CHAPTER VIII

HOST PARASITE RELATIONSHIP

 HOST PARASITE RELATIONSHIP

• On the basis of their life habits, microorganisms are

classified as saprophytes or parasites.
 Saprophytes : Mode of life of free-living organisms which
obtain their nourishment from soil and water. Saprophytes
in general do not require a living host.
 Parasites: organisms living on or in other higher organisms.
• The relationship between microorganisms and the
host is called symbiosis, a relationship between two
organisms in which at least one organism is
dependent on the other.
 The association may take one of the three forms:

1. commensalism, one of the organisms benefits, and the other is

unaffected.
 Many of the microorganisms that make up our normal micro
biota arc commensals.
2. Mutualism is a type of symbiosis that benefits both organisms.
 For example, the large intestine contains bacteria, such as
E. coli, that synthesize vitamin K and some B vitamins.
3. parasitism: one (the host) is harmed and the other(the parasite
) is benefited .
 Many disease-causing bacteria
 Host Susceptibility
• Susceptibility to bacterial infections depends on the
physiologic and immunologic condition of the host and on
the virulence of the bacteria.
• Susceptibility to some infections is higher in the very young
and the very old and in immunosuppressed patients.
– individuals with defective immune responses are prone to frequent,
recurrent infections with even the least virulent bacteria.
Host Resistance
• Numerous physical and chemical attributes of the host protect
against bacterial infection.
PATHOGENICITY Vs VIRULENCE
• The capacity of a bacterium to cause disease reflects its
relative pathogenicity.
• On this basis, bacteria can be organized into three major
groups.
i. primary pathogens
ii. Opportunistic pathogens
iii. Non pathogens
Virulence
• Virulence is a quantitative measure of pathogenicity and is
measured by the number of organisms required to cause
disease.
– The 50% lethal dose (LD50) is the number of organisms needed to kill
half the hosts, and the
– 50% infectious dose (ID50) is the number needed to cause infection in
half the hosts. The infectious dose of an organism required to cause
disease varies greatly among the pathogenic bacteria.
• The degree of virulence is related directly to the ability of the
organism to cause disease despite host resistance
mechanisms;
• are useful in comparing the relative virulence of
different bacteria.
• It is affected by numerous variables such as
– the number of infecting bacteria,
– route of entry into the body,
– specific and nonspecific host defense mechanisms,
– and virulence factors of the bacterium.
Bacterial Infectivity
• Bacterial infectivity results from a disturbance in the balance
between bacterial virulence and host resistance.
• The "objective" of bacteria is to multiply rather than to cause
disease; it is in the best interest of the bacteria not to kill the
host.
Host-Mediated Pathogenesis
• Tissue damage results from the toxic mediators released by
lymphoid cells rather than from bacterial toxins.
– Gram-negative bacterial sepsis,
– tuberculosis,
• The tissue damage in these infections is caused by toxic
factors released from the lymphocytes, macrophages, and
polymorphonuclear neutrophils infiltrating the site of
infection.
FIGURE: Generalized mechanisms of bacterial pathogenesis: bacteria-induced
toxicity or host-mediated damage.
 Virulence Factors
• Factors that are produced by a microorganism and evoke
disease .
– Allow the bacteria to multiply in their host or vector
without being killed or expelled by the host's defenses and
result sign and symptoms .
• Virulence factors help bacteria to (1) invade the host, (2)
evade host defenses and (3) cause disease.
 The following are types of virulence factors:
I. Adherence : Almost all pathogens have some means of
attaching themselves to host tissues at their portal of entry.
 this attachment, called adherence -is a necessary step in
pathogenicity.
• The attachment between pathogen and host is accomplished
by means of surface molecules on the pathogen called
adhesins or ligands that bind specifically to complementary
surface receptors on the cells of certain host tissues.
– Glycocalyx, fimbriae, and flagella
 II. Evade host defenses
Invasion Factors: Surface components that allow the bacterium
to invade host cells
• The microbes produce surface proteins called invasins that
rearrange nearby actin filaments of the cytoskeleton and
facilitate penetration into the Host Cell.
– The specific bacterial surface factors that mediate invasion are not
known in most instances
• Intracellular survival ; is an important attribute of certain
bacteria that enhances their ability to cause disease.
• Helps the bacteria evade host defense mechanism
– bacteria that can live within cells are protected from attack by
macrophages and neutrophils.
• on the basis of their invasive properties for
eukaryotic cells can be grouped in to three;
I. obligate intracellular parasites eg; Chlamydia and
Rickettsia.
II. facultative intracellular pathogens;
Mycobacterium, Legionella, Brucella, and Listeria.
III. Extra cellular parasites
• Intracellular bacteria must possess specialized
mechanisms to protect them from the harsh effects
of the lysosomal enzymes encountered within the
cell.
• These include ;
1 inhibition of the fusion of the phagosome with the
lysosome,
2inhibition of acidification of the phagosome, which reduces
the activity of the lysosomal degradative enzymes; and
3 escape from the phagosome into the cytoplasm, where
there are no degradative enzymes.
• Capsules: Some bacteria are surrounded by capsules
that protect them from opsonization and
phagocytosis.
III. cause disease(How Bacterial Pathogens
Damage Host Cell)
• microorganism can damage host cells in four basic
ways:
(I) by using the host's nutrients;
(2) by causing direct damage in the immediate vicinity of
the invasion;
(3) by producing toxins, and
(4) by inducing hypersensitivity reactions.
 (1). Using the Host's Nutrients: Siderophores
– Iron is required for the growth of most pathogenic
bacteria. However, the concentration of free iron in the
human body is fairly low because most of the iron is tightly
bound to iron-transport proteins, such as lactoferrin,
transferrin, and ferritin, as well as hemoglobin.
• When a pathogen needs iron, siderophores are released into
the medium where they take the iron away from iron-
transport proteins by binding the iron even more tightly
– Siderophores are iron-binding factors that allow some bacteria to
compete with the host for iron, which is bound to hemoglobin,
transferrin, and lactoferrin.
FIGURE: Competition between host cells and bacterial pathogens for iron,
illustrating the importance of siderophores. Since free iron is scarce in tissue
fluids and blood, bacterial siderophores compete effectively for Fe3+ bound to
lactoferrin and transferrin.
 (2). Direct Damage
• pathogens can cause direct damage
– the pathogens use the host cell for nutrients and produce
waste products.
– As pathogens metabolize and multiply in cells, the cells
usually rupture.
(3). The Production of Toxins
• Toxins are poisonous substances that are produced
by certain microorganisms.
• Toxins are of two general types, based on their
position relative to the microbial cell: exotoxins and
endotoxins.
• Exotoxins are produced inside some bacteria as part
of their growth and metabolism and are secreted by
the bacterium into the surrounding medium
• Exotoxins are proteins, and many are enzymes that
catalyze only certain biochemical reactions.
• Major categories include
 cytotoxins,
 neurotoxins, and
 enterotoxins.
Endotoxins
• Endotoxins are part of the outer portion of the cell wall of
gram-negative bacteria.
• Endotoxins are released when gram-negative bacteria die and
their cell walls undergo lysis, thus liberating the endotoxin.
• Antibiotics used to treat diseases caused by gram-negative
bacteria can lyse the bacterial cells; this reaction releases
endotoxin and may lead to an immediate worsening of the
symptoms.
• It induces the overproduction of cytokines, such as tumor
necrosis factor, interleukin-1, and nitric oxide from
macrophages, which causes the symptoms of septic shock,
such as fever and hypotension.
FIGURE: Basic structure of endotoxin (lipopolysaccharide) from Gram-
negative bacteria.
Table : Multiple biologic activities exhibited by the lipid component of endotoxin
 Genetic and Molecular Basis for Virulence

• Bacterial virulence factors may be encoded on chromosomal,

plasmid, transposon, or temperate bacteriophage DNA;
• virulence factor genes on transposons or temperate
bacteriophage DNA may integrate into the bacterial
chromosome.
• The transfer of genetic information can occur by either of the
three methods:
– Transformation; which a bacterium acquire DNA fragments
or genes from surroundings.
– Transduction; a virus (phage) acts as a vehicle for carrying
DNA from a donor bacterium to recipient bacterium.
– Conjugation; DNA is transferred from one bacterium to
another by cell to cell physical contact
FIGURE: Mechanisms of acquiring bacterial virulence genes.
Table: Genetic basis for virulence selected bacterial pathogens
 Defense mechanisms of the host
There are two defense mechanism of our body
1. Non-specific/ innate/ defence mechanisms
2. Specific / adaptive/ acquired/
1. Non-specific defence mechanisms
• Non- specific defense provides the first line protection
against potentially pathogenic microorganisms and are not
specific to pathogenic species.
• Most non-specific defenses are natural and offer
protection from the moment of birth.
– The non-specific defenses include:
– Physical barrier - Inflammatory
response
– Chemical barrier - Phagocytosis
– Normal microbial flora
 I. Physical barrier
a. Skin
– The outer surface of the skin layer is composed of keratin
which is not readily degraded by most microorganisms
– Also - prevents attachment.
- Impermeable to most pathogens.
b. Mucous Membranes
c. The whirling of system of bones
– Projected to nasal cavities
– Essential for trapping of entering microbes
d. Fluid flow
– Movement of fluids across the surface of body tissues
protects the body from accumulation of microorganisms.
Example, saliva washes microorganisms in the oral cavity to
the stomach. Tears continuously remove microorganisms
from the eye.
II. Chemical Barriers
• These are secretions of body which have an antimicrobial
activity. These include:
– Lysozyme
– Acidity
– Interferon
III. Phagocytosis
– Phagocytosis is a process of engulfing and destroying
an organism or other foreign body and digest with
enzyme contained in cytoplasmic (lysosomes)
granules of phagocytic cells.
– During Phagocytosis, the m/o is engulfed by
pseudopodia of phagocytic cell.
IV. Normal Micro flora
Normal microbial flora is microbial population
frequently found in association with particular tissue
that typically does not cause disease.
V. Compliments : are plasma proteins found in inactive
form and activated cascade reaction.
They are named from C1-C9
• Role of complements
– Opsonization: coating of pathogens and facilitates for
Phagocytosis e.g., C3a
– Chemo attractants e.g., C5a
– Bacteriallysis (C8C9)
VI. Inflammatory response
• Inflammatory response is a non specific immune response to
infection or injury and designed to remove cellular debris,
localizing invading microorganism and arrest the spread of
infection.
– Role of inflammation
• delivers additional cells of effector molecules to the site
of infection
• prevent the spread of infection
• promote the repair of injured tissue
• VII. NK cells / natural killers/ are lymphocytic in origin which
kill virus infected cells with put antigenic stimulation
 Adaptive
• It is occurred if the organism couldn’t overcome the disease
usually the innate defense mechanism
– Occurred due to or following exposure to foreign substances
– Is specific (response to particular pathogen)
– It is mediated by lymphocytes (T-cells and B-cells)
Accordingly:
1. Humoral immune response
2. Cell mediated immune response
1. Humoral immune response
– Is mediated by antibody which are produced by b-cells
(antigen stimulated cells i.e. plasma cells)
– involves five classes of immunoglobins IgA, IgD, IgE, IgG, IgM
Role of antibody
– Neutralization
– Opsonization
– Complement activation
2. Cell mediated: is immunity mediated by sensitized
(exposed to antigen) cells called T-lymphocyte and their
cyokines with out involvement of antibody.
• Cytokines are small soluble proteins secreted by cells
that can alter the behavior of the cell itself or another.
– T-cells includes
1. cytotoxic T-cells
- destroys infected cells
2. T-helper cells (CD4 cells)
- Th1- secret cytokines which activate
macrophages for interacellular killing
- Th2- activates B-cells for exteracellular killing
3. Suppressor T- cells
- regulate the function of the above T-cells
• Adaptive immunity can be
• Passive immunity
• Active immunity
1. Passive immunity
A. passive natural
- occurred due to natural transferred immunoglobulin
(IgG)
B. passive artificial
- occurred when Ab and lymphocytes are given to
individual which is deficient of them. (i.e., Ab and lymphocytes
of another person)
2. Active immunity
A. Active natural (contact with infection)
B. active artificial (immunization)
 Factors affecting host defence mechanism
1. Nutrition: Malnutrition predisposes to infection.
2. Age: The very old and the very young are particularly liable
to infection.
3. Sex: May be attributes to hormonal influence.
4. Impairment of the host immune response
– .radiotherapy
– Immunosuppressive drugs including steroids
– .Malignancy
– HIV
5. Race
6. Climate
7. Occupation
8. Drugs
9. Pregnancy
•
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