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Rules of Affinity
Fahrenholz Rule
Common ancestors of present-day parasites were themselves parasites of the common ancestors of
present-day hosts. Degrees of relationships between modern parasites thus provide clues to the
parentage of modern hosts.
Szidat Rule
The more specialized the host group, the more specialized are its parasites; conversely, the more
primitive or more generalized the host, the less specialized are its parasites. Hence among stable
parasites, the degree of specialization may serve as a clue to the relative phylogenetic ages of the
hosts.
Eichler Rule
When a large taxonomic group, for example, family of hosts consisting of many species is compared
with an equivalent taxonomic group consisting of few representatives, the large group has the
greater diversity of parasitic fauna.
Parasite Host Coevolution
Host–parasite coevolution is a special case of coevolution, which is defined as the reciprocal

adaptive genetic change of two antagonists (e.g. different species or genes) through reciprocal
selective pressures. Hosts and parasites exert reciprocal selective pressures on each other, which
may lead to rapid reciprocal adaptation.
Selection Dynamics
Host-parasite coevolution is characterized by reciprocal genetic change and thus changes in allele
frequencies within populations. These changes may be determined by two main types of selection
dynamics.
1. Negative frequency dependent selection:
To infect a large number of hosts the parasite should adapt to the most common host genotype. A
rare host genotype may then be favored by selection, its frequency will increase and eventually it
becomes common. Subsequently the parasite should adapt to the former infrequent genotype else it
will eliminated from the system.
2. Overdominant selection
Over dominance occurs if the heterozygote phenotype has a fitness advantage over both
homozygotes. One example is sickle cell anemia. It is due to a mutation in the hemoglobin gene
leading to sickle shape formation of red blood cells, causing clotting of blood vessels, restricted
blood flow and reduced oxygen transport. At the same time the mutation confers resistance to
malaria. The homozygote and heterozygote genotypes for the sickle-cell disease allele show malaria
Paper XIII: Parasitology 9.0: Evolution of Parasitism 3rd Semester

1
resistance, while the homozygote suffers from severe disease phenotype. The alternative
homozygote, which does not carry the sickle cell disease allele, is susceptible to Plasmodium. As a
consequence, the heterozygote genotype is selectively favored in areas with a high incidence of
malaria.
Adaptation of Pre-adaptations
Preadaptation describes a situation where a species evolves to use a preexisting structure or trait
inherited from an ancestor for a potentially unrelated function. One example of preadaptation is
dinosaurs having used feathers for insulation and display before using them to fly, or sweat glands in
mammals being transformed into mammary glands.
Progressive and Retrogressive Evolution
The progressive changes are those which some way improve an organ or enhance a function.
Conversely retrogressive changes are those which some way impair a function.
During the course of evolution the tapeworms lost their intestine which is look to be a retrogressive
change in term of evolution but actually it is a progressive change for the animal because it does not
need it now.
When we say that the animal get specialization in phylogeny that means it has extend in complexity
but there is a difference between specialization and progress. The specialization as improvement in
efficiency of adaptation for a particular mode of life, and progress as an improvement in efficiency of
living in general.
Origin of Protozoa
Entozoic protozoa may have been derived from ectoparasites, free-living forms first became
associated with hosts as casual commensals loosely attached to the skin or gills, and then gradually
fortified their position by moving into the mouth, gill chambers, anus, and other openings.
Another logical guess as to origins of these parasites is that they were derived from species
accidentally ingested by their future hosts. The protozoa that are steadily ingested with the food of
larger animals, and they find nutritional benefits and the protection and moisture provided by the
intestine, they established in the intestine, and then parasite could migrate to all other parts of the
body.
Also the secondary host evolved for example trypanosomes may have been taken up by tsetse flies
that began to transmit them mechanically to new vertebrate hosts, but when the flagellates adapted
themselves to development in the proboscis and salivary glands, tsetse flies became their new,
obligatory transport hosts.
Paper XIII: Parasitology 9.0: Evolution of Parasitism 3rd Semester

2
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Chronological and Biological Age
Your biological age is the age that most normal people would be when they have a body and mind
similar to yours. Compare this to your chronological age, which is the number of years you have
been alive.
Programs on the internet can calculate your Biological Age by asking questions about your
1. BMI (Body Mass Index) based on your weight and body fat
2. General health (especially digestion and immune system)
3. Outlook on life, mental health
4. Toxic load based on your diet, smoking, alcohol and the environment in which you live
5. Lifestyle including relationships, exercise and sexual habits
Food and Ageing
Each cell needs the proper food to keep it strong. Cells die and replace themselves at various
intervals. To understand anti-aging, understand that when a cell replaces itself it has three options
that it can replace itself with:
1. A cell may replace itself with a weaker cell each time. A cell will do this if it hasn't had the right
nutritional foods available to it. This process is called degeneration.
2. A cell can replace itself with the same strength cell. This means the body doesn't improve. That
is, you have a chronic condition.
3. The cell is capable of replacing itself with a stronger and better cell. This will happen only if the
cell has an abundance of energy and the right raw materials. This process is called regeneration.
It is anti-aging.
Aging process is controlled by a complicated and precise signaling network that involved in energy
homeostasis, cellular metabolism and stress resistance. Over the past few decades, research in
natural dietary compounds by various organism and animal models provides a new strategy for anti-
aging. Natural dietary compounds act through a variety mechanisms to extend lifespan and prevent
age-related diseases.
Antioxidants and Inflammation
Some foods and beverages contain powerful substances called phytonutrients that some believe are
capable of unlocking the key to longevity. Phytonutrients, which are members of the antioxidant
family, gobble up "free radicals" -- oxygen molecules that play a role in the onset of illnesses such as
heart disease, cancer, osteoporosis, and Alzheimer's disease.
As we age, we become more susceptible to the long-term effects of oxidative stress (a condition
where the body basically has too many free radicals) and inflammation on the cellular level. The
theory is that antioxidants and other age-defying compounds help cells ward off damage from free
radicals and minimize the impact of aging.
Paper XVI: Reproduction Biology 7.0: Food, Yoga and Ageing 3rd Semester
1
Calorie restriction
Caloric restriction (CR), or calorie restriction, is a dietary regimen that restricts calorie intake, where
the baseline for the restriction varies. Calorie restriction without malnutrition has been shown to
improve age-related health and to slow the aging process in a wide range of animals.
Yoga, Exercise and Ageing
Exercise training cannot restore tissue that has already been destroyed, but it can protect the
individual against a number of the chronic diseases of old age. More importantly, it maximizes
residual function. In some instances, biological age is reduced by as much as 20 years. Life
expectancy is increased, partial and total disability is delayed, and there are major gains in quality-
adjusted life expectancy. Exercise is thus a very important component of healthy living for the
senior citizen.
Talking about aging, there are several factors that leads to ageing (apart from age) - misuse of the
body, over-exaggeration of the mind, non-nutritious foods, poor posture while working, sedentary
lifestyle, and so on. However, you would be happy to know that our body has the unique ability to
renew or regenerate at the cellular level. The best way to attain this would be by practicing yoga
regularly.
Benefits of Yoga in Anti-Ageing
Yoga acts positively in maintaining the health of the human body. One of the most prominent
benefits of Yoga is the ability to be young once again. Apart from revitalizing the mind, Yoga
rejuvenates the body as well. People, who constantly practice Yoga, have found immense benefits
from it and feel better than what they felt in their younger years. There is a very famous concept in
Yoga philosophy. According to it, a person's age is determined by the flexibility of his spine, not the
number of years he has lived.
Yoga helps in slowing down the aging process, by providing elasticity to the spine, firming up the
skin, removing tension from the body, strengthening the abdominal muscles, eliminating the
likelihood of a double chin, improving the quality of loose arm muscles, correcting poor posture and
so on. Thus, of the numerous benefits of Yoga, anti-ageing is an important one. All you need is
patience (remember, there is no one day benefit policy!!) and the determination (you need to be
strong willed to practice every day) to practice Yoga.
Yoga increases the mental competence in a person, making him/her feel younger. It possesses the
power to fight the internal as well as the external diseases and dangers. This is the key to help an
individual to live longer. There are various types of Yoga, of which Hatha Yoga basically aims at
making people live long. Some of the anti-ageing properties of Yoga are long life, increased
resistance to diseases, increased vitality, and rejuvenation of glands, looking young, improvement in
vision and hearing and many other mental and emotional benefits.
Paper XVI: Reproduction Biology 7.0: Food, Yoga and Ageing 3rd Semester
2
Genetic and Physical Maps
A. A genetic map is a representation of the genes on a chromosome arrayed in linear order with
distances between loci expressed as percent recombination (map units, centimorgans). Also
called a linkage map.
1. Genes on the same chromosome are described as linked or syntenic.
 Humans have 24 linkage groups, corresponding to the 22 autosomes, plus X and Y
chromosomes.
 Groups of genes that are widely separated on a chromosome may show independent
assortment; however, all such groups can eventually be tied together by mapping
additional loci between them.
2. The genes on a chromosome can be represented as a single linear structure that goes from
one end of the chromosome to the other.
B. Genetic distance is measured by frequency of crossing over between loci on the same
chromosome.
1. One map unit = one centimorgans (cM) = 1% recombination between loci.
2. The farther apart two loci are, the more likely that a crossover will occur between them.
Conversely, if two loci are close together, a crossover is less likely to occur between them.
3. Recombination can only be detected between two loci, both of which are heterozygous.
 The dominant/recessive relationships must allow for detection of recombinants.
 The most useful systems involve codominant alleles.
 Efficient mapping requires polymorphic loci, i.e. loci with two or more common alleles.
Loci that have a single common allele are described as monomorphic.
 Any variations in DNA, whether in coding regions of genes or in noncoding regions, can
be used as genetic markers, i.e. as a label for a particular point on a chromosome.
4. If two loci are very far apart, two or more crossovers may occur.
 Even numbers of crossovers restore the original combinations of alleles and are counted
as zero crossovers.
 Odd numbers of crossovers create recombinant allelic combinations and are counted as
one crossover.
 A recombination rate of 50% corresponds to independent assortment. Therefore, only
distances less than 50 map units can be measured directly. Greater distances can be
constructed by adding up distances between closer loci.
5. Closely linked genes show association of alleles within families but not necessarily within
populations. Crossing over generates random haplotype combinations within populations. If
the loci are very close together, equilibrium among the possible combinations may take
many generations.
6. If two loci are linked, the alleles that are on the same chromosome are described as coupled;
alleles on opposite homologous chromosomes are in repulsion.
C. A physical map describes the physical location of genes on chromosomes.
1. Genes on the physical and genetic maps should be in the same order, but the scales need
not be identical, since crossing over may occur more often in some regions than in others.
Page No. 1 of 6 Gene Mapping 3rd Semester

2. Among the techniques for constructing physical maps are the following:
 Human/mouse cell hybrids tend to lose human chromosomes at random, leading
eventually to hybrid cell lines that have one or a few human chromosomes. If a gene is
always present or absent when one particular chromosome is present or absent, it can
be concluded that the gene is on that chromosome.
 Fluorescent or radioactive probes that bind to a particular gene can be observed
microscopically and can be used to localize the gene on a metaphase spread.
 Chromosomes from cells in metaphase can be sorted with high-speed electronic sorters.
One can make preparations of a particular chromosome. If a particular gene can be
shown to be in the preparation, it must be located on that chromosome.
D. Gene mapping has important applications.
1. It is useful for locating the position of genes on chromosomes, e.g. if two genes are closely
linked and the position of one is known, then the other must also be nearby.
2. It is useful in estimating genetic risk, e.g. if a gene cannot be tested directly, then variation at
a closely linked locus may indicate the presence or absence of a detrimental allele.
Map-Based or Positional Cloning
Positional cloning is a method of gene identification in which a gene for a specific phenotype is
identified, with only its approximate chromosomal location (but not the function) known, also
known as the candidate region. Initially, the candidate region can be defined using techniques such
as linkage analysis, and positional cloning is then used to narrow the candidate region until the gene
and its mutations are found. Positional cloning typically involves the isolation of partially overlapping
DNA segments from genomic libraries to progress along the chromosome toward a specific gene.
During the course of positional cloning, one needs to determine whether the DNA segment currently
under consideration is part of the gene.
Tests used for this purpose include cross-species hybridization, identification of unmethylated CpG
islands, exon trapping, direct cDNA selection, computer analysis of DNA sequence, mutation
screening in affected individuals, and tests of gene expression. For genomes in which the regions of
genetic polymorphisms are known, positional cloning involves identifying polymorphisms that flank
the mutation. This process requires that DNA fragments from the closest known genetic marker are
progressively cloned and sequenced, getting closer to the mutant allele with each new clone. This
process produces a contig map of the locus and is known as chromosome walking. With the
completion of genome sequencing projects such as the Human Genome Project, modern positional
cloning can use ready-made contigs from the genome sequence databases directly.
For each new DNA clone a polymorphism is identified and tested in the mapping population for its
recombination frequency compared to the mutant phenotype. When the DNA clone is at or close to
the mutant allele the recombination frequency should be close to zero. If the chromosome walk
proceeds through the mutant allele the new polymorphisms will start to show increase in
recombination frequency compared to the mutant phenotype. Depending on the size of the
mapping population, the mutant allele can be narrowed down to a small region (<30 Kb). Sequence
comparison between wild type and mutant DNA in that region is then required to locate the DNA
mutation that causes the phenotypic difference.

Modern positional cloning can more directly extract information from genomic sequencing projects
and existing data by analyzing the genes in the candidate region. Potential disease genes from the
candidate region can then be prioritized, potentially reducing the amount of work involved. Genes
with expression patterns consistent with the disease phenotype, showing a (putative) function
related to the phenotype, or homologous to another gene linked to the phenotype are all priority
candidates. Generalization of positional cloning techniques in this manner is also known as
positional gene discovery.
Fluorescence in Situ Hybridization
FISH (fluorescence in situ hybridization) is a cytogenetic technique used to detect and localize the
presence or absence of specific DNA sequences on chromosomes. FISH uses fluorescent probes that
bind to only those parts of the chromosome with which they show a high degree of sequence
complementarity. Fluorescence microscopy can be used to find out where the fluorescent probe
bound to the chromosomes. FISH is often used for finding specific features in DNA for use in genetic
counseling, medicine, and species identification. FISH can also be used to detect and localize specific
mRNAs within tissue samples.

Probes are derived from fragments of DNA that were isolated, purified, and amplified. The probe is
tagged directly with fluorophores, with targets for antibodies. Tagging can be done in various ways,
such as nick translation, or PCR using tagged nucleotides. Then, an interphase or metaphase
chromosome preparation is produced. The chromosomes are firmly attached to a substrate, usually
glass. Repetitive DNA sequences must be blocked by adding short fragments of DNA to the sample.
The probe is then applied to the chromosome DNA and incubated for approximately 12 hours while
hybridizing. Several wash steps remove all unhybridized or partially-hybridized probes. The results
are then visualized and quantified using a microscope that is capable of exciting the dye and
recording images.
If the fluorescent signal is weak, amplification of the signal may be necessary in order to exceed the
detection threshold of the microscope. Fluorescent signal strength depends on many factors such as
probe labeling efficiency, the type of probe, and the type of dye. Fluorescently-tagged antibodies or
streptavidin are bound to the dye molecule. These secondary components are selected so that they
have a strong signal.
Southern Blotting
A Southern blot is a method routinely used in molecular biology for detection of a specific DNA
sequence in DNA samples. Southern blotting combines transfer of electrophoresis-separated DNA
fragments to a filter membrane and subsequent fragment detection by probe hybridization.
Method
1. Restriction endonucleases are used to cut high-molecular-weight DNA strands into smaller
fragments.
2. The DNA fragments are then electrophoresed on an agarose gel to separate them by size.
3. If some of the DNA fragments are larger than 15 kb, then prior to blotting, the gel may be
treated with an acid, such as dilute HCl, which depurinates the DNA fragments, breaking the
DNA into smaller pieces, thus allowing more efficient transfer from the gel to membrane.
4. If alkaline transfer methods are used, the DNA gel is placed into an alkaline solution (typically
containing sodium hydroxide) to denature the double-stranded DNA. The denaturation in an
alkaline environment may improve binding of the negatively charged DNA to a positively
charged membrane, separating it into single DNA strands for later hybridization to the probe
(see below), and destroys any residual RNA that may still be present in the DNA. The choice of
alkaline over neutral transfer methods, however, is often empirical and may result in equivalent
results.
5. A sheet of nitrocellulose (or, alternatively, nylon) membrane is placed on top of (or below,
depending on the direction of the transfer) the gel. Pressure is applied evenly to the gel (either
using suction, or by placing a stack of paper towels and a weight on top of the membrane and
gel), to ensure good and even contact between gel and membrane. If transferring by suction 20X
SSC buffer is used to ensure a seal and prevent drying of the gel. Buffer transfer by capillary
action from a region of high water potential to a region of low water potential (usually filter
paper and paper tissues) is then used to move the DNA from the gel on to the membrane; ion
exchange interactions bind the DNA to the membrane due to the negative charge of the DNA
and positive charge of the membrane.

6. The membrane is then baked in a vacuum or regular oven at 80 °C for 2 hours (standard
conditions; nitrocellulose or nylon membrane) or exposed to ultraviolet radiation (nylon
membrane) to permanently attach the transferred DNA to the membrane.
7. The membrane is then exposed to a hybridization probe—a single DNA fragment with a specific
sequence whose presence in the target DNA is to be determined. The probe DNA is labelled so
that it can be detected, usually by incorporating radioactivity or tagging the molecule with a
fluorescent or chromogenic dye. In some cases, the hybridization probe may be made from RNA,
rather than DNA. To ensure the specificity of the binding of the probe to the sample DNA, most
common hybridization methods use salmon or herring sperm DNA for blocking of the membrane
surface and target DNA, deionized formamide, and detergents such as SDS to reduce non-
specific binding of the probe.
8. After hybridization, excess probe is washed from the membrane (typically using SSC buffer), and
the pattern of hybridization is visualized on X-ray film by autoradiography in the case of a
radioactive or fluorescent probe, or by development of color on the membrane if a chromogenic
detection method is used.
Result
Hybridization of the probe to a specific DNA fragment on the filter membrane indicates that this
fragment contains DNA sequence that is complementary to the probe.
The transfer step of the DNA from the electrophoresis gel to a membrane permits easy binding of
the labeled hybridization probe to the size-fractionated DNA. It also allows for the fixation of the
target-probe hybrids, required for analysis by autoradiography or other detection methods.
Southern blots performed with restriction enzyme-digested genomic DNA may be used to determine
the number of sequences (e.g., gene copies) in a genome. A probe that hybridizes only to a single
DNA segment that has not been cut by the restriction enzyme will produce a single band on a
Southern blot, whereas multiple bands will likely be observed when the probe hybridizes to several
highly similar sequences (e.g., those that may be the result of sequence duplication). Modification of
the hybridization conditions (for example, increasing the hybridization temperature or decreasing
salt concentration) may be used to increase specificity and decrease hybridization of the probe to
sequences that are less than 100% similar.

Chromosome Micro-Dissection and Micro-Cloning
Chromosome microdissection is a technique that physically removes a large section of DNA from a
complete chromosome. The smallest portion of DNA that can be isolated using this method
comprises 10 million base pairs - hundreds or thousands of individual genes.
Scientists who study chromosomes are known as cytogeneticists. They are able to identify each
chromosome based on its unique pattern of dark and light bands. Certain abnormalities, however,
cause chromosomes to have unusual banding patterns. For example, one chromosome may have a
piece of another chromosome inserted within it, creating extra bands. Or, a portion of a
chromosome may be repeated over and over again, resulting in an unusually wide, dark band
(known as a homogeneously staining region). Some chromosomal aberrations have been linked to
cancer and inherited genetic disorders, and the chromosomes of many tumor cells exhibit irregular
bands. To understand more about what causes these conditions, scientists hope to determine which
genes and DNA sequences are located near these unusual bands. Chromosome microdissection is a
specialized way of isolating these regions by removing the DNA from the band and making that DNA
available for further studies.
To prepare cells for chromosome microdissection, a scientist first treats them with a chemical that
forces them into metaphase: a phase of the cell's life-cycle where the chromosomes are tightly
coiled and highly visible. Next, the cells are dropped onto a microscope slide so that the nucleus,
which holds all of the genetic material together, breaks apart and releases the chromosomes onto
the slide. Then, under a microscope, the scientist locates the specific band of interest, and, using a
very fine needle, tears that band away from the rest of the chromosome. The researcher next
produces multiple copies of the isolated DNA using a procedure called PCR (polymerase chain
reaction). The scientist uses these copies to study the DNA from the unusual region of the
chromosome in question.

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Heat Shock Proteins
Heat shock proteins are present in cells under normal conditions, but are expressed at high levels
when exposed to a sudden temperature jump or other stress. Heat shock proteins stabilize proteins
and are involved in the folding of denatured proteins. High temperatures and other stresses, such
as altered pH and oxygen deprivation, make it more difficult for proteins to form their proper
structures and cause some already structured proteins to unfold.
Left uncorrected, mis-folded proteins form aggregates that may eventually kill the cell. Heat Shock
Proteins are induced rapidly at high levels to deal with this problem. Increased expression of HSps is
mediated at multiple levels: mRNA synthesis, mRNA stability, and translation efficiency. Most heat
shock proteins are molecular chaperones. Chaperones aid in the transport of proteins throughout
the cell's various compartments.
Factors that can Denature Proteins
Environmental stressors
1. Heat shock
2. Transition heavy metals
3. Inhibitors of energy metabolisms
4. Amino acid analogues
5. Chemotherapeutic agents
States of disease
1. Viral infection
2. Fever
3. Inflammation
4. Ischemia
5. Hypertrophy
6. Oxidant injury
7. Malignancy
Normal cellular influences

1. Cycle of cell division
2. Growth factors
3. Development and differentiation
Types of Heat Shock Proteins
HSP100
1. function as chaperones
2. solubilizes protein aggregates thereby dissociating them
3. facilitates proteolysis
4. essential in yeast for acquired thermo tolerance
5. essential for yeast prion propagation
Paper XII: Endocrinology 7.0: Heat Shock Protein 3rd Semester

1
HSP 90
1. stabilizes proteins prior to complete folding or activation
2. forms stable complexes with inactive glucocorticoid receptor and other transcription factors
3. most abundant non-ribosomal protein (cytosolic version)
4. most abundant protein in endoplasmic reticulum (ER version)
HSP70
1. Assists in protein transport into mitochondria and the endoplasmic reticulum
2. Protects proteins under stress
3. Stabilizes proteins prior to complete folding
4. transports across membranes and proteolysis
HSP60
1. mediate the native folding of proteins through cooperation of HSP70 and 60
Small Heat Shock Proteins

1. exhibit chaperone activity in vitro and thermo protection in vivo
2. produced at significant levels in cells experiencing heat stress
3. most are heat inducible, but some are synthesized in unstressed conditions-such as for cell
development
Paper XII: Endocrinology 7.0: Heat Shock Protein 3rd Semester

2
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v<qcfivn may Pbfts h a Su ctlinp , lD t')ssu deVada/aoh,
or lu q Cehceroun lyp. Voutn.
hache dcal prcstne / lcarasit= *a) tni h'alc tn;Hatateon
mcl3 cahc
fumanon 5/ cohnccdvc lisstt, ny >e/a4-tna
hosl h'ssq oy my tnlliak a uaib ,/ 6lncr 2sqch'o-ns.
.zqb-s/rtf tt
Z.
3F
Tkc P>cswc ma) c>+qkd ic fi a si ngte parasilc. qa
&La{ldey t}ovm oy hoty 6e ettakd g.0 %aLqo / *"ll
panaSih as a^;.lt hatn-ehdes
m funpn ycr-sAd.
Do>rus
Thc fl+ncral etF*r
r tnlalimt parosik a/1c qh th*<qseal
Plqs,4q Wkn leafoty,
lnh f.* lumen, deslntelqn U
tnvcosQ tS
/+eain7, $ bo>roDit7 or 6: ottscntvcnt orgqhs.
t Ptusi q te Viat \na - {Jtathcmi cat -Rc*pani!6e.1

- schishsotoq lu -S-bdl nyd,to..lyzcd.haelaaTto6in
/mn bost _
hactuAgwph.-Thc pwkin w Wcd {3 b" spancSs-b,

- Ntppasf:etytslus tn yak Wl--cslinc.disbt ileqn Cail,ue qyl
Ln cy6y7r4 t-ct l.e
ricno
8
. a |sorphân
/
* h t cv:,T;r#:,' :, { r:;;r'fr, ff:,
.7 "; : ir:*' r
*'
9 N A tevcl M goln Ia Wctcs Aad ilVer.
lh hds-l tisstl e.cal,M: lo
- kinelic pnpcrlics 1lt<c a[tinitt* fu, suislrak ts di&crrnt

su &stya Ic spect/a'ri ry u _diYaent
ac yw cd bbPe yi as
ttvtmv_|.o
- Pa/)qs) ks qnc hob diVskcl {: hoSl Chz1wil {caue-

- Pqrasit , pl"d,uc anianzynes brat- hrttt/ryack u)ln he-
host- ctl?-JmC5.
- batw, rnctaiolic pn>dttct- unitil host p>*bfutc adilfu
ovkr covcvning Darn pb"kct )t pot-
fl r27"))?Er
Vq.k-6ltt/tt
3.
u:::-::-- ..-38'
4 hoytnohEs n
- l71ghofru hac a
Canbalgd,N*qrr'i/qk" ,r!ccl,rt..A_c/er,za _
Ih Fpr."cia -#bduttiftv, (atarc ne$five elkct at
-
f'yqsik Prcsent lh )t^t < fihe- *ta:, b 4b rw ca.tiobydnk
a Sf, ** frnal f o, <)/is yrt

. - S*rcs< tS I
-
" ctit /l )<acr;6rs h, $ <<6l-s Jilrh ac pa)y?
h\n{rr, ltu pyqlfi4c_n etrtotiohs etb-.-_ l,efuct;m lcqds h
' CaWe q- Ail*
_ [qlL ncc qnd lw, y t e )<sb
r /.rcl* In b tacili<n (rqtt a /nat t, r l*e

arytan',nfl
i$t xri<l.ance tn /avnt, , 'tlr.-l\ rrk r,'ni**rrt gl frytqtiks
-Ouint ! e *S|--less hcr''
Pt"/' trt Uhicn b. e -?utcr t& _
.$/- adr v,rl .oY'rn, lt'trkl C' tqtsn 4aTtarl )nitlqnq' ,g__
?4,
PfrPIB :=ill .: PfrRnS/ro :y4tx. *of ill il
?-o : Hosr PARfrstrE
s PEct trlc/ry: 3H
]-tost P_arqsjtc s Fccirta'fo:
spcci/icitz Yc.fcrs b'tne hings /nql tnake q 4il.ne) dishnct
/1-* o.Lrqcr-g. hosL spcci/tcip vefcrs b Ycst>icbon V q
parasi l-c b oh e hosl .3-c hovrto XcnoL+t),. oY hoY-c fu? 4 t )
on1 ho.S"[ S.C hcl-cn^cnoUn.

fihign dcyrcc lrutt spcci/tzig hcans l'nal lnc adalokrh'ans
/
Cltt llost qnd lcarasi lz, Qne'sa clelt6a26 and lhhvwahcd, /uett
lnc D-qrasil* ttt Dttattc h Scnvtv.e on. o/uev hoJt sy'ccics.
This sftcci/.ki fo ts occw rn a)nt3 du c +a /r)o ),ta-roYls.
- l:iyst-.enVircnmcntaL atnd /tt; sl.-ql /or/-rrs. :f tncse;/acl^b
Arc a.ccidrnlJj Ktn.ovcol tne Pqn.a-sik n Atlc-lb Sll/t,tit'e t,
Aholn er hp ,f.l-
- Znd lS l'vtcability / PruqtiLc t'?, lhvacLc qhd {t,t,tviue ltr1 alrnet'
hosF
hc deTy-c.c,oy. ).ot ny.e-
"/- P* asik /-or iLs h."st tts- vatzr,l es
pavasiL lo pattasilc oT eu.ct4 th- di&cycnt slaga 7
l,f , gcle € haz q
/ ot sin ?-! c fp a4 ast'Le, Soyrye l)-ertast't
graotd mn/e host- and sa/4e-./zc"u haznou- yan/zc
/
the l> an as i L" ttdn 6v-a.q a1 Ya n 2f.
/ )4 os /' Sh o DE .lCvc/h?-4-
ss deV.rrc
/ SlputT.)g anll Lnc pavtotst l-c ha,o r)cncaD
X hosk' Shose hiTn dcfl>cc / tlr-ciTttg
rnc dcy yce o/ peci /1'-i fo d"l, ehd) - Qpon lmc mc-/a6o/ic
e
Yc q)il/)ctmcr)k o/ ln€ h ost.

hctasilz nx| ako Snous specificifu.-Sorne Skqins /
t-,t<e
Prnasit" .e\?cciue th q Sin 7ac Tnal yos{ ruarg" lc tp/ech'lc

tn ln kr rvti,d ial c h o s /' ea,ttqlry .
Dcarnplc thctqdes lnc Nc\t,k*etotu spccics / /rflaks

Ane/oUnd ohg tfi lnc ),tind7ul. krni ks c{nd Mq2j
7
Sp*ics g ciia[.d accw dvtry cqvvo o/ l4or,sc
siynifuirnr,
q
/ tf*fuafo ts h?dt ;t''lf nil a porusi ks h
speciT'o YanVc / host'
Zqb- lfttftt
i,f
-*g,eprukr' b / '?q{ntr d ir : t??ei, ,f uri/e a-

i___ h r.t.,
' anl qdabhallar lrtr fc|i t c',cs clp dr,.
qsn .: t,zplc ,iC,gg rn, A 6€Ct, :
t f S- t_C, g ,[;.t
i l*$ b e 't ,r{- tCL o .<l .i(,}. i liohlo*
I
l- e lo*tacl, Co :<r,.
I Z. Ere,oqk? t! far ns:.-
h a if.r'r'c t h',s!- ttvin? t .*at-a ..':b a,: ' , ,b k

h.e
'F.-. the, --
[Ccome t<atakd g
l_frflaphir", C,t/ t,l^ Cy {,r
Pqk-t/tl/tt
3
:.-. . ,--- : r: 3U
d Hps l spcci Rangc:
/.r'cij
if7r,c pauesib tngS 6e -uhabtc /o- dcu/opcd .m ahs,olnr-r- host
fr1tfi lyP, 4 lsalq{,ion tnqy 6c hapbcnll dilL h lna4y
YU15" hS:
A* E.nuitl nwtcttlott f,on d t'liow, .
lbc Speafuc chvirohmektel Onolt. liortE l4ttttcd 6J taey'an*tz
lil{c o-L, knlrtralutc., hte, oswah)c pvstt/ta b\g*LedlSeh} _
-Lk:-- hos?"
*a*.Nsklrura$ ttosl::
J/.trJ. 5![oDs Xsrsknce lo pAue*ik uitu Pma;ik:t"?u-qn6
yatcliohs qhd b lnqc),tcni cal tatnily- .__ _
so:me line pruqs;tq or/te a6teb liuc Gthd lu Vru ls|Lwin q

hosl 6Ltt lqcx_"/ suitabtc ynaqn b -kasyukstou ts a-6sertl.
,, -.: -)+ a pcmasil.-tnvadc tn Lnc ce-tts a hkue Lrt?caa-at){crfu

/
c>ckb q bmasit .ktua.a cahp,i h'rm and-a_ng_me/_h*
S. Pauasik pes[stah,ce: _
\he host hqt al] o/-auoWatlc b.rtd,tha, $1il. houe bc>cst",{tetbrc

b sholss bb*raslk it'st^|/ as throny2\atititj"U tiooaenltq.l
ptaess /
b ftw:asile hol- hosh
The gaaasil* yto.tt-Stl€rificiA fuaJt 6c a.tatng{. d,u7tr> qrg

ln*akon W lo, nost c/r loat,atik
.?qt---lf/tfr1
*- Kih4 / )lost laaaalla spui/aLlU.:

Kitld a/ host' powasth'c Spea/ab peaba fue kcasps
. d.tte h tsd tn knc- spa,V'cig - ctcsisk :
- Eco.loflcal SpcdftciA ,
Drr tniscase l*e poutasik W cn\qte ti:dyt ln a fo>ciyu
f hu*
6ut hatn atLy-hovot .ewh es -@c - k calnc rcal o"Vr al
/
-b n:,;crs'
- PhJi"oto-"7) mt sged|^cig:-
)h ltuD a,{SG l.ne
}teaasiU PtVsi"l@*U ard -Vruteh'cerb
, @uPqhllte bitrrt'bun4 has,L- 6u*-laaL u-)La *Y* 2 ost.
- El4taley'cal spcci /a ciP:
bncn pnysiob?n*t sPecLP"c)A, thuawe q /reltern /v
,.lcttaulawj\*u eaad ettotuy cd sla eclpbig,
. PUL, fa.ncic syaerqlt !9=l
-cA lnis (asc l-uo iost fiosscs ctaselJ Lalq k*d* /zrata"rrk
- .k,olJc cq we $&nctic xtoa bra, 6/ a hn,sk-$t* lccatu e l'arc
h;p h"sk ahd- jnulrw,4siL@ @c -lv.otucd la?ctzer
-qb-6/////
qh
Snfcch on ilnd &n)ta Paz]ays:
Thc.rc Wte sovnc ;/acl-ov qnd p>occsses l'nAt affect- /-?.1c
fiasl- Pctyctsitc sp*iilc;b occu/t ddng tne /n>-.
Y/)alov sruyu taTecliab:
/
Firs* st-ayc d l.r, Parasib h> hxl'.
frss;ocictDon /
The tn/cciuc slagtes o'c Sporct .7/, lartva ,s A rcSDn2
5fu7. Lshicn EatWc Some;fctclat-s /"zon /nebo-St th
ovdev h rcSuvnc dcvto?menl-- 1he nqlucc and /trcscncc dl
cLbscncc
7 b?tc/.achw dcttywine /hc, S/po,/'cig
- rhc pqrtasib u)ln divccl- lr'rlc flcte litre {st"vd) a hor1
e herif,c lrnan tnose
/ uti)'n lnkvlni aab hosl'
- Thc haLcni
"2 /r,c[o>rS
/s c5renhal frr e)cgsl-wryl'. rhaa
cr)€ thd.ttced fy h,st cu th colse d
fur^d
ehz;vnc- ol't ?sk / /anUal /o,ytcUoYt(S
/ frsh'yc
- Sccond h. rtssocrc/L)aa / p*rsiL. h /aosl:

sl-aye
/
-rho sRW ls tno,rl' cruciat tn dckrr")ng lnc yat4gc hosh.
7
The tuvand) ng ovTonisvq nW ktovc h, hercssay
fand
hul>rcnk lvt hosl 6 ad: .
' f-s* exawplc Sawc trp"1;aruS q Clqsvno{vqnfhas re.uu//) c)

Lne Uttcq / lrc tTosl fut- fud l-, nc$> h, mq)nktin
hovm4 ostnsh c ncti on.
/t
- l,loyvnohcs
? sonc fiosls elso pwbaby L^furrc hd/l
Suscc ph il\ib l-" lrq, qsi /c.
rtund sta7e
/ h. tssoc,thli* I pcnasilz, lT hw/':
Thrnct sk
W thvovc rvWtilot'.{h* q pq,aslkyb he
rcpn>fuactior. Rebwdurtizu Pwelcc /n/e*t ryb anal
hco 3ot4n7 fu, ha.l- %nvclQslrl The Pau?otsik h^)
hccd lne'hvtn),ianal , tnqct4anicat and kvwyl>q14/ e tonclilians
vqk-6//t/rr
6
4 bwhadirc tlast spaq;#"c,lb:
P)c qdttll tt
- q* hd -$cr. 4e-c/- he -bes/_,
lqli"
/\rou tnc nculS eweryad $ea have J." sccK o=at: foe h-o-s/.
t:hcn -lac pruipd_-?_-;tyq vahrn ts pt-t e n7*d br?cq tuqg_
Pzuasiu-m q-fr@cg otcci-dculat hpsl-- z,ra,s)aou,s hoc
f,t, han 4 Araa-el -Wkl% h_os* VnJP_rfu -
Vl
z. L) cc.'
- Licc aae-olh'qsl"ry-anal pubane4?*paaasib_ / 6)'.di ond
tuavnhoJs, Tuausf ov tD Qcclul he& 1. h,;-t/ hhru lzto
fum
hos]- 6od)es a4c lh-cbsc canhqct codtilhq (o-upttlqhbu ot
otui g fr"dia-p urfl
/.;, .
-[ttc-drr4hnlhpst-
^
ttav-enh6p-tv)uhs he. c)cqtn 4 fuc_chDn _
p-o/utati* lne lt^cc oyt ik $octa

/
Lke- Jtaztc/,>e -occua--allnatf- q$qls OhlJ oy:> tu-E hoSy'
Oy 0L Stylal) han{cx_X c}osclj..rc/.q/e-d- ,Qo,{y' fuw hrut
l'taNtot: wn ?" / h""S/ sloca'/z Clh
--r-clb-
1 6frt
i-
/tt
'r- l,: i t
S-*E-lics:
-- Inal'hynfils and {iyds- l, sf r i-s qtr l:Aza dlaZ ci; in' _

ktctbvlrrls ht{td i-t'yclS:- tTafL\vifu?ce rc ly,oye tcst^tZka
he#irs Fllnaurl
;a,thanf,e- ha_cJs_a
A. Tiryc qnd ' ib_r:

Parasite
An animal that lives upon (ectoparasite) or within (endoparasite) another living organism at whose
expense it obtains some advantage usually nourishment and protection.
Parasitic diseases include infections by protozoa, helminthes, and arthropods:
1. Protozoa: Malaria is caused by plasmodium, protozoa, and a single-cell organism that can only
divide within its host organism.
2. Helminthes: Schistosomiasis, another set of very important parasitic diseases, is caused by a
Helminth (a worm).
3. Arthropods: The arthropods include insects and arachnids (spiders, etc.), a number of which can
act as vectors (carriers) of parasitic diseases.
Parasitism is a type of antagonistic interspecific interaction in which smaller partner, called parasite,
derives food and shelter from larger partner, called host, at some expense.
Parasitology is the study of parasites, their hosts, and the relationship between them.
Types of Parasites
Ecto and Endoparasite

Ectoparasites stay out of the body and have special adaptations in the mouth organs for better
access to the target tissue. Mostly they feed on blood. These include ticks mites leeches mosquitoes
etc. Ectoparasites suck the body blood, or juice, or feed on living tissues from outside.
For e.g., Bugs, fleas, ticks, lice, numerous crustaceans etc. Petromyzon (sea lamprey) is a
sanguivorous agnathan, which attachés itself to the larger fish (such as shark) by the sucking action
of its buccal funnel, makes a hole in the hosts body with its rasping and toothed tongue mixes the
anticoagulant and sucks the blood. Pediculus (head louse), Xenopsylla (rat flea), Dermacentor (tick)
are common examples of human ectoparasites.
Endoparasites are those that live in the body of the host. They have various adaptations depending
upon the site of their existence. For e.g. tapeworms have hard epithelium that protect against
digestive juices in the body of the host. Examples include:
1. Taenia, Ascaris, Entamoeba etc. live in the intestine of man and cause taeniais, ascareasis and
amoebic dysentery respectively.
2. Plasmodium (malarial parasite) lives in the liver cells and RBCs of man and cause malaria.
3. Wuchereria (filarial worm) lives in the lymph vessel of man and cause filariasis (elephantiasis).
4. Trypanosoma lives in the cerebrospinal fluid of man and causes sleeping sickness.
E doparasites ca e ist i o e of t o for s: i tercellular i ha iti g spaces i the host’s ody or

intracellular i ha iti g cells i the host’s ody . Some animals show ectoparasitic and endoparasitic
interactions with great differences in morphology in the two phases. For e.g., Sacculina (root headed
barnacle).
Page No. 1 of 14 Parasitology 3rd Semester

Facultative Parasite
Facultative parasites are those which become a parasite only when they are in access to a host (or in
association with a host), otherwise they lead a free, independent life. A parasite whose life cycle can
be completed without a parasitic phase, but which may optionally include a parasitic phase under
certain circumstances. Example of facultative parasites includes:
1. Candida (fungus responsible for thrush in humans)
2. Naegleria fowleri (protozoan that lives freely but can also cause infection in human swimmers)
3. Prawn, Oyster etc.
Obligatory Parasite
Obligate parasites are those, which cannot live independently and necessarily need a host for food
and shelter. Obligate parasites are usually host specific. A parasite whose life cycle cannot be
completed without a parasitic phase at some stage. Example of obligatory parasites includes:
1. All viruses
2. Chlamydia bacterium
3. Taenia, Trypanosoma, Entamoeba etc.
Holoparasite and Hemiparasite

Holoparasites are those organisms, which are dependent upon their host for their entire nutritional
requirement. Example: Cuscuta a total parasite of Acacia
On the other hand, hemiparasites (or semi parasites) derive only a part of nourishment (usually
water and minerals) from their host and synthesize their own food by photosynthesis. Example:
Viscum (mistletoe) and Loranthus are partial stem parasites. Santalum is a partial root parasite.
Parasitic plants grow haustorial roots into the host plant tissues, which make connections with the
vascular tissue of the host plant and suck in the required nutrients.
Epiparasite and Hyperparasite

An epiparasite is a parasite that feeds on another parasite. The parasite that is being parasitized by
another organism is known as hyperpasasite or secondary parasite, and this relationship is
sometimes referred to as "hyperparasitoidism," especially in the insect world.
For example a wasp or fly larva may be an endoparasite of an Ichneumon wasp larva, which is in turn
an endoparasite of a wood-boring beetle larva. Therefore, the ovipositing adult female
hyperparasitoid must find the host of her host, namely the beetle larva, and oviposit into that beetle
larva, after which her egg hatches within the beetle larva and seeks out the Ichneumon larva,
ultimately burrowing into it and becoming an endoparasite. Hyperparasitoidism can be used for
biological control of the pest and parasites.
Pathogenic and Non-Pathogenic Parasite

Pathogenic parasites are those, which not only derive food from the host but also cause certain
diseases to the latter. Majority of the parasites are pathogenic.
For e.g., Bacterial parasites cause several diseases in man such as:

Fungi are known to cause rust, smut, and powdery mildew diseases in plants.
Non-pathogenic parasites are those, which derive only food from the host but do not cause any
disease to the latter.
Example: Several nematodes like hookworms, pinworms and roundworms are all non-pathogenic
parasites of man.
Temporary parasite and Permanent parasite

Temporary parasitism is also referred as partial or intermittent parasitism. Here, the parasite spends
most of its life cycle as independent free living organisms. Only a part of its life cycle is spent as a
parasite (usually the period of feeding).
Leech (Hirudinaria), bed bug (Cimex), mosquito (female Anopheles) is common temporary
ectoparasites of man.
Glochidium larva of Unio (fresh water mussel) undergoes metamorphosis as ectoparasite on a fresh
water fish.
Permanent parasitism is also referred as holoparasitic parasitism in this the organisms spend their
whole life cycle as parasites, which is of two types based on where the parasites are found i.e.
Ectoparasites and Endoparasites.
Accidental Parasite
The parasites which are found in the hosts other than those which they normally inhabit are referred
as accidental parasites. In other words, those parasites which attack unusual hosts are accidental
parasites.
Macroparasite and Microparasite

Macroparasites are multicellular parasites that are visible to the naked human eye, such as helminth
parasites (parasitic worms, such as flukes, tapeworms, and roundworms, or nematodes).
Microparasites are small, generally, unicellular and invisible to the naked eye, such as protozoan
parasites.
Necrotrophs
Necrotrophs are parasites that use another organism's tissue for their own nutritional benefit until
the host dies from loss of needed tissues or nutrients. Necrotrophs are also known as parasitoids.
Biotrophic parasites cannot survive in a dead host and therefore keep their hosts alive. Many
viruses, for example, are biotrophic because they use the host's genetic and cellular processes to
multiply.

Mesoparasite
Mesoparasites are the ones that penetrate external openings, such as the buccal cavity, cloaca,
external ear, and so forth.
Wandering Parasite
Wandering or aberrant parasites or erratic, instead of arriving at the site of infection in the definitive
host, reach an unusual place as a dead end, becoming unable to complete the life cycle. For
example, the tapeworm Taenia solium may migrate to the brain and remain there unless removed
via an operation.
Monogenic and Digenetic Parasite

Monogenic parasites complete the whole life cycle in one host, such as with Entamoeba histolytica.
A digenetic parasite needs, in addition to a primary host, also a secondary host to complete the
entire life cycle. Plasmodium vivax (malaria parasite) completes its asexual part of life cycle in people
and the sexual part in the female Anopheles mosquito.
Kleptoparasitism
Some parasites are social parasites, taking advantage of interactions between members of a social
host species such as ants or termites, to the hosts' detriment. Kleptoparasitism involves the parasite
stealing food that the host has caught or otherwise prepared. A specialized type of kleptoparasitism
is brood parasitism, such as that engaged in by many species of cuckoo. Many cuckoos use other
birds as lifetime "babysitters"; cuckoo young are raised and fed by adults of the host species, while
adult cuckoos fend for themselves.
Cheating Parasitism
Cheating or exploitation types of parasitism are often found in situations where there are
generalized, non-specific mutualisms between broad classes of organisms, such as mycorrhizal
relationships between plants and many types of fungi. Some myco-heterotrophic plants behave as
"mycorrhizal cheaters," establishing mycorrhiza-like interactions with a fungal symbiont, but taking
carbon from the fungus (which the fungus, in turn, gets from other plants) rather than donating
carbon.
Periodic Parasite
Periodic parasite one that parasitizes a host for short periods.
Protelean Parasites
Protelean parasites are insects in which only the immature stages are parasitic. Mermithid
nematodes and hairworms considered as protelean parasites.
Latent Parasites
Latent parasites are parasites which do not have any obvious effects on the host.
Interspecific and Intraspecific Parasites

When individuals of the same species parasitize individuals of the same species, they are referred to
as intraspecific parasites when species are different called interspecific parasites.

Monoxenous Parasites
Monoxenous parasites are parasites with direct life cycles (i.e., with one host).
Heteroxenous Parasites
Heteroxenous parasites are parasites with indirect life cycles requiring an intermediate host (i.e.,
involves 2 or more hosts).
Heterogenetic Parasites
Heterogenetic Parasites are parasites with alteration of generations e.g., Coccidian parasites and
Strongyloides.
Euryxenous Parasites
Euryxenous parasites are parasites with a broad host range.
Stenoxenous Parasites
Stenoxenous parasites are parasites with a narrow host range; e.g., host specific coccidian.

Host and Type of Hosts
Host
A host is an organism that harbors a virus, parasite, mutual partner, or commensal partner, typically
providing nourishment and shelter.
Definitive Host
A definitive host is usually the main host. For digenetic parasites, it is the host for the adult stage and
for the completion of sexual part of life cycle.
Intermediate Host
An intermediate or secondary host is a temporary environment, but one that is essential for the
completion of a particular parasite's life cycle. Such as host is found only in the case of digenetic
parasites for the completion of larval stage, asexual reproduction, and for transmission to the
definitive host.
Accidental Host
An accidental host may be one that can function as the normal host, but is infected only occasionally
for some reason, for example due to the lack of exposure or means of transmission.
Vector
A vector is usually the intermediate host playing an active role in the transmission of the parasite.
Permissive Host
A permissive host is either a definitive, intermediate, or accidental host that allows the parasite to
complete its life cycle in part or the whole.
Non-Permissive Host
A non-permissive host, on the other hand, is a host organism other than true definitive host, which
receives the parasite but the parasite finds itself in a dead end.
Paratenic Host
A paratenic host or transport host refer to a host organism other than true intermediate host that
receives the parasite in the position of intermediate host so that the parasite is helped to go to the
definitive host.
For example Echinococcus granulosus normally passes to a dog through an intermediate host, such
as a goat or sheep. But the parasite, instead of passing through the intermediate host, may come to
infect a human being and remain, causing hydatiditis, and a dog has no chance to get it from a
person.
Reservoir hosts
Reservoir hosts are permissive host alternatives to definitive hosts, such that the infective stage can
be passed from the host to the population of the definitive host.

Adaptations to Parasitism
Parasitic adaptations are responses to features in the parasite's environment and this environment is
the body of another organism, the host. This seems to be a difficult environment to invade but those
organisms that have done so have often been very successful both in terms of numbers of
individuals and numbers of species. Blood and tissues seem to be harder to invade than the gut, as is
shown by the smaller number of blood and tissue parasites. This is probably in part related to the
difficulties of getting eggs to the outside from sites within the host. Almost all phyla have some
parasitic members (at least 50% of all species are parasites). None of the deuterostome phyla are
truly parasitic (echinoderms, chordates, chaetognaths). Whilst amongst the protostomes, the only
groups that have no known parasitic members are the ectoprocts, endoprocts, phoronids and
brachiopods.
Morphological Adaptations
1. Size: many parasites are large compared with their free-living relatives. This could be related to
increased egg production.
2. Shape: most parasites are dorso-ventrally flattened and this is related to the need to cling on to
the host. Fleas are laterally flattened and rely on escape through the hairs. Nematodes are the
obvious exception to the trend of flattening in parasites and parasitic nematodes, as a whole,
show little morphological specialization.
3. In parasites and particularly in endoparasites there is loss of locomotory organs.
4. A characteristic feature of many parasites is organs of attachment. Despite the wide variety of
parasites there are only two trends running through the evolution of attachment organs, the
development of either hooks or suckers. Suckers occur in such widely divergent groups as
protozoa, monogeneans, digeneans, cestodes, parasitic crustaceans and parasitic annelids.
Spines and hooks are present in many parasitic groups and the elaboration of spines or suckers
or both into an eversible proboscis has occurred in the cestodes, acanthocephalans, and the
acarines (ticks). Other types of attachment organ include claws in parasitic insects and the
ctenidia (comb organ) of fleas. Penetrative filaments occur in a number of groups of parasite
(Oxyurid nematodes, Microspora protozoans).
5. In many parasites, particularly endoparasites, there is often a reduction in the CNS and sense
organs.
6. In endoparasites, again there is a trend to reduce the gut and absorb nutrients through the
whole body surface.
7. In those intestinal parasites, which do not absorb nutrients through the body surface, there is
usually a thick cuticle. So helminths tend either to loose their gut and absorb nutrients through
their teguments, or else retain their gut and have a thick resistant cuticle.
8. In many parasites there is a tremendous elaboration of the reproductive organs, associated with
increased gamete production. Cestodes, for example, basically consist of a small head and neck
region and the rest is serially repeated gonads. Parasites can be described as being solely
adapted for reproduction.
9. Parasitic protozoa are in an essentially isosmotic environment and so lack a contractile vacuole.
10. In parasitic insects there are often elaborate tracheal trunks, so the insect can remain air
breathing even when it is in its host.

Life Cycle Adaptations
1. There is usually an increase in reproductive potential compared with free-living relatives.
Parasites usually produce more eggs and sperm than their free-living relatives do and there may
be a great elaboration of the reproductive organs.
Other adaptations, which increase egg production, are hermaphroditism and parthenogenesis,
where every individual produces eggs and loss of seasonal reproductive cycles, so eggs and
sperm are produced all the year round. Rapid maturation and extended life span also increase
total reproductive capacity.
The reproductive potential of the parasite can again be increased by asexual reproduction at
different stages of the life cycle. One of the best examples are the digeneans where a single
sporocyst can give rise to daughter sporocysts each of which can give rise to several generations
of redia, before the cercariae are produced. It has been estimated that the reproductive
potential of a single liver fluke (Fasciola hepatica) is four hundred million offspring in its lifetime.
2. Infection of secondary and tertiary hosts. This has three advantages:
a. Increased reproductive potential, since asexual reproduction can take place in the
alternative host.
b. It increases the range of the parasite in space and time. That is infection of more than one
host can increase the geographical range of a parasite, particularly if one host is say
terrestrial and the other aquatic. By infecting more than one host species the parasite can
survive periods when one host is temporarily scarce.
c. An intermediate host can channel the parasite towards its definitive host since the
intermediate host is frequently part of the final host's food chain or else closely related
ecologically.
3. There is a marked trend amongst the major parasitic groups to reduce the extent of the free-
living phase of the life cycle (this avoids the variable external environment).
4. Many parasites have no provision for infecting new hosts beyond the provision of large numbers
of eggs or larvae. However, the infective stages of many parasites show adaptations that help to
increase their chances of infecting a host. These include:
a. Behavioural responses to locate favourable environments.
b. Responding to chemical stimuli from their host.
c. Changing the behaviour of the infected intermediate host to increase the chances of them
being eaten by the final host.
5. Integration of life cycles. There are many ways in which the life cycle of a parasite becomes
integrated with that of its host, but they fall into two broad mechanisms:
a. Regulation of infection by the host. Many parasites require a specific pattern of stimuli from
their host before they are able to infect them. This is particularly clear in those parasites that
infect their hosts passively via the gut in the form of cysts or eggs.
Such stages may require pre-digestion with host enzymes and the presence of specific bile
salts as well as the correct pH, temperature, redox potential, pO2 and pCO2 before they can
hatch.
b. Regulation of the adult parasite by the host. That is reproduction of the parasite is controlled
by hormonal or physiological changes in the host (e.g. the periodicity of microfilariae,
reproduction in Opalina and Polystoma in the frog).

Immunological Adaptations
Vertebrates react to the presence of foreign material in their tissues by the production of a humoral
and cell mediated response and this depends on the ability of the host to recognise the difference
between self and non-self. In mammals it takes approximately 9 days for the immune response to
become fully effective, so any parasite that persists for significantly longer than 9 days must have
some mechanism for avoiding or mitigating the hosts immune response. These include:
1. Absorption of host antigen
2. Antigenic variation
3. Occupation of immunologically privileged sites
4. Disruption of the host's immune response
5. Molecular mimicry
6. Loss or masking of surface antigens
Biochemical Adaptations
1. Energy metabolism. The energy metabolism of adult helminth parasites is essentially anaerobic
and helminths characteristically breakdown carbohydrate into a range of organic acids such as
acetate, lactate, succinate, propionate and branched chain fatty acids such as 2-methylbutyrate
and 2-methylvalerate. The TCA cycle is usually reduced or modified and many parasites fix
carbon dioxide and have a partial reversed cycle with phosphoenolpyruvate playing a central
role.. The cytochrome chain in helminths is often modified.
2. The reduction in the TCA cycle and cytochrome chain results in a low ATP production/mole
glucose catabolised. In Ascaris, for example, you get 6ATP/mole of glucose, compared with 36
ATP/mole in aerobic tissues. This low ATP/mole of glucose is often compensated for in parasites
by high rates of glucose utilisation.
3. In keeping with the anaerobic nature of adult helminth metabolism there is no beta-oxidation of
fatty acids in adult helminths and only limited amino acid catabolism.
4. So helminths would seem to be well adapted to live in anaerobic or microaerobic sites within the
body such as the gut or lumen of the excretory system. What is not clear is why this essentially
anaerobic metabolism is also found in helminths such as schistosomes that live in aerobic sites in
the body (in this case the blood stream).
5. Synthetic reactions. In general the synthetic capacities of parasites are reduced when compared
with their free-living relatives. This could be related to the low ATP/mole glucose produced in
parasites or to the abundant source of nutrients in the parasite's environment.
6. Nutrient uptake. A number of parasites such as cestodes and acanthocephalans have no gut and
produce no digestive enzymes of their own. Instead they rely on their host's digestive enzymes
to breakdown food to low molecular weight compounds (amino acids, monosaccharides, fatty
acids) which the parasites then absorb through their teguments. The absorption mechanisms of
cestodes and acanthocephalans compete with the uptake mechanisms of their hosts intestine
for the available nutrients. The amino acid, monosaccharide and fatty acid uptake mechanisms
of cestodes and acanthocephalans (and digeneans) are kinetically very similar to those of the
vertebrate intestine. So although there is a reduction of synthetic and catabolic pathways in
parasites, there is an elaboration of transport mechanisms.

Conclusions
Many of the morphological and biochemical reductions found in adult helminths do not necessarily
apply to the free-living stages of the same parasite. Such stages often have well developed
locomotory organs and sense organs. Intermediate stages also usually have a complete TCA cycle
and cytochrome chain and possess a functional beta-oxidation sequence.
The morphological and biochemical reductions found in adult parasites can be considered as an
economy of effort rather than a degenerate condition. Why, for example, maintain the elaborate
structure of the TCA cycle in the adult parasite when it may not be necessary, since there are ample
supplies of carbohydrate available to the parasite from the host? The information required to
synthesise the TCA cycle or the beta oxidation sequence, as well as sense organs, has not been lost
by the parasite, since it is expressed in the larval stages. In the adult parasite, that particular part of
the genome is simply not being expressed, but it has not been lost. Correlated with his is perhaps
the observation that the amount of non-repetitive DNA in a parasitic nematode such as Ascaris is 3
to 4 times higher than in free-living species. The amount of non-repetitive DNA in digeneans and
cestodes is again several times higher than in free-living turbellarians. The amount of non-repetitive
DNA in an organism gives a measure of its heterogeneity and hence of its information content. The
parasitic groups have higher information content than their free-living relatives and this is
presumably a reflection of their more complex life cycles.
In contrast to animal parasites with their complex life cycles, parasitic plants show a reduction in
biochemical ability and morphological specialization at all stages of their life cycle. In consequence
the non-repetitive DNA content of parasitic plants is less than that of their free-living relatives.
Parasitic adaptations are all responses to particular features of the parasite's environment, and with
the exception of the host's immune response, the same features are also found in free-living
environments. So few if any 'parasitic adaptations' are not also found in free-living organisms.
1. Animals that live in fast flowing streams and are in danger of being swept away are frequently
flattened dorso-ventrally or laterally and have developed hooks or suckers as organs of
attachment.
2. Reduction of sense organs is common in organisms that live in caves.
3. Absorption of nutrients through the general body surface is common in soft-bodied marine
invertebrates and a number of them have lost their guts.
4. Much of the biochemical modification found in adult helminths is related to the anaerobic or
near anaerobic conditions found in the vertebrate gut. Anaerobic conditions occur frequently in
free-living environments, in mud, in waterlogged soil, in bivalves when they close up as the tide
goes out. The intermediary metabolism of invertebrates living in these places is often extremely
similar to the intermediary metabolism of gut parasites, involving carbon dioxide fixation, partial
reverse TCA cycles and the production of organic acids such as succinate and propionate.
5. Organisms that live in transient environments, such as rainwater pools, have, like parasites,
developed resistant and dispersal stages and are often capable of asexual reproduction.
6. A characteristic feature of parasites is their high reproductive potential. But other organisms
that have hazardous phases in their life cycles, such as planktonic larvae, produce vast numbers
of offspring. But even in parasites there is a relationship between fecundity and parental care.
The monogeneans for example produce few well-provisioned eggs.

Parasitic adaptations in Helminthes
The helminthes are modified morphologically as well as physiologically to alive in their particular
environments. These modifications depend on the degree of parasitism.
(A) Morphological Adaptations:

The structural modifications or adaptations of helminthes have taken place along two lines.
(1) Degeneration or loss of organs.
(2) Attainment of new organs.
(1) Degeneration:
Endoparasites undergo simplification of unused organs or parts. In helminthes, the loss particularly
involves the locomotory and digestive organs.
(a) Locomotory organs: The helminth parasites live in the body of the host. So locomotory organs
are quite unnecessary for them. So the locomotory organs are totally reduced except in larval forms.
(b) Alimentation: As the helminth parasites live on digested and semi digested food of the host,
there is reduction in their elimination and digestive glands. The digested materials are absorbed
directly in the body.
(c) Sensory organs: The sensory organs of helminthes are also simple structures. Absence of
complicated sensory structures can also be co-related to sedentary life in a sheltered habitat,
especially in the endoparasite.
(2) Attainment of New Organs:
Parasitic existence leads to modification of old structures and attainment of new structures helpful
in food absorption, protection, attachment and vast reproduction.
(a) Cuticle: The outer integument or cuticle of helminth parasites becomes highly modified and is so
adapted as to resist against the digestive juice, passage of food and for adhesion.
(b) Musculature: The well developed musculature in tape worms enables them to distribute their
elongated snake-like bodies through-out the length of the intestine of their host. Similarly, power of
locomotion enables the roundworms to counteract gut parasites and to maintain their position in
the intestine. The advantage is that the worms cam obtains with greater ease of the pre-digested
nutrients of the host.
(c) Organs for attachment: Helminthes are variously modified for adhesion to the body of their
hosts. Suckers are for ed i all parasitic flat or s’ foe adhesio . I so e Cestodes a d
nematodes, hooks or hook like structures also develop in or near the cephalic end which help in
attachment. In some helminthes, as in miracidium and cercaria, unicellular secretory glands develop
which help during penetration in to the host.
(d) Vast reproduction: The reproductive organs show significant development and adaptation to
parasitism. There is vast increase in the reproductive capabilities through greater egg production.

Life history usually includes several larval stages for multiplication and for easy and sure transfer
from one host to another.
The nervous system in parasitic helminthes and excretory system, particularly in trematodes, show
little deviation or adaptation to parasitic mode of life.
(B) Physiological Adaptations:

(1) Intracellular digestion: The fluke as tissue elements and inflammatory exudates and have
probably intracellular digestion.
(2) Osmo-regulation: The osmotic pressure of the parasitic worms remains less than or same as
that of their hosts, so that there is no difficult in exchange of water. Cestodes have well developed
water osmoregulatory system and their Ph tolerance is high.
(3) Anaerobic respiration: The intestinal parasites live in an environment completely devoid of
free oxygen. Their evolutionary adaptation has resulted in a very low metabolic rate which requires a
minimum amount of oxygen. Moreover the respiration is of the anaerobic type, consisting of
extracting oxygen from the food stuffs they absorb and assimilate through their cuticle. The manner
in which oxygen is liberated from food is not clearly understood. In the absence of free oxygen,
energy is obtained by the fermentation of glycogen,, which is broken by glycolysis, into carbon
dioxide and fatty acids. The glycogen and lipid contents in their body tissues are high, where as the
protein content is less?
(4) Anti enzymes: Most of the helminth parasites, particularly intestinal parasites, secrete anti-
enzymes in order to protect themselves from the gastric juices and digestive enzymes of hosts. In
some strange evolutionary manner their ancestors developed these vital antienzymes and are
quickly digested by the host. Some of the new medicines aim at nullifying the protective effect of
these antienzymes resulting in the digestion of the worms by their hosts. In cestodes the bladder of
the cysticerous larva is digested y the host’s digestive juices, ut the scole re ai s u affected. The
eversio of the scole is also accelerated y the actio of the host’s ile.
Successful adaptation to parasitism brings a sort of equilibrium between the host and parasite and
consequently there is reduction in pathogenicity and where this equilibrium is disturbed, the
parasite causes considerable clinical symptoms.

Parasitic adaptations in Nematodes
The flatworms are morphologically and physiologically adapted to the parasitic and free living forms.
Morphological Adaptations
1. Locomotory organs are reduced except in larval forms which are free living.
2. Alimentary canal is reduced but absent in taenia. Taenia absorbs the food through general body
surface.
3. Protection from digested juice if flatworms are intestinal parasites such as taenia and fluke
larvae. They are provided with thick cuticle covering and thus become resistant.
4. Apparatus of attachment or adhesive: Acetabulam or sucking cups are present in all flatworms.
In taenia and roundworm hooks are accessory attachment apparatus. In both rostellum is also
present for attachment. Unicellular secretory glands in miracidium and cercaria larvae secrete
the lytic substance to penetrate the host tissue. Cystogenous unicellular glands in termatode
larvae for the formation of cyst.
5. Reproductive organs most significantly developed for the parasitic life. Internal body is mostly
occupied by the gonads.
6. Flatworms are mostly hermaphrodite with few exceptions. Ovary is branched for the production
of large number of eggs.
7. Self fertilization is common than cross.
8. Body of the flatworm is provided with about 900 segments. Each segment is representing an
animal known as proglottid.
Physiological Adaptations
1. Respiration is anaerobic
2. Secrete anti-enzymes for the protection of their body (in case of intestinal parasites).
3. Reduction of pathogenicity and parasite tries to maintain a sort of equilibrium.
4. Roundworms have well developed water osmoregulatory system for controlling the water
quantity in the body.

Disease Casual Agent Motion by Transmission
1. Amoebiasis Entamoeba Histolytica ( sarcodina) Pseudopodia Water, Food
2. Giardiasis Giardia Lambila ( Mastigophora) Flagella Water, Contact
3. Trichomoniasis Trichomonas Vaginalis ( Mastigophora) Flagella Sexual,Contact
4. African Sleeping Sickness Trypanosoma Brucei ( Mastigophora) Flagella Tsetse fly ( Glossina)
5. American Sleeping Sickness T.Cruzi (Mastigophora) Flagella Triatomid bug ( Triatoma)
6. Leishmaniasis ( Kala - azar ) Leishmania Donovani ( Mastigophora) Flagella Sandfly
(phlemotomus)
7. Balantidiasis Balantidium Coli ( Ciliophora) Cilia Food, Water
8. Toxoplasmosis Toxoplasma Gondii (Sporozoa) NA Domestic Cats, Food
9. Malaria Plasmodium Spp. (Sporozoa) NA Mosquito ( Anopheles)
10. Babesiosis Babesia Microti ( Sporozoa) NA Tick ( Ixodes)

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Post Transcriptional Modifications
RNA polymerase cannot distinguish the coding region of the gene from the nonsense, so it
transcribes everything. Thus, one posttranscriptional task is to remove the nonsense DNA from the
original transcript, in a process called splici g. Eukaryotes also tack special structures o to the ′-
a d ′-e ds of their RNAs. The ′-structure is called a cap, a d the ′-structure is a string of AMPs
called poly (A). All three of these events occur in the nucleus before the mRNA emigrates to the
cytoplasm.
5’-Cap Formation
The starting point is the unaltered 5' end of an RNA molecule. This features a final nucleotide
followed by three phosphate groups attached to the 5' carbon.
1. One of the terminal phosphate groups is removed (by RNA terminal phosphatase), leaving two
terminal phosphates.
2. GTP is added to the terminal phosphates (by a guanylyl transferase), losing two phosphate
groups (from the GTP) in the process. This results in the 5' to 5' triphosphate linkage.
3. The 7-nitrogen of guanine is methylated (by a methyl transferase).
4. Other methyltransferases are optionally used to carry out methylation of 5' proximal
nucleotides.
Post-Transcriptional Changes 3rd Semester

1
The 5' cap has 4 main functions:
1. Regulation of nuclear export.

2. Prevention of degradation by exonucleases.
3. Promotion of translation (see ribosome and translation).
4. Promotion of 5' proximal intron excision.
3'-end processing and polyadenylation
Polyadenylation is the addition of a poly (A) tail to an RNA molecule. The poly (A) tail consists of
multiple adenosine monophosphates; in other words, it is a stretch of RNA that has only adenine
bases. The 3'-most segment of the newly-made RNA is first cleaved off by a set of proteins; these
proteins then synthesize the poly (A) tail at the RNA's 3' end. The poly (A) tail is important for the
nuclear export, translation, and stability of mRNA. The tail is shortened over time, and, when it is
short enough, the mRNA is enzymatically degraded.
Mechanism
The cleavage is catalyzed by the enzyme CPSF. The binding site for CPSF contains the sequence
AAUAAA on the RNA. Two other proteins add specificity to the binding to RNA: CstF and CFI. CstF
binds to a GU-rich region. CFI recognizes a third site on the RNA the set of UGUAA sequences.
When the RNA is cleaved, polyadenylation starts, catalyzed by polyadenylate polymerase.

Polyadenylate polymerase builds the poly (A) tail by adding adenosine monophosphate units from
adenosine triphosphate to the RNA, cleaving off pyrophosphate.
Another protein, PAB2, binds to the new, short poly (A) tail and increases the affinity of
polyadenylate polymerase for the RNA. When the poly (A) tail is approximately 250 nucleotides long
the enzyme can no longer bind to CPSF and polyadenylation stops, thus determining the length of
the poly (A) tail.
RNA Splicing
In the process of splicing, the introns are removed from the primary transcript and the exons are
joined to form a continuous sequence that specifies a functional polypeptide.
Almost all the bacterial RNA is made up of continue stretches of exons but most of eukaryotes
consist of stretches of noncoding introns. Before the mRNA molecules are used in the cells the
introns must be removed and the exons must be spliced together.
The most of mRNA transcript are spliced by a large complex called spliceosome whereas some
introns are capable of self-splicing. These self-splicing introns are divided into two classes the Group
I introns and Group II introns.
Both group II introns and introns spliced by the spliceosome contain an adenine in the mid of intron
called ra ch poi t site. These i tro s also co tai a gua i e at ’ e d called ’ splice site a d
a other gua i e at ’ e d called ’ splice site.

2
Group II introns self-splicing
I the first reactio the ’ OH of ra ch poi t site of ade i e attack the phosphorus of guanine of
the ’ splice site. The reactio is tra sesterificatio i hich the phosphodiester li kage of the ’
spliced site is replaced with the new phosphodiester linkage between the branch point adenine and
phosphorus of gua i e of ’ spliced site.
In the second reaction the e ly li erated ’ OH of ’ e o attack the phosphorus of ’ e o splice

site. This tra sesterificatio reactio joi s the ’ a d ’ e o s a d li erates the i tro . The li erated
intron is lariat shape.
Spliceosome Splicing
The spliceosome consists of about 150 proteins and 5 RNA molecules called snRNA. Each of these
RNA molecules is complexes with several proteins to form complex called small nuclear ribonuclear
proteins (snRNPs).
Introns spliced by the spliceosome co tai the co served se ue ces at ’ spliced site a d ’ spliced
site in addition to the bases directly involve in the reaction. The highly conserved sequence is GU at
’ splice site a d AG at the ’ splice site a d A at the ra ch site.
1. First the U1 snRNP recog ize the ’ splice site usi g ase pairi g.
2. The the U AF U Au iliary Factor protei i d to the ’ splice site. The the su u it of U AF
i ds to the e d of ’ splice site.
3. Then U2AF recruit the BBP (Branch point Binding Protein) and it binds to the branch site. This
will form the early complex.
4. The U2 snRNP then replaces the BBP at branch site. This is called the A complex. The branch site
at that time forms a budge.
5. Then U2AF leaves the complex. The U4, U5, and U6 snRNPs joins the complex converting it into
B complex.U1 then leaves the complex and U replaces at ’ site. U is tha released fro the
complex allow U6 to interact with U2 producing the active site.

3
6. The ra ch site A attack the ’ site for i g a three ay ju ctio . U helps i ri g the ’ a d ’
site together by making transesterification reaction.
7. The spliceosome is than released the mRNA product and the lariat intron.

4
Group I introns self-splicing
Group I introns are capable of folding around themselves forming a secondary structure which
further fold into a tertiary structure. This tertiary structure contains two important features, a
guanine binding pocket and an internal guide sequence (IGS).
The IGS is capa le of ase pairi g ith the e o s at ’ e d of the RNA olecule. The guanine pocket
is capable of binding any guanine containing ribonucleotide including guanosine, GMP, GDP, GTP or
an RNA molecule that terminates with the guanine residue.
To begin splicing the free nucleotide containing guanine nucleotide binds to the guanine pocket. The
’ OH of this gua i e attack the ’ e d of the phosphate of the i tro . This tra sesterificatio
reactio fuses the gua i e to the free ’ e d of the i tro .
The free ’ OH of the e o tha attack the ’ e d of a other e o . This fuses the exons and releases
the introns.
RNA Editing
The sequence of nucleotides in mRNAs in coding regions can be modified after transcription in quite
dramatic ways by a phenomenon known as RNA editing. RNA editing occurs by two distinct
mechanisms:
Substitution Editing
The chemical alteration of individual nucleotides (the equivalent of point mutations) is called
substitution editing. These alterations are catalyzed by enzymes that recognize a specific target
sequence of nucleotides (much like restriction enzymes):
1. Cytidine deaminases that convert a C in the RNA to uracil (C-U Editing). An example of C-to-U
editing is with the apolipoprotein B gene in humans. Apo B100 is expressed in the liver and apo
B48 is expressed in the intestines. The B100 form has a CAA sequence that is edited to UAA, a
stop codon, in the intestines. It is unedited in the liver.

5
2. Adenosine deaminases that convert an A to inosine (I), which the ribosome translates as a G.
Thus a CAG codon (for Gln) can be converted to a CGG codon (for Arg) (A-I Editing).
Insertion/Deletion Editing
The insertion or deletion of nucleotides in the RNA is called as insertion or deletion editing. These
alterations are mediated by guide RNA molecules that Base-pair with the RNA to be edited and Serve
as a template for the addition (or removal) of nucleotides in the target RNA. It is also called as pan
editing.
1. First the base pairing of unedited primary transcript occurs with the guide RNA (gRNA). The
gRNA contains complementary sequences to the regions around the insertion/deletion points.
By the base pairing of gRNA and primary transcript a double stranded region is formed. Now the
editosome attaches to that region.
2. The editosome a large multi-protein complex which catalyzes the editing. The editosome opens
the transcript at the first mismatched nucleotide and starts inserting uridines. The inserted
uridines will base-pair with the guide RNA, and insertion will continue as long as A or G is
present in the guide RNA and will stop when a C or U is encountered. The inserted nucleotides
cause a frameshift and result in a translated protein that differs from its gene.

6
3. The mechanism of the editosome involves an endonucleolytic cut at the mismatch point then U-
transferase adds Us from UTP in the transcript.
4. A U-specific exoribonuclease removes the unpaired Us. After editing has made mRNA
complementary to gRNA, an RNA ligase rejoins the ends of the edited mRNA transcript.
Applications of RNA Editing
1. It is a mechanism to increase the number of different proteins available without the need to
increase the number of genes in the genome. So it can create proteins with slightly different
functions to use in specialized circumstances.
2. RNA editing may help protect the genome against some viruses and damage by
retrotransposons.
Nuclear export of mRNA
The nuclear export of mRNA transcripts can be broken down into distinct stages: first, pre-mRNA is
transcribed in the nucleus, where it is processed and packaged into messenger ribonucleoprotein
(mRNP) complexes; second, the mRNPs are targeted to and translocate through nuclear pore
complexes (NPCs) that are embedded in the nuclear envelope; and third, the mRNPs are
directionally released into the cytoplasm for translation.
Early mRNA processing events: assembly of mRNPs
The formation of an export-competent mRNP begins at transcription. During transcriptional

elongation, the nascent mRNA transcript is bound by a number of factors, some of which are part of
the family of heterogeneous nuclear ribonucleoproteins (hnRNPs). hnRNPs are highly abundant
nuclear RNA-binding proteins that are essential for various steps in the mRNA life cycle, including
packaging, export and translation.
Key steps in mRNA processing
There are four main processing events that occur during the formation of a mature mRNA transcript:
’ cappi g, splici g, ’-end cleavage and polyadenylation. Each of these modifications impacts export
in two ways. First, if an mRNA is not properly processed, it will not be exported and instead will be

7
targeted for degradation. Second, the processing events serve as triggers to recruit protein factors
that are necessary for export.
The first change that a nascent pre- RNA tra script u dergoes is ’ cappi g. Whe a tra script
reaches about 20-30 nucleotides in length, a 7- ethylgua osi e cap is added to the ’ e d, hich
protects the nascent pre-mRNA from degradation. The ’ cap is ou d y the cap i di g co ple .
Next, a transcript undergoes splicing, and a set of proteins is simultaneously deposited at the site of
exon fusion. These proteins are defined as the exon-junction complex (EJC). Capping and splicing are
both important for the recruitment of the transcription-export (TREX) complex. The TREX complex is
highly conserved and is essential for mRNA export. It consists of the THO complex and a set of export
factors that include Sub2 (an ATP-dependent DEAD-box RNA helicase) and UAP56 (also known as
HEL) and ALY (also known as REF) in human cells.
The THO complex associates with the nascent mRNA during transcription, and participates in both
transcription elongation and mRNA export. Once it is associated with the mRNA, the THO complex
then recruits the remaining TREX-complex components. The final pre-mRNA processing events are
’-end cleavage and polyadenylatio . A polyade ylatio site is recog ized i the ’-untranslated
region (UTR), resulting in pre-mRNA cleavage immediately downstream. The poly (A) tail is added by
a poly (A) polymerase and bound by a poly (A)-binding protein.
Recruitment of mRNA export factors, nuclear quality control and targeting to the NPC
The trafficking of most cargos that move between the nucleus and the cytoplasm involves
karyopherin-mediated receptors, and transport directionality is determined by a gradient of the
GTP-bound state of the small GTPase Ran. The Nxf1-Nxt1 heterodimer is recruited to the mRNP via
the TREX component ALY. ATP hydrolysis by UAP56 triggers the transfer of the mRNA to ALY and
results in an mRNP with bound export receptor.
Docking to and passage through the NPC
Following completion of proper nuclear processing and the recruitment of an export receptor, an
mRNP are considered to be export competent. This export-competent mRNP is specifically targeted
to the NPC via its export receptor.
The export receptor docks at the NPC by interacting with a discrete class of NPC proteins known as
the FG-Nups. Both the karyopherin receptors and Nxf1- Nxt1 mRNA export receptor directly bind to
the FG. Binding of the export receptor to the FGNups is required for NPC docking and translocation
of the mRNP. The binding of transport receptors to the FG-Nups is thought to mediate the
movement of the mRNP through the NPC by some type of facilitated diffusion mechanism.
Release into the cytoplasm and links to translation
The final step of mRNP translocation through the NPC involves directional release into the
cytoplasm. Cytoplasmic release is determined by the function of two conserved, essential mRNA
export factors, Dbp5 and Gle1, and soluble inositol hexakisphosphate (IP6). Dbp5 is an RNA-
dependent ATPase of the DEAD box protein family, and binds to the NPC cytoplasmic face by
interacting with the NPC protein Nup214. Gle1 specifically binds to IP6 and docks to a neighboring

8
NPC protein hCG1. As an mRNP reaches the cytoplasmic side of the NPC, it associates with Gle1 and
Dbp5. IP6-bound Gle1 stimulates the ATPase activity of Dbp5, thereby converting Dbp5 from an ATP-
to ADP-bound state.
It is thought that a conformational change induced by the Dbp5-ATP to Dbp5-ADP switch triggers the
removal of a subset of proteins from the mRNP, including the export receptor. As the mRNP enters
the cytoplasm, specific cytoplasmic mRNA binding proteins are incorporated.

9
z>
Roll No. Total Pages : 2
3524
MDQ/DX
ZOOLOGY
(Molecular Endocrinology)
Paper-XIV
Time : Three Hoursl fMaximum Marks : 70
Note : Question No" 1 is compulsory. Answer four questions
more, selecting tvvo from each section. All questions carry
14 marks each.
Compulsory Question
1. (a) Write the names of any three cholesterol derivatives of
reproductive importance. Give their molecular sffucture
as well.
(b) What is glycosylation and how does it differ from
glycation ? Give an exampie of each.
(c) Write the full version of the following :
(i) FSH
(iD ACTH
(iii) IP3
(iv) DAG.
(d) What are the eicosanoids and what are their forms of
hormonal importance? Explain.
(e) Write a brief note on the role of cholecystokinin in
digestive physiology.
(0 Differentiate between the hormonal defecte acromegaly
and dwarfism.
(g) Write a note on the importance of NO ( = nitric oxide)
as a hormone. 7 x7=tr4
3524fi001KD1764 IP.T.G
SECTION-A
2. Define a hormone, and write about the criteria used in the
classification of hormones. Add suitable examples. 14
3. What is signal transduction ? Describe one such mechanism
adopted by lipophilic group of hormones for affecting their
action. l4
4. Write brief notes on the following :
(i) Heat-shockProteins.
(ii) G-Proteins or Calmoduline. 7,7
5. Write notes on the following :
(i) Feedback control of hormone secretion.

(ii) Placental hormones.
(iii) Kidney as an endocrine organ. 5,5,4
SECTTON-B
6. Describe in detail, what possible physiological-cum-hormonal
changes are most likely to ensue, if a body (living) is in
short supply of carbohydrates. l4
7. Write short notes on the following :
(i) Leptin and its physiological effects.
(ii) Genes in honnonal disorders. 7,7
8. Write notes on the following : 7,7
(a) Nucleotides and their physiological functions.
(b) Role of DNA-binding proteins in gene transcription.
7,7
9. Explain, with the help of examples, the concept of 'Parallel
Pathway'. 14
3521fiOjlKD/764
\
Fnll No. Total Pages : 2
MDQ/D09 367 4
MOLECULAR ENDOCRINOLOGY
Paper-XIV
Time : Three Hoursl [Maximum Marks : 70
Note : Q. No. I is compulsory. Of the remaining questions,

answer four questions, selecting two questions from each
section.
(Compulsory Question)
1. Write concise notes on the following :
(a) Role of insulin in blood-glucose levels.
(b) Structural domains of nuclear receptors.
(c) Hormone-transport in plasma.
(d) Second messinger concept.
(e) Cross talk concept.
(D Hormone-nucleic acid interaction.
(gl Genomic action of hormones. 2x7=14
SECTION_A
2. Describe the pathway adopted by a body during the synthesis
of prostaglandin D. Add a short note on the biological activity
of this product. I4
3. Describe in detail biosynthesis of any pf,ptide hormone with

its modification(s) at the level of transcription and/or post-
transcription. 14
4. Discuss in details the role of hormones in the generation

and transduction of cell signals. 14
3674t50/KDt499 lP.T.O.
5. Write explanatory notes on the following :
(at Testicular steroidogenesis.
(b) Role of tyrosine in the synthesis of non-epinephrine.
7x2=14
SECTION-B
6. Discuss in detail the role of hormones in the regulation
of lipid metabolism. Add a short note on the role of the
hormone leptin. 14
7. Write an essay on Genetic bases of Hormonal Disorders.

t4
8. Enumerate some important sequence-specific DNA binding

proteins and explain their role in cell differentiation. 14
9. Write brief notes on the following :

(a) Non-genomic action of hormones.
(b) Interactive pathways (Parallel pathway). lx2=14
3674t50/KDt499 ,
Roll No. Total,Pages : 2
MDQ/D08 3,614
MOLECULAR ENDOCRINOLOGY
Paper*XIV
Tiine : Thtse Hours] tMaximum Marks : 70
Ndte : Qucstion No. I is cbmpulsory. Attempt y've qirestions in
all, sclecting t$'o questions from each Section.
ComPulsorY Question
l. Explain thc following :-
(i) Amino-acid derived hormone.
(ii) EndocrinoiogY.
(iii) Prostaglandins.
(iv) C-AMP.
(v) lnsutin secretion.
. (vi) Ca"*.
(vii) Lipase. 2x7=14
SECTION-A
2. Describe the rolcs of IP, and DAG as second messengcrs'
7+7
3. Discuss the role of cell structure in extracellular and

intracellular communication. 14
4, Describe the molecular mechanism of action of steroid

hormone. 14
(a) Post-translational'rnodifications. 7
(b) Nuclear receptors. 1
367460KD1750 lP.T,O.
SECTION-B
6; .
Discuss endocrine regulation of Lipid rnetabolism 14
7. Describe genetic basis of Hormona! disorders. 14
8. Describe the genomic and non-genomic action of a Peptide

hormone. t4
(a) Protein metabolism rcgulation. 7

(b) Zn.finger. 7
3674,50/KDl7s0
{)z?-
(
MDQ/DX 3523
MOLECULAR BIOLOGY
Paper - XIII
Time : Three Hoursl Maximum Marks : 70
Note : There are in all nine No. I

is compulsory.
questions. Q.
Remaining eight questions are from Section-A and
Section-B Gor each). The candidates is to attempt ,l,vo
questions from each section.
Note : All the /en questions are to be answered briefly :
l. (a) What is the -process in which DNA is changed ?

(b) What are the two main mechanisms in Mutations?
(c) In eukaryotic genome what makes exons different from
introns ?
(d) How is Transcription different from Translation ?
(e) What is the advantage of Gene silencing ?
(0 What are hotspots of mutation ?
(g) In which mode of replication does a parent circular

DNA molecule yield two daughter circles ?
(h) What two reactions are coupled when Nick translation
occur ?
(, What is m-RNA ?
0) Define Microcloning. lx10=10
3523tr00tr<D/1797 lP.T.O.
SECTION-A
2. Give an account of the historical developments in tha rrea
of Molecular Biology. 15
3. (a) Write in detail the mechanism of DNA replication. 1r/2

(b) Make a comparison of Eukaryotic and Prokaryotic
DNA replication. 7r/z
4. (a) Enlist various enzymes along with accessory proteins

associated in DNA replication. 7r/z
(b) Why has DNA replication been called "the most
complex process in a cell"? Discuss. 7Yz
5. What is the molecular mechanism of Gene silencing ?

Discuss in detail the post-transcriptional gene silencing. 15
SECTION-B
6. (a) What is a Genetic code ? Discuss in detail the role of
genetic codes in gene translation. 7y2
(b) Discuss the- similarities and differences between
Prokaryotic and Eukaryotic ffanslation. 7Y2
7. Give a detailed account of Initiation, Elongation and

Termination mechanism in protein synthesis. 15
8. (a) Discuss the molecular mechanism of disruption

of RNA structure and capping. lVz
(b) Give a detailed account of biochemistry of different
kinds of Ribozymes. 1Y2
9. Write in detail the molecular mechanism of the inhibition of

Splicing and Polyadenylation. 15
3523fiOOlKDll797
a
. MDQ/Do9 3673
MOLECULAR BIOLOGY
Paper-XIII
Note : Q. No. I is compulsory. Attempt rl4lo questions from

each Section, i.e., Section-A and Section-B.
1. Answer the following in about 20 words each :
(a) Why multiple origins of replication are required in

eukaryotes ?
(b) What do you mean by RNA editing ?
(c) Define Primosome and Replisome.

(d) What are the functions of miRNA and snRNA ?
(e) What is the role of capping and polyadenylation in
, RNA?
(f) Define Shine-Dalgarno sequence. Why initiated
formylated tRI{Amet is better than non-formylated in
prokaryotic translation ?
(g) What is DNA photolyase ?
(h) What is RecBCD complex ?
(i) What are hammerhead ribozyme and why it is

named so ?
() Define Genetic counselling. I x 10=10
3673t50tKDt498 lP.T.O.
SECTION-A
2. (a) How might continuous and discontinuous modes , ^
DNA replication be distinguished experimentally ?
(b) Enlist the proteins and enzymes that are involved in
DNA replication in E. coli and describe their known or
putative functions. 7+8
3. (a) Give an account of replication in eukaryotes.

(b) Describe post-transcriptional modifications. 9+6
4. (a) Give brief description on mRNA stability.

(b) Explain the mode of transcription termination in
prokaryotes and eukaryotes. 5+10
5. Write notes on any two of the following :
(a) Gene silencing.

(b) Mechanism of splicing.
(c) Transcriptional factors. 7r/x1Vt
SECTION-B
6. (a) How translation is initiated and terminated in
prokaryotes and eukaryotes ? Highlight the crucial
differences between both the systems.
(b) What do you mean by Genetic code ? Describe its
properties and write the various initiation and stop
codons and mention those codon differing in
mitochondrial and cytoplasmic nuclear DNA. 8+7
7. Write short notes on any two of the following :
(a) AFI?.
(b) FISH.
(c) Disease resistance molecular marker. 7r/t+lYz
367v5AKDt498 2
8. (a) Differentiate among Base excision, Nucleotide excision'
I
and Mismatch repairs.
(b) Elucidate the concept of antisense, and explain the
mechanism of antisense molecules with suitable
examples. 5+10
9. Explain the various types of ribozyme$, designing strategies

and applications. 5+5+5
36731sotKDt498
I-
( tt xo. Total Pages : 5
MDQ/DX 3525
PARASITOLOGY
Paper-XV
Time : Three Hours] [Maximum Marks : 70
Note : (i) Attemptfve questions, Question No. I is compulsory.

(ii) Rest /orzr questions are to be attempted, selecting
fwo questions from each section.
(iii) All questions carry equal marks.
1. Tick (/) the right answer:
(i) Of two hookfiorm human species:
(a) Ancylostoma is more pathogenic
(b) Necator is more pathogenic
(c) Both are equally pathogenic
(d) None is pathogenic.
(ii) Cysticercosis is caused by
(a) Diphyllobothrium
(b) Echinococcus
(c) Cysticercus
(d) Hymenolepis.
(iii) The. in{ective form of Fasciola hepatica is
(a) Egg
(b) Cercaria
(c) Sporocyst
(d) Metacercaria.
3525/rOO(KDt2069 lP.T.O.
t
(iv) In Plasrnodiurn vivax, schizogony lasts
(a) 48 hours
(b) 56 hours
(c) 62 hours
(d) 72 hours.
(v) Parasites have evolved from
(a) Free-living ancestors
(b) Symbiots
(c) Commensals
(d) Vectors.
(vi) Trophozoite stage of Giardia intestinalis multiplies ln
(a) Stomach
(b) Oesophagus
(c) Rectum
(d) Intestine.
(vii) Hypertrophy denotes
(a) Increase in cell size
(b) Cell destruction
(c) Accelerated rate of cell division
(d) None of these.
(viii)Vector for scrub typhus is
(a) Ensliniella
(b) Demodex
(c) Hydryphantes
(d) Trombicula.
3525/t00tKD/2069
1-ix) Fahrenholz's hypothesis denotes
(a) Hosts belonging to a large taxonomic group, will
harbour the greater diversity of parasites.
(b) The comnton ancestors of modern parasites were
themselves parasites of the common ancestors gf
present-day. hosts.
(c) The more evolutionarily specialized the host group,
the more specialized are the parasites.
(d) None of these.
(x) Schistosome cercarial dermatitis is caused by
(a)' Parasite secretion
(b) Parasite movement
(c) Mechanical interference
(d) Necrosis.
(xi) Vector of Japanese encephalitis is
(a) Aedes cabalus
(b) Culiseta .melanura
(c) Mansonia africana
(d) Culex tritaeniorhynchus.
(xiil Toxins produced by Yersinia pestis act on
(a) Golgi bodies
(b) Chromosomes
(c) Nucleus
(d) Mitochondrial membranes.
(xiii) Host's'hormones
(a) Make the parasite resistant to anthelmintics
(b) Make the parasite non-motile
(c) Kill the parasite
(d) Influence sexual development of the parasite.
3525t100/1ot2069. 3 lP.T.O.
!
(xiv)Densities and distribution of parasites are affec['J by
(a) Biologic factors
(b) Physical factors
(c) Chernical factors
(d) All the above. lxl4=14
SECTION_A
2. (i) Define the term Host. Describe with suitable examples,
the different types of hosts.
(ii) Define the term Parasite. Describe with suitable
examples, the different types of parasites. 7,7
3. Give an account of structural and functional modifications

among parasitic helminths. 14
4. Write short noteS on the following :

(i) Host cell reaction.
(ii) Biochemical responses in parasitism.
(iii) Host tissue reaction. 5,5,4
5. Write short notes on any three of the following :
(i) Visceralleishmaniasis.
(ii) Vivax malaria.
(iii) Giardiasis.
(iv) Amoebic dysentery. 5,5,4
SECTION-B
6. Write short notes on any three of the following :
(i) Hydatid disease.

(ii) Plague.
(iii) Rabics.
(iv) Q fever. 14
3525t100/KDt2069 4
7.( '' Write short trotes on the following :
(ii) Isolatiotr o1' Parasitc popr-rlatious'

(iii; Host parasite coevollttion' 5'5'4
8. Explain briefly any thrce of the following :
(i) Hookworm disease'

(ii) Filariasis.
(iii) Ascariasis.
(iv) Paragonimiasis. 5'5'4
g. Write short notes on the following:

(i) Mosquitoes and diseases'
(ii) Fleas and diseases'
. (iii) Blood-sucking mites' 5'5'4
35251100/KD/2069 5
Rolr No.
l
Total Pages : 3
MDQ/Doe 367 5
PARASITOLOGY
Paper-XV
Note : Attempt fue questionsin all. Q. No. I is compulsory.

Rest four questions ard to be attempted, selecting two
questions from each section. All questions carry equal
marks.
1. Answer the following in short :
(a) What is Fahrenholz's rule of evolution of parasitism ?
(b) Write four Helminthic diseases in man.

(c) What type of host specificity is found in fleas ?
(d) Name causative agent of Elephantiasis in man.

(e) Name two spp. of Liverfluke and its infective stage.
(0 Namo the blood fluke found in the urinary bladder
of man.
(g) [n Plasmodium falciparum, gametogony lasts for how
manydays? ' 2x7=14
SECTION-A
2. (a) Describe cellular and humoral immune response in
vertibrate host. 7
(b) How do parasites evade host immunity ? 7
3675t50/KD/500 IP.T.q.
3. (a) Describe hormonal effect on parasitism of
digestive tract. (7
(b) Discuss the physiological adaptations of nematodes
to parasitic mode of life,
Discuss the life-cycle, pathogenicity and control of

Trypanosomiasis in man. 14
5. (i) Define the term Host. 1
(ii) Describe the role of regular and irregular hosts in

5
(iii) Write notes on the following :
(a) Carrier. 2
(b) Vector. 2
(c) Reservof host. 2
(d) Primary host. 2
SECTION_B
(a) What is Parasite-host specificity ? Discuss the various
kinds of Parasite-host specificity. 7
(b). What is Progressive and Retrogress;ve evolution of

parasitism ? 7
7. (a) Write different types of adhesive organs of

Cestodes. 8
(b) Draw neat and well labelled diagram of cercarial

larva. 6
3675t50tKD/500
8. Describe the life-cycle, pathogenicity and control of
. Echinococcs granulosus. t4
9. Give an account of the following :
(i) Brucellosis 5
(ii) Fasciolopsis buski. 5
(iii) Amoebiasis. 4
3675t50/KD/500 I
RolI No. Total Pages : 2
3527
MDQ/DX
REPRODUCTION AND AGEING_I
Paper-XVI (ii)
Time : Three Hours] [Maximum Marks :70
Note : Attempt fve questions in all. Q. No. 1 is compulsory.
Attempt rruo questions each from Section A and Section B.
Compuslory Question
1. Explain the following :
(a) hCG.
(b) Sertoli cells.
(c) Medullarin
(d) Estrous.
(e) Mulation theory of Ageing.
(f) DNA acetylation.
(g) Age pigment. 2x7=14
SECTION-A
2. Describe the endocrine regulation of follicular $owth in
mammals. 14
3. Define Atresia. Explain its causes and elaborate on its

molecular mechanism. 14
4. Discuss Germ line-soma interactions during early

development. 14
3527t50tKDn504 lP.r.o.
5. Write notes on any two of the following :
(a) Testosterone.
7
(b) Ovularion.
7
(c) Neuro-hormones. 7
SECTION-B
6. Discuss general functional impairment during
ageing and
explain changes in behaviour.
t4
7. What are Isoenzymes ? Describe isoenzyme pattern
during
different stages of life with special reference
ro ageing. 14
8. Discuss Free Radical theory of ageing.
ru
9. Write notes on any two :
(a) Diet and Ageing.

7
(b) Anti,ageing Hormones.
7
(c) Wrinkling of Skin and Ageing. 7
3527/50/KDt1s04
1
MDQ/Do9 3677
REPRODUCTION AND AGEING_I
Paper-XVI (ii)
Note : Attempt lve in all. Q. No. I is compulsory.

questions
Attempt ,)4/o questions each from Section A and
Section B.
1. Explain the following :
(a) PMSG.
(b) Origin of PGCs.
(c) Leydig cells.
(d) Atresia and Fertility.
(e) Isoenzymes.
(fl Estrogen and Ageing.
(g) IDNA methYlation. 2x7=14
SECTION_A
) Discuss hypothalmo-pituitary-gondal axis in relation to
reproduction. t4
3. Describe the different types of cell to cell interactions in

mammalian testis. t4
4. Define Ovulation, and explain molecular mecnanism of

Ovulatory .process. T4
3677/50tKD/502 [P.T.O.
5. Write notes on any two :
(a) Apopotosis 7
(b) Germ cell migration. 7
(c) Follicular growth. 7
SECTION-B
6. Describe Chronological age and Biological age, and
explain how diet and exercise keep one young ? t4
7. Discuss enzyme changes during the process of ageing. 14
8. Describe the telomerase theory of ageing. 14
9. Explain (Any wo) :

(a) Collagen cross linking. 7
(b) Somatic mutation theorY. 7
(c) Age reversal effects of hormones. 7
3677t50tKD1502
Prostaglandin
A prostaglandin is any member of a group of lipid compounds that are derived enzymatically from
fatty acids and have important functions in the animal body. Every prostaglandin contains 20 carbon
atoms, including a 5-carbon ring.
Prostaglandins are not hormones, but autocrine or paracrine, which are locally acting messenger
molecules. They differ from hormones in that they are not produced at a discrete site but in many
places throughout the human body.
The name prostaglandin derives from the prostate gland. The prostaglandin was first isolated from
seminal fluid in 1935 by the Swedish physiologist Ulf von Euler. It was believed to be part of the
prostatic secretions. (In fact, prostaglandins are produced by the seminal vesicles). It was later
shown that many other tissues secrete prostaglandins for various functions.
In 1971, it was determined that aspirin-like drugs could inhibit the synthesis of prostaglandins.
Types of Prostaglandin
The following is a comparison of different types of prostaglandin, prostacyclin I2 (PGI2),

prostagla di E PGE , a d prostagla di F α PGF α .
PGI2: It has following receptors and functions:
IP: Vasodilation, inhibit platelet aggregation, bronchodilatation
EP1: Bronchoconstriction, GI tract smooth muscle contraction
EP2: Bronchodilatation, GI tract smooth muscle relaxation, vasodilatation
PGE2: It has following receptors and functions:

EP :↓ gastric acid secretio , ↑ gastric ucus secretion, uterus contraction (when pregnant), GI
tract s ooth uscle co tractio , lipolysis i hi itio , ↑ auto o ic eurotra s itters, ↑ platelet
response to their agonists a d ↑ atherothro osis i vivo
Unspecified: Hyperalgesia, pyrogenic
Page No. 1 of 5 Prostaglandin 3rd Semester

PGF2α: It has following receptors and functions:
FP: uterus contraction, bronchoconstriction
Biosynthesis

Functions of Prostaglandins
They have a variety of physiological effects on the body including:

1. Activation of the inflammatory responses at the sites of damaged tissue, and production of pain
and fever. When tissues are damaged, white blood cells flood the site to try to minimize tissue
destruction. Prostaglandins are produced as a result.
2. Blood clots form when a blood vessel is damaged. A type of prostaglandin called thromboxane
stimulates constriction and clotting of platelets. Also the opposite happens and prostaglandin 12
(PG12) is produced on the walls of blood vessels where clots should not be forming. (The body is
very, very clever. It knows what to do, where to do it and when.)
3. Certain prostaglandins are involved with the introduction of labour and other reproductive
processes, and the role of fertility. PGE2 causes uterine contractions and has been used to
induce labour.
4. Prostaglandins are involved in several other organs and systems such as the gastrointestinal
tract, cell growth and the immune system response.
Prostaglandins and Pain Messengers
Prostaglandins serve a variety of regulatory functions within the body. One of these functions is to
assist the transmission of pain signals to the brain so that you are readily alerted that damage or
dysfunction has occurred within the body.
When damage occurs to the body, certain prostaglandins are formed from the unsaturated fatty
acids released by damaged cells. The production of a particular group of prostaglandins amplifies the

amount of pain experienced by serving as a pain activator. They increase the sensitivity of the nerves
to pain impulses. By reducing the synthesis of prostaglandins, the amount of pain stimuli sent to the
brain is correspondingly reduced. This is usually achieved by the use of aspirin which blocks the
production of pain messenger prostaglandins.
Prostaglandins and Inflammation
Prostaglandins are known as local hormones - they are released from cells and bring about changes
in neighboring cells that carry specific prostaglandin receptors in their membranes.
The influence which prostaglandins have depends upon the type of tissue they are acting upon. Such
action may be direct, or as a result of modifying the actions of other signaling molecules.
As well as signaling and influencing pain messengers to the brain, prostaglandins will interact with
other chemicals in the body when there is damage. They will also intensify the effects of other
chemical mediators such as histamine.
Acting in concert these substances can bring about vasodilatation and an increase in the
permeability of capillaries supplying the damaged area, encouraging the migration of phagocytes
(Phagocytes are leukocytes - white blood cells - that engulf invading micro-organisms, and then kill
them. They are part of our natural defense against infection) from the blood through capillary walls
into the damaged tissue. As a result of these changes, the blood supply to the area increases, the
tissues swell, causing inflammation and pain subsequently occurs.
Prostaglandins and Womb Contractions
Primary dysmenorrhea (painful periods) is caused by cramping in the uterine muscles — the uterus is
a uscle a d like all uscles it co tracts a d rela es! Wo e do ’t usually feel these uscles
contract, unless it is a particularly strong contraction. With endometriosis the pain associated with
menstrual cramps is usually very intense and painful. During a contraction, blood supply to the
uterus can be temporarily cut off. This deprives the muscle of oxygen, which causes pain. But why do
the uterine muscles contract?
It is caused by the series two prostaglandins. Series two prostaglandins help the uterus to shed the
womb lining during menstruation by causing the contraction of the uterine muscles.
Understandably, if too many of these prostaglandins are produced, then the contractions will be
more severe and cause painful menstrual cramps — primary dysmenorrhea.
Prostaglandins and Infertility
One major group of hormones secreted by the normal endometrium is that of prostaglandins.
Prostaglandins are required for many bodily processes, including several stages of the menstrual
cycle and pregnancy.
Prostaglandins are required for ovulation, regression of the corpus luteum (i.e., ending the monthly
menstrual cycle), sperm motility, immune interaction, contraction of the uterus at birth and
menstrual cramps. Endometrial implants and the endometrium of the uterus are the richest source
of prostaglandin production in the body.
However, the problem with endometrial implants includes:
- Prostaglandins are released into the abdomen instead of inside the womb

- Prostaglandins release by the implants seem to be out of phase with their release by the uterus
- Prostaglandins are produced at the wrong time sending the wrong message
For instance, there is a normal surge in prostaglandin F production at the end of the menstrual cycle,
causing the effect of the corpus luteum of the ovary to die down and signaling the start of a new
menstrual cycle. The implants of endometriosis produce their own prostaglandin surge several days
after that of the womb lining. This may be one of the main causes of very early miscarriage.
If a women is a few days pregnant then the endometriosis implants producing prostaglandin F would
incorrectly signal the ovary to start a new menstrual cycle, causing the womb lining with the
implanted egg to be expelled - and the consequence is an early miscarriage.
Prostaglandins also play an important role in the contractions of womb and fallopian tubes. During
the normal menstrual cycle, the gentle contraction of the womb and fallopian tube aids the
movement of egg and sperm to the outer third of the fallopian tube where fertilization occurs. High
concentrations of endometriosis implants may prevent fertilization. An excess of PGF2 and PGE2
could cause contractions that are too strong and expel the egg too quickly.

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Telomerase Theory of Ageing
Chromosomes are long strands of DNA. At the end of each chromosome, there is a specialized structure called
telomeres. It keeps the chromosome protected and also prevents them from fusing with other DNA molecules. In
addition, telomeres play a vital role in cell division. During each cell division, DNA replication takes place where a new
DNA strand is formed from the template. However, some terminal part of the DNA may not be replicated due to the
limited amounts of telomerase enzyme unlike unicellular eukaryotes that possess unlimited amounts of telomerase
enzyme, and therefore, the telomeres get shorten with each cycle of cell division. This mechanism then limits
propagation of human cells to a restricted number of cell divisions by including replicative senescence, differentiation,
or apoptosis.
Diagram of factors affecting the telomere length in primary somatic cells from human tissues. According to the model
shown, telomeres i you g so atic cells have lo g tracts of telo ere repeats that favor foldi g i to a closed
structure that is invisible to the DNA damage response pathways and telomerase. As the telomere length at individual
chromosome ends decreases, the likelihood that telo eres re ai closed also decreases. At one point telomeres
become too short and indistinguishable from broken ends. Such ends will be processed by enzymes in the DNA repair
compartment (proposed to occupy a different nuclear domain than long telomeres). Depending on the cell type and
the genes that are expressed in the cell, a limited number of short ends can be elongated by limiting levels of
telomerase or recombination. However, with continued cell division and telomere loss, eventually too many short ends
accumulate for the limited capacity of these telo ere salvage path ays. At this poi t, defective telo eres ill trigger
levels of DNA damage signals such as p53 to which cells respond by either apoptosis or senescence. Rare (mutant) cells
that do not upregulate functional DNA damage responses (e.g., by loss of functional p53) continue cell divisions in the
presence of dysfunctional telomeres causing genome instability via chromosome fusions, chromosome breaks, and
repetitive break-fusion bridge cycles.
Paper XVI: Reproduction Biology 12.0: Telomerase Theory 3rd Semester

1
Interactions between Sertoli cells and germ cells in the testis
The production of mature spermatozoa requires a complex interaction between Sertoli cells and
germ cells. Sertoli cells regulate aspects of germ cell division and differentiation while germ cells
provide signals that modulate Sertoli cell functions.
There are several means by which this interaction may occur: (1) direct contact of components of
the plasma membrane may act as a signal. (2) Secondary messengers could be exchanged via gap
junctions. (3) The secretion of paracrine factors may facilitate intercellular communication.
Sertoli cell-germ cell contact

Sertoli cells and germ cells are in close physical proximity within the seminiferous tubules of the
testis.
Pachytene spermatocytes with Sertoli cells shows an increased secretion of androgen binding
protein (ABP) induced by follicle stimulating hormone (FSH).
In addition, a component of the germ cell plasma membrane was shown to increase the levels of
adenyl cyclase in Sertoli cells.
CAMs play a role in developmental events and maintenance of tissue architecture and may increase
adhesive contact between Sertoli cells and germ cells.
Sertoli cells could provide germ cells with factors essential for survival such as pyruvate, lactate, iron
and vitamins.
Intracellular secondary messengers such as Cu2+, cAMP, and inositol, 1, 4, 5 triphosphate could pass
between cells by connexons.
Proteins secreted by Sertoli cells

Sertoli cells are largely responsible for producing an environment suitable for germ cell survival,
meiotic division, and maturation. Sertoli cells secrete numerous proteins which can be subdivided
into several groups, including followings:
Transporters
Transferrin is an iron transport protein secreted by Sertoli cells and may be required for germ cell
division and subsequent development.
Similarly, ceruloplasmin is a copper transport protein which also acts as a feroxidase.
SPARC, a Secreted Protein that is Acidic and Rich in Cysteine, is a calcium binding protein that can
bind other divalent cations and is also made by Sertoli cells. SPARC may influence the shape of
Sertoli cells and thus facilitate movement of germ cells through the seminiferous epithelium during
spermatogenesis.
In addition to these ion transporters, Sertoli cells secrete androgen-binding protein (ABP), insulin-
like growth-factor-binding protein-3, and riboflavin-binding protein which may also have roles in
transport.
Proteases and protease inhibitors
Among the proteases secreted by Sertoli cells are plasminogen activator, metalloproteases, type IV
collagenase, and cyclic protein. They are involved in the remodeling of the seminiferous epithelium
subsequent to the movement of germ cells from the basal compartment to the adluminal
compartment.
Basement membrane proteins
Sertoli cells contribute type IV collagen, laminin, and proteoglycans to the composition of the
basement membrane of the seminiferous tubule.
Hormones and, growth factors
Numerous growth factors are secreted by Sertoli cells that may directly influence germ cell mitosis
and/or meiosis. For example, transforming growth factors (TGF-α) secreted by Sertoli cells could
have an effect on developing spermatogonia. Transforming growth factor-β (TGF-β) is also produced
by Sertoli cells that may act to suppress growth of spermatogonia prior to puberty.
Other growth factors produced by Sertoli cells include insulin like growth factor (somatomedin C),
which may have some influence on meiosis.
In addition, Sertoli cells produce interleukin-1α. Additional growth factors such as basic fibroblast
growth factor (bFGF), seminiferous growth factor, Sertoli cell-secreted growth factor, Mullerian
inhibitory substance, and prodynorphin, an endogenous opioid peptide, are also produced by Sertoli
cells.
Germ cell influence on Sertoli cell function

The presence or absence of germ cells has a profound effect on Sertoli cell behavior. This effect may
be the result of either direct cell contact or communication via gap junctions (as described above), or
via factors secreted by germ cells.
Germ cells apparently increase the overall synthesis and secretion of proteins by Sertoli cells. A
decrease in protein secretion by Sertoli cells occurred when germ cells were depleted. Moreover
when germ ceils was depleted from testes there was a decrease in binding of FSH to Sertoli cells.
In addition to increasing or decreasing the amount of protein secreted by Sertoli cells, germ cells
also increased phosphorylation and glycosylation of Sertoli cell proteins.
Several specific factors are apparently produced by germ cells. For example, the mRNA for β nerve
growth factor (βNGF), bFGF. Sertoli cells possessing the receptor for bFGF responded to bFGF with
increased secretion of transferrin.
Other Factors Transfer From Sertoli Cell To Germ Cell Are Following:
A. Transporters
Transferrin, Ceruloplasmin, SPARC, ABP, IGF Binding Protein, Riboflavin Binding Protein
B. Proteases And Protease Inhibitors
Plasminogen Activator, Metalloproteases, Type IV Collagenase, Cyclic Protein
C. Basement Membrane Proteins
Type IV Collagen, Laminin, Proteoglycans
D. Hormones And Growth Factors
TGF-α & β, Somatomedin C, Interleukin-1α, bFGF, Mullerian Inhibitory Substance, Prodynorphin

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Transcription in Eukaryotes
During transcription, an enzyme system converts the genetic information in a segment of double-
stranded DNA into an RNA strand with a base sequence complementary to one of the DNA strands.
Three major kinds of RNA are produced. Messenger RNAs (mRNAs) encode the amino acid sequence
of one or more polypeptides specified by a gene or set of genes. Transfer RNAs (tRNAs) read the
information encoded in the mRNA and transfer the appropriate amino acid to a growing polypeptide
chain during protein synthesis. Ribosomal RNAs (rRNAs) are constituents of ribosomes, the intricate
cellular machines that synthesize proteins.
RNA polymerases
1. RNA polymerase I: Present in Nucleolus and synthesized Pre-rRNA.

2. RNA polymerase II: Present in Nucleoplasm and synthesized messenger RNA (mRNA), small
nucleolar RNAs (snoRNAs), small nuclear RNAs (snRNAs), and microRNAs
3. RNA polymerase III: Present in Nucleoplasm and synthesized transfer RNA (tRNA), 5S ribosomal
RNA (rRNA), and some snRNAs.
RNA polymerase II has 12 subunits:
Core Subunits: Rpb1, Rpb2, Rpb3
Common Subunits: Rpb5, Rpb6, Rpb8, Rpb10, Rpb12
Non-essential Subunits: Rpb4, Rpb7, Rpb9, Rpb11
Promoter elements
RNA pol II core promoter has following element:
Upstream core promoter elements
1. TFIIB recognition element (BRE): Present at position − 7 to − having the TFIIB transcription
factor and (G/C) (G/C) (G/A) CGCC consequence sequence.
2. TATA box: Present at position − 1 to − having the TBP transcription factor and TATA (A/T) AA
(G/A) consequence sequence.
3. Initiator (Inr): Present at position -2 to +4 having the TAF1 (TAFII250), TAF2 (TAFII150)
transcription factor and PyPyA+1N (T/A) PyPy consequence sequence.
Transcription in Eukaryotes 3rd Semester

1
Downstream core promoter elements
4. Motif ten element (MTE): Present at position +18 to +27 having the TFIID transcription factor
and have the C (G/A) A (A/G) C (G/C), (C/A/G) AACG (G/C) consequence sequence.
5. Downstream promoter element (DPE): Present at position +28 to +32 having the transcription
factor TAF9 (TAFII40), TAF6 (TAFII60) and (A/G)G(A/T)(C/T)(G/A/C) consequence sequence.
Proximal promoter elements
6. CAAT box: Present at − to −7 position having the CBF, NF1, C/EBP transcription factor and
CCAAT consequence sequence.
7. GC box: Present at position − to −7 having the Sp1 transcription factor and GGGCGG
consequence sequence.
Enhancers and silencers
These elements are usually 700–1000 bp or more away from the start of transcription. The hallmark
of enhancers is that, unlike promoter elements, they can be downstream, upstream, or within an
intron. Enhancers increase gene promoter activity. Similar elements that repress gene activity are
called silencers.
Enhancers act through proteins that bind to them. These have several names: transcription factors,
enhancer-binding proteins, or activators. These proteins appear to stimulate transcription by
interacting with other proteins called general transcription factors at the promoter. This interaction
promotes formation of a preinitiation complex, which is necessary for transcription.
Silencers cause the chromatin to coil up into a condensed, inaccessible, and therefore inactive form,
thereby preventing transcription of neighboring genes.
Insulators
These are regulatory elements which shelter gene from inappropriate regulatory interactions.
Insulators can block interaction between an enhancer and a promoter when positioned in between
the two.
General transcription factors
1. TFIIB: Transcription factor for RNA polymerase II B: Stabilization of TBP–DNA interactions,

recruitment of RNA pol II–TFIIF, start site selection by RNA pol II.
2. TFIID: TBP: TATA-binding protein: Core promoter recognition, TFIIB recruitment.
3. TFIID: TAF: TBP-associated factor: Core promoter recognition or selectivity.
4. TFIIE: Transcription factor for RNA polymerase II E: TFIIH recruitment.
5. TFIIF: Transcription factor for RNA polymerase II F: Recruitment of RNA pol II to promoter DNA–
TBP–TFIIB complex.
6. TFIIH: Transcription factor for RNA polymerase II H: Promoter melting, helicase, RNA pol II CTD
kinase.
7. Mediator: Transduces regulatory information from activator and repressor proteins to RNA pol
II.

2
Specific transcription factors
Specific transcription factors contain the DNA binding domain which contains several motifs like:
1. Helix-Turn-Helix
2. Helix-Loop-Helix
3. Homeodomain
4. Zinc Fingers
5. Lucien Zipper
Elongation Factors
1. FACT: Facilitates chromatin transcription: Transcription-dependent nucleosome alterations

2. Elongator: Exact function in elongation unknown
3. TFIIS: Transcription factor for RNA polymerase II S: Facilitates RNA pol II passage through regions
that cause transcriptional arrest
Mechanism of Transcription
1. General transcription factors and preinitiation complex formation:

General transcription factors have been defined biochemically as factors required for the correct
initiation of RNA pol II transcription on a promoter with a classic TATA box and a strong initiator
(Inr) element. Assembling the general transcription apparatus involves a series of highly ordered
steps. Binding of TFIID provides a platform to recruit other general transcription factors and RNA
pol II to the promoter. These proteins assemble at promoter in the following order: TFIIA, TFIIB,
and TFIIF together with RNA pol II.
2. Transcription initiation complex formation:
Orderly addition of TFIIE and TFIIH form the transcription initiation complex. The whole structure
forms a closed complex around DNA. TFIIH is the most complex of all the general transcription
factors. TFIIH is the protein kinase that phosphorylates the CTD of RNA pol II. During this whole
process a marked conformational change occur in which 11 to 15 bp near the transcription start
point melted and unwind and form an open complex containing transcription bubble.
3. Promoter clearance and scaffold complex formation:
After pol II initiate the transcription TFIIB, TFIIF and pol II leave the promoter called as promoter
clearance but the remaining transcription factors remain associated with the promoter called as
scaffold complex. The scaffold complex facilitates the reinitiation of the process just by
recruitment of some transcription factors and RNA polymerase.
4. Phosphorylation of CTD (Carboxyl Terminal Domain):
TFIIH has an additional function during the initiation phase. A kinase activity in one of its
subunits phosphorylates Pol II CTD tail. Phosphorylation of the CTD is also important during the
subsequent elongation phase, and it affects the interactions between the transcription complex
and other enzymes involved in processing the transcript.

3
5. Elongation phase:
TFIIF remains associated with Pol II throughout elongation. During this stage, the activity of the
polymerase is greatly enhanced by proteins called elongation factors. The elongation factors
suppress pausing during transcription and also coordinate interactions between proteins
complexes involved in the posttranscriptional processing of mRNAs. Once the RNA transcript is
completed, transcription is terminated. Pol II is dephosphorylated and recycled, ready to initiate
another transcript.
The structure of the elongation complex is so efficient that the polymerase deal with the
problems of unwinding and rewinding its template, and of moving along its twisted (helical)
template without twisting its RNA product around the template.
RNA polymerase could accomplish this process in two ways. One way would be for the
polymerase and the growing RNA to rotate around and around the DNA template, following the
natural twist of the double-helical DNA, as transcription progressed. This would not twist the

4
DNA at all, but it would require considerable energy to make the polymerase gyrate that much,
and it would leave the transcript hopelessly twisted around the DNA template, with no known
enzyme to untwist it.
The other possibility is that the polymerase moves in a straight line, with the template DNA
rotating in one direction ahead of it to unwind, and rotating in the opposite direction behind it
to wind up again. But this kind of rotating of the DNA introduces strain. This process is called
supercoiling, and the supercoiled DNA is called a supercoil or superhelix. A class of enzymes
called topoisomerases can introduce transient breaks into DNA strands and so relax this kind of
strain.
6. Termination Phase:
Eukaryotic mRNA has to be processed in various ways before being exported from nucleus for
translation. One such process is take place during the termination phase of the transcription
cycle here lo g chai of ade i e is added to the ’ e d of the RNA tra script called
polyadenylation.
During this process CTD chain of pol II added two enzymes CPSF (Cleavage and Polyadenylation
Specificity Factor) and CstF (Cleavage stimulating Factor). When the pol II reaches at the end of
gene it face a poly A signal sequence. Once this sequence is transcribed it triggers the CPSF and
CstF. Once the CPSF and CstF bind to RNA additional cleavage factors are recruited leading to
cleavage of RNA.
An enzyme called Polymerase poly A (PAP) is then recruited which add about 200 adenine to the
e ’ e d produced y the cleavage of RNA.

5
Transcription in prokaryotes
During transcription, an enzyme system converts the genetic information in a segment of double-
stranded DNA into an RNA strand with a base sequence complementary to one of the DNA strands.
Three major kinds of RNA are produced. Messenger RNAs (mRNAs) encode the amino acid sequence
of one or more polypeptides specified by a gene or set of genes. Transfer RNAs (tRNAs) read the
information encoded in the mRNA and transfer the appropriate amino acid to a growing polypeptide
chain during protein synthesis. Ribosomal RNAs (rRNAs) are constituents of ribosomes, the intricate
cellular machines that synthesize proteins.
Initiation
Promoters
RNA polymerase binding sites on the DNA where the transcription begins are called promoters. The
promoter in the prokaryotes is present as consequence sequences because they represent the
probabilities. The first sequence is present about 10 bp upstream of the start of the transcription
called as -10 Box and second sequence present about 35 bp upstream of the start of the
transcription called as the -35 Box. Both together known as core promoter elements.
Mutations that destroy matches with the consensus sequences tend to be down mutations. They
make the promoter weaker, resulting in less transcription. Mutations that make the promoter
sequences more like the consensus sequences—usually make the promoters stronger; these are
called up mutations. The spacing between promoter elements is also important, and deletions or
insertions that move the –10 and –35 boxes unnaturally close together or far apart are deleterious.
RNA polymerase
E. coli RNA polymerase contains two very large subunits: beta (β) and beta-prime (β′ . The other RNA
polymerase subunits are called sigma (σ) and alpha (α). The subunit content of an RNA polymerase
holoe zy e is β′, β, σ a d α . Without the σ-subunit the holoenzyme is called as core enzyme.
β-subunit: The β-subunit of core polymerase is involved in phosphodiester bond formation, that the
β- a d β′-su u its participate i DNA i di g, a d that the α-subunit has several activities, including
assembly of the core polymerase. Both the β- a d β′-subunits are involved in DNA binding and that
two DNA binding sites are present: (1) an upstream, relatively weak site where DNA melting occurs
and electrostatic forces predominate; and (2) a downstream, strong binding site where hydrophobic
forces bind DNA and protein together.
α-subunit: The α-subunit is responsible for recognizing UP elements, and it also interacts with
activator proteins that bind to sites outside the promoter. But the N-terminal domain also plays a
key role in transcription by helping to organize the RNA polymerase. The order of subunit assembly
of the E. coli RNA poly erase is α → α → α β → α ββ′, hich suggests that α plays, a ce tral role.
Sigma (σ): The σ helps the holoe zy e to recog ize the authe tic RNA poly erase i di g sites o
the DNA called promoter region and to begin transcription there. The core polymerase is only
capable of binding loosely to the DNA because the holoenzyme, but not the core, can recognize
promoters for tight binding.
Transcription In Prokaryotes 3rd Semester

1
Structure of Sigma (σ): It contains four regions:
Regio 1: This regio is fou d o ly i the pri ary σ’s σ7 a d σ . Its role appears to be to prevent
σ fro i di g y itself to DNA. This is i porta t ecause σ i di g to pro oters could i hi it
holoenzyme binding and thereby inhibit transcription.
Regio : This regio is fou d i all σ-factors a d is the ost highly co served σ regio . Region 2 can
be subdivided into four parts, 2.1–2.4. Region 2.1 seems to be involved in binding to the polymerase
core a d regio . is respo si le for a crucial σ activity of recog itio of the pro oter’s –10 box.
Region 3: this region can form a helix-turn-helix DNA-binding domain.
Region 4: This region can be subdivided into subregions. Region 4 seems to play a key role in
promoter recognition. Subregion 4.2 contains another helix-turn-helix DNA-binding domain, which
suggests that it plays a role in polymerase–DNA binding.
RNA polymerase holoenzyme binds loosely to DNA at first. It either binds initially at a promoter or
scans along the DNA until it finds one. The complex with holoenzyme loosely bound at the promoter
is called a closed promoter complex because the DNA remains in closed double-stranded form.
Then the holoenzyme can melt a short region of the DNA at the promoter to form an open promoter
complex in which the polymerase is bound tightly to the DNA. This is called an open complex
because the DNA has to open up to form it. It is this conversion of a loosely bound polymerase in a
closed promoter complex to the tightly bound polymerase in the open promoter complex that
re uires σ, a d this is also hat allo s tra scription to begin.

2
Elongation
After i itiatio of tra scriptio is acco plished a d σ has left the sce e, the core co ti ues to
elongate the RNA, adding one nucleotide after another to the growing RNA chain.
The structure of the elongation complex is so efficient that the polymerase deal with the problems
of unwinding and rewinding its template, and of moving along its twisted (helical) template without
twisting its RNA product around the template.
RNA polymerase could accomplish this process in two ways. One way would be for the polymerase
and the growing RNA to rotate around and around the DNA template, following the natural twist of
the double-helical DNA, as transcription progressed. This would not twist the DNA at all, but it would
require considerable energy to make the polymerase gyrate that much, and it would leave the
transcript hopelessly twisted around the DNA template, with no known enzyme to untwist it.
The other possibility is that the polymerase moves in a straight line, with the template DNA rotating
in one direction ahead of it to unwind, and rotating in the opposite direction behind it to wind up
again. But this kind of rotating of the DNA introduces strain. This process is called supercoiling, and
the supercoiled DNA is called a supercoil or superhelix. A class of enzymes called topoisomerases can
introduce transient breaks into DNA strands and so relax this kind of strain.
Termination
When the polymerase reaches a terminator at the end of a gene it falls off the template, releasing
the RNA. E. coli cells contain about equal numbers of two kinds of terminators. The first kind, known
as intrinsic terminators, function with the RNA polymerase by itself without help from other
proteins. The second kind depends on an auxiliary factor called rho (q). Naturally, these are called
rho-dependent terminators.
Rho-Independent Termination
Rho-independent, or intrinsic, termination depends on terminators consisting of two elements: an

inverted repeat followed immediately by a T-rich region in the non-template strand of the gene. The
model of termination we will present later in this section depe ds o a hairpi structure in the
RNA transcript of the inverted repeat.

3
Consider this inverted repeat:
′-TACGAAGTTCGTA- ′
•
′-ATGCTTCAAGCAT- ′
Such a sequence is symmetrical around its center, indicated by the dot; it would read the same if
rotated 180 degrees in the plane of the paper, and we always read the stra d that ru s ′ → ′ left
to right.
Now observe that a transcript of this sequence
UACGAAGUUCGUA
is self-complementary around its center (the underlined G). That means that the self-complementary
bases can pair to form a hairpin as follows:
U •⋅ A
A•U
C•G
G•C
A•U
AU
G

4
As the T-rich region is transcribed, eight A–U base pairs would for et ee the A’s i the DNA
template strand and the U’s i the RNA product. The rU–dA base pairs are exceptionally weak.
The rU–dA pairs cause the polymerase to pause, allowing the hairpin to form and destabilize the
already weak rU–dA pairs that are holding the DNA template and RNA product together. This
destabilization results in dissociation of the RNA from its template, terminating transcription.
Rho-Dependent Termination
The rho as a protein that caused an apparent depression of the ability of RNA polymerase to
transcribe. This depression is simply the result of termination. The rho binds to the transcript
upstream of the termination site at a rho loading site.
Rho consists of a hexamer of identical subunits, each of which has ATPase activity. Binding of rho to
the RNA activates the ATPase, which supplies the energy to propel the rho hexamer along the RNA in
the 5′ → ′ directio , follo i g the RNA polymerase. This chase continues until the polymerase stalls
in the terminator region just after making the RNA hairpin.
Thus, when rho encounters the polymerase stalled at the terminator, it can unwind the RNA–DNA
hyrbid within the transcription bubble, releasing the RNA and terminating transcription.

5
Brucellosis
Brucellosis is an infectious disease caused by bacteria from the genus Brucella. This disease is also
called as Rock fever or Malta fever. This disease transmitted from certain animals to humans
(zoonotic disease). Brucellosis in humans is predominantly caused by four different species of
Brucella bacteria: B.melitensis (goats, sheep, camels), B.suis (pigs), B.abortus (cows, buffalo, camels),
and B.canis (dogs).
Transmission
Brucellosis is transmitted from animals to humans in several ways. The most common route of
transmission occurs when humans consume raw milk or cheese from infected sheep and goats.
Infected animals shed the organism into their milk, and if humans eat or drink unpasteurized dairy
products from these affected animals, they can develop brucellosis.
Brucellosis can also be transmitted to humans via inhalation of the organism or by direct contact
with infected animal secretions. The bacteria can gain entry into the body through the inhalation of
aerosolized secretions, through breaks in the skin, or through exposure of the mucous
membranes/conjunctiva from the splashing of infected secretions. With these routes of entry,
brucellosis is an occupational disease that can affect veterinarians, slaughterhouse workers,
butchers, hunters, laboratory personnel, and those individuals who work closely with livestock (for
example, farmers and shepherds).
Finally, an accidental injection with the livestock vaccine used against B.abortus can also lead to
brucellosis in humans. Human-to-human transmission is very rare (via sexual contact and
breastfeeding).
Symptoms
The symptoms and signs of brucellosis may develop from days to months after the initial exposure to
the organism (incubation period). While some individuals may develop mild symptoms, others may
go on to develop long-term chronic symptoms.
The signs and symptoms of brucellosis are extensive and they can be similar to many other febrile
illnesses. They include: fever, sweating, body aches, joint pain, fatigue, weakness, dizziness,
headache, depression and irritability, loss of appetite, weight loss, cough, difficulty breathing, chest
pain, abdominal pain, enlarged liver and spleen.
Diagnosis
In general, blood tests and tissue cultures are necessary for making the diagnosis of brucellosis.
Common blood tests used to make the diagnosis include testing for antibodies against the bacteria
and isolating the organism from blood cultures. A biopsy of body tissue (from the bone marrow or
the liver, for example) can also assist in making the diagnosis. Additional blood tests may
demonstrate anemia, low platelets, a low white blood cell count, and elevated liver function tests.
Other imaging studies and procedures may also be performed initially depending on the individual's
signs and symptoms. These tests may include CT scan, MRI, X-ray, ultrasound, lumbar puncture
(spinal tap), joint aspiration, or an electrocardiogram (ECG).
Page No. 1 of 7 Paper XIII: Parasitology: 10.0: Zoonosis 3rd Semester

Treatment
The cornerstone of treatment for brucellosis is antibiotics. Because of the high relapse rate
associated with the disease, the use of a multidrug (two or more) antibiotic regimen is
recommended. The antimicrobials most commonly used include doxycycline (Vibramycin),
streptomycin, rifampin (Rifadin), gentamicin (Garamycin), and trimethoprim-sulfamethoxazole
(Bactrim, Septra). The combination of antibiotics used will vary based on disease severity, age and
pregnancy. Rarely, surgical intervention may be needed for certain complications associated with
brucellosis, such as abscess formation or heart-valve infection.
Plague
Plague is an infectious disease caused by bacteria called Yersinia pestis. These bacteria are found
mainly in rodents, particularly rats, and in the fleas that feed on them. Other animals and humans
usually contract the bacteria from rodent or flea bites.
Forms of Plague
Bubonic plague
In bubonic plague, the most common form, bacteria infect the lymph system and become inflamed.
(The lymph or lymphatic system is a major component of body's immune system. The organs within
the lymphatic system are the tonsils, adenoids, spleen, and thymus.)
Bubonic plague affects the lymph nodes (another part of the lymph system). Within 3 to 7 days of
exposure to plague bacteria, person develops flu-like symptoms such as fever, headache, chills,
weakness, and swollen, tender lymph glands (called buboes—hence the name bubonic).
Bubonic plague is rarely spread from person to person.
Septicemic plague
This form of plague occurs when the bacteria multiply in the blood.
Symptoms include fever, chills, weakness, abdominal pain, shock, and bleeding underneath the skin
or other organs.
Septicemic plague is rarely spread from person to person.
Pneumonic plague
This is the most serious form of plague and occurs when Y. pestis bacteria infect the lungs and cause
pneumonia.
Symptoms usually develop within 1 to 3 days after you are exposed to airborne droplets of plague
bacteria. Pneumonia begins quickly, with shortness of breath, chest pain, cough, and sometimes
bloody or watery sputum. Other symptoms include fever, headache, and weakness.
Pneumonic plague is contagious. If someone has pneumonic plague and coughs, droplets containing
Y. pestis bacteria from their lungs are released into the air. An uninfected person can then develop
pneumonic plague by breathing in those droplets.

Transmission
Y. pestis is found in animals throughout the world, most commonly in rats but occasionally in other
wild animals. Most cases of human plague are caused by bites of infected animals or the infected
fleas that feed on them. In almost all cases, only the pneumonic form of plague can be passed from
person to person.
Diagnosis
A health care provider can diagnose plague by doing laboratory tests on blood or sputum, or on fluid
from a lymph node.
Treatment
When plague is suspected and diagnosed early, a health care provider can prescribe specific
antibiotics (generally streptomycin or gentamycin). Certain other antibiotics are also effective.
Left untreated, bubonic plague bacteria can quickly multiply in the bloodstream, causing septicemic
plague, or even progress to the lungs, causing pneumonic plague.
Rabies
Rabies is a disease caused by a virus that enters the body through the bite from infected animals and
causes brain swelling and, if not quickly treated, results in convulsions, respiratory failure, and death
in almost every person infected. Very rarely, rabies has been transmitted by saliva droplets from an
infected animal that contacts a skin break (abrasion or cut). Aerosols of saliva droplets or bat guano
may also rarely cause rabies.
Symptoms
After the first exposure (in most people, an animal bite), the symptoms of itching or discomfort like
pins or needles pricking the skin occur at the bite area. In addition, the person may develop fever
and a headache. Investigators suggest these symptoms may last from about two days to weeks. This
is the acute phase or the acute incubation phase of the disease.
Unfortunately, there is another incubation period before the next set of signs and symptoms
develop. The NIH (National Institutes of Health) suggests that the average latent incubation period is
about three to seven weeks, although they do report a range from seven days to 10 years, with the
longer time periods occurring infrequently.
The symptoms and signs of rabies in humans may consist of some or many of the following
according to the CDC and NIH: Anxiety, stress, and tension, Delirium, Drooling, Convulsions,
Exaggerated sensation at the bite site, Excitability or combative, Hallucinations, Loss of feeling in an
area of the body, Loss of muscle function, Low-grade fever (102 F or lower) , Muscle spasms,
Numbness and tingling, Pain at the site of the bite, Restlessness, insomnia, Swallowing difficulty
(drinking causes throat spasms and the person may become hydrophobic).

Causes
The virus that causes rabies is Lyssavirus (Lyssa is the Greek goddess of madness, rage, and frenzy)
rabies, a cylindrical or bullet-shaped virus that is enveloped and contains a negative-sensed RNA that
makes up its genetic material.
The virus is termed a neurotropic virus because it proliferates in nerve tissues, especially the brain
tissues of humans and animals. It proceeds from the bite or entrance wound along nerves to
eventually infect the brain. The treatment use of human immune globulin and vaccine is designed to
interrupt and kill the virus before it makes the journey to the brain.
The virus enters nerve cells, takes over the cells systems, and develops virus replicating sites (termed
Negri bodies that can be seen microscopically inside cells) that produce new viruses to continue viral
spread to other body sites like the brain and, most important for spreading the viruses to other
animals, the salivary glands.
The rabies life cycle is relatively simple; the virus is transmitted to a wild animal by bites or saliva,
the virus replicates in the bitten animal that, in turn, bites another animal and the cycle is
completed. Humans are incidentally infected and rarely transmit the virus so humans play almost no
role in the rabies life cycle.
Transmission
Almost every person who gets rabies has the virus transmitted to them by the bite of an infected
animal. The transmission of rabies from human to human is rare; the highest number recorded
happened when corneal transplants that were unknown before transplant to contain rabies virus
caused rabies in eight patients. Aerosols of infected saliva or bat guano may also transmit rabies. In
developing countries, the majority of people are infected by rabid dogs. Rabid dogs are often
aggressive and sometimes are drooling, but in other cases, they act very withdrawn.
Diagnosis
Most people have rabies definitively diagnosed by an immunofluorescence test that confirms the
presence or absence of rabies virus in tissue or saliva. These tests are usually done on people who
develop the severe symptoms of rabies; they are not done on people who undergo appropriate
treatment within 48 hours of exposure. Immunofluorescence tests can be performed on saliva,
serum, spinal fluid, and skin biopsies of hair follicles at the nape of the neck. In addition, saliva can
be tested by virus isolation or reverse transcription followed by polymerase chain reaction (RT-PCR).
Serum and spinal fluid can also be tested for antibodies to rabies virus. Skin biopsy specimens can
also be examined for rabies antigen in the cutaneous nerves at the base of hair follicles. Most labs
suggest that at least two positive tests from different body areas are required for a definitive

diagnosis. The vast majority of patients with a definitive diagnosis will die from the disease.
However, these tests are useful because they can help differentiate rabies from other diseases (for
example, tetanus, viral encephalitis causes, and poliomyelitis).
Treatment
Treatment for rabies (or more accurately, prevention of rabies before the latent symptoms can
develop) consists of giving a person an injection of rabies immune globulin and another injection of
rabies vaccine as soon as possible after the bite or exposure to saliva from an infected animal. As of
2010, the CDC recommends additional doses (injections) of rabies vaccine on the third, seventh, and
14th day after exposure. This schedule is for people who have had no previous treatment
(vaccination) against rabies. For people previously vaccinated against rabies, only two doses of the
vaccine are recommended; one as soon as possible after the exposure (no rabies immune globulin is
recommended) and one more three days later.
Japanese encephalitis
Japanese encephalitis is a viral disease that infects animals and humans. It is transmitted by
mosquitoes and in humans causes inflammation of the membranes around the brain. Domestic pigs
and wild birds (herons) are reservoirs of the virus; transmission to humans may cause severe
symptoms. One of the most important vectors of this disease is the mosquito Culex
tritaeniorhynchus.
Symptoms
The incubation period of JEV is 5 to 15 days. Illness usually begins with sudden onset of fever with
gastrointestinal symptoms and headache. Mental status or behavioral changes, focal neurologic
deficits, generalized weakness, and movement disorders may develop over the next few days.
Seizures are very common among children. Milder forms of disease such as aseptic meningitis or
fever with headache can occur, more commonly among adults.
Causes
The Japanese encephalitis virus has a life cycle involving domestic pigs and a specific type of
mosquito, Culex tritaeniorhynchus that lives in rural rice-growing and pig-farming regions. The
mosquito breeds in flooded rice fields, marshes, and standing water around planted fields. The virus
can infect humans, most domestic animals, birds, bats, snakes, and frogs through the bite of the
mosquito. After infection, the virus invades the central nervous system, including the brain and
spinal cord.
Diagnosis
Laboratory findings of JE include moderate leukocytosis (elevated white blood cell) count, mild
anemia, hyponatremia (low sodium), and an increased cell count in the cerebrospinal fluid (CSF)
(especially white blood cells). Laboratory diagnosis of JEV infection should be performed by using JE-
specific IgM-capture enzyme-linked immunosorbent assay (ELISA) on CSF or serum. JE-specific IgM
antibodies will be present in the CSF or blood of almost all patients 7 days following onset of
symptoms. The Centers for Disease Control or local health department can help with diagnosis.

Treatment
There is no specific antiviral treatment for JE; therapy consists of supportive care and management
of complications.
Vaccines
Two types of vaccines are commercially available in several Asian countries for humans and animals.
For horses, inactivated vaccines prepared from infected mouse brains or in cell cultures have been
used. For pigs, inactivated and live-attenuated vaccines are available.
Rickettsial Infections
Rickettsial infections and related infections (such as ehrlichiosis and Q fever) are caused by an
unusual type of bacteria that can live only in another organism.
Most of these infections are spread through ticks, mites, fleas, or lice. A fever, a severe headache,
and usually a rash develop, and people feel generally ill. Symptoms suggest the diagnosis, and
doctors use special cultures and blood tests to confirm it. Antibiotics are given as soon as doctors
suspect one of these infections.
Rickettsiae are an unusual type of bacteria that cause several diseases, including Rocky Mountain
spotted fever and epidemic typhus. Rickettsiae differ from most other bacteria in that they can live
and multiply only inside the cells of another organism (host) and cannot survive on their own in the
environment. Ehrlichia bacteria and Coxiella burnetii bacteria are similar to rickettsiae and cause
similar diseases.
People are the main host for some species of these bacteria. However, for most species, animals are
the usual host. These animals are called the reservoir of infection. Animals in the reservoir may or
may not be ill from the infection. Rickettsiae are usually spread to people through the bites of ticks,
mites, fleas, or lice that previously fed on an infected animal. Ticks, mites, fleas, and lice are called
vectors because they convey (transmit) organisms that cause disease. Q fever, caused by Coxiella
burnetii, can be spread through the air or in food. Each species of rickettsiae and related bacteria
has its own hosts and vectors.
In people, rickettsiae infect the cells lining small blood vessels, causing the blood vessels to become
inflamed or blocked or to bleed into the surrounding tissue. Where this damage occurs and how the
body responds determine which symptoms develop.
Symptoms
Different rickettsial infections tend to cause similar symptoms: Fever, Severe headache, a
characteristic rash, a general feeling of illness (malaise).
Because the rash often does not appear for several days, early rickettsial infection is often mistaken
for a common viral infection, such as influenza.
As severe rickettsial diseases progress, people typically experience confusion and severe weakness—
often with cough, difficulty breathing, and sometimes vomiting and diarrhea. In some people, the
liver or spleen enlarges, the kidneys malfunction, and blood pressure falls dangerously low. Death
can result.

Diagnosis
Because rickettsiae are transmitted by ticks, mites, fleas, and lice, a history of a bite from one or
more of these vectors is a helpful clue—particularly in geographic areas where rickettsial infection is
common. However, many people do not recall such a bite.
Often, doctors cannot confirm a rickettsial infection quickly because rickettsiae cannot be identified
using commonly available laboratory tests. Special cultures and blood tests for rickettsiae are not
routinely available and take so long to process that people usually need to be treated before test
results are available. Doctors base their decision to treat on the person's symptoms and the
likelihood of possible exposure.
Useful tests include immunofluorescence assay and polymerase chain reaction (PCR) testing, which
use a sample from the rash or blood. These tests make the bacteria easier to identify.
Immunofluorescence assays label foreign substances produced by the bacteria (antigens) with a
fluorescent dye that makes them easier to detect. PCR increases the amount of the bacteria's DNA.
Treatment
Rickettsial infections respond promptly to early treatment with the antibiotics doxycycline,
(preferred), chloramphenicol or tetracycline.
These antibiotics are given by mouth unless people are very sick. In such cases, antibiotics are given
intravenously. Most people noticeably improve in 1 or 2 days, and fever usually disappears in 2 to 3
days. People take the antibiotic for a minimum of 1 week—longer if the fever persists. When
treatment begins late, improvement is slower and the fever lasts longer. If the infection is untreated
or if treatment is begun too late, death can occur, especially in people with epidemic typhus or
Rocky Mountain spotted fever.
Ciprofloxacin and other similar antibiotics may be used to treat some rickettsial infections.
Scrub typhus
Scrub typhus is caused by Rickettsia tsutsugamushi, transmitted by mites and mite larvae (chiggers).
Rodents are the hosts. After an incubation of 6 to 21 days, symptoms begin suddenly, with fever,
chills, headache, and swollen lymph nodes. A black scab may develop at the site of the chigger bite.
A rash appears on the 5th to 8th day.
Q fever
Q fever is caused by the Coxiella burnetii, transmitted by inhaling infected droplets containing the
bacteria or by consuming contaminated raw milk. Sheep, cattle, and goats are the hosts. After an
incubation of 9 to 28 days, symptoms begin suddenly, with fever, severe headache, chills, extreme
weakness, muscle aches, loss of appetite, sweating, an unproductive cough, chest pain, and
inflammation of the airways (pneumonitis), but no rash.

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Parasite Host Coevolution

Host–parasite coevolution is a special case of coevolution, which is defined as the reciprocal

1. Negative frequency dependent selection:

Paper XIII: Parasitology 9.0: Evolution of Parasitism 3rd Semester

Progressive and Retrogressive Evolution

Paper XIII: Parasitology 9.0: Evolution of Parasitism 3rd Semester

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