Professional Documents
Culture Documents
Basic Principles
of Cellular and Organ
Pathology
Infection - I
http://www1.lf1.cuni.cz/~jdusk/
Jaroslava Dušková
Inst. Pathol. ,1st Med. Faculty, Charles Univ. Prague
Inflammation - causes
living
prions (?)
nonliving viral
physical bacterial
chemical mycotic
parasitic
AUTOIMMUNE
Interaction of Organism and
Microorganism – Terms
Bacteriemia (transient)
Sepsis/ Septicemia
Pyemia
Toxemia
Viremia
Bacteriemia
transient presence of
microbes in the
bloodstream
Sepsis / Septicemia
(Severe Bacteremia)
increasing numbers
of microbes (& their toxins)
in the bloodstream
Sepsis/Septicemia
Def.
systemic response to infection
manifestating as
tachypnoe > 20/min.
tachycardia > 90/min.
temperature > 39 st. C. (ev. < 36st.C)
leucocytosis > 15 000/1l (ev. < 4000/1l)
Sepsis – Pathogenetic Factors
Endotoxin, toxins G+ TNF, IL–1
Macrophages TNF, IL–1, IL–6
Cytokins NO synthesis
NO vasodilation
PAF (Platelets
Activating Factor) coagulation
Syndrome of Systemic
Inflammatory Response
Def.
systemic response to an AGENT
manifestating as
tachypnoe > 20/min.
tachycardia > 90/min.
temperature > 39 st. C. (ev. < 36st.C)
leucocytosis > 15 000/1l (ev. < 4000/1l)
General Successful
Natural transmission
defenses Site of attack
Inflammation Number of microorg.
Immune status Pathogenicity
Host Inflammation
– leucocytes
– macrophages
General -phagocytosis
– age, race, nutrition, other
diseases (diabetes) Immune status
Natural defenses – immunity (or lack of
it)
– skin, mucose integrity
active, passive
– mucus, cilliary action, immunisation, contact
unobstructed flow
– lymphocytes
– protective secretion
(lysosym in tears, gastric – immunoglobulins
acid, IgA – complement
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
INFECTION versus DISEASE
Pathogenicity (virulence)
Incubation Period
Carrier State
Agent – Host Interaction
cytocidal
stabilised (steady– state)
transformation –
ONCOGENS
Virus – Host Cell
Interaction
cytocidal
stabilised (steady– state)
transformation –
ONCOGENS
Inflammation - causes
infectious
prions
non viral
infectious bacterial
physical mycotic
chemical parasitic
AUTOIMMUNE
Infectious Agents of Humans
prions
viruses (DNA, RNA)
bacteria (incl. chlamydia, mycoplasma,
rickettsia – obligatory intracellular parasites)
fungi (yeasts, molds)
parasites (protozoa, helmints, ectoparasites-
insects: lice, mites, ticks; spiders)
Infectious Agents of Humans Bacteria
simple cells – prokaryotes
both DNA and RNA
cocci, bacilli (AFB!), spirochetes….
Gram positive /negative
extra- and/or intracellular
aerobic/ anaerobic
Infectious Agents of Humans Fungi
complex cells – eukaryotes
both DNA and RNA
yeasts, molds (hyphae, pseudohyphae…)
PAS, impregnation
extra- or intracellular
mostly opportune pathogens
Infectious Agents of Humans Parasites -1
Protozoa
complex cells – eukaryotes
both DNA and RNA
extra- or intracellular
(Amebas, Trichomonas,Trypanosoma,
Toxoplasma, Plasmodium, Pneumocystis…)
Infectious Agents of Humans Parasites -2
Metazoa (helmints and flukes)
multicellular
both DNA and RNA
flat and round worms
extracellular
(Taenia, Ascaris, Enterobius, Trichuris
Echinococcus, Clonorchis, Schistosoma,
Wuchereria…)
Infectious Agents of Humans Parasites -3
Insecta, Arachnida
multicellular
both DNA and RNA
extracellular
(Sarcoptes scabiei, fleas, ticks, lice……)