2. Terminologies
Terminology Explanation
Saprophytes Free-living microbes that live on dead or decaying organic matter. They are
usually found in soil and water and are generally unable to invade the living
host.
Parasites Microbes that live on a living host, derive nutrition from the host and also
cause harm to the host. They are of two types- microparasites (bacteria,
viruses, fungi and protozoa) and macroparasites (helminths).
Commensals Harmless microbes that harbour on a living host as normal flora of the host
without causing any injury to the host
4. Terminologies
Terminology Explanation
Infection Process in which a pathogenic organism enters, establishes itself,
multiplies and invades the normal anatomical barrier of the host;
resulting in disease.
Infectious disease When infection becomes apparent results in clinical
manifestation.
5. Terminologies
Terminology Explanation
Colonization Pathogenic organism enters, multiplies but does not invade, and
neither causes disease or nor elicits specific immune response. (not
same as normal flora).
• Commensals are limited to a particular anatomical site, e.g.
intestine, respiratory and genital tract. When they enter through
other routes, they may behave as pathogen. (Escherichia coli normal
flora in intestine, but when enters through respiratory tract can be
colonization or infection).
Infestation Distinct from infection in that it applies specifically to parasites of macroscopic
size, such as parasitic worms in intestine or arthropods (e.g. lice, itch mite etc.)
on the body surface.
6. Classification of infections
TERMINOLOGY EXPLANATION
Primary infection Initial infection with a pathogenic microorganism in a
host.
Reinfection Result of subsequent infection by the same microbe.
Secondary
infection
New pathogen sets up an infection in a host whose
immunity is already lowered by a pre-existing
infection.
7. Classification of infections
Terminology Explanation
Focal infection (or
focal sepsis)
Indicates a condition where, due to infection at localised sites
(such as in the appendix or tonsils), generalised effects are
produced.
Cross-infections When in a patient already suffering from a disease a new
infection sets up from another host or another external source.
8. Classification of infections
Terminology Explanation
Nosocomial
infections
Cross-infections occurring in hospitals are called
nosocomial infections.
Iatrogenic (or
physician induced)
Refers to the infections induced by the professional activity
of the physician or other health care workers resulting
from preventive, diagnostic, treatment.
9. Classification of infections
Terminology Explanation
Depending on the source of infection
Endogenous
infections
Source of infection is within the body, either normal flora if
breeches the anatomical barrier, or endogenous reactivation
of a latent infection.
Exogenous infections Source is outside the host's own body.
10. Classification of infections
Terminology Explanation
Based on the clinical manifestation produced
Asymptomatic or in-
apparent or subclinical
infection
Infection that is active but does not produce
noticeable symptoms.
Symptomatic or apparent
infections
o Acute infection- here, the symptoms last for a
short term period.
o Chronic infection- symptoms persist for a long
period.
11. Classification
of infections
Terminology Explanation
Based on the clinical manifestation
produced
Latent
infection
refers to an infection that is
inactive or dormant or in
hidden form; but capable of
reactivating later.
Atypical
infection
the usual manifestations of
the disease are not present.
Instead, atypical symptoms
may be present
12. Epidemiological Pattern of Infection
Terminology Explanation
Endemic Infections that occur at a persistent,
usually low level in a certain
geographical area.
Epidemic Infections that occur at a much
higher rate than usual in a particular
geographic area.
Pandemic Infection that spreads rapidly over
large areas of the world.
13. SOURCES AND RESERVOIR OF INFECTION
• Not always synonymous.
• Source- refers to the person, animal, or object from which a
microorganism is transmitted to the host.
• Reservoir - natural habitat in which the organism lives,
multiplies.
• Eg-
a) Tetanus- the reservoir and source are same, i.e. the soil
b) In typhoid fever, the reservoir may be a case or carrier,
but the source of infection is usually contaminated food
& water.
14. SOURCES OF INFECTION
HUMANS
• Carrier – harbours the pathogen
• Healthy carrier – harbours the
pathogen, but never suffered from
the disease
• Convalescent carrier – recovered
from disease and continues to
harbour the pathogen
15. SOURCES OF INFECTION
• Incubatory carriers - Person shed the organism during the
incubation period of disease (usually occurs in the last few days
of incubation period) e.g. measles, mumps, polio, diphtheria,
pertussis, hepatitis B, influenza, etc
16. SOURCES OF INFECTION
HUMANS
• Temporary carrier – less than six months
• Chronic carrier – several years
• Contact carrier – acquires pathogen from patient
• Paradoxical carrier – acquires pathogen from
another carrier
17. SOURCES OF INFECTION
ANIMALS
• Reservoir host – maintain the parasite in nature
• Zoonoses – diseases transmitted from animals to
human beings
19. Non living reservoirs
• Soil and inanimate matter can also act as
reservoir/source of infection.
• Example soil may harbour the agents of
tetanus, anthrax and some intestinal
helminths.
20. MODE OF TRANSMISSION
o Contact
oInhalation
oAirborne
oIngestion
oInoculation
oTransmission of Blood borne infections
oVector borne (mechanical or biological)
oVertical transmission
21. MECHANISM
OF
MICROBIAL
PATHOGENICITY
• 'Pathogenicity‘ - refer to the
ability of a microbial species to
produce disease.
• ‘Virulence' - relative degree of
pathogenesis (tissue damage),
which may vary between
different strains of the same
organism depending upon the
expression of the virulence
factors.
22. Exaltation- Enhancement of virulence is known as exaltation,
which can be induced experimentally by serial passage into
susceptible hosts.
Attenuation - Reduction of virulence which can be achieved by
passage through unfavourable hosts, repeated cultures in
artificial media, growth in high temperature or in the presence
of weak antiseptics, desiccation or prolonged storage in
culture.
MECHANISM OF MICROBIAL
PATHOGENICITY
23. MECHANISM OF MICROBIAL PATHOGENICITY
• Bacterial pathogenicity depends upon the sum total of several factors
as described below:
o Route of transmission of infection
o Infective dose of the organism
o Evasion of the local defences
o Adhesion
o Adherence
o Invasion
o Toxins
o Pathogenicity islands
o Bacterial secretory system
24. Microbial virulence factors are as follows:
Adhesion
Antiphagocytic factors
Invasiveness
Enzymes
Toxins
Inhibition of phagocytosis / Escape from hosts immune response
Genetic factors
Infecting dose
Route of infection
Communicability
Genetic factors
25. 1) ADHESION
• If organism did not adhere, it will be swept away by
mucus and other fluids.
• They allow pathogen to adhere only to receptors on
certain host epithelial cells.
• Eg) fimbriae,pili, flagella, LPS, Glycocalyx
26. Adherence allows organism to
1. colonize and multiply at a rate faster
than their removal.
2. Helps in penetrating body tissues and
cells.
3. provides focus for elaboration of
enzymes and toxins, delivered directly
to host cells.
27. 2)Antiphagocytic factors
• Capsule
• Bacterial surface antigens
• Streptococcal M- protein
à Mask the bacterial receptors from
antibacterial substances
28. 3) INVASIVENESS
• Entry of the bacteria into the host cells by
releasing digestive enzymes that allows them to
invade tissues.
• Highly invasive – spreading & generalised
diseases.(streptococcal infections)
• Less invasive – localized disease.(staphylococcal)
• Non invasive – produce toxins at site of
localization and may cause fatal
diseases.(tetanus)
29. 3) INVASIVENESS
• Entry of the bacteria into the host cells by
releasing digestive enzymes that allows them to
invade tissues.
• Highly invasive – spreading & generalised
diseases.(streptococcal infections)
• Less invasive – localized disease.(staphylococcal)
• Non invasive – produce toxins at site of
localization and may cause fatal
diseases.(tetanus)
30. 4) ENZYMES
• 1. Coagulase – form a fibrin shield around
bacteria
• 2. Hyaluronidase & Collagenase – break down
collagen and allow better penetration of
microorganisms into tissues.
• 3. Beta- lactamases – hydrolyse Beta lactam ring
of penicillin and cephalosporins, thus inactivating
the antibiotic.
31. 5) TOXINS
• Toxins produced by bacteria are classified
into two groups
1. Exotoxins
2. Endotoxins
36. 2) ENDOTOXINS
• Forms an integral part of the
cell wall of GNB
• Endotoxin activates the
clotting factor causing
formation of small blood
clots.
• These blood clots obstruct
capillaries, and cause
disseminated intravascular
coagulation (DIC)
• Response to endotoxin
include
• Fever
• DIC
• shock
• and even death.
38. Difference between endotoxin and
exotoxins.
Feature Endotoxins Exotoxins
Nature Lipopolysaccharides Proteins
Source Part of cell wall of Gram
negative bacteria
Secreted both by Gram
positive & negative
bacteria; diffuse into
surrounding medium
Released by Cell lysis
Not by secretion
Actively secreted by the
bacteria
Heat stability Highly stable Heat labile destroyed at
60oC
Mode of action ↑IL-1 and TNF Mostly enzyme like action
39. Feature Endotoxins Exotoxins
Effect Non-specific (fever,
shock, etc)
Specific action on
particular tissues
Tissue affinity No Specific affinity for tissues
Fatal dose Only large doses are fatal More potent, even
smaller doses- fatal
Antigenicity Poorly antigenic Highly antigenic
Neutralisation by
antibodies
Ineffective Neutralized by specific
antibodies
Used for vaccine No effective vaccine is
available using
endotoxin
Toxoid forms are used as
vaccine; e.g. tetanus
toxoid
Difference between endotoxin and
exotoxins.
40. 6) Inhibition of Phagocytosis
• Inhibition of chemotaxis,
attachment of phagocytes,
fusion of lysosome.
• Resistance to killing in
phagolysosome.
41. Escape
from
hosts
immune
response
• By antigenic variation - modify their
surface antigen and evade immune
response.
• Antibody cleavage – IgA protease
produced.
• Induction of blocking antibodies – which
bind on specific receptors on the surface
of bacteria and block access to the
effective antibacterial antibodies.