1. Infection - II General Pathology
Basic Principles of Cellular and Organ Pathology
Infection - II
Jaroslava Dušková
Inst. Pathol. ,1st Med. Faculty, Charles Univ. Prague

2. Inflammation - causes AUTOIMMUNE living nonliving prions (?) viral
physical
chemical
living
prions (?)
viral
bacterial
mycotic
parasitic
AUTOIMMUNE

3. Infectious Agents of Humans Viruses
virion
obligate intracellular
either DNA (adeno-, herpes-, pox-, cytomegalo-, EB, papova, HPV, ..
or RNA (picorna – entero-, polio-, coxsackie-, arbo-, rhino-, myxo-, paramyxo- RS, rubeola, rhabdo-, retro-,)

4. Virion
capsid
helical symmetry
icosaedral symmetry
genome
DNA
RNA

5. Host & Microorganism Encounter
General
Natural defenses
Inflammation
Immune status
Successful transmission
Site of attack
Number of microorg.
Pathogenicity

6. Host Inflammation Immune status General Natural defenses leucocytes
macrophages -phagocytosis
Immune status
immunity (or lack of it)
active, passive immunisation, contact
lymphocytes
immunoglobulins
complement
General
age, race, nutrition, other diseases (diabetes)
Natural defenses
skin, mucose integrity
mucus, cilliary action, unobstructed flow
protective secretion (lysosym in tears, gastric acid, IgA

7. Microorganism Successful transmission Site of attack
Number of microorg.
Pathogenicity invasiveness
toxin production
multiplication
resistence to host defence mechanisms
ability to cause necrosis
enzyme release

8. Virus – Host Cell Interaction
cytocidal
stabilised (steady– state)
transformation – ONCOGENS

9. Virus-Induced Injury cell entering - surface ligands – viral tropism
translocation of the entire virus
fusion of the viral envelope with the cell membrane
receptor mediated endocytosis
intracellular replicative phase – forming of virions using virus specific enzymes
virus assembly & release extracellular phase

10. Virus – Organism Interaction
infected cell
lysis by antibody and complement
cell mediated immunity lymphocytes macrophages interferon 

11. Virus-Induced Injury Host cell responses:
DNA, RNA and protein synthesis
metabolic derangements
cell lysis / cell fusion
multinuclear formation
viral inclusions

12. Infectious Agents of Humans Viruses
virion
obligate intracellular
either DNA (adeno, herpes, pox, cytomegalo, EB, papova, HPV, ..
or RNA (picorna – entero, polio, coxsackie arbo, rhino, arbo, myxo, paramyxo, RS, rubeola, rabdo, retro,)

13. The Herpes viruses Herpes simplex HSV 1,2
Varicella-Zoster chickenpox-shingles
Cytomegalovirus CMV infection
Epstein-Barr virus EBV infectious mononucleosis - glandular fever, Burkitt´s lymphoma

14. The respiratory viruses
Influenza influenza
Parainfluenza croup, pneumonia
RS bronchiolitis, pneumonia
Adeno pharyngitis, conjunctivitis
Rhino colds
Corona & Reo colds, SARS
colds (pl.) nachlazení

15. Viral Infections of Childhood
Measles – morbilli
Mumps – parotitis epidemica
German measles – rubeola
Fifth disease – erythema infectiosum- human parvovirus dis.
Measles 2 weeks incub. Red eyes, running nose, sneezing (kých), coughing

16. Poliomyelitis anterior acuta
Frequency
United States
No cases of wild-type poliovirus infection reported in the United States since 1979.
Until 1998, an average of 8-10 cases associated with the vaccine virus every year.
Four cases of vaccine-derived poliovirus were identified in 2005 among unvaccinated children in an Amish community in Minnesota.
International
The global incidence decreased by more than 99% since 1988.
No outbreaks reported in the western hemisphere since 1991
An outbreak in Haiti and the Dominican Republic in 2001.
Clusters of wild-type disease still found in some areas in Africa and Southeast Asia.
By 2004, the only 6 countries in which wild poliovirus transmission had not been interrupted were India, Egypt, Nigeria, Niger, Pakistan, and Afghanistan.
An increase in the number of cases was observed in 2006.

17. Tick Born Encephalitis
tick-borne encephalitis virus a member of the family Flaviviridae
virus initially isolated in 1937.
A closely related virus in Far Eastern Eurasia, Russian spring-summer encephalitis virus responsible for a similar disease with a more severe clinical course.

18. Marburg and Ebola Virus Infections
Pathogenesis
increase in vascular permeability
hemorrhagic diathesis
interstitial edema in visceral organs and brain
DIC
liver necrosis
renal tubular necrosis
terminal DIC/shock syndrome

19. Virus – Host Cell Interaction
cytocidal
stabilised (steady– state)
transformation – ONCOGENS

20. Oncogenic Viruses DNA HPV SV 40 – polyoma Adenoviruses Herpesviruses
Epstein– Barr
Hepatitis B
RNA
Rous sarcoma
Leukemia
HIV