Blood Safety: Current Risk and Emerging Infections

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Transcript Blood Safety: Current Risk and Emerging Infections

Weather Forecasting
Approach of Transfusion Services to
New Pathogen ( Emerging Infectious Agents )
Dr. R. N. Makroo
Director & Sr.Consultant
Dept. of Transfusion Medicine,Molecular Biology & Transplant Immunology
Indraprstha Apollo Hospitals
Introduction
• Over the past 10 to 15 years the leading
causes of allogeneic blood transfusionrelated morbidity and mortality have
shifted from being mainly due to
transfusion-transmitted infections (TTIs) to
the non-infectious events associated with
blood transfusions
Introduction
• Nonetheless, despite many advances in
the prevention of TTIs, TTIs continue to be
associated with on-going morbidity and
mortality.
• This is due to the emergence of new
pathogens (or re-emergence of known
pathogens) associated with TTIs.
Components of Blood Safety
• National and local
incidence/prevalence
• Criteria/Standards/
Guide-lines
• Selection of donor
population
•
Donor questioning
•
Laboratory testing
•
Product handling
•
Record keeping
•
cGMP/Quality
Outline
•
•
•
Status of blood donors
Current status of testing & risks
Emerging infections in Developed Vs Developing
countries
–
–
–
Background
Approach
Examples
•
VIRUSES, BACTERIAS, PRIONS,PARASITES, TICK BORN etc.
Emerging Infections
“Clinically distinct conditions
whose frequency in humans
has increased over the past
two decades”
Factors Contributing to
Emergence of Infectious Disease
•
•
•
•
Human demographics and behavior
Technology and industry
Economic development and land use
International travel and commerce
– Concept of global village
• Microbial adaptation and change
• Breakdown of public health measures
6
Days to Circumnavigate (
the Globe
350
5
300
4
250
200
3
150
2
100
50
1
0
0
1850
)
400
1900
1950
Year
World Population in billions (
)
Speed of Global Travel in Relation to
World Population Growth
2000
From: Murphy and Nathanson. Semin. Virol. 5, 87, 1994
Emerging Infections in Western
World
•
•
•
•
•
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New Agent
Expanding Range
Imported
Re-emergent
Newly recognized
Patient changes
– BSE/vCJD
– Babesia/Ehrlichia
– Chagas disease, WNV
– Malaria
– HHV-6, 8, TTV, SENV.
– CMV, B19?
NAT is performed on essentially all blood and plasma donations in the
United States
The decrease in risk over time for HIV, HCV, and HBV has
been truly dramatic.
Concern High,
Action Favored
HBV
vCJD
CJD
Ebola etc
Lyme
WNV
HCV
HIV
T.cruzi
HHV 8 Leishmania Babesia
B19
HAV
HHV 6
Malaria
Ehrlichia
Bacteria
HGV, etc
Chlamydia,
Leptospira
Bartonella, etc
RMSF
Benefit High
Action Favored
Blood is much safer, but is it safe enough?
All volunteer donors
25
HBsAg test
% Recipients Infected
20
15
AIDS high-risk exclusions
Anti-HIV test
10
ALT/HBcAb tests
Anti-HCV test
Improved
HCV tests
NAT
Implementation
5
0
1965
1970
Tobler and Busch, Clin Chem 1997.
1975
1980
1985
1990
1995
2000
Year of Transfusion
11
Infections in India: our problems
• HIV, HCV, HBV AND MALARIA: Major
problem to Blood safety
• NAT not Implemented to reduce the
incidence
Action Favored
HIV, HCV AND
HBV
New
Viruses
IS REALLY INDIA AT THE TOP IN BLOOD
SAFETY ???
NO
Very little concept of regular repeat V.B.D
Absence of Universal Hepatitis B core antibody Screening
WITH NO NAT
No Uniformity in the Blood Transfusion Services
ITS REALLY A LONG WAY TO GO
AND IT’S A STEEP HILL TO CLIMB
Indian Scenario
• BTS in India is mainly hospital based
• Blood Banking is governed by Drugs & Cosmetic Act
• 2609 licensed blood banks under different?? control
• Gap in demand and supply of blood
• Majority of blood donors are still replacement donors
• Voluntary donors constitute only 65% (NACO 2011)
• Majority of voluntary blood donors are first time donors
• Little concept of regular repeat voluntary blood donation
15
Challenges of Blood Screening in India
• Population ~1.2 billion includes 2.5 million with HIV, 15million with
HCV, and 43 million with HBV
• High blood donor seroprevalence of 0.3%,0.7%, and 1.4% for antiHIV-1, anti-HCV, and HBsAg, respectively increases transfusion
transmission risk of these viruses
• High percentage (~ 35%) of replacement donors compared to
volunteer donors
• 2609 ( 36%) government , (28%)private hospitals, (14%) NGO &
(21%)Stand alone private blood banks, many of which have poorly
regulated practices, collect about ~ 8 million donations annually.
• Currently nucleic acid testing (NAT) for screening is not mandatory
which would need to be adapted to our low volume setting
16
Threat to Safety of Blood Supply
• Current immunoassay blood screening tests detect
virus-induced antibodies or viral antigens, not the virus
itself – Window Period donations
• Window period between initial infection and detectable
seroconversion
• Chronic carrier state in asymptomatic donor - test
negative on antibody screen
• Atypical genetic variants of viruses
• Laboratory errors (very low: zero-0.05%, further
reduction by >1 assays)
17
Window Period
Window Period
Infection
HIV Ab Negative
HBsAg Negative
HCV Ab Negative
Detection by
Serology markers
18
Closing -the gap!
To enhance blood safety
• Implementation of new tests to narrow
down the window period
• Combining >1 assays - 2 assays
complement each other and decrease FP
and FN results
• Increasing regular repeat voluntary
donations (lower TTI incidence)
19
Why ID-NAT is preferred over Minipool?
High prevalence countries – Greater number of reactives
Low Regular Repeat Voluntary Donors – Higher
percentage of reactives
• Pooling results in a dilution of viremic samples
proportionate to the pool size
• MP-Reduces sensitivity. Release of infected units.
• MP requires additional process time, equipment,
manpower, lab space & environment for pooling and
resolution of positive pool.
• High prevalence countries have higher number of pools
reactive. Delayed release of negative blood units from a
positive pool. 1-2 days delay.
• Higher contamination and error chance.
•
•
20
In Asia: Why ID NAT
• Dr. J. P. Allain from Cambridge University- Global
Expert on Hepatitis B in Blood Transfusions quotes:
• Study with 143 samples from South East Asia showed:
• 70.7% of these would be missed in pools of 6 and
87.5% in pools of 10 assuming a sensitivity of 5 IU per
ml
• 37% of the donors had less than 5 IU/ml, and over
40% had between 5 and 30 IU/mL
• Additionally in India the predominant HBV is of
genotype D which is characterized by low viral load
with 10% having undetectable HBV DNA.
21
Why Nucleic Acid Testing? Reduction of Window
Period
Busch MP et al. Transfusion 2005;45:254-264, Assal A et al. Transfusion 2009;49:289-300,
Weusten J et al, Transfusion 2011;51:203-15
22
HIV-1 Minipool NAT Failures
Dwyre et al, Vox Sang 2011
23
HBV detection superiority with ID-NAT
Dwyre et al, Vox Sang 2011
24
TMA HCV superiority sensitivity
Sarrazin et al, Journal of Clinical
Virology 2002
Comandor et al, Am J
Gastroenterology 2001
20120919
Dr. Makroo Novartis Symposia
25
HCV Reactivity (April, 2006 – March 2012)
Profile of 7 HCV NAT Yields Total tested: 117,622
Need for NAT and IDT NAT
•0.39% (458) Sero prevalence for anti-HCV.
•0.17% (191) concordant Sero and NAT positives
•7 HCV NAT only yields1 , *4 Co-infections: HCV + HBV (ELISA HBV only)
•267 Serology yields - High false positivity of HCV ab tests2 - Need for NAT
S/N
1
2
3
4
5
6
7
Ultrio Discrim Assay
Reactive
HCV
HCV
HCV
HCV
HCV
HCV
HCV
Serology*
Non Reactive
Non Reactive
HBsAg
Anti HBc, Total
Anti HBc, total
Anti HBc, Total
Non Reactive
Viral Load IU/ml
56
52
97
58
62
99
53
• The low viral load of 52-99 IU/mL indicates the requirement of ID-NAT testing
1. Makroo RN,Chowdhry M,Minimole, Rosamma NL & Thakur U. Six years Experience on Impact of Individual Donor Nucleic Acid
Testing for Hepatitis C Viral RNA at a Tertiary Care Hospital of North India. 65th Annual AABB meeting Oct 6-9 Boston MA
2. Raghuraman et al. Occurrence of False Positives during Testing for Antibodies to Hepatitis C Virus among Volunteer Blood Donors in India,” J
.Clin. Microbiol. 2003; 41:1788-1790.
26
HBV Reactivity (April, 2006 – March 2012)
Total tested: 94,247 recalculate numbers
Profile of HBsAg, anti HBc and HBV DNA1
HBsAg ELISA
Anti HBc ELISA
Number
Percentage
HBV DNA- Percentage (Number)
Positive
Non reactive
156
0.16
Positive
Reactive
978
1.03
Negative
Reactive
8660
9.19
Negative
Reactive
0.007(#9) Occult NAT yields*
Negative
Non Reactive
0.006 (#8) WP NAT yields*
Positive
??
Positive
??
0.15 (#13)
0.75 (#887) Serology NAT*
concordants
0.37 (# 442) Sero yields*
• Presence of HBV DNA is indicative of infectivity
•99.85% of anti HBc reactive are negative by Procleix Ultrio HBV assay
•Very high attrition of donations if excluded for anti HBc at 9.19% positivity
27
ID-NAT YIELDS
RN Makroo et al. Indian J Med Res
127, February 2008, pp 140-147
Multicenter evaluation of individual donor nucleic acid testing (NAT) for simultaneous detection of
human immunodeficiency virus -1 & hepatitis B & C viruses in Indian blood donors
28
ID NAT Yield: 1 in 1500
67 in 100,000 donations
6700 infected donors per 10 million donations
Each donor infects 3 patients
6700 X 3 =
app. 20000 infections per 10 million donations
Annual cost of medical management
1.5-2.5 lacs/pt
= app. INR 400 crores annual expenditure
Cost of liver transplant = 20-25 lacs/pt + 10,000/month
If 2000 patients undergo LT/ yr
= app. INR 500 crores annual expenditure
= app. Cost for doing 10 million ID-NAT = 800 x 10 million
= INR 800 crores
29
30
NAT and Hepatitis
• Most transfusion-transmitted infections are caused by blood
donated during the early sero-negative window period, and
for HBV also during Occult status.
• Direct detection of viral nucleic acids by using the NAT
technologies significantly improves the blood safety by
shortening the window period and detecting occult cases.
• Since 1999, all developed and increasing number of
developing countries around the world have adopted routine
NAT blood screening. Countries have moved to ID-NAT
after including HBV.
• NAT on individual donations (ID NAT) provide the highest
level of safety to the blood supply.
31
HTLV-1 & 2
•
•
•
•
•
•
•
•
HTLV-I identified in 1978 in a Japanese patient.
Causes adult T-cell leukemia and lymphoma (ATL) and tropical spastic
paraparesis (TSP) also known as HTLV-I-associated myelopathy or HAM.
Prevalent globally but is endemic in Japan, the Caribbean, South
America, and West and Central Africa, where infection rates are above 1%.
HTLV-II identified in 1982 in a patient with hairy-cell leukemia
HTLV-II is found in American Indian populations and in some populations of
intravenous drug users
The overall incidence in first-time donors in the United States is around 40 per
100,000. In repeat donors a rate of approximately 1.6 per 100,000 person
years was identified from 1991 to 1996 Rossi’s principle of Transfusion Medicine. 4th Ed
In India its prevalence was found to be 0.18% and was concluded that
prevalence of HTLV-I/II carriers in India seems to be negligible and is not
a major public health hazard. Hence, routine screening of Indian blood
donors for antibody to HTLV-I/II is not warranted due to its low
prevalence.
Kumar H, Gupta PK. Is seroprevalence of HTLV-I/II among blood donors in India
relevant? Indian J Pathol Microbiol. 2006 Oct;49(4):532-4.
32
Malaria
•
Caused by plasmodium species
–
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•
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P. Falciparum: IP is 12 days, 40-60% malaria cases worldwide, >95% of all malarial deaths
P. vivax: 30-40% malaria cases, rarely fatal
P. ovale: West Afica
Others: P. malariae and P. knowlesi
Transmitted by : female anopheles mousquito
Transmitted by cellular blood components: whole blood or PRC or by
components contaminated with red cells
At 2-8 o C : P falciparum can survive for 2-3 weeks
Post transfusion malaria (PTM): severe disease in pregnant women and
immuno deficient individuals
33
Malaria
• Detection
–
–
–
–
–
Microscopic: blood films – gold standard
Macroscopic
Tests for malaria Ab: EIA, indirect immunofluoresence, western blot
Tests for malaria Ag: RIA, EIA
Tests for metabolic products: LDH ( all species) and HRP-2 (
falciparum)- method of choice for screening of blood donors
– Other : nucleic acid based tests and immunofluorscence for
detection of plasmodia within the erythrocytes
• Prevalence of Malaria at our centre in 2011: 0.019%
34
Cytomegalovirus
•
It is a herpes virus; sub-family: betaherpesvirinae
•
Incubation period: 4-8 weeks
•
Also known as HHV-5
•
CMV can manifest itself in many organs.
•
Therefore, CMV is a major problem in immuno-suppressed patients requiring
transfusion therapy.
•
95% of blood donors in India are sero positive for CMV
35
95% of blood donors in India are sero positive for CMV
36
Cytomegalovirus
• Patients who should receive components that are selected
or processed to minimize the risk of CMV infectivity include
the following:
–
–
–
–
–
Transplant recipients ( CMV negative)
Patients with severe immunodeficiency
Fetus (intrauterine transfusion)
CMV-negative pregnant females
Low birth weight premature infants and neonates
• It is essential for all blood banks to maintain a list of CMV
negative donors
• Leukoreduced blood (<5 X 106 Leukocytes) = CMV negative
blood
37
Cytomegalovirus
•
Donor testing
–
–
–
–
–
ELISA ( IgM or IgG or IgM + IgG )
Complement fixation test
Heamagglutination
Western blot
PCR based assays
38
Rossi’s principles of Transfusion Medicine,
4th
ed
Trypanosomiasis (Chaga’s disease)
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•
•
Causative Agent : Trypanosoma cruzi
Transmitted by triatomines or reduviid bugs (kissing bugs)
Acute phase lasts 4 to 6 weeks, characterized by mild symptoms such as fever,
malaise, and edema of the face, as well as lymphadenopathy and
hepatosplenomegaly.
The fatality rate in the acute phase is usually less than 5%.
Up to decades later, 15% to 30% of carriers will develop serious sequelae
involving the heart and gastrointestinal tract (mega-colon and megaesophagus).
Chagas’ disease kills an estimated 13,000 people annually, mostly from
cardiac complications. Barrett MP, Burchmore RJS, Stich A, et al. The trypanosomiases. Lancet 2003;362:1469-80
In India infections caused by T. evansi have been reported from
Maharastra India. Joshi PP et al Am. J. Trop. Med. Hyg., 73(3), 2005, pp. 491–495
Screening test: ELISA
Confirmatory testing :RIPA (not FDA approved)
Other methods: donor exclusion and pathogen inactivation
39
T. Cruzi in blood units
• Are platelets of greatest risk?
• few platelet units in look-backs
• transfusion cases: almost all involved
platelets
• survival and localization studies:
whole unit
platelets
red cells
plasma
< 7 days
< 4 days
< 2 days
none
Transfusion Transmitted Leptospirosis
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•
•
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•
•
Causative agent: Leptospira interrogans
Incubation period : 2-21 days
Endemic in : Maharashtra, West Bengal, Orissa, Gujarat, Tamil Nadu &
Andaman islands
Spreads by direct or indirect contact with urine of infected animals
Symptoms: influenza like illness
80% clear infection spontaneously, 10% suffer from complications while it is
fatal in another 10%
Methods of detection
– Dark field microscopy
– culture
– Detection of IgM antibody
– PCR based assays
41
Transfusion Transmitted Leptospirosis
Results
Of 794 DFM positive samples, 155 were
cultured on liquid EMJH medium.
42
Brucellosis
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•
•
•
•
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Causative agent: B. melitensis, B. suis and B. abortus
Zoonotic infection transmitted to humans primarily by consumption of
unpasteurized milk and milk products
Common presenting symptom are fever, fatigue, malaise, chills, sweats,
headaches, myalgia, arthralgia, and weight loss
Widespread in rural india
Transfusion transmitted brucellosis: severe infection in immuno supressed,
neonates and pregnant females
Diagnostic methods
–
–
–
–
Blood cultures
Antigen detection by ELISA
Antibody detection: IgM and IgG
Agllutination : Rose Bengal Plate agg. (RBPT )and standard tube agg test (SAT) for screening
purposes
It is suggested that, in areas endemic for brucellosis, blood donors should be questioned about symptoms
of brucellosis, and if suspected, serological tests for brucellosis should be indicated before blood
transfusion. At the same time, the prevalence of the disease among animals should be reduced with
effective animal disease control programs.
Akçakus M et al. Brucella melitensis in blood cultures of two newborns due to exchange transfusion.Turk J Pediatr. 2005 JulSep;47(3):272-4.
43
Creutzfeldt- Jakob disease (CJD)
•
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It is transmissible spongiform encephalopathies (TSEs), comprise a spectrum
of diseases in animals and humans.
In animals, these diseases include scrapie in sheep and goats, chronic wasting
disease in deer and elk, and transmissible mink encephalopathy.
Bovine spongiform encephalopathy (BSE) was first described in cattle in the
United Kingdom (UK)
In humans it causes fatal progressive dementia and motor disturbances
Iatrogenic transmission of sporadic CJD has occurred via neurosurgical
instrumentation and electroencephalogram (EEG) electrodes, corneal and dura
mater grafts, and cadaveric pituitary-derived growth and follicular stimulating
hormones.
Blood transfusion results in Variant CJD (vCJD), first described in 1996.
44
National CJD Surveillance Unit. CJD statistics Edinburgh, UK: NCJDSU, 2008. [Available at http://www.cjd.ed.ac.uk/fi gures.htm
(May 16, 2008).]
Creutzfeldt- Jakob disease (CJD)
•
Pathogenesis
– presence of abnormal prion protein (PrPTSE) within the central nervous system and
also in the follicular dendritic cells of peripheral lymphoid tissues including tonsils,
spleen, lymph nodes, and gut-associated lymphoid tissue
•
Donor screening methods
– Permanent deferral of donors
• family history of CJD
• Recipients of growth hormone and FSH of human origin
• Recipients of human dura matter and corneal grafts
• Permanent residents of U.K.
– Detection of PRPTSE peripheral blood
• Immunoblotting with proteinase K digestion and gel electrophoresis has been
enhanced using phosphotungstic acid precipitation and chemiluminescence
• Capillary immunoelectrophoresis following proteinase K digestion and
competitive antibody binding
45
Whole Blood
Distribution of TSE Infectivity
in Blood Components
Plasma
25 - 30%
Buffy Coat 35 - 45%
RBC
20 - 25%
Newer viruses: Dengue
•
Dengue is one of the most serious mosquito borne viral disease of humans.
•
Transmitted by : Aedes mosquito
•
Estimated number of Dengue cases per annum worldwide :50–100 million
Historical background
•
Estimated number of severe forms of the disease: 500.000 (0.5% a 1%)
•
Dengue like illness date back to more than 200 years ago
•
1779-1780 in Asia, Africa and North America
•
Viral etiology established by the 1940s
•
Global pandemic in Southeast Asia after World War II
47
Dengue : the virus
•
•
•
•
There are 4 distinct serotypes: DENV-1, DENV-2, DENV-3, DENV-4
Family: Flaviviridae; Genus: Flavivirus
All serotypes produce a similar illness and induce a life-long immunity that is
specific to the infecting serotype.
However, although the four serotypes are related, the humoral immune
response does not provide cross protective immunity against each other.
Transmission by Blood Transfusion
•In the 2001 one case of dengue transmission through bone marrow transplantation in
Puerto Rico
•In 2002 1 case transmitted by red blood cell transfusion were reported in Hong Kong.
•In both cases, donors made their donation during the viremic period but 1 to 2 days
before the onset of symptoms.
•Later they developed classical dengue disease.
48
A 52-year-old, asymptomatic, repeat blood donor gave blood on July 15, 2007.
An investigation of all recipients of his blood products was initiated after he
informed the blood bank that he had had a fever the day after donation. The
stored serum sample was positive for dengue virus type 2, as ascertained by
means of a polymerase-chain-reaction (PCR) assay.
Tambyah et al. Dengue Hemorrhagic Fever Transmitted by Blood Transfusion N Engl J Med 2008; 359:1526-1527
(National University of Singapore, Singapore 119074, Singapore)
Prevalent from centuries
Highly prevalent now49
Is there any impact of Dengue Epidemic on transfusion ?
•
Do not have a precise information on the percentage of individuals who is
asymptomatic during a given epidemic.
• Literature reports provide estimates from 30% to 70% of asymptomatic
individual at an epidemic.
• Also largely unknown is the level and length of viremic period among
asymptomatic individuals.
• It is obvious that a short and low level viremia will have a moderate impact on
the risk of dengue transmission by transfusion.
Therefore, The asymptomatic carriers may act as a source of platelets to the
symptomatic patients !
50
West Nile Virus
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Causative agent: a flavivirus, first recognized in 1937
Wide distribution: in Africa, Europe, Asia, Australia, and, in the past decade, in
Northern America.
WNV mainly infects birds and is normally transmitted by mosquito (Aedes)
The incubation period is between 3 and 15 days in humans
80% of infections being asymptomatic or with a mild flu-like illness. In rare
cases (fewer than 1% of those infected), a more severe disease results and
fatal encephalitis can occur.
Asking donors about pre-donation headache and fever was found to have no
effect on blood safety. (Orton SL et al. Self-reported symptoms associated with West Nile virus infection in RNApositive blood donors.Transfusion 2006;46:272-7).
•
•
•
The risk of transfusion transmission is associated with a period of viremia
occurring around 3 days after infection and lasting around a week.
Since July 2003, the US and Canadian blood supply has been screened using
WNV NAT
Both minipool and ID-NAT assays are available.
51
TT virus, SEN V, GBV-C/HGV
•
TT Virus
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–
–
–
–
•
SEN V
–
–
–
–
•
DNA unenveloped , non hepatotropic virus
named for the patient from whom it was first isolated in Japan
Genus Circoviridae.
Transmitted by orofecal and transfusion route
Transfusion route is not significant in TTV epidemiology
SENV is not 1 virus but rather 8 diverse strains;
2 of these strains (SENV-D and SENV-H): causes of transfusion-associated non-A–E hepatitis
SENV is clearly transmitted by Transfusion
Although SENV is clearly transmitted by transfusion, these data are insufficient to establish a
causal relationship between SEN V and TAH
GBV-C/HGV
–
–
–
–
Enveloped RNA virus
Virus genome similar to HCV
Transmitted through blood transfusion
High Risk groups:
• IV drug abusers
• Hemodialysis patients
• Multiple transfused patients
52
Bacterial contamination of blood
products
Popular organisms
RBC
•Y Enterocolitica
•Pseudomonas
•E. coli
•Klebsiella
•Proteus
•Propionibacterium
•Serratia sp
•Coag neg
staphylococcus
•Staph aureus
•streptococcus
Platelets
•Staph Epidermidis
•Bacillus sp
•Staph aureus
•Micrococcus
•Diphtheroids
Bacterial contamination of platelets
is specially problematic as they
are stored at RT
53
Sources of contamination
•
Donor bacteremia
•
Phlebotomy core
•
Skin surface contaminants
•
Containers and disposables
•
Environment
54
Comparison of Residual Risks
1:100
Transmission risk,
per unit
HIV
1:1000
Bacterial
Contamination
(platelets)
Clinical
Sepsis
(platelets)
HBV
1:10 000
HCV
Septic 1:100 000
Fatalities
(platelets)
1:1 000 000
1984
1986
1988
1990
Updated from: Goodnough LT e t al. NEJM 1999;341:126-7
1992
1994
1996
1998
2000
2002
Avoidance
eliminate
Bacterial
contamination
Contain/
inhibit
detect
56
Avoidance
•
•
•
•
•
Donor deferral
Skin decontamination before phlebotomy
Diversion of first 15 ml of blood
Closed system of component preparation
Apheresis products
57
Contain/
inhibit
• Storage time
– 24 hour hold
• Storage temperature
– Cool liquid stored platelets
– Frozen platelets
58
• Visual inspection
detect
– Discoloration
– Clumping
– Loss of swirling
• Biochemical parameters
– Platelet pH
– Glucose consumption
– Limulus amebocyte lysate assay
(yersinia endotoxin)
• Microscopy
– Gram stain
– Acridine orange
59
• Culture (gold standard)
detect
– BacT/Alert : CO2 production
– Pall BDS : O2 production
• Rapid tests
– Verax PGD
• Others
– PCR
– Chemiluminesence based
universal bacterial rRNA probe
60
eliminate
• Pathogen reduction technology
• Room temperature hold
• Filtration
61
STRATEGIES TO PREVENT INFECTION
Tracebility
Hemovigilance
Indications for transfusion
Storage
Pathogen inactivation
Screening tests
Processing quality control
Donor eligibility
Summary
•
Emerging infections may impact blood safety
•
Continuing, structured review of field needed
•
Risk assessment is performed as required
•
Selected agents are further evaluated in the field and the laboratory
•
Interventions: testing, interview, call-back
•
Partnerships with industry, public health agencies
63
The Road Ahead
 Commitment of blood banking
community to provide safe blood.
 Active involvement of health economists
keeping in mind that good quality costs.
64
BLOOD IS A PRICELESS
GIFT.....
.....but the final product costs !!
65
THANK YOU
Lets keep these unexpected
passengers out