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HEN > Microbiology > Flashcards

Microbiology Flashcards

1
Q

the species of orientia called?

A

O. tsutsugamushi

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2
Q

what different between orientia and rickettsia

A

in 16S rRNA sequence and cell wall structure

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3
Q

type of Rickettsia & Orientia

A

short bacilli

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4
Q

stain of Rickettsia & Orientia

A

Giemsa stain

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5
Q

culture of Rickettsia & Orientia and why this culture

A

tissue culture
embryonated eggs
experimental animals
because they are obligate intracellular

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6
Q

mode of transmission of Rickettsia & Orientia

A

by arthropods
ticks and mites inject bacteria to blood
lice and fleas in feces on skin

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7
Q

mention the Rickettsia & Orientia species and caused disease

A

R. prowazeki»>Epidemic typhus (man louse)
R. typhi»> Endemic typhus (rat flea)
O.tsutsugamushi»>Scrub typhus (rodents mites)
R. rickettsii»>Rockey mountain spotted fever (dogs and rodents tick)

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8
Q

symptoms of Epidemic typhus

A

prolonged fever
severe prostration
skin rash
enlargment of liver and spleen

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9
Q

mode of transmission and pathogenesis of Epidemic typhus

A

louse»feces>blood»capillary endothelium causing vasculitis in heart and brain» Disseminated intravascular coagulation and vascular occlusion

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10
Q

what is brill-zineser disease

A

It is caused when the rickettsia remains latent in lymph nodes for several years then activated due to lacking immunity to produce epidemic disease again

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11
Q

mode of transmission of R. typhi

A

is transmitted from rat to man by fleas

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12
Q

mode of trasmission of rocky mountain spotted fever

A

transovarian among ticks
Dogs and rodents are also resevoirs of infection

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13
Q

symptoms of rocky mountain spotted fever

A

non specific symptoms
The typical rash, which appears 2-6 days later, begins With macules that progress to petechiae that appear first on hands and feet then move to the trunk.
* CNS manifestations e.g. delirium, coma, D1C and circulatory collapse may occur in severe cases. It can be fatal if untreated.

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14
Q

diagnosis of rickettsial disease

A
  1. Direct detection in blood and skin biopsy specimens from the rash; by immuno-histochemical methods and PCR
    * 2. inoculation in pigs, mice, yolk sac of embryonated eggs which replaced by tissue culture
    * 3. serologic diagnosis
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15
Q

causes Q fever

A

Coxietta burnetii

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16
Q

difference between rickettsia and coxiella

A

coxiella is being more resistant to drying, disinfectants and UV

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17
Q

form endospores and its function

A

coxiella burnetti which make coxiella able to survive for months (in dried animal discharges (placental tissues or aminiotic fluid)
faeces, urine or milk

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18
Q

which phase is a virulent phase of Coxiella Burnetii

A

Phase 1

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19
Q

mode of infection of Coxiella burnetti (Q fever)

A
  1. inhalation of dust or aerosols contaminated with infected animal discharge and excreta
  2. consumption of unpasteurized infected milk
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20
Q

it not detected in blood (has negative blood culture result)

A

Coxiella burnetii

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21
Q

pathogenesis and clinical picture of Q fever

A
  1. infection of alveolar macrophages and a brief rickettsemia due to inhalation of infected aerosols
  2. acute disease begins with fever and influenza-like symptoms
  3. pneumonia and hepatitis
  4. Chronic Q fever can make life threatening endocarditis in abnormal patients
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22
Q

Diagnosis of Coxiella burnetii

A

serologic detection of a rising antibody titre to phase I or II
Indirect immunofluorescence , e.g. ELISA
PCR is useful in diagnosing culture negative endocarditis

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23
Q

best way to diagnose culture negative(of what) endocarditis

A

PCR

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24
Q

vaccine of Q fever

A

A formalin-killed whole cell, phase I C. burnetii vaccine is available for those occupationally at risk

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25
Q

Morphology of actinomyctes

A

filamentous branching Gram positive bacilli

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26
Q

the two genera of actinomyctes

A

Actinomyces and Nocardia

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27
Q

the diseases caused by actinomyctes

A

actinomycosis, nocardiosis and actinomycetoma

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28
Q

pathogenesis of Actinomyces israelii

A

it invades the tissues after local trauma causing actinomycosis, which is a chronic inflammatory, granulomatous lesion that drains pus through sinus tracts which contains yellow “sulphur granules”.

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29
Q

produce sulfur granules

A

Actinomyces israelii

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30
Q

morphology of Actinomyces israeli

A

These are composed of a central mycelial mass with a
peripheral zone of swollen clubs

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31
Q

most lesions of Actinomyces israelii

A

Actinomyces israeliicervico-facial (associated with poor dental hygiene or tooth extraction), abdominal or thoracic.

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32
Q

Diagnosis of Actinomyces israelii

A
  • Pus from lesions .
  • sulphur granules are seen with radially arranged clubs.
  • Gram staining will reveal filamentous branching Gram positive bacilli with bacillary and coccoid forms
  • Culture anaerobically on thioglycolate broth and brainheart infusion blood agar. Colonies are identified by morphology and immunofluorescent staining.
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33
Q

culture of A. israelii

A

thioglycolate broth and brainheart infusion blood agar

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34
Q

causes nocardiosis

A

Nocardia asteroides

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35
Q

pathogenesis of N.asteroides

A

Inhalation of the organism causing chronic pulmonary infections and brain and skin abscesses

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36
Q

diganosis of N. asteroides

A

detection of Gram positive bacilli, coccobacillary cells and branching filaments

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37
Q

culture of N. asteroides

A

brain-heart infusion agar

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38
Q

difference between actinomycotic and Eumycotic mycetoma in

  • causative agent
  • Granules
  • Microscopic examination
  • culture
  • treatment
A

P. 37 Lecture 1

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39
Q

morphology of Listeria monocytogenes

A

small gram positive, non-spore forming bacilli

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40
Q

characterized by tumbling movement

A

Listeria monocytogenes

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41
Q

the tumbling movement of Listeria monocytogenes is at which temp

A

22-28 C

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42
Q

what distinguishes Listeria monocytogenes from corynebacterium

A

tumbling movement of Listeria monocytogenes

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43
Q

catalase test of Listeria Monocytogenes

A

catalase positive

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44
Q

mode of transmission of Listeria monocytogenes to humans

A

1- Contact with domestic farm animals or their faeces, by ingestion of
contaminated unpasteurized milk or cheese and contaminated vegetables (i.e. food borne).

2- Vertical transmission can also occur transplacentally or during delivery

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45
Q

type of haemolysis of Listeria

A

Beta haemolysis

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46
Q

pathogenesis of listeria

A
  • has ability to invade mononuclear phagocytic cells. After internalization a listeriolysin O enzyme lyses the membrane of the phagolysosome and they escape destruction
  • It can move from cell to cell by means of actin rockets
  • Since it grows intracellularly, cell mediated immunity (CMI) is a
    more important host defense than humoral immunity
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47
Q

how Listeria move from cell to cell

A

by actin rockets

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48
Q

type of immunity initiated in Listeria infection

A

cell mediated immunity because Listeria grows intracellulary

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49
Q

diseases caused by listeria

A

1- Infection of pregnant women passes to the foetus transplacentally
causing granulomatosis infantiseptica characterized by pustular skin
lesions and intrauterine sepsis leading to abortion, still-birth or
premature labour.

2-Newborns infected during delivery from infected mothers, develop
neonatal meningitis.

3-Infection in immunosuppressed adults causes meningoencephalitis
and bacteraemia, specially in renal transplant patients.

4-Gastroenteritis which is characterized by watery diarrhoea, fever,
headache, myalgia and abdominal cramps but little vomiting.
Outbreaks are usually caused by contaminated dairy products.
Undercooked meats such as chicken and hot dogs have also been
involved.

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50
Q

Diagnosis of Listeria

A
  • Isolation from blood by blood culture and from CSF on blood
    agar and from stools on listeria selective media.
  • Isolation is enhanced if specimens are refrigerated for few
    days before inoculation “cold enhancement”.
  • Identification is done by gram stain and detection of tumbling
    motility and positive catalase.
  • It produces Beta- haemolysis, on sheep blood agar, which is
    enhanced in the vicinity of a streak of Staph, aureus, i.e. CAMP
    test positive
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51
Q

how listeria passes to fetus

A

transplacentally

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52
Q

what causes granulomatosis infantiseptica

A

Listeria

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53
Q

what causes neonatal meningits in newborns

A

listeria monocytogenes

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54
Q

what listeria do in immunosupressed patients

A

meningoencephalitis and bacteraemia

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55
Q

has tumbling motility

A

L. monocytogenes

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56
Q

causing undulant fever

A

Brucella

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57
Q

causing malta fever

A

Brucella

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58
Q

other names of brucellosis

A

undulant or Malta fever

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59
Q

Brucella

causing infection in goats and sheep

A

Br. melitensis

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60
Q

causing abortion of cattle

A

Br. abortus

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61
Q

Brucella causing infection in pigs

A

Br. suis

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62
Q

Borrelia causes infection in dogs

A

Br. canis

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63
Q

Morphology of Brucella

A

Gram negative short cocco-bacilli, non-motile, nonsporing and non-capsulated

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64
Q

media of brucella for growth

A

brucella agar,
brain heart infusion,
trypticase soy agar,
chocolate agar

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65
Q

which type of brucella require CO2 for growth

A

Br. Abortus

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66
Q

which brucella species produce H2S

A

Br. abortus and Br. suis

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67
Q

virulence and immunity of brucella

A
  • A lipopolysaccharide (LPS) is the major virulence factor as well
    as the major cell wall antigen. The LPS has endotoxic activity
    and elicits an antibody response (IgG, IgM, IgA) which may be
    protective.
  • Brucella can survive and multiply within host cell phagocytes
    i.e. facultative intracellular parasite, so immunity is mainly
    cell mediated
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68
Q

immunity triggered in brucella

A

cell mediated because brucella is facultative intracellular parasite

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69
Q

antibodies elicted in response to the LPS virulence factor of brucella

A

IgG, IgM, IgA

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70
Q

incubation period of brucella

A

1-6 weeks

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71
Q

brucella is found in

A

uterine discharges and milk of infected animals

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72
Q

mode of transmission of brucella

A

1- Ingestion of contaminated unpasteurized milk or milk products.

2- Direct through skin abrasions during handling of infected animals or their discharges.
Therefore brucellosis is an occupational disease affecting mostly butchers, farmers and veterinarians
3- inhalation of infected aerosol during handling of infected animals or their cultures in the
laboratories

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73
Q

what is undulant fever

A

disease caused by brucella characterized by an accute bacteraemic phase followed by chronic stage

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74
Q

what the brucella invade

A

The organism localizes in the reticulo-endothelial system; lymph nodes, liver, spleen and bone marrow.

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75
Q

undulant fever complicated by

A

osteomyelitis, meningitis or cholecystitis

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76
Q

which brucella biovar is more acute and which is more chronic

A

Br. melitensis infection is more acute and severe. Br. suis infection is more chronic

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77
Q

Blood cultures of brucella should not be discarded as negative before how many weeks

A

4 weeks

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78
Q

blood culture of brucella

A

brain heart infusion broth

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79
Q

diagnosis of brucella

A

Blood, bone marrow and lymph node biopsy for culture
1. blood culture: in brain heart infusion broth
2. serologic diagnosis:
Standard tube agglutination test (STAT)
A rapid slide agglutination test
ELISA for detection of IgG, IgM or IgA
**3. PCR: **
4. Brucellin test:

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80
Q

causes of false negative results of serologic tests of brucella

A
  • prozone phenomenon
  • presence of non-agglutinating IgA “blocking antibodies”
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81
Q

how to deal with prozone phenomnon

A

wide range of serum dilutions (up to 1/5120) shoud be done.

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82
Q

how to deal with the blocking antibodies IgA

A

Coomb’s antiglobulin method

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83
Q

What diseases caused by Borrelia

A

Relapsing fever and Lyme disease

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84
Q

has endoflagella

A

borrelia

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85
Q

culture of borrelia

A

Barbour-Stoenner-Kelly (BSK-II)
microaerophilic environment

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86
Q

a disease characterized by repeated bouts of fever alternating
with periods of apyrexia

A

Relapsing fever

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87
Q

Epidemic relapsing fever is caused by …… and transmitted by ….

A

B. recurrentis
lice

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88
Q

endemic relapsing fever is caused by ….. and transmitted by ……

A

B. duttoni and B. hermsii
ticks

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89
Q

Man is the only host for which species of Borrelia

A

B. recurrentis and B. duttoni

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90
Q

incubation period of Borrelia

A

3-10 days last for 4 days
then 3-10 days of afebrile period
which 3-10 relapses may occur

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91
Q

death in cases of borrelia due to

A

the spirochaetes invade many organs (heart, spleen, liver and kidney) with death generally due to myocarditis

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92
Q

diagnosis of Borrelia

A

1- During the febrile stage:
* Blood films stained with Leishman, Wright or Giemsa stains reveal large numbers of
spirochaetes.
2- During afebrile stage :
* Cultivation and mouse enrichment must be done as the organism is scanty in the
blood and blood films are negative.
* Diagnosis is done by injecting white mice intraperitoneally with the patient’s blood.
* After 2-4 days, films from tail blood are stained and examined for presence of
Borreliae.
* Mice blood is inoculated on BSKII medium.
3- DNA probes may be used for identification.

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93
Q

lyme disease is caused by

A

Borrelia burgdorferi
and is transmitted by ticks

94
Q

the main animal reservoir for lyme disease (Borrelia burgdorferi)

A

Rodents and deer

95
Q

the early and late manifestation of Lyme disease

A
  • The early stages are characterized by a distinctive skin lesion
    called “erythema migrans” associated with fever, chills, muscle
    pain and headache.
  • Late manifestations arthritis, myocarditis and neurologic manifestations e.g.
    meningitis.
96
Q

causes Erythema migrans

A

Borrelia burgdorferi

97
Q

morphology of Yersinia

A

gram negative bacilli

98
Q

causes plague in man

A

Yersinia pestis

99
Q

causes of human diarrhoeal diseases

A

Yersinia enterocolitica and Yersinia pseudotuberculosis

100
Q

How Yersinia pestis is transmitted

A

transmitted to man by the rat flea Xenopsylla cheopis

101
Q

Morphology of Yersinia pestis

A

Gram negative short ovoid, non-motile bacilli. In tissue, they form a
capsule-like outer envelope

102
Q

they show marked bipolar staining “safety pin appearance

A

Yersinia pestis

103
Q

staining of Yersinia pestis

A

Geimsa or methylene blue
gram negative

104
Q

Cultural characters of Yersinai pestis

A
  • Facultative anaerobes.
  • They grow on blood agar and MacConkey producing non-lactose fermenting colonies
  • rats die within few days when injected subcutaneosly
105
Q

Virulence factors of Yersinia pestis

A

1- A lipopolysaccharide endotoxin that causes endotoxic shock.

2- F1 antigen is antiphagocytic and induces protective antibodies.

3-V-W antigens are present in virulent strains and are encoded by genes on plasmids. They are antiphagocytic.

4-Yops (Yersinia outer proteins) have a variety of activities, including inhibiting phagocytosis, inhibiting platelet aggregation and preventing an effective inflammatory response.

5- Plasminogen activator protease degrades fibrin and extracellular proteins and facilitates systemic spread from the inoculation site.

6- An exotoxin lethal to mice

106
Q

pathogenesis of Yersinia plague

A

bubonic plague in lymph nodes
pneumonic plague or meningitis
septicaemic plagu: Dissemination is associated with endotoxic shock, DIC and cutaneous haemorrhages

107
Q

can be uesd in bioterrorism

A

Yersinia pestis

108
Q

cause of Primary pneumonic plague

A

due to inhalation of infected droplets from a patient.
Haemorrhagic consolidation, sepsis and death may occur

109
Q

diseases caused by Y. enterocolitica and Y. pseudotuberculosis

A
  • enterocolitis
  • mesenteric adenitis
  • bacteraemia and abscesses in liver or spleen
  • Immunologic sequelae e.g. reactive arthritis and erythema nodosum
110
Q

mode of transmission of Y. enterocolitica and Y. pseudotuberculosis

A

transmitted to humans by contamination of food with the excreta of domestic animals

111
Q

charachterized by peripheral zone of swollen club

A

Actinomyces israelii

112
Q

causing vasculitis in heart and brain

A

R. Prowazeki
Epidemic typhus

113
Q

causing DIC and vascular occlusion

A
  • R. Prowazeki Epidemic typhus
  • R. ricketsii rocky mountain spotted fever
114
Q

causes mesenteric adenitis

A

Y. enterocolitica and Y. pseudotuberculosis

115
Q

cause infection of alveolar macrophages

A

coxiella burnetti (Q fever)

116
Q

coxiella burnetti is transmitted between goats, sheep, cattle by

A

ticks

117
Q

incubation period of coxiella burnetti

A

2 weeks

118
Q

best method to diagnose coxiella burnetii

A

Indirect immunofluorescence

119
Q

pelvic actinomycosis due to

A

infection with women keeping an intrauterine device for a long period

120
Q

three different families of arbovirus

A
  • Togaviruses
  • Flaviviruses
  • Bunyaviruses
121
Q

Transmission of arboviruses by

A

blood-sucking arthropods e.g. mosquitoes, ticks,
or sandflies

122
Q

Common clinical pictures of arboviruses

A

Encephalitis, hemorrhagic fevers, myalgias, arthralgias, non hemorrhagic rash, lymphadenopathy

123
Q

Causes arbovirus encephalitis

A

togavirus and flavivirus groups are endemic

124
Q

Culture of arbovirus encephalitis

A

tissue culture
chick embryo
in mouse brain by intracerebral inoculation

125
Q

Pathogenesis of Arbovirus encephalitis

A

Infection is transmitted by a bite of the infective arthropod»>the virus multiplies in local lymphoid tissue then reaches the blood stream»> causing viraemia in same time with fever» leads to general lymphadenopathy and maculopapular rash» then it invaded the CNS causes encephalitis,
meningitis and myelitis

126
Q

Arboviruses causes cause mild meningitis disease

A

West Nile and Sindbis

127
Q

Fever characterized by jaundice and albuminuria

A

Yellow fever

128
Q

Causative organism and reservoir of yellow fever

A

Causative organism: flavivirus
Reservoir: monkeys

129
Q

Monkey to monkey transmission of yellow fever by

A

mosquito Aedes africanus in Africa and Haemagogus in South America

130
Q

Urban yellow fever is transmitted from man to man by

A

Aedes aegypti

131
Q

Can infected with it when you visit the jungle

A

Yellow fever

132
Q

Hematemesis is picture of what?

A

Yellow fever

133
Q

Vaccine of yellow fever

A

live attenuated vaccine called 17-D vaccine

134
Q

Contraindication of 17 D vaccine of yellow fever

A

Contraindicated for
* Infants less than 9 months
* Pregnancy
* persons with
* altered immune systems e.g. HIV or organ transplant patients

135
Q

Dengue viruses are transmitted principally between humans by the

A

Aedes aegypti

136
Q

How many antigenic types of Dengue viruses

A

Four

137
Q

The two types of dengue fever

A

Classic dengue (rarely fatal) and dengue hemorrhagic fever (fatal)

138
Q

Clinical picture of dengue hemorrhagic fever

A

Shock and hemorrhage

139
Q

Pathogenesis of Dengue virus

A

Forms virus-antibody complexes results in increasing virus permeability and thrombocytopenia
the antibodies increase the entry of virus into monocytes and macrophages with the consequent release of large amounts of cytokines vasoactive mediators causing DIC, haemorrhages and shock

140
Q

what listeria cause in renal transplant patients

A

meningoencephalitis and bacteraemia

141
Q

Which disease that its vaccine is given to animal

A

Rift valley fever

142
Q

Complications of Rift valley fever

A

retinitis, encephalitis and haemorrhagic
fever. Permanent loss of vision may occur.

143
Q

Causes sandfly fever

A

Bunyavirus transmitted by sandfly Phlebotomus papatasii

144
Q

Transmitted by culex

A

West Nile fever

145
Q

Fever that has no vaccine

A

West Nile fever

146
Q

The main reservoir of west Nile fever

A

Wild birds

147
Q

Mode of transmission of west nile fever

A

by culex mosquito from infected bird, infected traveller, infected mosquito in airplanes, or by blood transfusion or organ transplantation

148
Q

Screening of the donated blood by PCR in which fever

A

Wild Nile fever

149
Q

Infection that considered as endogenous

A

Brill Zinsser disease

150
Q

Most cases of rocky mountain spotted fever occur in which generation

A

In children

151
Q

Only rickettsia disease that man to man

A

R. prowazekii epidemic typhus

152
Q

We use immunohistochemistry in diagnosis of what

A

Rickettsial disease

153
Q

Type of HIV virus genome

A

diploid single stranded positive sense RNA

154
Q

gene encodes the core proteins
gene encodes the enzymes of HIV
gene encodes the envelope proteins of HIV

A

Gag gene
Pol gene
Env gene

155
Q

Surface glycoproteins of envelope of HIV
Internal structure proteins (core) of HIV

A

Gp120 & Gp41
P24 & P17

156
Q

Proteins (enzymes) of HIV

A

Reverse transcriptase, integrase, Protease

157
Q

Interacts with CD4 receptors on the cell surface

A

Gp120

158
Q

Gp protrudes from the surface

A

Gp120

159
Q

Mediates fusion between virus envelope and cell membrane of infected cells.

A

Gp41

160
Q

appears in the serum early after infection by HIV and is a serologic marker for virus replication

A

P24

161
Q

The most importance core protein of HIV

A

P24

162
Q

Matrix protein surrounds p24

A

P17

163
Q

Proteins encoded by pol gene:

A

Reverse transcriptase.
Integrase.
Polymerase.

164
Q

Function of pol gene proteins

A

After viral fusion with cell, RT transcribes the genome RNA into double stranded DNA (provirus), which integrates into the host cell DNA by the action of the integrase enzyme. Viral mRNA is transcribed from the proviral DNA and transported to the cytoplasm, where it is translated into large polyproteins. These are cleaved by the protease enzyme to produce the different viral structures and enzymes

165
Q

Mode of transmission of HIV

A

Sexual, blood, perinatal (trans-placentally, during delivery, breast feeding)

166
Q

What is Initial infection of HIV

A

The initial infection of the genital tract occurs in dendritic cells that line the mucosa, these migrate to local lymph nodes where helper T cells become infected by attachment to CD4

167
Q

A protein coreceptor on T cells that is required for infection of these cells.

A

CXCR4

168
Q

A coreceptor on macrophages, monocytes, dendritic cells is required for their infection

A

CCR5

169
Q

What cells response in the acute stage of HIV infection

A

cytotoxic CD8 lymphocytes (CTLs) and antibodies (humoral immunity) dramatically reduce HIV levels

170
Q

Viral mechanisms in the latent infection

A

a- Latent infection of host cells as a provirus.
b- Rapid genetic mutation.
c- Trapping of infectious virus in lymphoid tissues in and on the surface of follicular dendritic
cells, which act as reservoirs.

171
Q

II-Suppression of immune mechanisms which are more evident during late stages of infection of HIV

A

a-Deletion of CD4 T cells,
b-Deletion of HIV-specific CTL clones,
c- Dysfunction of CTLs due to; decreased production of IL-2, and decreased expression of
MHC-I by the action of viral genes, leading to decreased recognition of virus infected cells by
CTLs.
d- Impaired functions of APC.
e- Interference with humoral response which are T cell dependent

172
Q

Clinical picture of acute stage of HIV infection

A

begins 2-4 weeks after infection with a
mononucleosis-like picture of generalized
lymphadenopathy, fever, sore throat and a
maculopapular rash.

173
Q

fatigue, wasting, fever, chronic diarrhoea, and
persistent lymphadenopathy

A

AIDS Related Complex (ARC)

174
Q

The latent stage of HIV infection are clinically called as

A

AIDS Related Complex (ARC)

175
Q

Consequences of the late stage of HIV infections is AIDS

A
  • The most characteristic are Kaposi’s sarcoma and
    Pneumocystis jiroveci pneumonia.
  • Others are viral infections e.g. CMV, disseminated
    herpes simplex and herpes zoster infections; fungal
    infections such as C. albicans, cryptococcal
    meningitis; bacterial infections such as, M avium
    intracellular, M. tuberculosis;
  • protozoal infections such as toxoplasmosis
  • and cancer e.g.. non-hodgkin’s lymphoma and
    cervical cancer.
  • Many patients have neurologic problems e.g.
    dementia and neuropathy.
176
Q

Consequence of pediatric AIDS

A

Poor prognosis, present with clinical symptoms by 2 years of age; death follows in another 2 years from opportunistic infections,

177
Q

Laboratory diagnosis of HIV infection

A

1- Decreased CD4 cells count and inversion of the CD4/CD8 ratio.
2- Detection of HIV antibodies which appear 6-12 weeks after infection.
3- Detection of viral nucleic acid by PCR to know virus load
4-Virus isolation
5- Detection of viral antigens p24 by ELISA

178
Q

The antibody detection of HIV infection is confirmed by

A

the Western blot technique

179
Q

What is the Western blot technique

A

is more specific technique and it detects antibodies against viral core protein p24 or envelope glycoproteins gp 41, gp 120 or gpl60

180
Q

Diagnosis during the acute stage or pediatric AIDS of HIV infection

A

Diagnosis is made by viral isolation or by detection of viral RNA by PCR assay or by detection of p24
antigen

181
Q

treatment of choice for acute HIV infections

A

2 nucleoside analogues (reverse transcriptase inhibitors) in addition to a protease inhibitor

182
Q

Measures to reduce transmission of HIV infection from infected mothers to foetus

A

Screening of pregnant mothers for HIV,
those infected should receive treatment during pregnancy and delivery.
Neonates should receive the same drugs.
Delivery by cesarean section is recommended.
Infected mothers should not breast feed their infants

183
Q

Mechanism of cell transformation by tumor viruses

A
  1. Introduction of newtransforming genes i.e.
    “viral oncogenes”
  2. Activation or over expression of preexisting cellular genes “proto-oncogenes”
  3. Inactivation of a tumour suppressor gene
184
Q

What is the evidence of association between some viruses and human tumors?

A

a- Detection of virus nucleic acid integrated in the tumor cell chromosome or free in the
cytoplasm as in EB virus.
b- Detection of viral antigens in or on tumor cells.
c- The ability of viruses isolated from human tumors to cause transformation of cells in vitro e.g.
EBV, or to induce tumors in experimental animals.
d- The most definitive proof of a causal relationship is decreased tumor incidence by prevention
of viral infection e.g. HBV and HPV vaccination.

185
Q

Structure of Human papillomavirus HPV

A

dsDNA non-enveloped virus

186
Q

Mode of transmission of Human papillomavirus HPV

A

It is transmitted by direct and sexual contact

187
Q

Diseases caused by HPV

A

Types 6 and 11 cause anogenital warts; types 16 and 18, are implicated as the cause of carcinoma of the cervix

188
Q

Mechanism of oncogenesis of HPV

A

viral DNA integrated into host cell DNA leads to over-expressed E6 and E7 genes with
overproduction of E6 and E7 proteins which are HPV transforming proteins, which inactivates tumor suppressor proteins encoded by p35 and Rb genes and induce abnormal mitosis

189
Q

Prevention vaccine of HPV

A

HPV quadrivalent recombinant vaccine

190
Q

What is HPV quadrivalent recombinant vaccine

A

is composed of HPV LI proteins of types 6, 11, 16 and 18. It protects against cancer cervix and anogenital warts

191
Q

Way of given HPV vaccine and times

A

I.M. injections in three doses at a schedule of 0,1-2 and 6 months

192
Q

Vaccine of HPV for females

A

A bivalent vaccine containing types 16 and 18 is used for females only

193
Q

Diseases caused by Human T cell lymphotropic retrovirus (HTLV)

A

cutaneous T cell lymphomas and leukemias as well as tropical spastic paraparesis

194
Q

Mode of transmission of Human T cell lymphotropic retrovirus (HTLV)

A

blood transfusion, I.V. drug users, sexually in semen and from mother to infant in breast milk

195
Q

Causes cutaneous T cell lymphomas and leukemiasblood transfusion, I.V. drug users, sexually in semen and from mother to infant in breast milk

A

Human T cell lymphotropic retrovirus (HTLV)

196
Q

Causes nasopharyngeal carcinoma

A

Epstein-Barr

197
Q

Diseases caused by Epstein Barr

A

nasopharyngeal carcinoma, Burkitt’s lymphoma,
Hodgkins, non Hodgkins lymphomas and gastric cancer.

198
Q

Causes hepatocellular carcinoma (HCC)

A

Hepatitis B and C virus

199
Q

Causes Kaposi sarcoma

A

Human Herpesvirus 8

200
Q

What west nile virus and sindbis virus cause

A

mild meningitic disease

201
Q

What are the flaviviruses

A

YDW yellow fever, dengue fever, west nile fever

202
Q

Main reservoir of the yellow fever

A

monkeys

203
Q

Pathogenesis and clinical picture of
Yellow fever

A
  • The virus is introduced by the bite of an infective
    mosquito.
  • It multiphes in the local lymph nodes and spreads to
    the blood this coincides with sudden onset of fever,
    headache, myalgias and photophobia; some patients
    recover at this point.
  • The virus may reach the liver, spleen, kidney and bone
    marrow leading to their destruction.
  • This results in jaundice, haemorrhages and proteinuria.
    It may affect the heart or GIT leading to shock,
    prostration haematemesis (black vomit).
  • Death may result from kidney or liver failure.
204
Q

What are the bunya viruses

A

Rift valley fever and sandfly fever

205
Q

Man is infected with rift valley fever by

A

epizootic in domestic animals by coming in contact with infected animal body fluids or mosquito
bites.

206
Q

Animals infected with rift valley fever and how they infected

A

sheep and domestic animals infected with Aedes mosquito

207
Q

Person to person transmission of west nile fever by

A

Blood transfusion or organ transplantation

208
Q

grows on the chorioallantoic membrane of
chick embryo producing characteristic lesions
called “pocks”

A

Small pox virus

209
Q

What growing culture of small pox virus

A

grows on the chorioallantoic membrane of
chick embryo producing characteristic lesions
called “pocks”

210
Q

is the first disease to be controlled by
immunization

A

Small pox virus

211
Q

Reintroduced as biologic weapon

A

Yersinia pestis
Small pox virus

212
Q

Producing pocks lesions

A

Small pox virus

213
Q

Is the agent used for preparation of smallpox vaccine

A

Vaccinia virus

214
Q

Mode of transmission of small pox virus

A

The virus was transmitted by respiratory aerosol or by direct contact with skin lesions or contaminated fomites

215
Q

Vaccination of small pox virus

A

live vaccinia virus

216
Q

Clinical picture of small pox

A
  • It is a systemic disease with a viraemic stage and final localization in the skin causing the rash
  • The rash started on the face and extremities then appeared on the trunk.
  • The rash evolved through stages from macules to papules, vesicles, pustules and finally crusts in 2-3 weeks.
  • Crusts fell off leaving scarred area.
217
Q

Immunity followed the smallpox vaccine (vaccinia virus)

A

humoral and cell mediated immunity

218
Q

How small pox vaccine prepared

A

The vaccine is prepared from vesicular lesions (lymph) produced on shaved skin of calves or from virus grown on chick embryo; the final vaccine contains glycerol to stabilize the virus and phenol to destroy bacteria.

219
Q

Causes of successful eradication of
small pox

A

1- Man is the only host, and there is no animal
reservoir of infection
2- There is only one stable serotype of the virus
3- There is no carrier state or subclinical infection
4- Effective vaccine that is highly immunogenic and was used world wide
5- A surveillance-containment program was used by the WHO.
Smallpox cases are easily recognized clinically. Cases were traced and all susceptible contacts were
identified and vaccinated. The vaccine is protective if given within 4 days after exposure

220
Q

virus acquired by contact with wild animals killed for food or for their skins

A

Monkey pox

221
Q

Clinical picture of monkeypox

A

Symptoms are similar to smallpox, but differ in
occurrence of lymphadenopathy

222
Q

Causes pulmonary distress syndrome

A

Monkey pox

223
Q

How to differentiate monkeypox from smallpox

A

Monkeypox is antigenically distinct and produces
different lesions on the chorioallantoic
membrane of chick embryo

224
Q

Causes human warts (benign skin nodules)

A

Molluscum contagiosum

225
Q

How Molluscum contagiosum is transmitted

A

close contact and sexually

226
Q

Diseases caused by coxsackieviruses A

A

Herpangina
Acute hemorrhagic conjunctivitis
Handfoot and mouth disease

227
Q

Diseases caused by coxsackieviruses B

A

Pleurodynia
Myocarditis and pericarditis
Diabetes mellitus

228
Q

Diseases caused by coxsackieviruses A and B

A

Aseptic meningitis
Minor febrile illness
Diarrhea and hepatitis

229
Q

What causes Pleurodynia
What causes Acute hemorrhagic conjunctivitis
What causes Minor febrile illness

A

B Coxsackie
A Coxsackie
A&B Coxsackie

230
Q

What causes COX Diarrhea and hepatitis
What causes COX Diabetes mellitus
What causes Herpangina

A

A&B Coxsackie
B Coxsackie
A Coxsackie

231
Q

What causes COX Aseptic meningitis
What causes COX Myocarditis and pericarditis
What causes Handfoot and mouth disease

A

A&B Coxsackie
B Coxsackie
A Coxsackie

HEN (8 decks)

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