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[Immunohematology] Lec > [26] CHAPTER XI LESSON 1 > Flashcards

[26] CHAPTER XI LESSON 1 Flashcards

1
Q

is performed for hepatitis B surface antigen (HBsAg), antibody to hepatitis B core antigen (anti-HBc), antibody to hepatitis C virus (anti-HCV), antibodies to human immunodeficiency virus (anti-HIV 1/2), antibody to human T-cell lymphotropic virus types I and II (anti-HTLV-I/II), and syphilis.

A

Serologic testing

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2
Q

Each donor must also be tested at least once for antibodies to

A

Trypanosoma cruzi.

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3
Q

Required nucleic acid testing (NAT) is performed for:

A

HBV DNA, HIV-I RNA, HCV RNA, WNV RNA, and ZIKV RNA

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4
Q

Hepatitis is a generic term describing inflammation of the liver.

A
  1. Transfusion-Associated Hepatitis
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5
Q

Symptoms typically include jaundice, dark urine, hepatomegaly, anorexia, malaise, fever, nausea, abdominal pain, and vomiting.

A
  1. Transfusion-Associated Hepatitis
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6
Q

The clinical symptoms of hepatitis range from being asymptomatic to death.

A
  1. Transfusion-Associated Hepatitis
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7
Q

Hepatitis A virus (HAV) and hepatitis E virus (HEV) are mainly transmitted through the fecal/oral route.

A
  1. Transfusion-Associated Hepatitis
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8
Q

are primarily transmitted parenterally.

A

Hepatitis B virus (HBV), hepatitis C virus (HCV), hepatitis D virus (HDV), and hepatitis G virus (GBV-C or HGV)

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9
Q

HBsAg, IgM, and IgG antibody to HBc, HBV DNA

A

Hepatitis B

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10
Q

IgG antibody to HCV, HCV RNA

A

Hepatitis C

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11
Q

IgM and IgG antibody to HIV-1/2, HIV-1 RNA

A

HIV

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12
Q

IgG antibody to HTLV-I/II

A

HTLV

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13
Q

IgG or IgM antibody to T. pallidum antigens or nontreponemal serologic test for syphilis

A

Syphilis

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14
Q

WNV RNA

A

West Nile Virus

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15
Q

IgG antibody to T. cruzi (one-time testing)

A

Trypanosoma cruzi

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16
Q

ZIKV RNA

A

Zika virus

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17
Q

belongs to the Picornaviridae family of viruses and is a small, nonenveloped, single stranded RNA enterovirus.

A

Hepatitis A

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18
Q
  • Symptoms appear abruptly and last fewer than 2 months, but may persist for as long as 6 months in some individuals.
A

Hepatitis A

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19
Q
  • They may include nausea, vomiting, anorexia, fatigue, fever, jaundice, dark urine, and abdominal discomfort
A

Hepatitis A

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20
Q
  • Symptoms usually resolve within 3 weeks and are generally self-limiting.
A

Hepatitis A

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21
Q
  • Transmission is primarily through the fecal-oral route spread through water, food, and person-to-person contact.
A

Hepatitis A

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22
Q

Poor hygiene and poor sanitation contribute to the spread of HAV.

A

Hepatitis A

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23
Q

Because young children are generally asymptomatic, the disease is predominantly spread from person to person within the household.

A

Hepatitis A

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24
Q
  • The incubation period for HAV is 28 days on average, and the peak viremic period occurs 2 weeks before the onset of the elevation of liver enzymes or the appearance of jaundice.
A

Hepatitis A

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25
Q
  • The presence of IgM antiHAV antibody is required for diagnosis of hepatitis A.
A

Hepatitis A

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26
Q
  • IgG antibodies to HAV appear soon after IgM and may persist for years after the infection.
A

Hepatitis A

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27
Q

IgM antibodies are detectable at or prior to the onset of clinical illness and decline in 3 to 6 months.

A

Hepatitis A

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28
Q

Vaccination- The vaccine is produced from inactivated HAV

A

Hepatitis A

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29
Q
  • Immune globulin- can be used preexposure to protect those traveling to high HAVendemic areas or postexposure to prevent infection in those exposed within a family, after an outbreak at a day-care center, or from a common source of exposure such as a restaurant.
A

Hepatitis A

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30
Q
  • Other prevention methods include improvement in water purification, good hygiene, and improved sanitation
A

Hepatitis A

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31
Q

is a partially double-stranded circular DNA virus of the Hepadnaviridae family.

A

Hepatitis B

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32
Q
  • The individual may be completely asymptomatic or may present with typical signs of disease, including jaundice, dark urine, hepatomegaly, anorexia, malaise, fever, nausea, abdominal pain, and vomiting.
A

Hepatitis B

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33
Q

is transmitted through exposure to bodily fluids containing the virus from an infected individual.

A

Hepatitis B

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34
Q
  • Transmission may be sexual, parenteral, or perinatal.
A

Hepatitis B

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35
Q
  • A surface antigen protein, HBsAg, is on the outer envelope of the virus.
A

Hepatitis B

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36
Q
  • Antibodies can be produced to two proteins within the core: hepatitis B core antigen (HBcAg) and hepatitis B envelope antigen (HBeAg).
A

Hepatitis B

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37
Q
  • Hepatitis B vaccination
A

Hepatitis B

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38
Q
  • Hepatitis B immune globulin (HBIG)- injections and the vaccine given soon after exposure or within 12 hours of birth, if the mother is infected, may prevent infection.
A

Hepatitis B

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39
Q
  • Chronic infections are associated with cirrhosis and liver cancer.
A

Hepatitis B

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40
Q
  • Percutaneous transmission may occur through needle stick (drug use, occupational hazard, acupuncture, tattooing, or body piercing), hemodialysis, human bite, transfusion of unscreened blood or blood products, or sharing razors.
A

Hepatitis B

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41
Q
  • Permucosal transmission can occur through sexual intercourse or vertically from mother to infant (transplacental or through breast milk).
A

Hepatitis B

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42
Q

is the first marker to appear and can be detected by polymerase chain reaction (PCR) testing before HBsAg reaches detectable levels.

A
  • HBV DNA
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43
Q

is detectable 2 to 12 weeks postexposure during the acute stage and becomes undetectable in 12 to 20 weeks after development of anti-HBsAg.

A
  • HBsAg
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44
Q

appears after the HBsAg and, in recovering patients, disappears before HBsAg.

A
  • HBeAg
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45
Q

is present in the serum but is undetectable. However, IgM anti-HBc is the first antibody to appear, and it persists for about 6 months. Appearance of this antibody indicates current or recent acute infection.

A
  • HBcAg
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46
Q
  • Three other treatments licensed by the FDA are interferon (IFN)- α-2b, lamivudine, and adefovir dipivoxil.
A

Hepatitis B

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47
Q
  • The incubation period of HCV is 2 to 26 weeks.
A

Hepatitis C

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48
Q

can be transmitted percutaneously through needle stick, hemodialysis, human bite, transplant or transfusion, or by acupuncture, tattooing, or body piercing.

A

Hepatitis C

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49
Q
  • Diagnosis depends on biochemical changes suggestive of HCV, detection of HCV RNA or anti-HCV in serum, or a known exposure to the virus.
A

Hepatitis C

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50
Q
  • Currently there is no vaccine.
A

Hepatitis C

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51
Q

is a member of the Flaviviridae virus family and is caused by a virus with an RNA genome

A

Hepatitis C

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52
Q

is a member of the Flaviviridae virus family and is caused by a virus with an RNA genome

A

Hepatitis C

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53
Q

The average incubation period is 7 to 8 weeks, followed by seroconversion occurring in 8 to 9 weeks.

A

Hepatitis C

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54
Q

-Most HCV cases are asymptomatic.

A

Hepatitis C

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55
Q

Some cases report nonspecific symptoms such as anorexia, malaise, fatigue, or abdominal pain.

A

Hepatitis C

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56
Q

Most symptomatic cases are very mild.

A

Hepatitis C

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57
Q
  • It can also be transmitted permucosally through sexual intercourse, contact with an infected toothbrush or razor, or perinatally.
A

Hepatitis C

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58
Q
  • Transmitted mainly by exposure to contaminated blood, with IV drug use being the main source of infection.
A

Hepatitis C

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59
Q

-Recent increased cases have been reported from the HIV-positive men who have sex with men population

A

Hepatitis C

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60
Q
  • Today, anti-HCV testing via enzyme immunoassay (EIA) or chemiluminescent immunoassay (ChLIA) methodology and HCV RNA testing are performed on all donor units.
A

Hepatitis C

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61
Q
  • For supplemental confirmatory testing, the recombinant immunoblot assay (RIBA) is no longer available; however, blood centers may obtain FDA approval to use an alternate testing pathway, including line immunoblot.
A

Hepatitis C

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62
Q
  • Prevention consists of worldwide screening of blood and blood products; destruction or sterilization of needles and surgical or dental instruments; universal precautions; and education about the risks.
A

Hepatitis C

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63
Q
  • Optimal therapy for chronic HCV includes pegylated IFN and ribavirin combination
A

Hepatitis C

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64
Q
  • is a defective, single-stranded RNA virus that is found only in patients with HBV infection.
A

Hepatitis D

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65
Q
  • It requires HBsAg in order to synthesize an envelope protein and replicate.
A

Hepatitis D

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66
Q
  • It was previously called the delta antigen.
A

Hepatitis D

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67
Q
  • HDV is detected by testing for IgM or IgG anti-HDV or HDAg and HDV RNA in the serum.
A

Hepatitis D

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68
Q
  • As HDV cannot exist without HBV, testing for HBV will eliminate any infections with HDV.
A

Hepatitis D

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69
Q
  • Those at highest risk of infection are IV drug users.
A

Hepatitis D

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70
Q
  • This infection can also be transmitted sexually.
A

Hepatitis D

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71
Q
  • If a donor has HBV, the unit will not be used for transfusion
A

Hepatitis D

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72
Q
  • member of the Caliciviridae family of nonenveloped RNA viruses.
A

Hepatitis E

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73
Q
  • Symptoms are the same as for any hepatitis.
A

Hepatitis E

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74
Q

Generally, these cases are short-lived but can be prolonged.

A

Hepatitis E

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75
Q

causes an acute, self-limiting hepatitis that may last from 1 to 4 weeks in most people.

A

Hepatitis E

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76
Q

are responsible for acute, sporadic cases of infection that can be short-lived or prolonged.

A
  • HEV genotypes (G) 1, 2, and 4, 3
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77
Q

(usually occurring in developing countries)

A
  • HEV genotypes (G) 1, 2, and 4
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78
Q

(usually occurring in developed countries)

A

HEV G3

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79
Q

-The fecal- oral route is the most common form of transmission for

A

G1 and G2.

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80
Q

Transmission route are foodborne.

A

G3 and G4

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81
Q

is a major cause of hepatitis globally and is becoming a concern for transfusion transmission as more cases of transfusionassociated infections are reported in developed as well as underdeveloped countries.

A

Hepatitis E

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82
Q
  • Both IgM and IgG antibody to HEV (anti-HEV) may occur following HEV infection.
A

Hepatitis E

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83
Q

The titer of IgM anti-HEV declines rapidly during early convalescence; IgG anti-HEV persists and appears to provide at least short-term protection against disease.

A

Hepatitis E

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84
Q
  • Antibodies are usually identified using highly sensitive enzyme immunoassays that are recombinant and synthetic HEV antigens.
A

Hepatitis E

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85
Q
  • Meat such as pork, venison, and shellfish must be thoroughly cooked and water supplies must be cleaned and sewage disposal handled properly to prevent HEV infection.
A

Hepatitis E

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86
Q
  • Currently, no commercially available vaccine exists for the prevention of hepatitis E.
A

Hepatitis E

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87
Q
  • Ribavirin has been shown to be effective for treatment of chronic HEV, but its effectiveness for treatment of acute infection is not clear.
A

Hepatitis E

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88
Q

Some countries have introduced HEV screening for blood donations.

A

Hepatitis E

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89
Q

are two genotypes of the same enveloped RNA virus that belongs to the Flaviviridae family

A
  • GB virus C (GBV-C) and hepatitis G virus (HGV)
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90
Q
  • No evidence of liver disease, clinical or biochemical, was found.
A

Hepatitis G

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91
Q
  • In fact, there is some evidence that patients with HIV who have a coinfection with HGV have a slower progression to AIDS.
A

Hepatitis G

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92
Q
  • is transmitted by the bloodborne route.
A

Hepatitis G

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93
Q

-Parental transmission through contaminated blood and the presence of the virus in bile, stool, and saliva suggest transmission through the fecal-oral and respiratory routes.

A

Hepatitis G

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94
Q
  • Interferon-α treatment has been used with conflicting results.
A

Hepatitis G

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95
Q
  • Reverse transcription polymerase chain reaction (RT-PCR) for GBV-C/HGVRNA is used to diagnose a current, ongoing infection.
A

Hepatitis G

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96
Q
  • In most cases, the level of the GBV-C/HGV-RNA returned to normal levels once therapy was discontinued.
A

Hepatitis G

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97
Q

-Overall data do not support GBV-C/HGV as a major cause of liver failure.

A

Hepatitis G

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98
Q
  • Vertical or perinatal transmission from mother to child has been documented.
A

Hepatitis G

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99
Q
  • Only a small percentage of cases with low pretreatment viral loads had a predictable sustained response.
A

Hepatitis G

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100
Q

are well recognized as the etiologic agents of AIDS.

A

 HIV-1 and HIV-2

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101
Q

was first diagnosed in 1981, but the causative agent was not identified until 1984.

A

AIDS

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102
Q

is a retrovirus that is spherical in shape, with an approximate diameter of 100 nm.

A

 HIV

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103
Q

It consists of an envelope of glycoproteins, core proteins, and an inner core of viral RNA and reverse transcriptase.

A

 HIV

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104
Q

 The causative viruses, [?], are similar in structure, varying primarily in the envelope proteins

A

HIV-1 and HIV-2

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105
Q

Almost all cases in the United States result from infection with the

A

HIV-1 virus.

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106
Q

is prevalent in West Africa but is very rarely diagnosed in the United States

A

HIV-2

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107
Q

when it is diagnosed in the United States, it is usually linked to an association with West Africa.

A

HIV-2

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108
Q

 Symptoms may occur within 6 to 12 weeks of infection and persist for a few days to 2 weeks.

A

HIV Types 1 and 2

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109
Q

enters the cell by the binding of the virus glycoprotein 120 with cell surface receptors.

A

HIV Types 1 and 2

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110
Q

 During this period, antibody concentration and viral load reach equilibrium.

A

HIV Types 1 and 2

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111
Q

As the viral load increases and the CD4 count decreases, the patient progresses toward clinical AIDS.

A

HIV Types 1 and 2

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112
Q

 When the CD4 count is less than 200/µL, the patient is classified as having clinical AIDS.

A

HIV Types 1 and 2

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113
Q

is transmitted through sexual contact with an infected person, use of contaminated needles during drug use, and very rarely through transfusion of blood or blood components.

A

HIV

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114
Q

Congenital transmission may also occur.

A

HIV

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115
Q

 High-risk populations include men who have sex with men and IV drug users.

A

HIV

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116
Q

 The blood supply is most at risk from those individuals who have been recently infected with the virus but have not yet produced antibodies.

A

HIV

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117
Q

 infection may occur after receiving a single contaminated unit of whole blood or its components.

A

HIV

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118
Q

 The window period is that time after infection but before antibody or antigen is detectable by currently available testing procedures.

A

HIV

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119
Q

 It is possible for a donation to be infectious but to test negative for HIV-1/2 antibodies when the donor is in the window period.

A

HIV

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120
Q

 Antibodies are detectable at about 22 days after infection.

A

HIV

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121
Q

 EIA is used for the qualitative detection of HIV-1/2 in a ChLIA test.

A

HIV

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122
Q

Positive screening tests are repeated in duplicate, and if at least one of the duplicates also tests positive, a confirmatory test is performed.

A

HIV

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123
Q

 The confirmation of HIV-1/2 is performed using one or a combination of tests.

A

HIV

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124
Q

These include HIV-1 indirect immunofluorescence assay (IFA), HIV-2 enzyme-linked immunoassay, and a rapid diagnostic test used for HIV-1 and HIV-2 differentiation.

A

HIV

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125
Q

 In 2002 the first NAT test for HIV-1 RNA was approved (licensed) for use in the United States.

A

HIV

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126
Q

HIV-1 RNA testing closed the window period between time of infection and the detection of antibody to 7 to 10 days.

A

HIV

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127
Q

are RNA retroviruses.

A

HTLV-I and HTLV-II

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128
Q

causes a T-cell proliferation with persistent infection.

A

HTLV-I

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129
Q

 Once the RNA has been transcribed into DNA, it is integrated randomly into the host cell’s genome.

A

Human T-cell Lymphotropic Viruses Type I/II (HTLV-I/II)

130
Q

Once integrated into the DNA, the provirus can either complete its replication cycle or remain latent for many years

A

Human T-cell Lymphotropic Viruses Type I/II (HTLV-I/II)

131
Q

was the first retrovirus to be associated with a human disease. That association was with adult T-cell lymphoma/ leukemia (ATL), a highly aggressive, mature T-cell nonHodgkin’s lymphoma with a leukemic phase.

A

HTLV-I

132
Q

is also associated with the progressive neurological disorder known as HTLV-Iassociated myelopathy or tropical spastic paraparesis (HAM/TSP).

A

HTLV-I

133
Q
A

HTLV-I

134
Q

is transmitted vertically (breastfeeding), sexually (transmission from male to female more common), and parenterally (blood transfusion or IV drug abuse).

A

HTLV-I

135
Q

Because recipients of RBCs, platelets, and whole blood, but not fresh frozen plasma, have seroconverted, it is believed that transmission requires introduction of infected living white blood cells (WBCs).

A

HTLV-I

136
Q

This theory is supported by the fact that units stored for at least 7 days before transfusion are less likely to transmit the virus.

A

HTLV-I/II

137
Q

The risk of transmission through transfusion is less than 1:2,000,000 units transfused.

A

HTLV-I/II

138
Q

 Diagnosis is based on seroconversion after exposure because the majority of carriers are asymptomatic.

A

HTLV-I/II

139
Q

 Results are reported as reactive or negative for HTLV-I/II.

A

HTLV-I/II

140
Q

 The AABB and FDA have published guidelines on the use of the unit for transfusion and donor notification.

A

HTLV-I/II

141
Q

The guidelines state that if the donor is repeatedly reactive by the test of record (original EIA) but negative by the second licensed EIA of a different type (different manufacturer), the donor is still eligible for donation.

A

HTLV-I/II

142
Q

The donor can continue to donate as long as the test of-record EIA is negative on the next donation.

A

HTLV-I/II

143
Q

If the donor is repeatedly reactive by test of record on two separate occasions or on the same donation by the test-of-record assay and the different manufacturer’s EIA, the donor is indefinitely deferred.

A

HTLV-I/II

144
Q

 ATL does not respond well to treatment.

A

HTLV-I/II

145
Q

 The best prophylaxis is to prevent exposure.

A

HTLV-I/II

146
Q

is a member of the Flavivirus family and is a human, avian, and equine neuropathogen.

A

West Nile Virus

147
Q

 It is a single-stranded RNA lipid-enveloped virion that is common in Africa, West Asia, and the Middle East.

A

West Nile Virus

148
Q

 is a member of the Japanese encephalitis virus antigenic complex that includes St. Louis encephalitis virus prevalent in the Americas, Japanese encephalitis virus prevalent in East Asia, and Murray Valley encephalitis virus and Kunjin virus prevalent in Australia.

A

West Nile Virus

149
Q

 It is usually subclinical but may cause a mild flulike disease

A

West Nile Virus

150
Q

 It is capable of crossing the blood-brain barrier and can cause what is known as West Nile encephalitis, West Nile meningitis, or West Nile meningoencephalitis.

A

West Nile Virus

151
Q

 The risk of severe neurological disease increases markedly for anyone over the age of 50 years.

A

West Nile Virus

152
Q

 At least 65 species of mosquitoes have been found to carry WNV, the genus Culex is the chief vector.

A

West Nile Virus

153
Q

 The infection in humans has an incubation period of approximately 3 to 14 days following the mosquito bite, with symptoms lasting 3 to 6 days.

A

West Nile Virus

154
Q

 Although mosquito bites are the most common route of infection, there is a slight risk of contracting WNV from blood components, organ transplants, pregnancy, and breast milk.

A

West Nile Virus

155
Q

 Viremia usually lasts approximately 6 days and peaks around the onset of symptoms.

A

West Nile Virus

156
Q

Once clinical symptoms occur, the IgM WNV-specific antibody titer increases and the virus concentration in the bloodstream decreases.

A

West Nile Virus

157
Q

 IgM antibody-capture enzyme-linked immunosorbent assay (ELISA) was the method used to detect IgM antibody to the WNV in serum and cerebrospinal fluid (CSF).

A

West Nile Virus

158
Q

 Individuals should avoid mosquitoes and wear mosquito repellant and appropriate clothing if they are going to be in a mosquito-infested area.

A

West Nile Virus

159
Q

 Once infected, there is no licensed treatment, only supportive therapy.

A

West Nile Virus

160
Q

 Having survived the illness, a person is immune for life.

A

West Nile Virus

161
Q
A

West Nile Virus

162
Q

is an arbovirus in the Flavividae family, genus Flavivirus.

A

Zika virus (ZIKV)

163
Q

is transmitted by the Aedes aegypti and Aedes albopictus mosquitoes

A

Zika virus (ZIKV)

164
Q

symptoms include fever, headache, rash, and muscle and joint pain

A

Zika virus (ZIKV)

165
Q

 It has been associated with severe neurological complications including increased rates of microcephaly and fetal brain anomalies during pregnancy and GuillainBarre syndrome.

A

Zika virus (ZIKV)

166
Q

was first described in a rhesus monkey in 1947.

A

Zika virus (ZIKV)

167
Q

Human illness was confirmed in cases in Nigeria in 1953.

A

Zika virus (ZIKV)

168
Q

 Outbreaks of infections occurred in Micronesia and in French Polynesia in 2007 and 2013, respectively.

A

Zika virus (ZIKV)

169
Q

 Approximately 80% of infections are asymptomatic.

A

Zika virus (ZIKV)

170
Q

When symptoms do occur, the period of viremia without symptoms ranges from 3 to 12 days.

A

Zika virus (ZIKV)

171
Q

 ZIKV RNA has been found in asymptomatic blood donors, and there have been reported cases of probable transmission of ZIKV through transfusion.

A

Zika virus (ZIKV)

172
Q

 The FDA has established IT as a transfusion transmitted infection.

A

Zika virus (ZIKV)

173
Q

The February guidance included recommendations to defer donors for 28 days following travel to countries with active ZIKV transmission as well as donors who had sexual contact with men who traveled to those countries.

A

Zika virus (ZIKV)

174
Q

The FDA guidance also included recommendations for areas of active ZIKV transmission to import blood from nonactive areas or to test donor blood for ZIKV RNA using NAT or to use blood components that were pathogen reduced using an FDA-approved technology.

A

Zika virus (ZIKV)

175
Q

 Testing with NAT, PCR Diagnostic test and antibody testing such as ELIA and immunofluorescence assays.

A

Zika virus (ZIKV)

176
Q

Similar to WNV infections there is no medicine available for treatment of infection.

A

Zika virus (ZIKV)

177
Q

Avoidance of mosquito bites through use of insect repellent is recommended to reduce the risk of infection in areas of active Transmission.

A

Zika virus (ZIKV)

178
Q
  • member of the herpesvirus group and is found in all geographic locations and socio- economic groups, with a higher prevalence in developing countries.
A

Cytomegalovirus

179
Q
  • Once an individual is exposed, CMV can remain latent in the tissues and leukocytes for years, with reactivation occurring from a severe immune system impairment.
A

Cytomegalovirus

180
Q
  • Transmission occurs from person to person through contact with infected body fluids, which may include urine, semen, saliva, blood, cervical secretions, and breast milk.
A

Cytomegalovirus

181
Q
  • is the most frequently transmitted virus from mother to fetus.
A

Cytomegalovirus

182
Q
  • Those at the highest risk of a CMV infection are fetuses and immune- compromised individuals receiving allogeneic marrow transplants or solid organ transplants.
A

Cytomegalovirus

183
Q
  • Antibodies formed to CMV last a lifetime and can be detected by ELISA.
A

Cytomegalovirus

184
Q
  • Other laboratory tests include PCR, fluorescence assays, indirect hemagglutination, and latex agglutination.
A

Cytomegalovirus

185
Q
  • If the patient is symptomatic, active infection can be detected by viral culture of urine, throat swabs, and tissue samples
A

Cytomegalovirus

186
Q
  • Currently, there is no treatment for CMV for a healthy individual.
A

Cytomegalovirus

187
Q
  • Infants are being evaluated using antiviral drug therapy, and ganciclovir is being used for patients with depressed immunity.
A

Cytomegalovirus

188
Q
  • To prevent CMV transmission, leukocytereduced blood or blood from seronegative donors may be used.
A

Cytomegalovirus

189
Q
  • ubiquitous member of the herpesvirus family
A

Epstein- Barr Virus

190
Q
  • Infections occurring in infants or young children are usually asymptomatic.
A

Epstein- Barr Virus

191
Q
  • In adolescence and young adulthood, EBV causes infectious mononucleosis in 30% to 50% of patients.
A

Epstein- Barr Virus

192
Q
  • EBV was first discovered in 1964 in Burkitt’s lymphoma cells.
A

Epstein- Barr Virus

193
Q

Since then it has been associated with many illnesses besides infectious mononucleosis and cancers such as nasopharyngeal carcinoma, non-Hodgkin’s lymphoma, oral hairy leukoplakia in AIDS patients, T-cell lymphomas, and Hodgkin’s disease.

A

Epstein- Barr Virus

194
Q

has been called the “kissing disease” because the virus usually replicates in the cells of the oropharynx, possibly in infected B cells.

A

Epstein- Barr Virus

195
Q

Epstein- Barr Virus

A
196
Q
  • is a small, nonenveloped virus
A

Parvovirus B19

197
Q
  • Fifth disease presents with a mild rash described as “slapped cheek” when occurring on the face and a lacy red rash when occurring on the trunk and limbs.
A

Parvovirus B19

198
Q
  • As in all viral infections, the virus must enter the cell through a specific cell receptor.
A

Parvovirus B19

199
Q

enters the red blood cell (RBC) via the P antigen and replicates in the erythroid progenitor cells.

A

Parvovirus B19

200
Q

The cytotoxicity of erythroid precursors can lead to serious illness in individuals with chronic hemolytic anemia, such as sickle cell disease and thalassemia, who may have a transient aplastic crisis.

A

Parvovirus B19

201
Q
  • The viremic stage occurs shortly after infection.
A

Parvovirus B19

202
Q

A donor would be asymp-tomatic but capable of transmitting the virus during this period.

A

Parvovirus B19

203
Q

This is a concern for donor centers because the rate of seroconversion is high after exposure.

A

Parvovirus B19

204
Q
  • It causes a common childhood illness called “fifth disease” and is usually transmitted through respiratory secretions.
A

Parvovirus B19

205
Q
  • The FDA recommends manufacturers of plasmaderived products to engage in practices that will reduce the time between product collection and process testing in order for the collection establishments to be notified of positive test results within the in-date period of any blood components that are intended for transfusion.
A

Parvovirus B19

206
Q
  • In a study by Weimer and colleagues, plasmas were tested for B19 DNA levels by PCR, and those with high titers were eliminated from the pool used in the manufacture of antithrombin III (ATIII).
A

Parvovirus B19

207
Q

is a very common virus that causes a lifelong infection.

A
  • HHV-6
208
Q

virus replicates in the salivary gland and then remains latent in lymphocytes, monocytes, and perhaps other tissues.

A
  • HHV-6
209
Q

is not common in the population but has been seen in Africa.

A

HHV-8

210
Q

Is associated with several diseases that generally affect the immunesuppressed patient.

A

HHV-8

211
Q

These include Kaposi’s sarcoma (KS), primary effusion lymphoma, and multicentric Castleman’s disease.

A

HHV-8

212
Q
  • In childhood, it Tcauses roseola infantum, also known as “exanthem subitum” or “sixth disease.”
A
  • HHV-6
213
Q

: Spread is generally through sexual contact.

A

HHV-8

214
Q
  • In post-transplant patients who develop KS, it appears to be due to reactivation.
A

HHV-8

215
Q

The transmission of [?] has been associated with organ transplants and injection drug use.

A

HHV-8

216
Q

Symptoms are those of a mild, acute febrile disease

A
  • HHV-6
217
Q

EMERGING VIRUSES

A
218
Q
  • small enveloped single-stranded RNA virus of the family Togaviridae.
A

Chikungunya Virus (CHIKV)

219
Q
  • Primary disease symptoms include high fever, severe joint pain, headache, muscle pain, rash, and leukopenia.
A

Chikungunya Virus (CHIKV)

220
Q
  • The virus is vector borne, transmitted through mosquitoes mainly from the Aedes family.
A

Chikungunya Virus (CHIKV)

221
Q
  • Theoretically, CHIKV could be spread through transfusion, but there have been no reported cases of CHIKV transmission through transfusion even during outbreaks.
A

Chikungunya Virus (CHIKV)

222
Q
  • There is no medication for treatment of the disease and no vaccine for prevention.
A

Chikungunya Virus (CHIKV)

223
Q

-Similar to WNV and ZIKV, avoidance of mosquito bites is the recommenddation to reduce risk of infection.

A

Chikungunya Virus (CHIKV)

224
Q
  • small enveloped single-strand RNA virus in the genus Flavivirus
A

Dengue Virus

225
Q
  • Symptoms of disease usually occur 4 to 7 days following the bite of an infected mosquito.
A

Dengue Virus

226
Q
  • Illness usually presents with onset of fever, rash, a severe headache, lumbosacral aching pain followed by muscle pain, bone pain, anorexia, nausea, vomiting, and weakness.
A

Dengue Virus

227
Q
  • Severe dengue is rare and includes capillary leakage sequelae leading to shock with a subset demonstrating hemorrhagic manifestations.
A

Dengue Virus

228
Q
  • The virus is vector borne by the mosquitoes Aedes aegypti and Aedes albopictus.
A

Dengue Virus

229
Q
  • Transmission of DENV through transfusion and organ transplantation has been reported.
A

Dengue Virus

230
Q
  • There is currently no FDA or AABB guidance for donor deferral and no tests licensed for donor testing.
A

Dengue Virus

231
Q
  • Risk of DENV infection can be reduced by mosquito control and avoidance.
A

Dengue Virus

232
Q
  • Vaccines are in clinical trials, and there are no medicines for treatment of DENV illness other than those used in supportive care
A

Dengue Virus

233
Q

member of the family Filoviridae and can cause severe hemorrhagic fever

A

Ebola virus

234
Q
  • Symptoms of EVD include fever, severe headache, muscle pain, weakness, followed by diarrhea, vomiting, and abdominal pain.
A

Ebola virus

235
Q
  • Diffuse hemorrhage has been reported.
A

Ebola virus

236
Q

Symptoms occur most often within 4 to 10 days following infection and generally within 21 days

A

Ebola virus

237
Q
  • Due to the severity of EVD and the possibility of asymptomatic viremia, the FDA has determined that Ebola virus meets the criteria of a transfusion-transmitted infection.
A

Ebola virus

238
Q
  • Donors must be indefinitely deferred if they have a history of Ebola virus infection or disease.
A

Ebola virus

239
Q

Eight-week deferral periods are required from the date of the donor’s departure from a country with wide spread transmission of Ebola virus, after the last date of donor contact with a person infected with Ebola virus, after the last date of donor sexual contact with a person known to have recovered from EVD, or after notify-cation of exposure from a public health authority.

A

Ebola virus

240
Q
  • There are no FDAapproved therapeutics or vaccines for EVD.
A

BACTERIAL CONTAMINATION

241
Q
  • Common sources are from donor skin or from asymptomatic donor blood.
A

bacterial contamination

242
Q

-Platelets have been the most frequent source of septic transfusion reactions because room temperature storage promotes bacterial growth.

A

-Platelets

243
Q
  • The most common signs and symptoms of transfusion associated sepsis are rigors, fever, and tachycardia.
A

rigors, fever, and tachycardia.

244
Q
  • Other symptoms may include shock, low back pain, disseminated intravascular coagulation (DIC), and an increase or decrease in systolic blood pressure.
A

shock, low back pain, disseminated intravascular coagulation (DIC), and an increase or decrease in systolic blood pressure.

245
Q

usually originates with the donor, either through skin contamination at the phlebotomy site or an asymptomatic bacteremia.

A

BACTERIAL CONTAMINATION

246
Q
  • It may also occur through contamination during processing.
A

BACTERIAL CONTAMINATION

247
Q

is the most common risk of infection due to transfusion of blood.

A

BACTERIAL CONTAMINATION

248
Q

are the most common bacterial contaminants of blood.

A
  • Staphylococcus epidermidis or Staphylococcus aureus
249
Q
  • According to the CDC, [?] is the most common isolate found in RBC units, followed by the Pseudomonas species.
A

Yersinia enterocolitica

250
Q

, a common isolate of human skin, was the most common bacterial contaminant in RBCs.

A
  • Propionibacterium acnes
251
Q
  • Before the unit of RBCs or platelets is issued, the unit should be inspected for discoloration (dark purple or black), which strongly indicates contamination.
A

BACTERIAL CONTAMINATION

252
Q
  • To detect bacterial contamination, both the donor blood component and the recipient’s blood should be tested. s.
A

BACTERIAL CONTAMINATION

253
Q
  • The FDA has approved a psoralen/UV irradiationbased pathogen reduction method for use on apheresis platelets within 24 hours after collection.
A

BACTERIAL CONTAMINATION

254
Q
  • Use of apheresis platelets rather than pooled whole bloodderived platelets from multiple donors reduces the incidence of contamination occurring during phlebotomy.
A

BACTERIAL CONTAMINATION

255
Q
  • Leukoreduction of units can be helpful in removing phagocytized bacteria along with the leukocytes
A

BACTERIAL CONTAMINATION

256
Q
  • the causative agent is a spirochete.
A

Syphilis

257
Q
  • The standard serologic tests for syphilis (STS) usually do not detect a donor in the spirochetemia phase who has not yet seroconverted.
A

Syphilis

258
Q
  • Spirochetemia is short, and seroconversion usually occurs after this phase.
A

Syphilis

259
Q
  • The last reported case of transfusion-transmitted syphilis was 1996.
A

Syphilis

260
Q
  • It is usually spread through sexual contact but can be transmitted through blood transfusions.
A

Syphilis

261
Q
  • Polymerase chain reaction followed by Southern blotting and a labeled probe have been used to confirm the presence of treponemal antigen.
A

Syphilis

262
Q

The test is capable of detecting as few as one treponeme in CSF.

A

Syphilis

263
Q
  • Nontreponemal EIAs, fluorescent treponemal antibody absorption (FTAABS), T. pallidum immobilization (TPI), and T. pallidum hemagglutination (TPHA) are the methodologies utilized.
A

Syphilis

264
Q
  • Lyme disease is caused by the spirochete Borrelia
    burgdorferi, and RMSF (Rickettsia rickettsii) and ehrlichiosis (Ehrlichia species) are caused by bacteria that are obligate intracellular pathogens.
A

Tick-Borne Bacterial Agents

265
Q
  • Lyme disease, Rocky Mountain spotted fever (RMSF), and ehrlichiosis are all bacterial diseases spread by a tick bite.
A

Tick-Borne Bacterial Agents

266
Q

Transfusion- Associated Parasites

A
267
Q
  • Most cases of babesiosis are asymptomatic.
A

Babesia microti

268
Q
  • Symptomatic patients usually develop a malariatype illness characterized by fever, chills, lethargy, and hemolytic anemia.
A

Babesia microti

269
Q
  • Reported incubation periods for symptomatic patients range from 1 to 8 weeks after transfusion.
A

Babesia microti

270
Q
  • Babesiosis, a zoonotic disease, is usually transmitted by the bite of an infected deer tick. Infection is caused by the protozoan parasite, Babesia, which infects the RBCs.
A

Babesia microti

271
Q
  • Infected persons who donate blood during the asymptomatic period pose the greatest risk to the blood supply, as they probably have infectious organisms circulating in their bloodstreams.
A

Babesia microti

272
Q
  • Units of packed RBCs (liquid stored and frozen deglycerolized) and platelet units, which contain RBCs, have been associated with transmission.
A

Babesia microti

273
Q

can survive in refrigerated, uncoagulated blood for 21 to 35 days.

A

Babesia microti

274
Q
  • Thick and thin blood smears stained with Giemsa or Wright stain can be examined for intraerythrocytic organisms.
A

Babesia microti

275
Q
  • Serologic studies such as immunofluorescence assays can be used to detect circulating antibody.
A

Babesia microti

276
Q
  • Babesiosis can be effectively treated with antibiotic therapy.
A

Babesia microti

277
Q
  • There is no specific drug of choice, but quinine and clindamycin are very effective.
A

Babesia microti

278
Q
  • Combination of atovaquone and azithromycin can be as effective in patients without a life-threatening illness.
A

Babesia microti

279
Q
  • Apheresis has also been successful in patients who fail to respond to antibiotic therapy.
A

Babesia microti

280
Q
  • flagellate protozoan that is the etiologic agent of Chagas disease (American trypanosomiasis).
A

Trypanosoma cruzi

281
Q
  • The reduviid bug bite produces a localized nodule, referred to as a “chagoma.”
A

Trypanosoma cruzi

282
Q

The chagoma is usually painful and may take up to 3 months to heal.

A

Trypanosoma cruzi

283
Q
  • Clinical symptoms may be mild or absent; therefore, many cases are not diagnosed until the chronic phase of the disease.
A

Trypanosoma cruzi

284
Q
  • Symptoms include anemia, weakness, chills, intermittent fever, edema, lymphadenopathy, myocarditis, and gastrointestinal symptoms.
A

Trypanosoma cruzi

285
Q
  • Death may occur within a few weeks or months after initial infection.
A

Trypanosoma cruzi

286
Q
  • The disease is naturally acquired by the bite of a reduviid bug, thus making it a zoonotic infection.
A

Trypanosoma cruzi

287
Q
  • Insect transmission is the most common mode of infection, but the organism has also been transmitted by blood transfusion and organ transplants.
A

Trypanosoma cruzi

288
Q
  • Chagas disease can be transmitted congenitally, transplacentally, or through solid organ transplantation
A

Trypanosoma cruzi

289
Q
  • Chagas disease is endemic in Central and South America and some areas of Mexico.
A

Trypanosoma cruzi

290
Q
  • Acute Chagas disease is diagnosed by detecting the organism in the patient’s blood.
A

Trypanosoma cruzi

291
Q

Blood smears stained with Giemsa or Wright stain may be examined for the characteristic C- or Ushaped trypomastigote.

A

Trypanosoma cruzi

292
Q
  • Chronic Chagas disease is diagnosed serologically. Such testing includes complement fixation, immunofluorescence, and ELISA.
A

Trypanosoma cruzi

293
Q
  • The AABB TTD Committee has given T. cruzi an orange category rating. An orange category agent is considered a low scientific or epidemiological risk regarding blood saftey.
A

Trypanosoma cruzi

294
Q

was assigned a moderate rating by the TTD Committee based on public and regulatory attention to introducing blood donor screening.

A

Trypanosoma cruzi

295
Q
  • In the United States, medication for Chagas disease may be obtained only by contacting the CDC.
A

Trypanosoma cruzi

296
Q
  • intraerythrocytic protozoan infection, may be caused by several species of the genus Plasmodium
A

Malaria (Plasmodium species)

297
Q
  • Symptoms include fever, chills, headache, anemia, hemolysis, and splenomegaly.
A

Malaria (Plasmodium species)

298
Q

There may be variations in symptoms among the different species of Plasmodium.

A

Malaria (Plasmodium species)

299
Q
  • Malaria often mimics other diseases, and its diagnosis is often delayed due to lack of suspicion in nonendemic areas.
A

Malaria (Plasmodium species)

300
Q
  • Natural transmission occurs through the bite of a female Anopheles mosquito, but infection may also occur following transfusion of infected blood.
A

Malaria (Plasmodium species)

301
Q
  • Transfusion-associated malaria is acquired by receiving blood products from an asymptomatic carrier.
A

Malaria (Plasmodium species)

302
Q
  • Examination of thick and thin blood smears is performed to diagnose infection with malaria.
A

Malaria (Plasmodium species)

303
Q
  • Depending on the species of Plasmodium and the stage of the parasite’s life cycle, timing is crucial when evaluating the blood smear.
A

Malaria (Plasmodium species)

304
Q

A single negative smear does not rule out a diagnosis of malaria.

A

Malaria (Plasmodium species)

305
Q
  • According to FDA guidance documents, persons who have traveled to an endemic area are deferred for 1 year, and those who have had malaria or who have immigrated from or lived in an endemic area are deferred for 3 years.
A

Malaria (Plasmodium species)

306
Q
  • Chloroquine is generally effective for chemoprophylaxis and treatment of all four species of Plasmodium, except P. vivax acquired in Indonesia or Papua New Guinea, which is best treated with atovaquoneproguanil, with mefloquine or quinine plus tetracycline or doxycycline as alternatives.
A

Malaria (Plasmodium species)

307
Q

Prion Disease

A
308
Q
  • is one of the transmissible spongiform encephalopathies (TSEs)
A

Creutzfeldt- Jakob Disease

309
Q
  • These are rare diseases characterized by fatal neurodegeneration that results in sponge-like lesions in the brain.
A

Creutzfeldt- Jakob Disease

310
Q
  • The causative agent of all TSEs is believed to be a prion, which is described as a self-replicating protein.
A

Creutzfeldt- Jakob Disease

311
Q
  • The incubation period in humans varies from 4 to 20 years and may eventually prove to be longer in some cases.
A

Creutzfeldt- Jakob Disease

312
Q
  • There is no epidemio-logical evidence linking classic CJD to TTD.
A

Creutzfeldt- Jakob Disease

313
Q

However, in vCJD cases, prion particles have been found in lymphoreticular tissues, including the tonsils, spleen, and lymph nodes.

A

Creutzfeldt- Jakob Disease

314
Q

As blood is intimately involved with the lymphoreticular system, concerns arose regarding the ability of vCJD individuals to transmit the prion to recipients of blood or blood products.

A

Creutzfeldt- Jakob Disease

315
Q
  • Although a definitive diagnosis can be made only at autopsy, neurological signs and symptoms and disease progression are used to make a preliminary diagnosis.
A

Creutzfeldt- Jakob Disease

316
Q
  • Currently, there is no reliable diagnostic test that can detect asymptomatic individuals.
A

Creutzfeldt- Jakob Disease

317
Q

Therefore, deferral of donors with connection to the United Kingdom and parts of Europe as well as other associated risk factors is used to prevent transmission.

A

Creutzfeldt- Jakob Disease

318
Q

g for parasitic infections is not currently available that is why many blood banks have added questions to their donor questionnaire that address topics associated with risk for parasitic infection.

A
  1. Routine screening
319
Q

are in use for plasma and platelet products and under development for red cell products.

A
  1. Pathogen inactivation methods
320
Q

These methods remove or reduce the residual risk of transfusion-associated disease due to the window period, virus variants, laboratory mistakes, and new, emerging diseases.

A
  1. Pathogen inactivation methods
321
Q

is a process mandated by the FDA that directs collection facilities to notify donors who test positive for viral markers, to notify prior recipients of the possibility of infection, and to quarantine or discard implicated components currently in inventory

A
  1. Look-back

[Immunohematology] Lec (35 decks)

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