11. Lecture Flashcards

1
Q

how is a successful infection measuredd

A

Survival of viruses

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

extent of virus propagation in the host organism

A
  • Localized infection (certain tissues, organs)

* Generalized infection (spread by e.g. blood)

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

•Transcutaneous infection

A

•keratinized cells on the surface – no virus infection
•injuries: papilloma(ketratinized cells as well, rabies (bite)
•arthropod vector – arthropod-borne: arbovirus
→ mosquito, tick, fly, louse
- mechanic vector(transfer only, no multiplication in the vector) – biological vector (multiplication in the vector sometimes, overwinter, transfer to later generations - eggs also infected)
•special: conjunctiva (herpes) in humans

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

Airborne infection

A
– via the respiratory tract
•droplet infection 
•aerosol particles between 5 and 0.5 μm
•UV light, drying out
•defence systems
•mucosal immunity (IgA, lymphoid cells, alv. macrophage)
•temperature: 33°C – polymerase activity low
•microvilli
•respiratory diseases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Oral infection

A

Via the enteric system:
•oral cavity – lysozyme
•stomach: acidic pH, proteolytic enzymes
•small intestine: digestive enzymes, bile (detergent)
→ resistant viruses (mainly non-enveloped)
-proteolytic enzymes sometimes activate virus receptors!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Venereal infection

A

Via the urogenital tract
•sexual intercourses
•sensitive viruses too
•often cell-associated transmission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Transplacental- or intrauterine infection

A

Via the placenta
• different placenta structures – diff. barriers
• age / development of the embryo!
→ resorption, tolerance, abortion, mummification…

no immune response is developed against viruses - they can be recognized as the body’s own cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Germinative infection

A

Via the egg (birds)
• on the surface of the egg – at hatching (ie.: herpes)
• inside the egg - inside bird during development
• yolk immunity! (like immunity from placenta)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Latrogenic infection

A

– by veterinarians
• non-sterile equipment (papilloma-, flaviviruses)
• needle, syringe (flavi-, arteri-, retroviruses)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Mixed forms

A

•oronasal - influenza

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

Factors influencing the result of infection: susceptibility

A

•abortive infection – non pathogenic, not suitable route
→ host spectrum
•stenoxen (one)
•euryxen (multiple)

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

Factors influencing the result of infection: infectivity

A

•viral receptors, nucleic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Factors influencing the result of infection: amount of viruses

A

~chances of successful infection

~capacity of the immune system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Factors influencing the result of infection: pathogenicity

A

•overt disease ↔ adaptation

- interaction btw. virus and host e.g. co-evolution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Factors influencing the result of infection: virulence

A

degree of expression (pathogenicity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

types of virus infection: virus multiplication

A

•effect on the cell
•effect on the host organism
→ course of the disease

17
Q

types of virus infection: parameters

A
•presence of infectious virions in the host
•intracellular and extracellular
~ virus multiplication
•shedding of infective virions
~spread of the virus in the population
•clinical signs (disease)
•immune response (serum antibodies)
18
Q

acute infection

A

normalkurve
•Virus multiplication and shedding happen simultaneously
•Clinical signs occur at a certain virus concentration
•Immune response highest after recovery
•Can lead to death
•Can turn into a chronic infection

19
Q

Latent infection

A

chronic infection
• Acute phase: virus replication, immune response, shedding, clinical signs
• Weak antigens – antireceptor induce low level of antibodies, and decrease further quickly -> body is not protected against infection
• Immune response occur after acute phase but decrease quite quickly, when low a reactivation of the virus can occur

20
Q

tolerated infection

A

chronic infection
• Usually happen at second trimester of pregnancy -> self recognision phase (which ag’s part of body) -> no reaction against viruses as they are though to be part of the body -> no neutralization -> continous shedding -> constant source of infection in a herd until death
• Clinical signs might be seen during whole life
• Sigmoid curve

21
Q

direct (viruses) and indirect (antibodies) are seen in beginning and later in: tolerated infection

A

indirect: –
direct: ++

22
Q

direct (viruses) and indirect (antibodies) are seen in beginning and later in: acute infection

A

indirect: -+
direct: -+

23
Q

direct (viruses) and indirect (antibodies) are seen in beginning and later in: non-infected

A

indirect: –
direct: –

24
Q

persisting infection

A

chronic infection
• hidden neutralization antigen
• Acute phase with clinical signs – may lead to death
• If survive virus multiplication and immune response occur whole life, but shedding and clinical signs are seen from time to time
• Shedding even with antibodies in body by hiding at specific places such as CNS, hoof, bladder
• Ig not effective
• hidden virus

25
Q

slow infection

A

chronic infection, retroviruses, e.g. HIV
• Integration with genome – slow
• Frequent antigenic changes – difficult to clear the viruses from the body

HIV:
• Virus multiplication increasing thoughout life
• Clinical symptoms in older age, infection at young age typically
• Immune response but inefective bc of the destruction of the immune system – new antibody prod as the antigens change
• Shedding here and there at young age, constant at old age
• Prions
- No antigenic prod agains prions -> accumilation in brain -> e.g. changes in behavior or other clinical symptoms depending on where in the brain the infection occur