3. WHAT IS
INFECTION
• An infection is the colonization of a host by
Microbial species. Infecting Microbes seek to
use the host's resources to reproduce, often
resulting in disease.
• Infections are usually considered to be caused
by microscopic organisms like viruses, prions,
bacteria, and viroids, though larger organisms
like macro parasites and fungi can also infect.
4. BASIS OF CLASSIFICATION OF
INFECTIONS
• Infections are classified in multiple ways. They are
classified by the causative agent as well as by the
constellation of symptoms and medical signs that
are produced.
• An infection that produces symptoms is an
apparent infection.
• An infection that is active, but does not produce
noticeable symptoms, may be called in apparent,
silent, or subclinical.
• An infection that is inactive or dormant is called a
latent infection
6. WHAT CAUSES AN INFECTIOUS
DISEASE
• Infection is caused
by microorganism
• The
microorganism
may be a bacteria,
a virus, a parasite
or a fungus
Bacillus anthracis bacteria–
Public Health Image Library
Dr.T.V
.Rao MD
5
7. OVERVIEW
• Types of Microorganisms
• Principles of Infection
– Transmission
– Host resistance
– Virulence and pathogenicity
– Control of transmission and infection
• Development of Infection
– Onset and course
– Clinical signs and symptoms
– Diagnostic tests
• Antimicrobial Drugs
• Example of Infection: Influenza
8. CONDITIONS REQUIRED FOR INFECTION
TO SPREAD FROM ONE PERSON TO
ANOTHER
• 1. One person must be infected with a
microorganism
• 2. The other person must be susceptible
to infection with that microorganism
• 3. The microorganism must be able to
leave the body of the infected person and
enter the body of the susceptible person.
9. TYPES OF
INFECTION
• Colonization – infection present on surface of
body –
– Organism propagating at a rate sufficient to
maintain its numbers without producing identifiable
evidence of any reaction in host
• Inapparent or subclinical infection
– organism not only multiplying but also causes a
measurable reaction that is however not clinically
detectable
• Symptomatic infection
– Organism causes clinically detectable reaction
10. TIME PARAMETERS OF
INTERACTION
• Latency Period = the time between
infection agent and onset of
infectiousness
• Incubation Period = the time
between infection and onset of
symptoms
• Latency period may not be the
same as the incu
Dr.T
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.V
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ion period 9
11. DEFINITIONS
• Disease and Infectious Disease
–Disease
• Any deviation from a condition of
good health and well-being
–Infectious Disease
A disease condition caused by the
presence or growth of infectious
microorganisms or parasites
12. DEFINITION
S
• Pathogenicity and Virulence
– Pathogenicity
• The ability of a microbe to cause disease
• This term is often used to describe or
compare species
– Virulence
• The degree of pathogenicity in a
microorganism
• This term is often used to describe or
compare strains within a species
13. DEFINITIONS
• Acute infection vs. chronic infection
–Acute Infection
• An infection characterized by sudden onset,
rapid progression, and often with severe
symptoms
– Chronic Infection
• An infection characterized by delayed onset
and slow progression
14. DEFINITIONS
• Primary infection vs. secondary
infection
–Primary Infection
• An infection that develops in an
otherwise healthy individual
–Secondary Infection
• An infection that develops in an
individual who is already infected with
a different pathogen
15. DEFINITIONS
• Localized infection vs. systemic infection
– Localized Infection
• An infection that is restricted to a specific
location or region within the body of the
host
– Systemic Infection
• An infection that has spread to several
regions or areas in the body of the host
16. .DEFINITION
S
• Clinical infection vs. subclinical
infection
•–Clinical Infection
•An infection with obvious observable
or detectable symptoms
•–Subclinical Infection
•An infection with few or no obvious
symptoms
Dr.T.V
.Rao MD 15
17. DEFINITION
S
• Opportunistic infection
– An infection caused
by microorganisms
that are commonly
found in the host’s
environment This
term is often used to
refer to infections
caused by organisms
in the normal flora
18.
19. DEFINING
• The suffix “-emia”
–A suffix meaning “presence of an infectious
agent”
• Bacteremia = Presence of infectious
bacteria
• Viremia = Presence of infectious virus
• Fungemia = Presence of infectious fungus
• Septicemia = Presence of an infectious
agent in the bloodstream
20. DEFINITIONS
• The suffix “-itis”
– A suffix meaning “inflammation of”
• Examples:
–Pharyngitis = Inflammation of the pharynx
–Endocarditis = Inflammation of the heart
chambers
–Gastroenteritis = Inflammation of the
gastrointestinal tract
21. DEFINITION
S
• Epidemiology
– The study of the transmission of disease
• Communicable Disease
– A disease that can be transmitted from one individual to
another
• Contagious Disease
– A communicable disease that is easily spread from one
individual to another
• Non communicable Disease
– A disease that is not transmitted from one individual to
another
22. DEFINITION
S
• Endemic Disease
– A disease condition that is normally found in a
certain percentage of a population
• Epidemic Disease
– A disease condition present in a greater than
usual percentage of a specific population
• Pandemic Disease
– An epidemic affecting a large geographical area;
often on a global scale
23. DEFINITION
S
• Reservoir of Infection
– The source of an infectious agent
• Carrier
– An individual who carries an infectious agent
without manifesting symptoms, yet who can
transmit the agent to another individual
• Fomites
– Any inanimate object capable of being an
intermediate in the indirect transmission of an
infectious agent
24. DEFINITION
S
• Animal Vectors
– An animal (nonhuman) that can transmit an
infectious agent to humans
– Two types: mechanical and biological
• Biological animal vectors: The infectious agent must
incubate in the animal host as part of the agent’s
developmental cycle; eg, the transmission of malaria
by infected mosquitoes
• Mechanical animal vectors: The infectious agent is
physically transmitted by the animal vector, but the
agent does not incubate or grow in the animal; eg, the
transmission of bacteria sticking to the feet of flies
25. DEFINITIONS
• Direct Mechanisms
of Disease
Transmission
– Directly From Person
to Person
– Examples:
Direct Skin Contact
Airborne (Aerosols)
– From Mother to
fetus
27. THE NORMAL FLORA OF HUMANS
• Types of Symbiosis
–Mutualism
• A symbiotic relationship in which both species
benefit
–Commensalism
• A symbiotic relationship in which one species
benefits, and the other species is neither helped
nor harmed
28. THE NORMAL FLORA OF
HUMANS
• Types of Symbiosis (cont.)
– Parasitism
• A symbiotic relationship in which one
species benefits, and the other species
is harmed
• Generally, the species that benefits
(the parasite) is much smaller than the
species that is harmed (the host)
29. . THE NORMAL FLORA OF
HUMANS
• Normal flora is present
in
– skin
– upper respiratory tract
– oral cavity
– intestine, especially large
intestine
– vaginal tract
• Very little normal flora
in eyes & stomach
30. THE NORMAL FLORA IS ABSENT
• Notably absent in most all internal organs
– Absent in:
• lower respiratory tract
• muscle tissue
• blood & tissue fluid
• cerebrospinal fluid
• peritoneum
• pericardium
• meninges
31. THE NORMAL FLORA OF HUMANS
• Benefits of the normal
flora
– Nutrient
production/processing
eg Vitamin K production by
E. coli
– Competition with
pathogenic microbes
– Normal development of
the immune system
• Normal flora and
opportunistic infections
32. DEVELOPMENT OF INFECTION:
ONSET
AND COURSE
• Incubation period
– Organism present; no
clinical signs,
symptoms
• Prodromal period
– Symptoms; don’t feel
like yourself
• Acute period
– Fully developed
infection
33. DEVELOPMENT OF INFECTION:
CLINICAL SIGNS AND SYMPTOMS
• Local signs
– Inflammation
– Purulent exudate if bacterial infection; serous
exudate if viral
– Tissue necrosis
– Lymphadenopathy
– Respiratory effects
• Systemic signs
– Fever, fatigue, headache, nausea
34. GENERALIZED STAGES OF
INFECTION
1. Entry of Pathogen
– Portal of Entry
2. Colonization
– Usually at the site of entry
3. Incubation Period
– Asymptomatic period
– Between the initial contact with the microbe
and the appearance of the first symptoms
35. GENERALIZED STAGES OF
INFECTION
4. Prodromal Symptoms
– Initial Symptoms
5. Invasive period
– Increasing Severity of Symptoms
– Fever
– Inflammation and Swelling
– Tissue Damage
– Infection May Spread to Other Sites
– Acme (Fastigium)
38. VIRULENCE AND
PATHOGENICITY
• Pathogenicity: capacity of microbes to cause
disease
• Virulence: degree of pathogenicity of specific
microbe
– Based on:
• Invasive qualities
• Toxic qualities
• Presence of pili or fimbriae for adhesion
• Ability to avoid host defenses (mutate)
Dr.T.V
.Rao MD 38
39. VIRULENCE FACTORS AND
TOXINS
• State of the
Host Immune
System
• Number of
Pathogenic Cells
encountered by
the Host
–Infectious Dose
Dr.T.V
.Rao MD 39
41. VIRULENCE FACTORS AND
TOXINS
• Adhesion Factors
– Examples:
• Protein A
(Staphylococcus
aureus)
• Protein M
(Streptococcus
pyogenes)
42. VIRULENCE FACTORS AND
TOXINS
• Exotoxins
– A type of bacterial toxin with the following
properties:
• May be produced by either gram-positive or gram-
negative bacteria
• Is secreted by the bacteria
• The action of the exotoxin does not necessarily
require the presence of the bacteria in the host
• Most exotoxins are peptide or protein
• Most exotoxins are heat sensitive (exception:
enterotoxin of Staphylococcus aureus)
43. VIRULENCE FACTORS AND
TOXINS
• Exotoxins (cont.)
– Classes of exotoxins: Neurotoxic, cytotoxic, or
enterotoxic exotoxins
• Neurotoxins: Interfere with proper synaptic
transmissions in neurons
• Cytotoxins: Inhibit specific cellular activities, such as
protein synthesis
• Enterotoxins: Interfere with water reabsorption in
the large intestine; irritate the lining of the
gastrointestinal tract
44. VIRULENCE FACTORS AND
TOXINS
• Endotoxins
– A type of bacterial toxin having the following
properties:
• Produced only by gram-negative bacteria
• Endotoxins are a component of the gram-negative
cell wall
• The action of endotoxin requires the presence of
the bacteria in the host. The endotoxin may be
released from the cell wall as the cells die and
disintegrate
45. VIRULENCE FACTORS AND
TOXINS
• Endotoxins (cont.)
• Endotoxin is composed
of Lipid A: Part of the
lipopolysaccharide
layer
• Mode of action:
Irritation/inflammation
of epithelium, GI
irritation,
capillary/blood vessel
inflammation,
hemorrhaging
46. DEVELOPMENT OF
INFECTION:
DIAGNOSTIC TESTS
• Cultures and stains
– bacteria
• Blood tests
– Bacteria
• Leukocytosis
– Virus
• Leukopenia
– Increase in neutrophils w/
acute; increase in
lymphocytes and monocytes
w/ chronic
• Radiologic exams
47. STEPS TO MINIMIZE RISK OF
INFECTION
• Locate, remove reservoir
host
• Block portal exit of
microbes from reservoir
• Know mode(s) of
transmission of specific
infections
• Block portals of entry
• Cleaning
• Sterilization
• Disinfectants
• Antiseptics
48. HOSPITAL ACQUIRED
INFECTIONS
• Infection which was
neither present nor
incubating at the time
of admission
• Includes infection which
only becomes apparent
after discharge from
hospital but which was
acquired during
hospitalisation (Rcn,
1995)
• Also called nosocomial
infection
49. MODES OF SPREAD
Two sources of infection:
• Endogenous or self-infection - organisms
which are harmless in one site can be
pathogenic when transferred to another
site e.g., E. coli
• Exogenous or cross-infection - organisms
transmitted from another source e.g.,
nurse, doctor, other patient, environment (Peto,
1998)
50. 1ST PRINCIPLE OF INFECTION
PRÉVENTION
at least 35-50% of all nosocomial infections are associated
with patient care practices:
• Use and care of urinary catheters
• Use and care of vascular access lines
• Therapy and support of pulmonary functions
• Experience with surgical procedures
• Hand hygiene and standard precautions
51. BASIC STEPS IN PREVENTION OF
INFECTION
• There are possible
treatment and
prevention to stop
the infection cycle.
This is through
adequate hygiene,
sanitary
environment
maintenance and
health education.
52. and have no effect on viral ones.
ANTIMICROBIAL AGENTS IN
INFECTION
• Anti-infective drugs such as antibiotics,
antiviral, antifungal and ant tubercular drugs
suppress infection. It can be administered by
mouth, topically or intravenously depending
on the infection extent and severity.
Sometimes, if drug resistance is known,
multiple drugs are used to stop drug
resistance and increase drug effectiveness.
Antibiotics only work for bacterial infection
56. ACUTE
INFLAMMATION
■ Immediate and early response to tissue
injury (physical, chemical, microbiologic, etc.)
■ Acute inflammation has two major components :
■ Vascular changes
■ Cellular events
58. VASCULAR
CHANGE
■ The main vascular reactions of acute
inflammation are increased blood flow
followed by vasodilation and increased
vascular permeability:
■ warmth and redness
■ Opens microvascular beds and protein-rich
fluid moves into extravascular tissues
■ Migration of leukocytes (principally neutrophils)
59. INCREASED VASCULAR
PERMEABILITY
■ This will leads to the
movement of protein-rich
fluid and blood cells into the
extravascular tissue.
■ The resulting protein-rich
accumulation is called an exudate.
■ Increases interstitial osmotic
pressure contributing to
edema.
60.
61. VASCULAR
LEAKAGE
■ several mechanisms may contribute to
increased vascular permeablity:
■ Endothelial cell contraction that leading to
intracellular gaps of venules
This occur after binding of histamines and
bradykinins, and many other mediators and
is usually short-lived (15 – 30 min.)
62. VASCULAR
LEAKAGE
■ Cytokine mediators (TNF, IL-1) induce
endothelial cell junction retraction through
cytoskeleton reorganization
■ This reaction may take 4 – 6 hrs to develop
,and lasting for 24 hrs or more
63. VASCULAR
LEAKAGE
■ Endothelial injuries result in vascular
leakage by causing direct endothelial cell
necrosis, detachment making them leaky
until they are repaired or may cause
delayed damage as in thermal, certain
bacterial toxins or Ultraviolet injury.
64. VASCULAR
LEAKAGE
■ Certain mediators such as vascular
endothelial growth factor (VEGF) may
cause increased transcytosis via
intracellular vesicles which travel from the
luminal to basement membrane surface of
the endothelial cell
■ All or any combination of these events
may occur in response to a given
stimulus
66. LEUKOCYTE CELLULAR
EVENTS
■ Leukocytes leave the vascular lumen to the
extravascular space through the following
sequence of events:
■
■
■ Margination and rolling along the vessel wall
Firm adhesion and transmigration between
endothelial cells
Chemotaxis and activation
67.
68. MARGINATION AND
ROLLIN
G
■
■ With increased vascular permeability, fluid
leaves the vessel causing leukocytes to
settle-out of the central flow column and
“marginate” along the endothelial surface
Endothelial cells and leukocytes have
complementary surface adhesion molecules
which briefly stick and release causing the
leukocyte to roll along the endothelium until it
eventually comes to a stop as mutual
adhesion reaches a peak
69. MARGINATION AND
ROLLIN
G
■ Early rolling adhesion mediated by
selectin family of adhesion molecules:
■ E-selectin (on endothelium cell)
■ P-selectin (present on platelets, endothelium)
■ L-selectin (on the surface of most leukocytes)
70. ADHESION
■ The rolling leukocytes are able to sense
change on the endothelium that initiate the
next step in the reaction of leukocytes, which
is firm adhesion to endothelial surface
Occur as leukocytes adhere to the endothelial
surface and is mediated by the interaction of
integrins on leukocytes binding to IG-family
adhesion proteins on the endothelium.
■
71. TRANSMIGRATION
(DIAPEDESIS)
■ Is the movement of leukocyte across
the endothelial surface
■ Occurs after firm adhesion and
mediated by palatelete endothelial cell
adhesion molecules-1 (PECAM –1)
on both leukocyte and endothelium
72. CHEMOTAXIS
■
• Leukocytes follow chemical gradient to
site of injury this process called
(chemotaxis)
• Chemotactic factors for neutrophils,
produced at the site of injury, include:
■
■
■
■ Bacterial products
Components of complement system especially (C5a)
Cytokines.
73. PHAGOCYTOSI
S
■ Phagocytosis is the ingestion of
particulate material by phagocytic cell
■ neutrophils and monocytes-macrophages
are the most important phagocytic cells
74. ■ Phagocytosis consists of three steps:
■ Recognition and attachment of the particle
■ Engulfment (form phagocytic vacuole)
■ Killing and degradation of the ingested
materials.
75. DEFECTS OF LEUKOCYTE FUNCTION
■ Defects of leukocyte adhesion:
■ Leukocyte adhesion deficiency type I :
is associated with recurrent bacterial
infections.
■ Leukocyte adhesion deficiency type 2 :
is associated with recurrent bacterial
infections and result from mutations in the
gene that required for the synthesis of
sialyl-lewis X on neutrophils.
76. DEFECTS OF LEUKOCYTE
FUNCTION
■ Defects of chemotaxis/phagocytosis:
■ Microtubule assembly defect leads to
impaired locomotion and lysosomal
degranulation (Chediak-Higashi Syndrome)
79. POSSIBLE OUTCOMES OF
ACUTE INFLAMMATION
■ Complete resolution of tissue structure
and function:
■
■
■ When the injury is limited or short-lived.
There has been no or little tissue damage
When the injured tissue is capable of regeneration
■ Scarring (fibrosis):
■
■ When inflammation occur in tissues that do not
regenerate
The injured tissue is filled with connective tissue
82. CHRONIC
INFLAMMATIO
N
■ Is inflammation of prolonged duration (week
to years) in which continuing inflammation,
tissue injury, and healing, often by fibrosis,
proceed simultaneously.
83. CHRONIC
INFLAMMATIO
N
■
■
■
■ Is characterized by a different set of
reactions:
Lymphocyte, macrophage, plasma cell
(mononuclear cell) infiltration
Tissue destruction by inflammatory cells
Repair with fibrosis and angiogenesis (new
vessel formation)
84. ■
CHRONIC INFLAMMATION MAY
ARISE IN THE FOLLOWING
SETTING :
■
■
■ Persistent injury or infection (ulcer, TB)
Prolonged toxic agent exposure (silica)
Autoimmune disease states (RA, SLE)
86. CHRONICINFLAMMATORY
CELLS AND MEDIATORS
■ Macrophages
■ The dominant cells.
■ Scattered all over (Kupffer cells, sinus
histiocytes, alveolar macrophages, etc.
■ Derived from circulating blood monocytes
and reach site of injury within 24 – 48 hrs
and transform to macrophages.
87. CHRONICINFLAMMATORY
CELLS AND MEDIATORS
■
■
■ Two majors pathways of macrophage
activation:
Classical macrophage activation:
induced byT cell-derived cytokines, endotoxins, and other products of
inflammation
Alternative macrophage activation:
induced by cytokines produced by T lymphocytes and other cell including
mast cell and eosinophils
88. CHRONICINFLAMMATORY
CELLS AND MEDIATORS
■
■
■
■ Macrophages have several roles in host
defense and inflammatory reaction:
Ingest and eliminate microbes and dead
tissue.
Initiate the process of tissue repair.
Secrete mediators of inflammation such as
cytokines.
89. CHRONICINFLAMMATORY
CELLS AND MEDIATORS
■ Lymphocytes (T - B )
■ Antigen-activated (via macrophages and dendritic
cells)
■ Lymphocytes and macrophages interact in
a bidirectional way and these interaction play an
important role in propagating chronic inflammation
lymphocyte release macrophage-activating
cytokines (in turn, macrophages release
lymphocyte-activating cytokines until inflammatory
stimulus is removed)
90. CHRONICINFLAMMATORY
CELLS AND MEDIATORS
■ Eosinophils
■ Found especially at sites of parasitic
infections, and as part of immune reaction
mediated by IgE
■ Typically associated with allergies.
92. GRANULOMATOUS
INFLAMMATION
■ Is a distinctive pattern of chronic
inflammation characterized by
aggregates of activated macrophages
and scattered lymphocytes.
93. ■ Granulomatous Inflammation can form
under three setting :
■ Persistance T-cell response to certain
microbes (such as TB)
■ In some immune mediated inflammatory
diseases (Crohn disease)
■ In sarcoidosis disease in response to
relatively inert foreign bodies(suture or
splinter)
95. SYSTEMIC
EFFECTS
■ Fever
■
■
■ The most prominent manifestation of acute-phase
response.
Fever is produced in response to pyrogens which
stimulate prostoglandine synthesis.
PGE stimulate the production of neurotransmitters
to reset the temperature at a higher level.
96. SYSTEMIC EFFECTS
(CONT’D)
■ Leukocytosis
■
■ Is a common feature of inflammatory reaction,
espicially those induced by bacterial infection
Elevated white blood cell count.
■ Other manifestations include:
■
■
■ Increased heart rate and blood pressure.
Decreased sweating.
Sepsis in severe bacterial infection.
