Updated: 10/31/96
Updated: 10/31/96
To understand the nature of disease, particularly infectious disease.
To learn the ways bacteria have of invading and producing the disease state.
An ID agent must be able to grow on or in a host and it must do harm to that host. Every ID is characterized by the SYMPTOMS produced in the average victim of that ID. These symptoms, referred to as the CLINICAL SYMPTOMS, are used by physicians and health care personnel to identify a particular ID or group of IDs. For example, one set of symptoms identify common upper respiratory diseases (colds). However, the mumps virus has a UNIQUE set of symptoms that are used in diagnosing this particular infectious agent. That is, a single pathogen may produce a clear set of symptoms that allows its easy recognition, whereas a set of identical symptoms (e.g. the "runs", colds, pneumonia) may be produced by a number of different ID agents. Finally, some ID agents cause a variety of different symptoms in different hosts of the same species; AIDS and tuberculosis are two such examples.
In describing an ID the agent is identified, if known, the symptoms are described, along with the prognosis and the manner in which the ID is contracted. Molecular biology has given us tools to rapidly identify the probable etiological agent of many common diseases. The combination of DNA fingerprinting and PCR make it possible to obtain an accurate diagnosis from as little as 10 micro liters of a patient's body fluid (blood, urine, spit, etc.) within a few hours rather than the days it has taken in the recent past. New techniques are in the pipeline that will cut diagnosis time down to a FEW SECONDS in many cases. While it is crucial, diagnosis only IDENTIFIES the etiological agent, but it does not explain how the disease process works or how the patient contacted the ID agent in the first place.
Once introduced to a suitable place, the IA begins to grow. At this point the NDS of the body often eliminates the intruders without harm, but if the pathogen has the proper arsenal of weapons it can establish itself and render serious harm on the host. The experimental questions scientists ask today are about the mechanisms that a pathogen employs to establish itself and produce the subsequent disease. These disease-inducing factors are called VIRULENCE FACTORS or VIRULENCE DETERMINANTS (VD). Identification of a pathogen's VDs and an understanding of their molecular mechanisms of action, allows us to design ways to neutralize or destroy the VD, thus rendering the pathogen harmless; we can "pull its teeth".
SEPTACEMIA:
This describes the case where the pathogen grows massively within the host.
In effect the host becomes a virtual "test tube" for the bacterium. Bacteria
will be found in the blood and all the organs. Death usually ensues when
this happens.
Virulence determinants come in many forms, but I will describe only some of the MAJOR ones:
TOXINS:
Toxins are products of a pathogen that destroys one or more vital component
of the host which allows it to survive and flourish. EXOTOXINS
are toxins that are SECRETED from the
cell or leak out of the cell after is dies. Generally they are soluble
proteins and thus are carried throughout the body in the blood or lymph,
doing damage at a distance from the infection. Toxins tend to target specific
cells in the body. Some are enzymes and others are proteins that bind to
and inhibit crucial cellular activities which eventually lead to the death
of cells. A special group of toxins, produced only by G- bacteria, are
called ENDOTOXINS. Examples of toxic
VD include:
Diphtheria
toxin: an enzyme that blocks protein synthesis in many cells. The bacterium
producing this potent toxin grows mainly in the throat. Botulism
Toxin: Inhibits acetylcholine release from motor nerve endings and kills
the nerve cells. As will be discussed in the section on "Food Borne Diseases",
this is the most deadly toxin known. This is an exception to the "infection
rule", since C. botulinum does not have to infect for the toxin
to kill. Tetanus
toxin: Blocks the function of certain nerve cells leading to spastic paralysis.
The bacterium that produces this toxin usually grows locally in a puncture
wound, such as that from a nail or rose thorn, yet it readily kills full
grown horses or humans.Endotoxins
are composed of LPS
which
is only produced by G- bacteria. Endotoxins have a general basic structure,
but differ significantly in composition between species. Endotoxins are
released in relatively small amounts as the cells grown, but in copious
amounts when the cells die. Different endotoxins differ in their toxicity,
but all are heat stable and can tolerate autoclaving.Endotoxins harm many systems in the body and hence are very dangerous. They are often responsible for the cause of death of infections by G- cells.
ENZYMES:
Pathogens use a variety of enzymes to assist them in establishing infection
and producing a disease. There are VD enzymes that dissolve the glue between
cells, thus allowing the bacteria to spread rapidly through the tissue.
There are enzymes (hemolysins) that lyse
red blood cells and others that lyse white blood cells. There are enzymes
that degrade DNA and others that dissolve proteins.
ATTACHMENT
SYSTEMS:
Since many of the NSD involve mechanically flushing away pathogens, a common
VD are cell components that stick the bacteria to the target cells. Like
the attachment
or
docking proteins of viruses, these systems stick things to one another.
Two general attachment-systems have been found. The pili are short protein
rods or curled protein strands that have binding proteins on the ends that
attach firmly to receptor molecules on the surface of other cells. The
other system is that of the capsule. Capsules,
as you recall, are composed of sugar polymers (occasionally of protein
polymers) that tend to be sticky. These capsules are often produced in
large quantities which entrap microbes in sticky masses. For example, the
plaque on out teeth is generally composed of a group of microbes acting
symbiotically together, through the production of pili and capsules, to
stick (like super-glue) to our teeth, gums and tongue. Figure 1 illustrates
the action of attachment systems.
Figure 1. Attachment system that bind pathogens to their hosts. On the left binding proteins, usually pili, of the pathogens attach to the receptor molecules on the surface of the host cells. The pathogen may simply use this are an anchor by which it keeps from being flushed away by a flow of material like urine or mucous or this may be the first step in a process of attacking and destroying the target cell. On the right bacteria are shown embedded within a capsule which binds to the surface of a target cell. Again, the bacterial cells may use this as a way of not being washed away or it may be the preliminary step in a process that leads to the death of the target cell.
INFECTION
= The pathogen establishes itself in or on the host. It overcomes or avoids
the NDS and gains a "foothold" which allows it to grow and reproduce. No
symptoms are yet present and the host is unaware of the infection. However,
with newer molecular biology methods (PCR),
we may soon be able to detect the presence of a pathogen at this early
stage when it is more vulnerable. In many case the host mounts a successful
counter attack once the infection gets large enough for the host to detect
it. For example, this is the case with ZITS.
INCUBATION
PERIOD
= This is the period of time it takes for the pathogen to establish itself
to the point where the first disease symptoms appear. This varies widely,
for most bacteria it takes 2 to five days, but for some like T.B. or leprosy
it may be 20 to 30 years. For many viruses it is 3 days to two weeks, but
for rabies it may take several weeks or even months, whereas AIDS takes
up to 10 yrs to clinically develop.
INITIAL
SYMPTOMS
= These refer to the first symptoms that clearly demonstrate an illness.
Since symptoms vary widely between hosts this is a statistical matter.
One person many have a subclinical case, where they feel mildly ill, but
with no clear symptoms, to others that show unusual symptoms that can be
mistaken for other diseases.
ACUTE
= This refers to the classical clinical or text book symptoms, where the
disease is in full flower and the patient is usually seriously or clearly
ill.
The intensity of the illness varies with the disease, the strain of the
etiological agent and the condition of the patient. Some diseases like
chickenpox and the "common cold" are almost always relatively mild and
without complications. Others, like bubonic plague or measles are usually
severe and can be life threatening. Some, like rabies and AIDS are close
to being 100% fatal. In general, and with few exceptions, every disease
is survivable and every disease can prove fatal to some.
The symptoms and outcome of every disease is dependent on a mixture of
many factors. Some of the more obvious include the GENETICS of the host
and the IA, the PHYSICAL CONDITION of the host, the STRESS encountered
by the host during the disease and the AGE & SEX of the host. The complex
interplay of these factors makes it difficult to predict the outcome of
a disease of an individual. Disease data is ENTIRELY STATISTICAL, like
a horse race or the lottery.It
is very common for people to have a disease and not show any identifiable
symptoms and yet to become as immune as another person who almost dies
from the same disease. When this is the case, the individual is said to
have had a SUBCLINICAL case.RECOVERY
= Period where the symptoms decline and the patient recovers. Recovery
may take many paths.
In many cases the etiological agent is totally eliminated and the patient
returns to full health.
In other cases, the patient shows a full recovery but the IA is
still present. Under these conditions the patient becomes a CARRIER
and remains capable of shedding (spreading) the virulent form of the IA
for some period, perhaps for the remainder of their lives. This is the
case for diseases like Typhoid, Herpes and HPV.
Some carriers appear to be fully recover, but the disease may be progressing
slowly towards a fatal outcome, such as may occur with syphilis, HIV
and tuberculosis. Magic Johnson is probably such a case.
Some carriers, like those with herpes and hepatitis have occasional outbreaks
of the disease throughout their lives, but they are rarely fatal.
In many cases a disease becomes CHRONIC.
The victim makes a partial recovery, but they are still less well than-normal
and continuously demonstrate symptoms of ill health or have frequent relapses.
Many infestations (worms and other large parasites) take this path. Lyme
disease can become chronic.
In other cases, the patient recovers and eliminates the IA, but their immune
system has been damage and they subsequently fall victim to an autoimmune
disease like rheumatoid arthritis.Click here if you want a brief introduction to a large list of bacterial infections.
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