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

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

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-,)

Virion capsid helical symmetry icosaedral symmetry genome DNA RNA

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

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

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

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

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

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

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

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,)

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

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

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

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.

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.

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

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

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