page 2
Introduction
Teacher's Notes
INFECTIOUS
DISEASES
Infectious disease is still a major influence on the
quality of life experienced by most of humanity. We
are all familiar to some extent with the effect they
have on us. Just over 50 years ago, however, one
of the main functions of our hospitals was isolation
of patients who were suffering from incurable
contagious diseases. Fortunately things have
improved for us and we only occasionally
experience such diseases. This is not the case in
other less developed countries, where the sight of
people either suffering from or presenting the
results of infections is common. The contrast we
experience in travelling from one society to the
other is often really dramatic. We would experience
the same thing if we travelled back in time.
Duration: 30 mins
One can question whether anything has really
changed. Right now there are over 300 million
sufferers of malaria world-wide and one million die
from the disease annually. Each year an estimated
3 million people die of AIDS, with a conservative
estimate of 40 million people infected. People
suffering from hepatitis, one of the most common
infections, number over 400 million. Further, over
the past 20 years we have witnessed the
emergence or the re-emergence of some 20 viral
infections, and quite a number of bacteria have
rapidly developed resistance to a range of
antibiotics. In fact, although the twentieth century
appeared to be the golden age for the treatment
of infectious human diseases, scientists are
warning that the battle is certainly not over.
The Video
Infectious Disease
Before anyone had any understanding of infectious
diseases, in their ignorance and fear, people
blamed them on punishment from God, bad air and
on the position of the stars and planets. This
slowly began to change and the change was a
reflection of the emergence of the Scientific
Revolution. Causes of events, including disease,
could be investigated and understood.
CAUSES & CONTROLS
Years: 11 +
page 3
From 1348 to 1350, the Black death killed one third
of the population of western Europe. In England
the population fell from 3.8 million in 1348 to 2.1
million in 1374, It was devastating, and it took the
next 200 years for the population to again reach
the numbers of 1350.
We begin with the invention of the microscope and
Anton van Leeuwenhoek’s first description of
microscopic organisms in 1676. Although Edward
Jenner carried out the first scientific small pox
vaccination in 1796, this strange new world of
organisms wasn’t linked with disease until 1835,
when Italian Agostino Bassi found that a
microscopic fungus caused disease in silkworms.
Later, in 1857, the French scientist Louis Pasteur
found that micro-organisms were responsible for
fermentation and spoilage in wine making. He
reasoned that killing the microbes would prevent
the spoilage and became convinced that similar
organisms could also cause disease. In completing
his experiments on spoilage he also concluded
that spontaneous generation could not occur and
also developed the process of sterilisation that
page 4
became known as pasteurisation.
Between 1864 and 1876 the role of bacteria in
natural cycles had been suggested and their
classification had begun.
In 1876 Robert Koch, working under Ferdinand
Cohn, publishes a paper on his work with anthrax,
describing a bacterium as its cause, and thus
validating the germ theory of disease. Soon it
became clear that many other illnesses were also
caused by infection and in 1894 Alexandre Yersin
isolated the bacterium Yersinia (Pasteurella) pestis
as the organism that is responsible for bubonic
plague. Research methods had been established
and the mechanism of infection by micro-organisms
was generally accepted.
Causes of infectious diseases
Today, we recognise many different agents of
infectious disease. They are known collectively as
“pathogens”, after the Greek word “pathos”,
meaning suffering.
Pathogens vary greatly in their characteristics, but
they are all able to survive in or on a living host,
multiply, and harm the host in some way. Other
relationships exist where the infecting organism
does not damage the host and is not pathogenic.
In fact there is a whole range of relationships, right
through to mutualism where neither organism can
survive without the other.
The relationship of a pathogen to its host is a
parasitic one, and in its simplest form is one of
consumption. One organism eats the other and the
eater generally benefits at the expense of the
eaten. Each parasite is well adapted to its very
specific environment. Free living organisms are not
normal able to survive inside another, as happens
to a fly that you may accidentally swallow.
In examining pathogens it is convenient to begin
with those we are able to see.
page 5
Macro-parasites
Macro-parasites are multicellular, complex
organisms. Those that live on the outside of the
host are known as external or ecto-parasites.
Many ectoparasites, including head lice, bite the
skin and suck the blood of their host.
Some, like the paralysis tick secrete a dangerous
toxin as they feed off the host. The relationship is
simple.
Other parasites live in quite different
environments at different periods of their life cycle
and are adapted to each. The first host may not
be inconvenienced, yet the parasite is a pathogen
in the second. The hydatid worm, Echinococcus, is
an example worth examining as it has very
special, highly adapted features which increase its
chances in reaching a new host. In its
intermediate host, usually a sheep, pig, or
kangaroo, it invades and damages the liver and
forms cysts where it multiplies into many
tapeworm heads. If the cyst is eaten by a dog on
the death of the host, each tapeworm head
attaches itself to the intestine of the dog and
grows into an adult tapeworm. If the new host is
a human, the cysts that form often grow very
large and have to be removed surgically. But as
humans are not usually eaten by dogs, this
becomes the end of this parasite’s life, which is
perhaps little consolation to the human sufferer.
Fungi
Fungi are a diverse group of organisms, many of
which are beneficial for the environment, and for
people. The fungi that cause disease are
microscopic. They are generally grouped into
simple single celled organisms called yeasts, or
more complex structures known as moulds. The
more common fungal infections cause inflammation
of bodily surfaces, such as ringworm caused by
moulds, and
thrush, a yeast infection, seen in the video in the
throat of a patient.
page 6
Protozoa
Protozoa are a large group of single celled
organisms. Like the other pathogens above,
protozoa are eukaryotic, which means their cells
have a well-defined nucleus. Their size range is
within that of the microscopic fungi.
Protozoa damage living tissue and produce toxins
or poisons. Plasmodium, the cause of malaria,
enters the bloodstream via the saliva of a
mosquito. From there, it invades first liver cells
and then red blood cells. It multiplies inside the
cell, then bursts forth, killing the cell in the
process. The relationship between plasmodium
and its hosts are quite complex and indicate an
historically long association. As indicated earlier,
malaria is one of the most common infections of
humans and worthy of more study.
Other protozoan such as Pfiesteria have a far
more complex and even extraordinary lives.
Pfiesteria which can take on at least 20 different
forms, can be responsible for the death of millions
of estuarine fish in one year.
Bacteria
Bacteria are another diverse group of single
celled organisms. Bacteria are prokaryotic,
meaning they lack a membrane bound nucleus
and are generally smaller than protozoa. They
occur everywhere that life exists and further. Most
of the1000 different bacteria are essential to the
continuation of life as they are involved in the
cycling of matter in the biosphere. We have more
bacteria on our skin surface that there are
humans on Earth and in one gram of soil there
are from between 10 5 to 10 9 organisms. There are
about 4000 per m 3 free floating or on dust
particles in the air. Only a few form pathogens.
If we examine a common bacteria Escherichia coli
(E coli) under a microscope at x1200, we see the
individual bacteria as small rod shaped
structures. They are present in our gut where
they feed on left over food, and are always
present in human faeces. Thus they are used as
page 7
an index in monitoring the quality of water,
disappearing over time in unpolluted water. Water
with an E. coli count of 1 per 100 ml is fit to drink.
Although they do not become pathogens and are
harmless, other bacteria which are more difficult to
detect may accompany them. They, like most other
bacteria reproduce very rapidly, from 1 to 100,000
in one day, when in a moist nutrient media at 37°k.
In the absence of moisture, some bacteria form
spores to protect them against desiccation. The
formation of spores also protects against changes
in temperature and lack of nutrients. Each
bacterium has a relatively specific favourable
environment, which is a distinguishing
characteristic; different combinations of
temperature, oxygen concentration, aerobic or
anaerobic environments, and acidity-alkalinity
strengths suit different bacteria. Each can be
cultivated in specific artificial growth media, most
are heterotrophic while others are photosynthetic
or chemosynthetic autotrophic. The colonies they
form when grown on solid cultures are generally
distinct which helps in their identification.
Heterotrophic bacteria feed on animal wastes and
dead organisms and some of these are pathogenic
and cause disease directly. They harm their host by
multiplying in the host’s tissues, altering them and
using the product as food. Some also produce
toxins which in most cases are the disease causing
agents. Toxins are poisonous secretions that can
do considerable damage to the host, even killing
them. With some, the products are fatal to the
bacteria itself. The bacteria producing a toxin that
causes tetanus, Clostridium tetani, produces
spores that survive in soil. They are killed by
excess oxygen. When these spores enter a wound
where other bacteria are using the available
-9
oxygen, they germinate and grow. 5 x 10
grams
of its toxin is enough to kill a guinea pig, so it is a
powerful substance. Most toxins are proteins that
act as complex metabolic poisons and are tissue
destroying. They can be either exotoxins that are
secreted , or endotoxins that are liberated on the
death of the bacteria.
The examples used in the video are Mycobacterium
page 8
tuberculosis which destroys lung tissues, and the
bacterium that causes cholera, which produces a
toxin that attacks the gut, causing diarrhoea and
severe dehydration. Both are classic examples and
worthy of further study by students.
Viruses
Viruses are generally much smaller than bacteria,
with the smallest viruses (around 10 nanometres)
being about one thousandth the size of the largest
bacteria (around 10 micrometres). Their size made
viruses invisible to humans until the invention of
the electron-microscope in the 1930’s. Their
discovery was first made by inference. By the end
of the 19th century, work by Pasteur, Koch and
others had shown that many infectious diseases
were associated with specific bacteria and it was
assumed that this was the case for all diseases.
However there remained a number of mysterious
diseases for which no organisms could be found.
In 1892 Dmitri Ivanowski published the first
evidence of the filterability of a pathogenic agent,
which was later shown to be the virus of tobacco
mosaic disease, but he was not sure that he had
identified a new region of study. In 1897 Martinus
Beijerinck recognized “soluble” living microbes, a
term he applied to the discovery of tobacco mosaic
virus.. He pressed the juice from tobacco leaves
infected with the disease, which gave the leaves a
mottled appearance, and found that a filtrate free
of bacteria retained the ability to cause this
disease in healthy plants even after repeated
dilutions. The infecting agent seemed to multiply in
the second plant and was therefore not a toxin. He
called the invisible cause “living fluid infect ant” and
from this came the name filterable virus.
In 1900 following the work of Walter Reed, where
he found that yellow fever is transmitted by
mosquitoes, it was demonstrated that Yellow Fever
is caused by a filterable virus transmitted by them.
The agent is similar to that reported in 1898 by
Loffler and Frosch for foot and mouth disease of
cattle. This was the first report of a viral agent
page 9
known to cause human disease.
Viruses are now known to be made up of a protein
matrix around a core of RNA or DNA. Some viruses
have an additional outer lipid layer. These are
known as enveloped viruses. Viruses are not
considered true living organisms, because they
have no other organelles or any metabolic
enzymes and can only metabolise and multiply
inside specific cells of a living host. In reproducing,
the viral nucleic acid directs the cytoplasm of the
host cell to construct new viruses which are
eventually liberated by the bursting or lysis of the
host cell. In another form, some can be crystallised
and still retain their disease causing properties
when returned to the host cell. Some may not
cause serious harm to the host at all. Some called
bacteriophages, cause disease in bacteria and are
generally plentiful where bacteria are plentiful.
The Herpes simplex viruses replicate in the cell
nucleus. Their protein coat is completed in the
cytoplasm, then the viruses are released from the
cell. This process kills the host cell, giving rise to
the well known symptoms of disease, cold sores.
Around 90% of our adult community carries this
infection.
Prions
Much smaller than the smallest known virus, prions
are the most recently identified type of pathogen.
Prions are abnormal forms of a usually harmless
protein found in the brain.
They are unusual, in that they have no genetic
material at all. They multiply by triggering other
protein molecules in the brain cells to take on their
abnormal shape. This destroys normal brain
tissue, causing devastating diseases such as
bovine spongiform encephalopathy, commonly
known as mad cow disease.
A list of diseases is attached as part of the
supplementary material (digital version only).
Inspection of the list of the 200 most common
infectious diseases shows the relative numbers of
members in each of the above groups. Eight are
page 10
page 11
macro-parasites, fourteen are fungi, five are
yeasts, 85 are bacteria, and 82 are viruses, while a
few diseases have several causes.
believed to be transmitted through respiratory
droplets during prolonged close contact with an
infected person.
Transmission of infectious diseases
The normal healthy body is inhabited by millions of
bacteria and fungi. Found mainly on the skin and in
the nose, mouth and gut, these organisms are
known as our “normal flora”, and usually they
cause us no harm. But they can turn into
pathogens if our body is weakened in some way.
Staphylococcus bacteria from the skin can easily
enter a wound, where they are able to damage the
exposed internal tissue.
The so-called faecal-oral route of transmission
occurs when pathogens originating from faecal
material are delivered to our mouths by our hands,
our utensils, or via contaminated food or water.
In 1854, London was gripped by a deadly epidemic
of cholera. Its source was a mystery until physician
John Snow noticed that people in the affected area
all obtained their water from the same well – a
well that was being contaminated with faeces from
a nearby cess-pool. Dr Snow ordered the removal
of the handle from the water pump, and the
epidemic came to an end.
Today, contamination of water is rare in developed
countries but it remains a serious problem in many
poorer nations.
So certain infectious diseases can originate from
our own bodies. Mostly, however, they occur when
pathogens are transmitted to our bodies from
other sources.
Direct transmission occurs when there is physical
contact between a healthy person and an infected
person or animal. This includes skin contact, as
with head lice and ringworm, mixing of saliva, as in
the virus that causes glandular fever, and sexual
contact. HIV and the hepatitis B & C viruses can
also spread by indirect contact, such as mixing of
blood.
Other forms of direct transmission, not shown in
the video, include in utero and peri-natal
transmission (direct transmission from a mother to
a child before or during birth) and transmission via
breast milk.
Indirect transmission occurs in many different
ways. One of the most common is via the air,
whereby pathogens breathed out in tiny drops of
fluid are inhaled by another person. A person
infected with the measles or influenza virus can
emit enough virus particles in a single cough to
infect several other people. The common cold
viruses also spread very easily, not only by air, but
also via items contaminated with nasal secretions.
Much less infectious is leprosy – a bacterial disease
Another major route of transmission is by animals
that act as carriers, or vectors of disease.
The black death, or bubonic plague, is transmitted
by fleas that feed on rats infected with plague
bacteria. These days, the mosquito is the most
important animal carrier of disease, particularly in
tropical and subtropical regions. It is estimated
that between 75 and 100 million people are
infected by mosquitoes with malaria every year
and 1 million of these people will die from the
disease.
As well as malaria, mosquitoes transmit serious
viral diseases, including dengue fever, yellow fever
and encephalitis which is a severe inflammation of
the brain.
Another form of indirect transmission, not shown in
the video, is entry of pathogens into wounds via
contaminated objects or soil (eg tetanus).
page 12
The response to infection
Natural resistance
Fortunately for us, simply being exposed to a
pathogen doesn’t always mean that we get sick.
To cause disease, the pathogen must first
overcome our system of bodily defences. Our first
line of defence consists of a series of barriers. Our
skin is a physical barrier, plus its acid pH and its
population of micro-organisms discourage the
growth of pathogens. The acid environment in our
stomach kills many ingested pathogens. And in
our respiratory tract, foreign particles are trapped
by mucous and flushed to the surface by tiny hairs
known as cilia.
But sometimes pathogens get past these “frontline” defences and enter the tissues of the body,
such as bacteria that pass down into the lungs or
bacteria that enter through cuts and scratches.
This stimulates our second line of defence –
chemicals and cells that seek out and attack the
invader.
Both the first and second lines of defence against
infection are possessed by everyone, and are
directed at any pathogen. They are sometimes
referred to as our “ natural” or “innate”
resistance and the response is called our innate
immune response.
Acting in this response are special white blood
cells, called macrophages, neutrophils and natural
killer (NK) cells. These are scavengers that engulf
and destroy the pathogen in a process known as
phagocytosis. Another component of this
response, termed the complement, consists of
some twenty special protein molecules which
assist in destroying the pathogens.
For clarity we include here some information about
the origin of these cells in our body.
Both red and white cells are produced from the
division of stem cells in the bone marrow. The
process is complex and involves the action of
page 14
page 13
specific growth factors and colony simulating factors
to produce a variety of cells:
white cells
Û
Û
lympoid stem cell
T-cells
lymphocytes
R-cells
stem
cells
neurophils
granulocytes
basophils
monocytes
macrophage cells
eosinoprils
Û
myeloid stem cell
platelets
red cells (erythrocytes)
Acquired resistance
Our next level, a more specific line of defence, is
known as the “adaptive immune response”, or our
“acquired resistance”.. The adaptive immune
response has three main features:
Memory, where recovery from infection by one
pathogen frequently protects us against
subsequent infections by the same organism, The
term “immunity” is used to summarise this
protection.
Specificity, where recovery from infection by one
pathogen does not usually provide us with
protection against another, unless the organisms
are closely related in some way.
Diversity, where responses can be made against
a multitude of different organisms and foreign
substances.
Although it can involve many of the body’s
defences, the adaptive immune response is the
result of antigen-antibody reactions. An antigen
(antibody generator) is a complex molecule
associated with a pathogen or foreign molecule,
and is either a protein or a polysaccharide that
stimulates the production of an opposing antibody.
Each antigen is unique. Bacteria, viruses and even
red blood cells may have the same unique antigen
molecule repeated many time over their surface.
Fortunately most pathogens have one or more
antigens.
This immune response or reaction only develops
when our body is exposed to the antigens. The
immune response is then aimed at that particular
pathogen through the production of antibodies
which are large protein molecules called
immunoglobins. There are nine recognised
antibodies, including the following five most
common:
Antitoxins which absorb toxins produced by a
pathogen and render them harmless,
Agglutinins which agglutinate or clump particles
such as bacteria together,
Precipitins which precipitate soluble antigens out of
solution,
Cytolysius which leads to the breakdown of foreign
cells,
and Opsonins which render particles available for
phagocytosis.
Each is produced in a specific and complex pathway
that involves a combination of several different
kinds of cells acting in our immune system.
The immune response relies on special white blood
cells called lymphocytes, which are closely
associated with the organs of our immune system
that are positioned throughout our body. The
organs include: tonsils and adenoids, the thymus,
lymph nodes, spleen, Peyer’s Patches, appendix,
lymphatic vessels, and the bone marrow. They are
known as lymph organs because they are
concerned with the growth, development and
deployment of lymphocytes, of which there are two
main kinds: B cells, produced in the bone marrow,
and T cells, also produced in the bone marrow but
which mature in the thymus. The organs of the
immune system are connected to one another and
to other body organs by a system of lymphatic
vessels that are similar to blood vessels. The
material in the lymphatic system is constantly
circulating through our body, rejoining the
bloodstream via the large veins to the right of the
heart to later move back into the intercell fluid.
The active cells of the immune system and any
foreign matter are conveyed through the system in
page 15
the clear lymph fluid which also surrounds the
body’s tissues. Along the lymphatic vessels are
the lymph nodes where the immune cells
congregate and where they can encounter
antigens.
Our body’s response to an infection (or injury)
begins with the damaged tissue’s rapid attraction
of white blood cells (lymphocytes) as they respond
to signalling molecules. These act as
chemoattractants and a large number these cells
enter the affected tissue. Other signalling
molecules escape into the blood stream. They
stimulate bone marrow to produce more
leucocytes or white cells. Some macrophages and
lymphocytes are also produced near the affected
tissue and in the lymphatic system.
There are two chief immune responses that occur
in us: the humoral (fluid) response where
antibody production occurs in the fluids
surrounding the infected area, and the cellmediated response. The distinction reflects the
roles of the two types of lymphocytes, B cells and
T cells.
A B cell is only able to make one specific antibody.
As they encounter their specific antigen, they
engulf it, process it and with the assistance of T
cells, develop into plasma cells. Plasma cells make
the antibodies which are released into the
surrounding fluid. These molecules attach to the
foreign antigen as bound antibodies to facilitate
their destruction particularly by macrophages,
killer cells and by the reactions involved in the
complement system. Thus B cells are particularly
effective against pathogenic cells, viruses and
toxins free in the blood and lymph.
T cells recognise two antigens on the pathogen or
the infected cell that their receptors bind to. This
activates them to divide to produce both
lymphocytes that are involved in the immediate
immune response and memory cells. Activated T
cells are more complex in their response than B
page 16
cells. One variety of T cell produced is the cytotoxic T
cell which destroys the antigen-carrying cell. Other
accessory T cells and macrophage cells are also
usually involved. The often complex process
deactivates the invading pathogen, or triggers other
cells and chemicals to destroy it. With viruses,
matured T cells either destroy the pathogens
themselves, or attract other forms of T cells and
scavengers to finish off the invader and the infected
cells.
Our immune response doesn’t always stop us from
getting sick, but without it we wouldn’t get better.
For some diseases, such as chicken pox, it also
prevents us from getting the same disease again
because certain B and T cells have special memory
functions and remain primed to attack more strongly
if the pathogen appears again. Such immunity often
remains with us for life.
Other pathogens are more evasive. The influenza
virus frequently changes its structure so that the
immune system no longer recognises it. This means
we can get a new flu every year. It also means that
the virus can suddenly appear in a more dangerous
form, as it did in 1918, when it killed over 20 million
people, many more than the battlefields of World
War 1.
Vaccination
Immunity is attained in a variety of ways. Hereditary
immunity is a genetically determined resistance.
Naturally acquired immunity appears as either
actively acquired from natural exposure to the
infectious pathogen or passively acquired from the
transfer of antibodies from mother to offspring.
Artificially acquired immunity can also be active or
passive, but is usually the result of introducing
(inoculating) a non-disease producing dose of a
disease organism or its toxin into a body. This
stimulates the body’s defence mechanisms against
the disease so that a later invasion of the pathogen
can be successfully resisted and the body recovers.
page 17
In 1796 the English physician Edward Jenner
noticed that milkmaids who suffered from a mild
disease called cowpox never contracted the much
more serious illness known as smallpox. Amid great
controversy, Jenner went on to protect other
people by deliberately exposing them to material
from a cowpox pustule. This was the first
equivalent of modern day vaccination, or use of a
relatively harmless substance to trigger an immune
response that prepares the body to fight a
particular pathogen.
These days, vaccines are made using dead
pathogens, a live but harmless strain of the
pathogen, or just a part of the pathogen that still
triggers an antibody response. Widespread use of
vaccines has rid the world of the devastation of
small pox, and has greatly reduced the incidence of
other diseases such as measles, mumps and polio.
Blood extracts, commonly called serum, that contain
antibodies are sometimes used to give temporary
effects such as in the use of Tetanus antitoxin
obtained from horse’s blood.
Some diseases are more challenging to control by
vaccination. The changing structure of the influenza
virus means that the virus must be carefully
monitored and the vaccine regularly updated.
For some pathogens, such as HIV and plasmodium,
their biology is so complex that so far a vaccine
eludes us.
Disease prevention
One of the fundamental principles of disease
prevention is maximising our resistance to infection.
This means looking after our bodies, and
vaccinating where appropriate. This is particularly
important for the people whose disease resistance
may be decreased, such as the elderly.
The other side of prevention is keeping away from
pathogens. This is becoming more difficult as
population growth forces people to live closer
together, and global movement of people allows
pathogens to spread over greater distances.
Pathogens that spread through the air are
page 18
especially difficult to control because we are often
sharing air space with other people. And
quarantining ourselves at home is often not very
practical.
Also challenging are those diseases where the
carrier seeks us out. Even using bed nets and
insecticide, mosquitoes are hard to avoid,
especially since mosquitoes are showing increasing
resistance to insecticides. Nevertheless, for many
pathogens, the risk of infection can be reduced
through basic hygiene. This includes: preventing
contamination of water supplies, pasteurisation of
milk and use of clean food processing techniques,
disinfection of wounds and sterilisation of medical
instruments,
and use of physical barriers, such as gloves and
condoms for prevention of many sexually
transmitted diseases.
Our personal hygiene also reduces the risk of
transmitting pathogens to other people. This is
important whether we’re sick or healthy, because
we may pass on a potentially harmful organism
without showing signs of illness.
In the developed world, we tend to take disease
control for granted. But we need only look at places
ravaged by natural disaster or conflict to see how
quickly diseases can emerge when sanitation and
health services break down.
Treatment
History records the use of special chemicals to
combat disease, some with measurable amounts of
success. Peruvians drank a bark infusion as a
protection from malaria. The derivative quinine,
formed the basis for much of the modern treatment
of this disease. Paul Ehrlich in 1911 discovered a
synthetic compound that has a destructive effect
on syphilis. In 1928 Gerhard Domagh discovered a
synthetic compound which enabled test animals to
survive doses of Streptococcus, the bacterium that
caused blood poisoning. When his daughter
became infected he used the drug to save her life.
page 19
The drug was sulphanilamide. In 1928 Alexander
Fleming discovered the effect penicillin has on gram
positive micro-organisms.
In 1939, a group of scientists led by Howard Florey
produced a usable form of penicillin. This natural
product of the mould “penicillium” was the first
substance to be widely used for treatment of
bacterial infections. Since this breakthrough,
intensive research has given us hundreds of drugs
that kill, or disable particular bacteria, protozoa and
fungi. These drugs have greatly reduced suffering
and the threat of death from infection.
But their widespread use has presented us with
another major problem. Many pathogens have
adapted to become resistant to these drugs. We
are seeing the evolution of pathogens for which we
have no effective antibiotics.
It’s crucial that we try to slow the emergence of
further resistance, for example, by using antibiotics
only when they are really needed. For viral
infections, there are relatively few specific
treatments available. Since viruses interact so
closely with host cells, it’s hard to develop a
chemical that affects the virus without also affecting
the host. Some anti-flu drugs avoid this problem by
inactivating the viral enzyme that frees virus
particles from infected cells which reduces the
spread of the virus and helps our immune system to
eliminate the pathogen.
With HIV infection, the immune system itself is the
centre of the attack and is weakened and cannot
destroy the virus. Currently available drugs need to
be taken constantly, just to keep the virus under
control.
Over the last 200 years, we have made remarkable
progress in understanding and controlling infectious
diseases. The arrival of gene technology has given
scientists even greater powers to develop new
drugs, vaccines and other disease control
strategies.
page 20
page 21
Nevertheless, since you started watching this
program, around 50 people will have died of
malaria, AIDS will have claimed nearly 200 lives,
and countless people will have contracted some
kind of infectious disease. We also live with such
possibilities as the return of a killer flu, or the use
of pathogens such as anthrax as instruments of
terrorism. Clearly, we still face many challenges in
gaining the upper hand against infection.
Credits
Writer/producer
Corinna Klupiec
Editor
Dominique Fusy
But infectious diseases are not the only form of
debilitating illness we in the western world
experience. Statistics over the past century show a
dramatic shift in the causes of death. And partly in
response to this, the level of research and the
amount of money spent on research on infectious
disease is small compared to that spent on the
other forms of disease. This is another story.
Footage provided courtesy of:
Natural History New Zealand Limited
PAHO Archives (copyright PAHO)
Getty Images/Archive Films
CSL Limited
CSIRO Australia
CARE Australia
Grant Davies/ Pumpkin Television
Linda Blagg
Moviebank Film Stock Research Australia
Yersinia pestis and HIV images copyright Russell
Kightley Media, rkm.com.au
Malaria animations courtesy of the Walter and Eliza
Hall Institute of Medical Research
Flu drug animation courtesy of CSIRO and Glaxo
Smith Kline Australia
Stills provided courtesy of:
Norbert Fischer
Martin Billeter & Roland Kirk/”Molmol” (prion image)
Fred Cohen, University of California, San Francisco
(prion images)
Bristol Biomedical Image Archive & Massey
University (hydatidosis)
F.A. Murphy School of Veterinary Medicine UC Davis
(virus micrographs)
Department of Veterinary Pathobiology Texas A&M
University (fungi)
Online editor/Graphics/Animations
Roddy Balle
Sound
Dominique Fusy, Philip McGuire
Consultant/Teachers Notes
John Willis
Executive Producer
John Davis
Copyright
CLASSROOM VIDEO (2002)
and Orders:
Classroom Video
1/1 Vuko Place
Warriewood, NSW, 2102
Ph: (02) 9913 8700 Fax: (02) 9913 8077
email: orders@classroomvideo.com.au
UK:
Phone: (01454) 324222 Fax: (01454) 325222
Canada:
Phone: (604) 5236677 Fax: (604) 5236688
USA:
Phone: 1800 665 4121 Fax: 1800 665 2909
New Zealand
Phone/Fax: (09) 478 4540
Students activities and questions
Key words
The Black death, pestilence, less developed countries, bacterium, Leeuwenhoek, microscope, microscopic organisms, disease, fungus, Agostino Bassi,
macro-parasites, fungi, protozoa, bacteria, viruses, prions, Robert Koch, infection, Louis Pasteur, fermentation, anthrax bacteria, prokaryotic, yeasts,
pathogens, multicellular, inflammation, tuberculosis, mycobacterium, cholera, electron-microscope, metabolise, living host, Herpes simplex, cytoplasm,
symptoms of disease, normal flora, staphylococcus, direct transmission, indirect contact, contaminated, faecal-oral route, contaminated food or water,
epidemic, John Snow, vectors of disease, malaria, bodily defence, physical barrier, acid pH, population of micro-organism, ingested pathogens, tissues
of the body, white blood cells, macrophage, neutrophil, phagocytosis, natural or innate resistance, immune response, ,acquired resistance, antigens,
lymphocytes, B cells, T cells, antibodies, influenza, Edward Jenner, cowpox, smallpox, vaccination, measles, mumps, polio, HIV, plasmodium, prevention,
resistance, quarantine, basic hygiene, pasteurisation, disinfection, sterilisation, transmitting pathogens, Howard Florey, penicillin, resistant, enzyme
Introductory activities
1. Make a list of common diseases that you are familiar with. Divide them into “infectious” and “other forms” of disease. Find out how common each
disease is in two contrasting countries.
2. Make a working definition of the terms: disease, infectious disease.
3. Conduct an interview with a person who has suffered from an infectious disease or has specific knowledge of such a disease.
4. Prepare a report regarding the disease topic from your interview and your research. Present the report to the class
5. Identify the factors that cause a particular disease as well as treatments and cures.
6. Conduct research using the Internet and print materials regarding a disease topic.
7. Gather materials and plan a game to demonstrate the transmission of an infectious disease. Issue each student with an envelope, one of which is
marked with a cross to signify the first infected individual. Give out envelopes containing either blue squares to simulate no infection, red squares to
simulate infection. Students simulate contact by shaking hands and transferring a paper square. On receiving a red square the student must continue
to hand on red squares. Check the distribution after say three handshakes. Continue with discussion. (Many variations can be invented to show the
exponential growth of the infection)
8. Discuss what parts of the environment contain microorganisms that can cause disease.
9. Grow moulds. Label 4 petri dishes A, B, C, and D. Place some moist, rich, garden soil in each one and then sprinkle some rolled oats on the top.
Some students may wish to add a few drops of sugar solution. Put the lid on each dish. The dishes should be kept under the following conditions. A in
a warm dark place B in a cold, dark place C in a warm, dark place D in a warm, light place.
Observe each dish carefully each day for a number of days. Record the observations, and check these with other groups in the class. Report the
effect of (a) temperature (b) amount of light on the growth of fungi.
10. Make yoghurt. Find a recipe for making yoghurt and then make a batch of yoghurt. Record the method and the results and outline the part played
by microbes in this process.
11. A compost heap. Examine a compost heap by vertically dissecting it. What processes can be observed?
page 22
Viewing the video
1 Identify the use of the key words in the video on the initial viewing. Begin building a glossary.
2. Did the discovery of the microscope help early scientists identify the causes of disease?
3. What causes disease? How do microbes (germs) cause disease in an animal’s body?
4. Are all microorganisms disease producing?
5. A new born baby will have contact with diseaes causing microbes. How is a newborn baby prepared to fight disease right when it is born?
6. Why is an animal’s body such a favourable place for the growth of microbes?
7. What is a parasite?
8. Why can all disease-causing microbes be regarded as parasites?
9. What is meant by the word ‘infection’?
10. What is a disinfectant? Give some examples. What is the effect of disinfecting and sterilizing?
11. What is meant by the word ‘septic’? What is an antiseptic? Give some examples.
12. What precautions are now taken in hospitals, and by doctors themselves, to prevent infection by disease-causing microbes?
13. Our body has several forms of defence to help prevent harmful microbes entering it.
Two of these are (a) the skin (b) tears.
Why are they called our first line of defence? Describe how each of these carry out this job.
14. What is the part played by white blood cells in preventing disease?
15. What are antibodies? How are they produced? How do they help us?
16. How can parasites enter our body? Is there any sure ways of stopping them?
17. Does “immunity” to a disease mean the disease-causing parasite does not harm us? What is meant by immunity to a disease’?
18. There are two types of immunity, depending on how they are acquired.
(a) active immunity (b) passive immunity.
What is the difference between them? How is each acquired?
19. What is a vaccine? What is meant by vaccination?
Give some examples of diseases which can be prevented by vaccination.
Can all infectious diseases be prevented by using vaccines?
20. Not long ago there were no antibiotics. How was life in our community different compared to the present day? What is an antibiotic? What are
some common antibiotics? How are they produced? What are they used for?
page 23
Discussion questions
1. It has been stated that:’Microbes do more harm than good.’ Do you agree with this statement? Give reasons for your answer.
2. In 1665, the Great Plague swept through London. In this epidemic 97 000 people died. In the worst week, 8297 people died. Do you think it likely
that such an event could ever happen again? Explain your answer.
3. Diseases caused by bacteria can usually be cured by antibiotics. Suppose a particular kind of bacterium proved difficult to kill. How could a doctor
try to get rid of the bacteria involved? What might happen if some bacteria were still able to survive this further treatment?
4. Ringworm is a disease caused by a fungus. How would you prevent a ringworm infection from spreading?
5. Most country towns and city councils employ health inspectors. What activities do you think these people should pay particular attention to?
6. What is meant by the word ‘quarantine’? Why is a quarantine station useful in fighting disease? Some overseas travellers coming to Australia
complain bitterly when their pets are immediately quarantined on entry. Are these people justified in complaining?
7. In our daily activities, we are often advised to follow certain rules of hygiene. What are these rules? Why is following them good practice?
8. In a number of your experiments on microbes, you have used controls. What is a control? Look back and find activities in which they have been
used. Why was the control necessary in each case?
9. Microbes often cause things to decay. In what ways is this
(a) useful to us (b) harmful to us?
Do microbes always cause things to decay? Explain your answer using the terms ‘parasite’ and ‘saprophyte’.
Further research
1. Viruses. Write a brief account of viruses under the following headings. (a) discovery (b) structure and size (c) properties (d) known plant viruses
(e) known human and animal viruses
2. Bacteria. Find out as much as you can about (a) the uses of bacteria in industry (b) disease-causing bacteria. Write an account of your findings.
3. Fungi and Moulds. Describe as many important functions of moulds as you can.
4. Write a brief account of the life and work of each of the following scientists. (a) Anton van Leeuwenhoek (b) Agostino Bassi (c) Louis Pasteur (d)
Joseph Lister (e) Edward Jenner (f) Alexander Fleming (g) Sir Macfarlane Burnet.
5. How are microbes involved in the following? (a) food poisoning (b) the production of penicillin (c) the disease tuberculosis (d) treatment of sewage
(e) outbreaks of pimples (f). our body-odour
6. Find out about the Commonwealth Serum Laboratory.
7. Choose a vaccine such as the Salk polio vaccine and write a report on how it was developed.
8. What does the word ‘quarantine’ mean? Why and when is quarantine necessary? What sort of quarantine regulations apply in Australia? Research
newspapers to find reports of the latest outbreak of disease that involved the use of ‘quarantine’.
page 24
page 2
1676 Antony Leeuwenhoek observes “little
animals”.
become putrefied. “antiseptic” meaning “against
putrefication”
1796 Edward Jenner carries out first scientific Small
pox vaccination.
1870 Thomas H. Huxley’s Biogenesis and
Abiogenesis address is the first clear statement
to offer powerful support for Pasteur’s claim to
have experimentally disproved spontaneous
generation.
1835 Italian Agostino Bassi found that a
microscopic fungus caused disease in silkworms.
Teacher's Notes
INFECTIOUS
DISEASES
Timeline of events
in the development
of microbiology
1677 to 1942.
Years: 11 +
Duration: 30 mins
page 3
1850 Ignaz Semmelweis advocates washing hands
to stop the spread of disease.
1872 Ferdinand J. Cohn publiishes a discussion
of the role of microorganisms in the cycling of
elements in nature.
1857 Louis Pasteur describes lactic acid
fermentation due to microbe action and using
microscopic studies shows that different
fermentation results are caused by different
microbes.
1875 Cohn publishes an early classification of
bacteria, using the genus name, Bacillus, for the
first time.
1861 Pasteur introduced the terms aerobic and
anaerobic in describing the growth of yeast at the
expense of sugar in the presence or absence of
oxygen. He observes that more alcohol is produced
in the absence of oxygen when sugar is fermented,
which is now termed the Pasteur effect. Disprovs
spontaneous generation through his classic
experiment using swan-necked flasks.
1864 Pasteur supports Germ Theory of disease,
through study of diseases in silkworms. Develops
method of heating wine for a few minutes at 50 to
60 °C prevents spoiling of wine. The process is
later known as Pasteurisation.
1865 After twenty years of freedom from the
disease, Great Britain experiences an epizootic
(epidemic) of rinderpest; which results in the death
of 500,000 cattle in two years. Government
inquiries highlights contemporary views on
epidemiology and the germ theory of disease.
1867 Joseph Lister practices antiseptic surgery
using spray of carbolic acid (at the time used to
treat sewage) and dressings soaked in carbolic
acid. The treatment is effective and fewer wounds
The German botanist Brefeld grows fungal
colonies from single spores on gelatin surfaces.
The method allowed the isolation of pure
cultures of microbes and was an improvement on
the earlier methods of Schroeter who used slices
of potato incubated in a moist environment.
1876 Robert Koch, working under Ferdinand
Cohn, publishes a paper on his work with
anthrax, describing a bacterium as the cause of
this disease, validating the germ theory of
disease.
1877 Jean Jacques Theophile Schloesing proves
that nitrification is a biological process in the soil
by using chloroform vapors to inhibit the
production of nitrate. Applied to the treatment of
sewerage.
Koch dries films of bacteria, stains them with
methylene blue, uses cover slips and prepares
permanent visual records using photographs.
John Tyndall publishes his method for fractional
sterilization and clarifies the role of heat
resistant factors (spores) in putrefaction.
Tyndall’s conclusion adds a final footnote to the
work of Pasteur and others in proving that
spontaneous generation is impossible.
page 4
1878 Thomas Burrill demonstrates for the first time
a bacterial disease of plants; Micrococcus
amylophorous causes pear blight.
Joseph Lister publishes his study of lactic
fermentation of milk, demonstrating the specific
cause of milk souring. His research is conducted
using the first method developed for isolating a
pure culture of a bacterium, which he names
Bacterium lactis.
Albert Neisser identifies Neisseria gonorrhoeoe, the
pathogen that causes gonorrhea. Perhaps the first
to attribute a chronic human disease to a microbe.
1880 Louis Pasteur develops a method of
attenuating a virulent pathogen, the agent of
chicken cholera, so it would immunize and not
cause disease.
This is the conceptual break-though for establishing
protection against disease by the inoculation of a
weakened strain of the causative agent. Pasteur
uses the word “attenuated” to mean weakened.
As Pasteur acknowledged, the concept came from
Jenner’s success at smallpox vaccination.
C. L. Alphonse Laveran finds malarial parasites in
erythrocytes of infected individuals and shows that
the parasite enters the organism and replicates.
1881 Robert Koch uses solidified culture media,
firstly aseptically cut slice of a potato, then gelatin
added to the culture media, poured onto flat glass
plates and allowed to gel. Isolates pure cultures of
bacteria from colonies growing on the surface of
the plate.
Paul Ehrlich refines the use of the dye methylene
blue in bacteriological staining and uses it to stain
the tubercule bacillus. He shows the dye binds to
the bacterium and resists decoloration with an acid
alcohol wash..
Koch systematically investigated the efficacy of
chemical disinfectants demonstrating that carbolic
acid used by Lister in aseptic surgery was merely
bacteriostatic and not bactericidal. He first
page 5
recognized that disinfection depended on the
chemical concentration and contact time. Anthrax
spores were dried on silk threads, exposed to
disinfectants, washed with sterile water and
cultured to evaluate a range of chemicals.
1882 Angelina Fannie and Walther Hesse in Koch’s
laboratory use agar, an extract of algae, as a
solidifying agent to prepare solid media for growing
microbes. Fannie suggests the use of agar-agar
after leanring of it from friends who cook. Agar
replaces gelatin because it remains solid at
temperatures up to 100 °k, it is clear, and it resists
digestion by bacterial enzymes.
Koch isolates the tubercule bacillus, Mycobacterium
tuberculosis. The search for the tubercule bacillus is
more difficult that anthrax. He finally isolates the
bacillus from the tissues of a workman and stains
them with methylene blue, yielding blue colored
rods with bends and curves. He injects the tissues
from people who had died into animals and then
grows the bacilli he isolates into pure cultures.
1883 Edward Theodore Klebs and Fredrich Loeffler
independently discover Corynebacterium diphtheriae,
which causes diphtheria. Loeffler later shows that
the bacterium secretes a soluble substance that
affects organs beyond sites where there is physical
evidence of the organism.
Ulysse Gayon and Gabriel Dupetit isolate in pure
culture two strains of denitrifying bacteria. They
show that individual organic compounds, such as
sugars and alcohols, can replace complex organics
and serve as reductants for nitrate, as well as
serving as carbon sources.
1884 Ilya Ilich Metchnikoff demonstrates that
certain body cells move to damaged areas of the
body where they consume bacteria and other
foreign particles. He calls the process phagocytosis.
He proposes a theory of cellular immunity.
Robert Koch puts forth a set of postulates, or
standards of proof involving the tubercle bacillus.
Three major facts: 1) the presence of the tubercule
page 6
bacillus (as proved by staining) in tubercular
lesions of various organs of humans and
animals, 2) the cultivation of the organisms in
pure culture on blood serum, and 3) the
production of tuberculosis at will by its
inoculation into guinea pigs
Hans Christian J. Gram develops a dye system
for identifying bacteria [the Gram stain].
Bacteria which retain the violet dye are
classified as gram-positive. The distinction in
staining is later correlated with other
biochemical and morphological differences.
Together with Pasteur, the French firm
Chamberland’s Autoclave, develops a chamber
to sterilize materials using superheated steam.
1885 As part of his rabies research, Louis
Pasteur oversees injections of the child Joseph
Meister with “aged” spinal cord allegedly
infected with rabies virus. Pasteur uses the
term “virus” meaning poison, but has no idea of
the nature of the causitive organism. Although
the treatment is successful, the experiment
itself is an ethical violation of research
standards. Pasteur knew he was giving the
child successively more dangerous portions.
Paul Ehrlich espouses the theory that certain
chemicals, such as dyes, affect bacterial cells
and reasoned that these chemicals could be
toxic against microbes, work that lays the
foundation for his development of arsenic as a
treatment for syphilis.
Christian Gram develops Gram stain
Theodor Escherich identifies a bacterium, that is
a natural inhabitant of the human gut, which he
names Bacterium coli. He shows that certain
strains are responsible for infant diarrhea and
gastroenteritis.
1886 Theobald Smith and D. E. Salmon inject
heated killed whole cell vaccine of hog cholera
into pigeons and demonstrate immunity to
subsequent administration of a live microbial
culture. The organism is a bacterium and
unrelated to hog cholera or swine plague disease,
which is caused by a virus.
John Brown Buist devises a method for staining
and fixing lymph matter from a cowpox vesicle.
Although he believes the tiny bodies he sees are
spores, he is nonetheless the first person to see
(and photograph) a virus.
SergeiW inogradsky studiesBeggiatoa and
determines that it can use inorganic H2S as an
energy source and CO2 as a carbon source. He
establishes the concept of autotrophy and its
relationship to natural cycles.
Julius Richard Petri working in Koch’s laboratory,
introduces a new type of culture dish for semi-solid
media. The dish has an overhanging lid that keeps
contaminants out.
1888 The Institut Pasteur is founded in France in
November.
Emile Roux and Alexandre Yersin show that
Cornyebacterium diphtheriae affects tissues and
organs by a toxin. They use a filtrate from cells that
can directly kill laboratory animals.
Martinus Beijerinck uses enrichment culture, minus
nitrogenous compounds, to obtain a pure culture of
the root nodule bacterium Rhizobium,
demonstrating that enrichment culture creates the
conditions for optimal growth of a desired
bacterium.
Hellriegel and Wilfarth describe symbiotic nitrogen
fixation by nodulated legumes.. The 1888
publication with Wilfarth is considered to be “the
classical paper.”
1889 A. Charrin and J. Roger discover that bacteria
can be agglutinated by serum.
Kitasato obtained the first pure culture of the strict
anaerobic pathogen, the tetanus bacillus
Clostridium tetani. Taking advantage of the fact that
the spores of the organism are extremely heatresistant, he heated a mixed culture of C. tetani
and other bacteria at 80 °k for one hour, then
cultivated them in a hydrogen atmosphere.
1890 Emil von Behring and Shibasaburo Kitasato
working together in Berlin in 1890 announce the
discovery of diphtheria antitoxin serum, the first
rational approach to therapy of infectious diseases.
They inject a sublethal dose of diphtheria filtrate
into animals and produce a serum that is
specifically capable of neutralizing the toxin. They
then inject the antitoxin serum into an uninfected
animal to prevent a subsequent infection. Behring,
trained as a surgeon, was a researcher for Koch.
Kitasato was Koch’s first student at the Institute of
Hygiene.
Sergei Winogradsky succeeds in isolating nitrifying
bacteria from soil. During the period 1890-1891,
Winogradsky performs the major definitive work on
the organisms responsible for the process of
nitrification in nature.
1891 Paul Ehrlich proposes that antibodies are
responsible for immunity. He shows that antibodies
form against the plant toxins ricin and abrin.
1892 Dmitri Ivanowski publishes the first evidence
of the filterability of a pathogenic agent, the virus
of tobacco mosaic disease, launching the field of
virology. He passes the agent through candle
filters that retain bacteria but isn’t sure that he has
identified a new region..
William Welch and George Nuttall identify
Clostridium perfringens, the organism responsible
for causing gangrene.
1893 Theobald Smith and F.L. Kilbourne establish
that ticks carry Babesia microti, which causes
babesiosis in animals and humans. This is the first
account of a zoonotic disease and also the
foundation of all later work on the animal host and
the arthropod vector.
1894 Richard Pfeiffer observes that a heat stable
toxic material bound to the membrane of Vibrio
Cholerae is released only after the cells are
disintegrated. He calls the material endotoxin, to
distinguish it from filterable material released by
bacteria.
Alexandre Yersin isolates Yersinia (Pasteurella)
pestis, the organism that is responsible for
bubonic plague. Shibasaburo Kitasato also
observes the bacterium in cases of plague.
Martinus Beijerinck isolates the first sulfatereducing bacterium, Spirillum desulfuricans
(Desulfovibrio desulfuricans).
1895 Sergei Winogradsky isolates the first freeliving nitrogen-fixing organism, Clostridum
pasteurianum.
David Bruce describes in great detail the Tsetse
fly disease (Nagana - means loss of spirits,
depression, in Zulu) in Zululand. He also
describes the parasite (drawings of tryp and of
tsetse) and demonstrates transmission by
infected blood or fly bite.
1896 Max Gruber and Herbert Durham extend
the 1889 observation of Charrin and Roger to
show the agglutination of bacteria by serum is
specific. This was recognized as a new disease
diagnostic tool.
Christan Eijkman, while searching for an
infectious agent, he discovers that beriberi is
the result of a vitamin deficiency.
1897 Paul Ehrlich proposes his “side-chain”
theory of immunity and develops standards for
toxin and antitoxin.
Edward Buchner helps launch the field of
enzymology by publishing the first evidence of a
cell-free fermentation process using extracts
isolated from yeast. This discovery refutes
Pasteur’s claim that fermentation requires the
repsence of live cells.
Waldemar Haffkine produces immunity against
the plague with killed organisms.
Almwroth Wright and David Sample develop an
effective vaccine with killed cells of Salmonella
typhi to prevent typhoid fever.
Friedrich Loeffler and Paul Frosch prove that
foot-and-mouth disease in livestock is caused
by organisms tiny enough to pass through
bacteriological filters and too small to be seen
through a light microscope.
Jules Bordet discovers that hemolytic sera acts on
foreign blood in a manner similar to the action of
antimicrobic sera on microbes by precipitating the
material from solution. He shows there are two
factors, a heat-labile substance found in normal
blood and a bacteriocidal material present in the
blood of immunized animals.
B. R. Schenck presents the first unequivocal case
of sporotrichosis and includes a description of the
organism that was first isolated from the patient.
This organism was later named Sporotrichum
schenckii.
W. Ophuls and H. C. Moffitt correctly identify the
etiologic agent of coccidioidomycosis, Coccidiodes
immitis, as a mold. This was formerly described as
a protozoan.
1899 Ronald Ross shows that the malarial
parasite undergoes a cycle of development in
mosquitoes and that the disease is transmitted by
the bite of female mosquitoes.
Martinus Beijerinck recognizes “soluble” living
microbes, a term he applies to the discovery of
tobacco mosaic virus. A filtrate free of bacteria
retains ability to cause disease in plants even after
repeated dilutions.In 1897 he had pressed the
juice from tobacco leaves infected with tobacco
mosaic disease, which gave the leaves a mottled
appearance.
The organizing meeting of the Society of American
Bacteriologists is held at Yale, December 28, 1899.
The Society is the first independent organization
devoted to the promotion and service of
bacteriology in the United States. It later becomes
the American Society for Microbiology.
1903 William Leishman observes Leishmania
donovani in the spleen of a soldier who dies from
Dum-Dum fever. Charles Donovan helps to identify
the protozoan causing the disease.
F. G. Novy cultivates trypanosomes isolated in the
blood of rats.
1900 Based on work of Walter Reed, it is
demonstrated that Yellow Fever is caused by a
filterable virus transmitted by mosquitoes. The
agent is similar to that reported in 1898 by Loffler
and Frosch for foot and mouth disease of cattle.
This is the first report of a viral agent known to
cause human disease. Based on the findings of the
Yellow Fever Commission the mosquito was
eradicated.
1901 Jules Bordet and Octave Gengou develop
the complement fixation test. They show that any
antigen-antibody reaction leads to the binding of
complement to the target antigen.
E. Wildiers publishes the first description of a
microbial growth factor, opening the field of vitamin
research. He finds that a water soluble extract of
yeast has a compund that is required for the
growth of yeast. The material is later found to be
a B vitamin.
1904 Martinus Beijerinck obtains the first pure
culture of sulfur-oxidizing bacterium, Thiobacillus
denitrificans. Under anaerobic conditions it uses
carbon dioxide as a source of carbon.
Cornelius Johan Koning suggests that fungi play
an important role in the decomposition of organic
matter and the formation of humus.
1905 Franz Schardinger isolates aerobic bacilli
which produce acetone, ethanol, and acetic acid.
These are important industrial chemicals.
Fritz R. Schaudinn and Erich Hoffman identify
Treponema pallidum, the cause of syphilis. The
bacterium is isolated from fluid leaking from a
syphylitic chancre and is spiral in appearance.
Shigetane Ishiwata discovers that the cause of a
disease outbreak in silkworms is a new species of
bacteria, later called Bacillus thuringiensis, or Bt.
Ishiwata called the organism “Sotto-Bacillen.”
(“Sotto” in Japanese signifies sudden collapse.)
Sir Roland Biffen shows that the ability of wheat to
resist infection with a fungus is genetically
inherited.
1906 August von Wasserman describes the
“Wasserman reaction” for the diagnosis of
syphilis in monkeys. The test uses complement
fixation and becomes the basis for the general
uses of complement tests as diagnostics.
N. L. Sohngen presents groundbreaking work on
methane-using and methane-producing bacteria.
This is the first proof that methane can serve as
an energy and carbon source.
A newly appointed pathologist in the Panama
Canal Zone, Samuel Darling, performs an autopsy
on a patient with a disease resembling
tuberculosis and an agent resembling Leishmania
sp. He recognizes significant differences between
the etiologic agent and Leishmania sp., and
names the organism Histoplasma capsulatum,
believing that it is a protozoan. It is now known
to be a fungus.
1907 Erwin Smith and C.O. Townsend discover
that the cause of crown galls is a bacterium
called Agrobacterium tumefaciens.
1909 Howard Ricketts shows that Rocky
Mountain spotted fever is caused by an organism
that is intermediate in size between an virus and
a bacterium. This organism, Rickettsia, is
transmitted by ticks. Ricketts dies from typhus,
another rickettsial disease, in 1910.
Sigurd Orla-Jensen proposes that physiological
characteristics of bacteria are of primary
importance in their classification.
Carlos Chagas discovers the trypanosome, which
he named Trypanosoma cruzi, and its mode of
transmission, via reduviid bugs, as the cause of
the human disease named for him.
Charles Henry Nicolle demonstrates that typhus
fever is transmitted from person to person by the
body louse. This information was used in both
world wars to reduce the incidence of typhus.
Raimond Sabouraud summarizes about twenty
years of his systematic and scientific studies of
dermatophytes and dermatophytoses in a classic
treatise, Les Teinges. He introduces a medium for
the growth of pathogenic fungi.
1911 Francis Peyton Rous discovers a virus that
can cause cancer in chickens by injecting a cell free
filtrate of tumors. This is the first experimental
proof of an infectious etiologic agent of cancer. In
1909 a farmer brought Rous a hen that had a
breast tumor. Rous performed an autopsy,
extracted tumor cells and injected them in other
hens, where sarcoma developed.
Paul Ehrlich announces the discovery of an
effective cure (Salvarsan) for syphilis, the first
specific chemotherapeutic agent for a bacterial
disease. Ehrlich was a researcher in Koch’s lab,
where he worked on immunology. In 1906 he
became head of the Research Institute for
Chemotherapy. He sought an arsenic derivative.
The 606th compound worked. He brought news of
the treatment to London, where Fleming became
one of the few physicians to administer it.
The first discovery of bacteriophage, by Frederick
Twort. Twort’s discovery was something of an
accident. He had spent several years growing
viruses and noticed that the bacteria infecting his
plates became transparent.
Chaim Weizmann, using the knowledge of
Pasteur’s discovery that yeast ferments sugar,
uses Clostridium acetobutylicum to produce
acetone and butyl alcohol. These were essential to
the British munitions program during World War I.
McCrady establishes a quantitative approach for
analyzing water samples for coliforms.
1917 Felix d’Herrelle independently describes
bacterial viruses and coins the name
“bacteriophage.”
J. N. Currie discovers how to produce citric acid in
large quantities from the mold Aspergillus niger-by
employing a growth limiting medium rich in iron.
1918 Alice Evans establishes that members of the
genus Brucella. are responsible for the diseases of
Malta Fever, cattle abortion, and swine abortion.
She reports that the bacteria are bacilli and not
micrococci.
In the fall of 1918, as World War I was ending, an
influenza pandemic of unprecedented virulence
swept the globe, leaving some 40 million dead in
its wake. A search for the responsible agent began
in earnest that year, leading to the first isolation of
an influenza virus by 1930.
1919 Theobald Smith and M. S. Taylor describe the
microbe, Vibrio fetus n. sp., responsible for fetal
membrane disease in cattle.
James Brown uses blood agar as a medium to
study the hemolytic reactions for the genus
Streptococcus and divides it into three types, alpha,
beta, and gamma.
1920 The SAB committee presents a report on the
Characterization and Classification of Bacterial
Types that becomes the basis for the classic work
of D. H. Bergey, later published in 1923.
1923 Michael Heidelberger and O. A. Avery show
that carbohydrates from the pneumococcus can
serve as virulence antigens and are serologically
specific. This overturns the current wisdom that
only proteins or glycoproteins are antigenic.
1924 George and Gladys Dick describe the “Dick
test”, a skin test for scarlet fever. They purify a
soluble extoxin from hemolytic Streptococccus
pyogenes and use it as a diagnostic. They use
Koch’s postulates to show that scarlet fever is
caused by streptocoocci, recover the bacteria from
all cases of the disease and infect others with
cultures of the bacterium.
Albert Calmette and Camille Guerin introduce a
living non-virulent strain of tuberculosis (BCG) to
immunize against the disease. This is the result of
work begun in 1906 on attenuating a strain of
bovine tuberculosis bacillus. More than 200
subcultures were grown before the resulting strain
was tested.
Albert Jan Kluyver publishes an article “Unity
and Diversity in the Metabolism of Microorganisms” that demonstrates common
metabolic events occur in different microbes.
The processes he refers to are oxidation,
fermentation and biosynthesis. Klyuver also
points out that life on earth without microbes
would not be possible.
1926 Thomas Rivers distinguishes between
bacteria and viruses, establishing virology as
a separate area of study. This paper was
published after he presented it at an SAB
meeting held in December of 1926.
Albert Jan Kluyver and Hendrick Jean Louis
Donker propose a universal model for
metabolic events in cells based on a transfer
of hydrogen atoms. The model applies to
aerobic and anaerobic organisms.
Everitt Murray isolates from rabbits a
bacterium that is responsible for listeriosis in
man. The organism can grow at low
temperatures and frequently is found in food.
He names it Bacterium monocytogenes. It is
later renamed Listeria monocytogenes.
1928 Frederick Griffith discovers
transformation in bacteria and establishes the
foundation of molecular genetics.
1929 Alexander Fleming publishes the first
paper describing penicillin and its effect on
gram positive microorganisms. This finding is
unique since it is a rare example of bacterial
lysis and not just microbial antagonism
brought on by the mold Penicillium. Fleming
kept his cultures 2-3 weeks before discarding
them. When he looked at one set he noticed
that the staphylococcus bacteria seemed to
be dissolving. The mold that contaminated the
culture was a rare organism called penicillium.
He left the culture on the lab bench and went
on vacation. While he was away the culture
was subjected to a cold spell followed by a
warm one – the only conditions under which
the discovery could be made. When penicillin is
finally produced in major quantities in the 1940s,
its power and availability effectively launch the
“Antibiotics Era,” a major revolution in public
health and medicine.
1930 Henning Karstrom begins to identify the
phenomena of enzyme adaptation and of
constitutive synthesis, in which synthesis of an
enzyme either is increased in response to the
presence of the substrate of the environment or
is independent of the growth medium. His work is
based on studies of carbohydrate metabolism in
Gram negative enteric bacteria.
1931 Rene Dubos working with Oswald Avery
discovers Bacillus brevis, an organism that breaks
down the capsular polysaccharide of Type III S.
pneumocci and protects mice against pneumonia.
C. B. van Niel shows that photosynthetic bacteria
use reduced compounds as electron donors
without producing oxygen. Sulfur bacteria use H2S
as a source of electrons for the fixation of carbon
dioxide. He posits that plants use water as a
source and release oxygen.
Margaret Pittman identifies variation, such as
encapsulated forms, and type specificity, such as
type b, of the Haemophilus influenzae as
determinants of pathogenicity.
William Joseph Elford discovers that viruses range
in size from large protein molecules to tiny
bacteria.
Alice Woodruff and Ernest Goodpasture devise a
technique of cultivating viruses in eggs.
1932 R. Stewart and K. Meyer describe the
isolation of Coccidiodes immitis from soil located
near where several patients were thought to
have become infected. This establishes that the
soil is a reservoir for the fungus.
1933 Rebecca Lancefield describes a method of
producing streptococcal antigens and sera for use
in precipitin tests and suggests that this approach
can be used epidemiologically to identify the
probable origin of a given strain.
duirng the fermentation of glycerol. This is the
first report of carbon dioxide fixation by a
heterotrophic bacterium.
1934 Ladislaus Laszlo Marton is the first to
examine biological specimans with the electron
microscope, which achieves magnifications of 200300, 000x. Later in 1937, he publishes the first
electron micrographs of bacteria.
Alice Evans accomplishes the first typing of a
strain of bacteria with bacteriophage.
William de Monbreun describes the dimorphic
nature of Histoplasma capsulatum after being
surprised by the growth of a mold from patient
tissues displaying yeasts.
Gerhard J. Domagk uses a chemically synthesized
antimetabolite, Prontosil, to kill Streptococcus in
mice. It is later shown that Prontosil is hydrolyzed
in vivo to an active compound, sulfanilamide. One
of the first patients to be treated with Protonsil
was Domagk’s daughter who had a streptococcal
infection that was unresponsive to other
treatments. When she was near death, she was
injected with large quantities of Protonsil and she
made a dramatic recovery.
Wendell Stanley crystallizes tobacco mosaic virus
and shows it remains infectious. However, he does
not recognize that the infectious material is nucleic
acid and not protein.
William A. Hinton, chief of the Wasserman
laboratory at Harvard, publishes the first major
text on syphilis, Syphilis and its Treatment, which
includes reference to the Davies-Hinton test to
detect syphilis in spinal fluids.
1938 Field tests of Max Theiler’s vaccine
against yellow fever prove successful. The
vaccine is based on a mouse passaged virus.
The Rockefeller Foundation manufactures
more than 28 million doses by 1947.
1936 J. D. Bernal, F. C. Bauden, N. W, Pirie, and I.
Pankuchen demonstrate that isolated
preparations of tobacco mosaic virus contain
phosphorus as a component of a phosphoribonucleic acid. They also isolate ribonucleic
acids.this challenges the claim by Stanley that the
TMV is composed only of protein
Harland Wood and Chester Werkman show that
CO 2 is consumed by Propionibacterium arabinosum
1939 E. L. Ellis and Max Delbruck establish the
concept of the one-step viral growth cycle for
a bacteriophage active against E. coli.
1940 Pathologist Howard Florey and
biochemist Ernest Chain produce an extract of
penicillin, the first powerful antibiotic. They
isolate the antibiotic from Fleming’s mold
cultures and demonstrate that it can cure
infections in animals. Florey and Chain began
their research by focusing on the discovery by
Fleming of lysozyme. In the course of
reviewing Fleming’s papers, Chain read the
description of penicillin.
Ernest Chain and E.P. Abraham describe a
sustance from E. coli that can inactivate
penicillin. It was the first bacterial product that
was recognized to mediate resistance to an
antibacterial agent.
Helmuth Ruska uses an electron microscope to
obtain the first pictures of a virus.
Charles E. Smith and his colleagues
demonstrate the usefulness of a tuberculinlike preparation of Coccidiodes immitis in
detecting prior exposure to the fungus. This
preparation allowed for the delineation of the
endemic area for the fungus.
Donald O. Woods describes the relation of
para-aminobenzoic acid to the mechanism of
action of sulfanilamide, which was used by
Domagk to treat Streptococcal infections in
mice.
Selman Waksman and H. Boyd Woodruff
discover actinomycin, the first antibiotic
obtained pure from an actinomycete, leading to
the discovery of many other antibiotics from that
group of microorganisms. After Renee Dubos
discovered two antibacterial substances in soil,
Waksman decided to focus on the medicinal uses
of antibacterial soil microbes.
1941 George Beadle and Edward Tatum jointly
publish a paper on their experiments using the
fungus Neurospora crassa to establish that
particular genes are expressed through the action
of correspondingly specific enzymes.
Charles Fletcher first demonstrates that penicillin
is non-toxic to human volunteers, by injecting a
police officer suffering with a lethal infection.
McFarlane Burnet proposes that descendents of
antigen reacting cells produce antibodies specific
to the antigen.
George Hirst demonstrates that influenza virus
agglutinates red blood cells. Since the cell
attachment proteins of most viruses also
agglutinate red blood cells, this property provides
a rapid, accurate and quantitative method of
counting virus particles.
1942 Selman Waksman suggests the word
“antibiotic” (coined in 1889 by P. Vuillemin) after
Dr. J. E. Flynn, the editor of Biological Abstracts
asked him to suggest a term for chemical
substances, including compounds and
preparations that are produced by microbes and
have antimicrobial properties.
Although there is no journal citation, Waksman
recalled the incident in his book The Antibiotic Era.
Because the word was accepted quickly and the
meaning became confused, Waksman published a
comprehensive definition in 1947: “an antibiotic is
a chemical substance produced by microbes that
inhibits the growth of and even destroys other
microbes (and is active in dilute solutions)” was
added later.
The term “antibiotic” now also includes synthetic
and semi-synthetic substances.
List of infectious diseases and their disease
agents
Acanthamoeba - (Parasitic)
Cryptosporidiosis - Cryptosporidium parvum or
Cryptosporidium coccidi (Protozoan parasite)
Giardiasis - Giardia lamblia (Protozoan parasite)
Leishmaniasis - Leishmania (Parasitic)
Scabies - Sarcoptes scabiei (Mites)
Toxoplasmosis - Toxoplasma gondii (Sporozoan)
Trichinosis - Trichinella spiralis (Nematode)
Trichomoniasis - Trichomonas vaginalis (Protozoan)
Aspergilloma / Aspergillosis - Aspergillus (Mould)
Athlete’s Foot - Dermatophytes (Mould)
Darling’s Disease - Histoplasma capsulatum (Mould)
Dermatomycoses - Dermatophytes (Mould)
Gardener’s Disease - Sporothrix schenckii (Mould)
Gilchrist’s Disease - Blastomyces dermatitidis
(yeast and mould forms)
Histoplasmosis - Histoplasma capsulatum (Mould)
Jock Itch - Dermatophytes (Mould)
Phaeohyphomycosis - Dematiaceous Fungi (Mould)
Phycomycosis - Mucor species (Mould)
Ring Worm - Dermatophytes (Mould)
Sporotrichosis - Sporothrix schenckii (Mould)
Tinea - Dermatophytes (Mould)
Zygomycosis - Mucor species (Mould)
Candidiasis - Candida (Yeast)
Moniliasis - Candida species (Yeast)
Mycotic Vulvovaginitis - Candida species (Yeast)
Thrush - Candida species (Yeast)
Vulvovaginitis, Mycotic - Candida species (Yeast)
Actinobacillosis - Actinobacillus spp. (Bacterial)
Actinomycosis – Actinomyces spp.
Anisakidosis - Anisakis simplex (Bacterial)
Anthrax - Bacillus anthracis (Bacterial)
Arthritis, Septic - Staphylococcus aureus, or
Neisseria gonorrhoeae (Bacterial)
Blastomycosis - Blastomyces dermatitidis (Bacterial)
“Black death” (plague) - Yersinia pestis (Bacterial)
Botulism - Clostridium botulinum (Bacterial)
Brazilian purpuric fever - Haemophilus
aegyptius (Bacterial)
Bronchitis - (Bacterial)
Brucellosis - Brucella (Bacterial)
Bubonic Plague - Yersinia pestis (Bacterial)
Cellulitis – Various bacteria (Bacterial)
Chancroid - Haemophilus ducreyi (Bacterial)
Chlamydia - Chlamydiae trachomatis (Bacterial)
Cholera - Vibrio cholerae (Bacterial)
Desert Rheumatism - Coccidioides immites
(Bacterial)
Diphtheria - Corynebacterium diphtheriae
(Bacterial)
Dysentery - Shigella (Bacterial)
Ear Infection - see Otitis Media
Ehrlichiosis - Ehrlichia (Bacterial)
Endocarditis - various bacterial pathogens
(Bacterial)
Epiglottitis - Haemophilus influenzae or
Streptococcus pyogenes (Bacterial)
“Flesh Eating Bacteria” - Necrotizing fasciitis
(NF) - Group A Strep (Bacterial)
Food Poisoning - various bacterial pathogens,
and some toxins
Gas gangrene - Clostridium perfringens
(Bacterial)
Gonorrhea - Neisseria gonorrhoeae (Bacterial)
Granuloma Inguinale - Calymmatobacterium
granulomatis (Bacterial)
Impetigo - Streptococcus pyogenes or
Staphylococcus aureus (Bacterial)
Legionnaire’s Disease (Legionnaire’s
pneumonia) - Legionella pneumophila
(Bacterial)
Leprosy (Hansen’s disease) - Mycobacterium
leprae (Bacterial)
Leptospirosis - Leptospira interrogans
(Spirochetes, Bacterial)
Listeriosis - Listeria moncytogenes (Bacterial)
Lyme disease - Borrelia burgdoferi (Spirochetes,
Bacterial)
Malta fever - Brucella sp. (Bacterial)
Melioidosis - Pseudomonas pseudomallei
(Bacterial)
Meningitis, bacterial - Neisseria meningitidis
(Bacterial), Haemophilus influenzae (Bacterial),
Listeria monocytogenes (Bacterial), Streptoccoccus
pneumoniae, Group B streptococcus (Bacterial)
Middle Ear Infection - see Otitis Media
Necrotizing fasciitis (NF) - Group A Strep (Bacterial)
Nocardiosis - Nocardia (Bacterial)
Otitis externa - Pseudomonas aeruginosa
(Bacterial)
Otitis media - Streptococcus pneunomiae, or
Haemophilus influenzae, or Moraxella catarrhalis, or
Staphylococcus aureus (Bacterial)
PCP - Pneumocystis carinii (Bacterial)
Pelvic Inflamatory Disease - various Bacterial
pathogens (Bacterial)
Peritonitis - Escherichia coli, or Bacteriodes
(Bacterial)
Pertussis - Bordetella pertussis (Bacterial)
Pharyngitis: Streptococcus pyogenes (Bacterial)
“Pink eye” conjunctivitis - see Conjunctivitis
Plague - Yersinia pestis (Bacterial)
Pneumocystis carinii Pneumonia - Pneumocystis
carinii (Bacterial)
Pneumonic Plague - Yersinia Pestis (Bacterial)
Pontiac fever - Legionella pneumophila (Bacterial)
Posadas-Werincke’s Disease - Coccidioides immites
(Bacterial)
Pseudomembranous colitis - Clostridium dificile
(Bacterial)
Psittacosis - Chlamydia psittaci (Bacterial)
Q fever - Coxiella burnetti (Rickettsial)
Red Eye - see Conjunctivitis
Reticuloendotheliosis - Histoplasma capsulatum
(Bacterial)
Rheumatic Fever - Streptococcus pyogenes
(Bacterial)
Rocky Mountain Spotted Fever (RMSF) - Rickettsia
rickettsii (Rickettsial)
Salmonellosis - Salmonella species (Bacterial)
San Joaquin Fever - Coccidioides immitis (Bacterial)
Scarlet fever - Streptococcus pyogenes (Bacterial)
Schistosomiasis - Schistosomiasis mansoni
(Bacterial)
Sepsis - various Bacterial Pathogens (Bacterial)
Septic Arthritis - Staphylococcus aureus, or
Neisseria gonorrhoeae (Bacterial)
Shigellosis - Shigella species (Bacterial)
Shipping fever - Pasteurella multocida (Bacterial)
Strep Throat - see Pharyngitis
Strongyloidiasis - Strongyloides stercoralis
(Bacterial)
Swimmer’s Ear - See Otitis Externa
Syphilis - Treponema pallidum (Spirochete bacteria)
Tetanus - Clostridium tetani (Bacterial)
Thrombophlebitis - Staphylococcus species
(Bacterial)
Toxic Shock Syndrome - Staphylococcus aureus or
Streptococcus pyogenes (Bacterial)
Trachoma - Chlamydia trachomatis (Bacterial)
Tuberculosis - Mycobacterium tuberculosis
(Bacterial)
Tularemia - Francisella tularensis (Bacterial)
Typhoid fever - Salmonella typhi (Bacterial)
Undulating fever - Brucella species (Bacterial)
Urinary Tract Infection (UTI) - various Bacterial
Pathogens (Bacterial)
Urethritis - Chlamydia trachomatis (Bacterial) , or
Trichomonas vaginalis (Protozoan), or Herpes
Simples Virus (Herpesvirus), Ureaplasma
urealyticum (Mycoplasma)
Vaginosis - Gardnerella vaginalis (Bacterial), or
Bacteroides species (Bacterial), or Streptococcus
species (Bacterial)
Valley Fever - Coccidioides immitis (Bacterial)
Whooping Cough - Bordetella pertussis (Bacterial)
Wool sorters’ disease - Bacillus anthracis
(Bacterial)
Acute hemorrhagic conjunctivitis - Coxsackie A-24
virus (Picornavirus: Enterovirus), Enterovirus 70
(Picornavirus: Enterovirus)
Acute hemorrhagic cystitis - Adenovirus 11 and 21
(Adenovirus)
AIDS / Acquired Immune Deficiency Syndrome human immunodeficiency virus (Retrovirus)
Bornholm disease (pleurodynia) - Coxsackie B
(Picornavirus: Enterovirus)
Bronchiolitis - Respiratory syncytial virus
(Paramyxovirus), Parainfluenza virus
(Paramyxovirus)
California encephalitis - California encephalitis
virus (Bunyavirus)
Cat Scratch Fever - Bartonella henselae
(Bacterial)
Cervical cancer - human papilloma virus
(Papovavirus)
Chicken pox - varicella zoster virus
(Herpesvirus)
Colorado tick fever - Colorado tick fever virus
(Reovirus)
Conjunctivitis - Haemophilus aegyptius or
Chlamydiae trachomatis (Bacterial) or
Adenovirus (Adenovirus) or Herpes Simplex
Virus (Herpesvirus)
Cowpox - vaccinia virus (Poxvirus)
Croup, infectious - parainfluenza viruses 1-3
(Paramyxovirus)
Dengue - dengue virus (Flavivirus)
“Devil’s grip”(pleurodynia) - Coxsackie B
(Picornavirus: Enterovirus)
Eastern equine encephalitis - EEE virus
(Togavirus)
Ebola hemorrhagic fever - Ebola virus
(Filovirus)
Erythema infectiosum - Parvovirus B19
(Parvovirus)
“Fifth” disease (erythema infectiosum) Parvovirus B19 (Parvovirus)
Foot and Mouth Disease (Hand-foot-mouth
disease) - Coxsackie A-16 virus (Picornavirus:
Enterovirus)
Gastroenteritis - Norwalk virus (Calicivirus),
rotavirus (Reovirus), or various bacterial
species
Genital HSV - Herpes Simples Virus
(Herpesvirus)
Gingivostomatitis - HSV-1 (Herpesvirus)
Hand-foot-mouth disease - Coxsackie A-16
virus (Picornavirus: Enterovirus)
Hantavirus hemorrhagic fever / HantaanKorean hemorrhagic fever - Hantavirus
(Bunyavirus)
Hepatitis:
Hepatitis A - hepatitis A virus (Picornavirus:
Enterovirus)
Hepatitis B - hepatitis B virus (Hepadnavirus)
Hepatitis C - hepatitis C virus (Flavivirus)
Hepatitis D - hepatitis D virus (Deltavirus)
Hepatitis E - hepatitis E virus (Calicivirus)
Herpangina - Coxsackie A (Picornavirus:
Enterovirus), Enterovirus 7 (Picornavirus:
Enterovirus)
Herpes, genital - HSV-2 (Herpesvirus)
Herpes labialis - HSV-1 (Herpesvirus)
Herpes, neonatal - HSV-2 (Herpesvirus)
HIV - human immunodeficiency virus (Retrovirus)
Infectious myocarditis - Coxsackie B1-B5
(Picornavirus: Enterovirus)
Infectious pericarditis - Coxsackie B1-B5
(Picornavirus: Enterovirus)
Influenza - Influenza viruses A, B, and C
(Orthomyxovirus)
Japanese encephalitis virus - JEE virus (Flavivirus)
Junin Argentinian hemorrhagic fever - Juninvirus
(Arenavirus)
Keratoconjunctivitis - Adenovirus (Adenovirus),
HSV-1 (Herpesvirus)
Koch-Weeks - see Conjunctivitis
LaCrosse encephalitis - LaCross virus
(Bunyavirus)
Lassa hemorrhagic fever - Lassavirus (Arenavirus)
Machupo Bolivian hemorrhagic fever Machupovirus (Arenavirus)
Marburg hemorrhagic fever - Marburg virus
(Filovirus)
Measles - rubeola virus (Paramyxovirus)
Meningitis, aseptic - Coxsackie A and B
(Picornavirus: Enterovirus), Echovirus
(Picornavirus: Enterovirus), lymphocytic
choriomeningitis virus (Arenavirus), HSV-2
(Herpesvirus), Mycobacterium tuberculosis
(Bacterial)
Microsporidiosis - Microsporidia - (single cell
Parasites)
Molluscum contagiosum - Molluscum (Poxvirus)
Mononucleosis - Epstein-Barr virus (Herpesvirus)
Mononucleosis-like syndrome - CMV (Herpesvirus)
Mumps - mumps virus (Paramyxovirus)
Orf - Orfvirus (Poxvirus)
Pharyngoconjunctival fever - Adenovirus 1-3 and 5
(Adenovirus)
Respiratory Synytial Virus (Paramyxovirus:
Pneumovirus)
Influenza Virus (Orthomyxovirus)
Parainfluenza Virus (Paramyxovirus)
Adenovirus (Adenovirus)
Epstein-Barr Virus (Herpesvirus)
Pleurodynia - Coxsackie B (Picornavirus:
Enterovirus)
Pneumonia, viral - respiratory syncytial virus
(Paramyxovirus), CMV (Herpesvirus)
Polio, Poliomyelitis - Poliovirus (Picornavirus:
Enterovirus)
Progressive multifocal leukencephalopathy - JC
virus (Papovavirus)
Rabies - rabies virus (Rhabdovirus)
Roseola - HHV-6 (Herpesvirus)
Rubella - rubivirus (Togavirus)
Rubeola - see Measles
Septic Thrombophlebitis - see Thrombophlebitis
Shingles (zoster) - varicella zoster virus
(Herpesvirus)
Sinusitis - various Bacterial Pathogens (Bacterial)
Smallpox - variola virus (Poxvirus)
“Slapped cheek” disease (erythema infectiosum) Parvovirus B19 (Parvovirus)
St. Louis encephalitis - SLE virus (Flavivirus)
Temporal lobe encephalitis - HSV-1 (Herpesvirus)
Varicella - varicella zoster virus (Herpesvirus)
Western equine encephalitis - WEE virus
(Togavirus)
Yellow fever - Yellow fever virus (Flavivirus)
Zoster - varicella zoster virus (Herpesvirus)
Borna Diease - Borna Diease Virus (Unassigned
Virus)