Unit 2: Bacteriology
06
Lecture 1 – General Microbiology
Microbiology in Medicine & Host – Parasite
Relationship
Microbiology: is the study of microorganisms, which are
tiny organisms that live around us & inside our body. An
infection is caused by the infiltration of a disease-causing
microorganism known as a Pathogenic microorganism.
Some pathogenic microorganisms infect humans, but not
other animals & plants. Some pathogenic microorganisms
that infect animals or plants also infect humans. Not all
microorganisms are pathogens. In fact many
microorganisms help to maintain homeostasis in our
bodies and are used in the production of food in our
intestines that assist in the digestion of food & play a
critical role in the formation of vitamins such as vitamin
B & vitamin K. They help by breaking down large
molecules into smaller ones.
The History of Infectious Diseases
The Past
Infectious diseases have been known for thousands of
years, although accurate information on their etiology has
only been available for about a century. In the medical
teachings of Hippocrates, the cause of infections
occurring frequently in a certain locality or during a
certain period (epidemics) was sought in “changes” in the
air according to the theory of miasmas. This concept, still
reflected in terms such as “swamp fever” or “malaria,”
was the predominant academic opinion until the end of
the 19th century, despite the fact that the Dutch cloth
merchant A. van Leeuwenhoek had seen and described
bacteria as early as the 17th century, using a microscope
he built himself with a single convex lens and a very short
focal length. At the time, general acceptance of the notion
of “spontaneous generation”—creation of life from dead
organic material—stood in the way of implicating the
bacteria found in the corpses of infection victims as the
cause of the deadly diseases. It was not until Pasteur
disproved the doctrine of spontaneous generation in the
second half of the 19th century that a new way of thinking
became possible. By the end of that century,
microorganisms had been identified as the causal agents
in many familiar diseases by applying the Henle-Koch
postulates formulated by R. Koch in 1890.
The Henle–Koch Postulates
The postulates can be freely formulated as follows:
The microorganism must be found under conditions
corresponding to the pathological changes and clinical
course of the disease in question.
It must be possible to cause an identical (human) or
similar (animal) disease with pure cultures of the
pathogen.
The pathogen must not occur within the framework of
other diseases as an “accidental parasite.”
These postulates are still used today to confirm the cause
of an infectious disease.
However, the fact that these conditions are not met does
not necessarily exclude a contribution to disease etiology
by a pathogen found in context. In particular, many
infections caused by subcellular entities do not fulfill the
postulates in their classic form.
The Present
The frequency and deadliness of infectious diseases
throughout thousands of years of human history have kept
them at the focus of medical science. The development of
effective preventive and therapeutic measures in recent
decades has diminished, and sometimes eliminated
entirely, the grim epidemics of smallpox, plague, spotted
fever, diphtheria, and other such contagions. Today we
have specific drug treatments for many infectious
diseases. As a result of these developments, the attention
of medical researchers was diverted to other fields: it
seemed we had tamed the infectious diseases. Recent
years have proved this assumption false. Previously
unknown pathogens causing new diseases are being found
and familiar organisms have demonstrated an ability to
evolve new forms and reassert themselves. The origins of
this reversal are many and complex: human behavior has
changed, particularly in terms of mobility and nutrition.
Further contributory factors were the introduction of
invasive and aggressive medical therapies, neglect of
established methods of infection control and, of course,
the ability of pathogens to make full use of their specific
genetic variability to adapt to changing conditions.The
upshot is that physicians in particular, as well as other
medical professionals and staff, urgently require a basic
knowledge of the pathogens involved and the genesis of
infectious diseases if they are to respond effectively to
this dynamism in the field of infectiology. The aim of this
textbook is to impart these essentials to them.
Unit 2: Bacteriology
06
Pathogens: Prokaryotic and Eukaryotic
Microorganisms
According to a proposal by Woese that has been gaining
general acceptance inrecent years, the world of living
things is classified in the three domains: bacteria,
archaea, and eucarya. In this system, each domain is
subdivided into
kingdoms. Pathogenic microorganisms
are found in the domains bacteria and eucarya.
Bacteria. This domain includes the kingdom of the
heterotrophic eubacteria and includes all human pathogen
bacteria. The other kingdoms, for instance that of the
photosynthetic cyanobacteria, are not pathogenic. It is
estimated that bacterial species on Earth number in the
hundreds of thousands, of which only about 5500 have
been discovered and described in detail.
Archaea. This domain includes forms that live under
extreme environmental conditions, including thermophilic,
hyperthermophilic, halophilic,and methanogenic
microorganisms. The earlier term for the archaea was
archaebacteria (ancient bacteria) , and they are indeed a
kind of living fossil. Thermophilic archaea thrive mainly in
warm, moist biotopes such as the hot springs at the top of
geothermal vents. The hyperthermophilic archaea, a more
recent discovery, live near deep-sea volcanic plumes at
temperatures exceeding 100 °C.
Eucarya. This domain includes all life forms with cells
possessing a genuine nucleus.The plant and animal
kingdoms (animales and plantales) are all eukaryotic life
forms. Pathogenic eukaryotic microorganisms include
fungal and protozoan species.
Classic bacteria.
These organisms reproduce asexually by binary transverse
fission. They do not possess the nucleus typical of
eucarya. The cell walls of these organisms are rigid (with
some exceptions, e.g., the mycoplasma).
Chlamydiae. These organisms are obligate intracellular
parasites that are able to reproduce in certain human cells
only and are found in two stages: the infectious,
nonreproductive particles called elementary bodies (0.3
µm) and the noninfectious, intracytoplasmic, reproductive
forms known as initial (or reticulate) bodies (1 µm).
Rickettsiae. These organisms are obligate intracellular
parasites, rod-shaped to coccoid, that reproduce by binary
transverse fission. The diameter of the individual cell is
from 0.3–1 µm.
Mycoplasmas. Mycoplasmas are bacteria without rigid
cellwalls. They are found in a wide variety of forms, the
most common being the coccoid cell (0.3–0.8
µ
m).
Threadlike forms also occur in various lengths.
Fungi and Protozoa
Fungi. Fungi (Mycophyta) are nonmotile eukaryotes with
rigid cell walls and a classic cell nucleus. They contain no
photosynthetic pigments and are carbon heterotrophic,
that is, they utilize various organic nutrient substrates (in
contrast to carbon autotrophic plants). Of more than 50
000 fungal species, only about 300 are known to be
human pathogens. Most fungal infections occur as a result
of weakened host immune defenses.
Protozoa. Protozoa are microorganisms in various sizes
and forms that may be free-living or parasitic. They
possess a nucleus containing chromosomes and organelles
such as mitochondria (lacking in some cases), an en-
doplasmic reticulum, pseudopods, flagella, cilia,
kinetoplasts, etc. Many parasitic protozoa are transmitted
by arthropods, whereby multiplication and transformation
into the infectious stage take place in the vector.
Animals
Helminths. Parasitic worms belong to the animal
kingdom. These are metazoan organisms with highly
differentiated structures. Medically significant groups
include the trematodes (flukes or flatworms), cestodes
(tapeworms), and nematodes (roundworms).
Subcellular Infectious Entities
Prions (proteinaceous infectious particles). The evidence
indicates that prions are protein molecules that cause
degenerative central nervous system (CNS) diseases such
as Creutzfeldt-Jakob disease, kuru, scrapie in sheep, and
bovine spongiform encephalopathy (BSE) (general term:
transmissible spongiform encephalopathies [TSE]).
Viruses. Ultramicroscopic, obligate intracellular parasites
that:
contain only one type of nucleic acid, either DNA or RNA
possess no enzymatic energy-producing system and no
protein-synthesizing apparatus, and
Force infected host cells to synthesize virus particles.
Arthropods. These animals are characterized by an external
chitin skeleton, segmented bodies, jointed legs, special
mouthparts, and other specific features. Their role as direct
causative agents of diseases is a minor one (mites, for
instance, cause scabies) as compared to their role as vectors
transmitting viruses, bacteria, protozoa , & helminths.
Unit 2: Bacteriology
06
Basic Terminology of Infectiology
The terms pathogenicity and virulence are not clearly
defined in their relevance to microorganisms. They are
sometimes even used synonymously. It has been proposed
that pathogenicity be used to characterize a particular
species and that virulence be used to describe the sum of
the disease-causing properties of a population (strain) of a
pathogenic species.
Pathogenicity and virulence in the microorganism
correspond to susceptibility in a host species and
disposition in a specific host organism, whereby an
individual may be anywhere from highly disposed to
resistant.
Host–Pathogen Interactions
The factors determining the genesis, clinical picture and
outcome of an infection include complex relationships
between the host and invading organisms that differ
widely depending on the pathogen involved. Despite this
variability, a number of general principles apply to the
interactions between the invading pathogen with its
aggression factors and the host with its defenses. Since
the pathogenesis of bacterial infectious diseases has been
researched very thoroughly, the following summary is
based on the host–invader interactions seen in this type of
infection. The determinants of bacterial pathogenicity
and virulence can be outlined as follows:
Adhesion to host cells (adhesins).
Breaching of host anatomical barriers (invasins) and
colonization of tissues (aggressins).
Strategies to overcome nonspecific defenses, especially
antiphagocytic mechanisms (impedins).
Strategies to overcome specific immunity, the most
important of which is production of IgA proteases
(impedins), molecular mimicry, and immunogen
variability.Damage to host tissues due to direct bacterial
cytotoxicity, exotoxins, and exoenzymes (aggressins).
Damage due to inflammatory reactions in the
macroorganism: activation of complement and
phagocytosis; induction of cytokine production
(modulins).
The above bacterial pathogenicity factors are
confronted by the following host defense mechanisms:
Nonspecific defenses including mechanical, humoral, and
cellular systems. Phagocy- tosis is the most important
process in this context.
Specific immune responses based on antibodies and
specific reactions of T lymphocytes.
The response of these defenses to infection thus involves
the correlation of a number of different mechanisms.
Defective defenses make it easier for an infection to take
hold. Primary, innate defects are rare, whereas acquired,
secondary immune defects occur frequently, paving the
way for infections by microorganisms known as
“facultative pathogens” (opportunists).
Determinants of Bacterial Pathogenicity and Virulence
Relatively little is known about the factors determining
the pathogenicity and virulence of microorganisms, and
most of what we do know concerns the disease -causing
mechanisms of bacteria.
There are five groups of potential bacterial contributors to
the pathogenesis of infectious diseases:
1) Adhesins. They facilitate adhesion to specific target cells.
2) Invasins. They are responsible for active invasion of the
cells of the acroorganism.
3) Impedins. These components disable host immune
defenses in some cases.
4) Aggressins. These substances include toxins and tissue-
damaging enzymes.
5) Modulins. Substances that induce excess cytokine
production (i.e., lipopolysaccharides of Gram-negative
bacteria, superantigens, murein fragments).