11. Lecture Flashcards
how is a successful infection measuredd
Survival of viruses
extent of virus propagation in the host organism
- Localized infection (certain tissues, organs)
* Generalized infection (spread by e.g. blood)
•Transcutaneous infection
•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
Airborne infection
– 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
Oral infection
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!
Venereal infection
Via the urogenital tract
•sexual intercourses
•sensitive viruses too
•often cell-associated transmission
Transplacental- or intrauterine infection
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
Germinative infection
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)
Latrogenic infection
– by veterinarians
• non-sterile equipment (papilloma-, flaviviruses)
• needle, syringe (flavi-, arteri-, retroviruses)
Mixed forms
•oronasal - influenza
Factors influencing the result of infection: susceptibility
•abortive infection – non pathogenic, not suitable route
→ host spectrum
•stenoxen (one)
•euryxen (multiple)
Factors influencing the result of infection: infectivity
•viral receptors, nucleic acid
Factors influencing the result of infection: amount of viruses
~chances of successful infection
~capacity of the immune system
Factors influencing the result of infection: pathogenicity
•overt disease ↔ adaptation
- interaction btw. virus and host e.g. co-evolution
Factors influencing the result of infection: virulence
degree of expression (pathogenicity)
types of virus infection: virus multiplication
•effect on the cell
•effect on the host organism
→ course of the disease
types of virus infection: parameters
•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)
acute infection
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
Latent infection
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
tolerated infection
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
direct (viruses) and indirect (antibodies) are seen in beginning and later in: tolerated infection
indirect: –
direct: ++
direct (viruses) and indirect (antibodies) are seen in beginning and later in: acute infection
indirect: -+
direct: -+
direct (viruses) and indirect (antibodies) are seen in beginning and later in: non-infected
indirect: –
direct: –
persisting infection
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
slow infection
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
