Infectious disease Flashcards

1
Q

Malarial diseases

A
  • Plasmodium Falciparum- Vivax- Malariae- Ovale- Knowlesi
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the primary malarial vector?

A
  • Anolpheles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the 4 HIV genes and what does each contain?

A
  • Gag - P24 (capsid), P17 (matrix)- Pro - Protease- Pol - RT, Integrase- Env - Gp 120 and 41
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the HIV gene regulatory regions and what do they regulate?

A
  • 5’ - RNA transcription initiation- 3’ - termination and polyanenylation - Important for integration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe the Herpesvirus genome and function.

A
  • 100 genes- Immediate early genes - Shut off host cell protein synthesis and distruction of mRNA and DNA- Early genes - Replication of DNA and formation of concatemers- Late genes - Formation of envelop and capsid proteins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the diseases caused by EBV?

A
  • Infectious mononucleosis- Nasopharyngeal carcinoma- Burkitt’s lymphoma- Hodgkins lymphoma- Gastric carcinoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the pathogenesis of EBV?

A
  • Infects B cells and epithelial cells of the oropharynx- Acts as mitogen to B cells increasing proliferation and release of heterophile antibodies through the binding of CD21 and MHC 2.- T cells respond against infected cells through rapid proliferation (lymphocytosis) and produce atypical CTL’s (Downey bodies)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How do patients present with EBV?

A
  • Children normally asymptomatic- Teens and adults present with lymphadenopathy (especially posterior cervical and auricular), fatigue and flu like symptoms.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the isotype of the heterophile antibody that is produced in EBV and what complications does this create?

A
  • IgM- Antibodies can develop against ampicillin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What type of herpesvirus is EBV?

A
  • Gamma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What type of herpes virus is MCV?

A
  • Beta
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What diseases are associated with MCV?

A
  • Infectious mono- Congenital abnormalities - AIDS- Organ transplant patients
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does CMV evade CTL’s?

A
  • Inhibits translation of MHC 1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does transmission differ between MCV and EBV?

A
  • EBV - salivary transmission- MCV - Often sexual transmission
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How does presentation differ for MCV?

A
  • Pharyngitis with exudate rarely seen- Heterophile antibody negative
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How does MCV effect immunocompromised patients?

A
  • Transplant - latent in many tissues, fever, leukopenia, hepatitis, pneumonitis, esophagitis, gastritis, colitis and retinitis. Graft rejection- AIDS - intestinal tract. Colitis and diarrhea, meningoencephalitis.
17
Q

How is MCV diagnosed?

A
  • Culturing, PCR, immunofluorescence, histological stain with owl eye inclusions.
18
Q

In EBV what antigens remain following the loss of heterophile antibodies?

A
  • Viral capsid antigen (VCA)- Early antigen
19
Q

What are the hemorrhagic fever viruses?

A
  • Flavivirus - Dengue - +ssRNA- Filovirus - ebola and marburg -ssRNA
20
Q

What are the five types of ebola viruses?

A
  • Human - Zaire, Sudan, tai forrest and Bundybugyo- Primate - Reston VA
21
Q

What caused the Marburg outbreak in Germany?

A
  • African Green monkey’s
22
Q

What is the structure of the filovirus?

A
  • Helical capsid within an envelope which contains Glycoprotein that mediates attachment and entry of virion into host cell.- Within envelope - RNA dependent RNA polymerase, transcription factor (VP 30) and polymerase cofactor (VP 35)
23
Q

Pathogenesis of filovirus

A
  • Infects and replicates within DC’s and macrophages- Inoculation site to regional lymph nodes to spleen and liver and other lymphoid tissue - Impaired antibody production allowing virus to proliferate. - Systemic release of cytokines leads to systemic inflammation and increased vascular permeability.- Activation of TF leads to systemic clotting- DIC, shock, systemic hemorrhage and multiorgan failure.
24
Q

Flavivirus structure

A
    • ssRNA- Icosahedral, enveloped- Envelope made of M protein and E dimer
25
Q

How is the Dengue fever transmitted?

A
  • Mosquito transmission- Aedes aegypti
26
Q

Dengue pathogenesis

A
  • DC’s of skin and fibroblasts- Lymph nodes - monocytes and WBC- Dissemination throughout blood
27
Q

Dengue disease progression

A
  • Febrile illness - fever, myalgia, deep bone pain, rash, HA and pain behind eyes, lymphadenopathy, vomiting and diarrhea- Severe dengue - Typically <15 yo, Plasma leakage, severe bleeding (GI, skin, mucosa), Dengue shock syndrome
28
Q

How is Dengue fever diagnosed?

A
  • Isolation of virus - Serologic test- NAT (PCR)