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Grade: 12

                        

the microscopic proteinaceous infection agent are calleda protozoab fungic prionsd bacteria

3 years ago

Answers : (2)

Vasanth SR
askIITians Faculty
1310 Points
							Prions536-1464_pathogens_med.jpeg
						
3 years ago
SR Roy
128 Points
							
Microbes and Infectious Disease
Introduction
Terminology
Scale of Sizes
Agents of Infectious Diseases
Prions
Viruses
Bacteria
Rickettsiae &
Chlamydiae
Fungi
Other Parasites
Protozoa
Helminths
Sexually Transmitted Diseases
Treating Disease
Arthropods
Introduction
Infectious diseases can be the
result
of the colonization of the body by various microbe
s. There are many similar
disease states that can arise from different causes
, i.e., pneumonia can be caused by viruses, many ty
pes of bacteria,
protozoa, and even fungi. In this chapter, we will
look at the various types of microbes and some of t
he diseases they
cause.
Terminology
A
host
is any organism capable of supporting the nutritio
nal and physical requirements of another. A
microbe
is a microscopic organism. The presence and multipl
ication of an organism on or within a host is calle
d
colonization
or
infection
.
We refer to the colonization of one organism by ano
ther as
symbiosis
. If the symbiotic relationship benefits
both organisms, it is called
mutualism
. On a macroscopic level sharks and remora fish hav
e a mutual symbiotic
relationship; the fish clean the teeth of the shark
s, which maintain the sharks’ oral health while pro
viding food for
the fish. Clover, peas, and soybeans root systems a
re populated by a class of bacteria. The bacteria f
ix the inert gas
nitrogen in the soil and convert it into a form tha
t can be utilized by the plants. This effectively f
ertilizes the plants
and increases their rates of growth. Clearly, both
the host and bacteria benefit from this relation.
Commensalism
is a symbiotic relation in which one organism bene
fits and the other is not harmed. Our bodies
are populated by an extremely large number of bacte
ria that can, but don’t always, benefit us. The bac
teria always
benefit. The
E. coli
in our colon are examples.
Parasitism
occurs when the infecting organism benefits and th
e host is harmed. If the host sustains injury or
pathological changes in response to the parasite, t
he process is an
infectious disease
. Anything causing disease is
said to be a
pathogen
.
These three characterizations of symbiosis are not
as cut-and-dried and they might seem. As an example
, many
of the bacteria living in or on our bodies cause us
no harm when they live in certain regions of the b
ody. But, when
they grow in other regions, they cause disease.
Agents of Infectious Diseases
There are many agents of infectious diseases, rangi
ng in size from microscopically small to macroscopi
cally
large.
Scale of Sizes
Since most microbes are really, really small, we n
eed to get a feeling for the units in which they ar
e measured,
nanometers
. One nanometer is one-billionth of a meter. Suppos
e we
shrunk
a meter by a factor of one billion. The
result would be one-billionth of a meter or one-mil
lionth of a millimeter. Knowing that a dime is abou
t a millimeter
thick, this means you’d need to slice the dime para
llel to its faces into a million equal slices, each
of which would be
one nanometer thick. If you get tired slicing and s
top at 100 slices, that thickness would be the size
of a eukaryotic
cell.
Going in the other direction, suppose your computer
monitor is about 40 cm. on a side and we
increase
each
side by a factor of one billion. Then it would be 4
00 million meters = 400,000 kilometers on a side. T
hat would be
large enough for the moon to orbit the earth within
the plane of the front face, with a little room to
spare!
Viruses can range in size from 28–200 nm and they h
ave from 5K–500K bases. Bacteria run from 1000–2000
nm in size and contain 1000K–9000K base pairs.
If a small virion (30 nm) were one inch long, a lar
ge bacterium would be over 5 feet long, and a five-
foot tall
person would stand about 800 miles high—well beyond
the extent of the earth’s atmosphere.
The following picture (from the University of Queen
sland website) shows the relative scale of sizes of
a virus,
tobacco smoke, a bacterium, a fungal spore, a plant
spore, and a raindrop. The measurements in the pic
ture are given
in microns, which are millionths of a meter, or one
thousand nanometers.
 
©PGB
2
Comparison of the relative sizes of various microbe
s with tobacco smoke, spores, and
a rain droplet.
Prions
During the 1950s, anthropologists studying the Fore
people in Papua, New Guinea recorded the presence
of a
strange fatal disease, called
kuru
, which attacked the brain. Victims lost coordinati
on, fine motor control, and the
ability to swallow. They developed tremors and show
ed signs of dementia
1
. Of a population of 35,000, fully 3700
cases of this disease were recorded among this trib
e. It seemed to center almost exclusively on adult
females,
although it was present at lower levels equally in
boys and girls. Some villages suffered so many deat
hs, they had
triple the number of living males as females. Recor
ds indicated the disease took between four and fort
y years to
manifest itself. After extensive epidemiological st
udy, it became apparent that there was a very stron
g association
between kuru and the practice of ritual cannibalism
, whereby the relatives “honored” the recently dece
ased member
of the family by consuming her/his body in its enti
rety. Almost exclusively adult women practiced the
details of the
ritual—men rarely participated. Women and children
would bake the internal organs, brain, and bone, gr
ind the
results into a powder, and then they would mix the
powder with vegetables and eat the results. Men, on
the other
hand, would consume the muscle tissue, i.e., the me
at. In 1957, the study group brought pressure to be
ar on the tribal
elders to cease the practice and no cases have been
seen in those born
after
1960, although the last death due to kuru
occurred in the 1990s. A recent study of all health
records between 1996 and 2004 identified 11 people
living in the
affected area who had kuru.
Researchers referred to this form of disease as a
transmissible spongiform encephalopathy
(TSE).
Scrapie
is a disease of goats and sheep that has been pres
ent in Europe for at least two centuries. The disea
se
migrated from England to Canada and made its Americ
an debut in 1947. Transmission is thought to be fro
m the ewe
to her offspring or to other lambs due to contact w
ith placental materials and fluids. Symptoms do not
appear for two
to five years.
Infected sheep seem to suffer from an interminable
itch. They frequently “scrape” themselves against a
tree or
fence post until they wear off the outer layers of
tissue. This is accompanied by a loss of coordinati
on and
corresponding difficulties in walking.
The disease is widespread in Europe (200–600 indivi
dual cases per year in the UK, endemic in other cou
ntries),
the US (900 flocks infected to date), and the Middl
e East. There do not seem to be any infections in e
ither Australia
or New Zealand. There are recorded transmissions fr
om sheep to goats.
1
The Fore described the disease as having three sep
arate stages: “walk-about yet,” “sit down finish,”
and “sleep finish.”
 
©PGB
3
A sheep showing the effects of scrapie.
Prions
are proteins. In fact, the name comes, dyslexicall
y, from
pro
teinaceous
in
fectious particle. Prionic
proteins come in two forms: cellular PrP
c
and scrapie-like PrP
sc
. The later can force conformational changes in
proteins by altering the natural protein-folding me
chanism—proteins with different foldings can have r
adically
different effects in the body. These misfolded prot
eins likely cause human neurodegenerative diseases
such as kuru,
variant Creutzfeldt
2
-Jakob disease (vCJD
3
), Gerstmann-Sträussler-Scheinker syndrome (GSSS),
and fatal familial
insomnia (FFI)
4
.
The amino acid sequences for PrP
c
and PrP
sc
proteins are identical, only their shapes differ.
Cellular PrP
c
is rich
in so-called
α
-helices (corkscrew-shapes), whereas in scrapie-lik
e PrP
sc
these helices have been flattened to so-called
β
-regions. These conformational changes render PrP
sc
resistant to protein-digesting protease enzymes, i
.e., they are
not all broken down during digestion. Not all confo
rmational changes are the same, neither from mammal
species to
species or within a given species.
More recent research (2/2008) that a prionic infect
ion of neurons increases the free cholesterol conte
nt in the
cell membranes and this may be part of the mechanis
m that causes neurodegeneration.
In the not too distant past, the feed industries in
the United Kingdom used ground waste parts, usuall
y
intestines, glands, spinal tissue, and brains, from
slaughtered sheep and cows as feed for other cows.
Suddenly, cows
were acting strangely (they suffered severe disorie
ntation, staggering, and an inability to stand) and
died for no
apparent reason. Upon autopsy, it was found that th
e brains of such “mad cows” were not solid masses,
but more
closely resembled sponges, complete with holes cont
aining no neurons but rather filled with glial cell
s. This
mad
cow disease
was officially named
bovine spongiform encephalopathy
, BSE. These cows were also ground into
feed for other (herbivorous) cows. Only in recent t
imes has there been a “ban” on such practices
5
.
Prions are extremely robust with respect to sterili
zation. They are known to resist radiation, boiling
,
microwaves, and chemical agents. Surgical instrumen
ts used on Creutzfeldt-Jakob disease patients that
had been
carefully sterilized have shown traces of PrP
sc
. Iatrogenic vCJD is estimated to comprise 5% of al
l cases. There are
documented transmissions due to corneal transplants
, liver transplants, dura mater graft transplants,
and
contaminated instruments and electrodes.
Disease has been induced by an injection of small d
oses of PrP
sc
and feeding meat of infected animals to
animals of the same and different species. Epidemio
logical studies have shown a very strong link betwe
en the
ingestion of brain and spinal cord tissue from infe
cted animals, mostly cattle, and variant Creutzfeld
t-Jakob disease.
Ordinarily, CJD occurs in about one in a million pe
ople. It has no standard single course of progressi
on of
symptoms. Its first signs of incidence are rare in
those under forty years-of-age, more common in thos
e aged 50 to
75, and rare again for those over 75. The average a
ge at death is about 60. Most brain damage occurs i
n the
cerebellum. There is an indication that the disease
may have an incubation period at least as long as
thirty or as
many as fifty years, but once the protein refolding
starts, it proceeds at an accelerating rate and pa
tients rarely live
more than two years. Nevertheless, some people infe
cted in the 1990s showed symptoms (and died) much f
aster.
2
Talk about coincidences: Creutzfeldt worked as an
assistant to Alois Alzheimer.
3
As of December 1, 2006, there were 165 cases in th
e United Kingdom, 21 in France, 3 in the US, 2 in t
he Netherlands, and one
each in Canada, Ireland, Italy, Portugal, Saudi Ara
bia, and Spain.
4
There is no known transmission of FFI outside of t
he 28 families in which it is an inherited disease.
Also, studies of the brains
of sufferers have not found the characteristic spon
giform lesions.
5
Of course, the “invisible hand” of the market push
es producers to skirt any such ban, especially in t
his day and age.
 
©PGB
4
The most recent research has shown that the human p
rion protein gene arises in one of three types. It
can
encode the protein containing the amino acid methio
nine (M), both methionine and valine (V), or only v
aline as
position 129. Thus unaffected people can be classif
ied as 129MM, 129MV, or 129VV. In 2008 a group foun
d a new
sporadic prion disease, which they thought affected
only one of these types. Further research publishe
d in 2010
found that all three types can be affected. The new
disease is, like CJD, a dementing disease and has
been named
Variably Protease-sensitive Prionopathy (VPSPr).
As a confounding effect, research has associated th
e proliferation of PrP
sc
with an excess of manganese together
with a deficiency of copper in the diets of sheep a
nd cows. Furthermore, specific RNA molecules have b
een shown
to be highly associated with the transition from no
rmal prionic proteins to their mutant scrapie-like
form.
Nevertheless, artificially made prionic proteins (I
n theory, these should not be contaminated with any
other
organisms.) have been shown to induce the equivalen
t of BSE in lab animals—but these results remain
controversial. There is some good news on this fron
t. In mid-March 2005, the Pall Corporation applied
to the Food
& Drug Administration’s Blood Products Advisory Com
mittee for approval of a filtration system that red
uces both
white blood cells and prions in blood. The approved
product is the Pall Leukotrap® Affinity Plus Prion
and
Leukocyte Reduction Filter System. Reducing the num
ber of white cells alone decreases the risk of a tr
ansmissible
encephalopathy by 40%, whereas this method removes
99% of the prions present. A reduction of this magn
itude will
leave the remaining prions undetectable by the so-c
alled Western Blot test (more about that in a later
chapter). It is
also fairly gentle on red blood cells, so their the
rapeutic value is not degraded.
Currently, there is a major spread of animal Chroni
c Wasting Disease (CWD) throughout much of North
America. It has been endemic for many years in elk,
mule deer, and white-tailed deer
6
in southeastern Wyoming,
northeastern Colorado, Saskatchewan, Alberta, and s
mall parts of Nebraska, Wisconsin, and Illinois. It
is moving
from west to east, causing concerns that it may soo
n reach the eastern US white-tailed deer population
and seriously
damage the hunting industry. Although it is a spong
iform encephalopathy (a disease that leaves holes i
n the brain), it
has
not been established
that this is a prionic disease. Nor has there been
any
proven
instance of transmission from a
hunted animal to a human. Nevertheless, hunters wou
ld be wise not to consume meat from such animals.
There are TSEs that affect mink and cats. In the la
b, goats, mice, and a host of other animals have al
so been
infected.
Viruses
A
virus
is an
obligate intracellular
parasite
(meaning that it
must
exist within the cells of its host in order to
replicate). A virus is metabolically inert outside
a cell.
Viruses are not living cells.
They cannot provide their own
nutrition, nor can they replicate on their own.
Viruses have no organized cellular structures but s
imply a protein coat, called the
capsid
, surrounding a nucleic
acid core, called a
genome
, of either RNA or DNA, but
never
both. The capsid together with the genome is calle
d
the
nucleocapsid
. The nucleocapsid may be surrounded by an
envelope
that is composed of a lipid bilayer
containing protein spikes. An entire virus particle
is called a
virion
. Viruses are classified by the categories: DNA or
RNA; single strand or double strand; enveloped or n
on-enveloped; by their symmetry—helical, icosahedra
l, or
complex; family; and species.
The following are the steps in many, but not all, c
ases of viral replication.
Attachment
to a cell by connecting to a cellular receptor or
docking site
Penetration
or
Entry
into a cell. This can occur in one of three ways:
o
Direct translocation of the virion across the cell
membrane
o
Fusion of the viral and cell membranes
o
Uptake of the virion into a cellular phagosome and
release within the cell
Uncoating
: Once inside the cell, the virus removes its coat
Replication
of viral nucleic acid within the cell
Migration
of the viral genome to the nucleus of the cell
Integration
of the viral and host nucleic acids to form a
provirus
DNA/RNA nuclear transport
Synthesis
of proteins used in the virus coat
Assembly
of structural subunits
Reencapsidation
6
It also affects farmed mink, domestic cats, cougar
s, and zoo-dwelling ungulates like bison, kudu, and
oryx.
 
©PGB
5
Release
of the virions. Frequently the virions
bud
off the cell surface. Sometimes they are released
during
cell
lysis
, wherein the cell bursts and disperses the reprodu
ced virions
Maturation
of the released virions
An electron-micrograph of virions budding from
the host cell
In order to attach to a cell, a virion’s surface at
tachment proteins must fit, certain special protein
molecules,
called
receptors
, on the cells they infect. Viruses are specific wi
th regard to the types of cells to which they can
attach and infect. Viruses cannot bind to receptors
on tissue for which there is not an adequate fit.
For this reason,
they are said to have
host and tissue specificity
and can only infect certain tissues in certain spe
cies. As examples,
the influenza virus is specific to sialic acid whic
h is heavily expressed on respiratory epithelial ce
lls; an Epstein-Barr
virion can only bind to receptors in the oral and/o
r nasal mucosa; and herpes virus infects cells of t
he nervous
system.
The virus hijacks the reproductive mechanism of the
host cell to produce more virions and eventually t
he host
cell weakens and either lyses (bursts) or the newly
formed viruses bud off the surface of the host cel
l. The time it
takes for the virus to sap the strength of its host
cell varies with disease. Thus, some viral disease
s are associated
with a large proportion of carriers, e.g., hepatiti
s B and C.
On the other hand, infecting viruses can transform
the genome of a host cell and convert it into a cel
l that
becomes cancerous, which will not die and exhibits
uncontrolled growth patterns. Some examples are giv
en below.
Virus
Cancer
Human T cell leukemia virus (type I) Adult T cell l
eukemia
Epstein-Barr virus
Burkitt’s lymphoma
Nasopharyngeal carcinoma
Hepatitis B & C viruses
Hepatocellular carcinoma (l
iver cancer)
 
©PGB
6
Papilloma virus
7
Skin and cervical cancers, warts
Human Herpes Virus, HHV-6
Polio Virus
The bacteriophage shown above is a virus that uses
a bacterium as its host. Each phage uses its syrin
ge-like
design to inject its nucleic acid into a bacterium,
thus turning it into a veritable virus factory for
producing more
phages. Recent research suggests that phages keep m
any bacteria from growing exponentially. These phag
es are
extremely plentiful—estimates suggest at least ten
times as many of them as there are bacteria.
There are poxviruses that infect mammals, snakes,
and insects. In fact, some experts attribute the co
ntrol of the
exponential growth of insects to the presence of su
ch viruses.
As viruses go, smallpox, with its 187,000 bases an
d about 200 genes, is well armed to confront its ho
sts. Its 11–
14 day incubation period gives it ample opportunity
to spread itself far and wide in this time of rapi
d travel. The
influenza virus, which is transmitted on exhaled ae
rosol droplets, is no slouch either.
Much in the news is the norovirus or Norwalk-like
virus, which has been responsible for gastrointesti
nal
disorders frequently seen aboard cruise ships. Worl
dwide, the virus causes 23,000,000 infections per y
ear and has an
infectious dose of between 5 and 100 virions—far fe
wer than almost any other virus (except smallpox wh
ich can
infect a person with around a dozen virions). So fa
r, no one has been able to grow a norovirus for the
length of time
needed to research possible vaccines.
Another particularly frightening microbe is the Eb
ola virus which causes a particularly lethal hemorr
hagic
(causing internal bleeding) disease. It is known to
infect humans, gorillas, chimpanzees, and small an
telopes called
duikers. In outbreaks among humans it has had a hig
h mortality rate (>60%) but killed only around a th
ousand
7
Human Papillomavirus (HPV) DNA has been identified
in 99.7% of cervical cancers. HPV 16 accounts for
50–60% of cervical
cancers, HPV 18 accounts for 10–15%, and HPV 31, 33
, 45, 52, and 58 account for 18% of such cancers. H
PV 6 and 11 are
noncancer-causing, but are associated with external
anogenital warts, low-grade genital dysplasias, an
d recurrent respiratory
papillomatosis. The vaccine Gardasil targets HPV 6,
11, 16, and 18, while Cervarix targets HPV 16 and
18.
 
©PGB
7
people as of January 2008
8
. On the other hand, it has attacked western lowlan
d gorillas and killed at least 5500 and
perhaps as many 30,000 of them.
Influenza is caused by an RNA virus whose genome i
s constructed of eight separate fragments (which co
de for
11 proteins). The latest version making the rounds
is characterized as an A:H1N1 virus. As virions bre
ak, the eight
fragments can intermingle with those of other forms
of influenza, thus contributing to antigenic drift
and antigenic
shift.
Once a virus has infiltrated a cell and been trans
formed to a provirus, that cell is fully infected.
As an indication
of the ramifications of this, in May 2004 an organ
donor diagnosed with a brain hemorrhage died and fi
ve people
received the harvested organs. It turns out the don
or was infected with the rabies virus and each of t
he transplanted
organs were likewise infected. One recipient died o
f surgical complications, but the other four died o
f rabies in June
of 2004.
Viruses and cells of other species of microbe can
mutate. The RNA-based influenza virus has a 10 gene
,
segmented genome, meaning that instead of a single
piece of nucleic acid, it is composed of several pi
eces. If two
different varieties of influenza infect the same ce
ll, these pieces can get intermixed resulting in an
entirely different
form of the virus. This is precisely how antigenic
shift occurs among strains of influenza viruses.
2 years ago
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