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4.2 Blood Transfusion Science > Transusion Transmitted Infections > Flashcards

Transusion Transmitted Infections Flashcards

1
Q

When did we introduce hepatitis E testing?

A

Testing introduced in January 2016

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2
Q

What is Hepatitis E

A

A small, nonenveloped, single-stranded RNA virus of the family Hepeviridae, a Hepevirus

There are 4 main strains HEV1-4

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3
Q

Talk about the four different strains of hepatitis E virus

A

HEV1 and HEV 2 infections in developing countries -> waterborn infection

HEV3 and 4 infections endemic in the developing world - zoonotic infections, under reported, many cases subclinical

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4
Q

Talk about the prevalence of HEV

A

Prevalence of 1:5000 donors approximately

HEV1 and 2 causes 3.4 million sympotomatic cases nicluding 70,000 deaths and 3, 000 stillbirths

Significant proportion of symptomatic cases are misdiagnosed or unrecognised especially with HEV3 and HEV4

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5
Q

What was originally thought about hep e

A

it was thought to originally be due to alcoholism i.e. alcoholic cirhhosis

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6
Q

What is the main zoonotic source of Hepatitis E

A

Pigs

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7
Q

What are some HEV1 and 2 endemic areas

A

China
India
Rural Malasia

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8
Q

What are the main sources of hepatitis E

A

Human hosts, certain animal species including pigs and wild boar

There is evidence of zoonotic transmission via the food-borne route

Consumption of uncooked meat including pig, wild-boar, deer etc

Elevated seroprevalence in pig farmers, abattoir workers and veterinarians

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9
Q

Who do we see chronic hepatitis E infections in?

A

Immuno-compromised patients
Solid-organ transplant recipients
Patients with haematological disease
HIV infection with low CD4 cell counts <100/mm^3

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10
Q

How does hepatitis E manifest in the immuno-compromised?

A

Rapid progression of liver fibrosis, chronic hepatitis after 15 months, cirrhosis E after 3 years

Extra-hepatic manifestations including neurological complications

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11
Q

When did we become concerned with hepatitis E

A

We didnt think it was an infectious virus so we didnt really bother with it

We only started after two studies carried out in the UK and US revealed that between 3 and 13% of suspected drug-induced liver injury was in fact HEV3 infection

After this Ireland was quick to develop an assay for HEV -> we have a large pork industry and large prevalence so we didnt want to be cought with this as we had been HCV

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12
Q

What is HTLV 1 and 2

A

Oncogenic viruses causative of adult T-Cell leukaemia and lymphoma (in chronic)

They may also cause a tropical spastic paraparesis

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13
Q

What is tropical spastic paraparesis?

A

A progressive degeneration of spinal cord neurones

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14
Q

How is HTLV transmissed

A

HTLV1 is transmitted by cellular blood components but not by cell free
Both 1 and 2 are transmitted by sexual contact, needles and breast milk

NB: blood storage decreases risk

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15
Q

What is the incubation period and seroprevalence of HTLV 1 and 2

A

30-90 days incubation
Seroconversion and possible disease up to 40 years after infection
IgM first produced then IgG
20 million people are infected worldwide, 3-8 million are in Africa
In the US prevalence of 0.016 percent of donors have it
Remains in the body for life, once in your system it can reactivate whenever immunosuppressed etc

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16
Q

When did we start screening for HTLV

A

Screening donors since 1996
But weve only had 4 HTLV donors in 22 years

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17
Q

What is cytomegalovirus

A

Herpes virus 5
It usually causes an asymptomatic infection which resolves on its own and is replaced by anti-CMV antibody
thus the Ab is a marker for infection
Many donors and patients are therefore exposed to the virus and only the immunosuppressed are of concern

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18
Q

Talk about the seroprevalence of CMV

A

26% of Irish donors - low compared to other -> can be up to 90% in certain countries
-> 29% in females, 24% in males

Seroconversion rate was 1.55% -> i.e. donors tat were previously neg that are now pos

Prevalence is highest in over 60s

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19
Q

Talk abou CMV in the immunocompromised

A

Immunosuppressed or neonates get CMV- blood

Its a common cause of fatality in HIV
-> causes hepatitis like infection
-> terrible encephalitis and eventually death
-> historic cause of death though

antiviral medications may stop the replication of the virus but will not destroy it

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20
Q

What problems are associated with CMV

A

Virus can remain latent in healthy donors - donors arent excluded from donating

reactivation of virus upon transfusion in immunocompromised

Cellular blood components are the potential transmitters

Window period of 6-8 weeks

CMV DNA is present weeks to months before the antibody appears

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21
Q

Why do we still use CMV+ units?

A

This is because immunecompetent people cannot get CMV from LD blood -> it is considered CMV safe to give to healthy people

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22
Q

Who should be given CMV negative blood?

A

Intra-uterine foetuses
Exchange transfusion infants
Neonates up to 1 year
Bone marrow recipients
PBSC recipients
Other organ transplants
Seronegative pregnant mothers
HIV patients, not yet infected
Patients immunosuppressed in general

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23
Q

What is West Nile Virus, how is it transmitted

A

A mosqiuto botn virus carried by birds
Lipid enveloped RNA virus
Its not that dangerous but 1% of people get encephalitis
Transmitted from humans then to birds and from birds to other parts of america etc

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24
Q

Talk about the initial outbreak of WNV

A

Initial outbreak in USA in 1999
It used to be unheard of until the early 2000s where we had our first cases
There was first an outbreak in a NY blood bank

Transplanted organs gave 4 recipients WNV
>30 cases of transplant/transfusion cases
Incidence of 1.5 cases per 10000 donors are positive

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25
Q

Talk about the European outbreak of west nile virus

A

Outbreak occureed in Denmark
Associated with imported tires
Mosquitos on old tires were infected with virus

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26
Q

How do we test for WNV

A

Tested using PCR

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27
Q

How do we test for WNV?

A

tested using PCR
We used to just defer people from america but one it became a european disease we had to start testiing

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28
Q

What is the incubation period of WNV?

A

2-21 days post transfusion

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29
Q

How do we test for WNV?

A

Tested using PCR

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30
Q

What encephalitis viruses are we concerned with?

A

Concerned wiith flaviviruses such as:
- West Nile Virus
- Japanese Encephalitis
- St. Louis Encephalitis
- Murray Valley Encephalitis

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31
Q

What is significant about japanese encephalitis

A

It has a 33% fatality rate

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32
Q

How did we deal with the WNV outbreak

A

The WNV outbreak is a great example of a rapidly emergent agent but a succefful intervention
We were able to get WNV out of the blood bank system very quickly - we were on top of it very quickly

In 2002 USA had 23 transfused cases but in recent years we have had o

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33
Q

What kind of disease does WNV cause, comment on its mortality

A

80% of cases are asymptomatic
18-20% cause mild illness, fever, headache, malaise
1-2% cause encephalitis

In 2003 the CDC recorded 9862 cases in 46 states and 264 deaths

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34
Q

How do you remove WNV from a pack?

A

Low pH, high temperature and SD treatment
Hence why we use SD treated plasma and we test for WNV in summer moths so it wont be present in plasma or red cells
We dont do pathogen inactivation of platelets though

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35
Q

When do we test for WNV?

A

May to December testing

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36
Q

What three viruses are the future threat to TTI

A

St. Louis Encephalitis
Japanese Encephalitis
Dengue virus

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37
Q

Talk about Dengue virus

A

The most common insect spread virus in the world
Used to be killed by DTT pesticides in the 1950s however these caused a lot of childhood deformities so their use was stopped
Were now seeing a resergence in numbers -> 50x more cases in US from 1980 to 1999
Migration from south america into southern states has resulted in more serious infections etc

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38
Q

Comment on the prevalence and mortality of JEV

A

33% mortality
20-50,000 cases per year in china

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39
Q

Talk about SARS in transfusion

A

Both SARS and Covid arent transfusion related
Would have been a problem as we found covid in packs

40
Q

Why are we concerned with flaviviruses

A

As their vectors, mosquitos are starting to move into Europe
Now were wondering if we need to srart viral inctivation

41
Q

Talk about Ebstein Barr Virus

A

EB virus also known as HHV 4 is a herpes like C<V virus endemic
It causes infectious mononucleosis/glandular fever
90% of donors have antibodies against it which can coesxist with latent virus -> you can have it but never have an infection -> can become dormant and can flare up
Transfusion transmission is rare -> usually very sick if you have it
Questionnarie deferral

42
Q

Talk about parvo virus

A

Small single stranded DNA non enveloped virus
It doesnt cause chronic infection and is resolved in 1-2 weeks
It dosnt cause serious infection, most people have had it and cleared it, most have antibodies against it
Causes fifth disease in children
One of the most commom reasons for IUT can cause aplasia and anaemia in unborn babies

43
Q

Talk about Parvo virus in blood products

A

Rarely transmitted in blood products as donor or recipient will usually have antibodies against it

Since its a non-envloped virus its not affected by SD treatment

if you pool plasma and on unit is positive then the antibodies in al 999 others will subdue the singular positive

44
Q

When was parvo virus first detected in blood products?

A

First detected while testing for HBsAg in Australia
-> P antigen receptor in cells

45
Q

Talk about parvo in children

A

Causes fifth disease in children
Red rashed cheeks
Usually cleared in a couple of weeks

46
Q

Talk about Parvo in pregnancy

A

In pregnancy it can effect erythrocyte progenitor cells and cause aplasia in the unborn
This causes a problematic anaemia
One of the most common causes of IUT
Risk of foetal loss is about 10% if infection occurs before week 20 of gestation

47
Q

Talk about parvovirus B19

A

Non-envelope viruses
Resistant to chemical and physical inactivation
Targets red cell progenitors, replicates within them, causing a variety of haemolytic crises, especailly in the young

48
Q

Talk about the prevalence of Parvo B19

A

High prevalence - up to 90% have had it, anti-B19
Many never know thy have it
Most of us clear it without any problems

49
Q

How do we prevent parvo B19 being transmissed?

A

We rely on the fact that your not sick when you donate
But we dont test for it or do viral inactivation of plate;et etc
Assumption that antibodies in pooled plasma overpower etc

50
Q

How does prion disease occur

A

Human tissue contains prion protein PrP
Natural cellular form PrPc or as a variant pathological form PrPsc (scrapie isoforms)
Both forms have identical amino acid sequence but differ in secondary structure
The pathological form is able to change other normal proteins to the abnormal aggregates that cause spongiform degeneration in the brain

51
Q

When was prion disease first noted

A

discoved in tribes in papa new guinea
Cooru disease - Males would drink the ashes of those whove died -> caused similar disease to VcJD

This caused initial confusion as whatever was causing the disease wasnt destroyed through cremation

52
Q

What are prions, how do they become diseased

A

Background/filler proteins in cells
They normally form globular structures -> which stuff can move around normally

They can develop into abnormal structure, beta sheets which form filaments

Thes filaments damage the cells

The cells then atrophy and die

53
Q

Where did vcjd originate

A

Variant form of pions fund in sheep and deer -> known as scrapey as it caused these animals to start scraping the group before going mad

sprad to humans when cattle were fed sheep meat - mad cow disease -> disease didnt occur when humans ate the affected sheep but only when affected cow was eaten -> prions werent close enough to our prions

Takes like 2 years to develop symptoms
Evidence of familial spead - eating same food but not transfused

54
Q

What does cjd stand for

A

Creutzfeldt-Jakob disease

55
Q

How was CJD spread, how long to develop symptoms etc

A

Sporadic
Familial
Not transmitted by blood transfusion

Acquired:
- growth hormones, dura mater graphs, corneal grafts
- can take 60 years to develop symptoms
- can cause memory loss and confusion

56
Q

Talk about vCJD in humans

A

Started with Bovine spongeform E
It then crossed the species barrier to cause vCJD in humans
It affects younger people
Peaked in 1996 last case reported in 2004 - releastically anyone living in UK during this time who had eaten beef will have prions
PrPsc has been found in tonsils, spleen, lymph nodes and appendix
Not everyone will develop the disease - certain muatations are more likely to develop cjD -> certain types tend to lend to switching
Mutation at 129

57
Q

How do we test for vCJD?

A

There is no blood test available
We use a sickical amplification assay but this requires a tissue
No test in BT for it

58
Q

Talk about the first transmissed vCJD case in the UK

A

1st patient was 62 years old -> he recieved 5 units in 2000
6.5 years later he became irritable and depressed
13 months later he died

One of his initial donors was aged 24 died 3 years 4months later of vCJD

There has been 4 cases in the UK of suspected transfusion related vCJD

59
Q

How have we prevented vCJD

A

We initially thought it was in leucocytes but we were wrong -> it is only in 3%
Hence why we introduced LD
But now we know 68% of CJD is found in plasma

NB:Hence we introduced ligand filtered plasma which binds any prions

60
Q

What has recent research on VJCD revealed?

A

New research looked at tonsils of people who had died and found that there was actally a high prevalence of the disease

However some people were more susceptible than others ie. wasnt the cause of death

=> its present in the community but its not causing infections - indicating vCJD carrier status

Only recently we allowed people who lived in the UK to donate again

61
Q

What is the vjd filter called?

A

P-Capt filter

62
Q

How does the P-Capt filter work

A

Use of affinity resin
Resin coated in ligands for prions
Red cells wont bind but prions will
This removes all detectable infectivity from plasma products

63
Q

What technolog is incorporated into P-Capt filter

A

PRDT
Pathogen Removal and Diagnostic Technologies

64
Q

Talk about bacterial contamination of products

A

Bacteria are usually prevented from growing due to antibacterial properties of blood

Complement attaches to bacteria and are phagocytosed by white cells during storage

However platelet contamination is common -> way more common then red cells

Autologous blood contamination can also occur

Can be endogenous or exogenous

65
Q

What is one way of preventing bacterial contamination thats suggested but not recommended?

A

Adding antibiotics to blood

66
Q

Currently how do we prevent bacterial contamintion

A

Clean the site of donation thoroughly
Divert first few mls of blood
Store blood at room temperature for 24 hours after donation as this allows wbcs to be active at 22 degrees and kill any bacteria that may be present
Store blood at 4 degrees to prevent growth

67
Q

How frequent is bacterial transfusion transmitted infections?

A

There was 97 suspected bacterial TTI investigations reported to SHOT in 2018

Only one was a probable S. epidermidis

68
Q

what is the rate of SAR to bacterial contamination of red cells?

A

1:500,000

69
Q

What bacteria are most likely to contaminate products

A

Red cells: P. fluorescens (26.5%), Psuedomonas putida (4.1%), Yersinia enterocolitica (51%), treponema pallidum (4.1%)

Yersinia contaminated 51% -> grows well at 4 degrees, uses citrate as a source of energy and requires iron -> thus red cells are ideal growth medium

Psuedomonas is also capable of growing in cold temperatures

70
Q

How would a contaminated blood pack look?

A

RC looks unhealthy very quickly
Blood will congeal
White spots in back etc

71
Q

Talk about yersinia infected blood packs

A

Yersinia has caused fatal reactions
Live beacteria can survive in leucocytes

72
Q

What bacteria most commonly infect platelets

A

Staphylococcus epidermidis (25%)
Salmonella cholerasuis (13.5%)
Serratia marescens (9.6%)
Stapylococcus aureus (5.8%)
Bacillus cereus (5.8%)
Streptococcus viridans group (3.5%)
Other species (36.5)

NB: staph, strep, serratia, flavobacteria

73
Q

Talk about platelet contamination rates

A

Rate of SAR to bacterial contamination of platelets 1:5000

Due to storage at 22 degrees

74
Q

How do we prevent platelet contamination

A

BacT for all platelets

75
Q

Talk about malaria contamination of products

A

Any product that contains red cells can transmit malaria
Malaria can survive in stored blood 1 week and longer but then it dies in the pack

76
Q

Talk abou the prevalence of malaria

A

300 million cases of infection per year
More than 1 million fatalities per year

Frequency of transmission of 0.2 per million in the US -> 3 cases per year -> especially in southern states

77
Q

How do we test for malaria

A

ELISA testing as microscopy sens is poor

we also defer

78
Q

What is chagas disease

A

Trypanosoma Cruzi
Endemic to Latin America
Used to be associated with mud huts but now endemic to urban areas
50-90% recover on their own with no sequelae -> no condition associated
Once infected an individual generaly remains infected for life

79
Q

Talk about the prevalence of chagas disease

A

8 to 11 million people in Mexico, Central America and South America have Chagas disease, most of whom do not know they are infeced

its not an uncommon disease
Seen in USA an spain
Just hasnt been a problem yet in Ireland
Only transmissed in America

80
Q

How do we avoid transmission of Chagas disease

A

We defer -> any one from south America
Never take blood from those from Bolivia where 68% of people are ELISA positive

125mls of Gentian/crystal vioelt can be added to packs

81
Q

What are some examples of emerging infections?

A

HIV and vCJD -> previously unknown diseases that emerged

Inluenza - change in microorganism

WNV, Chik V, malaia, Q fever, Dengue fever -> change in habitat with organism spreading to new area

XMRV -> identification that disease is caused by infection

Mycobacterium TB -> an old infection thats re-emerging

Chronic fatigue syndrome -> ME -> lasts for years -> thought to be caused b certain viruses but we dont knoww which ones -> will probably have a test for this in the future

82
Q

What are the two methods of heat inactivation of pathogens?

A

Dry heat at 80 degrees for 72 hours destroys HIV and hep

Pasteurisation also destroys these organisms

83
Q

Give an example of a virus not destroyed by heat treatment

A

Non enveloped viruses arent destroyed such as Parvovirus B19

84
Q

What does solvent detergent treatment involve?

A

Solvent = tri-(n-butyl) phosphate TNBP
Detergent = Triton X

85
Q

What is the issue with SD treatment

A

Non-enveloped viruses are not inactivated

Its currently used on plasma and coagulation factors and fibrinogen but theres still problems

86
Q

What is an alernative to SD treatment with TNBP?

A

Heating with n-heptane at 60 degrees for 20 hours
But this is also not effective on non-enveloped viruses

87
Q

What is an alternaive to SD treatmenet?

A

Methylene Blue treatment

88
Q

How does methylene blue treatment work?

A

MB is a virucidal agent with high affinity for viruses and nucleic acids

On exposure to light adjacent molecules are destroyed

89
Q

Give two examples of MB treatment

A

Intercept or mirosol (vitamin B6)

90
Q

What pathogen inactivation is being developed for rbcs?

A

s59 -> amotosalen
?????

91
Q

Intercept is available for what two products

A

Platelets and plasma but we dont do this

92
Q

How does Intercept work?

A

Works via covalent bond crosslinking

S-59 targets helican region of single-or double-stranded DNA or RNA

Intercalation

Crosslinking

Multiple crosslinks block strand separation and replication

93
Q

What protozoa are potentially transmissible through blood?

A

Plasmodium species (malaria)
Trypanosoma cruzi (Chagas disease)
Toxoplasma gondii (toxoplasmosis)
Babesia (microti/divergens) (babesiosis)
Leishmania species (Leishmaniasis)

94
Q

How do we prevent protozoal contamination of blood?

A

Mostly done by deferal -> no testing for these other than malaria

95
Q

What test could potentially be included in he IBTS in the next few years

A

Lyme disease screnning especially in those from the west of Ireland

96
Q

What are some issues with introducing a test in the IBTS

A

Screening test - sensitivity versus specificity
Confirmatory Tests
Mandatory testing or not
Donor counselling -> what do you do if positive
Acquisition of anti-viral Ig
Viral inactivation procedures
Surveillance
Donor look backs -> when you introduce a test are you going to go back and re test old samples etc

4.2 Blood Transfusion Science (18 decks)

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