-What is host - pathogen interaction? -Define terms includes pathogenicity, lethal dose, infection etc. -Duration of symptom - Pathogens and steps involved in mechanism of pathogenesis 1. Microbial adherence 2. Invasion 3. Colonization 4. Evasion 5. Damage to host 6. Exiting the host 7. Survival outside the host 8. Transmission - Host -pathogen interaction in plants and animals - Defence system in plants and animals

1. HOST PATHOGEN INTERACTION
Presented by :-
Rashmi Bhandari
M.Sc. Microbiology(1st sem)

2. HOST PATHOGEN INTERACTION
• The host–pathogen interaction is defined as how microbes or viruses sustain
themselves within host organisms on a molecular, cellular, organismal or
population level.
• This term is most commonly used to refer to disease-causing microorganisms
although they may not cause illness in all hosts.
• Host:-The source from which the parasite takes nutrients.
• Pathogens are organisms that can cause disease.
• Virulence is a pathogen’s or microbe’s ability to cause damage to a host.
• Infectivity: The level at which a microorganism is able to infect or invade a host.
• Transmissibility: The measure of a microorganism’s ability to spread from one
host to the next. This can include both distance and number of affected
individuals.

3. Pathogenicity
• . It is the capability of microbial species to cause disease—is determined by
its virulence factors.
• Primary pathogen is microbe or virus that causes disease in healthy
individual
-Diseases such as plague, malaria, measles, influenza, diphtheria,
tetanus, tuberculosis, etc.
• Opportunistic pathogen (opportunist) causes disease only when body’s
innate or adaptive defenses are compromised or when introduced into
unusual location
- Can be members of normal microbiota or common in environment
(e.g., Pseudomonas)
• Virulence refers to degree of pathogenicity
• Virulence factors are traits that allow microorganism to cause disease

4. Infection
Term infection refer the most intimate way in which a
microorganismis may cause disease
• Infectious disease yields noticeable impairment :-
– Symptoms are subjective effects experienced by patient (e.g., pain
and nausea)
– Signs are objective evidence (e.g., rash, pus formation, swelling)
• Can be subclinical: no or mild symptoms
• Initial infection is primary infection
• Damage can predispose individual to developing a secondary
infection (e.g., respiratory illness impairing mucociliary escalator)

5. • Characteristics of Infectious Disease
• Communicable or contagious diseases easily spread
• Infectious dose is number of microbes necessary to establish
infection
ID50 is number of microorganism that infects 50% of population
• Shigellosis results from ~10–100 ingested Shigella
• Salmonellosis results from as many as 10⁶ ingested Salmonella
enterica
• – Difference partially reflects ability to survive stomach acid

6. • All the infectious diseases begin at some surface of the host, whether it
be the external surface such as the skin or internal surface such as
mucous membranes of respiratory tract, intestine or urogenital tract.
• In most infectious disease the pathogen is penetrates the body surface
and gain access to the internal tissue.
• In some kinds of infection the pathogen may remain localized, growing
near its point of entry into the body.
• In other it may be transported to other body sites.
• Some pathogens may cause generalised infections, in which the
pathogen becomes widely distributed and grows throughout the body.
• Some pathogens may be capable of growth within host causing severe
distruption of normal physiological process.

7. • In order to cause infectious disease a pathogen must accomplish the following:-
• It must enter the host.
• It must metabolize and multiply on or in the host tissue
• It must resist host defense
• It must damage the host
Lethal dose
• The virulence of a pathogen is usually measured by determining its LD50 dose for
a particular type of laboratory animal.
• The LD50 dose is defined as that number of organism which, when administered
to a number of laboratory animals, will kill 50% of them.

8. Course of Infectious Disease
• Incubation period: time between infection and onset
-Varies considerably: few days for common cold to even years
for Hansen’s disease (leprosy)
- Depends on growth rate, host’s condition, infectious dose
• Illness: signs and symptoms of disease
-May be preceded by prodromal phase (vague symptoms)
• Convalescence: recuperation, recovery from disease
• Carriers may harbor and spread infectious agent for long periods of
time in absence of signs or symptoms

9. Duration of Symptoms
• Acute infections: symptoms develop quickly, last a short time (e.g., strep throat)
• Chronic infections: develop slowly, last for months or years (e.g., tuberculosis)
• Latent infections: never completely eliminated; microbe exists in host tissues without
causing symptoms
- Decrease in immunity may allow reactivation
- Chicken pox (acute illness) results from Varicella-zoster virus; immune response
stops, but virus takes refuge in sensory nerves, can later produce viral particles resulting in
shingles

10. Types of pathogens
Pathogens include bacteria, fungi, protozoa, helminths and viruses.
Each of these different types of organisms can be further classified as a
pathogen based on its mode of transmission. This includes the
following:- food borne, airborne, waterborne, blood-borne and vector-
borne.
Many pathogenic bacteria, such as food borne Staphylococcus
aureus and Clostridium botulinum, secret toxins into the host to cause
symptoms.
HIV and Hepatitis B are viral infections caused by blood-borne
pathogens. Aspergillus, the most common pathogenic fungi, secrets
aflatoxin which acts as a carcinogen and contaminants many foods,
specially those grown underground ( nuts, potatoes, etc.)

11. Mechanism of pathogenesis
• Microbial Adherence:-
- Adhesins attach to host cell receptor
- Often located at tips of pili (called fimbriae)
- Can be component of capsules or various cell wall proteins
- Binding highly specific; exploits host cell receptor
• 1) Tissue tropism :-pathogens that prefer specific tissues over others e.g. Streptococcus mutans is abundant in
dental plaque and S. salivarius which is attached to epithelial cells of the tongue
• 2) Species specificity :- pathogens that only infect certain species , e.g. Nisseria gonorrhoeae infections are
limited to humans; E. coli K-88 infections are limited to pigs
• 3) Genetic specificity :-surface mutations that occur so previous antibodies do not recognize the invading
pathogen. They are genetically immune to a pathogen , e.g. Certain pigs are not susceptible to E. coli K-88
infections; Susceptibility to Plasmodium vivax infection (malaria) is dependent on the presence of the Duffy
antigens on the host’s redblood cells.
• If a microorganism cannot adhere to a host cell membrane, disease will not occur.

12. • Invasion :-
1. Penetrating the Skin
Difficult barrier to penetrate; bacteria rely on injuries
e.g. Staphylococcus aureus enters via cut or wound;
Yersinia pestis is injected by fleas
2. Penetrating Mucous Membranes
Entry point for most pathogens
a) Directed Uptake by Cells :-Pathogen induces cells
to engulf via endocytosis
e.g. Salmonella uses type III secretion system
to inject effector proteins (invasins); actin molecules
rearrange, yield membrane ruffling.

13. b) Exploiting Antigen-Sampling Processes :-
- Some pathogens use M cells to cross
intestinal barrier
- e.g. Shigella survives phagocytosis by
macrophages; induces apoptosis; binds to
base of mucosal epithelial cells and induces uptake
- Some invade by alveolar macrophages
e.g. Mycobacterium tuberculosis produces
surface proteins, directs uptake, avoids macrophage
activation

14. • Colonization:- Colonization is the multiplication of pathogenic
organisms where toxins are produced and the normal flora are
overcome. During this stage, pathogens compete with normal flora
for space and nutrients.
• During colonization, the host begins to show signs of septicemia (i.e.,
blood infection where bacteria are reproducing).
e.g. 10-100 for Shigella and 1,000,000 for Salmonella

15. Evasion of host defense:-
1. Hiding Within a Host Cell :- Allows avoidance of complement proteins, phagocytes,
and antibodies
e.g. Shigella directs transfer from intestinal epithelial cell to adjacent cells by causing
host cell actin polymerization
2. Avoiding Killing by Complement System Proteins :- Serum resistant bacteria resist
e.g. Neisseria gonorrhoeae hijacks host system, binds complement regulatory proteins
to avoid activation of membrane attack complex
3. Avoiding Destruction by Phagocytes :-
a) Preventing Encounters with Phagocytes :-
C5a peptidase: degrades chemoattractant C5a
e.g. Streptococcus pyogenes
b) Membrane-damaging toxins: kill phagocytes,
other cells
e.g. S. pyogenes makes streptolysin O

16. c) Surviving Within Phagocytes
• Escape from phagosome: prior to lysis with lysosomes
e.g. Listeria monocytogenes produces molecule that forms pores in membrane;
Shigella species lyse phagosome
• Prevent phagosome-lysosome fusion: avoid destruction
e.g. Salmonella sense ingestion by macrophage, produce protein that blocks fusion process
• Survive within phagolysosome: few can survive destructive environment
e.g. Coxiella burnetii (Q fever) can withstand; delays fusion, allows time to equip itself to
survive
d) Avoiding Antibodies
IgA protease: cleaves IgA, found in mucus secretions
e.g. Neisseria gonorrhoeae
Antigenic variation: alter structure of surface antigens, stay ahead of antibody production
e.g. Neisseria gonorrhoeae varies antigenic structure of pili
Mimicking host molecules: cover surface with molecules similar to those found in host cell,
appear to be “self”
e.g. Streptococcus pyogenes form capsule from hyaluronic acid, a polysaccharide found in
tissues

17. Damage to the Host
• Direct or indirect effect
1. Direct (e.g., toxins produced)
2. Indirect (e.g., immune response)
Damage may help pathogen to exit and spread
e.g.- Vibrio cholerae induces watery diarrhea, up to 20 liters/day, which can contaminate water supplies
- Bordetella pertussis triggers severe coughing, pathogens released into air
• Exotoxins :- protein secreted by pathogens
that causes damage to the host tissue.
e.g. batolinum toxin, tetanus toxin, hemolysin
(rupture red blood cells)
• Endotoxins:- toxic substance that are released
when a cell is killed

19. • Damaging Effects of the Immune Response
• Damage Associated with Inflammation
-Phagocytic cells can release enzymes and toxic products
• Damage Associated with Adaptive Immunity
-Immune complexes: antigen-antibody complexes can form
settle in kidneys and joints, and activate complement system leading to
inflammation
– E.g. acute glomerulonephritis following skin, throat infections
of S. pyogenes
-Cross-reactive antibodies: may bind to body’s own tissues,
promote autoimmune response
e.g. acute rheumatic fever following S. pyogenes infection

20. • Exiting the Host:-A pathogen must exit the body. This occurs
through various routes. Examples include sneezing,
coughing, diarrhea, coitus, pus, blood, or insect bites.
• Survival Outside the Host:-Finally, a pathogen must be able
to survive in the environment long enough to be transmitted
to another host. Some are hardy and can survive for several
weeks before a new host is found. There are others that
survive in animal reservoirs or require direct contact because
they are fragile.

21. • Transmission:- In order to begin infection and eventually cause disease, pathogens must
find a transmission route.
Transmission of an infectious agent can occur in many ways:-
• Direct contact:- Droplet spread (produced by sneezing, coughing, or even talking)
• Indirect :- Airborne, Vehicleborne, Vectorborne (mechanical or biologic)
Airborne transmission occurs when infectious agents are carried by dust or droplet
suspended in air.
Measles, for example ( the measles virus remained suspended in the air)
Vehicles that may indirectly transmit an infectious agent include food, water, biologic
products (blood), and fomites (inanimate objects such as handkerchiefs, bedding, or surgical
scalpels)
Improperly canned foods provide an environment that supports production of
botulinum toxin by Clostridium botulinum.
Vectors such as mosquitoes, fleas, and ticks may carry an infectious agent through
purely mechanical means or may support growth or changes in the agent.
Examples of mechanical transmission are flies carrying Shigella on their appendages and
fleas carrying Yersinia pestis, the causative agent of plague, in their gut.
In contrast, in biologic transmission, the causative agent of malaria or guinea worm
disease undergoes maturation in an intermediate host before it can be transmitted to
humans

22. Host pathogen interaction in plants
The contact between the plant and the pathogenic microorganisms leads to a
particular chain of events. Communication requires a mobile 'systemic signal’ .
Interaction leads to two types of response:-
1. Compatible response:- successful infection leading to disease
2. Incompatible interaction :-successful plant defence
Types of pathogen based on effects:-
1. Necrotrophic pathogen:- They kill the plant cell immediately.
e.g. Gray mold fungus Botrytis cinerea
Bacterial pathogen Erwinia carotovora
2. Biotrophic pathogen :- Plants cell remain alive
e.g. Fungus Blumeria graminis
Bacterial pathogen Xanthomonas oryzae
3. Hemibiotrophic pathogen :- plants cell initially alive and later killed
e.g. Fungus Magnaporthe grisea

23. Plant Defenses
Constitutive defence. Induced defence
Elicitors of defense respons:- Any substance that has a capability of activating defense response in
plants. It includes components of the cell surface as well as excreated metabolites.
ELICITORS
General specific
• Cell wall
• Waxy epidermal cuticle
• Bark
• Thorn, Spines
• Toxic chemicals
• Pathogen degrading enzymes
• Deliberate cell suicide
• Systematic resistance
1. Oligosaccharides elicitors
2. Protein/ Peptide elicitors
1. Avr gene product

24. Classes of plant immune response:-
1. Basal response:- transcription of gene is response to PAMP recognition
2. Hypersensitive response:- apoptosis of cell at the site of infection
3. Systematic aquired immunity:- The entire plant becomes resistant to
infection.
Steps in plant pathogen interaction
1. Recognition :- depends on generation of elicitors by the pathogen
(diseases or non diseases)
2. Transduction:- signal transduction at cellular level refers to
movement of signal
3. Perception:- is a surface level phenomenon in which elicitors from
the pathogen are recognised by host receptor
4. Signalling
5. Response

25. Plant immunity system

26. Animal-Pathogen Interactions
• Commensalism:- Commensalism is defined as a host-microbial interaction
that does not result in perceptible, ongoing, and/or persistent host damage.
However, it is notable that this may not be absolute, since the initial acquisition
of commensal organisms may elicit damage in some hosts.
• Distructive association:- Pathognic microbes interact with animals including
man and causes many diseases.
e.g. Cryptosporidium causes Cryptosporidiosis disease in Calves
Bacillus anthracis cause anthrax disease
Streptococcal Pharyngitis (“Strep Throat”)
Streptococcus pyogenes is a β-hemolytic Gram-positive coccus that causes strep
throat .Strains that produce SPEs (streptococcal pyrogenic exotoxins) can cause
scarlet fever.
For example, E. coli is acquired shortly after birth and this encounter places
some infants at risk for E. coli meningitis during the first month of life

27. • Rabies- a frightening example of a pathogen modifying host behaviour
• Rabies virus release a toxin that has the ability to alter behaviour in
animals through inhibition of nicotinic acetylcholine receptors present in
the central nervous system.
• Fatal attraction :-
. The parasites Toxoplasma gondii increase dopaminergic activity by
directly producing an enzyme required for the synthesis of L-DOPA (a
dopamine precursor) in its mouse host.
Increase dopamine levels have been associated with changes in fear
perception.

28. Host Defenses system
• A microorganism will not be able to invade unless it overcomes an
animal’s or individual’s host defenses.
• Specific host defenses may include:
• Skin and mucosal secretions
• Non-specific local responses (e.g., pH)
• Non-specific inflammatory responses
• Specific immune responses (e.g., lymphocytes)
The ability for a pathogen to overcome host defenses can be
accomplished by two distinct components: a primary pathogen (causes
disease in a healthy host) or opportunistic pathogen (causes disease if
host is immunocompromised).

29. Host immunity system
There are two types of immune system
1. Innate immune system:- it is the first line of defense against
pathogens and is initiated by genome- encoded pattern recognition
receptors (PRPs) that recognize PAMP
• Non specific and does not confer long- lasting immunity
• Immune cells :- dendritic cells and macrophages, intestinal epithelial
cells and myofibroblast
2. Adaptive immunity:- it is a second line of immune response, highly
specific, confers long lasting
• One cell determines one antigenic determinant
• T lymphocytes

30. Innate immunity: mechanisms
• Mechanical barriers / surface secretion
• skin, acidic pH in stomach, cilia
• Humoral mechanisms
• lysozymes, basic proteins, complement, interferons
• Cellular defense mechanisms
• natural killer cells neutrophils, macrophages,, mast cells,
basophils, eosinophils
Neutrophil
NK Cell Monocyte
Macrophage
Basophils &
Mast cells
Eosinophils

31. Adaptive immunity: mechanisms
• Cell-mediated immune response (CMIR)
• T-lymphocytes
• eliminate intracellular microbes that survive within
phagocytes or other infected cells
• Humoral immune response (HIR)
• B-lymphocytes
• mediated by antibodies
• eliminate extra-cellular
microbes and their toxins
Plasma cell
(Derived from B-lymphocyte,
produces antibodies)

32. Cell-mediated immune response
1. Cytotoxic T-cell
• recognizes peptide antigen on
macrophage in association with major
histo-compatibility complex (MHC) class
• identifies molecules on cell surfaces
• helps body distinguish self from non-self
2. T-cell goes into effectors cells stage that is
able to kill infected cells
T lymphocytes 2 types
Helper T- lymphocytes (CD4+)
CD4+ T cells activate phagocytes to kill microbes
Cytolytic T-lymphocyte (CD8+)
CD8+ T cells destroy infected cells containing
microbes or microbial proteins

33. Humoral immune response
1. B lymphocytes recognize
specific antigens
• proliferate and differentiate
into antibody-secreting
plasma cells
2. Antibodies bind to specific
antigens on microbes; destroy
microbes via specific
mechanisms
3. Some B lymphocytes evolve
into the resting state - memory
cells

35. Conclusion :-
• Microorganisms are located everywhere, and there are many more
microbes than hosts. The goal for both host and microbe is survival.
Infection can be localized, focal, or occur systemically. Several factors
affect the balance between health and infectious disease.
Pathogenesis depends on genetics, the state of host health, age, and
stress.

36. References
• Casadevall A, Pirofski LA (2000). “Host-pathogen interactions: Basic
concepts of microbial commensalism, colonization, infection, and
disease”. Infect Immun. 68 (12).
• Rendtorff, R. C. (1954). “The experimental transmission of human
intestinal protozoan parasites. II. Giardia lamblia cysts given in
capsules”
• Eugene W. Nester -“Microbiology:-A Human Perspective”
• Joanne M. Willey - “Prescott’s Principles of MICROBIOLOGY”

37. THANK YOU