous disorder of unknown aetiology affecting multiple organ systems especially in young adults

Incidence

Male = Female
Blacks more than whites
Usually aged 20 - 40 years

Pathology

Granulomata are non caseating with predominantly epithelioid cells but also lymphocytes, granulocytes and plasma cells.
Granulomas may occur in any organ- May increase in size, decrease in size or remain static.
Lesions resolve by fibrosis
Involvement of bone in the absence of other clinical involvement or X-Ray manifestations is highly unusual
Osteoporosis most common feature with cortical thinning and striations, coarsened trabeculae along with lytic lesions

Clinically: (highly variable)

Leads principally to bilateral hilar adenopathy, pulmonary infiltrates and skin or eye lesions
General: malaise, fever

Skeletal

Acute poly arthritis (symetrical & peripheral) and tenosynovitis
May get osteosclerosis either nodular or generalised especially affecting the axial skeleton (differentiate from Pagets)
Hand most commonly involved site - May be associated with symmetrical small joint erosive poly-arthropathy affecting DIPJs particularly
Chronic poly arthritis may develop with relapsing and remitting caurse eventually ® subchondral collapse and permanent disability

Myopathy

CNS & PNS involvement

Skin

granulomas (erythema nodosum)

Respiratory

Cough and dyspnoea
Asymptomatic hilar lymphadenopathy

GIT

hepato-splenomegaly

Eye

granulomatous uveitis
Symptoms usually resolve in 4-6/52

Investigations

ESR usually increased
Kveim test positive ® granulomatous reaction

Diagnosis

Diagnosis historically by non-caseating epithelioid-cell granulomas

Differential Diagnosis

Skull abnormalities ® EG or neoplasm
Spinal ® infection
Joints ® RA, gout, septic arthritis
Cyst like lesions of MC and phalanges
Gout TB
Fungal disease RA
Metastasis Xanthomatosis
Myeloma Tubero sclerosis
Hyperparathyroidism Fibrous dysplasia
Haemangiomas Enchondromatosis (Olliers')

Polymyalga Rheumatica

Usually middle aged women ® marked post inactivity stiffness
Pain most often around pelvic and pectoral girdles
Tenderness in muscles rather than joints
ESR almost always increased

Pathology

Form of giant cell arteritis and associated with temporal arteritis, therefore risk of ® blindness

Treatment

Corticosteroids ® rapid and dramatic relief

SLE

Definition:

Chronic inflammatory condition characterised by the presence of anti-nuclear antibodies.

Incidence

Prevalence 3-400 / 100,000
Occurs mainly in young women
Male : Female ® 1:9 increases to 1:30 in child bearing years
Probable viral trigger in genetically susceptible individual

Aetiology

Genetic or environmental mediators may ® triggers

Pathology

Fibrinoid necrosis of small vessels ® variety of inflammatory lesions in the kidney, spleen, lungs, and other organs
Fibrinoid deposits in synovium ® mild inflammation
Cartilage destruction is seldom severe

Clinically

Malaise, anorexia, weight loss and fever
Non destructive, non deforming arthritis -Joint pain is usual but not a salient feature
May be tenosynovitis rather than arthritis
May ® tendon ruptures
Severe cases may resemble rheumatoid
Aseptic necrosis of the hip and other joints is not uncommon (? related entirely to steroid therapy)
Associated with skin rashes (butterfly rash) and ulceration
Raynauds syndrome
Hepatosplenomegaly

Associated with

Nephritis (50% of patients)
Pericarditis (30% patients)
Myocarditis (25% of patients)
Pleuritis (40-50% of patients)
Normochromic normocytic anaemia (common)
Thrombocytopenia (25% of patients)
Hepatitis, splenomegaly and chorea

Investigations

Anaemia, leucopoenia and increased ESR are common
Anti-nuclear factor always positive
Rh factor also positive in 25%

Treatment

Steroids both topical and systemically administered
NSAIDs for minor clinical manifestations of SLE
Antimalarials also used for mild systemic disease, cutaneous and musculo-skeletal manifestations

Prognosis

Survival 85% at 5 years and 65% at 10 years
Death usually secondary to renal failure

Scleroderma

Definition

Uncommon generalised disorder of connective tissue affecting primarily the skin, lungs, GIT, heart, kidneys and musculo-skeletal system

Incidence

Female : Male 4:1
Usually 30 - 50 years at onset

Aetiology:

Chromosomal abnormalities have been noted in as many as 90% of patients
? significance

Pathogenesis

Abnormal regulation of connective tissue synthesis
Primary event seems to be endothelial cell damage ®narrowing, decreased distensibility ® obliteration of vessels

Pathology

Target organ oedema ® fibrosis
Hyper-gammaglobulinaemia and ANF are frequent findings

Clinically

Raynauds
Skin ® firm, thickened and leathery
Lower limbs relatively spared
Taut skin over fingers ® limit extension and may ® FFD
Resorption of bone of terminal phalanx may occur
Facial skin contracture ® unable to open mouth fully
CREST syndrome: Subcutaneous calcinosis, Raynauds, oesophageal abnormalities, sclerodactyly and telangiectasia
Greater than 50% ® pain / stiffness of fingers and knees
Systemic poly arthritis similar to rheumatoid may occur
Associated with intestinal malabsorption
Pulmonary fibrosis and pulmonary hypertension may occur
Cardiac involvement ® degree of heart block & arrhythmias
Acute and chronic pericarditis may occur ®cardiac tamponade and accounts for 15% of deaths
Renal failure is the leading cause of death and is usually evident within 3 years of the onset of the disease

Investigations

Increased ESR
Normochromic, normocytic anaemia
ANF evident in 40-90% of patients

Treatment

No specific treatment effective
® use appropriate treatment for the organ systems involved

Rheumatic Fever

Systemic non supperatve inflammatory disease often recurrent and most likely related to prior infection with a group A b haemolytic strep.
® auto-immune response
Affects joints, the heart, skin, serosa, lungs
Joints are involved most often but the most significant effects are on the heart as the other effects are nearly always benign and transient
4% ® bacterial endocarditis ® prophylactic antibiotics

Peripheral arthropathy is also sometimes seen with

Serum sickness
Haemochromatosis
Hyperthyroidism
Giant cell arteritis
Occult neoplasm
Self limited viral illness
Hypertrophic osteodystrophy
Tietzes' syndrome
Erythema nodosum
Erythema multiformae

Pigmented Villo-nodular Synovitis

Usually occurs in the knee as a mono-articular proliferative process

Incidence

2 per 1,000,000 population
Knee involved more frequently than other joints and in diffuse rather than localised form
Male : Female ® 1:1 (Male may be slightly more than )

Pathogenesis

Inflammation with haemosiderin laden macrophages
? triggering mechanism
May be a benign neoplastic condition

Pathology

Histological

lesion characterised by fibrous stroma, deposition of haemosiderin, histiocyte infiltration and giant cells occurring in the synovial membrane of tendon sheaths and large joints
Sub-synovial nodular proliferation of larger round polyhedral or spindle cells with prominent cytoplasm and pale nuclei
Phagocytic, histiocytic cells are also present
Lipid laden foam cells and multi-nucleated giant cells are interspersed with haemosiderin laden cells

Gross

Most lesions are a single nodular outgrowth more likely pedunculated than sessile with a firm elastic consistency

Clinically

Two forms: Localised, nodular
Diffuse
Mon-articular arthritis affecting adults in the 3rd to 4th decade
Onset insidious
50% or less recall an episode of trauma
Associated with a joint effusion
No abnormality may be evident or only evidence of effusion

X-Rays

Soft tissue mass
Cysts or bony erosions in ~ 33%
Diffuse bony lesion in ~ 25%
Arthrography may identify the synovial mass
Arteriography ® richly vascular soft tissue masses
MRI ® may give typical picture due to haemosiderin

Treatment

Recurrence more common in the diffuse form
Local excision acceptable for isolated lesions
Radiotherapy, wide excision arthrodesis and grafting have been used for diffuse disease
No treatment has ® universally good results
Radiotherapy best early or when lesions are vascular rather than later when they become fibrosed
Most commonly reported technique is wide synovectomy but ® high incidence of recurrence
Diffuse form associated with significant morbidity but total synovectomy seems the treatment of choice

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POLIO

The Story Behind the Polio Vaccine
http://articles.mercola.com/sites/articles/archive/2015/01/18/history-vaccination.aspx

Another prime argument for the justification and support of today’s highly aggressive vaccination program is the alleged success of the polio vaccine. But here again, the historical perspective fails to support the vaccination paradigm. "The story behind polio is absolutely fascinating when you look at the politics that went on researching the vaccine, and how scientists were fired if they disagreed with the program going on through the National Foundation of Infantile Paralysis (NFIP) in the late 1940s and early 1950s. That was the vaccine that Jonas Salk developed," Dr. Humphries says. Before the Salk vaccine became available, if you were admitted to the hospital any doctor could diagnose you with polio based on two physical examinations within 24 hours, to check for paralysis in one or more muscle groups. We now know that a number of viruses can cause paralysis, but back then, all instances were thought to be due to polio virus.

When the polio vaccine was developed, a problem emerged. Swedish scientists were trying to tell the US scientists that formaldehyde inactivation was not going to work as planned. Their warning, however, fell on deaf ears. This was unfortunate, as they turned out to be correct. Live poliovirus, which was put in an injectable vaccine, would appear to be inactivated right after it was made, but sometimes it would "resurrect" in the vial... In essence, the formaldehyde did not kill off all the polioviruses in these vaccines, which led to live polio viruses being injected. As a result, more people developed paralysis from the vaccine in 1955 than would have developed it from a wild, normal natural poliovirus. Something had to be done to make it appear as though the vaccine was working. So what they did was change the diagnostic criteria for polio. Sadly this is a very common practice in medicine. When the observations don’t fit your expectations, change or rig the system so that they do. With polio, the original criteria was two examinations within 24 hours. This was changed to two examinations within 60 days. This was helpful in cooking the books, because within 60 days, most people recover from their bout with poliomyelitis. "All those people who were formerly called polio were no longer categorized as polio because they recovered from their paralysis within that time," Dr. Humphries explains.

Then there was the issue of testing. Prior to the vaccine, there was no testing done on blood or stool samples. After the vaccine came along, there was an epidemic in Michigan around 1958. About 2,000 people were diagnosed with polio. In disbelief over the outbreak, serological testing was done, and they discovered that the polio virus was found in only a small minority—about one-quarter of those who displayed symptoms of infection. Interestingly, in the remainder they discovered a different virus or no virus at all! And, subsequently, those patients were no longer "counted" as having polio. "So simply by doing the diagnostic testing and changing the diagnostic criteria, the rates of polio plummeted, whether or not there was ever a vaccine. These were the kind of things that were going on back then," Dr. Humphries says. Oral Polio Vaccine Propagates Transmission of Vaccine Virus It’s important to realize that the injected polio vaccine does nothing to prevent transmission of the virus, and after an oral polio vaccine you become a reservoir of virus that can mutate or combine with other bowel viruses, creating new strains that are often more virulent to those around you. According to Dr. Humphries, the only thing the injectable vaccine theoretically does is give you some blood immunity, similar to tetanus. This means it is only going to be effective if your blood meets the virus before the virus meets your nervous system.

Once vaccine makers realized just how difficult it was to inactivate the polio virus, and many people ended up contracting polio from the vaccine, they decided to abandon the injectable polio vaccine and create an oral vaccine instead, which is more similar to the natural route of infection. Again, controversy ensued. The oral vaccine did interrupt transmission of the wild type virus, but it propagated transmission of the vaccine virus instead. "The fact of the matter is that you can attenuate a virus all you want, which means that you pass it through different animals to make it mutate enough that it's not quite as lethal or virulent at some point. But once you put that vaccine or that virus back into its natural host, it mutates back to the way it was," Dr. Humphries explains. "You can give a baby an oral polio vaccine and it can be attenuated. But even in the vial, before you give it to that baby, those viruses are starting to revert back to their former problematic state. And then once the baby swallows that, the baby will generate some immunity in the intestine. But what's going to come out of that baby is going to be mutated vaccine virus.

Oftentimes this is problematic, especially in people who are immunosuppressed." In the 1990s the US quit using the oral vaccine, and switched back to the injectable vaccine. To address the hazards of injecting improperly or inadequately inactivated polio virus, certain adjustments to the formulation were made. Modern polio vaccines are propagated and inactivated differently from earlier versions, and different countries also use different strains of the polio virus.
Older polio viruses used to contain three strains of the virus. Today, some countries will only use one or two.

Polio Was 'Eradicated' NOT by the Vaccine But Through Redefinition As noted by Dr. Humphries, it's very easy to defeat the polio vaccine argument, as most incidences of polio disappeared because the disease was redefined—not because there was an actual change in disease prevalence. In fact, it could be argued that the vaccine did more harm than good, since some versions caused polio, and others propagated new mutated strains of the virus. According to Dr. Humphries, at one point, the only polio cases in the US were vaccine-induced. Yet even though there are no cases of wild polio being discovered, the polio vaccine remains part of the US vaccine program... "Even today, you can just go on to the CDC website and the Morbidity and Mortality Weekly Report (MMWR). You can see that cases of polio in this country by and large occur when people get the oral vaccine in another country and then come here. When they say that polio is only a plane ride away, the truth is that disease from polio vaccine is also a plane ride away... Like I said, the injected vaccines do not interrupt propagation of the virus. If somebody comes to this country who has recently had an oral polio vaccine and he's shedding a highly virulent strain, people in this country can start passing it around."

Polio Epidemic Historically Related to Increase in Sugar Consumption

Here's another interesting tidbit that no one ever talks about: In the past, it has sometimes been suggested that a large part of the polio epidemic was related to increases in sugar consumption. Dr. Benjamin Sandler wrote an entire book about this, and Dr. Humphries refers to his work in her book as well. She explains the connection as follows: "Polio's an enterovirus [i.e. a virus that enters the body through the gastrointestinal tract and thrives there]. The integrity and the flora population in your bowel is extremely important when it comes to dealing with any kind of bowel infection. A diet that's high in sugar is going to 1) impair your cell-mediated immune system and 2) trash your gut flora... [It was] shown that in populations who cut back on their sugar intake, the rates of polio plummeted... But it was so unbelievable that nobody really listened to him. It was the same as when Dr. Frederick Klenner tried to say that he cured 100 percent of patients with intravenous vitamin C and [it] just didn't register. The... low-sugar diet was very effective because of the effect it has on the immune system and on the bowel flora.

The same with dichlorodiphenyltrichloroethane (DDT); DDT really trashes the bowel, the intestinal walls, and the flora.... Not only can DDT give you all the symptoms of polio all by itself, it can also make the poliovirus much more virulent and active in the body for the same reason: it disturbs the normal function of the bowel."
DDT exposure has also been linked to Alzheimer's disease, and it's worth noting that the contemporary equivalent of DDT, glyphosate, according to Dr. Don Huber, professor emeritus at Purdue University, is far more toxic than DDT. It definitely has been shown to decimate your microbiome, and glyphosate preferentially kills bacteria known to be beneficial for human health.

A Lot More Than Five Senses

Humans Have a Lot More Than Five Senses

DAVEN HISKEY

Today I found out humans have a lot more than five senses. It turns out, there are at least nine senses and most researchers think there are more like twenty-one or so. Just for reference, the commonly held definition of a “sense” is “any system that consists of a group of sensory cell types that respond to a specific physical phenomenon and that corresponds to a particular group of regions within the brain where the signals are received and interpreted. The commonly held human senses are as follows:

Sight: This technically is two senses given the two distinct types of receptors present, one for color (cones) and one for brightness (rods).

Taste: This is sometimes argued to be five senses by itself due to the differing types of taste receptors (sweet, salty, sour, bitter, and umami), but generally is just referred to as one sense. For those who don’t know, umami receptors detect the amino acid glutamate, which is a taste generally found in meat and some artificial flavoring. The taste sense, unlike sight, is a sense based off of a chemical reaction

Touch: This has been found to be distinct from pressure, temperature, pain, and even itch sensors. Pressure: Obvious sense is obvious.

Itch: Surprisingly, this is a distinct sensor system from other touch-related senses. Thermoception: Ability to sense heat and cold. This also is thought of as more than one sense. This is not just because of the two hot/cold receptors, but also because there is a completely different type of thermoceptor, in terms of the mechanism for detection, in the brain.
These thermoceptors in the brain are used for monitoring internal body temperature.

Sound: Detecting vibrations along some medium, such as air or water that is in contact with your ear drums.

Smell: Yet another of the sensors that work off of a chemical reaction. This sense combines with taste to produce flavors.

Proprioception: This sense gives you the ability to tell where your body parts are, relative to other body parts. This sense is one of the things police officers test when they pull over someone who they think is driving drunk. The “close your eyes and touch your nose” test is testing this sense. This sense is used all the time in little ways, such as when you scratch an itch on your foot, but never once look at your foot to see where your hand is relative to your foot.

Tension Sensors: These are found in such places as your muscles and allow the brain the ability to monitor muscle tension. Nociception: In a word, pain. This was once thought to simply be the result of overloading other senses, such as “touch”, but this has been found not to be the case and instead, it is its own unique sensory system.

There are three distinct types of pain receptors: cutaneous (skin), somatic (bones and joints), and visceral (body organs).

Equilibrioception: The sense that allows you to keep your balance and sense body movement in terms of acceleration and directional changes. This sense also allows for perceiving gravity. The sensory system for this is found in your inner ears and is called the vestibular labyrinthine system. Anyone who’s ever had this sense go out on them on occasion knows how important this is. When it’s not working or malfunctioning, you literally can’t tell up from down and moving from one location to another without aid is nearly impossible.

Stretch Receptors: These are found in such places as the lungs, bladder, stomach, and the gastrointestinal tract. A type of stretch receptor, that senses dilation of blood vessels, is also often involved in headaches.

Chemoreceptors: These trigger an area of the medulla in the brain that is involved in detecting blood born hormones and drugs. It also is involved in the vomiting reflex.

Thirst: This system more or less allows your body to monitor its hydration level and so your body knows when it should tell you to drink.

Hunger: This system allows your body to detect when you need to eat something.

Magentoception: This is the ability to detect magnetic fields, which is principally useful in providing a sense of direction when detecting the Earth’s magnetic field. Unlike most birds, humans do not have a strong magentoception, however, experiments have demonstrated that we do tend to have some sense of magnetic fields. The mechanism for this is not completely understood; it is theorized that this has something to do with deposits of ferric iron in our noses. This would make sense if that is correct as humans who are given magnetic implants have been shown to have a much stronger magnetoception than humans without.

Time: This one is debated as no singular mechanism has been found that allows people to perceive time. However, experimental data has conclusively shown humans have a startling accurate sense of time, particularly when younger. The mechanism we use for this seems to be a distributed system involving the cerebral cortex, cerebellum, and basal ganglia. Long term time keeping seems to be monitored by the suprachiasmatic nuclei (responsible for the circadian rhythm). Short term time keeping is handled by other cell systems.

VERTIGO. -HLA B27- Meniere's Disease

See your primary care doctor immediately if vertigo is accompanied by any of the following signs or symptoms: Headache that is unusual or severe for you
Double vision or loss of vision
Speech impairment

Diseases and Conditions
Meniere's disease
By Mayo Clinic Staff
The primary signs and symptoms of Meniere's disease are: Recurring episodes of vertigo. Vertigo is similar to the sensation you experience if you spin around quickly several times and suddenly stop. You feel as if the room is still spinning, and you lose your balance. Episodes of vertigo occur without warning and usually last 20 minutes to two hours or more, up to 24 hours. Severe vertigo can cause nausea and vomiting. Hearing loss. Hearing loss in Meniere's disease may fluctuate, particularly early in the course of the disease. Eventually, most people experience some degree of permanent hearing loss. Ringing in the ear (tinnitus). Tinnitus is the perception of a ringing, buzzing, roaring, whistling or hissing sound in your ear. Feeling of fullness in the ear. People with Meniere's disease often feel aural fullness or increased pressure in the ear. A typical episode might start with a feeling of fullness in your ear, increasing tinnitus and decreasing hearing followed by severe vertigo, often accompanied by nausea and vomiting. Such an episode might last 20 minutes to four hours, after which signs and symptoms improve. Episodes often occur in clusters, with long periods of mild or no symptoms (remission) between. Still, the severity, frequency and duration of each of these sensory perception problems vary, especially early in the disease. For example, you could have frequent episodes with severe vertigo and only mild disturbances in other sensations. Or you may experience mild vertigo and hearing loss infrequently but have frequent tinnitus that disturbs your sleep. When to see a doctor See your doctor if you experience any signs or symptoms of Meniere's disease. Because any one of these problems may be the result of other illnesses, it's important to get an accurate diagnosis as soon as possible. Vertigo is an uncommon but possible sign of other disorders, such as stroke, brain tumor, multiple sclerosis, or diseases of your heart or blood vessels (cardiovascular disease). See your primary care doctor immediately if vertigo is accompanied by any of the following signs or symptoms: Headache that is unusual or severe for you
Double vision or loss of vision
Speech impairment
Leg or arm weakness
Loss of consciousness
Falling or difficulty walking
Numbness or tingling Chest pain

http://www.entjournal.com/article/hla-b27-associated-bilateral-m-ni-re-disease

HLA-B27-associated bilateral Ménière disease

March 1, 2010 by Shamila G. Rawal, MD, Kunal H. Thakkar, MD, Kasra Ziai, BS, Peter A. Santi, MD, and Hamid R. Djalilian, MD

Abstract
We describe 2 cases of bilateral Ménière disease with features resembling autoimmune inner ear disease in patients who were found to be carriers of human leukocyte antigen (HLA) B27. For immunohistochemical analysis, mouse inner ear sections were used as the tissue substrate for reaction with serum. Both patients demonstrated an increased immunofluorescence reaction compared with a normal control. We suggest that an antibody-mediated mechanism may be responsible for HLA-B27-associated Ménière disease.