Classification of Organisms pdf - D. Haider

Classification of organisms microbiology

Carl Woese devised three classification groups called domain. A domain is larger than a
kingdom

Domains
· Eubacteria: Bacteria that have peptidoglycan cell walls. (Peptidoglycan is the molecular
structure of the cell walls of eubacteria which consists of Nacetyglucosamine, N-
acetylmuramic acid, tetrapeptide, side chain and murein).

· Archaea: Prokaryotes that do not have peptidoglycan cell walls

· Eucarya: Organisms from the following kingdoms:

Kingdoms

· Protista: Examples- Algae, protozoa.

· Fungi: Examples- one-celled yeasts, multicellular molds and mushrooms.

· Plantae: Examples- moss, conifers, ferns, flowering plant, algae.

· Animalia: Examples- insects, worms, sponges and vertebrates.

Host-pathgen relations

Introduction:

The pathogenesis of bacterial infection includes initiation of the infectious process and the
mechanisms that lead to the development of signs and symptoms of disease. Characteristics
of bacteria that are pathogens include transmissibility, adherence to host cells, invasion of
host cells and tissues, toxigenicity, and ability to evade the host's immune system. Many
infections caused by bacteria that are commonly considered to be pathogens are inapparent
or asymptomatic.

Adherence (adhesion, attachment):

The process by which bacteria stick to the surfaces of host cells. Once bacteria have entered
the body, adherence is a major initial step in the infection process.

Carrier: A person or animal with asymptomatic infection that can be transmitted to another
susceptible person or animal.

Infection: Multiplication of an infectious agent within the body. Multiplication of the bacteria
that are part of the normal flora of the gastrointestinal tract, skin, etc, is generally not
considered an infection; on the other hand, multiplication of pathogenic bacteria (eg,
Salmonella species)—even if the person is asymptomatic––is deemed an infection.

Invasion: The process whereby bacteria, animal parasites, fungi, and viruses enter host cells or
tissues and spread in the body.

Nonpathogen: A microorganism that does not cause disease; may be part of the normal flora.

Opportunistic pathogen: An agent capable of causing disease only when the host's resistance
is impaired (ie, when the patient is "immunocompromised").

Pathogen: A microorganism capable of causing disease.

Pathogenicity: The ability of an infectious agent to cause disease.

Toxigenicity: The ability of a microorganism to produce a toxin that contributes to the
development of disease.

Virulence: The quantitative ability of an agent to cause disease. Virulent agents cause disease
when introduced into the host in small numbers. Virulence involves invasion and toxigenicity

Normal Microbial Flora of the Human Body

The term "normal microbial flora" denotes the population of microorganisms that inhabit the
skin and mucous membranes of healthy normal persons. It is doubtful whether a normal viral
flora exists in humans.

The skin and mucous membranes always harbor a variety of microorganisms that can be
arranged into two groups: (1) The resident
flora consists of relatively fixed types of microorganisms regularly found in a given area at a
given age; if disturbed, it promptly reestablishes itself. (2) The transient flora consists of
nonpathogenic or potentially pathogenic microorganisms that inhabit the skin or mucous
membranes for hours, days, or weeks; it is derived from the environment, does not produce
disease, and does not establish itself permanently on the surface. Members of the transient
flora are generally of little significance so long as the normal resident flora remains intact.
However, if the resident flora is disturbed, transient microorganisms may colonize, proliferate,
and produce disease.

Transmission of Infection

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Microorganisms can be transmitted from environment (human or animals) and affected

another host by aerosol route, oral route, or nosocomial infection and urogenital route these
processes can be occurred by several ways:

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1- direct contact from infected animal to susceptible person (zoonotic disease). Like

Bacillus anthracis (caused anthrax).

2- rodents borne disease like Yersinia pestis.

3- nosocomial disease by hand personal.

The Infectious Process

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Once in the body, bacteria must attach or adhere to host cell, usually epithelial cells. After
the bacteria have established a primary site of infection, they multiply and spread directly
through tissues or via the lymphatic system to the bloodstream. This infection (bacteremia)
can be transient or persistent. Bacteremia allows bacteria to spread widely in the body and
permits them to reach tissues particularly suitable for their multiplication.

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Pneumococcal pneumonia is an example of the infectious process. S pneumoniae can be
cultured from the nasopharynx of 5–40% of healthy people. Occasionally, pneumococci
from the nasopharynx are aspirated into the lungs

Adherence Factors

Once bacteria enter the body of the host, they must adhere to cells of a tissue surface. If they
did not adhere, they would be swept away by mucus and other fluids that bathe the tissue
surface. Adherence, which is only one step in the infectious process, is followed by
development of microcolonies and subsequent steps in the pathogenesis of infection.

The  interactions  between  bacteria  and  tissue  cell  surfaces  in  the  adhesion  process  are
complex. Several factors play important roles: surface hydrophobicity and net surface charge,
binding molecules on bacteria (ligands), and host cell receptor interactions. Bacteria and host
cells  commonly  have  net  negative  surface  charges  and,  therefore,  repulsive  electrostatic
forces.  These  forces  are  overcome  by  hydrophobic  and  other  more  specific  interactions
between bacteria and host cells.

Bacteria also have specific surface molecules that interact with host cells. Many bacteria have
pili,  hair-like  appendages  that  extend  from  the  bacterial  cell  surface  and  help  mediate
adherence of the bacteria to host cell surfaces. For example, some E coli strains have type 1
pili,  which  adhere  to  epithelial  cell  receptors  containing  D-mannose;  adherence  can  be
blocked in vitro by addition of D-mannose to the medium. E coli organisms that cause urinary
tract infections commonly do not have D-mannose-mediated adherence but have P-pili, which
attach to a portion of the P blood

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Therefore the important adherence factors include:



capsule



2-pili like P pili of E.coli



interaction between bacterial cell components (ligands) and specific host receptors.



different charges between bacterial surface and host cell surface (electrostatic force)

Invasion of Host Cells & Tissues

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For  many  disease-causing  bacteria,  invasion  of  the  host's  epithelium  is  central  to  the
infectious  process.  Some  bacteria  (eg,  salmonella  species)  invade  tissues  through  the
junctions  between  epithelial  cells.  Other  bacteria  (eg,  yersinia  species,  N  gonorrhoeae,
Chlamydia  trachomatis)  invade  specific  types  of  the  host's  epithelial  cells  and  may
subsequently enter the tissue. Once inside the host cell, bacteria may remain enclosed in a
vacuole composed of the host cell membrane, or the vacuole membrane may be dissolved
and  bacteria  may  be  dispersed  in  the  cytoplasm.  Some  bacteria  (eg,  shigella  species)
multiply within host cells, whereas other bacteria do not.

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"Invasion"  is  the  term  commonly  used  to  describe  the  entry  of  bacteria  into  host  cells,
implying  an  active  role  for  the  organisms  and  a  passive  role  for  the  host  cells.  In  many
infections,  the  bacteria  produce  virulence  factors  that  influence  the  host  cells,  causing
them to engulf (ingest) the bacteria. The host cells play a very active role in the process.

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Toxin production and other virulence properties are generally independent of the ability of
bacteria to invade cells and tissues. For example, Corynebacterium diphtheriae is able to
invade the epithelium of the nasopharynx and cause symptomatic sore throat even when
the C diphtheriae strains are nontoxigenic.

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M cells normally sample antigens and present them to macrophages in the submucosa.
Shigellae are phagocytosed by the M cells, pass through the M cells, and escape killing by
macrophages.

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L  monocytogenes  from  the  environment  is  ingested  in  food.  Presumably,  the  bacteria
adhere to and invade the intestinal mucosa, reach the bloodstream, and disseminate. The
pathogenesis  of  this  process  has  been  studied  in  vitro.  L  monocytogenes  adheres  to  and
readily  invades  macrophages  and  cultured  undifferentiated  intestinal  cells.  The  listeriae
induce engulfment by the host cells.

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Toxins

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Toxins produced by bacteria are generally classified into two groups: exotoxins and
endotoxins.

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Exotoxins

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Many gram-positive and gram-negative bacteria produce exotoxins of considerable medical
importance. Some of these toxins have had major roles in world history. For example,
tetanus caused by the toxin of C tetani killed as many as 50,000 soldiers of the Axis powers
in World War II. Many exotoxins consist of A and B subunits. The B subunit generally

mediates adherence of the toxin complex to a host cell and aids entrance of the exotoxin
into the host cell. The A subunit provides the toxic activity.

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C botulinum causes botulism. It is found in soil or water and may grow in foods (canned,
vacuum-packed, etc) if the environment is appropriately anaerobic. An exceedingly potent
toxin (the most potent toxin known) is produced. It is heat-labile and is destroyed by
sufficient heating.

Some S aureus strains growing on mucous membranes or in wounds, elaborate toxic shock
syndrome toxin-1 (TSST-1), which causes toxic shock syndrome. The illness is characterized
by shock, high fever, and a diffuse red rash that later desquamates; multiple other organ
systems are involved as well. TSST-1 is a super antigen and stimulates lymphocytes to
produce large amounts of IL-1 and TNF. The major clinical manifestations of the disease
appear to be secondary to the effects of the cytokines. TSST-1 may act synergistically with
low levels of lipopolysaccharide to yield the toxic effect.

Negative Bacteria

Lipopolysaccharides of Gram

The lipopolysaccharides (LPS, endotoxin) of gram-negative bacteria are derived from
cell walls and are often liberated when the bacteria lyse. The substances are heat-
stable, have molecular weights between 3000 and 5000 (lipooligosaccharides, LOS) and
several million (lipopolysaccharides), and can be extracted (eg, with phenol-water).

The pathophysiologic effects of LPS are similar regardless of their bacterial origin
except for those of bacteroides species, which have a different structure and are less
toxic. LPS in the bloodstream is initially bound to circulating proteins which then
interact with receptors on macrophages and monocytes and other cells of the
reticuloendothelial system. IL-1, TNF, and other cytokines are released, and the
complement and coagulation cascades are activated. The following can be observed
clinically or experimentally: fever, leukopenia, and hypoglycemia; hypotension and
shock resulting in impaired perfusion of essential organs (eg, brain, heart, kidney);
intravascular coagulation; and death from massive organ dysfunction.

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Differences between exo and end

endotoxin

exotoxin

proberty

Bacterial

chromosome

Plasmid or

bacteriophage

Gene location

lps

proteins

composition

Non specific fever

and shock

specific

Action

Stable at 100 C° for

1 hr

Labile destroyed at

60C°

Heat stability

yes

diffusibility

Weak

Strong

Antigenicity

Weak

Strong

Toxicity

Yes

Convertibility to

toxoid

Gram -ve

Mainly G+ve

Produced by

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Peptidoglycan of Gram-Positive Bacteria

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The peptidoglycan of gram-positive bacteria is made up of cross-linked macromolecules
that surround the bacterial cells. Vascular changes leading to shock may also occur in
infections due to gram-positive bacteria that contain no LPS. Gram-positive bacteria have
considerably more cell wall-associated peptidoglycan than do gram-negative bacteria.
Peptidoglycan released during infection may yield many of the same biologic activities as
LPS, though peptidoglycan is invariably much less potent than LPS.

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Enzymes

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Many species of bacteria produce enzymes that are not intrinsically toxic but do play
important roles in the infectious process for examples : -

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Tissue-Degrading Enzymes

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Many bacteria produce tissue-degrading enzymes. The best-characterized are enzymes
from C perfringens), S aureus , group A streptococci , and, to a lesser extent, anaerobic
bacteria. The roles of tissue-degrading enzymes in the pathogenesis of infections appear
obvious but have been difficult to prove, especially those of individual enzymes. For
example, antibodies against the tissue-degrading enzymes of streptococci do not modify
the features of streptococcal disease.

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In addition to lecithinase, C perfringens produces the proteolytic enzyme collagenase,
which degrades collagen, the major protein of fibrous connective tissue, and promotes
spread of infection in tissue.

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S aureus produces coagulase, which works in conjunction with serum factors to coagulate
plasma. Coagulase contributes to the formation of fibrin walls around staphylococcal
lesions, which helps them persist in tissues. Coagulase also causes deposition of fibrin on
the surfaces of individual staphylococci, which may help protect them from phagocytosis or
from destruction within phagocytic cells.

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Hyaluronidases are enzymes that hydrolyze hyalouronic acid, a constituent of the ground
substance of connective tissue. They are produced by many bacteria (eg, staphylococci,
streptococci, and anaerobes) and aid in their spread through tissues.

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IgA1 Proteases

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Immunoglobulin A is the secretory antibody on mucosal surfaces. It has two primary forms,
IgA1 and IgA2, that differ near the center, or hinge, region of the heavy chains of the
molecules. IgA1 has a series of amino acid in the hinge region that are not present in IgA2.
Some bacteria that cause disease produce enzymes, IgA1 proteases, that split IgA1 at
specific proline-threonine or proline-serine bonds in the hinge region and inactivate its
antibody activity. IgA1 protease is an important virulence factor of the pathogens N
gonorrhoeae, N meningitidis, H influenzae, and S pneumoniae. .

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Antiphagocytic Factors

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Many bacterial pathogens are rapidly killed once they are ingested by polymorphonuclear
cells or macrophages. Some pathogens evade phagocytosis or leukocyte microbicidal
mechanisms by adsorbing normal host components to their surfaces. For example, S
aureus has surface protein A, which binds to the Fc portion of IgG. Other pathogens have
surface factors that impede phagocytosis—eg, S pneumoniae, N meningitidis; many other
bacteria have polysaccharide capsules. S pyogenes (group A streptococci) has M protein. N
gonorrhoeae (gonococci) has pili. Most of these antiphagocytic surface structures show
much antigenic heterogeneity. For example, there are more than 90 pneumococcal
capsular polysaccharide types and more than 80 M protein types of group A streptococci.
Antibodies against one type of the antiphagocytic factor (eg, capsular polysaccharide, M
protein) protect the host from disease caused by bacteria of that type but not from those
with other antigenic types of the same factor.

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A few bacteria (eg, capnocytophaga and bordetella) produce soluble factors or toxins that
inhibit chemotaxis by leukocytes and thus evade phagocytosis by a different mechanism.

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Intracellular Pathogenicity

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Some bacteria (eg, M tuberculosis, brucella species, and legionella species) live and grow in
the hostile environment within polymorphonuclear cells, macrophages, or monocytes. The
bacteria accomplish this feat by several mechanisms: They may avoid entry into
phagolysosomes and live within the cytosol of the phagocyte; they may prevent
phagosome-lysosome fusion and live within the phagosome; or they may be resistant to
lysosomal enzymes and survive within the phagolysosome.

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Antigenic Heterogeneity

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The surface structures of bacteria (and of many other microorganisms) have considerable
antigenic heterogeneity. Often these antigens are used as part of a serologic classification
system for the bacteria. The classification of the 2000 or so different salmonellae is based
principally on the types of the O (lipopolysaccharide side chain) and H (flagellar) antigens.
Similarly, there are more than 100 E coli O types and more than 100 E coli K (capsule)
types. The antigenic type of the bacteria may be a marker for virulence, related to the
clonal nature of pathogens .

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