Lecture 2a Microbe Host Relationship

21/03/2022
MICROBE – HOST
RELATIONSHIP
RENZ AMADOR I. BAGAS, RMT

MICROBIOLOGY & PARASITOLOGY DIVISION
RTRMF COLLEGE OF MEDICAL TECHNOLOGY
THE HUMAN MICROBIOME PROJECT
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WHAT IS SYMBIOSIS?
• Symbiosis, or a symbiotic relationship, is defined as the living together or
close association of two dissimilar organisms (usually two different
species).
• Symbionts - organisms that live together in such
a relationship
• Microbial Symbiosis – symbiotic relationship formed
by microorganisms with other microorganisms
or with higher form of organisms that could be
both detrimental and beneficial on both ends.
• Types of Microbial Symbiosis: Neutralism, Mutualism, Commensalism,
Parasitism
Topic 2: Microbe Host Relationship rabagas,RMT
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TYPES OF MICROBIAL SYMBIOSIS

• NUETRALISM
➢symbiotic relationship in which neither symbiont is affected by the
relationship
➢ e.g. existence of two organisms in the same ecological niche
• MUTUALISM
➢symbiotic relationship that is beneficial to both symbionts
➢ e.g. Escherichia coli and human being
➢ e.g. Termite and Oxymonadida and the Parabasalia
➢ e.g. Algae and Fungi in Lichens
TYPES OF MICROBIAL SYMBIOSIS

• COMMENSALISM
➢symbiotic relationship that is beneficial to one symbiont and of no
consequence (i.e., is neither beneficial nor harmful) to the other
➢ Host – the organism that harbors the microorganism
➢ e.g. indigenous microbiota and host organism(humans or animals
• PARASITISM
➢symbiotic relationship that is beneficial to
one symbiont (the parasite) and detrimental
to the other symbiont (the host)
➢ e.g. malarial parasite and human host
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INDIGENOUS MICROBIOTA OF HUMANS

• “indigenous microflora” or “normal flora”
• Includes all bacteria, fungi, virus, protozoans
that reside on and within the person
• Estimated to be around 100 trillion cells with composed of 500 – 1000 species
• Moist and warm conditions provides excellent growth for this indigenous microbiota
• Transient Microbiota – microorganisms that take up a temporary residence on and within humans
• Destruction of microbiota destroys the balance between the host and other microorganisms
❖ Superinfection - overgrowth or population explosion of an organism that is usually present in
low numbers
❖ e.g. Candidiasis or Moniliasis infection in mouth and
vagina by Candida albicans
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• MICROBIAL FLORA IN THE SKIN
➢ estimated to have 300 species mostly anaerobes
➢ inhabits the deeper layers of skin, hair follicles,
and sweat and sebaceous glands
➢ The most common bacteria on the skin are
species of Staphylococcus
(especially S. epidermidis and other
coagulase-negative staphylococci),
Corynebacterium, and Propionibacterium
➢ Factors for growth: anatomical location, presence of moisture,
pH, temperature, salinity, presence of chemical waste,
presence of other microbes
➢ Superinfection is imminent in cases of immunosuppressed state

• MICROBIAL FLORA OF EYES AND EARS
➢ internal ear and middle ear are sterile
➢External ear and ear canal are inhabited mainly
by S. epidermidis, S. aureus and Corynebacterium spp.
➢The external surface of the eye is lubricated,

cleansed, and protected by tears,
mucus, and sebum.
➢ Tears contains lysozyme and other
antimicrobial enzymes
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• MICROBIAL FLORA OF THE RESPIRATORY TRACT
➢ The nasal passages and throat are
areas provide moist, warm mucous
membranes that furnish excellent
conditions for microbial growth.
➢Healthy carriers
• harbor virulent (disease-causing)
pathogens and do not have the
diseases but can them to
susceptible persons
e.g. diphtheria, meningitis,
pneumonia, and whooping cough.

• MICROBIAL FLORA OF THE RESPIRATORY TRACT
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• MICROBIAL FLORA OF THE ORAL CAVITY
➢ The anatomy of the oral cavity (mouth)
affords shelter for numerous anaerobic
and aerobic bacteria.
➢ Anaerobic microorganisms flourish in
gum margins, crevices between the teeth,
and deep folds (crypts) on the surface
of the tonsils.
➢ Bacteria thrive especially well in particles
of food and in the debris of dead
epithelial cells around the teeth.
➢ most common indigenous microflora of the
mouth are various species of alpha hemolytic
streptococci.

• MICROBIAL FLORA OF THE GASTROINTESTINAL TRACT
➢ STOMACH: Gastric enzymes and extreme
acidity (pH1.5) prevent growth of microbiota
➢ Helicobacter pylori – common cause of ulcer
➢ SMALL INTESTINE: Few grow in the duodenum;
Jejunum and Ileum contains bile salts and acids
➢ COLON: largest number and variety of microbiota
• Obligate, Aerotolerant and Facultative Anaerobes
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• MICROBIAL FLORA OF THE GENITOURINARY TRACT
➢ The genitourinary (GU) tract (or urogenital tract)
consists of the urinary tract (kidneys, ureters,
urinary bladder, and urethra) and the various parts
of the male and female reproductive systems.
➢Distal Urethra and the external opening of urethra
harbors many microbes (bacteria, yeast, fungi and virus).
➢ Urethritis (UTI) are commonly caused by STD’s such as
Neisseria gonorrheae, Chlamydia trachomatis and
mycoplasma.
➢ FEMALE RS: During puberty and after menopause –
alkaline vaginal secretion supporting the growth of
diphteroids, streptococci, staphylococci and coliforms

➢ Child bearing years: Acidic vaginal secretions (pH 4-5) supporting the growth of selected
bacterial species: Actinomyces, Bacteriodes,
Lactobacillus, Mycoplasma, Prevotella, Proteus,
Pseudomonas, Staphylococcus and
Streptococcus.
➢ Lactobacillus acidophilus key player for acid-
production in the vagina.
➢ Decrease in its lactic acid production increases
the chance of Bacterial Vaginosis (BV).
➢ Vaginal Candidiasis is one of the examples
of microbial overgrowth after the decreased
activity of L. acidophilus.
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➢ Child bearing years: Acidic vaginal secretions (pH 4-5) supporting the growth of selected
bacterial species: Actinomyces, Bacteriodes,
Lactobacillus, Mycoplasma, Prevotella, Proteus,
Pseudomonas, Staphylococcus and
Streptococcus.
➢ Lactobacillus acidophilus key player for acid-
production in the vagina.
➢ Decrease in its lactic acid production increases
the chance of Bacterial Vaginosis (BV).
➢ Vaginal Candidiasis is one of the examples
of microbial overgrowth after the decreased
activity of L. acidophilus.
➢ Vaginitis Vs. Vaginosis
ROLES OF INDIGENOUS MICROBIOTA

• BENEFICIAL AND HARMFUL ROLES OF INDIGENOUS MICROBIOTA
➢ Certain intestinal microbes produce useful compounds needed by
the body such as Vitamin K and B12, biotin, pantothenic acid,
and pyridoxine.
➢ Stimulator of the immune system and prevents colonization of
harmful microorganisms – microbial antagonism.
➢ Microbial Antagonism – serve as a beneficial role because it prevents
transient microbes form colonizing the body.
➢ Mechanism includes production of antibiotics and antimicrobial
peptides such bacteriocin
➢ Opportunistic Microorganism – normal microbial flora causes patho-
genic infection once the host’s immune system weakens and
is found outside its original site of colonization.
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ROLES OF INDIGENOUS MICROBIOTA

• BENEFICIAL AND HARMFUL ROLES OF
INDIGENOUS MICROBIOTA
➢ Biotherapeutic Agents – aka as probiotics
are used to restore the balance of
microorganisms in the gut after infection or
chemical intervention for treatment of
infection (Lactobacillus casei Shirota strain,
Bifidobacterium, Enterococcus and
Saccharomyces).
➢ Fecal Transplant is used
to treat recurrent
C. difficile infection
and restoration of gut
microbiome.
MICROBE TO MICROBE INTERACTION

• MICROBIAL COMMUNITIES (BIOFILMS)
➢ In nature, microbes are often organized into what are
known as biofilms—complex and persistent communities
of assorted microbes.
➢ A bacterial biofilm consists of a variety of different
species of bacteria plus a gooey extracellular matrix
that the bacteria secrete, composed of
polysaccharides, proteins, and nucleic acids.
➢ They grow in bones,heart valves, tissues, and inanimate
objects such as artificial heart valves, catheters, and
prosthetic implants.
• Microbes commonly associated with biofilms on MUST-TO-REMEMBER!!!!
indwelling medical devices include the yeast C. These biofilms causes the
albicans and bacteria such as S. aureus, coagulase- microorganism to become sessile –
negative staphylococci, Enterococcus spp., evading the functions of antibiotics and
Klebsiella pneumoniae, and Pseudomonas the actions of immune system.
aeruginosa.
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• MICROBIAL SYNERGISM
➢

• MICROBIAL INTERRELATION
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MICROBIAL
PATHOGENECITY AND
INFECTION MECHANISM
INFECTION MECHANISM
INFECTION VS. INFECTIOUS DISEASE
➢ In medical perspectives, both terms connotes the same meaning
➢ Microbiological Perspectives:
▪ INFECTION – colonization and establishment of residence of
a microorganism in the host cell
▪ INFECTIOUS DISEASE – development of pathogenic
manifestations caused by the materials such as toxins and
enzymes released by the microorganism
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INFECTION MECHANISM
FACTORS THAT AFFECTS DEVELOPMENT OF INFECTION
1. The site where the microbe established residence cannot support its
growth.
2. Receptors for their colonization is not present.
3. Antibacterial factors released by the host destroys the microbial
inhabitants.
4. Microbial antagonism which are actions of indigenous microbiota.
5. Host nutritional and health status influences the pathogen – host
encounter.
6. Active immune response and status of the patient destroys the harmful
pathogens.
INFECTION MECHANISM
FOUR PHASES
OF AN
INFECTIOUS
DISEASE
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INFECTION MECHANISM
FOUR PHASES OF AN INFECTIOUS DISEASE
Incubation Period Prodromal Period Period of Illness Convalescent Period

The time elapses The time of early The time where The time where the
between arrival of onset of the patient host recovers from
the pathogen symptoms experiences the the infection.
and the onset of indicating start of typical symptoms “Period of Healing”
symptoms. disorder. of the disease.
INFECTION MECHANISM
SIGNS VS. SYMPTOMS
SYMPTOMS SIGNS
Subjective (perceived by Objective (can be
the patient) measured)
Discussed in Medical Discussed in Physical
History Examination
Non-specific indication of Definite indication of
the infection infection
e.g. diarrhea, vomiting, e.g. sore, boils, rash,

body malaise, hemoptysis nodules, lumps
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INFECTION MECHANISM
DIFFERENT TERMS IN INFECTION MECHANISM
LOCALIZED VS SYSTEMATIC
▪ Localized – infection is contained in one area (pimples, boils, abscess)
▪ Systemic – aka generalized infection, when the infection reaches the blood stream
and has spread all through out the body
ACUTE, SUB-ACUTE AND CHRONIC DISEASES
▪ Acute – rapid onset of infection, and usually followed by a relatively rapid recovery
(e.g. mumps, measles, influenza, colds, cough)
▪ Chronic – slow onset of infection and can last for a long time (e.g. tuberculosis,
leprosy, HIV)
▪ Subacute – sudden onset of infection that can develop into long-lasting disease
(e.g. bacterial endocarditis)
INFECTION MECHANISM
PRIMARY VS SECONDARY INFECTION
▪ Primary Infection – “first disease” infection caused by
a primary infectious agent (e.g. bacterial pneumonia)
▪ Secondary Infection – “second disease” infection
caused by a secondary infectious agent following the
primary infection (e.g. viral pneumonia)
LATENT AND TERTIARY INFECTION
▪ Latent Infection – there is an active infection but
no signs and symptoms are manifested by the host
▪ Tertiary Infection – Systemic spread of the infectious
agent and manifestation of signs and symptoms
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INFECTION MECHANISM
▪ Pathogenicity - ability of microbial species to
cause a disease
▪ Carrier - a person or animal with asymptomatic
infection that can be transmitted to another
susceptible person or animal
▪ Virulence
- quantitative ability of an agent to cause disease
- involves adherence, invasion, and toxigenicity
▪ Toxigenicity - ability of a microorganism to
produce a toxin that contributes to the
development of disease
INFECTION MECHANISM
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INFECTION MECHANISM
INFECTION MECHANISM
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INFECTION MECHANISM
https://slideplayer.com/slide/13054861/
INFECTION MECHANISM
• Portal of Entry of Microorganisms
1. External Surfaces (Skin, conjunctiva)
2. Internal Surfaces
• mucous membrane of:
▪ Respiratory tract, Urogenital tract
• Penetration of Epithelial Cell Layers

• Active – penetrates to tissues by itself
• Passive – introduced through breach
in body surfaces (wound, burns, etc.)
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INFECTION MECHANISM
▪ Microbial Adherence
• attachment of pathogens to the
surfaces of the host (e.g. N.
gonorrhea)
• some are introduced through vectors
▪ Growth in underlying tissues

▪ Infection of the lymphatic system
▪ Infection of the blood (septicemia)
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VIRULENCE FACTORS
VIRULENT, VIRULENCE & VIRULENCE FACTORS
▪ Virulent: ability of microbe to cause harm;
pathogenic, toxigenic
▪ Virulence: (1)Expresses a measure or
degree of pathogenicity
(2) Compares the severity of
the infectious disease
caused by pathogens.
▪ Virulence factors: the physical attributes
(phenotypic) or properties of pathogens
that enables them to escape various
host’s defenses.
VIRULENCE FACTORS
❖ ADHERENCE FACTORS
▪ attachment to the host cell is necessary for
colonization and invasion to host body
▪ Classifications of Adherence Factors:
1. Receptors & Integrin
➢ molecules (often glycoprotein) on the
surfaces of the host cell
➢ point of attachment/recognition of
pathogen
2. Adhesins & Ligands
➢ molecules that are found on the
surfaces of pathogens that is able to
recognize and bind to a particular
receptor
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VIRULENCE FACTORS
❖ ADHERENCE FACTORS
3. Bacterial Fimbrae (Pili)
➢ “attachment pili”; colonization factor
➢ thin, hair-like flexible structure enabling the
bacteria to attach on surfaces
➢ e.g. M protein of S. pyogenes: protects the
cell from phagocytosis and adherence to
pharyngeal cells
❖ INTRACELLULAR PATHOGENS
➢ Obligate: requires host cell for survival
➢ e.g. Rickettsia spp. – leaky membrane, Chlamydia –
energy parasite, Plasmodium & Babesia – infects the
RBC
➢ Facultative: they can survive with or without host cell
VIRULENCE FACTORS
❖INTRACELLULAR PATHOGENS
▪ INTRACELLULAR SURVIVAL MECHANISM
1. Escape from Respiratory Burst:
catalase, superoxide dismutase
2. Presence of extracellular
appendages: mycolic acid (M.
tuberculosis) & capsule
3. Inhibition of phagolysosome
formation: Toxoplasma gondii
(prevention of phagolysosome
formation), Rickettsia (release of
phospholipases that destroys the
vacuole
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VIRULENCE FACTORS
❖ANTIPHAGOCYTIC FACTORS
▪ CAPSULE
➢ thick layer of glycocalyx polymers covering the bacteria
➢ evades the phagocytosis due to lack of surface receptors
for phagocyte binding
➢ S. pneumoniae, N. meningitidis, K. pneumoniae,
Haemophiles influenzae & Cryptococcus neoformans
▪ FLAGELLA
➢ thread-like locomotor appendages making the bacteria
motile and invade the aqueous areas in the body
▪ M PROTEIN
➢ mediates evasion of phagocytes; present in
Streptococcus pyogenes
▪ PROTEIN A
➢ cellular component of cell wall that inhibits phagocytosis
and coagglutinates IgG subclasses.
VIRULENCE FACTORS
❖EXOENZYMES
➢ enzymes that are produced within the microbial cell and release to
cause pathogenesis such as (1) evasion of immune function, (2)
invasion of tissues, and (3) damage to the tissues
A. NECROTIZING ENZYMES
✓ Necrotizing fasciitis: caused by the release of proteases and
other enzymes that destroys the soft tissues ( S. pyogenes)
✓ Gas gangrene (myonecrosis): release of proteases and lipases
that dissolves the fat and muscles (Clostridium perfringens)
B. COAGULASES
✓ binds with prothrombin to form staphylothrombin that converts the
fibrinogen to a solid fibrin clot
✓ clotting will provide a sticky coating to the bacteria to evade immune
function
✓ Staphylococcus aureus
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VIRULENCE FACTORS
C. KINASES (FIBRINOLYSIN)
✓dissolve the fibrin clot
✓ Staphylokinase (S. aureus) & Streptokinase (Streptococcus):
used to for treating blood clots
D. COLLAGENASE
✓ break down the collagen; e.g. gas gangrene (C. perfringes)
E. HEMOLYSINS
✓ enzymes that damage the RBC to harm the host and obtain
iron
✓ β-hemolytic (complete), α-hemolysis (partial), γ-hemolysis (no
hemolysis
F. LECITHINASE
✓ breaks down lecithin that destroys the membrane of cells & RBC
✓ causes a destruction of extensive areas of tissues
VIRULENCE FACTORS
G. HYALOURODINASE “spreading factor”
✓ Breaks down the hyaluronic acid enabling the pathogen to spread to
connective tissues
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VIRULENCE FACTORS
VIRULENCE FACTORS
❖ TOXOIDS & TOXINS
➢
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VIRULENCE FACTORS
▪ EXOTOXINS Flaccid Paralysis
➢ causes organ-specific toxicity

➢ TYPES:
1. Neurotoxin – affect the CNS
a. Botulinum toxin – blocks the nerve impulses
causing flaccid paralysis (C. botulinum)
b. Tetanospasmin – affects control of nerve
transmission leading to spastic, rigid paralysis Tetanus
(C. tetani)
2. Enterotoxin – toxins that affect the GIT causing
diarrhea and vomiting
e. g. Cholera toxin, Salmonella Toxin, Shigella toxin,
C. difficile toxin: pseudomembranous colitis
VIRULENCE FACTORS
3. Cytotoxin – kills the cells (epithelial linings)
a. Diptheria Toxin A: pseudomembrane formation
b. Staphylococal TSST-1: affect the capillary walls
c. Exfoliative toxin: affects the epidermal layer of skin
(Scalded Skin Syndrome)
4. Erythrogenic Toxins (Hemolysins) – affects/lyse the RBC

a. S. pyogenes Hemolysin: Scarlet fever
5. Leukocidin – destroys the white blood cells (phagocyte)

a. Panton Valentine Leukocidin : MRSA Infection
6. Other Toxins
a. Pseudomonas aeruginosa toxin: inhibits protein
synthesis
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VIRULENCE FACTORS
▪ ENDOTOXINS
➢found in the cell wall of Gram-negative microbes
➢released upon cell lysis
➢LPS (lipopolysaccharide) – LIPID A
➢effects:
a. Pathogenicity
✓change in body temperature due to the release of pyrogen
✓ Septic Shock
b. Blood changes
✓damage of blood platelet
✓Hemorrhage
✓ Disseminated Intravascular Coagulation
VIRULENCE FACTORS
❖ MECHANISM BY WHICH PATHOGENS ESCAPE IMMUNE RESPONSE
A. ANTIGENIC VARIATION
➢ Some pathogens are able to periodically change their surface antigens by
shedding the old antigens
➢ Influenza virus, HIV, Borrelia recurrentis (relapsing fever), Trypanosomes
B. CAMOUFLAGE & MIMICRY
➢ Camouflage: microbes will coat themselves with host protein to evade immune
function (e.g. adult schistosomes)
➢ Molecular Mimicry: pathogens has the ability to produce antigens that closely
resembles host antigen (e. g. Hyaluronic acid in S. pyogenes capsule and in
human connective tissue)
C. ANTIBODY DESTRUCTION
➢ IgA Proteases: cleaves the secretory IgA (Streptococcus, H. influenzae & N.
gonorrheae)
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VIRULENCE FACTORS
VIRULENCE FACTORS
❖ MOBILE GENETICS & PATHOGENECITY ISLAND
• Plasmids
➢ are extrachromosomal pieces of
DNA and are capable of replicating
• Transposons
➢ highly mobile segments of DNA that
can move from one part of the DNA
to another.
➢ can result in recombination between
extrachromosomal DNA and the
chromosome
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VIRULENCE FACTORS
• Bacteriophages & Transduction
➢Transfer of these mobile genetic
elements between members of
one species
➢Transfer of these mobile genetic
elements between species can
result in transfer of virulence
factors, including antimicrobial
resistance genes
VIRULENCE FACTORS
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VIRULENCE FACTORS
VIRULENCE FACTORS
• PATHOGENECITY ISLAND
➢they have one or more
virulence genes
➢they are present in the
genome of pathogenic
members
➢ absent in the nonpathogenic
members
➢originate from gene transfer
from foreign species
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VIRULENCE FACTORS
❖ OTHER MECHANISM FOR VIRULENCE
A. Bacterial Secretion System
➢involved in cellular functions such as the transport
of proteins that make pili or flagella and in the
secretion of enzymes or toxins
B. Antimicrobial Resistance
➢ ability to evade the actions of
antibiotic/antimicrobial agents
➢ chromosomal & extra-chromosomal origins
➢ Drug Efflux pumps (gram negative bacteria)
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21/03/2022

RENZ AMADOR I. BAGAS, RMT

THE HUMAN MICROBIOME PROJECT

Topic 2: Microbe Host Relationship rabagas,RMT

TYPES OF MICROBIAL SYMBIOSIS

Topic 2: Microbe Host Relationship rabagas,RMT

TYPES OF MICROBIAL SYMBIOSIS

Topic 2: Microbe Host Relationship rabagas,RMT

INDIGENOUS MICROBIOTA OF HUMANS

Topic 2: Microbe Host Relationship rabagas,RMT

INDIGENOUS MICROBIOTA OF HUMANS

Topic 2: Microbe Host Relationship rabagas,RMT

INDIGENOUS MICROBIOTA OF HUMANS

Topic 2: Microbe Host Relationship rabagas,RMT

INDIGENOUS MICROBIOTA OF HUMANS

➢The external surface of the eye is lubricated,

Topic 2: Microbe Host Relationship rabagas,RMT

INDIGENOUS MICROBIOTA OF HUMANS

Topic 2: Microbe Host Relationship rabagas,RMT

INDIGENOUS MICROBIOTA OF HUMANS

Topic 2: Microbe Host Relationship rabagas,RMT

INDIGENOUS MICROBIOTA OF HUMANS

Topic 2: Microbe Host Relationship rabagas,RMT

INDIGENOUS MICROBIOTA OF HUMANS

Topic 2: Microbe Host Relationship rabagas,RMT

INDIGENOUS MICROBIOTA OF HUMANS

Topic 2: Microbe Host Relationship rabagas,RMT

INDIGENOUS MICROBIOTA OF HUMANS

Topic 2: Microbe Host Relationship rabagas,RMT

INDIGENOUS MICROBIOTA OF HUMANS

Topic 2: Microbe Host Relationship rabagas,RMT

ROLES OF INDIGENOUS MICROBIOTA

Topic 2: Microbe Host Relationship rabagas,RMT

ROLES OF INDIGENOUS MICROBIOTA

Topic 2: Microbe Host Relationship rabagas,RMT

MICROBE TO MICROBE INTERACTION

MICROBE TO MICROBE INTERACTION

Topic 2: Microbe Host Relationship rabagas,RMT

MICROBE TO MICROBE INTERACTION

Topic 2: Microbe Host Relationship rabagas,RMT

Topic 2: Microbe Host Relationship rabagas,RMT

Topic 2: Microbe Host Relationship rabagas,RMT

Topic 2: Microbe Host Relationship rabagas,RMT

Incubation Period Prodromal Period Period of Illness Convalescent Period

Topic 2: Microbe Host Relationship rabagas,RMT

e.g. diarrhea, vomiting, e.g. sore, boils, rash,

Topic 2: Microbe Host Relationship rabagas,RMT

Topic 2: Microbe Host Relationship rabagas,RMT

Topic 2: Microbe Host Relationship rabagas,RMT

Topic 2: Microbe Host Relationship rabagas,RMT

Topic 2: Microbe Host Relationship rabagas,RMT

Topic 2: Microbe Host Relationship rabagas,RMT

Topic 2: Microbe Host Relationship rabagas,RMT

Topic 2: Microbe Host Relationship rabagas,RMT

• Penetration of Epithelial Cell Layers

Topic 2: Microbe Host Relationship rabagas,RMT

▪ Growth in underlying tissues

Topic 2: Microbe Host Relationship rabagas,RMT

Topic 2: Microbe Host Relationship rabagas,RMT

Topic 2: Microbe Host Relationship rabagas,RMT

Topic 2: Microbe Host Relationship rabagas,RMT

Topic 2: Microbe Host Relationship rabagas,RMT

Topic 2: Microbe Host Relationship rabagas,RMT

Topic 2: Microbe Host Relationship rabagas,RMT