1. The science of biology. The importance of biology in medical education.

Biology is a complex science (botany, zoology, physiology, anatomy, anthropology, mycology,

ichthyology ...). It studies the morphology and structure of organisms, the features of their functioning,
the interrelationships of organisms with the environment and other organisms. The term "biology",
suggested Lamarck in 1802.

The tasks of biology and medical biology:

a) Study of the basic rules for the organization and functioning of organisms, including

rights b) The discovery of forms of interrelation and interaction (interdependence)

c) Establishment of biological parameters (characteristics) and possibilities

d) Prediction of the consequences of exposure. It is reasonable to use. Critically rethink what has
been done.

Medicine is a complex science of pathological processes. The system of knowledge about the causes of
the pathological process, methods of diagnosis and prevention of pathologies, methods of treatment
at certain stages of development of human society.

2.The concept of life. Characteristics of living things. Life forms.

There are living and non-living things. The characteristics of living things are:
1. Cellular organization
2. Reproduction
3. Metabolism
4. Homeostasis
5. Heredity
6. Response to stimuli
7. Growth and development
8. Adaption through evolution
There are cellular and non-cellular forms of life. Cellular organisms include prokaryotes and eukaryotes.
Non-cellular organisms include viruses and prions.

3.Levels of organization of the living world. Their importance in medicine

Biology is the study of life. Since life is such a broad topic, scientists break it down into several different
levels of organization to make it easier to study. These levels start from the smallest unit of life and
work up to the largest and most broad category.

Molecule->Cell->Tissue->Organ->Organ system->Organism->Ecosystem->Biosphere
4.The cell theory, present state. The importance of the cell theory in medicine. General plan of
cellular organization common to all cells.
The cell theory states that:

1. All living things are one or more cells

2. Cells are fundamental and structural unit of life.
3. All cells originate from pre-existing cells (omnis cellula ex cellula)
4. The chemical reaction of living cells take place within cells.
It is one of the most basic principles in the reductionist approach to biology and tries to view
the living systems with functional units as cells, the interactions between the cells, the
intra- cellular processes etc.
The cellular organization common to all cells are: DNA, plasma membrane, cytoplasm
and ribosomes.

5.The cell: basic structural and functional unit of life. Prokaryotic and eukaryotic cells

Prokaryotic cells are structurally simple. They are found only in single-celled and colonial organisms.
Bacteria and cyanobacteria (blue-green algae) belongs to prokaryotes. Prokaryotes are distinguished
from eukaryotes on the basis of nuclear organization, specifically their lack of a nuclear membrane.
Prokaryotes also lack most of the intracellular organelles and structures that are characteristics of
eukaryotic cells (an important exception is the ribosomes, which are present in both prokaryotic and
eukaryotic cells). Most of the functions of organelles, such as mitochondria, chloroplast, and the
Golgi apparatus, are taken over by the prokaryotic plasma membrane,

Eukaryotic cells have organelles with their own membranes. Single-celled eukaryotic organisms such
as amoebae and some fungi are very divers, but many colonial and multicellular forms such as plants,
animals, and brown algae also exist.

6. Techniques used to study cell structure and function.

Microscopy is the most common technique used to study cell structure and its functions.
Light microscopy is useful for examining cells and cellular structure in order of 200-300nm or
larger. High resolution can be obtained by using electro-microscope.

7. The chemical composition of cells

Cells are composed of carbohydrates, lipids, protiens, nucleic acids and water. Water is the
most abundant molecule in cells, accounting 70% or more of total mass of cell.
8. Morphology and physiology of Eukaryotic cell, Cytoplasm and Double membranous organelles.
EUKARYOTIC CELL
(1) Eukaryotic cells have membrane bound true nucleus.
(2) They have plasma membrane
(3) They have numerous membrane bound organelles, mitochondria, endoplasmic reticulum (smooth ER
and rough ER) , Golgi apparatus and chloroplasts.
E.g.: Yeast and Amoeba.
CYTOPLASM
(1) Entire region of cell between plasma membrane and nuclear envelope.
(2) It is composed of organelles suspended in gel-like cytosol, the cytoskeleton and various
chemicals. (3) Consists of proteins, simple sugars, polysaccharide, amino acid and fatty acids.

DOUBLE MEMBRANOUS ORGANELLES: Organelles which have outs and inner membranes are
called double membranous organelle.

MITOCHONDRIA
(1) Mitochondria has inner and outer membrane.
(2) Inner membrane is folded for a large surface area for chemical reactions to take
place. (3) Aerobic respiration takes place in mitochondria and it stores ATP (energy).

9.Single membranous organelles.

(1) LYSOSOME: Small spherical organelle that enclose digesting enzymes within single membranes.
Function: Digests molecules, foreign substances and is known as recycling center found in
both animal and plant cells.
(2) PEROXISOME: Single membrane bound vesicle which takes part in metabolism in fatty acids.
Function: Involve formation and decomposition of hydrogen peroxide.
(3) ENDOPLASMIC RETICULUM: A system of membrane channels continuous with outer membrane
of nuclear envelope:
A: Rough Endoplasmic Reticulum: Ribosomes are present.
Function: The main function is synthesis of proteins.
B: Smooth Endoplasmic Reticulum: Ribosomes are absent on its surface hence the name ER.
Function: Synthesis of lipids.
(4) GOLGI APPARATUS: Consists of flattened curved saccules.
Function: They are helpful in protein synthesis.
10. Non-membranous organelles. Locomotor organelles. Cytoplasmic inclusions.
(1)RIBOSOME
Structure: (a) Made of protein and RNA.
(b) No membrane
(c) Made in nucleus

Function: (1) Acids in protein synthesis

(2) Free ribosomes makes proteins used by the cell
(3) Ribosomes in r.ER makes proteins for export to other
cells. (2) CENTROSOME
Structure: (a) Small region of cytoplasm, made up of
microtubules. (b) No membranes.

Function: (1) Helps the cell divide.

(3) CYTOKELETON
Structure: A network of thin, fibrous elements made up of microtubules and micro filaments.
Function: (1) Maintains a cell shape
(2) Acts as support system for organelles

LOCOMOTER ORGANELLES
(a) Flagella and Cilia:
Structure: Contains proteins and microtubules which are composed of linear polymers of
globular proteins called tubulin.
Function: Move materials over the surface of the cell.

(b) Pseudopodia:
Locomotion and the capturing of prey.
Pseudopodia are critical in censing prey that can be engulfed.

CYTOPLASMIC INCLUSIONS: Inconstant components of cell which may appear or disappear

depending metabolic process of cells.
11. Cell Membrane. Chemical composition; structure and functions. Glycocalyx.
Cell membrane: The thin outside layer that surrounds the cytoplasm of a cell and controls
the movement of materials into and out of the cell.
Found in both prokaryotic and eukaryotic cells.
Chemical composition:
- Phospholipids - Proteins
- Glycolipids - Glycoproteins
- Cholesterol
Membrane Structure: The fluid mosaic model
The lipid bilayer is fluid because individual
phospholipid molecules don’t bind to one
another, membrane proteins are anchored
into the lipid bilayer by their non-polar regions
Functions:
- Transport across membrane (selective permeability)
- Cell- cell interactions
- Cell division into compartments
Glycocalyx: Thick outer covering of the plasma membrane. It is composed of strands of sugars
and proteins bound together. The result is a thick, sticky layer that helps cells stay put in
environments with lots of physical stress

12. Transport across cell membrane. Its medical importance.

Passive transport: does not include chemical energy(ATP) and substances can only move
only down the concentration gradient.

1. Simple diffusion: movement of Gas exchange in the lungs and tissues

hydrophobic (nonpolar) and small polar
molecules.

2. Facilitated diffusion: transport of Absorption of substances in small intestine.

substances by a transmembrane protein
molecule. Absorption of glucose in cells.

3. Osmosis: the diffusion of water across a Water reabsorption in kidneys.

membrane but always down the
concentration gradient. Usage of physiological solution NaCl.
 Active transport: uses ATP to force substances through the membrane AGAINST
their concentration gradient. It requires (i) a transmembrane protein (ii) energy

1. Ion pumps: the pumping of substances To maintain membrane potential

across a membrane by a highly specific
transmembrane protein molecule. Na reabsorption in kidneys

Endocytosis: the transport of materials into the cell.

1. Phagocytosis: cell eating Cell immunity

2. Pinocytosis: cell drinking Using of human egg cells

Mothers milk immunoglobin uptake

Cholesterol
3. Receptor-mediated endocytosis: the
cytoplasm membrane folds inwards to Some viruses (polio, herpes)
form coated pits.

Exocytosis: the transport of materials out of Secretion of mucus, hormones, enzymes.

cell.

13. The cell as an open system. Substances and energy flow in cells. Cellular energy supply.

METABOLISM: Sum of all the chemical and physical changes that take place within the body.
Metabolism can be divided into two types
- Anabolism
- Catabolism

ANABOLISM: A constructive metabolic process whereby energy is consumed to synthesize or

combine simpler substances, such as amino acids, into more complex organic compounds,
such as enzymes and nucleic acids.

CATABOLISM: A type of metabolic process by which complex molecules are broken down
to produce energy and reducing power.
14. Structure and functions of the nucleus. Euchromatin and Heterochrimatin. Hierarchies
in eukaryotic genome organization. Sex Chromatin.

EUCHROMATIN HETEROCHROMATIN
Dispersed extended portion Clumped coil portion
Poorly staining Densely staining
Genetically active portion Genetically inactive portion
Contains unique sequences Contains repetitive sequences
Loss of even a small part of portion results in Loss of even big part of portion doesn’t result in
change of phenotype or organism death. change of phenotype or death of organism.
The euchromatrin is in the central region of nucleus The heterochromatin is close against the inside
of the nuclear membrane
High frequency of recombination Low frequency of recombination
Includes genes which are determined qualitative Includes genes determined quantitative traits
traits

Name Organization Function

Nuclear Double layered membrane. The Encloses the contents of the nucleus
1 envelope space between the layers- during cells life cycle. Pores regulates
perinuclear space & appears to the passage of the molecules between
connect with the rough E.R. the nucleus and cytoplasm
The envelope is perforated
with nuclear pores.
In nucleoplasm many substances are
Nuclear matrix A network of the fibers-
dissolved which are required for
2 nuclear matrix is found in
chemical reactions.
nucleoplasm- a highly viscous
liquid of nucleus.
1. The synthesis of specific for
particular organism RNA molecules.
Chromatin It is dense string like fibers of 2. The transmissions of hereditary
3 DNA and proteins properties to daughter cells.

Dense fibers of chromatin

4 Nucleolus inside nucleus 1.The synthesis of rRNA
2. The construction of ribosomes
Hierarchies in eukaryotic genome organization

Level Characteristics
Nucleosome Coiling of DNA double helix around histone
protein beds. i.e.nucleosomes.

Solenoid level Nucleosome undergo coiling to form chromatin

fibers-solenoid

Looped domain Chromatin fiber in turn form loops

Metaphase chromosome Supercoiling to form metaphase chromosome

SEX CHROMATIN: a small condensed mass of the inactivated X-chromosome usually located
just inside the nuclear membrane of the interphase nucleus; the number of sex chromatin
bodies
per nucleus is one less than the number of X-chromosomes; normal males and females
with
Turner syndrome (XO) have none (sex chromatin negative), normal females and males
with Klinefelter syndrome (XXY) have one, and XXX-females have two. For technical
reasons only about half the cells in a preparation show typical masses

15. Chromosome composition and morphology. Chromosomes during the cell cycle.
Polytene chromosomes.

Morphological types of chromosomes ( as seen in metaphase)

1. METACENTRIC- A chromosome having its centromere in the middle. It’s the type of
chromosome with a centrally placed centromere that divides the chromosome into 2
arms having approximately equal length.
2. SUB METACENTRIC- A chromosome whose centromere lies between its middle and its
end but closer to the middle.
3. ACROCENTRIC- A chromosome with the centromere near one end so that one
chromosomal arm is the short and one is long
4. TELOCENTRIC- A chromosome like a straight rod with the centromere in terminal position
(such chromosomes aren’t in human karyotype by standards)

Chromosome during cell cycle:

Cell cycle is the cycle of events in a eukaryotic cell from one cell division to the next. It
consists of interphase and Mitosis.
During interphase, chromatin is in its least condensed state and appears loosely distributed
throughout the nucleus. Chromatin condensation begins during prophase and chromosomes
become visible. Chromosomes remain condensed throughout the various stages of mitosis.
The chromosomes are shortest and most visible during metaphase

Polytene chromosomes:
In tissues of most species, chromosomes aren’t visible during interphase. One exception is the
giant chromosomes in the salivary glands of many dipteran (two-winged) flies, discovered in
1933. Polytene chromosomes are much larger than the chromosomes of other cells in the
larva. The giant size of polytene chromosomes is 3000mcm lengthways, 15-20 mcm in
thickness. They began as normal chromosomes, but through repeated rounds of DNA
replication without any cell division (called endoreplication), they become large, banded
chromosomes. Thus single chromosome consists of many chromatids (about 1000) because of
process of continuous replication.
16. Human karyotype. Human chromosome classification. Medical Application of
chromosome analysis.
Human karyotype is the number, size and the shape of the chromosomes of a somatic cell
arranged in a standard manner.
Chromosomes are arranged in pairs and ordered by its size. Somatic cells have 23 pairs of
chromosomes which makes the diploid (2n) number 46. The haploid (n) number is the number
of chromosomes in a gamete- sex cell.
There are two types of chromosomes:
(i) Autosomes: Chromosomes other than sex chromosomes.
Occurs in pairs in diploid cells.
(ii) Heterochromosomes: Sex chromosomes.
Determines the gender of the individual.
Chromosomes differ in Male and Female. In Male XY and in Female XX. (Y is
smaller in size than X.
Human karyotype for male is 44X+ XY (22 pairs of autosomes + pair of hetero
chromosome)
Human karyotype for female is 44XX

MAIN PRINCIPLE OF CHROMOSOME ANALYSIS

1. Chromosomes are studied on stage of prophase, metaphase or anaphase.
2. Making of the specimens Chromosomes are studied on tissue section, but squashes and smears
are more suitable.
3. Chromosomes are stained with basic dyes. Two principle staining techniques.
(i) Conventional staining techniques- Used to uniformly stain chromosomes and leave the
centromeres constricted, thus enabling measurement of chromosome length, centromeric position
and arm ratio.
(ii) Banding or differential staining techniques used to facilitate the identification of specific
abnormalities. Most commonly used- G-Banding. It yields series of lightly and darkly stained bands.
The dark region tend to be heterochromatic, the light region tend to be euchromatic cytogenetics
employs several techniques (C,Q,R,T banding) to visualize the different aspects of specific
chromosome abnormalities.
4. The metaphase plate with good allocation of chromosomes and without the considerable layer
are appropriate for analysis.

5. Depending on the research purpose the chromosome analysis is carried with or without karyotyping.
6. Except shape and length two additional parameter are used for characteristics of
chromosomes. (a) Centromere index (CI) ratio of short arm length to total length of chromosome
( its 0.5 for
metacentric chromosome )
(b) Ratio of arms ( its 1 for metacentric chromosome )

- Denver and Paris classification of chromosomes include chromosomal features such as length of
chromosomes, centromere position ad relative length of arms for conventionally stained
chromosomes.
- Some of the main indications for performing chromosomal analysis are parental (before the birth)
postnatal (after the birth).
17. Ultrastructural pathology of the cell.
Cancer of lymphatic tissue (lymphoma): Hollow
metaphase. Skin Cancer (squamous cell carcinoma): Tipolar
mitosis.

18: Molecular level of organization of genetic information.

Nucleic acid structure and function.
Characterizing different levels of DNA organization.
Level 1- Nucleosome- coiling of DNA double helix histone protein beads i.e.
nucleosome. Level 2- 30nm Fiber- Nucleosome undergo coiling to form chromatin
fibers- solenoid. Level 3- Looped domain- chromatin fibers turn loops (looped domain)
Level 4- supercoiling to form metaphase chromosome.
Nucleic acids are molecules that allow organisms to transfer genetic information from
one generation to the next. These are two types of nucleic acids: Deoxyribonucleic acid (DNA)
and Ribonucleic acid (RNA)

NUCLEIC ACIDS: NUCLEOTIDES

Nucleic acids are composed of nucleotide monomers linked together. Nucleotides contain three parts:
a) Nitrogenous base
b) Pentose sugar
c) A phosphate group

DNA is composed of a phosphate-deoxyribose sugar backbone and four nitrogenous base:

adenine A, guanine G, cytosine C and thymine T. In double stranded DNA, adenine pairs
with thymine (AT) and guanine pairs with cytosine (GC)
Function: DNA is the cellular molecule that contains instructions for the performances of all cell
functions. When a cell divides, its DNA is copied and passed from one cell generation to the
next generation. DNA is organized into chromosomes and found within the nucleus of our cells.
It contains the programmatic instructions for cellular activation. When organisms produce
offspring, these instructions in are passed down through DNA.

RNA most commonly exists as a single stranded molecule. RNA is composed of a phosphate
ribose sugar backbone and the nitrogenous bases adenine, guanine, cytosine and uracil. When
the DNA is transcribed into a RNA transcript during DNA transcription, guanin pairs with
cytosine (GC) and adenine pairs with uracil (AU)
Function: RNA in essential for synthesis of proteins. Information contained within the genetic
code is typically passed from DNA to RNA to the resulting proteins. There are several types of
RNA. Messenger RNA (mRNA) in the RNA transcript or RNA copy of the DNA message
produced during DNA transcription.
mRNA is translated of mRNA in protein synthesis. rRNA is a component of ribosomes and is
also involved in protein synthesis.
 19: Modes of genetic transfer in bacteria transformations, transduction and
conjugation. Medical importance.
- TRANSFORMATION: the transfer of genetic material from one cell to another and can alter
the genetic makeup of recipient cell.
- TRANSDUCTION: the transfer of part of DNA molecule from a bacterium (donor) to
other bacterium (recipient) by bacteriophage.
- CONJUGATION: the process in which DNA is transferred from a bacterial donor cell to
a recipient cell by cell-to cell contact.

20: Organization of eukaryotic and prokaryotic genomes structural and regulatory genes.
The tRNA rRNA genes mobile genetic elements.
HOUSEKEEPING GENES: are typically constitutive genes that’re required for the maintenance
of basic cellular function and are expressed in all cells of an organism under normal patho
physiological conditions.
LUXURY GENES: are tissue specific or organ specific, which means they’re not expressed in
all cells. They are not constantly expressed only when their function is needed.
STRUCTURAL GENES: genes encoding the amino acid sequence of a protein, non
regulatory gene.
REGULATORY GENES: genes that control protein production.
GENES OF tRNA: genes that encode for a transfer RNA. Unlike most of other genes encoding
the proteins, they are represented in multiple copies of the genes in human genome.
GENES OF rRNA: genes that code for a ribosomal RNA. The nucleolus organizer, special regions
known as nuclear organizing regions (NOR) are on some chromosomes.

21. Organization of the flow of genetic information in the cell . DNA replication. DNA repair.

-Organization of the flow of genetic information in the cell

The flow of genetic information follows the "Central Dogma" of molecular biology: DNA is copied as
messenger RNA (mRNA) which in turn is the template for protein synthesis (uses rRNA and tRNA).
Genes (DNA) specify the amino acid or nucleotide sequences of functional cellular proteins and RNAs.
-DNA Replication
It is the process of copying the double-strand DNA prior to cell division.

Significance of Replication; to make copies of DNA molecule

Enzymes and their functions:

TOPOISOMERASE - unwinds and uncoils the DNA double helix

HELICASE - cuts and rejoins one strand of DNA helping the separation of DNA helix
DNA-POLYMERASE - forms a new DNA chain in the 5’ to 3’ direction
DNA-LIGASE - links up the short DNA segments (known as Okazaki fragments) after replacing the
RNA primers with deoxy ribonucleotides
RNA-PRIMASE - catalyzes the polymerization of RNA building blocks (A,U,G,C) into the primer
RNA-PRIMER - is a short chain of RNA that is formed on the DNA template of lagging strand
STABILIZING PROTEINS(SSB PROTEINS) - stabilize the unwound parental DNA

Stages of DNA replication

Stage Characteristics
1 Initiation -Activation of deoxy ribonucleotides (mono-triphosphate)
-Recognition of initiation point
-Unwinding of DNA molecule
2 Elongation -Exposure of parent DNA base
-Base pairing
-Conversion of deoxy ribonucleotide monophosphate
-Formation of new DNA chains
3 Termination -New 2 daughter DNA molecules are produced & then they
become spirally coiled to form a double helix (Helix formation)
-DNA Repair
The process of restoration of the DNA structure

Significance of DNA repair; to repair mistakes in DNA structure

DNA repair mechanisms

Photo reactivation Excision repair

Factor of UV (ultraviolet) 1)X-rays
damage 2)HNO2
3)free radicals
4)some antibiotics
5)yperite (mustard gas)
DNA repair Enzyme photolyase in bacteria breaks 1)Endonucleases- recognition of damage,
mechanism the chemical bonds created by UV light incision of DNA single strand
between adjacent thymidine bases 2)Exonucleases- excision of damaged
(dimers) fragment
3)DNA-polymerase- polymerization
(synthesis of the correct fragment)
4)Ligases- ligation (linkage)

Diseases caused by disorder of DNA repair;

-Xeroderma pigmentosum (XP)

Cockayne Syndrome (CS)
Hutchinosm-Gilford progeria syndrome
Werner syndrome (WS) “Adult progeria”
Breast cancer
Colon cancer
22. Important properties of genetic code
GENETIC CODE - The biochemical basis of heredity consisting of triplets (codons) in DNA and
RNA that determine the specific amino acid sequence in proteins.

Characteristics

-The genetic code is a triplet code (A sequence of 3 nucleotides named “codon” codes for 1 amino acid).

-The genetic code is universal: given codon specifies the same anticodon in protein synthesis in
different species of organisms.

-The genetic code is redundant (degenerate) but unambiguous. It means two or more codons may
code for the same amino acid but neither of them ever specifies any other amino acid. Redundant
codons typically differ in their third positions.

-The genetic code is non-overlapping code: a nitrogenous base of one codon is not a part of
adjacent one.

-The genetic code is collinear. Linear order of codons in the mRNA corresponds to the linear orders
of amino acids in polypeptide chain.

-Biosynthesis of all proteins in prokaryotic and eukaryotic cells begins translation from start codon AUG
(methionine).

- Three codons: UAA, UGA & UAG are stop codons or termination codons. They do not encode
any amino acid, but signal the end of a polypeptide chain.

23. Protein synthesis steps. Transcription

-Protein synthesis steps

1. Transcription
2. Translation

-TRANSCRIPTION: the synthesis of RNA by the enzyme RNA-polymerase (synthesis of poly

ribonucleic strand) on DNA template (a gene).

Transcription occurs in the nucleus. Transcription takes the information encoded in DNA
and encodes it into mRNA, which heads out of the cell's nucleus and into the cytoplasm.
During translation, the mRNA works with a ribosome and tRNA to synthesize proteins.

SIGNIFICANCE OF TRANSCRIPTION: It generates RNA containing the information to synthesize a

specific protein.
Steps of transcription;

Stage Characteristics
1 Initiation DNA & RNA polymerase binding. The DNA unwinds & the RNA polymerase
binds at an initial binding site called the “promoter region.”

2 Elongation RNA polymerase makes an elongation chain of RNA nucleotides, each new
RNA nucleotide is complementary to the DNA nucleotide. (i.e., each
ribonucleotide inserted into the growing RNA strand follows the base
pairing rules. There is no thymine (T) in RNA). The RNA polymerase
proceeds down one strand moving in the 3’5’ direction but the synthesis
of the RNA proceeds in the 5’3’ direction.
3 Termination The completed mRNA molecule is released from RNA polymerase-DNA
complex and can begin translation. In eukaryotic cells this means first
moving from the nucleus into the cytoplasm. In prokaryotic cells (bacteria),
ribosomes can bind and begin translation before polymerase has
completed of the new mRNA strand.

Features Transcription DNA replication

Principal enzyme RNA Polymerase DNA Polymerase
Nucleotides ACGU (Deoxy) A C G T
Pairings C-G ….A-U C-G…A-T
Strand “copied” Lower strand (template) Both strands
Regions “copied” Specific regions all

24. Translation: Initiation, Elongation and Termination steps. Post translational protein modification.

-TRANSLATION: The synthesis of polypeptide using the genetic information encoded in mRNA molecule.

SIGNIFICANCE OF TRANSLATION: process provides the production of all types of proteins necessary for
an organism’s vital functions.
REQUIREMENT FOR PROTEIN SYNTHESIS: mRNA, tRNA, amino acids, ribosome, ATP, enzymes (and Mg2+
ions for amino acylation)
STEPS:
-Proceeds with preparatory stage acylation.

Stage Characteristics
1 Initiation -Leading codon AUG of mRNA associate with small subunit of ribosome.
-The AUG codon associate with UAC anticodon of aminoacyl-tRNA which bears
amino acid, methionine.
-Small subunit of ribosome associate with large subunit of ribosome
2 Elongation -Appropriate aminoacyl-tRNA molecules associate with A site on large
ribosomal subunit.
-Peptide bonds forms between amino acids at P and A site.
3 Termination -Step 1 to 3 are repeated until a stop codon on mRNA arrives at A site and a
releasing factor associates with it detaching the completed protein

-POST TRANSLATIONAL PROTEIN MODIFICATION:

Includes protein folding and chemical modification of a protein after its translation. It is one of the
later steps in biosynthesis for many proteins.

1. PROTEIN FOLDING: is the folding of polypeptide chain into their correct three-dimensional structures
after protein synthesis. The folding is provided for such enzymes as foldases and isomerases.
Sometimes specific proteins (chaperonins or chaperone proteins) take place in folding.

2. CHEMICAL MODIFICATION: may involve the formation of disulfide bridges and attachment of any of a
number of biochemical function groups, such as acetate, phosphate, various lipids and carbohydrates.
Enzymes may also remove one or more amino acids from the amino end of the polypeptide chain, or
cut the polypeptide in the middle of the chain.

Types of post translational modification includes;

-PHOSPHORYLATION: the addition of a phosphate group, usually to serine, tyrosine, threonine

or histidine

-ACETYLATION: the addition of an acetyl group, usually at the N-terminus of the protein

-ALKYLATION: the addition of an alkyl group (eg: methyl, ethyl)

-METHYLATION: the addition of a methyl group, usually at lysine or arginine residues (this is a
subtype of alkylation)

-GLYCOSYLATION: the addition of a glycosyl group to either asparagine, hydroxylsine, serine

or threonine, resulting in a glycoprotein.
25. Gene expression in prokaryotes and eukaryotes. Exon-intron structure of eukaryotic
genes. Processing, splicing.

Gene expression in prokaryotes and eukaryotes

All the genetic information of prokaryotic is usually contained in a circular DNA molecule-
the bacterial chromosome (nucleoid) and eukaryotic nuclear DNA is organized in non-closed
molecules-chromosomes, whereas mitochondrial DNA and plastid DNA are circular.
Prokaryotic genomes are short.
Eukaryotic genomes are redundant. Because they contain a lot of copies of some genes, “silent”
genes, and long non-coding inserts within genes (introns) and between them spacers.
Bacterial chromosome has histone-like proteins whereas eukaryotic chromosomes have
histone proteins.
In eukaryotes, regulation of gene expression is more complex and precise than in prokaryotes.
-EXONS: Coding part of gene

-Exon contains the code for producing protein and is copied and spliced together with other
such sequences to form mRNA

-Each exons codes for a specific protein of the complete protein

-Exons are separated by introns

-INTRONS: Non-coding part of gene that is initially transcribed into the primary RNA transcript and
is removed by splicing.

-PROCESSING, SPLICING: All the primary transcripts produced in the nucleus must undergo
processing steps to produce functional RNA molecules for export to the cytosol.

Significance of processing: formation of “mature” functional mRNA-a template for translation.

Alternative splicing allows many gene products with different functions to be produced from a
single coding sequence, so it is a major protein diversity.
 Steps of RNA processing:

-CAPPING (SYNTHESIS OF THE CAP): Cap is a mutilated guanine (G) which is attached to the 5’ end of
the pre-mRNA. The cap protects the RNA from enzymes-nuclease. Cap helps in the arrangement of
‘mature’ mRNA in ribosome.

-SPLICING: Removal of introns present in the pre-mRNA by enzymes nucleases and splicing of
the remaining exons by enzymes ligases

-POLYADENYLATION (SYNTHESIS OF THE POLY (A) TAIL): This is a sequence of adenine (A) 30-300
nucleotides long. This completes the mRNA molecule, which is now ready for export to the cytosol.
(The remainder of the transcript is degraded, and the RNA polymerase leaves the DNA

The removal of introns and splicing of exons is done with spliceosome- a complex of several
small nuclear RNA (snRNA) molecules and some 145 different proteins.

Enzymes that take part in processing:

-NUCLEASES: enzymes that catalyze the break-down of nucleic acids by cleaving the bonds
between adjacent nucleotides.

-LIGASES: link up the fragments of nucleic acids in single strand.

26. Regulation of gene expression in prokaryotes and eukaryotes.

Prokaryotic gene expression is primarily controlled at the level of transcription. It occurs in

cytoplasm of a cell due to the lack of a defined nucleus; thus DNA is freely located within
the cytoplasm.
Eukaryotic gene expression is controlled at the level of epigenetics, transcription, post
transcription and post translation. It occurs in both the nucleus and cytoplasm. In
eukaryotes, regulation of gene expression is more complex and precise than in prokaryotes.
27. Genetic engineering and biotechnology.

Genetic engineering, also called genetic modification, is the direct manipulation of an organism
genome using biotechnology. It is a set of technologies used to change the genetic makeup of cell,
including transfer of genes within and across species boundaries to produce improved organism.

28. Cell life, its courses and periods, cell cycle. Interphase.

cell is the basic unit of life. Each type of cell has its own life span. Example: RBC – 4 months.

Cell cycle or cell division: the cycles of events in eukaryotic cell from one cell division to the next.
It consists of interphase and mitosis.

Interphase: the stage of a cell between two successive mitotic. It is a phase defined only by the
absence of cell division. Cells during interphase may or may not growing. There are 3 parts of
interphase.

1. S-PHASE: synthesis of DNA (production of centrosome) during which the DNA is replicated.
2. G2 PHASE: is the second growth phase, also the preparation for mitosis. Synthesis of
tubulins (mitotic spindle proteins). The G2 phase is a period in the cell cycle where cell exists
in a quiescent state.
3. M-PHASE: or mitotic and cytokinesis, the actual division of the cell into two daughter cells.

29. Cell division, Mitosis

Mitosis is a process of nuclear division in a living cell by the chromosomes are exactly replicated and
the two copies distributed to identical daughter nuclei.

1. PROPHASE: the first mitotic stage of mitosis, during which the mitotic spindle apparatus forms
2. METAPHASE: the chromosomes arranged to migrate to the equator of the spindle.
3. ANAPHASE: at first, the centromere joining each pair of sister chromatids separate, freeing
the sister chromatids from each other. After the chromatids physically separate, they are
pulled to opposite poles of the cell by the microtubules attached to their centromere.
4. TELOPHASE: the mitotic apparatus is disassembled; the nuclear envelope reforms and
the chromosomes uncoil.
5. CYTOKINESIS: when mitosis is complete, the cell divides into two so that the two sets
of chromosomes separated by cell mitosis end up a different daughter cell.
30. Mitotic abnormalities. Somatic mutations. Amitosis.

The mitotic abnormalities are formed as a result of placing the cells in unfavorable conditions
during different phases.

Physical agent such as temperature. Radiations and chemicals like narcotics and enzyme inhibitors,
can easily produce mitotic deformities.

Somatic mutation, genetic alteration acquired by the cell. That can be passed to the progeny of
mutated cell in the course of cell division. Somatic mutations are inherited genetic alterations that
occur in the germ cells caused due to environmental factors such as exposed to UV radiation or other
chemicals.

Amitosis is cell division by simple cleavage of the nucleus and division of the cytoplasm without
spindle formation of appearance of chromosomes.

31. Cell cycle regulation. Cell growth. Growth factors. Mitotic activity in the tissues.

The cell cycle is controlled by the interaction of three types of regulatory proteins, which initiate and
or introduce progression through cell cycle:

1. Cyclin-dependent kinases (CKD)

2. Cyclin that interacts with CKD with formation of complexes
3. Inhibitors of cyclin-dependent kinase complexes

Regulation of cell cycle is carried out by the reversible phosphorylation of regulatory proteins.

Growth factors: proteins which regulate cell growth, cell proliferation, differentiation and

mutation.

1. Epidermal GF (EGF)
2. Fibroblast GF (FGF)
3. Platelet derived GF (PD6F)
4. Insulin-like GF (IGF-I)
5. Vascular growth factors.
Violation of normal mitotic course and incorrect distribution of chromosomes among daughter cells
can result in cells with unbalanced karyotype, causing mutations and in particular. Somatic aneuploidy.

There are three types of mitotic abnormalities classified according to morphological principles:
1. Abnormalities caused by chromosome damage
2. Abnormalities caused by damage of mitotic apparatus
3. Violation of cytokinesis
32. Cell death: apoptosis and necrosis.
APOPTOSIS: of programmed cell death, process of cellular self-destruction. Eg: death of RBC.
NECROSIS: the cell death which can be caused by variety of chemical and toxic substances. Eg:
frostbite.

33. Cell and tissue cultures, cell cloning. Application of cell culture in medicine.

Cell and tissue culture is a process by which cells are grown under controlled conditions,
generally outside their natural environment. Cell conditions may vary from each cell type.

Cloning in biotechnology refers to processes used to create copies of DNA fragments

(molecular cloning), cells (cell cloning), or organisms.

Fundamental to the manufacture of viral vaccines and other products of biotechnology. Culture of
human stem cells is used to expand the number of cells and differentiate the cells into various
somatic cell types for transplantation.
34.Subject and objectives of Human Genetics and Medical Genetics. Pharmacogenetics and
Immunogenetics.
Human genetics: Study of inheritance of characteristics by children from parents.
Objectives:
-Formulate the significance of human genetics
-Study pedigree analysis for inheritance and distribution of certain genetic traits in human beings on
the basis of heredity principles discovered by G.Mendel
-Evaluate probabilities of birth of healthy or affected child in family with heredity pathology
-Determine a mode of inheritance of human traits.
Pharmacogenetics: Science that studies drug responses and their genetically controlled variations. It
allows us to combine pharmacology and genomics to develop effective and safe medication dosages
which are specific to an individual’s DNA makeup. Therefore, minimizing the side effects from the
drugs.
Immunogenetics: Study of the genetic basis of the immune response. It includes the study of normal
immunological pathways and the identification of genetic variations that result in immune defects,
which may result in the identification of new therapeutic targets for immune diseases.
35.Human genotype. System of interacting genes.
Human genotype: A person’s genotype refers to the types of genes he or she has for particular
inheritable trait. Genotype determines which characteristics an individual will express, for example:
whether they have freckles, if they are lactose intolerant or if their eyes will blue, brown or another
color.
A specific allelic combination for a set of gene is called Genotype
There are two types of gene interactions:
-Interaction of allelic genes (Complete dominance, Incomplete dominance, Super dominance (over
dominance) & Codominance
-Interaction of non-allelic genes (Complementation, Epistasis, Polygeny)
Mechanism of gene interaction: Two genes are interacting to produce a single phenotype according to
interaction of proteins, which are coded by this genes.
 36.Human Phenotype:
Complex of specific and individual characters and features of an organism. Quantitative and qualitative
traits.
Human Phenotype: Environmentally and genetically determined observable physical appearance of an
organism. For example: Sound of your voice, height, eye color.
Phenotype can be determined by observation
Quantitative traits: It’s a measurable phenotype that depends on the cumulative actions of many
genes and the environment. These traits can vary among individuals, over a range, to produce a
continuous distribution of phenotypes. They are usually determined by a larger number of genes.
Example: Height & blood pressure.
Qualitative traits: Feature, that is either present, or not present, depending on whether the gene
responsible for that trait is present (or functional) or absent (or non-functional). They are usually
encoded by one gene or sometime by few number of genes. These traits usually don’t change in
response to the environment. (1) Qualitative traits are discrete values, so they can be analyzed by
counts and ratios. (2)
Example: Flower color (which could be red, brown, green or yellow) & Blood group
Note:
1. Example: If a flower is genetically programmed to produce blue flowers, it will continue to produce
blue flowers no matter where and how they are grown.
2. For example, the number of blue flowers in a plant can be counted exactly, and flowers to plant
ratios can be determined precisely.
37.Principles of inheritance in monohybrid cross.
Mendel’s law of segregation. Mendelian traits. Monogenic traits in humans.
Mendel’s law of segregation: When an organism makes gametes, each gamete receives just one gene
copy, which is selected randomly.
38.Principles of inheritance in di- and trihybrid crosses.
Mendel’s law of independent assortment.
Mendel’s law of Independent assortment: The alleles of two (or more) different genes get sorted into
gametes independently of one another. In other words, the allele a gamete receives for one gene does
not influence the allele received for another gene.
39.Multiple alleles. Blood type genetics. Their medical importance.
Multiple alleles: Phenomenon when more than two allelic form of wild type are located on the same
locus in a given pair of chromosomes.
Example: Human blood type. Blood type exists as 4 possible phenotypes: A, B, AB & O. Alleles are
different forms of one gene, for example; there can be 3 alleles (A, B & O) that to contribute blood
types on humans.
Blood type genetics: The A and B antigen molecules on the surface of red blood cells are made by two
different enzymes. These two enzymes are encoded by different versions, or alleles, of the same gene.
The A allele codes for an enzyme that makes the A antigen, and the B allele codes for an enzyme that
makes the B antigen. A third version of this gene, the O allele, codes for a protein that is not
functional; it makes no surface molecules at all.
Everyone inherits two alleles of the gene, one from each parent. The combination of your two alleles
determines your blood type.
All possible combination of blood type alleles
Medical importance:
-Blood testing can detect possible risks to fetal health in advance, by checking whether the fetus'
blood type is compatible with the mother's.
-Blood transfusion
If someone with group B antigen receives red blood cells from someone with group A antigen, their
body will reject the transfusion. This is because patients with B antigen on their red blood cells have
anti-A antibody in their plasma. The anti-A antibody in the plasma then attacks and destroys the A
antigen donor red blood cells. This can be fatal.
40.Interaction of allelic genes: Complete dominance, incomplete dominance, over dominance,
codominance
Complete dominance: Type of inheritance in which both heterozygotes (Aa) and dominant
homozygotes (AA) have the same phenotype.
Incomplete dominance: Type of inheritance in which a cross between organisms with two different
phenotypes produces offspring with a third phenotype that is a blending of the parental traits
Over dominance: Type of inheritance in which dominant allele in heterozygote condition (Aa) is more
active than homozygous one (AA).
Codominance: Type of inheritance where a cross between organisms with two different phenotypes
produces offspring with a third phenotype which both of the parental traits appear together.
41.Interaction of noon-allelic genes: complementation, epistasis.
Non- allelic genes: Alleles that are in different loci of homologous chromosomes or in the non-
homologous chromosomes.
Complementation: Kind of gene interaction in which manifestation of a character is determined by
presence of two dominant genes of different allelomorphic pair simultaneously
Epistasis: Type of inheritance when the action of one gene masks the effect of another. There are two
types of epistasis:
1.Recessive epistasis: inhibition effect is due to influence of recessive allele in homozygous condition.
(Eg. Bombay phenotype)
2.Dominant epistasis: one dominant gene suppresses the manifestation of other non-allelic dominant
gene.
42.Polygenic inheritance in humans. Pleiotropy.
Polygenic inheritance occurs when a trait is controlled by several gene pairs, usually results in
continuous variation. Polygenic traits are controlled by an unknown number of genes. The gene
expression is influenced by a variety of factors including gender, nutrition, breed, rate of growth and
amount of exercise. These traits are qualitative traits- that’s a wide range within the population. Such
traits include height, weight, character, working abilities and some gender defects.
Pleiotropy: Phenomenon, in which a single gene produces multiple phenotypic effects.
There are two types of pleiotropy.
1.Primary pleiotropy: in this pleiotropy gene shows own multiple action simultaneously. Example:
Osteogenesis imperfecta, Marfan’s syndrome, Hartnup disease.
2.Secondary pleiotropy: in this pleiotropy there is one primary phenotypic appearance of gene, which
leads to multiple secondary effects developed one for other.
Example: Sickle-cell anaemia, phenylketonuria, galactosemia.
43.Linked inheritance(T.H Morgan law).Crossing over. Genetic and cytological maps of chromosome.
Genes that are inherited together with the other gene(s) as they are located on the same
chromosome. Supplement. When a pair or set of genes are on the same chromosome, they are usually
inherited together or as a single unit.
Crossing over: Crossing over involves the exchange of chromosome segments between non-sister
chromatids during the production of gametes. often called recombination. It occurs during meiosis.
Distance between any two genes are measured in terms of mapunits. One map unit is also known as
centimorgan being equal to 1% of crossing over.
44.Chromosomal theory of inheritance.
1)Genes are located on chromosomes
2) Genes in chromosome are arranged in linear order
3) genes of same chromosome tend to be inherited together
4) genes of same chromosome compose linkage group.
5) gene linkage can be broken down under crossing over.
6) Distance between genes in chromosome is proportional to percentage of crossing over between
them.
45.Human genome research, present state. Genetic maps of human chromosomes.
NHGRI's mission in formal terms is to "support the NIH component of the Human Genome Project, a
worldwide research effort designed to analyze the structure of human DNA and determine the
location of the ..
A graphic representation of the arrangement of a gene or a DNA sequence on a chromosome. A
genetic map is used to locate and identify the gene or group of genes that determines a particular
inherited trait. ◇ Locating and identifying genes in a genetic map is called genetic mapping.
46.Genes of autosomes and sex chromosomes. Sex linked traits, sex influenced traits, sex limited
traits, hemizygosity.
Humans have a diploid genome that usually contains 22 pairs of autosomes and one allosome pair (46
chromosomes total).
Sex chromosomes: Chromosomes which differ in males and females.
Males (XY) and females (XX)
Sex linked traits: traits which are controlled by genes which align on sex chromosomes
Sex limited traits: Traits expressed in only one sex. E.g.: beard growth or mammary gland
Sex influenced traits: They are expressed in both male and females but variously E.g. pattern baldness,
singing voice
Hemizygosity: When gene exists only in one copy
47. Genetics of sex. Genetic mechanism of sex determination. Gene dosage. Gene position effect.
sex determination is genetic: males and females have different alleles or even different genes that
specify their sexual morphology.
Genetic mechanism of sex determination
1) Chromosomal or genetic level(fertilization)
2) Gonadal sex(9-16 weeks after fertilization)
3) Phenotypic sex(8 weeks after fertilization)
4) Gender identify (from childhood)
Gene dosage is the number of copies of a particular gene present in a genome.
Gene Position effect is the effect on the expression of a gene when its location in a chromosome is
changed, often by translocation. This has been well described in Drosophila with respect to eye color
and is known as position effect variegation (PEV).
48.Variation, its forms. The ontogenic and evolutionary significance of variation.
variation is ability to exist in different forms.
Forms:- 1) heritable (genetics)
2) Non- heritable (modifications)
Significance
The Evolutionary Significance of Variation in Traits Subject to Ontogenetic Change and Maternal
Environmental Effects. ... The strength and ubiquity of these sources of variation are important to
evolutionary biologists because they can mask the expression of genetic variation in such traits.
49. Modifications, their characteristics. Reaction norm.
Non heritable or somatic variations occur in the somatic cells of individuals due to influence of
environment.
Visible or otherwise measurable properties of heritable traits are called phenotypes, while the genetic
factors responsible for creating the phenotypes are called genotypes. The most basic question to be
asked about a trait is whether or not the observed variation in the character is influenced genes at all.
The Norm of Reaction is a curve that relates, for a given genotype, the contribution of environmental
variation to observed phenotypic variation.
50.multifactorial principle of phenotypic appearance. Role of environmental factors in gene
expression, penetrance, expressivity. Phenocopies.
polygenic or multifactorial traits occurs when a trait is controlled by several gene pairs usually results
in continuous variation. Example height, mass, intelligence skin and eye color in human are polygenic
traits.
The expression of genes in an organism can be influenced by the environment, including the external
world in which the organism is located or develops, as well as the organism's internal world, which
includes such factors as its hormones and metabolism.
Penetrance: Frequency of expression of an allele when it is present in genotype of the organism.
Expressivity: Variation in allelic expression when the allele is penetrant.
Phenocopies: an individual showing features characteristic of a genotype other than its own, but
produced environmentally rather than genetically.
51.Genotypic variation, its forms. Combinative variation. The mechanism of its appearance and
significance.
genotypic variation is the variation in genotypes either between individuals of the same species or
between different species as a result of genetic mutation, gene flow, or something that occurred
during meiosis.
1)combinative
2)mutation
Combinative variation
Genotypical variation includes recombination’s of genes during meiosis and fertilization (combinative
variability) and mutations. Combinative variability can arise by two mechanisms: independent
assortment and crossing over leading to recombination.
Significance
Genetic variation in humans, as for the purposes of this section, will refer to any variance in phenotype
which results from heritable allele expression, mutations, and epigenetic changes. ... The trait is still
the result of variance in genetic sequence between individuals as a result of inheritance from their
parents.
52. Mutations and their phenotypic manifestations. Mutation theory. Classification of mutations.
Mutations in the genetic material may be gross or point alterations.
Mutations result from errors during DNA replication or other types of damage to DNA.
Mutation can result in many different types of change in sequences. Mutations in genes can either
have no effect, alter the product of a gene, or prevent the gene from functioning properly or
completely. Mutations can also occur in non genic regions.
Mutation theory
1. Mutations or discontinuous variations are the raw material of evolution.
2. Mutations appear all of a sudden. They become operational immediately.
3. Unlike Darwin’s continuous variations or fluctuations, mutations do not revolve around the mean or
normal character of the species.
4. The same type of mutations can appear in a number of individuals of a species.
5. All mutations are inheritable.
Medical importance
When a mutation alters a protein that plays a critical role in the body, it can disrupt normal
development or cause a medical condition. ... It is important to note that genes themselves do not
cause disease—genetic disorders are caused by mutations that make a gene function improperly.
53.Mutagens. Classification of mutagens. Genetic monitoring. Risk-reducing factors of mutation.
Natural or human made agent, which can alter the structure or sequence of DNA.
Mutagens are classified into:
1) Physical ( ionized radiation, uv radiation, temperature)
2) Biological ( viruses, bacterial toxins, fungal toxins)
3) Chemical mutagens ( nitrous acid, hydrocarbons from cigerrate smoke)
Genetic monitoring; the use of molecular markers to (i) identify individuals, species or populations, or
(ii) to quantify changes in population genetic metrics (such as effective population size, genetic
diversity and population size) over time.
Risk reducing factors
Natural exposure of an organism to certain environmental factors, such as ultraviolet light and
chemical carcinogens (e.g., aflatoxin B1), also can cause mutations. A common cause of spontaneous
point mutations is the deamination of cytosine to uracil in the DNA double helix.
54. Gene mutations, mechanism of their appearance. Monogenic diseases.
Mutations in single gene (point mutation- alteration in DNA at molecular level) or several genes.
Example: albinism, hemophilia etc.
Mechanism
gene
Modified gene
Monogenic diseases are caused by single mutant gene(Albinism, hemophilia). Their modes of
inheritance follow Mendel laws of inheritance and segregation.
55.Chromosome aberrations. Mechanism of their appearance. Example of human diseases due to
chromosome aberrations.
A chromosome abnormality, disorder, anomaly, aberration, or mutation is a missing, extra, or irregular
portion of chromosomal DNA. It can be from an atypical number of chromosomes or a structural
abnormality in one or more chromosomes.
Mechanism of appearance are:
1)deletion: loss of portion of one chromosome
2)duplication: when portion of chromosome is repeated
3)inversion: A segment separates from chromosome and re inserted at same place but reverse.
4)insertion: Extra chromosome segment is added into another site.
5)Translocation: A portion of one chromosome is transferred to another chromosome
Examples: Cri du chat, down’s syndrome, turners syndrome
56.Mechanisms of genomic Mutations( polyploidy, haploidy, polysomy, and monosomy).
Mutations can occur spontaneously owing to several different mechanisms, including errors of DNA
replication and spontaneous damage to the DNA. Mutagens are agents that increase the frequency of
mutagenesis, usually by altering the DNA.
Polyploidy: Polyploid cells and organisms are those containing more than two paired (homologous)
sets of chromosomes. Most species whose cells have nuclei (Eukaryotes) are diploid.
Haploidy: organisms whose cell has single pair of chromosome is known as haploid.(sperm, ova)
Polysomy: is a condition found in many species, including fungi, plants, insects, and mammals, in
which an organism has at least one more chromosome than normal, i.e., there may be three or more
copies of the chromosome rather than the expected two copies.
 Monosomy: is a form of aneuploidy with the presence of only one chromosome from a pair.
57.Classification of human hereditary diseases. Principle of their diagnostics.
hereditary diseases are classified into 5 categories:
1)Gene diseases
!)Monogenic diseases(albinism, hemophilia)
!!) polygenic diseases(gout, diabetes)
2)Chromosome diseases ( cri du chat, down syndrome)
3)Multifactorial disease ( atherosclerosis, hypertension)
4)Gene disease of somatic cells (cancer, autoimmune disorders)
5)Diseases due to incapability of genes(hemolytic disease)
Principle of diagnosis is Bio-chemical methods and genealogical method
59. Genealogical method. Modes of inheritance.
The study of particular trait begins with a person first found to exhibit the trait known as proband.
The procedure starts with gathering info of disorder, age of onset, duration of complaints and any
other major illness.
The second step is to collect info regarding first degree relatives, parents, sibs, offspring of proband.
The following info is to be recorded – name, surname, date of birth, age, age of death, cause of death,
still birth and abortions.
The data collected from family over no of generations can be represented in genealogical chart
(pedigree, family tree) using international conventional symbols.
Modes of inheritance: Autosomal dominant/ recessive
X-linked Dominant/ recessive
Y-linked
61.Monogenic disorders due to primary pleiotropy.
Primary pleiotropy: when a gene effects two or more traits directly. E.g.: marfan syndrome, ehlers
Danlos syndrome
Single-gene disorders: occur when an alteration occurs in a gene causing one gene to stop working.
An example of a single gene disorder is sickle-cell anemia.
.
62.Non chromosomal hereditary. Mitochondrial genome. Mitochondrial diseases.
Ans Non chromosomal disorders: are rare disorders caused by mutations in non-chromosomal DNA
located within the mitochondria. (The mitochondria are subcellular organelles.) These disorders can be
found to affect any part of the body including the brain and the muscles
Mitochondrial genome: The mitochondrial genome is the full genetic complement of a
mitochondrion. Mitochondrial DNA is only a small portion of the total DNA of a eukaryotic cell and in
most species is solely inherited from the mother. In humans mitochondrial DNA contains
approximately 16,600 base pairs encoding 37 genes.
Mitochondrial diseases: Mitochondrial diseases are inherited only from mother to all the children. (
example cardiomyopathy(MMC), Alzheimer’s disease, maternal myopathy)
63.hereditary diseases due to unknown primary bio chemical defect.
An inborn error of metabolism is defined as genetically determined biochemical disorder in which a
specific enzyme defect produces a metabolic block that may have pathological consequences.
The clinical picture is result of disorder brought about by the metabolic block which leads to:
1)Accumulation of precursor just preceding the step where there is a block.
2) stoppage of subsequent steps in the metabolism.
64. Disorders caused by numerical abnormalities of autosomes and sex chromosomes. Mechanism
of their origin and principles of laboratory diagnostics.
Abnormalities of autosomes
Down’s syndrome( Trisomy21, Mongolism)
Karyotype: 47, XX or XY, +21
Patients with Downs syndrome have 47 chromosomes instead of normal 46.
Diagnostics: 1) congenital heart diseases
2)mental retardation
3)abnormal ears/pelvis
Edwards syndrome(trisomy 18, E trisomy)
Karyotype: 47, XX or XY, +18
Diagnostics: 1)mental and growth retardation
2)congenital heart defects
3) Abnormal dermatoglyphic

Patau’s syndrome(trisomy 13 or D trisomy)

Karyotype: 47, XX or XY, +13
Diagnostics: 1)microcephaly
2)cleft lip/plate

4)double ureter
Sex chromosome Abnormalities
1) Turner’s syndrome(ovarian dysgenesis)
Karyotype: 45, XO

Diagnostics: 1)short height

2)wide and webbed neck
3)Absence of menstrual cycle
4) Abnormal bone development
2)Klinefelter’s syndrome
Karyotype: 47, XXY
Diagnostics: 1)wide hips
2)poor beard grow
3)frontal baldness absent
4) mental retardation

65.Germ and somatic mutations, their importance. Mosaicism.

germinal mutation, is any detectable variation within germ cells. Mutations in these cells are the only
mutations that can be passed on to offspring,
Somatic mutations are a result of changes in the DNA of somatic cells
66.Genetic heterogeneity of hereditary diseases. Genocopies.
There are two types of genetic heterogeneity: allelic heterogeneity, which occurs when a similar
phenotype is produced by different alleles within the same gene; and locus heterogeneity, which
occurs when a similar phenotype is produced by mutations at different loci.
hereditary diseases: a specific gene from one or both parents leads to an abnormality.
67.Genetic predisposition (susceptibility) to a disease. The concept of multifactorial diseases.
A genetic predisposition (sometimes also called genetic susceptibility) is an increased likelihood of
developing a particular disease based on a person's genetic makeup. A genetic predisposition results
from specific genetic variations that are often inherited from a parent
the concept of multifactorial diseases :Common medical problems such as heart disease, type 2
diabetes, and obesity do not have a single genetic cause—they are likely associated with the effects of
multiple genes (polygenic) in combination with lifestyle and environmental factors
68.Importance of family medical history for genetic counseling. Medical genetic counseling.
knowing your family history can help you reduce your risk of developing health problems. Family
members share their genes, as well as their environment, lifestyles, and habits. ... Risks for diseases
such as asthma, diabetes, cancer, and heart disease also run in families.
69.Prenatal diagnosis of hereditary diseases. Newborn metabolic screening programs.
Prenatal screening tests: These tests can tell you the chances that your fetus has an aneuploidy and a
few additional disorders. FAQ165 “Prenatal Genetic Screening Tests” focuses on these tests. ... These
tests are done on cells from the fetus or placenta obtained through amniocentesis or chorionic villus
sampling (CVS).
The Newborn Metabolic Screening Programme screens for rare but potentially serious disorders such
as phenylketonuria (PKU), cystic fibrosis, and congenital hypothyroidism. A blood sample is taken from
your baby's heel at or as soon as possible after 48 hours of age
70.Prevention and treatment of hereditary diseases. Perspectives of gene therapy.
Check regularly for the disease. Follow a healthy diet. Get regular exercise. Avoid smoking tobacco and
too much alcohol. Get specific genetic testing that can help with diagnosis and treatment.
perspective of gene therapy :The skin, and in particular epidermal cells, are particularly suited to
genetic manipulation and follow-up of therapeutic effects. Cutaneous gene therapy may be effective
for skin defects and systemic abnormalities.
71.Reproduction as universal characteristics of life. Types and forms of reproduction. Possibilities of
organism cloning.
there are many types of reproduction two important are : Sexual reproduction requires two parents.
Each parent contributes a gamete - a sex cell that has half of the normal DNA of a regular body cell. In
males, the gametes are sperm and in females, the gametes are eggs.
Asexual reproduction requires only one parent.
72.Meiosis. Genetic variation due to meiosis.
Meiosis :a type of cell division that results in four daughter cells each with half the number of
chromosomes of the parent cell.
Genetic variation is increased by meiosis. During fertilisation, 1 gamete from each parent combines to
form a zygote. each gamete contains a different set of DNA. This produces a unique combination of
genes in the resulting zygote.
73.Gametogenesis: spermatogenesis, oogenesis.
Gametogenesis:the process in which cells undergo meiosis to form gametes.
Spermatogenesis: is the process by which haploid spermatozoa develop from germ cells in the
seminiferous tubules of the testis. This process starts with the mitotic division of the stem cells located
close to the basement membrane of the tubules.
Oogenesis :occurs within the embryo sac and leads to the formation of a single egg cell per ovule. In
ascaris, the oocyte does not even begin meiosis until the sperm touches it, in contrast to mammals,
where meiosis is completed in the estrus cycle.
74.Human sex cells, their cytogenetic characteristics. Differences between gametes and somatic
cells.
in humans, the male gamete is called sperm, and the female gamete is called an egg. When the
gametes join they form a cell called a zygote. Human sperm and eggs contain 23 chromosomes.
In humans, a diploid cell has 46 chromosomes. Gametes are sex cells, so the egg and sperm. They are
considered haploid because each gamete contains half the number of chromosomes that an
organism's somatic cells will have. Produced through meiosis, human gametes each have 23
chromosomes.
75.Fertilization. Parthenogenesis. Biological features of human reproduction.
parthenogenesis is a natural form of asexual reproduction in which growth and development of
embryos occur without fertilization.
Normal egg cells form after meiosis and are haploid, with half as many chromosomes as their mother's
body cells. Haploid individuals, however, are usually non-viable, and parthenogenetic offspring usually
have the diploid chromosome number. Depending on the mechanism involved in restoring the diploid
number of chromosomes, parthenogenetic offspring may have anywhere between all and half of the
mother's alleles. The offspring having all of the mother's genetic material are called full clones and
those having only half are called half clones. Full clones are usually formed without meiosis. If meiosis
occurs, the offspring will get only a fraction of the mother's alleles since crossing over of DNA takes
place during meiosis, creating variation.
Parthenogenetic offspring in species that use either the XY or the X0 sex-determination system have
two X chromosomes and are female.
76.Ontogenesis, its periods. Embryogenesis, its steps. Extraembryonic organs.
The ontogenesis is divided into prenatal and postnatal periods.
Embryonal stage or the prenatal embryogenesis includes development of an organism from a
fertilization of an ovum up to the going out of a new organism from an egg or from the uterus of a
maternal organism into environments.
The embryogenesis includes the following basic stages:
1. Fertilization and cleavage of an ovum.
2. Gastrulation with germinal layers is formed.
3. Histogenesis and organogenesis are the formation of tissues and organs.
Extraembryonic organs protect and nourish the embryo. All terrestrial vertebrates have four
extraembryonic membranes: the chorion, allantois, yolk sac, and amnion. Although they develop from
the germ layers, these membranes are not part of the embryo proper and are discarded at birth. The
extraembryonic membranes are adaptations to the challenges of embryonic development on land.
During development they protect the embryo, prevent the embryo from drying out, and help it to
obtain food and oxygen and eliminate wastes.
77.Genetic control of development. Differentiation of cells, germ layers and tissues. Embryonic
induction. Cell and tissue cloning.
Germ layer, any of three primary cell layers, formed in the earliest stages of embryonic development,
consisting of the endoderm (inner layer), the ectoderm (outer layer), and the mesoderm (middle
layer). The germ layers form during the process of gastrulation, when the hollow ball of cells that
constitutes the blastula begins to differentiate into more-specialized cells that become layered across
the developing embryo. Hence, each germ layer eventually gives rise to certain tissue types in the
body.
The endoderm is so called because it is the innermost of the three germ layers. Cells derived from the
endoderm eventually form many of the internal linings of the body, including the lining of most of the
gastrointestinal tract, the lungs, the liver, the pancreas and other glands that open into the
gastrointestinal tract, and certain other organs, such as the upper urogenital tract and female vagina.
Endoderm cells give rise to certain organs, among them the colon, the stomach, the intestines, the
lungs, the liver, and the pancreas. The ectoderm, on the other hand, eventually forms certain “outer
linings” of the body, including the epidermis (outermost skin layer) and hair. The ectoderm also is the
precursor to mammary glands and the central and peripheral nervous systems.
Cells derived from the mesoderm, which lies between the endoderm and the ectoderm, give rise to all
other tissues of the body, including the dermis of the skin, the heart, the muscle system, the
urogenital system, the bones, and the bone marrow (and therefore the blood). The mesoderm allows
more highly evolved organisms to have an internal body cavity that houses and protects organs,
bathing them in fluids and supporting them with connective tissue.
Embryonic induction describes the embryonic process in which one group of cells, the inducing tissue,
directs the development of another group of cells, the responding tissue. Induction directs the
development of various tissues and organs in most animal embryos; for example, the eye lens and the
heart.
Cloning is a set of laboratory methods and techniques that allows us to reproduce any biological
material as many times as we want, specifically cells, DNA, etc.
Stem cells are undifferentiated or unspecialized cells without a specific function because they have not
yet changed into specific tissue cells. Stem cells are different to other body cells because during
division they present the following characteristics:
They produce new copies of themselves indefinitely.
They produce new cells that under the right stimuli can develop into different tissues of which the
human body is composed of.
They can colonise and repair sick tissues or organs, replacing sick cells with healthy cells.
Stem cells are cells from which each of us developed after the ovum is fertilized by the spermatozoon.
Stem cells are the cells that gave rise to all the tissues and organs that make up our body when they
were subjected to specific stimuli. All our organs and tissues maintain a “small reserve” of these cells
that allow for the maintenance and repair of tissues and organs.
78.Features of human prenatal development. Critical periods of embryonic development.
Environmental teratogens.
Prenatal development is the process in which an embryo and later fetus develops during gestation.
Prenatal development starts with fertilization, the first stage in embryogenesis which continues in
fetal development until birth.
In human pregnancy, prenatal development, also known as antenatal development, is the
development of the embryo following fertilization, and continued as fetal development. By the end of
the tenth week of gestational age the embryo has acquired its basic form and is referred to as a fetus.
The next period is that of fetal development where many organs become fully developed. This fetal
period is described both topically (by organ) and chronologically (by time) with major occurrences
being listed by gestational age.
In pregnancy, each part of the baby’s body forms at a specific time. During these times, the body can
be very sensitive to damage caused by medications, alcohol or other harmful exposures. We call this
specific time the “critical period of development” for that body part.
critical periods of embryonic development include fertilization, implantation, gastrulation,
differntiation of germ layers, differntiation of axial organs, placentation and organogenesis.
teratogenesis is the production of developmental malformations. there are 3 types of teratogenic
influences. 1-physical (radiation, X-rays, hyperthermia, mechanical trauma, electromagnetic
influence). 2-chemical (alcohol and drugs, industrial solvents, medicines (thalidomide, antibiotics)). 3-
biological (infectious agents, viruses, bacterial toxins, protozoans).
 79.Congenital disorders, their classification: hereditary, exogenic, and multifactorial disorders,
embryopathies and fetopathies; abnormalities due to phylogenetic and non-phylogenetic factors.
congenital diseases are disorders present at birth as a result of the following:
1- genetic factors, e.g., chromosomal disorder as downs syndrome; gene disorder as hemophilia etc.
2- acquired in utero from environmental factors, e.g., congenital syphilis from maternal infection.
3- combined genetic and environmental factors, e.g., cleft palate, congenital heart disease.
although the factors responsible for some congenital diseases are present at birth, the signs and
symptoms of these conditions may not develop until a varying period of time. in some instances this
may be many years (polycystic kidney).
according to a mutation type, mode of gene interaction and environmental factors, all genetic
disorders are classified into 5 categories:
1- gene disease caused by mutation in a single gene (e.g., point mutation - alteration in DNA at
molecular level) or several genes. examples are albinism, hemophilia, partial color blindness. gene
diseases subdivide in monogenic and polygenic ones:
a- monogenic diseases are caused by a single mutant gene (albinism, hemophilia). their modes of
inheritance follow mendels law of inheritance and segregation.
there are 3 groups of diseases resulting from mutations affecting single genes do not follow the
mendelian rules of inheritance:
i) diseases caused by triplet repeat mutations (e.g., fragile x syndrome, huntingtons chorea).
ii)diseases caused by mutations in mitichondrial genes (e.g., lebers hereditary optic atrophy).
iii) diseases associated with alteration of imprinted regions of the genome (e.g., prader -willi syndrome
and angelman syndrome).
b- polygenic diseases are determined by a number of genes, each having minor effect in expression of
a single trait (gout, diabetes mellitus). they follow the pattern of polygenic inheritance for
transmission from generation to generation.
2. chromosome diseases caused by chromosomal and genomic mutations. examples are a cri-du-chat
syndrome, turners syndrome, downs syndrome.
3- multifactorial diseases, where both genetic and nongenetic, or environmental, factors are involved
in determining the trait and these factors are multiple. examples are atherosclerosis, ulcer diseases,
and hypertension.
4- gene diseases of somatic cells (e.g., cancer, autoimmune diseases).
5- diseases due to incompatibility of genes, example is hemolytic disease of newborns, in which fetal
red blood cells die earlier due to the action of antibodies formed by a mother against fetal RH-antigen.
80.Human postnatal development, its periods.

81.Interrelation of ontogenesis and phylogenesis. Biogenetic law (recapitulation theory) and its
interpretation by A.N. Severtzov.

82.Phylogenesis of integument, skeleton, digestive, respiratory, circulatory, nervous, excretory and

reproductive systems of vertebrates. Congenital disorders due to ontophylogenetic conditions.

83.Neurohumoral regulation of growth and development.

84.Growth and differentiation in postembryonic period.

85.Ageing as a stage of ontogenesis. Theories of ageing.

ontogenesis : the development of an individual organism or anatomical or behavioural feature from the
earliest stage to maturity.
86.Life expectancy and longevity problems. The concept of gerontology and geriatrics.
gerontology : the scientific study of old age, the process of ageing, and the particular problems of old
people. Geriatrics : relating to old people, especially with regard to their health care.

87.Clinical death and biological death. clinical

death : is when the heart stops pumping and can be revived if early medications were given.
Biological death : formal death for the body when the whole system fails but some certain organs
continue to function for a while.

88.Tissue and organ regeneration. Types of regeneration. Regenerative biology and medicine. 3 types
of regeneration : physiological, reparative and autotomy . Physiological : replacement of the cells that
are lost daily by day-to-day activities (example : RBC’s regeneration, regeneration of skin cells) .
Reparative : This is the replacement of lost parts or repair of damaged body organs. In this type of
regeneration, wound is repaired or closed by the expansion of the adjoining epidermis over the
wound.(example : healing of wounds) Autotomy : In
some animals like starfish, some part of the body is broken off on being threatened by a predator. This
phenomenon of self-mutilation of the body is called autotomy(example : starfish or octopus cutting of a
leg)

89.Features of regenerative processes in humans, their medical importance. Typical and atypical
regeneration. Neoplastic growth.

- Neoplasia : is a type of overgrowth of tissues .

90.Regulation of regenerative process.

91.Tissue and organ transplantation. Types of transplantation. Tissue incompatibility and its
management.

Autotransplantation, Allotransplantation, Xenotransplantation, Isotranplantation.

92.The concept of homeostasis. Homeostatic regulatory mechanisms at the different levels of

organization of life.

Hemostasis is the natural process in which blood flow slows and a clot forms to prevent blood loss
during an injury, with hemo- meaning blood, and stasis meaning stopping. During hemostasis, blood
changes from a fluid liquid to a gelatinous state. Steps of Hemostasis- Hemostasis includes three steps
that occur in a rapid sequence: (1) vascular spasm, or vasoconstriction, a brief and intense contraction of
blood vessels; (2) formation of a platelet plug; and (3) blood clotting or coagulation, which reinforces the
platelet plug with fibrin mesh that acts as a glue to hold the clot together. Once blood flow has ceased,
tissue repair can begin.

93.Modern evolutionary theory: synthesis of darvinism and population genetics.

The theory of evolution by natural selection, first formulated in Darwin's book "On the Origin of Species"
in 1859, is the process by which organisms change over time as a result of changes in heritable physical
or behavioral traits. Changes that allow an organism to better adapt to its environment will help it
survive and have more offspring.
94.Biological species concept. Species: reality and dynamics. Species criteria. Gene pool of species.
Biological species concept defines species in terms of interbreeding. For instance, Ernst Mayr defined a
species as follows: "species are groups of interbreeding natural populations that are reproductively
isolated from other such groups." The biological species concept explains why the members of a species
resemble one another, i.e. form phenetic clusters, and differ from other species. When two organisms
breed within a species, their genes pass into their combined offspring. As this process is repeated, the
genes of different organisms are constantly shuffled around the species gene pool. The shared gene
pool gives the species its identity. By contrast, genes are not (by definition) transferred to other species,
and different species therefore take on a different appearance.
95.Species structure. Population: a structural unit of species. Population characteristics:
morphological, ecological, genetic ones. Gene pool of population.

96.Idealized and real populations. Law of a constancy of genetic structure of idealized populations
(Hardy-Weinberg law). Its use in calculation of allelic frequencies of real populations and human
population.

The idealized population: With using a number of simplifying assumptions. Models of idealised
populations are either used to make a general point, or they are fit to data on real populations for which
the assumptions may not hold true
Hardy_Weinberg law: allele and genotype frequencies in a population will remain constant from
generation to generation in the absence of other evolutionary influences
Real population: is all the organisms of the same group or species, which live in a particular
geographical area, and have the capability of interbreeding

97.The concept of microevolution. Population: an elementary unit of species.

Microevolution is the change in allele frequencies that occurs over time within a population.This change
is due to four different processes: mutation, selection (natural and artificial), gene flow and genetic drift.
Organism level: The organism is an elementary unit of life. There is a great variety of all kinds of
organisms on the Earth (the amount only of animals runs to about 2 million species).

98.Factors of evolution, their interaction.

Sexual selection

small population

migration

mutation

natural selection

99.Natural selection as a driving force of evolution. Types of natural selection.

Natural selection is the differential survival and reproduction of individuals due to differences in
phenotype. It is a key mechanism of evolution, the change in the heritable traits characteristic of a
population over generations
Types:

Stabilizing selection

Directional selection

Disruptive Selection

100.The results of evolution: speciation, genetic polymorphism, adaptation.

Evolution: is a process that results in changes in the genetic material of a population over time. It gives
rise to biodiversity at every level of biological organism, including the levels of species, genetics and
individual organisms. •Speciation: is the
formation of new and distinct species. •Genetic polymorphism:
is the occurrence of two or more genetically determined phenotypes in a population.
•Adaptation: is process by which any living organism becomes fitted to its environment. This process is a
result of natural selection’s acting upon heritable variation.

101.Types of speciation.

•Allopatric: geographically isolated populations.

•Peripatric: a small population isolated at edge of large population.

•Parapatric: a continuously distributed population.

•Sympatric: within the range of ancestral population.

102.Genetic heterogeneity and genetic polymorphism of natural populations as a basis of their

evolutionary plasticity.

Genetic heterogeneity: is the production of single or similar phenotypes through different genetic
mechanisms. There are two types of genetic heterogeneity: •Allelic heterogeneity: occurs when a
similar phenotype is produced by different alleles within the same gene. •Locus heterogeneity: occurs
when a similar phenotype is produced by mutations at different loci.

Genetic polymorphism: Is a case where more than one allele occupies the gene’s locus within a
population.

103.Genetic load of human populations.

104.Adaptation of organisms to their habitat. Origin of biological expedience.

105.Human population. Population structure of mankind. Large and small populations (deme, genetic
isolates). population is
group of individuals living in particular geographic area and inter bearding in nature.
population structure: geographic area , size , density , sex ratio , age ratio.

106.The effect of marriage structure and demographic rates on gene pool of human populations.

the marriage of individuals having difference genotype effect the gene pool of a small population
107.The effect of mutagenesis, isolation, migration on genetic structure of population and genetic
constitution of humans. Genetic drift in isolates.

mutation causes loss of genes in populations. the average rate of mutation is 1 in 100000

isolation: it reduce the heterozygote and increase the homozygote.

migration: it causes exchange of genes of two groups.

genetic drift in isolates: causes a effect in gene frequent for small population but not for large one.

108.Features of natural selection in human populations. Selection and counter-selection.

important for evolution. the ability to transmit genes for the next generation.

109.Genetic and phenotypic polymorphism of mankind. Types of genetic polymorphism: adaptive

(ecological) and balanced (heterozygous).

110.The concept of macroevolution. Interaction of macro- and microevolution.

Macroevolution refers to evolution above the species level. Macroevolution encompasses the grandest
trends and transformations in evolution, such as the origin of mammals and the radiation of flowering
plants

Change in allele frequencies resulting from natural selection, genetic drift, gene flow, and mutation.
Microevolution happens on a small time scale — from one generation to the next. When such small
changes build up over the course of millions of years, they translate into evolution on a grand scale — in
other words, macroevolution!

The four basic evolutionary mechanisms — mutation, migration, genetic drift, and natural selection —
can produce major evolutionary change if given enough time.

111.Taxonomic position of Homo sapiens species within the living world. Qualitative features of
humans. Biological and social factors during anthropogenesis.

Human taxonomy on one hand involves the placement of humans within the Taxonomy of the hominids
(great apes), and on the other the division of archaic and modern humans into species and, if applicable,
subspecies.

big brains, opposable thumbs, speech, upright posture, clothing etc.

Anthropogenesis, meaning the process or point of becoming human, is also called hominization.

112.The origin of the human races as a result of adaptive laws of human development. The unity of
mankind.

113.Parasitism. Morphophysiological adaptations of parasites. Evolution of parasitism.

Parasitism is where one organism benefits at the expense of another.

Morphological:
1.Specialized manner of obtaining food:
a) loss or reduction of locomotor ability by some parasitic animals. (eg: fasciola and taenia)
b) absence of degeneration of feeding organs and sometimes even of the alimentary canal (taenia)
c) development of highly specialized mouth parts in some ectoparasitic animals (insects Pulex,
Pediculus.)
2. with penetrating or maintaining contact with:
a) the host development of boring devices to effect entry (eg, hexacanth worm embryos, many round
worms)
b) the host development of holdfast organs by which to cling securely (eg, hooks and suckers of Taenia
tapeworm, suckers of Fasciola, teeth of hookworms, claws of biting lice)
3. with offering resistance to host reactions:
a) the development of thick resistant outer covering in some parasitic animals
4. with great constancy of the parasite’s environment:
a) the tendency for regeneracy of the sensory organs (eg, Taenia.
Physiological:
1. Nutritional process:
a) Production of exo-enzymes by parasitic animals which digest host tissues external to the
parasite (eg, Taenia, plasmodium)
b) Production of anti-coagulants by blood-feeding parasitic animals (eg, Pulex)
c) Pronounced chemosensitivity in in order to reach the right site in a host’s body (eg,
Plasmodium in a mosquito, Fasciola in a herbivorous animal)
2. Reistance to host reactions:
a) Production of anti-enzymes in order to reach parasitic animals (eg, gut parasites)
3. Conditions of low oxygen tension:
a) Increased ability to respire efficiently in comparatively low oxygen concentrations (eg, gut
parasites)
114.Principles of the parasites classification: obligate, facultative, temporary, permanent,
monoxenous, heteroxenous, specific and nonspecific parasites, endo- and ectoparasites.

Obligate: completely dependent on the host during a segment or all of its life cycle (Plasmodium spp)
Facultative: an organism that exhibits both parasitic and non-parasitic modes of living and hence does not
absolutely depend on the parasitic way of life, but is capable of adapting to it placed on a host (eg,
Naegleria fowleri)
Temporary: free-living during a part of their life cycle
Permanent: parasitic throughout life
Monoxenous: a parasite so exacting that only a single species can supply the requirements (eg,
Ancylostoma duodenale, Taenia solium parasitize in human only.
Heteroxenous: when it requires some hosts to complete its complete its life cycle (eg, human and a female
Anopheles mosquito for Plasmodium, causing malaria.
Specific:
Nonspecific:
Endoparasites: in association with a host, a parasite that live inside host body within cells (cytozoic),
tissues (histozoic), or cavities (coelozoic) (eg, Plasmodium of red blood cells and liver cells, maggots of
fly Wohlfartia magnifica on necrotic tissue and larvae of tapeworm Taenia solium in brain tissue, Ascaris
lumbricoides of human intestine, etc)
Ectoparasite: these parasites may be situated externally upon it, either affixed to the superficial tisuues
(eg, the tick, wandering about on its surface, the flea.
115.The effects of a parasite on a host.

The relationship between a parasite and its host is beneficial to one, harmful to the other. Parasites may
even kill their hosts. But the death of its host is a disadvantage and often a disaster for a prasaite.

a. Takes away food, vitamins and micro elements.

b. Effects the mechanical actions of tissues and organs
 c. Toxic action on cell metabolism and organ functions
d. Causes allergies
e. Disturbs the intestinal micro flora
f. Aggravates other diseases
g. Clears the way for pathogenic microorganism
h. Changes metabolic processes
116.Pathogenicity and virulence of the parasites.

Pathogenicity refers to the ability of an organism to cause disease (ie, harm the host). Virulence is the degree of
pathogenicisty and it depends on invasiveness and toxigenecity of the parasire. Certain factors as dose
and route of invasion also work on pathogenicity of organism. For example: invasive dose in Lambliosis
varies from 10-100 mature cysts. In Helmintic invasions pathological manifestations depends on the size,
number activity and metabolism of the worms.

a. Incubation period: time interval between the entry of a parasite and the onset of the first signs
of the disease. Some disease may have an incubation period so slow that it takes months before
symptoms appear.
b. Prodromal periods: in which characteristic symptoms of the disease are absent and non-specific
symptoms develop common to many diseases.
c. Clinical period is characterized by a specific clinical manifestation
d. Invasion oucome: which can end in death, recovery or chronic invasion.
117.The effects of a host on a parasite.

The host must provide conditions for the development of the parasite. The parasite has a specific
inhabitation. During transition to parasitism the relations of the organism and the environment become
simpler. The temperature of the hosts plays a vital role in the reproduction and maturation of the
parasite. Also auto invasion increases high chances for its sexual reproduction The host is like a link
between the parasite and the external environment. The temperature of the hosts plays a vital role in
the reproduction and maturation of the parasite. Also auto invasion increases high chances for its sexual
reproduction.

118.Modes, routes and mechanisms of a parasite transmission.

They all have complex life cycles to accommodate to their different stages of life cycles to employ
specialized reproductive phases in the life cycle. They produce enormous number of off springs to
increase their successful dissemination of offspring among new hosts and have a high resistance to
external factors. A parasite must be able to find all of its nutritional requirements in the materials of its
hosts body in the food which a host acquires itself. In some cases parasites may utilize a variety of hosts
for this purposes. They sometimes use hosts as vectors.

a. Definitive host: in this the parasite lives its adult and sexual stage
b. Intermediate host: in which a parasite lives as the larval and asexual stage.
c. Additional Host: 2nd intermediate host (predatory fish for larvae of fish tapeworms)
d. Reservoir host: hosts that harbor the parasite and thus ensure its continuity of the parasites life
cycle and act as additional sources of human infestation.
e. Obligate parasite: when it can only live only as a parasite and dies with the death of the host.
f. Facultative Parasite: when it can live both in a host and as well as in free form.
119.Life cycles of parasites. Alternation of parasitic generations and phenomenon of the host
alternation. Definitive, intermediate, additional, reservoir, obligate, and facultative hosts of parasites.

120.Biological and mechanical vectors of causative agents of diseases.

Biological : is a vector that has more association between vector, pathogen and host. The disease agent
replicates inside the vector .

Mechanical : for example when an insect is feeding on faeces and it carries some bacteria physically
(might stick to its body) and transfer it to human food for example (important : no replication inside the
vector)

121.Organism as a habitat for parasites. Autoinvasion and reinvasion.

Autoinvasion : is when the infected person can get infected again from themselves because of bad
personal hygiene for example (not cleaning properly after defecation)(example : Entrobius vermicularis)
.

Reinvasion : maybe is when the person gets infected again by the same pathogen but not from himself
from other people .

122.Parasitocenology science. Human being as a main component of the symbiocoenosis.

123.Transmissive and natural focal diseases. The concept of obligate and facultative transmissive
diseases.

Natural : it means that the disease is found in the nature and can be obtained from a bite of a blood
sucking insect for example .

Transmissive : the pathogen should be transferred from an infected organism to the new non-infected
organism
Obligate : is a parasite that can’t complete its lifecycle without a host as a part of it
Facultative : is an organism that shows parasitic characteristics but doesn’t totally depend on a host.

124.E.N. Pavlovsky's theory of natural focality (nidality) of transmissive diseases. A natural focus and
its components: a causative agent, its vector and reservoir hosts.

it’s a group of diseases which are reserved in wild animals (rodents, birds etc.) and are transmitted by
blood-sucking arthropods

125.Types of natural foci. Synanthropic foci. Anthroponoses and zoonoses.

Natural focus is the ecology (the environment that relates to living organism) that is best suited to a
biological system. E.g. an insect-borne disease; the area in which the disease naturally flourished.
A synanthrope (from the Greek syn-, "together with" + anthro, "man") is a member of a species of wild
animals and plants of various kinds that live near, and benefit from, an association with humans and the
somewhat artificial habitats that humans create around them. Those habitats include houses, gardens,
farms, roadsides, garbage dumps, and so on. Anthroponoses (Greek “anthrópos”
= man, “nosos” = disease) are diseases transmissible from human to human. Examples include rubella,
smallpox, diphtheria, gonorrhea and trichomoniasis.
Zoonoses are diseases, pathogens of which are transmitted from one animal to the other. Major modern
diseases such as Ebola virus disease and salmonellosis are zoonoses.

126.Biological principles of eradication of transmissive and natural focal diseases.

Biological principles of eradication of diseases are:

Control: The reduction of disease incidence, prevalence, morbidity or mortality to a locally acceptable
level as a result of deliberate efforts;

Elimination of disease: Reduction to zero of the incidence of a specified disease in a defined

geographical area

Elimination of infections: Reduction to zero of the incidence of infection caused by a specific agent in a
defined geographical area.

Eradication: Permanent reduction to zero of the worldwide incidence of infection caused by a specific
agent Example: smallpox.

Extinction: The specific infectious agent no longer exists in nature or in the laboratory Example none.

127.Essentials of prevention of parasitic diseases. Prophylaxis of parasitic diseases: biological,

immunological, ecological, and public methods.

A. Biological measures: using their “natural” enemies. For example, breeding the mosquitofish, which
feeds on larvae of malaria mosquitoes.

B. immunological measures: use of antibiotics

C. ecological measures: habitat disruption e.g. draining the water where mosquito breed.

D. public methods:

128.Factors of distribution of parasitic diseases. Human migration and dispersion of parasitic diseases.

Climatic Factors that have a profound effect on the epidemiology of parasitic infections
are temperature, humidity, rainfall, sunlight and wind. These factors determine the geographical
distribution of both host and parasite.

Man appeared in East Africa some three and a half million years ago and then migrated to
Europe, Asia, and later to the Americas, thus beginning the differentiation process.

Wars, spontaneous migrations and forced migrations (slave trade) led to enormous
mixtures of populations in Europe and Africa and favoured the spread of numerous parasitic
diseases with specific strains according to geographic area.

For example, the three human plasmodia (Plasmodium falciparum, P. vivax, and P.
malariae) were imported from Africa into the Mediterranean region with the first human
migrations, but it was the Neolithic revolution (sedentarisation, irrigation, population
increase) which brought about actual foci for malaria.
129.Famous parasitologists and their contributions to science.

J. Harold Drudge, Widely acknowledged for his numerous contributions to the field of parasitology,
Drudge is especially known for the significance of his work in equine helminthology (the study of
parasitic worms).

Anita Hoffmann was a Mexican specializing in acarology and parasitology. She is a pioneer in the
study of arachnids and acari in Mexico

Erasmus M. Nighbert Upon completing his doctorate, the U.S. Department of Agriculture’s
Bureau of Animal Industry (BAI) appointed Nighbert as a field agent in meat inspection and tick
eradication.

130.Subkingdom Protozoa. Classification, structure, and medical importance of representative

species.
protozoa are eukaryotic, unicellular organisms. Major classes of subphylum protozoa are class lobosea
(amoeba proteus, E.histolytica( amoebic dysentery) , zoomastigophora(euglena, lamblia(giardiasis),
sporrozoa ( plasmodium, toxoplasma(toxoplasmosis) and litostomatea(paramecium,
Balantidium(balantidiasis).
Structure of organisms of class lobosea:- NO definite shape, reproduce exclusively asexually by
variations of mitosis. Production of cyst in one of the stages in life cycle.
Class zoomastigophora: they are fixed oval, elongate or spherical shape. Reproduction is by
longitudinal fission and sexual one.
Class sporozoa: -reproduce sexually and asexually
Class litostomatea: they have macro micro-nucleus. Reproduce sexually and asexually by transversal
fission.
131.Entamoeba histolytica.
1.Classification(Taxonomy):Phylum:Sacromastigophora,Class:Lobosea 2.Latin name: Entamoeba
Histolytica 3.Disease: Amoebiasis {amoebic dysentery} 4.Geographical distribution: Its widespread in the middle
east , India , Indo-China, North and Central Africa, Indonesia, South America, etc. 5.Morphology: E.Histolytica
occurs in human body in 3 vital forms, two trophozoites and a cyst. (a)Forma magna- it’s a vegetative large tissue
form which feeds on the erythrocytes. Size 30-45 mcm. (b)Forma minuta- a vegetative small commensal form
which lives in the lumen of the large intestine and feeds on bacteria. (c) cyst- it develops form the small vegetative
form. Occurs within the clonic lumen, never outside the body. Spherical in shape, Size 8-16 mcm in diameter,
Mature cyst contains four nuclei 6.Localization inside human body: Large intestine 7.Invasive stage for a human:
Cysts 8.Route and factors of transmission: Route: peroral, Factors: food products and water contaminated with
cysts -Person to person contact through dirty(unwashed) hands -In anal-oral sexual intercourse. 9.Source of
invasion:Infected human 10.Life cycle: Trophozoites emerge from the cyst in the small intestine and then pass on
to the colon, where they multiply by binary fission. E. hystolytica invades the colonic epithelium and it produces
proteole enzymes which cause lysis of cells tissue. Parasites grow and become capable of phagocytizing
erythrocytes. It penetrates (forma magna) the mucous, submucous and muscular coat invades the intestinal vessel
and reach to liver. 11.Pathogenicity: Lesions of large intestine,Main clinical manifestation is diarrhoea,Patients
stool has appearance of “raspberry jelly” as it contains blood. Complications- liver abscess, necrosis lung and brain
abscess. 12.Labatory diagnosis: Detection of E.hystolitica cyst in faeces(dysymptomic form). In acute amoebiasis
vegetative forms are revealed in diarrheic (liquid) stool with blood or mucous. (asymptomic form).
13.Prophylaxis:Reveal the cyst carriers and to treat sick people ,Protection of food products from flies,
cockroaches (vector of cyst).
132.Facultative parasitic amoebae of medical importance. Non-pathogenic amoebae.
1.Classification(Taxonomy):Phylum:Sacromastigophora, Class:Lobosea. 2.Latin name:Entamoeba coli
3.Disease:Non-pathogenic.4.Distribution:Worldwide, in temperate and tropic zone. 5.Morphology: Cysts
are large, has 8 nuclei. Entamoeba coli trophozoite has a single nucleus with its eccentric endosome and irregular
chromatin is visible. Size 20-40 mcm.
6.Localization:Large intestine.7.Invasive Stage: Cyst.8.Route and Factors: Same as E.Histolytica
9.Source of Invasion: Infected human.10.Life Cycle: Same as E.Histolytica. 11.Pathogenicity: commensal
but can produce mild diarrhea.12.Laboratory:Detection of cysts in stool.
13.Prophylaxis:Same as E.Histolytica.
133.Lamblia intestinalis.
1.Classification(Taxonomy):Phylum Sarcomastigophora, Class Zoomastigophora. 2.Latin name:Lamblia
intestinalis. 3.Disease: Lambliasis (Lamliosis)(giardiasis). 4.Distribution:Every where.
5.Morphology:1-CYST: immature cyst 2 nuclei, mature cyst 4 nuclei.2-TROPHOZOITE: two nuclei, 4 flagella.
6.Localization:Small intestine (duodenum) and sometimes gall bladder.7.Invasive Stage: Cyst
8.Route and Factors: Route: peroral, Factors: water and food stuff contains cyst, dirty (unwashed hands).
9.Source of Invasion: People who discharge cysts with faeces. 10.Life Cycle: Lamblia cyst get into human
organisms through mouth. The chitin membrane of the cyst dissolves on entering the intestine. The vegetative
forms multiply in small intestine and penetrate into the duodenum and gall bladder. The parasites from cysts,
which excrete with faeces. 11.Pathogenicity: Causes waterborne diarrhoeal disease. Also causes asymptomatic
colonization or acute or chronic diarrhoea – steatorrhea (pale fatty stool). Dyspeptic syndrome (nausea,
anorexia, pyrosis, hypoacidity). Weight loss, dehydration, and general emaciation cholecystitis and hepatitis
develop frequently. 12.Laboratory: Microscopical examination of duodenal contents where trophozoite are
revealed or faeces to find the cysts and vegetative form. 13.Prophylaxis: To reveal the cysts carriers and to
treat them, Protection of water and food stuffs, Health education of the population aimed at introducing of
hygienic habits.
134.Trichomonads.
Trichonomas Vaginalis
1.Classification(Taxonomy): Phylum Sacromastigophora,Class Zoomastigophora.2.Latin name: Trichomonas
vaginalis. 3.Disease:Urogenital trichomoniasis. 4.Distribution:Everywhere.5.Morphology: T.vaginalis
(trophozoite) is both phagocytotic and pinocytotic. Diagnostic features include jerky motility, induced by anterior
flagella, a rigid microtubular staining reveals a nucleus parabasal body and large number of dense granules.
Metabolism anaerobic and fermentative although it tolerates oxygen. 6.Localization: Lower parts of genital
apparatus and urethra. 7.Invasive Stage: Vegetative form (trophozoite). 8.Route and Factors: In sexual
intercourses. via toilet material like sponge. 9.Source of Invasion: Sick people and trichomonad carriers
10.Life Cycle: Is simple, multiplication begins by longitudinal binary fission. No resistant cyst, no intermediate or
reservoir host are included. 11.Pathogenicity: Invasions of trichomonads parasites occurs in the form of acute,
subacute or chronic urethritis and in women, also vaginitis. The disease is asymptomatic in 90% of men and 50%
of woman infected with parasite
Clinical manifestation: Frothy Vaginal discharge, Mild vulvovaginal itching and burning, Vaginal discharge usually
pale yellow to grey-green and has musty odour. , Lower abdominal pain, Urethritis and more rarely ,
epididmititis or prostatilitis can develop in infected males.
Re infection is common. 12.Laboratory: The smears are made of discharge from the vagina and urethra.
13.Prophylaxis: Practice safer sex, All sexual partners need to be tested even if there are no symptoms
Trichomonas Hominis
1. Classification(Taxonomy): Phylum Sacromastigophora, Class: Zoomastigophora. 2. Latin name: Trichomonas
hominis. 3. Disease: Non-pathogenic. 4. Geographical distribution : Worldwide5. Morphological features: Only
one morphological features: Trophozoite forms, 4 flagella ,No cysts. 6. Localization inside of human body: Large
intestine. 7. Invasive stage for human: Trophozoite. 8. Route and factors of transmission: Peroral
9. Source of invasions: Sick humans. 10. Life cycle: Trophozoite reproduce by binary fission and does not from
cysts 11. Pathogenicity: Non-pathogenic, commensal, sometimes associated with diarrhoea
12. Laboratory diagnosis:Microscopical examination of stool (trophozite).13. Prophylaxis: personal hygiene
Trichomonas Tenax
1. Classification(Taxonomy): Phylum: Sacromastigophora, Class: Zoomastigphora
2. Latin name: Trichomonas Tenax 3. Disease: Periodental gingivitis 4. Geographical distribution: Worldwide
5. Localization in human body: Oral cavity, sometimes lungs, stomach
 6. Morphology: No cysts, parasite have 4 flagella. Multiplication of trophozites occur by binary fission.
7. Invasive stage for human: trophozite 8. Route and factors of transmission: peroral
9. Source of invasion: sick humans 10. Life cycle: Trophozites are present in mouth cavity. Multiply by
longitudinal binary fission 11. Pathogenicity: Ulcers in mouth 12. Laboratory diagnosis: Microscopic
examination of smears from salivary in oral cavity 13. Prophylaxis: Hygiene/good hygiene habit and keep mouth
cavity clean.
135.Causative agents of cutaneous and visceral leishmaniasis.
Leishmania Tropica
1.Classification (Taxonomy): Phylum-Sacromastigophora, Class-Zoomastigophora
2. Latin name: Leishmania tropica minor/major/Mexicana complex. 3.Disease: Cutaneous Leishmaniasis also
known as Baghdad boil, Delhi boil, aleppo boil etc. 4. Geographical distribution: Leishmania tropica occurs in
Africa, the middle east, Asia, Polynesia, Leishmania Mexicana in the New world.5.Morphological form: In infected
tissue leishmania parasites occur as oval organisms without flagella (amastigote) cytoplasm contains one or several
vacuoles, a large Romanowsky- griemsa method stains the cytoplasm light blue, the nucleus bright red and
blepharoplasty dark-red. Flagellate (promastigote) form are produced in a body of invertebrate vector- sandfly
6. Localization inside human body: Subcutaneous fat. 7. Invasive stage for human: Promastigote form
8. Route and factors of transmission: Route- Transmissive. Invasion is conveyed by the sandfly vector of the genus
phlebotomus. Factor- bite of sandfly. 9. Source of invasion: sick humans and domestic dogs, wild rodents gebil,
ground squirrel. 10. Life cycle: the insect (vector) becomes infected when takes a blood meal containing infected
monocytes and macrophages. They transform into promastigotes and reproduce rapidly. When
Insect takes a blood meal, the promastigotes are injected into the mammalian host where they are phagocytosed
into vacuole by macrophages. They resist digestion and are released into the cytoplasm, where promastigotes
transform into amastigotes and start reproducing by binary fission. Heavily parasitized macro-phages rupture to
release their amastigotes which infect new macrophages.11. Pathogenicity: two forms of cutaneous leishmaniasis
(a) The dry form(late ulcerating leishmaniasis) is caused by leishmania tropica minor .Copper-coloured spot
appears on the skin of face, neck, hands and legs.The spot gradually develops into a tubercle which grows and
necrotized tissue forms in its centre.
(b) The moist form(acute necrotizing leishmaniasis) is caused by tropica major. Form papules (small pimple) are
oedernatous and the ulcer dges are loose and with an uneven outline.
Produce lymphangitis and lymphadenitis
Invasion of pinna (chidero’s ear caused by L.mexicana result in gross destruction of the external ear).
12. Laboratory diagnosis:
Is made by microscopic examination of the contents from cutaneous ulcer for finding of leishmania amastigotes
13. Prophylaxis: Use of insect repellent on exposed part of the body, Early diagnosis of disease and treatment of
infected humans, Extermination of sandflies, dog and rodent infected with leishmanias. Vaccination. Immunization
produces a stable immunity.
Leishmania brasiliensis
1. Classification (Taxonomic):Phylum Sacromastigophora, Class Zoomastigophora. 2. Latin name: Leishmania
brasiliensis. 3. Disease: Mucocutaneous leishmaniasis. 4. Geographical distribution: Central and South America
(Mexico, Gutaemala, Brazil, Venezuela and Panama). 5. Morphological features: same as Leishmania tropical
minor 6. Localization inside human body: Skin and rare mucous membrane 7.Invasive stage for human:
Promastigote form 8.Route and factors of transmission: Route: Transmissive, Invasive is conveyed by the vector of
genus Lutzomyia 9. Source of invasion: A reservoir of the American cutaneous leishmaniasis are sick humans,
rodents and domestic animal. 10. Life cycle: same as Leishmania Tropical minor 11. Pathogenicity: Mucocutaneous
leishmaniasis occur on the exposed parts of the body and runs a benign course. After an initial skin lesions, its
spontaneous heals and chronic ulcer appear after months or years on the skin, mouth and nose.
Tissue destruction with disfigurement can be very severe.
Mucosal lesions become painful gradually and can become sites of infection sometimes leading to sepsis.
Untreated these lesions can result in terrible deformity and complications are sometimes fatal.
12. Laboratory diagnosis: microscopic examination of the contents from cutaneous ulcer for finding of leishmanial
amastigotes 13. Prophylaxis: same as Leishmania tropical minor except vaccination.
136.Causative agents of trypanosomiasis.
Trypanosoma brucei gambiense
1. Classification (Taxonomy):Phylum Sacromastigophora, Class zoomastigophora
2. Latin name: Trypanosoma brucei gambiense. 3. Disease: African trypanosomiasis also sleeping sickness,
chronic form. 4. Geographical distribution:West Africa, but also Southern Sudan and Uganda
5. Morphological features: Trypanosoma can be seen as spindle shaped cell with pointed flagella at the end.
Cytoplasm stains light blue with Romanowsky- Gremza stain, while the nucleus blepharoplast and flagella stain
red. In the life cycles of Trypanosomes variety of different forms appear distinguished mainly by the position of
flagella: (i) Trypomastigote (Trypanosoma flagellum posterior of nucleus). (ii) Epimastigote flagellum anterior of
nucleus. (iii) Metacyclic Trypamastigotes small and stumpy and lack a free flagellum
6. Localization inside human body: Present in blood plasma, in tissue particularly in the muscles and the
cerebrospinal fluid. 7. Invasive stage: Metacyclic form. 8. Route and factors of transmission:
Route: Transmissive by the bite of Tsetse fly (Glossina palpalis). Factor: bite of Tsetse fly.
9. Source of invasion: patients with manifest and latent form of trypanosomiasis; cattle are reservoir of the
causative agent. 10. Life cycle: In vector organism T.b.gambiense passes, the following stages of development-
Trypomastigote, epimastigote and metracyclic form. In human organism T.B.Gambiense parasites are only in
promastigote form. Tsetse fly inoculates the human with metacyclic trypomastigotes. The parasites enter the
lymphatic system and pass into the bloodstream. Inside the host, they quickly transform into long slender
trypomastigotes are carried to other blood fluids like lymph and spinal fluid and continue multiplication asexually
by binary fission. 11. Pathogenicity: Invasion with Trypanososmes gives rise to Gambian or mid an west African
sleeping sickness which is characterized by cachexia, anaemia fever, oedema of the brain, chronic
leptomeningitis, haemorrhages and kidney lesions. Reaches coma at certain time and patients even die from this
disease. 12. Laboratory diagnosis: (a) microscopic examination of blood(during fever period). (b) examination of
the cerebrospinal fluid during the stage of and lethargy
13. Prophylaxis: Recognition and treatment of infected people. Vector control and protection of the population
from the bites of tsetse flies. Use of insect repellent, bed nets, chemotherapy, extermination of vector flies.
Trypnasoma brucei rhodesiense
1. Classification(taxonomy):Phylum Sacromastigophora, Class Zoomastigophora
2. Latin name: Trypnasoma brucei rhodesiense. 3. Disease: African trypnasomiasis
4. Geographical distribution: East Africa from Ethopia in the north to Botswana in the South
5. Morphoogical feature: See T.b.gambiense. 6. Localization of inside human body: Parasites are present in the
blood, lymph, lymph nodes in the tissue of spinal cord and brain, in the cerebrospinal fluid
7. Invasive stage for human: Metacyclic form. 8. Route and factors of transmission: Route – Transmissive by
tsetse fly, Factor- bite of tsetse fly (glossina morsitance). 9. Source of invasion Patient with manifest and latent
forms of the disease. Acute form of antelopes, zebras etc.10. Life Cycle: see T.B.Gambiense.11. pathogenicity: It
gives rise to Rhodesian or East African sleeping sickness, which is characterized by an acute course fever is high,
emacitation more rapid and lymphatic involvement less evident. 12. Laboratory diagnosis: Microscopic
examination of blood. See gambiense
13. Prophylaxis: Recognition and treatment of patients, Protection of population form the bites of tsetse flies,
the use of insect repellents, extermination of vector flies, chemoprophylaxis.
Trypanosoma cruzi
1.Classification(Taxonomy): Phylum Sacromastigophora, Class Zoomastigophora
2. Latin name: Trypanosoma cruzi. 3.Disease: Trypanosomiasis (Chagas disease)
4. Geographical distribution: South and Central America, Southern Texas (USA)
5. Morphological features: see Trypanasoma brucei gambiense
6. Localization inside human body: The parasites may be detected in the peripheral blood,but they multiply not
in the blood but in the tissues of the striated and cardiac muscles and in CNS.
7. Invasive stage for human: Metacyclic form 8. Route and factors of transmission:
Route: transmissive by bite of various bug species of family Triatomidae and contamination of vulnerable
surfaces with faeces of infected vectors. Less commonly infection may spread via transfusion of infected blood,
organ transplantation, transplacental. 9. source of invasion: Patients with American Trypanosomiasis natural
reservoir of disease is the domestic cats, dogs and wild animals (opossums, anteaters, armadillos, racoons,
rodents and monkey). 10. Life Cycle: Human are infected usually night time when the insect take blood meal and
infected faeces are rubbed into the skin abrasion of mucosal suface conjunctiva. Inside the host metacyclic
trypnomastigotes invade cell near the sites of inoculation where they transform into intracellular amastigotes
Amastigotes multiply by binary fission and eventually change into more trypomastigotes within the cell.
Trypomastigotes then breakout of the infected cells and migrate into the blood stream.
It will infect other surrounding tissues where they become amastigotes again
Replication occurs only when the parasite enters another or are ingested by another vector.
The kissing bug becomes infected by feeding on humans or animals blood that cointain circulating parasites.
Ingestion trypomastigotes transform in epimastigotes in vector’s midgut. Parasite multiply and differentiate into
infective metacyclic trypomastigots. 11. Pathogenicity: Acute phase – acute myocarditis and
meningoencephalitis. Chronic stage- serious cardiac, gastrointestinal problems. 25% patients develop chronic
myocarditis which may lead to sudden death. In adults disease is accompanied with rise of body temperature,
face odeama, enlargement of the thyroid gland, lymph nodes, spleen and liver. Transplacental transmission of
T.cruzi results in cogenitl Chaga’s disease with premature birth and development delay in survivors.
12. Laboratory diagnosis: Examination of a patients blood smears; PCR. 13. Prophylaxis: Involves the regular
spraying of houses with benzene hexachloride for extermination of bugs; the use if the bed nets; vector control;
blood screening is vital to prevent infection through transfusion and organ transplantation.
137.Malaria parasite. Control and elimination of malaria. Goals of the modern antimalarial service.
Species of malarial plasmodia.
1. Classification(taxonomy): Phylum Apicomplexa, Class Sporozoa
2 and 3. Latin name and disease:
Plasmodium Vivax (Tertian malaria)
Plasmodium malaria quartan malaria
Plasmodium falciparum tropical malaria
Plasmodium Ovale tertian malaria or ovale-malaria
Plasmodium Knowlei by knowlesi malaria
4. Geographical distribution:
P.Vivax is major species in temperate zones
P.Ovale occurs in tropical west Africa and rarely in the western Pacific.
Plasmodium knowlesi has been found in Malaysia, Borneo and Thailand
5. Morphological features and life cycle.
When a human being is bitten by anopheles mosquito female (infected with malarial plasmodia) the parasites
enter the blood with mosquito saliva
Invasive stage named sporozite is morphologically a thread-like cell.
Sporozites invade the liver process is extremely rapid, starting within a few minutes and being largely complete
within 30 min.
Exoerythrocytic Stage
In liver cell sporozites multiply (schizogony).
Numerous daughter nuclei are first formed transforming the parasite into schizont within an infected liver cell.
Schizont give rise to merozoites
Then the erythrocytic merozoite are liberated in their thousands from each parenchymal cell into the
blood stream.
Romanowsky-Giemsa stain dyes the cytoplasm light-blue and nucleus red.
P.falciparum undergo one cycle of tissue schizogony and P.vivax two cycles.
Sporozites of P.vivax and Ovale can remain in a latent form in liver as hypnozoites.
Endoerythrocytic stage
In blood stream merozoites attack to and invade circulating erythrocytes.
Merozoites become trophozite start digesting haemoglobin.
After gaining the entrance into erythrocyte, the young erythrocyte (ring-form stage) grows larger vacuole
of amoeboid trophozite movement
As it grows, a pigment appears Ca product of haemoglobin break
Mature schizont becomes round and pulls in its pseudopodia and the time of complete maturation.
Merulation takes place at this stage i.e. the nucleus and cytoplasm divide forming from 4 to 32
merozoites
On the completion of the merualtion, the erythrocytes are destroyed and the merozites are released into
the blood plasma.
Plasmodium species differ in their ability to invade RBCs. P.vivax and P.ovale preferentially invade
reticulocyte and young RBCs, whereas P.malariae invades senescent RBCs
p.falciparum is capabl of invading all RBCs, especially young.
 Each cell in the RBCs terminates with rupture of the cells and release of merozites into the circulation.
An average number of merozites produced in 40000 in P.Falcioarum and just 2000 in P.ovale.
At certain age, merozoites transform into sexual form-female(macrogamonts), male (microgamonts).
Gametogony
Microgamonts fertilize the macrogamonts and as a result form ookinete
The latter penetrates into the stomach wall where it transform into an oocyst.
The mature oocyst is filled with sporozite. It bursts and the soporozites are released into the mosquito
body cavity.
They accumulate in salivary glands and are introduced into the human body through a bile
6. Localization inside human body: Liver cell, erythrocytes.
7. Invasive stage for human: Sporozites in principal mode of transmission
Erythrocytic schizont in blood transfusion
8. Route and factors of transmission:
Route-Transmissive; transplacental, blood fusion, needle stick injury.
Factor- bite of female anopheles mosquito; blood of infected people.
9. Source of invasion: Patients with manifest and latent form of malaria.
10. life cycle: refer to textbook
11.Pathogenicity :
Malaria attack(paroxysia)
Several clinical forms of malaria (coma, central oedama).
Enlargement if spleen
Development if anaemia
Melanosis of internal organs and tissue
In P.falciparum infection, complication such as cerebral malaria may occur, its characterized by severe headache
impaired unconsciousness, ultimately coma.
12. Laboratory diagnosis:
Microscopic examination of the Gimsa-stained blood smear to reveal schizonts and gametocysts.
13. Prophylactic measures:
Personal- attacking the source of infection
Use of insecticides. For water control water reservoir are treated with HCCH chemicals and Gambusia fish which
destroy mosquito larva.
Individual
Protection formites of vector
Prophylactic chemotherapy
Vaccination.
138.Toxoplasma gondii.
1. Classification: Phylum Apicomplexa, Class sporozoa. 2.Latin name: Toxoplasma gondii
3. Disease: Toxoplasmosis. 4. Geographical distribution: Worldwide 5. Morphological features: pear or oval
shaped, exists in several forms, endozide(multiples intracellularly), young forms (pseudocyst) accumulate in cells
during multiplication, cysts, the result of intracellular multiplication, oocyst excrete with cat faeces can stay in
soil for month in certain temperature and humidity.6. Localization inside human body: The parasites are present
within various cells of histophagocytic system, nerve tissue, liver, placenta etc. 7. Invasive stage for human:
endozoide cyst, oocyst, pseudocyst.8.Route and factors of transmission: Major routes: Peroral, percutaneous
route, and transplacental (cogenital). Minor routes: parental route by transfusion or from transplanted organ
route. Factors: food stuffs contaminated with cat faeces or lamb or pork meat contaminated with T.gondii cysts,
meat, milk and dairy products of animals sick with toxoplasmosis, water contaminated by sick animals.
9. Source of invasions: cats and other animals of family Felidae, infected with causative agent of toxoplasmosis.
10. life cycle: T.gondii is an obligate intracellular parasite that has heteroxenous life cycle. Fertilization of
macrogamete by microgamete occurs within the host cell, results in formation of oocyst. Oocysts are passed in
cat faeces. These non-infective oocysts undergo process known as sporogony outside body and become
infections. The sporulated oocyst remain invasive months in shaded moist.
11.Pathogenicity: Immune system of healthy adults and children is enough to prevent 23 parasites from causing
serious illness. In some cases, acute acquired toxoplasmosis in adults can lead to flu-like symptoms headache,
 aching muscles (myalgia), fever of 38 degrees Celsius, tiredness, swelling of lymph nodes, particularly in throat or
armpits. There may be myocarditis, pericarditis, pneumonia, hepatitis, nephritis or encephalitis . Ocular
toxoplasmosis leads to reduced vision blurred vision, redness of eye. Congenital toxoplasmosis causes
microcephaly, eye lesions(chorioretinitis), pneumonia, hepatitis, nephritis, high (39-40-degree Celsius) or sub
febrile body temperature are also typical manifestations. 12. Laboratory diagnosis: Serological methods, imaging
(MRI, CT scanning for brain lesions of cerebral toxoplasmosis). Fluorescent antibody techniques are more reliable
than examination of stained smears identification of T.gondii. 13. Prophylaxis: Recognition of cases carriers
among domestic animals and their isolation and treatment. Milk must be boiled, meat of animal having
toxoplasmosis must be heat and treated, eggs must be cooked for five minutes. Health education on personal
hygiene is taught among population. Pregnant woman and young children should avoid close contact with cats.
139.Balantidium coli.
1.Classification(Taxanomy):Phylum ciliophoran, Class Litostomatea
2.Latin name: Balantidium coli. 3. Disease: Balantidiasis. 4. Geographical distribution: disease of tropics, although
it is also found in cooler temperate climates. 5. Morphological features: The parasite has asymmetrical oval body
covered with cilia. Parasite multiplies by horizontal binary fission. 6. Localization inside human body: Large
intestine. 7.Invasive stage for human: Cyst. 8. Route and factors of transmission: Route:peroral, Factors: food and
water contaminated with cyst. 9. Sources of invasion: Pigs, grey rats, patients with manifest forms of balantidiasis
and cyst carriers. 10. Life cycle: B.coli have two stage life cycle comprising motile ciliated forms that parasitize the
colon and cysts. Cyst pass through host digestive system until it reaches large intestine where excystation occurs
and trophozoites are released. They multiply by transversal binary fission or by conjugation. Trophozoites are
passed with faeces and encyst to form new cyst. Encystation takes place in rectum of host.
11. Pathogenicity: Common symptoms include chronic diarrhoea, occasional dysentery, Balantidium causes colitis,
lesions of colon, ulcers, blood and mucous in stool, causes liver abscess, loss of appetite and weight, nausea, foul
breathe, abdominal pain, headache and emaciation.
12. Laboratory diagnosis: Trophozoites in fresh stools (unfixed smear)
13. Prophylaxis:Sanitary-hygienic measures, protection of food and water from contamination with swine faeces
and observation of individual hygiene when taking care of animals.
140.Phylum Plathelminthes (Flatworms). Classification, structure, and medical importance of
representative species.

141.Features of helminth life cycles. Geohelminths, biohelminths, contact helminths.

Helminths form three main life-cycle stages: eggs, larvae and adults. Adult worms infect definitive hosts (those in
which sexual development occurs) whereas larval stages may be free-living or parasitize invertebrate vectors,
intermediate or paratenic hosts.
Biohelminthes: develop with alternation of host.
Geohelminths: develop without alternation of hosts and the part of life cycle passes in soil.
Contact helminths: all stages of development occur in human organism.
142.Liver fluke.
1. Classification: Phylum Platyhelminthes (flatworm), Class Trematoda (flukes) 2. Latin name: Fasciola hepatica
(liver fluke) 3. Disease: Fascioliasis 4. Geographical distribution: worldwide
5. Morphology: Adult fluke (marita) is 30-50mm in length, Mouth at anterior end is surrounded by muscular disk
forming anterior sucker consists of ventral sucker with digestive system, Excretory pore at posterior end 6.
Localisation inside human body: Bile ducts of liver
7. Invasive stage for human: Adolescaria 8. Route & factor: Peroral, Factor; water and aquatic plants
contaminated with adolescaria larva 9. Source of invasion: herbivorous animals (sheep, pigs, cattle). Very rarely
infect human
10. Life cycle:
-Animal excrete eggs in their faeces
-Those eggs that reach to warm water develop to become ciliated larva (miracidia)
-These larva enter the intermediate host- freshwater snail of class Gastropoda
-In the intermediate host larval development takes place (sporocyst, 1st and 2nd redia generation and cercaria
stage)
-Cercaria is released an encyst on aquatic or surface vegetation
-When mammalian host ingest parasites excyst, migrate through the intestinal wall, the body cavity and penetrate
the liver capsule.
-Immature fluke reaches bile duct and produce 5000 eggs by single individual
-Adult fluke remain in duct for many years
11. Pathogenicity: Fever, Malaise (feeling of discomfort), Weight loss, Right upper quadrant pain relate to
migration of fluke. Occur 2-3 months after ingestion
-Secondary symptoms (2nd phase): Jaundice, cholangitis, fluke maybe found in lung, brain and skin 12. Lab
diagnosis: Detection of ova in duodenal aspirate or serological test
Ova not found in stool until 2nd phase of illness. Why? Because it takes 3 months for the parasite to become an
adult.13. Prophylaxis: Health education, Boiling or purifying drinking water, Avoid raw or under-cooked salads
made from aquatic plants, Control of snail population
143.Cat fluke.
1. Classification: Phylum Platyhelminthes (flatworm), Class Trematoda 2. Latin name: Opisthorchis felineus (cat
fluke) 3. Disease: Opisthorchiasis 4. Geographical distribution: Central, East, South Europe, South-East Asia 5.
Morphology: Adult fluke 4-13 mm in length, 3-5mm in width, eggs are yellowish brown and oval with an
operculum. Size of egg is smallest among helminthic eggs.They contain miracidia when laid.6. Localization inside
human body: Biliary tree of liver, gallbladder, and rarely pancreatic duct.7. Invasive stage for human:
Metacercaria 8. Route and factors of transmission: Peroral, Factors; Raw or undercooked freshwater fish
containing metacercaria 9. Source of invasion: Fish-eating mammals
10. Life cycle:
-Developed eggs are passed out in faeces and upon reaching to water they are eaten by snails (Bithynia spp, first
intermediate host)
-The snail hatches and the miracidia in snail develop further through the stages of sporocyst, redia, cercaria
-Cercaria is released from snail to freshwater after 6-8 weeks
-It penetrates the muscles of freshwater fish to develop into metacercariae
-Metacercaria mature and become infective stage in 6 weeks
-Definitive host (humans, dogs, cats) ingest this infected freshwater fish
-Metacercaria are liberated by digestion, they enter duodenum then migrate to bile ducts where they mature
withing 4 weeks and produce eggs.
-Life span is 10 years 11. Pathogenicity: Obstruction of biliary tract, Necrosis of hepatic cells, Gallbladder enlarged
up to 10-20cm in length and contains white bile.
12. Lab diagnosis: Finding egg in faeces, bile or duodenal fluid, Immunodiagnosis is useful
13. Prophylaxis: Health education, Avoid eating raw or undercooked fish, Improve sanitation

144.Lung fluke.
1. Classification: Phylum Platyhelminthes, Class Trematoda 2. Latin name: Paragonimus westermani (Lung fluke) 3.
Disease: Paragonimiasis 4. Geographical distribution: East Asia, Japan, Taiwan, China, Philippines, West Africa,
South & Central America 5. Morphology: Adult flukes are reddish-brown and coffee bean shaped. 0.8-1.6 cm in
length, consists of cuticular spines on integument. Typically encapsulated in cysts adjacent to the bronchi. 6.
Localization inside human body: Lung parenchyma 7. Invasive stage for human: Metacercaria 8. Route and
factors of transmission: Peroral, Factors; raw, pickled or poorly cooked freshwater crustaceans 9. Source of
invasion: Crayfish-eating mammals

10. Life cycle: -Adult

fluke lives in lung, Ova are expelled from bronchi and expectorated with sputum and swallowed and passes to
faeces -Hatch in freshwater
after few weeks resulting miracidia in few various species of freshwater snail which form sporocyst, redia and
daughter redia (1st intermediate host) -Crabs and crayfish ingest
metacercariae (2nd intermediate host) -When human eats such
infected crabs and crayfish, they get infected -Metacercaria excyst in
peritoneal cavity, diaphragm and pleural cavity and encyst in lung parenchyma -Life span 20-25 years 11.
Pathogenicity: Chronic cough with jam-like brownish-red sputum, Breathlessness, chest pain, pleural effusion,
Extrapulmonary cerebral, abdominal paragonimiasis may occur 12. Lab diagnosis: Observing characteristics of ova
in sputum, pleural effusion or stool. (Eggs are golden brown and ovoid in shape), Chest radiographs for multiple
cysts in lungs, Computer tomography of chest 13. Prophylaxis: Health education, Controlling and eradicating
intermediate host, changing the social and dietary customs, Treatment of infected people in endemic area

145.Chinese liver fluke.

1. Classification: Phylum Platyhelminthes, Class Trematoda 2. Latin name: Clonorchis sinesis (Chinese liver fluke) 3.
Disease: Clonorchiasis (Clonorchosis) 4. Geographical distribution: Southeast of Asia, Common in China and also
found in Hong Kong, Vietnam, Taiwan, Korea and Japan 5. Morphology: Adult fluke has spindloid body 10-20x4-6
mm, branchy testes, egg looks same as O. felineus, and eggs are elongated ovoid in shape with attenuated anterior
end 6. Localization inside human body: Bile duct 7. Invasive stage for human: Metacercaria 8. Route and
factors of transmission: Peroral, Factor; ingestion of raw undercooked fresh cyprinoid fish or freshwater fish
containing metacercaria9. Source of invasion: Fish eating mammals like cats, tigers, dogs, foxes 10. Life cycle:
Same as O. Felineus with few variations. Variations are: -Intermediate host include both cyprinoid fish and
freshwater crayfish -Reservoir hosts includes cats, tigers, dogs, fox, badgers and mink
-lifetime in human organism come to 40 years 11. Pathogenicity: -Irritation of bile ducts which become dilated
and deviated -Enlargement of liver, necrotic and impaired function -Indifestion, epigastric discomfort, anemia -
Slightly jaundice, edema –Diarrhea -Cholangitis, cholangiohepatitis, cholangiocarcinoma 12. Lab diagnosis: Finding
egg in faeces, bile or duodenal fluid, Immunodiagnosis is useful 13. Prophylaxis: Health education, Avoid
eating raw or undercooked fish, Improve sanitation
146.Lancet fluke.
1. Classification: Phylum Platyhelminthes, Class Trematoda 2. Latin name: Dicrocoelium lanceolatum (Lancet fluke)
3. Disease: Dicrocoeliasis 4. Geographical distribution: Europe, Egypt, Iran, China and other countries 5.
Morphology: Transparent, flat measuring 5-15x1.5-2.5mm, Eggs are dark brown, slightly flattened on one side,
thick wall with large operculum and contain a fully developed miracidium when laid 6. Localization inside human
body: Bile duct 7. Invasive stage for human: Metacercaria in infected ants 8. Route and factors of transmission:
Peroral, Factors; infected ants found in grass, herbs, raw fruit, vegetables or even drinking water 9. Source of
invasion: Sheep and cattle, very rarely human 10. Life cycle: Complex lifecycle with 2 intermediate host- land snail
(Genus Helicella) & ant (Genus Formica) -Adult fluke lives in biliary passages of sheep and cattle. The eggs are
passed out in faeces. When land snail ingest their eggs, it undergo a development cycle (sporocyst, redia, cercaria
stage). Cercaria are released in slime balls shed by snail -Second intermediate host, and ant swallows a cyst loaded
with hundreds of lancet flukes. Parasite enter the gut and drift through its body. Cercaria grow in ant’s abdomen
and develop into infective metacercaria

-When metacercaria moves to head of the ant, ant becomes “zombie ant”. They climb up plants stems and attach
themselves there. Herbivorous mammals eats the plants together with the ant

11. Pathogenicity: Gastrointestinal disturbances-abdominal distress, biliary colic, vomiting, diarrhea or

constipation, enlargement of liver, spurious human infections 12. Lab diagnosis: Detect ova in faeces, bile or
duodenal fluid. Recovery of adult flukes after anthelminthics. 13. Prophylaxis: Clean plants, fallen fruits, raw
vegetables from attached ants in endemic areas, not to chew grass blades.

147.Blood flukes&148.Minute intestinal fluke.

1. Classification: Phylum Platehelminths, Class Trematoda (flatworms).2. Latin name: (1) Schistosoma mansoni (2)
Schistosoma Japonicum (3) Schistosoma Hematobium3. Disease: (1) Intestinal Schistosomiasis (S. mansoni &
S.Japonicum) (2) Urinary Schistosomiasis (S.Hematobium)4. Geographical distribution: Mainly in Africa, Middle
east, China, South America, Caribbean, parts of South-east Asia5. Morphology: Unlike other trematods,
schistosomes have separate sexes. Male and female worms are 1-2cm long are morphologically distinct. The
shorter and flatter male envelopes female in its gynaecophoric canal and the pairs remain permanently coupled,
with male attaching itself to venule wall by means of ventral suckers. Both sexes absorbs nutrients and ingest
blood (Blood flukes). Eggs of S.hematobium are ellipsoid and have sharp terminal spine. Eggs of S.mansoni have
distinctive lateral spine. Eggs of S.japonicum spherical with small knob.6. Localization inside human body:
S.mansoni & S.japonicum are found in mesenteric veins. S.masoni is found more often in veins that drain larger
intestine. S.japonicum is found in veins that drain small intestine. S.hematobium is found in pelvic veins, occurring
usually in venous plexus of bladders. 7. Invasive stage for human: Cercaria 8. Route and factors of transmission:
Route; mainly percutaneous. Peroral route poorly explored. Factors; by swimming in lakes, ponds and other
freshwater sources which are infected with snails (Genera Biomphalaria for S.mansoni, Bulinus for S.hematobium
and Oncomelania for S.japonicum) 9. Source of invasion: Infected humans, in case of S.hematobium these are
humans and nonhuman-primates for S.japonicum such as cattle, pigs, dogs and rodents 10. Life cycle: Cercaria
released from infected snails into water penetrate directly through skin of vertebrate host while eggs passed out in
excreta of infected vertebrates hatch upon contact with water to release larval miracida, which invade new snails.
11. Pathogenicity: (1) Eggs with sharp spine traumatize tissues of organs, cause ulcers, inflammatory process,
allergization. (2) Cercaria and schistosomulum(adolescent)- When cercaria repeatedly penetrate skin it may cause
itching and a rash (swimmer’s itch). Pneumonitis, urticarial. (3)Adult blood flukes- abdominal pain, bloody
diarrhea, dysuria, hematuria, fever (in Aisa called Katayan fever), myalgia, malaise. 12. Lab diagnosis: Based on
microscopy finding eggs. Concentrated stool samples for S.japonicum and S.mansoni. Urine sediment at fixed time
(10am-2pm) for S.hematobium. Immunologica tests. Computer tomography, scanning, ultra sonograph. 13.
Prophylaxis: If contact with water, skin should be rubbed vigorously with towel. Water should not be allowed to
evaporate as this may aid cercarial penetration. Health education, Mass chemotherapy. Biological control of snail
populations.

149.Nanophyetus salmincola.

150.Pork tapeworm.
1. Classification: Phylum Platyhelminthes, Class Cestoidea 2. Latin name: Taenia Solium (pork tapeworm) 3.
Disease: Taeniasis & Cysticercosis 4. Geographical distribution: Common in Sub-Saharan Africa, China, India other
parts of Asia 5. Morphology: Length 3-5m. Gravid proglottids longer than wide. Scolex has rostellum with double
circlet of 22-32 small and large hooks. 3 lobed ovary.6. Localization inside human body: In taeniasis-adult worm in
small intestine. In cysticercosis- cysticerci larvae in tissues (muscles, eyes, brain) 7. Invasive stage for human:
Taeniasis- cysticercus larva. In cysticercosis- egg 8. Route and factors of transmission: Peroral Factors; In taeniasis-
insufficiently cooked pork. In cysticercosis- food or formites contaminated with eggs 9. Source of invasion:
Infected human 10. Life cycle: If eggs with oncospheres are swallowed by pig, shells and embryophores are
digested in duodenum and hexaeanth embryos are free. With their sharp hooksm they bore into gut wall and enter
blood or lymphatic vessels in which they are carried around the body. They soon leave circulation and enter
voluntary muscles particularly in tongue and limbs. In muscle hooks are caste off and embryo develops into
cysticercus. The raw or undercooked meat must be eaten by a human being (brown spots on beef “measly pork”).
Bladder-worm (cysticercus) is not digested by stomach juices of human, it proceeds to fix itself to wall, casts off
bladders and start proliferating proglottides. Each proglottid of adult tapeworm produces thousands of eggs. 11.
Pathogenicity: Abdominal pain, indigestion, vomiting, constipation, loss of appetite, nervous disorders 12. Lab
diagnosis: In taeniasis- detection of proglottids in faeces. In cysticercosis- serological tests. 13. Prophylaxis:
Destruction of eggs and larvae. To reveal sick humans and to treat them. Inspection of pork by health officials.

151.Beef tapeworm.
1. Classification: Phylum Platehelminthes, Class Ceistoidea (Tapeworm) 2. Latin name: Taeniarhyncus saginata
(beef tapeworm) 3. Disease: Taeniarhyncosis 4. Geographical distribution: Highest prevalence in Africa, Middle
East, South America, South-east Asia, Europe and former USSR 5. Morphology: 4-8 m in lenth. Gravid proglottid is
longer than wide. Gravid uterus have 17-35 lateral branch. Scolex have no rostellum, No hooks. 2-lobed ovary 6.
Localization inside human body: Small intestine 7. Invasive stage for human: Cysticercus larvae 8. Route and
factors of transmission: Peroral, Factors; by eating insufficiently cooked beef 9. Source of invasion: Infected
human 10. Life cycle: Gravid proglottids are passed at defecation, free eggs also occur in faeces. Cattle have access
to human faeces in farms. In cattle cysticerci occur in striated muscles, they are whitish, oval, contain invaginated
protoscolex with no hooks. Infected meat eaten by man, Adult tapeworms in intestine. Gravid proglottids in
faeces. 11. Pathogenicity: Multiple worms are more common in higher transmission areas. Might be active worm
migration through anus. Nausea, upper abdominal pain.12. Lab diagnosis: Detection of proglottids on faeces.13.
Prophylaxis: -Reveal and treat sick people
-Sanitation and hygiene on cattle farms

-Proper sewage treatment

152.Cysticercosis. Routes of transmission and prophylactic measures.

Route of transmission: Peroral Factors: Unwashed hands, food & water containing egg

Prophylaxis: Improved sanitation, treat infected people, proper sanitation, proper sewage treatment and disposal,
personal hygiene.

- After ingestion of T.solium eggs, either in contaminated food or auto-infection (anus-hand-mouth). The
oncospheres are transported from gut via bloodstream and liver to capillaries, where they encyst at
random throughout body. They often show predilection for eye and brain, may cause blindness, epilepsy,
paralysis or even death. If lie in muscle, some muscular pain but after few years, they die and are then
calcified.
153.Dwarf tapeworm.
1) Taxonomic classification
Phylum: Platyhelminthes
Class: Cestoidea
2) Latin name: Hymenolepis nana (dwarf tapeworm)
3) Disease: Hymenolepiasis
4) Geographic distribution: worldwide because it’s a contact helminth
5) Morphology:
• length 25-40mm, 4 suckers.
• Rostellum with single circlet of 20-30 minute hooks.
• Gravid uterus is bilobed; 2 lobed ovary
6) Localization inside human body:
Small intestine
7) Invasive stage for human:
Embryonated egg
8) Route and factors of transmission
Route: peroral
Factors: through person-person contact and fomites
9) Source of invasion: infected human
10) Life cycle:
The lifecycle involves only human. Fully embryonated infective egg are passed in feces. Infection is commonly
direct, but also by fecal-oral routes. Eggs hatch in jejunum and hexacanth embryo bore into villus where it
transform into cysticercoid larva. After 4-6 days re-enter gut and attaches to mucosa. Eggs appear in feces within
12 days.
11) Pathogenicity:
Mucosal damage caused by both larval and adult worm lead to protein loss and sometime malabsorption.
Abdominal pain, anorexia.
12) Laboratory diagnosis:
Eggs can be detected in feces. Proglottids are found in feces after treatment.
13) Prophylaxis
• Reveal and treat sick humans.
• Protection of food and water from contaminating with eggs.
• Health education
154.Echinococcus species: E. granulosus and E. multilocularis.
1) Taxonomic classification
Phylum: Platyhelminthes
Class: cestoidea
2) Latin name: Echinococcus granulosus (dog tapeworm)
3) Disease:
Cystic echinococcosis (hydatidosis, hydatid disease)
4) Geographic distribution:
Whole Euro-Asian land mass in Northern and eastern Africa, South America, Canada and Australia
5) Morphology:
Adult 3-9mm long, has 3 or 4 segments (proglottids)
Scolex is armed with 2 ring of hooks and 4 suckers
6) Localization inside human body:
Internal organs (mainly liver and lungs) also in brain, heart, spleen, kidney, bones and even in uterus in women.
7) Invasive stage for human:
egg
8) Route and factors of transmission
Route: peroral
Factors: contaminated food, fruits, vegetables and drinking water
9) Source of invasion:
Carnivorous canids (domestic and wild dogs. e.g. wolves, jackals, coyotes etc)
10) Life cycle:
Human being- accident host (intermediate)
Eggs are passed in feces on to ground where herbivorous incidentally ingest them while grazing. Human beings
ingest them after handling dogs with contaminated hair, or by consuming unwashed vegetables or water
contaminated with dog feces. Carnivorous acquire parasite by consuming infected viscera of intermediate host.
Most commonly occur when dogs devour sheep livers and lungs.
In intermediate host, eggs hatch in duodenum and emerged hexacanth embryo (3 pairs of cephalic hooks) passes
through intestinal wall into portal and lymphatic system and then most commonly to liver or lungs, but may pass
from lungs to any other organ of the body. When it settle embryo develop into cyst (single with clear fluid) with
outer elastic, inner germinal layer of epithelial cells from which bud broad capsules. Both capsules and
protoscoleces may break off forming ‘hydatid sand’ on floor of cyst.
11) Pathogenicity:
Early stages of infection are asymptomatic. Anaphylaxis, which may be fetal, can follow hydatid cyst rupture.
Spontaneous or traumatic cyst rupture and spillage of viable parasitic tissue.
If cyst in lungs rupture into bronchi, intense cough may develop, followed by vomiting hydatid material and cystic
membranes.
12) Laboratory diagnosis:
Radiographic examination (chest X-ray), ultra-sonography, immunodiagnosis, CT scan
13) Prophylaxis
• Protection of food from contamination with parasitic eggs.
• Control of stray dogs
• Wash hands after handling dogs
• Health education
1) Taxonomic classification:
Phylum: Platyhelminthes
Class: cestoidea
2) Latin name:
Echinococcus multilocularis
3) Disease:
Alveolar echinococcus (alveolar hydatid diseases)
4) Geographic distribution:
North America, former USSR, Japan, central Europe, Turkey
5) Morphology:
Adult 3-3.4mm. the scolex is armed with 2 ring of hooks and 4 suckers.
Cyst is “alveolar” or honey combed shape.
6) Localization inside human body:
Usually in liver, rarely in other organs.
7) Invasive stage for human:
egg
8) Route and factors of transmission
Route: peroral
Factors: contaminated food (wild berries), contact with dogs and feces of killed foxes.
9) Source of invasion:
Foxes, dogs, cats and other carnivorous.
10) Life cycle:
Life span- 189 days. Definitive host- (foxes, cats and dogs).
Acquire parasite by consuming infected viscera of intermediate host (rodents).
Adult worms are located in small intestine of carnivores.
Eggs become invasive in 35 days after definitive host infection. The gravid proglottids are passed in feces on
ground. People contract with alveolar hydatid disease after ingestion of E.multilocularis eggs with oncospheres,
while gathering of wild berries, field working in result contact with dogs and jackets of killed foxes, oncospheres
are transported from gut via blood stream to the liver.
11) Pathogenicity:
Anaphylaxis, which can be fatal, can follow rupture but bronchopulmonary or hepato-bilary obstruction and
failure. Long bone lesions may result in spontaneous fracture.
12) Laboratory diagnosis:
Radiographic examination, ultrasonography, immunodiagnostics.
13) Prophylaxis
Prevention of infection of dogs.
Protection of food stuffs from contamination with eggs.
Health education.
155.Broad fish tapeworm.
1) Taxonomic classification
Phylum: Platyhelminthes
Class: Cestoidea
2) Latin name: Diphylobothrium latum (broad fish tapeworm)
3) Disease: Diphyllobothriasis
4) Geographic distribution: Finland, Siberia, Switzerland, Korea, Japan
5) Morphology: adult is 9-10m long. Has scolex with two bothria (sucking groove), one dorsally, one ventrally.
6) Localization inside human body: small intestine
7) Invasive stage for human: plerocercoid larva.
8) Route and factors of transmission
Route: peroral
Factors: insufficiently cooked fresh water fish
9) Source of invasion: fish eating mammals and human.
10) Life cycle: when human consume raw fish such as pike, perch and salmonids that have plerocercoid larvae. In
human intestine plerocercoid larva develops into an adult (one per person). Adult produces million eggs each day.
In freshwater eggs embryonate to coracidium, which is taken by cyclops and develop into procercoid larvae. This
larva then infects fresh water fish, which in-turn are eaten by large salmond fish in which plerocercoid develops
which are found in muscle of fish
11) Pathogenicity: abdominal discomfort, fatique, diarrhea, dizziness. Tapeworm pernicious anaemia (caused by
Vit B12 deficiency)
12) Laboratory diagnosis: eggs in stool
13) Prophylaxis:
• not to eat insufficiently cooked fish.
 • Real and treat sick humans.
156.Phylum Nemathelminthes (Roundworms). Classification, structure, and medical importance of
representative species.
The species of this phylum occur in seas, fresh water, in soil and ocean. Nemathelminths includes five
classes. One of them is class Nematoda.
They have non-segmented body. Body has 3 germ layers (triploblastic). They have pseudo coelom
(primary body cavity). They have separate sexes. (adults are sexually dimorphic). Nematodes always
have 4 larval stages during their life of cycles.
Medical significance: Ascariasis, toxocariasis, trichocephaliasis, enterobiasis etc.
157.Maw worm.
1) Taxonomic classification
Phylum: Nemathelminthes
Class: Nematoda
2) Latin name: ascaris lumbricoides (maw worm)
3) Disease: Ascarsis
4) Geographic distribution: worldwide
5) Morphology: male are shorter with curled tail. 15-25cm. female are longer without a curved tail (20-40cm).
adult worms are cylindrical with tapering ends. A. lumbricoides is white in colour. Mouth is at anterior end,
surrounded by three lips with minute teeth.
6) Localization inside human body:
Small intestine
7) Invasive stage for human:
Invasive egg
8) Route and factors of transmission
Route: peroral
Factors: vegetables and fruit contaminated with invasive eggs, unwashed (soiled) hands.
9) Source of invasion: infected human
10) Life cycle: when invasive eggs are ingested, the infective larva hatches out in the small intestine → intestinal
wall → portal circulation (liver) → hearth via pulmonary artery → lungs. From lungs it reaches to alveoli → bronchi
→ trachea.
At this time when you cough and swallow the sputum, the larva re-enter to the small intestine. It moults to
become sexually mature worm. Life-span 1 year.
11) Pathogenicity:
• Fever
• Intestinal colic
• Nausea
• Vomiting
• Diarrhea
• Central nervous disorder
• Pneumonitis
• Bronchospasm
• Intestinal obstruction
12) Laboratory diagnosis:
Detection of eggs in feces.
13) Prophylaxis
• To reveal and to treat sick humans
• To destroy flies and cockroaches as vectors of helminthic eggs
• Not to drink un-boiled water
• Don’t eat unwashed (soiled) vegetables
• Health education
158.Larval ascarids: causative agents of human diseases (larva migrans syndrome).
Ascaris lumbricoides is the causative agent of human larval ascarid diseases.
Scheme of ascaris larvae migration in human body

intestine intestinal capillaries liver portal circulation right heart pulmonary artery lungs
bronchial tree throat oesophagus stomach intestine

159.Pinworm.
1) Taxonomic classification
Phylum: Nemathelminthes
Class: Nematoda
2) Latin name: Enterobius Vermicularis (pin worm)
3) Disease: Enterobiasis
4) Geographic distribution: world-wide
5) Morphology: Male is shorter in size than that of female (Male- 7mm and Female- 10-13mm)
Gravid female has two distended uteri. Male has a single spicule and curved tail. Eggs are 50-60mcm in lenghth,
and has a thick, transparent shell.
6) Localization inside human body: caecal region
7) Invasive stage for human: eggs
8) Route and factors of transmission
Route: peroral
Factors: fomites contaminated with invasive egg
9) Source of invasion: infected human
10) Life cycle: larva matures into an adult in the lumen of the intestinal tract. Lifecycle is completed in about 6
weeks. Female deposits its egg on anus and perianal skin. Not visceral migration.
11) Pathogenicity: pruritus ani. Persistent itching may lead to inflammation and secondary bacterial infection.
Insomnia, emotional disturbance anorexia, weight loss in children
appendicittes
12) Laboratory diagnosis: eggs are found mostly around anus so eggs are found by swabbing or using cellulose
adhesive tape.
13) Prophylaxis attention to peroral hygiene.
Keep nails short and wash hands with soap and water after defecation.
Bed cover and sleeping garment should be changed every day and keep the floor in the bed-room clean.
160.Whipworm.
1. Taxonomic classification: Phylum Nemathelminthes, Class Nematoda 2. Latin name:
Trichocephalus trichiurus (whip worm) 3. Disease: Trichocephaliasis 4. Geographical distribution:
World-wide 5. Invasion stage for human: Invasive egg 6. Morphological features: Adult is a bit shorter
than female in size (Male is 30-45mm; Female is 35-50 mm), commonly called whip worm as anterior
portion is this and elongated while the posterior portion is bulbous and fleshy, produce barrel- shaped egg
7. Location inside body: Caecal region, upper part of large intestine 8. Route and factors of
transmission: Route- Peroral, Factors- Vegetables contaminated with invasive egg, soiled hands 9.
Source of invasion: Infected human
10. Life cycle:
- After ingesting of invasive egg the larva doesn’t undergo visceral migration but penetrates to the gut
- The worms attach themselves to the large intestine
- Period of development in the host- 3 months 11. Pathogenicity: Light infection- asymptomatic. Severe
infections- lesions of large intestine, diarrhea, in children leads to anemia, edema and cardiac failure,
acute appendicitis and poor growth in height
12. Laboratory diagnosis: Finding the characteristic barrel shaped eggs in the faeces
13. Prophylaxis: to reveal and to treat sick humans, to destroy flies and cockroaches as vectors of
helminthic eggs, not to drink unboiled water, don’t eat unwashed (soiled) vegetables and health education
on personal hygiene.
161.Hookworms.
hookworms are parasitic nematodes that parasitizes in small intestine of their host, which maybe a
mammal, such as dog, cat or human.
Two species of hookworms infect humans, Ancylostoma duodenale(Ancylostomiasis) and Necator
Americanus(Ancylostomiasis).
162.Palisade worm.
 163.Trichina worm.
1. Taxonomic classification: Phylum Nemathelminthes, Class Nematoda (round worms)
2. Latin name: Trichinella spiralis 3. Disease: Trichinosis 4. Geographical distribution: World wide 5.
Morphology: Male is 14-18 cm, Female is viviparous and about twice as long as male, Muscle larvae are
1mm long 6. Location inside human body: Larvae are into streated muscles, adult helminth in small
intestine 7. Invasive stage for human: Encysted larva 8. Route and factors of transmission: Route-
Peroral, Factors- uncooked meat of pork, pork products, wild boar and bears 9. Source of invasion: Pigs
and carnivorous animals
10. Life cycle:
- Human beings become infected by eating improperly cooked pork products, after 8 ingestion, larvae are
liberated in small intestine and mature into adults.
- Female deposits larvae in intestinal tissues into blood stream into striated muscles of body. After
penetration larva undergo 3 moults and gets enclosed in thick walled cyst
- Pigs become infected by eating scrap and garbage and carcasses of infected rats
11. Pathogenicity: Enteral disorders, abdominal pain, nausea, vomiting and diarrhea, edema of face,
fever, its lethal; can cause myocardiac failure 12. Laboratory diagnosis: Serological test, muscle biopsy
13. Prophylaxis: Larvae in pork can be killed by freezing at 18 C for 24 hours, thorough cooking of pork

164.Guinea worm. L.M. Isaev’s contribution to eradication of dracunculiasis foci.

1. Taxonomic classification: Phylum Nemathelminthes, Class Nematoda 2. Latin name: Dracunculus
medinesis 3. Disease: Dracunculiasis 4. Geographical distribution: Africa, Middle East, Indian
subcontinent 5. Morphology: Largest nematode to infect man, Female is 70-120cm long and Male is 12-
30 cm long 6. Localization in human body: Subdermal and subcutaneous connective tissue of
extremities 7. Invasive stage for human: Larva 8. Route and factors of transmission: Peroral, water
containing copepod crustaceans infected with parasitic larvae 9. Source of invasion: Infected humans,
dogs 10. Life cycle:
- Infection is acquired when copepod, crustaceans, containing infected larvae of D. medenesis are
ingested in drinking water
- Larvae are released into intestine, migrate to body cavity, mature and mate, after which males
disappear. Between 9-14 months later females migrate within subdermal and subcutaneous connective
tissues, usually reaching extremities. There female produce a chemical which causes formation of a
blister, where ulcer form at site through which worm produce releasing rhabiditiform larvae, when
immersed into the water. Larvae are actively digested by copepod.
11. Pathogenicity: Infected individuals remain asymptomatic in first period of disease, during migration,
symptoms are nettle rash, dyspnea, sometimes diarrhea and bronchial asthma
12. Laboratory diagnosis: Early stages are not diagnosticated. After formation of blisters, determination
of the disease is not difficult 13. Prophylaxis: Not to drink water from unprotected ground water sources
165.Filariidae (Wuchereria bancrofti, Brugia malayi, Loa loa, Onchocerca volvulus).
1. Taxonomic classification: Phylum Nemathelminthes, Class Nematoda 2. Latin name: Loa Loa
3. Disease: Loiasis 4. Geographical distribution: West and central Africa 5. Morphology: Adult worms
are smooth, thread like, creamy- white. Males are 30mm long. Females are 50 mm long. Females are
viviparous. 6. Localization in human body: Adult worms are in subcutaneous and subconjunctival and
periorbital tissues. Larvae are in blood 7. Invasive stage for human: Microfilariae 8. Route and factors
of transmission: Route- Transmissive 9. Source of invasion: Infected human
10. Life cycle:
- Human is definitive host
- Deerfly vectors of genus chrysops is intermediate host
- Bite of female chrysops, microfilariae are introduced into skin of human host and tend to migrate in
subcutaneous tissues. They have predilection for conjunctival and periorbital tissues.
11. Pathogenicity: Calabar swellings, which are painless, soft tissue swellings near joints. Urticaira,
pruritus, lymphedema, arthritis may occur. Picture resembling meningo-encephalitis that occur only during
treatment is tough to be allergic reaction.
12. Laboratory diagnosis: Finding microfilariae in peripheral blood smear. Serological tests
13. Prophylaxis: Extermination of vectors, to protect open parts of body from biting of vectors, reveal sick
humans and treat them.
166.Dirofilaria species.
 167.Laboratory diagnosis of helminthic invasions. Ovo-, larvo-, helminthoscopy.

168.Phylum Arthropoda. Classification, structure, and medical importance of representative species.

The phylum Arthropoda includes 3 classes, such as insecta, crustacea and arachnoidea.
Arthropods are metamerically segmented, triploblastic, bilaterally symmetrical, coelomate animals.
Chitinous cuticle thickened or impregnated to form strong exo skeleton. There are jointed segmental
jointed limbs, at least one pair functioning as jaws. Cephalization has been carried much further, and
six segments constitute the head.
2)Species of class crustacea acts as intermediate host of parasitic diseases such as dracunculus
medinesis
Species of class insecta may cause various diseases such as housefly can act as mechanical vector of
hepatitis A and salmonella and sand fly is a vector of leishmaniasis.
Species of class arachnoidea, such as ticks and mites can cause relapsing fever and tick can cause
rickettisal tick- borne disease.
169.Class Crustacea: general characteristics. Crustaceans of medical importance.

170.Class Arachnoidea: general characteristics. Arachnids of medical importance.

171.Venomous arthropods. Mites of medical importance.

172.Ticks of medical importance.

173.Class Insecta. Morphology, features of life cycles, and medical importance of representative
species.
Class Insecta includes arthropods which have tracheal system for breathing. The body is divided into
three parts, head, thorax abdomen. Head has segments, with one pair of antennae. Head has sense
organs and jointed mouth parts. They have 3 pairs of walking legs. Sexual dimorphism is seen.
Most of the species of the class insecta have complete metamorphosis life cycle, for example (
Mosquito, deer fly, sand fly, black fly)
Few of them have incomplete metamorphosis life cycle such as bed bugs, kissing bug, and louses.
174.Flies: species and medical importance.

175.Cockroaches: species and medical importance.

Polio virus, Mechanical vector of hepatitis and salmonellosis

176.Lice: species, body structure and medical importance.

177.Fleas: features of body structure and development. Species of fleas.

178.Bugs: medical importance.

179.Mosquitoes: species, features of body structure and development, medical importance.

180.Sandflies. Biting midges.

181.Molluscs (snails) as intermediate hosts of helminths.

182.Venomous animals. Poisonous plants and fungi.
•Venomous animals (Active): Scorpion, Black widow spider, Rattle snake, Royal cobra
•Venomous animals: (Passive): Fugue fish, snowtrout fish
•Poisonous plants: Agave genus, corn cockle, wood anemone, Mexican poppy, belladonna, angel’s
trumpet, wild calla, yellow oleander, greater celandine, wild carrot, death-of-man, Natal lily, autumn
crocus, lily of the valley, Daphne genus, Datura genus, Delphinium genus, snowdrop, European holly,
Siberian iris, bleeding heart, lily, lupine, pasque flower, false acacia, calla lily.
•Poisonous fungi: Death cap, destroying angles, fools mushroom, deadly webcap, fool’s webcap and
several species from the genus Galerina, Lepoita and Conocybe.
183.The biosphere and noosphere theories of V.I. Vernadsky. Living matter of biosphere and its
functions.
Living matter of biosphere (Biotic component): It’s the plants, animals and human beings. Biotic
component can be divided into three groups:
1.Producers: Photosynthesizing organisms. They are any kind of green plant. Green plants make their
own food by taking sunlight and using the energy to make sugar.
2.Consumers: Any organism that can’t make its own food. They have to feen of producers or other
consumers to survive.
3.Decomposers: An organism that primarily feeds on dead organisms or the waste from living
organisms.
184.Biogeochemical cycles and energy flow in biosphere.
•Biogeochemical cycles: The ways in which an element—or compound such as water—moves
between its various living and nonliving forms and locations in the biosphere.
•Biogeochemical cycles important to living organisms include the water, carbon, nitrogen,
phosphorous, and sulfur cycles.
•Energy flows through an ecosystem and is dissipated as heat, but chemical elements are recycled.
185.Ecology. The concept of environment. Types of environment: aerial, aquatic, terrestrial, and
internal.

186.Medical and biological aspects of biosphere impact on human health. Biofields and biological
rhythms, their medical significance.
•Ecology: Study of interactions that organisms have with each other, other organisms and with abiotic
component of their environment.
•Environment: Surroundings, in where organisms live. It has three components
1.Abiotic component: All non-living elements which are essential for survival of all living organisms
(Lithosphere, atmosphere and hydrosphere). Mineral nutrients, gases and nature are three basic
requirements of organic life.
2.Biotic component: Plants, animals and human beings.
3.Energy: Vital component, which is essential for reproduction and generation of all biological life on
earth.
•Types of environments:
1.Aerial:
2.Aquatic:
3.Terrestrial: The earth’s land area, including its manmade and natural surface and sub-surface
features, and its interfaces and interactions with the atmosphere and the oceans.
4.Internal:The medium in which all body cells are bathed and which maintains a constantenvironment
in terms of pH, osmotic pressure, etc.
187.Ecological factors. Unity of an organism and environment
Ecological factors affecting human beings include:
1-Abiotic: factors of inanimate nature directly or indirectly affecting the organism (light, temp,
humidity)
2-Biotic: influence of surrounding living organisms
3-Anthropogenic: forms of human activity that come to change the nature as the habitat of other
species.
188.Human genetic variation due to biological and geographical features of habitat.

189.Human adaptive ecotypes, their characteristics: arctic, tropical, temperate zone, desert, high
altitude ecotypes.
Ecotype: a population of a species that survives as a distinct group through environmental selection
and isolation and that is comparable with a taxonomic subspecies.
Characteristics:
-Arctic: short, round persons with short arms and legs, flat faces with fat pads over the sinuses, narrow
noses, and a heavier-than-average layer of body fat. These adaptations provide minimum surface area
in relation to body mass for minimum heat loss, minimum heat loss in the extremities (which allows
manual dexterity during exposure to cold and guards against frostbite), and protection of the lungs
and base of the brain against cold air in the nasal passages.
-Tropical: height variability, elongated torso, increased length of limbs, decreased size and volume of
ribcage dimensions, decreased volume of muscle mass, increased perspiration, decreased volume of
base metabolism and fat synthesis.
-Temperature zone: Excessive sweating, tall and thin, so that he has maximum surface area for heat
radiation. He has little body fat; often a wide nose, since warming of the air in the nasal passages is not
desirable; and usually dark skin, which shields him from harmful solar radiation and may serve to
lower his sweating threshold.
-Dessert: can sweat freely but must deal with the water loss involved; hence, he is usually thin but not
tall. This adaptation minimizes both water needs and water loss. Skin pigmentation is moderate since
extreme pigmentation is good protection from the sun but allows absorption of heat, which must be
lost by sweating.
-High altitude (Mountain): high rate of metabolism, elongated tubular bones, wide ribcage, increase in
lung tissue, high blood oxygen capacity due to increased number of erythrocytes, high hemoglobin
level.

190.Human adaptation to extreme conditions (the Arctic, deserts, space, etc.).

-Arctic: short, round persons with short arms and legs, flat faces with fat pads over the sinuses, narrow
noses, and a heavier-than-average layer of body fat. These adaptations provide minimum surface area
in relation to body mass for minimum heat loss, minimum heat loss in the extremities (which allows
manual dexterity during exposure to cold and guards against frostbite), and protection of the lungs
and base of the brain against cold air in the nasal passages.
-Deserts: can sweat freely but must deal with the water loss involved; hence, he is usually thin but not
tall. This adaptation minimizes both water needs and water loss. Skin pigmentation is moderate since
extreme pigmentation is good protection from the sun but allows absorption of heat, which must be
lost by sweating.
-Space:
191.Hereditary differences in human response to environmental factors. The concept of
ecogenetics.
Eco genetics- a branch of genetics that study genetic traits to the response to environmental
substances.
192.Qualitative parameters of the environment and their effects on human health.
Qualitative methods are commonly used in the social sciences and in a variety of disciplines related to public
health. Several articles published as editorials or commentaries in public and environmental health journals in
recent years have advocated for the use of more qualitative methods in environmental health research.
Environmental parameters “influence the distribution, abundance and activity of animals and plants,” according
to the Natural Resource Institute. “Local meteorological conditions such as air temperature, rainfall or sunlight
may affect the behaviour of terrestrial organisms, and water current, dissolved oxygen, suspended material and
river bed topography may influence aquatic species.” They can include currents and water turbulence,
temperature, salinity, nutrient element (productivity), dissolved oxygen levels, and depth and substance type.
For example a coral reef distribution is limited by (requires) sunlight, temperature, full salinity, saturation state,
and low nutrients. Recent articles on the value of qualitative data in the study of environmental health argue
that qualitative methods are especially important to community-based environmental health research because
of their ability to engage residents regarding local environmental health problems. Qualitative methods “provide
a way to produce community narratives that give voice to individuals and characterize the community in a full
and complex fashion”.
193.Healthy (comfort), unhealthy (discomfort), and extreme environments. Adequate and
inadequate environmental conditions.

194.The concept of stress. Functional types of human response to the environmental factors
(“sprinter”, “stayer”, “mixt”).
Stress is an adaptive response to an external situation that results in physical, psychological or
behavioral deviations for organizational participants.
195.Human activity as an ecological factor. Basic directions and consequences of anthropogenic
environmental changes. Environmental protection.
Basic direction and consequences of anthropogenic environmental changes
diseases of marine invertebrates and vertebrates and two recently-emerged viral zoonoses, Nipah
virus disease and West Nile virus disease. These exemplify the varied etiology, pathogenesis, zoonotic
potential and ecological impact of wildlife EIDs. Strikingly similar underlying factors drive disease
emergence in both human and wildlife populations. These are predominantly ecological and almost
entirely the product of human environmental change. Since human environmental changes are largely
responsible for their emergence, the threats wildlife EIDs pose to biodiversity and human health
represent yet another consequence of anthropogenic influence on ecosystems.
Environmental protection.
Environmental protection is a practice of protecting the natural environment on individual,
organization controlled or governmental levels, for the benefit of both the environment and humans.
Due to the pressures of overconsumption, population and technology, the biophysical environment is
being degraded, sometimes permanently. This has been recognized, and governments have begun
placing restraints on activities that cause environmental degradation.
196.The major ecological problems of Ukraine.
Environmental issues in Ukraine. Soviet policies of raising industrial and agricultural productivity with
little regard to ecological considerations have had a devastating effect on the environment. Air
pollution is especially severe in such industrial centers as Zaporizhzhya, Luhans'k, and Donetsk.