Microbial Structures and Functions Moicroorganisms

1.
Microbial structures and Functions
Moicroorganisms
Are living organisms of microscopic size.
• Based on architectural differences microorganisms
can be divided into:
1. Eukaryotes- fungi, algae and protozoa- cells with
membrane bounded nucleus
2. Prokaryotes-bacteria (eubacteria) and archae
(archaeobacteria)–cells lacking a definite nucleus.
Microorganisms with prokaryotic
Archae and bacteria
• The distinction between these: is based on fundamental
biochemical differences.
• The archae- consists of several physiological types
1. thermophilic: growing only under very hot (as high as 90o
C) conditions
2. Thermoacidophilic: growing only under very hot and highly
acidic conditions
3. Methanogens : producing methane from carbondioxide and
live only in places molecular oxygen is completely absent.
4. Halophilic: growing in highly saline environments
The Bacteria
• extremely diverse collection of prokaryotic microorganisms
• exhibiting greatly diverse morphologies, and physiologies.
Shape of bacteria-
• Spherical,
• rod,
• spiral or
• pleomorphic
Size
Typical size range from 0.2-1.5 micrometer
Arrangement characteristic cellular arrangement
• cocci may be arranged:
• inpairs: diplococci,
• in chains: streptococci,
• groups of four: tetrads,
• or eight sarcina,
• as grape like clusters staphylococci.
Some bacilli may be arranged in chains: streptobacilli,
• others at an angle to each other
The type of arrangement is determined by the plane of division
and tendency to remain attached after division.
Bacterial cells: structures and function
Cell wall: The outer layer of cell envelope.

• Is a very rigid structure that gives shape
to the cell
• prevents the cell from expanding and
eventually bursting
• Chemically: peptidoglycan/murein
• N-acetylglucosamine, N-acetyl muramic acid
Peptidoglycan N-acetyl muramic acid and N- acetylglucosamine
molecules alternating in chains. They are crossed by peptide chains
Gram positive cell envelope:
cell wall differs in gram positive and gram negative

bacteria.
• Gram positive-Greater amount of peptidoglycan,
bascally a polymer of N-acetylglucosamine, N-
acetylmuramic acids , Teichoic acid
• Gram negative bacteria-Cell wall of gram negative
bacteria is more complex than those of gram positive
–peptidoglycan layer is thin,
• outer membrane is made of phospholipids and
lipopolysaccharide (LPS)
Cellular structures
Cell membrane/cytoplasmic membrane:

• Is a thin (5-10nm) semipermeable membrane
• controlling in flow and outflow to and from the protoplasm
• Chemically lipoprotein, small amount of carbohydrate
Cytoplasm: Is a colloidal system of organic and in organic

solutes
• No protoplasmic streaming
• No endoplasmic reticulum or mitochondria
• Contains ribosomes-center of protein synthesis
• Mesosomes multinucleated structures formd as invagination of
plasma membrane, site of respiratory enzymes.
• Slime layer and capsule-
• Viscid material around the cell surface organized into sharply defined
structure known as capsule.
• When it is loose undemarketed secretion is known as Slime layer
• Flagella: Motile bacteria posses one or more unbranched long sinuous
filaments called flagella.
• Fimbriae(pili) –hair- like surface appendages. They are shorter and
thinner than flagella.
• Are organ of adhesion
• In Conjugation Fimbriae (pili) serve as conjugation tube.
• Spore: Some bacteria have the ability to form highly resistant resting
stages called Spores.
Growth and multiplication
• Bacteria divide by binary fission.

• The interval between two cell divisions known as
generation time
• The generation time varies from species to species
• In many medically important bacteria the generation
time is 20 minutes.
• Some bacteria are slow growing, the generation time
about 20 hrs tubercle bacilli,
• 20 days for M. leprae
Bacterial growth curve
Curve shows the following phases:
• Lag phase-the initial period is the time required for

adaptation to the new environment
• Log phase/exponential phase: The cell start dividing
and their numbers increase exponentially.
• Stationary phase: cell division stops due to depletion of
nutrients and accumulation of toxic products
• Phase of decline: Population decreases due to cell
death
Curve shows the following phases:
• Lag phase-the initial period is the time required for

adaptation to the new environment
• Log phase/exponential phase: The cell start dividing
and their numbers increase exponentially.
• Stationary phase: cell division stops due to depletion of
nutrients and accumulation of toxic products
• Phase of decline: Population decreases due to cell
death
Bacterial nutrition
• The principal constituent of bacterial cells is water,

proteins, polysaccarides, lipids, nucleic acid,
mucopeptides and low molecular compounds.
• Bacterial metabolism is similar to the metabolism of
higher organisms with only some differences.
• For growth and multiplication minimum nutritional
requirements are water, source of carbon, source
of nitrogen and some inorganic salts.
Bacterial nutrition
classified nutrionally based on their energy requirements,

their ability to synthesize essential metabolites:
• Phototrophs: energy derived from sunlight
• Chmotrophs: energy derived from chemical reactions
• Autotrophs: can synthesise their organic compound
• Hetrotrophs: unable to synthesise their own organic
compound
Oxygen requiremnt and metabolism:
• Aerobic bacteria
• Anaerobic bacteria
• Microaerophilic
Bacterial nutrition
The influnce of free oxygen is related to the metabolic

character of the bacteria:
Aerobic respiration : In the case of aerobes ultimate electron
acceptor is atmospheric oxygen
• the carbon and energy source is completely oxidised to carbon
and water,
• ADP converted to ATP- the process is oxidative
phosphorylation
Anaerobic respiration: Anaerobic bacteria use as electron
acceptors nitrates, sulphates, etc instead of oxygen
Fermentaion: anaerobic metabolism in which the carbon and
energy source are both electron donor and electron acceptor
Eukaryotic Microorganisms
• Fungi, algae and protozoa :

are microorganisms with eukaryotic cells
• The cells of these organisms are structurally similar
to multicellular organisms (plants and animals)
• Fungi-Their cells are cell walls composed of chitin
and other polysaccharides.
• Some are unicellular, eg.yeasts and others are
multicellular with filamentous, eg. molds.
Eukaryotic Microorganisms
• Protozoa- Are unicellular eukaryotic microorganisms

Various groups of protozoa exhibit different strategy
for locomotion.
• Algae-Are photosynthetic eukaryotic
microorganisms.
• Many are unicellular, but some are multicellular and
organized filaments.
1.1.Microbial Genetics
• Genetics is the study of heredity.

• the replication and expression of the cells hereditary
information.
• The double helical nature of the DNA macromolecule
is critical for its replication.
• The information within the DNA determines the
metabolic and structural nature of the organism.
Microbial Genetics
• DNA is organized in all cells into structures referred

to as chromosomes.
• bacterial and archaeal cells also may have plasmids
• and eukaryotic cells may also have episomes
(extrachromosomal elements).
• The genetic information contained in the
chromosomes, plasmids or episomes are referred to as
the cells genome (totality of genetic information).
• The replication of the double helical DNA a
semi conservative process
• two new daughter DNA double helices
contains one strand from the parental DNA
• and one newly synthesized
complimentary strand.
Microbial Genetics
• microoganisms includes prokaryotes and (mainly

unicellular) eukaryotes
• eukaryotes have diploid genes
• The two copies are similar, but not identical. We call
each member of the set an allele.
• prokaryotes are haploid-each gene is present in
only a single copy
Microbial Genetics
• bacteria multiply by binary fission ,so in

principle, each progeny cell is a clone of the
parent.
• But in reality, mutations happen. Progeny
cells may not be clones.
• binary fission produces clones, but mutations
can arise
• the bacterial chromosome is circular molecule of
DNA, located within the nucleoid.
Exception-
• streptomycets have linear chromosome.
• Agrobacterium tumefacins has one circular
chromosome, one linear chromosome and several
plasmids
• Vibrio cholera. It is super coiled within the
cytoplasm.
• Similarly the archaeal chromosome is a single circular
loop.
• PLASMIDS-These are circular strands of DNA.
• A bacterium may contain more than one plasmid.
• They replicate independently of the cell’s chromosome.
• Their size is only 1%-5% to that of the cell’s
chromosome
• Each plasmid carries information to replicate it’s self.
• Plasmids confer advantages to the cells that carry them.
• TYPES OF PLASMIDS
• F Plasmid – .also called an F factor. These
factors carry instructions for conjugation.
• conjugation transfers genes from one bacterium
to another.
• R Factors - also called Resistant factors, carry
genes for resistance to drugs, heavy metals and
toxins.
• Bacteriocin Factors - carry genes for
proteinaceous toxins called Bacteriocidins.
• Virulence Plasmids – contain instructions for
structure, enzymes, or toxins that help a bacterium to
become pathogenic.
• Cryptic Plasmids -“Cryptic Plasmids” are plasmids
that do not code for any.
Transmission of Genetic Material
GENETIC RECOMBINATION & TRANSFER

• when genes are exchanged between two different
organisms to form a new combination it is called
Genetic Recombination .
• Three methods of gene transfer and recombination
are:
• Transformation
• Transduction and
• Conjugation.
TRANSFORMATION
• Is the transfer of genetic material from the
environment.
• When a bacterial cell dies, the cell will lyse out and
the DNA is released into the environment.
• A recipient cell can take up some of the DNA from
that environment.
• A cell has to be “Competent” to take up free DNA
from the environment.
• Examples of bacterial cells: Streptococcus,
Haemophilus, Neisseria, Bacillus,
Staphylococcus and Pseudomonas.
TRANSDUCTION-
• is the transfer of a portion of DNA from one bacteria
to another by a bacteriophage infecting a bacterium.
• A bacteriophage has an affinity only for bacteria and
will not infect eukaryotic cells at all.
• Stage 1: The phage attaches to the bacterial host cell.
• The phage synthesizes lysozyme, which breaks the cell wall

• and the phage dsDNA is injected in the bacteria’s cytoplasm.
• Stage 2: The phage DNA now directs the bacterial cell to

respond to it’s needs.
• From the bacterium’s cytoplasmic pool, phage DNA and
phage proteins are synthesized.
• Stage 3: The host cell now synthesizes new phages that pack
phage DNA into the newly formed capsid.
BACTERIAL CONJUGATION
• is the process by which donor bacterium make
physical contact with recipient bacterium and transfer
genetic material.
• Conjugation needs the help of a plasmid that contains
an F factor, which is the “Fertility factor”. This type
plasmid is self-replicating and contains genes.
• These plasmids are found in bacteria as well as yeast
with the name of “Saccharomyces cerevisiae”, also
known as Baker’s Yeast
Host Parasite interaction during microbial infection
• Parasitic organisms are those which live in /on a

living host.
• Many of the parasitic organisms live on the
external or internal surfaces of the host with out
causing disease.
• These are called commensals.
• Parasitic microorganism that multiply in the host
tissue causing disease is called pathogenic
microorganism.
Infection and Disease

• Infection is the process by which the parasite enters
into a relationship with the host.
Its essential steps are the following.
• 1. Entrance of the parasite into the host
• 2. Multiplication of parasites within the host
Factors that govern disease production

The outcome of infection depends on interactions betwen:-
1/ Microbial factors: pathogenicity and virulence
2/ host resistance factors: natural and acquired resistance
(immunity)
Microbial Factors
Pathogenicity: is the capacity of an organism to cause disease.
• It requires the attributes of transmissibility or communicability
from one host or reservoir to a fresh host,
Infectivity: is the ability to breach the new host’s defences.
Virulence : is the degree of pathogenicity
• Virulence in the clinical sense is a

manifestation of a complex parasite–host
relationship
• Virulence is measured in terms of the number
of organisms or micrograms (ug) of toxins
necessary to kill a given host
• the LD50 (the number of organisms or
micrograms of toxins needed to kill 50% of the
organism.
Virulence factors:
• These are certain structures or products to overcome host
defence mechanisms and cause disease.
Adherence factors-Structures or substances that help their adhesion
to host cell mucous membranes to start disease process.
• The pili of N.gonorrhoeae and E. coli attachment of the
organism to the urinary tract.
• Invasiveness- This is the ability to invade tissues, multiply and
spread rapidly.
• This is may be partly due to certain surface components
polysaccharide capsule
• The M proteins of Streptococcus pyogenes.
.
Toxin production – are bacterial products which have a direct

harmful action on tissue cells.
They fall into 2 groups:
Extoxins- toxins are produced and diffuse freely into the
surrounding medium i.e they are extracellular toxins.
• Bacteria such as Cl.tetani, C.diphtheria, Cl.botulinum
produce exotoxins.
Endotoxins-These are part of bacterial cell wall.
• Typical endotoxins are that of gram negative organisms.
• O antigen which is lipopolysaccharide of the cell wall.
4. Extracellular enzymes: These are substances produced by

some bacteria
• help the spread, invasion, and establishment of the
microorganisms into the tissue.
• Collagenase-produced by Cl.perfringens and breaks down
collagen fibes and promotes spread of infection.
• Coagulase-is produced by S. aureus. It coagulates plasma
with deposition of a fibrin wall around staphylococcal lesions
which help them to persist.
• Fibrinolysin (Striptokinase )-is produced by Strep. pyogenes
It causes lysis of fibrin clots and assist in spread of organisms
in tissue.
Host resistance factors (Immune system)

• The main function of the immune system is to
prevent or limit infections by microorganisms.
The immune system is divided into two functional
divisions
• the innate immune system
• and the acquired immune system.
• 1/ innate immune system- acts as a first line

of defence against infectious agents before
they cause overt infection.
• Innate immunity is natural inborn
• non specific, acting against all microorganisms
• not acquired through previous contact with
the infectious agents.
• If this first defence fails, the acquired immune
is called upon.
Host Parasite interaction during microbial
infection
I/ First line defence-
• 1. Mechanical barriers at portal of entry: skin and
mucous
• 2. Chemical barriers at the portal of entry include
sweat and sebaceous secretions in the skin.
• Their acid pH and high faty acid
• Hydrolytic enzyme in the saliva,
• HCl of the stomach,
• proteolytic enzyme in the small intestine
• Lysozyme that dissolves bacterial cell wall
• 3. Normal bacterial flora present at the portal of entry.

• These suppresses the growth of many pathogenic bacteria and
fungi.
II/ Second line of natural-non-specific defence:
• bactericidal substances in serum and body fluids.
• lysozyme present in all body fluids.
• Complement. It is a group of proteins in serum and body
fluids.
• It plays an important role in facilitating phagocytosis and
promoting inflammation.
• It includes components which bind to the surface of bacteria
and cause their lysis.
• Phagocytosis
• ii.Polymorphonuclear leukocytes (neutrophils)-are
most abundant phagocytic cells in circulating bloods.
• They are produced in the bone marrow.
• They are continuously present in circulating blood,
• affording protection against the entry of foreign
material.
• They live only for few days.
• ii/ Mononuclear cells (macrophages)-Monocytes are
larger than neutrophils, they are precursors of
macrophages.
infection
• Natural Killer (NK) celles
• These are larger granular lymphocytes which
have a non-specified cytotoxic activity on
tumor cells,
virus infected cells and graft cells.
infection
Acquired Specific Immunity:
• Acquired immunity is specific.
• mediated by either antibody (humoral)
• or lymphoid cells (cellular)
• occurs when a host is exposed to infectious agent.
infection
Actively acquired immunity
• An individual can actively produce his own
antibody on exposure to foreign or infective agent.
• The immunity develops slowly,
• it lasts for long time.
• It can be naturally acquired or artificially induced.
• Naturally active immunity occurs following clinical

or sub clinical infections:
• e.g. after measles or mumps infection long lasting
immunity develop.
Artificial active Immunity
• occurs after vaccination with live or killed infectious
agents or their product
infection
Passive acquired immunity –
Ready made antibodies are transferred to individuals.
• This gives rapid protection.
• However immunity is short lasting .
• There are two types-
• Natural passive –Immunity occurs when antibodies are
transferred from mother to foetus through placenta.
Artificial passive- Immunity as in treatment or
prophylaxis against several diseases e.g. injecting
antitoxic serum in treatment of diphtheria prophylactic
in gamma globulins to protect contacts of cases of
measles or poliomyelitis.
Antimicrobial agents and mechanism of
resistance to drugs
• Antimicrobial agents -Selective chemicals that
inhibit the growth of or kill microorganisms include
naturally occurring antibiotics, semi synthetic
antibiotics and some synthetic chemical compounds.
• Antibiotics are natural substances produced by an
organism to kill or inhibit the growth of another
organism.
Types of action of antimicrobial agents-
• 1. Bactercidal drugs are these which have a rapid

lethal action.
• Kill and destroy the bacteria e.g. penicillin,
cephalosporin, amino glycosides.
• 2. bacteriostatic drugs – these merely inhibit the
division i.e. growth of organisms e.g. sulphonamides,
tetracycline and chloramphenicol.
Properties of an ideal chemotherapeutic or antibiotic
• Selective toxicity -toxic to the bacterial cell at doses those are
not toxic to the host cell.
• Kills that target cell –bactericidal superior to bacteriostatic
• Target cell does not develop resistance.
• Broard spectrum- having a wide range of activity against
most of gram positive and gram negative bacteria
• Diffusible into remote areas of the body with slow rate of
excretion
Range of action of antimicrobial agents-
They fall into 3 main categories-
1. Active against gram positive organisms e.g.

penicillin, erythromycin, linomycin.
2. Active mainly against gramnegative organisms
e.g. polymyxin and nalidixic acid
3. Active against both gram positive and gram
negative organisms(broad spectrum activity) e.g.
tetracyclines, chloramphenicol, ampicilin
Mechanism of action of antimicrobial agents
1. Inhibition of cell wall synthesis –Some antibiotics

interfere with cell wall synthesis and cause
bacteriolysis,
• e.g.i/ Pencillins are produced either naturally by
species of the fungus Penicillium or synthetically or
by modifications of pencillinic acid.
• The penicillins are effective primarily against gram
positive and limited number of gram-negative
bacteria.
• e.g.ii/ Cephalosporins are produced by species of the

fungus Acremonium ( formerly called
Cephalosporium).
• They are structurally similar to the penicillins in that
they contain the B-lactam ring.
• e.g.iii/ Vancomycins produced by species of
Streptomyces
• Effective against gram-negative bacteria by inhibiting
peptidoglycan formation.
2. Inhibition of cytoplasmic membrane function

• Some antibiotics cause disruption of the cytoplasmic
membrane and leakage of cellular proteins and
nucleotides leading to cell death.
• e.g.i/ polymixins are produced by Bacillus polymyxa
• inhibit the normal function of the bacterial cell
membrane.
• polymxin B and polymyxin E too toxic for internal
use and are used only as tropical antibacterial agents.
• e.g.ii/. Nystatin and amphotericin B which are

produced by streptomyces species, are
clinically useful as antifungal compounds
3. Inhibition of Protein Synthesis-
Many antibiotics block protein synthesis by setting on
the 30s or 50s subunits of the bacterial ribosome.
• E. g. i/ the aminoglycosides inhibit protein synthesis in

bacteria by binding to ribosome.
• a/ streptomycin binds to the 30s subunit of bacterial
ribosome
• b/ amikacin , kanamycin,neomycin,gentamycin and
torbamycin.
• ii/the tetracycline broad spectrum antibiotics produced
by streptomyces species.
• iii. Chloramphenicol is the only naturally occurring
antibiotic that contains nitrobenzene which accounts for
its toxicity to bacterial and mammalian cells.
• It combines with 50s subunit of bacterial ribosome
• iv. Erythromycin produced by Streptomyces

erythreus.
• the molecules bind to the 50s subunits of ribosomes
and interfere with peptidotransferase activity
• V. Lincomycin –it is similar to erythromycin action.
Cindamycin is a synthetic modification of lincomycin
used in the treatment of infections caused by
anaerobic bacteria.
• 4. Inhibition of transcription and nucleic

acid synthesis
• These can act on any of the steps of DNA or
RNA replication-
• Rifamycin- synthetic derivative of rifampin
which is a potent inhibitor of DNA- dependent
RNA polymerase in bacteria.
• The synthesis of all forms of RNA is
inhibited .
• Chloroquine is an important antiprotozoan.

• It also inhibits nucleic acid synthesis in
mammalian cells ,
• intracellular levels in protozoa which
concentrate the drug are much higher than
in human cells.
F. Competitive inhibition
• They compete with an essential metabolite for the
same enzyme.
• Sulphonamides are structural analogues to para
aminobenzoic acid(PABA)
• so they enter into the reaction in place of PABA and
compete for the active centre of the enzyme
• thus inhibits folic acid synthesis by bacterial cells.
• Folic acid is required as a coenzyme in transfer of 1-
carbon units between molecules.
Mechanism of resistance to antimicrobial agents
1.The organism produces enzymes that destroy the

drug
e.g. production of B-lactamase that destroys penicillin
by penicillin resistant staphylococci .
2.The organism changes its permeability to the drug
by modification of protein in the outer cell
membrane
• thus impairing its active transport into the cell e.g.
resistance to polymyxins.
Mechanism of resistance to antimicrobial agents
3.The organism develops an altered receptor

site for the drug
e.g. resistance to aminoglycosides
4.The organism develops an altered metabolic
pathway that bypasses the reaction inhibited
by the drug
e.g. sulphonamide resistant bacteria acquired the
ability to use preformed folic acid with no
need for extra cellular PABA.
Origin of resistance to antimicrobial agents
• Non genetic drug resistance Metabolic inactivity –

Most antimicrobial agents act effectively only on
replicating cells.
Non genetic drug resistance
• Metabolic inactivity – Most antimicrobial agents act
effectively only on replicating cells . Non multiplying
organisms are phenotypically resistant to drugs.
• Loss of target structure- L-forms of bacteria are
penicillin resistant ,having lost their cell wall which is
the structural target site of the drug.
Genetic drug resistance
1.Plasmid mediated resistance

– Plasmids frequently carry genes that code for
the production of enzymes that inactivate or
destroy antimicrobial agents e.g. B-lactamase
which destroy the B-lactam ring in penicillin and
cephalosporins.
– Plasmids may result in epidemic resistance
among bacteria by moving from one to the
other by conjugation , transduction or
transformation.
2. Transposons (are DNA elements that jump from

one place in DNA to another) mediated resistance-
Many transposons carry genes that code for drugs
resistance.
• As they move between plasmids and chromosomes
they can transfer this property by bacteria
• This process is called tansposition.
3. chromosomal drug resistance. This develops as a

result of :
a. spontaneous mutation in agene that controls
susceptibility to an antimicrobial agent.
b. the most common results of chromosomal mutation is
alteration of receptors for a drug
e.g. streptomycin resistance can result from a mutation
in the chromosomal gene that controls the receptor
for streptomycin ,located in the 30s bacterial
ribosome
Complication of antimicrobial Agents
• 1. Development of drug resistance

• The emergence of resistant mutants is
encouraged by
• inadequate dosage,
• prolonged treatment,
• the presence of closed focus in infection
and the abuse of antibiotics without in-vitro
susceptibility testing.
• 2. Drug toxicity
• Many of the antibacterial drugs have toxic side
effects.
• This can be due to overdosage ,
• prolonged use or narrow margin of selective toxicity
e.g.streptomycin affects the 8th cranial nerve leading
to deafness ,
• chloramphenicol may cause depression of the bone
marrow, the
aminoglycosides(e.g.garamycin,tobramycin ) are
nephrotoxic.
• 3.Superinfection
• a. superinfection may occur by pre-existing resistant
strains Staph. aureus in hospital infection.
• b. Another type of super infection is due to
suppression of normal flora by antibiotics
• e.g.overgrowth of candida in the vagina causing
vaginitis or in the mouth causing oral thrush.
• .
Prolonged oral chemotherapy leading to suppression

of intestinal flora
• and overgrowth staphylococcal entercolitis or
clostridium difficile which causes
pseudomembranous colitis.
• Over growth of gram negative organisms
naturally drug resistant e.g. pseudomonas,
proteus may cause respiratory tract infection
• 4. Hypersensitivity –
• The drug may act as a hapten ,binds to
tissue proteins and stimulate an
exaggerated immune response leading to
tissue
Choice of an antimicrobial agent
• while waiting for the result of sensitivity

test
• in closed lesion when there is no available
sample.
II. Bacterial pathogens causing eye, ear
and skin infections.
Eye Infections
• Various microbes including bacteria,
viruses and fungi may cause eye
infections.
• Among bacteria, N.gonorrheae,
Chlamydia, Staph.aureus, H.influzae,
Str.pneumoniae are the most common
pathogens.
Eye Infections: Opthalmia neonatorum
• N.gonorrheae is the cause of sexually

transmitted disease gonorrhoea.
• It commonly presents as a purulent infection of
mucous membrane of urethra and also the
cervix of the female
• Opthalmia neonatorum-Babies born to infected
woman may suffer conjunctivitis, opthalmia
neonattorum,
• and in young girls a vulvovaginitis.
Eye Infections: Opthalmia neonatorum
• Opthalmia neonatorum-Babies born to infected woman may

suffer opthalmia neonatorum.
• This may occur when the eyes are coated with gonococci as
the baby passes down the birth canal of infected woman.
• A severe purulent eye discharge with periorbital oedema
occurs within a few days of birth.
• If untreated, opthalmia will lead rapidly to blindness.
• prevented in areas of high prevalence by insillation of 1%
aqueous silver nitrate in the eye of newborn babies.
Eye Infections Trachoma
• Chlamydia trachomatis is the causative agent.

• Are small Gram-negative bacteria
• are obligate intracellular parasite.
• They differ from most true bacteria in that they have no
peptidoglycan in their cell wall
• and lack the ability to produce their own ATP.
• Morphology and growth cycle
• The chlamydiae has two forms-
• Elementary body - is extra cellular, infectious metabolically
inert form which is 300- 350 nm.
• Reticulate body- This is non-infectious but metabolically
active particle which is 800-1000 nm.
• Once chlamydiae cell have come into contact of the

organism,
• it enters the cell within the vesicle.
• In the vesicle the elementary body loses its dense
DNA core and the particle size increases and
becomes reticulate body.
• In the vesicle the reticulate body divides by binary
fission to yield pleomorphic organism.
• Trachoma has been known for thousands of years.

• it is still found in countries where standards of
sanitation and hygiene are poor and flies abound.
• C. trachomatis ,A, B, Ba, and C are the usual
causal agents.
• In endemic areas children are often infected
before their second birthday.
Eye Infections: Trachoma
• Scaring of tarsal conjunctiva

• Inturned eyelashes
• Corneal opacity
• The disease is spread mainly by flies and fingers.
• Adult inclusion conjunctivitis (paratrachoma) is
caused by serotypes D-K. It is most prevalent in
sexually active young people and is spread from
genitalia to eye.
Eye Infections: Trachoma
• Blindness due to this cause is still a problem in the

trachoma belt,which stretches from North Africa to
South –East Asia. Key signs of the progression of the
disease-
• Medium trachomatis inflammation in the conjunctiva
with follicular inflammation
• Intense inflammation with diffuse thickening of the
conjunctiva
Eye Infections: Chlamydial ophthalmia
• Chlamydial ophthalmia neonatorum

(inclusion blennorrhoea) develops in
infants 5-21 d after birth.
• The source of infection is infected genital
tract of the mother, and the child is
infected during passage through the birth
canal.
Chlamydiae
• Laboratory
• Chlamydiae may be isolated in either
embryonated eggs or tissue culture.
• The presence of the organisms is detected by
staining for inclusion or elementary bodies.
• The disadvantage of culture is that it only
detects viable organisms.
• ELISA, and fluroscent antibody will
demonstrate elementary bodies.
Chlamydiae
• Treatment and control

• Vaccine has not been successful.
• Antibiotics can be used in the treatment of
chlamydia infections.
• The antibiotics of choice are tetracycline
in adults and erythromycin in babies
Skin infection
• Human skin acts as an excellent barrier to

infection.
• Some parasites, such as hookworm larvae
and schistosome cercariae can penetrate to
initiate infection
• Primary skin infection may gain access by
abrasions,
• or specialized adaptation to grow well in
keratinized tissue.
Skin infection
• Bacterial infection of skin

Staphylococcal impetigo –Is a
superficial, discrete, crusted spot that
lasts up to two weeks.
• Impetigo may be caused by
Staphylococcus aureus and by Str.
pyogens.
• Stapylococcus aureus- causes a wide
range of major and minor infections in
man and animals.
Skin infection Staphylococcal impetigo
• Staph. aureus is a Gram-positive coccus

about 1mu in diameter.
• The cocci are mainly arranged in grape-
like clusters but some occur as a single or
pairs.
• It is coagulase positive, B-haemolytic on
blood agar.
Staphylococcal impetigo
• Pathogenesis-
• Staph aureus is present in the nose and on the
skin of a viable proportion of healthy people.
• It is opportunistic pathogen in that it causes
infections most commonly at sites of lowered
host resistance,
• e.g. damaged skin or mucous membranes or
haematoma in the cancellous tissue of a long
bone.
Staphylococcal VIRULENCE FACTORS
• Virulence factors-Staph. aureus strains possess

• a large number of cell-associated and extracellular
factors ,
• Staphylococcal toxins
• Epidermolytic toxins –Two kinds of epidermolytic
toxin(type A and B)
• are commonly produced by strains mainly belonging
to phage group II.
• The strains in this group cause blister diseases.
Staphylococcal blisters
• Pemphigus neonatorum or the flattened

blisters of Impetigo
• Blistering results from splitting within the
plane of the epidermis induced by the
Epidermolytic toxins.
• Such blisters range in severity from trivial
to the distended blister of Pemphigus
neonatorum or the flattened blisters of
Impetigo.
Staphylococcal Scalded skin syndrom
Scalded skin syndrom

• The most dramatic manifestation of epidermolytic toxin is
the scalded skin syndrome.
• In this case the toxin spreads systemically in individuals
that lack neutralizing antitoxin.
• Extensive areas of skin surface are affected.
• Enterotoxins-five types of enterotoxin (types A-E) are
commonly produced by up to 65% of strains.
These are heat stable toxins.
• When ingested as preformed toxins induce nausea,
vomiting, and diarrhoea.
EAR INFECTIONS
• Most common ear infection is otitis media or infection of

the middle ear in children
• Otitis media- is an inflamation of middle ear with
formation of pus, leading to pressure and pain.
• Organisms most commonly incriminated in infections of
the middle ear are:
• Streptococcus pneumoniae
• Streptococcus pyogens
• Haemophilus influenzae type b
•
EAR INFECTIONS
SINUSITIS
• Sinusitis- is an infection of nasal sinuses. Most of
the organisms commonly incriminated in infections
of the nasal sinuses are those found in the otitis
media:
• Streptococcus pneumoniae
• Streptococcus pyogens
• Staphylococus aureus
• Haemophilus influenzae type b
EAR INFECTIONS
• direct extension of microorganisms from

nasopharynx into the frontal and maxillary
sinuses in adults and into the middle ear in
children is common.
• It is assumed that severe pain and
discharge of pus from the nose or ear is
suggestive of bacterial infection
EAR INFECTIONS
• obtaining adequate material for

microbiological examination is difficult and
requires the expertise of ear ,nose and throat.
• Hence antibiotics are usually given to cover
streptococci and H. influenzae.
• In adults with recurrent or chronic sinusitis ,
anaerobes such as peptostreptococci,or
bacteroids are often found in sinus washings.
Streptococci
Streptococci- Streptococci are gram positive bacteria

arranged in chains of varying length,
• each cell is approximately 1.0 um in diameter,
• non –motile, non-sporing, and may be capsulate.
Streptococci
• The majority are facultative anaerobes,

• but there are species that are strictly
anaerobic.
• They are catalase –negative.
• The majority of the ß -haemolytic
streptococci cause primary infection in
man and animals.
Table 6 principal types of Streptococci and enterococci involved
in human infections
Speies Lancefield group Type of haemolysis

blood agar
Str.pyogenes A ß
Str.agalactia B ß
Str.equisimilis C ß
Str.zooepidemicus D ß
Str.faecalis D ß or none
Str. bovis D ß or none
Str.equinus D ß or none
Str.pneumoniae None α
Str.pyogene
• based on polysaccharide antigens they

contained in their cell wall Lancefield
identified a number of different groups lettered
sequentially A-H and K-V.
• Str.pyogene belongs to Lancefield group A.
Str.pyogene
• The most common route of entry of
Str.pyogenes is the upper respiratory tract.
• They usually establish primary infection in
the throat,
• but only a proportion of infected individuals
develop tonsillitis or pharyngitis.
• The others may have mild atypical
infection or become symptomless carriers.
Diagnosis
• Culture : Fluid collected from ear tissue inoculated

onto blood agar, chocolate agar
• incubated for 24 hours both aerobically and
anaeobically because Group A strains only
haemolysin O fails to haemolysis on aerobic culture.
• Identification of ß –haemolytic streptococci
• Gram stain can also be prepared to observe Gram
posistive cocci,but of little help in the dignosis of
streptococci
Haemophilus influenzae
• Haemophili are pleomorphic Gram negative

rods.
• In clinical specimens H. influenzae is most
commonly seen as a small, uniform coccobacilli,
• but large spherical bodies or fusiforms may be
seen.
• Some strains of H. influenzae produce a
capsule which can be demonstrated by Quellung
reaction.
• The dependence of H. influenzae on blood for growth
on laboratory culture media
• is based on a requirement for two factors, X and V.
• X factor –haemin is required for the synthesis of
iron-containing respiratory enzymes cytochrome C,
cytochrome oxidase,catalase and peroxidase
• V factor is nicotinamide adenine dinucleotide
(NAD) or phophate(NADP).
• The differential requirements of X and V factors are
important criteria for defining Haemophilus species.
• Culture ordinary blood agar contains X and V factors
but growth of H.influenzae on this medium is poor
• heating blood agar (chocolate agar) will liberate extra

X and V factor into the medium.
• Streaking an organism which excretes an excess of
these factors will produce stimulation in its vicinity
(satellitism)
• Biochemical reaction-Haemophili are catalase
positive,oxidase positive,and ferment glucose and
galactose.
• They can be divided into eight biotypes on the

basis of indole production,urease activity and
ornithine decarboxylase reactions.
• The capsular polysaccharide antigen divides six
distinct antigenic types :designated a-f.
• The most important of these is Type b.
• Strains possessing this type are associated with
most invasive infections seen with this species.
• Pathogenesis
• H. influenzae is exclusively a human
parasite which resides principally in upper
respiratory tract.
• Invasive diseases caused by H. influenzae
type b include epiglottitis, meningitis,
bacteraemia,septic arthritis,pneumonia
and cellulites.
• The infections are unusual in the first 2

months of life, but are otherwise mainly
seen in early childhood.
• Most cases occur in children under 2
years of age,
• but acute epiglottitis tend to present in
slightly older children between 2-4 years of
age.
Laboratory culture – Cultured on heated blod

agar Chocolate agar
• Heating blood releases the growth factors
• a requirement for two factors, X and V.
• X factor –haemin is required for the synthesis of
iron-containing respiratory enzymes cytochrome
C, cytochrome oxidase,catalase and peroxidase.
• Treatment
• H. influenzae is sensitive to a wide range of
antibiotics and usually inhibited by low
concentration of ampicillin, chloramphenicol,
tetracycline, sulphonamide, and trimethoprim.
Epidemiology of invasive diseases
• H. influenzae is an important cause of serious
serious systemic bacterial diseases in children
through out the world.
Str. pneumoniae
Description
• Str.pneumoniae (Diplococcus pneumoniae)
• is a member of Lactobacillaceae.
• It is a gram positive, non-motile, encapsulated,
ovoid or lanceolate coccus
• tends to occur in pairs,
• Most strains are facultative anaerobic although
occasional glucose and 5-10% Co2 is required.
Str. pneumoniae
• pathological specimens- ear discharge
• Blood cultures are of value
• The culture media used is 5% blood agar.
• Identification is demonstrated by its susceptibility
to optocin,
• and bile solubility distinguish from other α-
haemolytic streptococci.
• The presence of capsular polysaccharide in
capsular swelling test /quellung reaction
demonstrated by type specific antisera for
virulent serotype.
Str. pneumoniae
• Treatments
• Str. pneumoniae is sensitive to wide range
of antimicrobial agents.
• These include the penicillins,
cephalosporins,
erythromycin,tetracycline,clindamycin,vanc
omy,teicoplanin,chloramphenicol and
sulphonamides.
Gastro-intestinal infections
• Gastrointestinal infections may be caused by bacteria,
viruses and protozoa.
Common bacterial causes of gastrointestinal
diseases-
• Salmonella spp.
• Campylobacter spp.
• Shigella spp.
• Escherichia coli (ETEC,EIEC, EPEC, EHEC)
• Vibrio cholerae
• Vibrio parahaemolyticus
• Yersinia enterocolitica
Gastro-enteritis and food poisoning
• Acute gastroenteritis is characterized by

vomiting,abdominal pain diarrhoea and fever.
• It can be caused by ingestion of a wide variety of
bacteria or their products.
• Salmonellae are a major cause of food-borne infection world –wide.
• Description
• Salmonellae are typical members of the enterobacteriacea,
facultatively anaerobic, Gram negative bacilli,
• distinguished from other members of the family by their biochemical
characteristics, and antigenic structure.
• Their normal habitat is the normal intestine.
BIOCHEMICAL REACTION
organism motility Gas from Acid from Urease citrate H2S Indole
glucose lactose ONPG
Sh.dysenteriae 1 - - - - - - +
-
Sh.dysenteriae 2-10 - - - - - V V
-
Sh.flexneri1-5 - - - - - V -
-
Sh.flexneri 6 - - - - - - -
V
- - - - - V -
Sh.boydii -
- - + - - - - +
Sh. sonni
+ - - - - + - +
Salmonella typhi
+ + - - + + - -
Salmonella(other spp)
+ + + - -- - + +
Esch.coli
Citrobacter spp. + + + - + V V +
- + + + + - V +
Klebsiella spp
+ V - + V V V -
Proteus spp
Salmonella
• Antigens- have somatic or O antigen and

flagellar or H antigen.
• Some salmonella also produce a surface
polysaccharide, of which the Vi antigen of
Salmonella typhi is the most important
example.
• The antigenic structure of any salmonella
is expressed as an antigenic formula
Salmonella antigen
• which has three parts:

• O antigen, the phase 1 H antigen and
phase 2 H antigen in that order.
• The three parts separated by colon
and the component antigens in each
part by commas.
The antigenic structure of some representative Salmonella
S. typhi 9,12, (vi) : :

d 1,2
S. paratyphi B 1,4,5,12 : :
b 1,2
S.typhimurium 1,4,5,12 : :
i 1,7
S. enteritidis 1,9,12 : :
G,m 1,2
S.virchow 6,7 : :
r l,w
S.kedougou 1,13,23 : :
i e,n,x
S.hadar 6,8 : :
Z10 1,2
H.heidelberg 1,4,5,12 : :
r 1,5
S.infantis : :
6,7,14 r 1,2
S. newport : :
6,8,20 e,h 1,5
Salmonella
• All the 2000 or so serotypes can cause
human infection,but S.cholerae-suis,
S.dublin are more irregular.
• Over 2000 serotypes have so far been
described.
Pathogenesis and clinical manifestations
• Salmonella infection is initiated by ingestion of
sufficient number of organisms to overcome
body defences, in particular gastric acidity, and
to colonize the small intestine.
Salmonella
The infective dose is regularly below 103

organisms and sometimes less than a 100
bacteria.
• Many factors influence the infective dose.
• Such as strain to strain variation in
virulence,
• vehicle of ingestion.
Salmonella
• Once the bacteria enter the lumen of the
intestine they are able to multiply.
• Some bacteria attach to the microvilli of
the ileal mucosa by means of adhesions
on the bacterial surface,
• which adhere specially to mannose –
containing receptors on the epithelium.
• Attachment is followed by degeneration of
microvilli.
Salmonella
• Attachment is followed by degeneration of
microvilli. Further multiplication in these
cells macrophages of the peyer’s patches.
• Some bacteria penetrate into the sub-
mucosa and pass to the local mesentric
lymph nodes.
• All the clinical manifestations of
salmonella infection, including diarrhoea
begin after ileal penetration.
Salmonella
Enteric fever( typhoid fever).
• Enteric fever is mostly caused by S. typhi or S.

paratyphi A, B or C.
• The clinical features tend to be more severe with
S. typhi ( typhoid fever).
• Human infections with these organisms is
characterized by a long incubation period of 10-
14 days
• followed by septicaemic illness ,enteric
fever,quite unlike the diarrhoea and vomiting
that are characteristic of food poisoning.
Salmonella
Laboratory diagnosis
• Depends on isolation and identification of
causal salmonella from a specimen.
• Enteric fever can be isolated from blood
culture, stool and urine culture.
• Widal test –serological test for specific O
and H antibodies
Salmonella
Treatment
• Enteric fever
• Chloramphenicol introduced in 1948 still
effective. Chloramphenicol resistance in S.typhi
may be treated with ampicillin and
cotrimoxazole.
• Gastro-enteritis
• Management of salmonella gastro-enteritis
• includes replacement of fluids and electrolytes
and control of nausea, vomiting and pain .
• the role antibiotics in this condition is limited.
Shigella (Bacillary dysentery)
• Dysentery: is a clinical entity characterized by frequent

passage of blood-stained mucopurulent stools.
• Bacillary dysentery is caused by members of the genus
Shigella.
• Shigellae are typical members of the Enterobacteriaceae
• Shegellae are Gram negative bacilli indistinguishable
from other enterobateria microscopically.
• They are non-motile and non-capsulated and non-
lactose fermenting.
• The genus Shigella is subdivided on

biochemical and serological grounds into
four
species-
• Shigella dysenteriae, Sh.flexneri,
Sh.boydii and Sh.sonni.
Pathogenesis
• Shigellae are pathogens of man and other
primates.
• The infective dose is small, between 10 and 100.

• After reaching the large intestine the shigellae
multiply in the gut lumen .
• Many bacteria adhere to the epithelial cells of
the gut mucosa and induce the cells to ingest
them.
• The shigellae multiply within the epithelial cells
and spread laterally to the adjacent cells and
deep into the lamina propria.
• Patches of the necrotized epithelial cells are

sloughed and ulcer forms.
• Dysentery bacilli rarely invade other tissues.
• Althogh the main determinant of pathogenicity
in shigella infection is invasion of the wall of the
large intestine,with its consequent inflammatory
reaction,
• many strains have been shown to produce an
exotoxin able to cause secretion of water and
electrolyte.
• Infections with Sh.dysenteriae is usually

associated with severe illness.
• The special virulence of Sh.dysenteriae has
been ascribed to its ability to produce a potent
exotoxin.
• The illness caused by members of the
Sh.flexneri and Sh. boydii group may be
prostrating as that caused by Sh. dysenteriae.
• At the other end the illness associated with
Sh.sonnei is mild.
Shigella
• Epidemiology
• Bacillary dysentery is usually spread faecal-orally by
fingers.
• The carrier may also handle and infect food that is eaten,
or eating utensils that are used by another person who is
thereby infected.
• In communities without satisfactory methods of sewage
disposal, insects can gain access to infected human
excreta and transfer shigellae mechanically to foodstuffs.
• Occasional epidemics of bacillary dysentery have been
traced to water supplies when chlorination of the supply
has not been instituted or has been defective.
Shigella
• Hand washing and disinfecting skin after

visiting toilet, can reduce the dysentery
bacilli from the hands, but cannot be
guarantee to remove all the bacilli from the
hands.
Shigella Laboratory Diagnosis
• The faeces are inoculated on macConkey

or SSA or other enteric agar medium
• and after incubation at 37 0C for 18-24 h.
• Non-lactose fermenting pale colony
• tested biochemically for characteristic
reactions.
• Colonies that give characteristic reactions
confirmed by serological investigation with
species- specific sera.
Shigella
Treatment
• Most cases of shigellosis especially those

due to Sh. Sonnei are mild and donot
require antibiotic therapy.
• Oral rehydration salt solution is all that is
required.
• In severe infections ampicillin, co-
trimoxazole, tetracycline,or ciprofloxacin
are appropriate provided that they are
active in vitro test.
Cholera
• Cholera is typically characterized by
sudden onset of effortless vomiting and
profuse watery diarrhoeae.
• The causative agent is Vibrio cholerae
• The genus vibrio is the most extensively
characterized and medically important
group within the family Vibrionaceae.
V.cholerae
• The members of the genus Vibrio are
short gram negative curved,motile
bacteria.
• They are fermentative and
• nearly all are oxidase positive.
• The genus can be divided into non-
halophilic and halophilic.
• V.cholerae is non halophilic and can grow
in media without added salt.
V.cholerae
• The biochemical reactions and antigenic
structure are important in identification of
V.cholerae.
• There are over 80 different somatic (O) antigens
in strains of V.cholerae,
• but the causative organism of epidemic cholera
is defined by possession of O1 antigen and
known as V.cholerae O1.
• Strains of other serogroups are collectively
known as non-O1 V.cholerae ( known in the past
as non-agglutinable vibrio or non-cholera
V.cholerae
• Pathogenesis
• Choleral is typically characterized by
sudden onset of effortless vomiting
and profuse watery diarrhoeae.
• Rapid dehydration and hypovolaemic
shock which may cause death in 12-24h
are related to the profuse
watery,colourless (rice water
stools)stools.
V.cholerae
• Cholera toxin consists of five B subunit and a
single A subunit.
• The B subunit binds to a specific receptor on
the cells lining the villi and cryps of the small
intestine.
• It is thought that insertion of the B subunit into
the host cell membrane forms transmembrane
channel
• through which the toxic A subunit can pass into
the cytoplasm.
V.cholerae
• The cholera vibrio are ingested in drink or
food.
• After passing the acid barrier of the
stomach
• the organisms begin to multiply in the
alkaline environment of the small intestine
where they produce a potent enterotoxin,
cholera toxin.
V.cholerae
• The cholera enterotoxin causes transfer of
adenosine diphosribose(ADP ribose) from
nicotinamide adenine dinucleotide(NAD)
• to a regulatory protein which is part of the
adenylated cyclase enzyme responsible
for the generation of intracellular cyclic
adenosine monophosphate.(cAMP).
V.cholerae
• This inturn causes i/ inhibition of uptake of
Na+ and Cl by cells lining the villi,
• ii\ hypersecretion of Cl- and HCO3- ions.
• Therefore the up take of water , normally
accompanied by Na+ and Cl- absorption
is blocked
• and there is a passive outflow of water
across mucosal cells leading to serious
loss of water and electrolytes.
V.cholerae
• Laboratory diagnosis
• Stool specimens are inoculated into
alkaline peptone water in which vibrios
grow rapidly and accumulate on the
surface.
• inoculated on thiosulphate-citrate-bile
-salt-sucrose(TCBS).
V.cholerae
• V.choleae strains appear as yellow
sucrose fermenting colonies.
• The colonies can be tested for oxidase
production
• and agglutination in O1 antiserum prior to
biochemical confirmation.
cholera
• Treatment
• Priority is given to fluid and electrolyte
replacement.
• Oral rehydration therapy is often sufficient
• but severe cases may require intravenous
rehydration.
• Tetracycline, chloramphenicol and co-
trimoxazole
• given to reduce the period of excetion of
V.cholerae in the stools of patients.
cholera
• Epidemiology
• Infection is generally spread by way of contaminated water or
certain foods such as uncooked sea food or vegetables.
• The source of the contamination is usually the faeces of carriers or
patients with cholera,
• but in non endemic areas probably originate from natural aquatic
reservoirs.
• Cholera is characteristically an infection of communities with poor
standard of hygiene.
• Communities with shared communal water supplies such as tanks,
ponds ,canals or rivers.
• In general ,those public health measures used in the control of any
oro-faaecal disease spread can have value in cholera control.
Diarrheagenic
Escherichia coli
• Strains of Escherichia coli are Gram
negative coliform bacteria
• predominant among the aerobic
commensal flora of human and animals
intestines.
• are usually motile, grow well in non
selective media, forming smooth
colourless colonies 2-3 mm in diameter.
Diarrheagenic
Escherichia coli
• On MacConkey agar they produce large
red colonies, may be haemolytic on blood
agar.
• They ferment lactose, with production of
acid and gas in 24-48 h.
• They have O, H, and K antigens.
Diarrheagenic
Escherichia coli
• diarrheagenic Strains fall into at least six
groups.
• Enteropathogenic Esh. Coli(EPEC)
• Enterotoxigenic Esh. Coli (ETEC)
• Entero-invasive Esh. Coli (EIEC)
• Enterohaemorrhagic(EHEC)/
Verocytotoxic Esh. Coli ( VTEC)
• Enteroaggregative Esh. Coli(EAEC)
1.EPEC
• EPEC are an important category of diarrheagenic Esh. coli which

has been linked to infant diarrhoea in the developing world.
• The ability of EPEC strains to cause diarrhoae has been
confirmed by oral administration of the organisms to babies and
adults. Most strains do not produce ST,LT,VT.
2. Enterotoxigenic Esch. Coli (ETEC)

• These strains produce a heat stable enterotoxin(ST) or a heat
labile enterotoxin(LT) or both.
• In addition ,they possess colonization factors that are specific for
the host animal species and which enable the organisms to
adhere to the epithelium of the small intestine.
3. Enteroinvasive Esch.coli(EIEC)
• EIEC causes diarrhoea identical to

bacillary dysentery caused by Shigellae.
• The organisms penetrate the epithelial
cells of the large intestine by inasive
mechanism.
• In order to survive the hostile upper
intestine, along their passage,
• they must resist the effects of gastric
acidity, bile salts and pancreatic enzymes.
4. Verocytotoxigenic Esch.coli(VTEC)
• Esch. Coli O157 is by far the most common

serogroup found in human VTEC infections.
• These organisms produce one or both of two
verocytotoxins(VT1 and VT2).
• VT1 is closely related to the so called shiga
toxin produced by Shigella dysenteriae1.
• VTEC cause a range of symptoms from mild
watery diarrhoea
• to severe diarrhoea with large amounts of fresh
blood in the stool(haemorrhagic colitis).
Laboratory Diagnosis
of Esch. Coli
• diagnosis of Esch. Coli, is culture of

faecal specimen on suitable media such
as MacConkey agar.
• Identification is done using slide
agglutination with polyvalent antisera for
the different serogroups.
• Those with positive reactions are tested
with monovalent antisera.
diagnosis of Esch. Coli
• inoculation into animal tissues like
Chinese hamster cells for detection of LT
toxins,
• immunological techniques including
ELISA, Radio immunoassay,
• Injection of enterotoxin preparation into
ileal loop of rabbits can be used for the
diagnosis of ETEC.
diagnosis of Esch. Coli
• Guinea-pig eye or Sereny test,
• tissue culture methods can be used for
diagnosis of EIEC.
• Verocytotoxigenic Esch. Coli (VTEC) may
be detected by Sorbitol fermentation within
24 h using sorbitol - Ma cConkey agar for
primary culture
• followed by agglutination with an O157
antiserum.
Treatment and control
• Esch. coli is naturally sensitive to many
antibiotics such as ampicillin,
cephalosporins, tetracycline,
streptomycine, chloramphenicol,
kanamycin, gentammicin, trimethoprim
and cephalexin.
Sexually Transmitted Diseases
• Sexually transmitted bacterial pathogens

include
• N.gonorrhoeae,
• Chlamydia trachomatis,
• Haemophilus ducreyi,
• Treponema pallidum,
Calymmatobacterium grannulomatis and
Ureaplasma urealyticum.
Gonorrhoea
• Gonorrhoea is a sexually transmitted

disease caused by Neisseria gonorrhoeae
• Neisseriae are gram-negative diplococci
of which meningococcus and gonococcus
pathogens.
• They are gram negative, bean shaped
occurring in pairs
N.gonorrhoeae
• Pathogenesis
• N. gonorrhoeae is exclusively human
pathogen although chimpanzees have
been infected artificially.
• The commonest clinical presentation is
acute urethritis in male a few days after
unprotected sexual intercourse.
N.gonorrhoeae
• Dysuria and a purulent penile discharge

make most sufferers seek treatment
rapidly.
• In woman with vaginal infection,
• only half may have symptoms of vaginal
discharge and dysuria.
N.gonorrhoeae
• At menstruation or after instrumentation,

particularly termination of pregnancy,
• gonococci ascend to the fallopian tubes to
give rise to acute salpingitis,
• followed by pelvic inflammatory disease
and sterility if inadequately treated.
N.gonorrhoeae Diagnosis
• N.gonorrhoeae can be recovered from

culture of urethral discharge.
• N.gonorrhoeae is a fastidious organism
requiring humidity, 5-7% carbon dioxide
and complex media.
• Commonly used media for cultivation of
N.gonorrhoeae is Thyermartin Agar or
Chocolate agar
N.gonorrhoeae
Treatment
• Antimicrobial susceptibility testing
• is essential since the susceptibility of
isolates to commonly used antibiotics
varies from time to time and from place to
place.
syphilis.
• T.pallidum is the causative agent of
syphilis
• Infection is usually acquired by sexual
contact with infected individuals
• and is commonest in the sexually active
age group of 15-30 years old.
Pathogenesis
• T. pallidum enters tissues by
penetration of intact mucosae or
through abraded skin.
• The bacterium rapidly enters the
lymphatics is widely disseminated via
blood stream and may lodge in any
organ.
• The exact infectious dose for man is not known
but in animal experiment animals less than 10
organisms.
• The bacterium multiply at initial entry site
• a lesion characteristic of primary syphilis-a
chancre forms following an average incubation
of 3 weeks.
• The chancre is Painless and most frequently on
the external genitalia,
• but it may occur on other areas
• Secondary syphilis- The primary chancre heals
within 3-6 weeks,
• and 2-12 weeks later the symptom of Secondary
syphilis develop.
• The symptoms include macular or pustular
lesions widespread involving different parts of
the skin, particularly on the trunk and
extremities.
• Secondary syphilis is highly infectious.
• The symptoms of Secondary syphilis gradually
resolve.
• Latent infection- is a period of no clinical
manifestations but in which serological
evidences persist.
• Tertiary syphilis- After decades of primary
infection, a slowly progressive, destructive
inflammatory disease that may affect any organ
develops.
• The three most common forms of late syphilis
are neurosyphilis, cardiovascular syphilis and
gummatous syphilis-a rare granulomatous lesion
of the skeleton,skin or mucocutaneous tissues.
• Laboratory Diagnosis
• Bacteriological methods -It is impossible to diagnose by this
method. Treponemes can be observed with phase contrast
microscopy from primary or secondary lesions.
• Serological Tests
• Infection with T. pallidum results in the rapid production of two types
of antibodies.
• 1. Specific antibodies- these are directed primarily at polypeptide
antigens of the bacterium.
• These can be tested by Flurescent treponemal antibody test (FTA-
Abs).
• Flurescent treponemal antibody test (FTA-Abs) is an indirect
immunoflurescence assay in which T.pallidum antigen is used.
• 2. Non specific antibodies that react with
a non-treponemal antigen called
cardiolipin.
• The Veneral Disease Reference
Laboratory (VARL) test is a non-specific
serological test for syphilis.
• It uses a mixture of cardiolipin, cholesterol
and lecithin as an antigen.
• Treatment
• All pathogenic treponemes are sensitive to
benzylpenicillin, prolonged high dose procaine
penicillin.
• In case of allergy erythromycin tetracycline or
chloramphenicol may be used.
• Antibiotic therapy of syphilitic patient with
antibiotics may induce a systemic response
called the Jarsch-Herxheimer reaction.
• This is due to release of an endogenous
pyrogen from the spirochates.
Chancroid
• Haemophilus ducreyi are pleomorphic Gram negative

rods, most commonly seen as small, uniform coccobacilli
• is responsible for the sexually transmitted disease called
chancroid
• that can be seen in materials from ulcer or in pus from
lymph node aspirate .
• Patients present with painful penil ulcer (soft sore or soft
chancre) and inguinal lymphadenitis.
• It is likely that the lesions of chancroid have facilitated

the transmission of HIV in some tropical countries
• An unrelated Gram-negative rod,
Calymmatobacterium grannulomattis
causes a somewhat similar sexually
transmitted disease, granuloma inguinale
in parts of the tropics.
• Intracellular organism known as Donovan
bodies can be demonstrated in the stained
smear from the lesions.
• Treatment
• Chancroid has traditionally been treated
with sulphonamides (alone or in
combination with streptomycin),
tetracycline, erythromycin, co-trimoxazole,
co-amoxiclav, cefotaxime and
ciprofloxacin have been shown to be
effective, but resistant strains occur.
Urinary tract infections (UTI)
Common organisms
Eschercia coli
Proteus mirabilis
Klebsiella spp.
Staphylococus
S. saprophyticus
S. epidermidis
Enterococci
Other coliforms
Pseudomonas
aeruginosa
UTI
• Esch. Coli is commonly implicated in
infections of the urinary tract
• and is by far the most common cause of
acute uncomplicated urinary tract infection
outside hospitals.
• Esch. Coli that cause UTI often originate
in the gut of the patient and the infection is
thought to occur in an ascending manner.
UTI (Esc.coli)
• The ability of Esc.coli to infect the urinary tract is
associated with fimbriae the specifically mediate
adherence to the uroepithelial cells.
• Urinary tract infection is much commoner in
females than in males since the shorter, wider
female urethra appears to be less effective in
preventing access of the bacteria to the bladder.
• The high incidences in pregnant women can be
attributed to impairment of urine flow due to
partly hormonal changes and partly to pressure
on the urinary tract.
UTI (Esc.coli)
• Clinical specimen cultured on suitable media for
identification and sensitivity testing.
• Treatment
• Esch. Coli is naturally sensitive to many antibiotics.
• Many strains, however, have acquired plasmids
conferring resistance to one or more antimicrobials.
• Extra-intestinal Esch.coli infections are treated preferably
guided by antimicrobial susceptibility test.
UTI (Klebsiella)
Klebsiella, Enterobacter, Proteus and other
enterobacteria that cause UTI
Klebsiella:
• Klebsiella are a fairly common cause of urinary tract
infection.
• The genus klebsiella are member of the
enterobacteriaceae.
• and are straight rods about 1-2µm long and 0.5-0.8 µm
wide.
• capsule material is produced in greater amount
of media rich in carbohydrate.
• Spp. include K.oxytoca, k.pneumoniae,
k.aerogenes, k. ozaenae, and K.
rhinoscleromatis .
• Cases are sporadic and usually occur in
members of the general population rather than in
hospital patient.
• Klebsiella infection of the urine often responds to
trimethoprim nitrofurantoin, or cephalosporins.
Enterobacter
• Enterobacter
• have many feature in common with those of
genus Klebsiella, but are readily
distinguished by their motility .
• Most infections are of the urinary tract, although
members of the genus are an important cause of
bactermia in some hospital.
Proteus,Providencia,and
Morganella
• These organisms are linked and they are best considered
together.
• Genetic evidences and enzyme studies show that a
separate genus is justified with a single species
Morganella morgani.
• Proteus and providencia are now separate species.
• All these organisms grow well on ordinary nutrient media.
• A notable property of Pr. Vulgaris and Pr. Mirabilis
strains is their ability to swarm on sold media.
•
Proteus,Providencia,and
Morganella
• M.morganii and proteus and providencia have
the almost unique ability to oxidatevely
deaminate amino acids,
• tested in a medium containing Phenylalanine.
• Proteus mirabilis are a prominent cause of
urinary tract infection in children and domiciliary
practice.
Treatment
• Susceptability should be guided by antimicrobial
susceptibility test finding.
Bacterial Pathogens Causing
Central Nervous System (CNS)
Meningeal irritation may occur in association with
other acute infections Bacterial agents that
cause meningitis include:
• Neisseria meningidis,
• H. influenzae,
• Str.pneumoniae,
• Esch. Coli,
• Listeria monocytogenes.
Neisseria meningidis
• N.meningitidis and N. gonorrheae are so similar
in their morphological and culture characters.
• They are gram negative, oval cocci occurring in
pairs with the apposed surfaces flat or even
slightly concave (bean shaped)
• In pus from inflammatory exudates,such as CSF
or urthral discharge the diplococci are found in
polymorphonuclear cells.
• Pathogenic neissariae are demanding in
their growth requirements
• The addition of heated blood or ascitic
fluid, or both to nutrient agar
• incubation in moist atmosphere containing
5-10% carbon dioxide 35-36 oC will
ensure a good growth.
• Serologic Classification
• Meningococci are divisible into three
main serological groups: A,B,C.
• Group A is ,in most countries ,the
serogroup associated with epidemic
cerebrospinal meningitis .
Pathogenesis
• The natural habitat of the meningococcus is the human
nasopharynx.
• Surveys of normal population show that around 5-10%
are carriers of meningococci,over half which are non-
capsulate strains.
• The route of spread of the meningococci from the
nasopharynx to the meninges is controversial:
• the organism may either spread directly through the
cribriform plate to the subarachnoid space by the
perineural sheaths of the olfactory nerve
• or much more probably, it passes through the
nasophryngeal mucosa to enter the blood stream.
• CSF is cultured on heated blood (chocolate )
agar and on Blood Agar. These cultures are
incubated overnight at 37 oC in an atmosphere
of 5-10 % Carbon dioxide.
• If Gram stained from the resulting growth show
gram negative diplococci.
• Colonies on solid medium are oxidase positive.
Direct slide agultination test may be carried with
out on suspensions of colonies picked from solid
medium
• Treatment
• It is important to perform sensitivity test on
meningococcal isolates.
Epidemiology
• Meningococcal infections which occur world
wide ,are notifiable in most countries.
• Epidemic strains of group A or B may give rise
to a high incidence of disease in susceptible
individuals who acquire such strains.
Chemoprophylaxis
• Outbreaks of diseases may be controlled
either by Chemoprophylaxis alone or
combined with Vaccination
Vaccination
• A vaccine containing group A ,B and C
polysaccharides alone is adequate in most
countries.
Animal and Arthropod Transmitted
Bacterial, Chlamydial and Rickettsial
Infections
Zoonoses
• Diseases that primarily affect wild and
domestic animals
• can be transmitted to humans by direct
contact with infected animals
• by ingesting contaminated meat,
• or more frequently by arthropod vectors,
which are carriers of disease agent.
PLAGUE
• Plague is caused by Yersinia
pestis( Formerly Pasteurella pestis).
• Yersinia pestis is a gram negative,
• non-motile, non-sporing, pleomorphic or
short coccobacillus, 1.5x0.7
• occuring singly ,in pairs or in chains.
PLAGUE
• Y. pestis grows both aerobically and
anaerobically
• but it is somewhat sensitive to oxygen and
smll inocula may not grow readily in
ordinary culture media when grown
aerobically.
• Growth occurs within a temperature range
of 14-37oC.
PLAGUE
Antigens
• There are two main antigenic complexes
that are associated with virulence and
immunogenicity of the organism.
• These are Somatic (heat stable) and
Capsular and heat- labile.
PLAGUE
Pathogenensis
• There are three severe forms of human plague
:bunonic, pneumonic and septicaemic plague.
• Bubonic Plague: The transfer of Y.pestis from rats to
man through the bits of infected fleas
• may occasionally result in a localized infection,
• known as pestis minor, with mild constitutional
symptoms.
• Painful swellings or buboes occur at inguinal axillary
or cervical regions depending on the position of the
flea bite.
PLAGUE
• From the primary buboes the plague bacilli
may spread to all parts of the body.
• In the absence of antibiotic therapy the
fatality rate may be as high as 50%.
Pneumonic plague-This develops as a
result of droplets infected with Y.pestis
being passed from person to person. A
severe bronchopneumonia develops.
PLAGUE
• Septicaemic plague-This may occur as a
primary infection
• or as a complication of bubonic or
pneumonic plague.
• The plague bacilli may spread throughout
the body and the outcome is invariably
fatal.
PLAGUE
• Epidemiology
• Bubonic plague is a zoonosis.
• The bacilli are transmitted from animal to animal
and from animal to man by fleas, Xenopsylla
cheopis an ecto parasite of rats.
• When a flea feeds on the blood of a sick animal,
• plague bacilli are sucked into the insect’s mid
gut where they multiply to such an extent that
they block the proventriculus.
•
PLAGUE
• On the death of the animal the flea seeks an
alternative host which may be another rodent or
man.
• In cool humid weather, fleas multiply and plague
spread rapidly whereas in hot dry weather the
fleas die and the spread of infection is limited.
• The sputum of a person suffering of pneumonic
plague rapidly spread infection by droplet in
community.
PLAGUE
• Bipolar –stained coccobacilli from exudates or
sputum are confirmed as Y.pestis
• by culture of appropriate specimens on Blood
agar and incubating at 27o C.
• Characteristic colonies growing on blood agar
plates are identified as those of Y.pestis by
various cultural and biological tests.
• .
PLAGUE
• Treatment
• Mesentric adenitis is usually self-limiting
septicaemic demands parenteral treatment
with ampicillinor tetracycline
Rickettsial Infections
• Rickettiaceae include a diverse group of
organisms
• share common features such as
intracellular growth and use of arthropod
vectors.
• Rickettsiae are typically defined as
obligate intracellular Gram negative
bacteria.
• Rochalimaea Quintana (can be grown in
cell free culture)
• and Coxiella burnetti (does not require an
arthropod vector to maintain itself in
nature)
• traditionally considered to be members of
rickettsiaceae
• The genus Rickettsia is divided into three
antigenically distinct groups:
• the typhus group,
• the spotted fever group,
• and the scrub group.
Species and disease Geographic distribution Means of transmission Primary vectors Important vertebrate hosts
Typhus group
R.prowazekii(epidemic typhus Africa North and South America Louse faeces Pediculus humanus Humans, possibily other
mammals(flying squirrels
R.typhi(murine typhus) Primarily tropics and sub-tropics Flea faeces Xenopsylla cheopis and other fleas Rodents and other small
mammals
Spotted fever group
R.akari (rickettsialpox USA, USSR, Korea Bite of mouse mite Liponyssoides sanguineus House mice(Musmusculus)
possible other rodents
R.australis (Queens land tick Australia Bite of tick Ixodes holocyclus Small marsupials
typhus
R.conorii(butonneusfever) Europe,Africa,Middle East,India Bite of tick Rhipicephalus etc Rodents, possiblydogs and other
small mammals
R.japonica(oriental spotted Japan Probably tick unknown unknown

fever
R.rickettsii(Rockymountain North and South America Bite of tick Dermacentor etc Rodents and other small
spotted fever) mammals
R.sibirica(northAsian tick Northern Asia Bite of tick Dermacentor etc. Rodents and other small
typhus mammals
Scrub typhus
R.tsutsugamushi(scrub typhus Asia,ustralia,islands of SW Bite of larval mite Chiggers(Leptotrombidium Rodents (particularly rats)
Pacific and Indian Oceans
• Typhus and spotted fever group rikettsiae are
closely related as indicated by DNA-DNA
hybridization studies,
• both have a typical Gram- negative bacterial cell
wall
• The polysaccharide antigens distinguish
the two groups.
• Electrophoresis has demonstrated a
number of distinct proteins in typhus group
rickettsiae.
• The spotted fever group differs slightly
• The scrub typhus rickettsiae appear to be

fundamentally different
• There is no genetic relationship or
antigenic similarities between
R.tsutsugamushi and other members of
the genus.
• The cell wall lacks lipopolysaccharide,
peptidoglycan or slime layer
• and appears to derive its structural
integrity from proteins linked disulphide
bonds.
• Pathogenesis
• Rickettsiae normally enter the body through the
bite or faeces of an arthropod vector.
• They enter endothelial cells by induced
phagocytosis, multiply intracellularly and
eventually destroy their host cells.
• In the cases of R.typhi or R.prowazekii the
rickettsiae continue to multiply until the cell is
packed with organisms and then bursts.
• .
• Spotted fever group rickettssiae seldom
accumulate in large numbers and do not cause
lysis of the host cells
• but appear to induce the formation of filopodia
which the rickettsiae enter and escape.
• Infected cells exhibit signs of membrane
damage.
• Scrub typhus also escape from host cells soon
after infecting them,
• but little is known about the mechanism by
which these organisms damage cells
• Rickettsial disease
• Epidemic typhus and Murine typhus- Initial
symptoms of the disease are headache and
fever 6-15 d after being exposed to
R.prowazekii.
• A macular rash,often noted 4-7 d after patients
become ill,first appear on the trunk and axillaries
and then spreads to the extremities.
• In mild cases the rash may begin to fade after 1-
2 d, more severe cases it may last much longer
and become haemorrhagic.
• Tick-borne spotted fever- There are many
clinical similarities among the tick-borne
rickettsiosis of the spotted fever group.
• Although all can be life-threatening, the most
severe is Rocky Mountain spotted fever.
• Early symptoms include fever and severe
headache, often accompanied by mayalgia,
anorexia, vomiting, abdominal pain, diarrhoea,
photophobia and cough.
• Rickettsialpox-is relatively mild infection and clinical
course is similar to other spotted fevergroup infections.
• Scrub typhus – Infection with scrub typhus rickettsiae
may be inapparent or fatal,depending on host
factorsandvirulence of the infecting strains.
• Symptoms develop 6-18 d afterbeing bitten by infected
mite (chigger).
• Enlargement of local lymphnodes
• Progression of the diseasemay be accompanied by
interstitial pneumonitis,generalized
lymphoadenopathy,splenomegaly and rash.
• Laboratory methods can be divided into
serological tests, isolation of rickttsia from
blood and tissue.
• Isolation of the organism in cell culture
• Isolation of the organism in cell culture or
susceptible lab animals such as guinea
pigs or mice.
• Serological methods
• The indirect haemagglutination, immunofluorescence,
and latex agglutination appears to have the greatest
clinical application.
• Weilfelix test Relies on agglutination of the somatic cell
of non-motile
• Proteus species widely available but has low level of
sensitivity and specificity.
• Treatment
• Rickettsial infections may be treated with tetracycline or
chloramphenicole.
• Both are rickettsiostatic and allow the patient’s immune
system time to respond and control the infection.
Chlamydiae
• Are small Gram-negative bacteria which are
obligate intracellular parasites.
• There are three species agreed by an
international committee:
• Chlamydia trachomatis can be divided into those
• causing trachoma,and inclusion
conjunctivitis(TRIC)
• Those causing lymphogranuloma venerum(LGV)
and
• the one causing mouse pneumonitis(MoPn)
• Chlamydia psittaci(ornithosis)
• in man is caused by infection with avian
strains of C. psittaci.
• The illness is an influenza like syndrome
with generalized malaise, fever
anorexia,rigors,sore throat headache and
photophobia.
•
• It may be a severe illness typhoidal state,
delirium and pneumonia.
• The avian strain of C.psittaci has caused
respiratory infection of shepherds.
• Birds with respiratory and intestinal infections
shed the organism in nasal secretions and
droppings.
• The nasal secretions may contaminate the
feathers, where they dry and produce an
infected dust in which can survive for months
• .
• Similarly the organism has been in sheep
droppings, milk, on the placenta.
• Aerosols can be produced and are hazard to
shepherds, who may develop a respiratory
infection, and to pregnant women and can cause
miscarriage.
• Range of natural hosts infected by C.psittaci
and diseases reported to date are shown in
Table below.
Table 10 Examples of the range of diseases
caused by C. psittaci in natural hosts
host cojunct Intestinal Respiratory Placental Seminal infertility polyart Meningo- mastitis
ivitis in fections infections infection infection hritis enceephali
abortion tis
birds + + + - - - - - -
sheep + + + + + - + + +
cattle + + + + + + + + +
Goats _ + + + - - - - +
Cats + + + - - - - - -
Guinea + _ - - - + - - -
pigs
Koala + _ - - - + - - -
bears + _ - - - + - - -
• Chlamydiae may be isolated in either
embryonated eggs or tissue culture.
• The presence of the organism is detected by
staining for inclusions or elementary body.
• staining of smears by fluorescent antibodies will
demonstrate elementary bodies and the ELISA
test can detect antigens.
• DNA probe,serology are also among the
possible methods.
• Treatment
• Antibodies can be used in the treatment of
chlamydial infections.
• The antibiotics of choice are tetracycline
in adults and erythromycin in babies.
MYCOLOGY
• The study of Fungi is called Mycology.
• I. THE BIOLOGY OF FUNGI
• Fungi constitute diverse group of eukaryotic
organisms which exist as saprophytes, parasites
or commensals.
• They have membrane-bound organells, internal
membrane systems,
• and a well defined cell wall which is made up of
polysaccharides and chitin.
• They can be divided into two main groups:
Moulds and Yeasts.
I. THE BIOLOGY OF FUNGI
• Moulds are filamentous or mycelial fungi.
• They are composed of branching filaments known as

hyphae.
• They grow by extension of apical interwoven mass called
mycelium.
• In most fungi the hyphae have regular cross –walls
called septa,
• but in lower fungi these are absent and called aseptate
fungi.
• Moulds produce asexually by means of spores or
sexually.
• In laboratory cultures they produce asexual spores.
. THE BIOLOGY OF FUNGI
• Yeasts
• Yeasts are unicellular fungi.
• Most reproduce by an asexual process
called budding.
• Some yeasts produce chains of elongated
cells (pseudomycellium)
• that resemble the mycelium of moulds,
species also produce true mycelium.
THE BIOLOGY OF FUNGI
• Dimorphic fungi. Fungi that are capable

of changing their growth to either a
mycelial or yeast phase
• Many of these fungi are pathogens.
THE BIOLOGY OF FUNGI
• Identification
• Identification of moulds is by detailed
study of macroscopic and microscopic
morphology of fungi and their spore types.
• Yeasts are primarily identified according
to their ability to ferment sugars and
assimilate carbon and nitrogen
compounds.
II. FUNGAL PATHOGENS INVOLVED IN
DISEASES OF MAN
• Fungal disease in man and animals is

called mycosis
Types of Mycoses
• Fungal diseases can be divided into:
• Superficial mycoses
• Subcutaneous Mycoses
• Systemic mycoses
• Mycotoxins
I. Superficial mycoses-
• These are diseases of the skin, hair, nails and mucous membranes.
• They are the most common of all fungal infections and have world
wide distribution.
• Ringworm (Dermatophytosis) –This is a complex diseases which
affects the keratinous of hair,nail,and the horny layer of the skin.
• It is caused by a group of closely related moulds called
dermatophytes.
• These fungi have the ability to colonize and digest Keratin.
• They have no tendency to invade the deeper structures of the body.
• There are three important genera: Microsporon,
Tricophton, and Epidermophton
• Microspora are the most common cause of
ringworm of the scalp and may give to ring worm
in other parts of the body.
• Trichophta may cause ring worm of the scalp,
beard, skin, or nails.
• The organisms are found as chains of spores
inside or on the surface of hairs taken from
affected areas.
• Epidermophta- Are largely responsible for
ringworm of the body hands, feet, and
nails.
• They grow only in the epidermis when they
appear as interlacing threads.
• They do not invade the hairs.
• Tinea captis (Ringworm of the scalp)
occurs most often in children and is highly
communicable disease.
. may spread directly from person to person
or by articles of apparel.
It occurs in domestic animals from which it
can be transmitted to man.
Tinea cruris is the ringworm of the groins.
Tinea pedis- a ringworm of the feet (atlete’s foot)
is contracted from footwear, lockers, floors, etc.,
and is difficult to control.
Laboratory Dignosis
• The laboratory dignosis of dermatomycoses
depends on
• demonstrating the fungi in the hair and skin
scraping by direct microscopic examination or by
cultural methods.
• visible by soaking the material to be
examined in from10-20 percent sodium or
potassium hydroxide before examining
Yeast infection
• These affect the skin nail and mucous
membranes of the mouth and vagina,
• are usually caused by Candida
species.e.g C. albicans.
• Yeast infections are generally endogenous
in orgin
• but can be transmitted sexually.
• Malassezia furfur causes an infection of
the skin called pityriasis versicolor.
II. Subcutaneous mycoses
• These are mycosis of the skin

subcutaneous tissues and bone
• They show slow localized spread and
occur mainly in tropics and subtropics.
• The fungi are saprophytic and inoculated
from soil or decaying vegetation into the
subcutaneous tissue.
The principal subcutaneous mycoses are:
• Mycetoma,
• chromomycosis
• and sporotrichosis
• Sporotrichosis
• Sporotrichosis is a chronic infection usually
limited to the skin and the underlying tissue .
• It is charactrized by the formation of gumma-like
growths that slowly undergo softening and
ulceration.
• It may be caused by several species of fungi
• The most important of these is Sporotrichum
schenckii.
• The fungi is cigar-shaped structures and
found within the mononuclear cells.
• They can be demonstrated only by
cultural methods.
Mycetoma
• Is a chronic, granulomatous infection of the skin
subcutaneous tissues, fascia and bone which
most often affects the foot or hand.
• It may be cause by one of a number of different
actinomycetes (actinomycetoma) or moulds
(eumycetoma).
• The disease follows traumatic inoculation of the
organisms into the subcutaneous tissue from soil
or vegetable sources usually on thorns or
splinters.
• Consequently the disease occurs in agricultural
workers in whom minor skin injuries are
common.
• Species of organisms include
• Exophiala,
• Acremonium,
• Actinomadura,
• Nocardia,
• and Streptomyces.
• .
• Within the host tissues the organisms develop to
form compacted colonies (grains) 0.5-2mmin
diameter
Chromomycosis/Chromoblastomycosis
• Is a chronic, localized disease of the skin and
subcutaneous tissues characterized by crusted
warty lesions usually involving the limbs.
• The disease is mainly encountered in the
tropics.
• The principal causes are
• Fonsecaea pedrosoi,
• F.compacta,
• Phialophora verrucosa,
• Exophiala dermatitidis and
• Cladosporium carrionii.
• Like the mycetoma, the disease is seen most often among males in rural
areas.
The principal causes are
• Fonsecaea pedrosoi,
• F.compacta,
• Phialophora verrucosa,
• Exophiala dermatitidis and
• Cladosporium carrionii.
• Like the mycetoma, the disease is seen most often among males in rural
areas.
Systemic mycoses
• generally acquired by inhalation of air borne
spores of moulds
• They are saprophytes in soil and plant materials.
• They are mostly dimorphic fungi
• The principal disease are:
• coccidioidomycosis,
• Blastomycosis
Histoplasmosis,Paracoccidioidomycosis
• coccidioidomycosis, Blastomycosis
Histoplasmosis, Paracoccidioidomycosis
•C. immitis cause coccidioidomycosis,
•Blastomyces dermatitidis- Blastomycosis
•H.capsulatum-Histoplasmosis
• paracoccidioides brasiliensis-
Paracoccidioidomycosis
Pathogenesis and immunity
• Direct microscopy
• Most specimens are examined in wet
mount
• after a partial digestion of the tissue with
10-20 percent potassium hydroxide.
• Gram stain can also be used for yeasts
cells and Giemsa staining for
H.capsulatum.
• Culture
• Most pathogenic fungi are easy to grow in culture.
• most commonly used are Sabourauds glucose agar
(SDA),
• 4% Malt extract agar with supplemented
• Chloramphenicol (50 mg/l) to minimize bacterial
contamination
• and cycloheximide (500mg/l to reduce saprophytic fungi.
• Fungal pathogens incubated at25-30 0C and 37 0C.
•
• Brain –heart infusion or blood agar are
used to promote growth of dimorphic fungi
which helps the yeast phase.
• Cultures are incubated at least for 2-3
weeks.
• Yeasts usually grow within 1-5 d.
• Moulds are identified by their microscopic
and macroscopic morphology
• yeasts are identified by biochemical tests.
• Treatment
• There are relatively few antifungal agents
compared to the large number of antibacterial
agents.
• This is because man and fungi are both
eukaryotes
• and most substances that kill or inhibit fungal
pathogens are also toxic to the host.
• Most antifungal agents exploit differences in the
sterol composition of the fungal cell membrane.
• Most antifungal agents are available only for
topical use
• relatively few can be used systemically.
Ketoconazole and terbinafine are administered
orally.
• Others like amphotericin B and miconazole are
given parentally.
• Flucytosine, fluconazole, and itraconazole are
available for oral or parental administration.
THE BIOLOGY AND CLASSIFICATION OF
VIRUSES
Definition
• viruses are the smallest of the infective agents
Structure of viruses
• The basic infectious particle of a virus is known
as the virion.
• this consists of Nucleic acid and a surrounding
protein coat called Capsid.
• The combination of nucleic acid and capsid is
called nucleocapsid
• The capsid is composed of distinct
morphological units called capsomers.
• Capsomers are assembled from viral proteins.
• The arrangement of the capsomers and the
nucleic acid determines the symemetry of the
virion.
• Some viruses are enclosed within an envelope
derived from host cell membranes
• but modified by the inclusion of viral
glycoprotein.
Viral Infection
• Productive-infection results in viral replication with

the production of viruses
• that can infect other compatible cells.
• This is called cytolytic as the host cell lyses when
the progeny virions are released.
• This occurs if the host cell is permissive cell.
• In few cases the viruses are produced from infected
cells
• but host cells are not killed the infection is
• productive but nonlytic.
• Abortive- The replication of virus does not
occur.
• This happens if the host cell is non
permissive
• or because replication produce viral progeny
that are incapable of infecting other host
cells.
• This could be due to mutation in the virus so
that some essential function is lost ,
• or to the production of defective particles, or
action of interferons.
• Restrictive -Occurs when the host cell
is non permissive and the infection is
non productive.
• Viruses which enter cells but are not
produced by infected cells,
• the virus is maintained within the cell
in the form of DNA which replicates in
association with the host cell DNA.
Viral replication
• specific details of viral replication vary from one virus to
another,
• the general strategy of replication is the same for most
viruses.
stages in viral replication include:
• Attachment,
• penetration of the virus into the host cell,
• release of the viral genome from the capsid
• synthesis of viral proteins,
• synthesis of viral nucleic acid,
• assembly of viral progeny called virions and release of
viruses from the host cell.
Viral replication
• Attachment- viral replication begins with the
attachment (adsorption) of a virus to the surface
of a susceptible host cell.
• Attachment of a virus to a host cell involves the
binding of specific sites on the surface of the
virus to specific sites on the surface of the host
cell.
• The binding constituents on the host cell surface
typically a glycoprotein receptor.
• Viral receptors are part of the normal surface
structure of a particular cell and have other
functions.
Viral replication
• Penetration of the virus into the host cell-
Entry of a virus into a host cell occurs very
shortly after attachment.
Entry of the virus into the host cell depends on
viral type and may involve:
1/ transport of the entire virus across the
cytoplasmic membrane by endocytosis,
2/simultaneous penetration, uncoating and transfer
of only the viral genome across the cytoplasm
3/fusion of a viral envelope with the cytoplasmic
membrane of the host cell.
Viral replication
• Expression and replication of viral genomes
• The expression of the viral genome to
synthesize viral proteins and the replication of
the viral genome within the host cell are viral
replication.
• Some viruses such as papoviruses and
papiloma viruses rely on host enzymes to
replicate the viral genome.
• Most viruses such as herpsvirus use viral
proteins to replicate the viral genome.
Viral replication
• Viruses may stimulate transcription of their
own gene within the infected cell
• Viruses which contain DNA and replicate
in the nucleus can use cellular enzymes
solely for transcription and translation.
• All other viruses require to synthesize
their mRNA by processes other than those
found in uninfected cells.
VIRAL PATHOGENESIS
• Viral virulence often is due to multiple

factors.
• Each of which contribute to the efficiency
of viral replication
• and the degree to which viral replication
disrupts normal host cell functioning.
VIRAL PATHOGENESIS
• Tissue tropism- The affinity of a virus toward

specific tissue reflects the ability of viruses to
replicate within the cells of those tissues.
• The adsorption of viruses onto specific receptor
sites of human cells establishes the necessary
prerequisite for up take of viruses by host cells,
• replication, disruption of the normal host cell
function, and production of disease symptoms
by the invading viral pathogens
• Ability to down-regulate host cell
activities- Virulence of viruses depends
on their ability to down-regulate host cell
activities
• while up-regulating activities involved in
viral replication.
• In this manner the rates of viral replication
is optimized.
VIRAL PATHOGENESIS
• Presence of external spikes that aid in their attachment to host

cells- Some viruses, such as adenoviruses have external spikes
that aid in their attachment to host cells.
• Accumulation of capsid proteins- Accumulation of capsid
proteins late in the viral replication cycle can kill the host cell,
leading to release of the assembled viruses.
• Avoidance of immune defenses- The virulence of
many viruses is attributed at least in part to their ability to
evade the body’s immune defense system.
• Viruses exhibit diverse mechanisms for subverting the
immune defenses.
VIRAL INFECTION OF THE
RESPIRATORY TRACT
ADENOVIRUS
Description
• Adenovirus is an icosahedral, 20 sided regular
solid with triangular faces.
• The virion is 70-75 nm in size .
• double stranded DNA
• mw approximately 20x106 ,
• equivalent to 35-45 kilobase pairs.
Classification
• Human adenoviruses are further
subdivided into six subgenera:
• (A-F) based on DNA homology.
• Within each subgenus, serotypes are
defined by cross-reactivity in neutralization
test.
ADENOVIRUS
Replication
• The virus attaches to susceptible cells by the
apical fibres and is then taken into the cell
• It then passes to the nucleus ,losing the
peripentones at the nuclear membrane.
• Inside the nucleus the DNA is released and the
process of replication initiated.
• Following production of new viral DNA
ADENOVIRUS
Replication
• the remaining genes are transcribed from
it to form ‘late’ proteins.
• These are produced in quantity in the
cytoplasm are mostly structural
• and are later transported back to the
nucleus where new virus particles are
assembled.
ADENOVIRUS
• The effect of the shutting down of the host

cell metabolism
• and the accumulation of thousands of
new virions results in rupture of (lysis)
• and death of the infected cell with release
of the particles.
ADENOVIRUS
Clinical features
• Diseases by adenoviruses are mild upper
respiratory tract infections
• with fever, runny nose and cough.
• These infections are rarely serious but,
may progress to pneumonia.
• The majority of these pneumonias occur in
young children.
•
ADENOVIRUS
• In older children and young adults labelled as

colds
• but epidemics of adenoviruse infection with
respiratory symptoms and fever are common
• example in military camps.
• The majority are due to type 1-7, although higher
serotypes may be involved sporadically.
• Type 1,2, 5 and 6 are more commonly
associated with endemic infections while 3,4and
7 are more epidemic.
ADENOVIRUS
Electron microscopy
Finding virus in faece by electron microscopy.
Virus antigen
• The presence of a viral antigen in nasopharynx by
immuoflurescence using group specific antibodies
• (polyclonal or monoclonal)_
• other serological tests also available
• Cell culture
• Virus can be grown in cell culture from respiratory
specimen.
ADENOVIRUS
• Treatment
• There is no antiviral drug available for
treatment of adenoviral infections.
Infections are usually self-limiting.
INFLUENZA VIRUSES (ORTHOMYXOVIRIDAE)
Orthomyxoviruses comprise:
• influenza A, B, and C viruses which infect man.
• Influenza A viruses can infect a variety of
different host species.
• Influenza C is little studied ,and although
assumed to be primarily a human
• infection,
• it has recently been isolated from pigs in China.
INFLUENZA VIRUSES
(ORTHOMYXOVIRIDAE
• Description
• The virions are spherical ,80-120nm
indiameter
• a helical nucleocapsid with a core of eight
segments of single –stranded RNA with weight
of 5x106
• Within the virion RNA-dependent RNA
polymerase
• An envelope which contain lipids derived from
plasma membrane
INFLUENZA VIRUSES
(ORTHOMYXOVIRIDAE)
• From the envelope project spikes which attach the virion to
cell receptor haemagglutinin (H).
• Haemagglutinin interact with membrane
receptors called N-acetylneuraminic acid(NANA)
• Between the haemagglutinin spikes there are mushroom-
shaped protrusions of neuraminidase(N).
• The neuraminidase activity also important in the final release
of new virus particles from the infected cells.
INFLUENZA VIRUSES
(ORTHOMYXOVIRIDAE)
Cultivation
• Primary isolation are on primary monkey kidney or human
embryo kidney cells
• Embryonic chick cells and those from species mammals are
susceptible.
Replication
• Specific attachment of virion’s haemagglutinin trimers with
NANA-containing component of the cell surface
• Virions are then taken into the cell vesicles
• Fusion of the viral envelope with the membrane
INFLUENZA VIRUSES
(ORTHOMYXOVIRIDAE)
• This leads the release of nucleocapsid into the cytoplasm
• Transcrption of the viral RNA molecules produces 10 mRNA
species as RNA segments.
• mRNA are processed within the cell nucleus.
• Assembly of the new viral components takes place in the
nucleus of the host cell.
• The viral matrix proteins migrate to the cell
membrane
• and are joined by the haemagglutinin and
neuraminidase glycoproteins.
• Release occurs by budding.
INFLUENZA VIRUSES
(ORTHOMYXOVIRIDAE)
• Pathogenesis
• inhaled virus is deposited on the mucous membrane lining the respiratory
tract or directly into the alveoli,
• virus attaches to the surface of the respiratory epithelial cell
• and the intracellular replication cycle is initiated.
• The major site of infection is ciliated columnar epithelial cells.
• Alteration of form of these cells, disintegration of the nucleus, inclusion
body and the cilia are lost.
• Release of the virus from the cells allows it to spread via the
mucous blanket to other areas of the respiratory tract.
INFLUENZA VIRUSES
(ORTHOMYXOVIRIDAE)
• The cell damage initiates an acute inflammatory
response.
• Influenza A–In classical influenza the incubation
period may vary from 1to 4d.
Clinical features
• The illness is characterized by a sudden onset
of systemic symptoms such as chills, fever,
headache, myalgia and anorexia.
• Respiratory symptoms are less common but
second place to the systemic
INFLUENZA VIRUSES
(ORTHOMYXOVIRIDAE
• The infection with Influenza B- symptoms is milder
• and some studies have shown more involvement of the
gastrointestinal tract,with the term ‘gastric flu’.
• Influenza C- Infection is comparatively rare compared with
influenza A and B
• upper respiratory tract infection infection usually confined to
young children.
• Epidemiology
• Typically, there is a sudden appearance of
cases of respiratory disease,
• these occur for several weeks and then
suddenly cease
• The major pandemics are associated with
antigenic shifts- when the viral H or N or
both ,are changed.
• The shift results from the acquisition of a
complete new RNA segment 4 and/or 5.
• Influenza B virus do not undergo antigenic shift
as there is no animal reservoir.
• There is antigenic change that results from
mutation,
• the changes are the cause of antigenic drift.
• Peak number of cases are seen with
appearance of a new strain.
• This is followed at varying intervals of a year or
two by the appearance of virus which has drifted
antigenically from the parent type.
• Control
• Immunization is the only approach
available for the prevention of influenza,
both in individuals and the community.
• This protects against infection, but only
with strains closely related to those in the
vaccine.
PARAMYXOVIRUSES
• The paramyxoviruses are a family of enveloped
viruses
• contains single stranded RNA as a single piece.
• They resemble the orthomyxoviruses in both
morphology and affinity for sialic acid receptors
on mammalian cells
• but they are larger and more fragile.
• Included in here are several genera with several
members:
Parainfluenza viruses:
• Mumps virus,
• Newcastle disease virus (NDV)
• and simian virus 5 (sv5),
• morbillivirus (measles,canine distemper virus and rinderpest
virus)
• and pneumovirus (respiratory syncytial (RS) virus).
Description
• Nucleocapsid contain single stranded negative-sense
RNA with molecular weight of 7x106.
• Diameter varies from 80-350nm,but giant filamentous
forms up to 800nm occasionally occur
• pleomorphic envelope with a lipoprotein membrane
• surface projections carries haemagglutinin and
neuraminidase functions(HN)
• and F(the fusion protein) glycoproteins.
Replication
• Viruses attach via haemagglutin into sialic
acid containing receptors on cell surface,
• Fusion of F protein of the viral envelope
with the cell membrane,
• Release of nucleocapsid into the cell,
• The negative –stranded RNA cannot act as
mRNA,
• thus mRNAs are produced with the help of
RNA-dependant RNA polymerase.
• The messenger RNA transcripts are
translated to produce virus specific proteins.
• These include RNA polymerase, which
copies back positive RNA to negative
strands for transcription of later mRNA
• Assembling of viral components and
incorporation of H N and F,
• Release(buding off) by the action of
neuraminidase action.
MUMPS
• Is a typical paramyxovirus, the spikes on
the envelope carry either HN or F protein
• the envelope also contains a matrix (M)
protein.
Replication
• Indistinguishable from that already
described for parainfluenza viruses.
Clinical features and pathogenesis
• It is a common childhood infection
• Involvement of salivary glands is a frequent feature.
• Infection is probably by droplet into the respiratory tract.
• The incubation period is 14-1d
• followed by generalized ‘flue- like’ illness with fever, malaise
• and localized swelling of the salivary glands, usually the
parotids.
• Neurological involvement is common in mumps(over 50% of
infections) though the majority are not clinically apparent.
Laboratory DX
• Typical mumps doesnot usually require lab.confirmation
• but mild cases with little parotid swelling may not be noticed
until complications develop.
• Diagnosis will depend on growing the virus from throat
swabs, saliva or affected glands or from the cerebrospinal
fluid.
Epidemiology and control
• Mumps is a worldwide disease,with man the only known
reservoir
• Most infections are in school age children,
• in adults more severe and more complications.
• Has now vaccine incorporate into a triple vaccine
against measles ,mumps,and rubella (MMR).
• All the three components are live attenuated viruses.
MEASLES
• The spikes on the measles viruses envelope carry a

haemagglutinin but not neuraminidase.
• There is F protein which is also a haemolysin.
• A matrix protein M
• Measles virus is related to canine distemper virus (CDV) and
rinder pest virus in cattle.
• There is partial cross–protection between measles and CDV.
• Similar cross-reactivity is found with rinder pest virus.
• Pathogenesis
• Measles is acute febrile illness mostly
in childhood,
• after incubation period of 10-12d.
• The onset is flue-like with high
fever,cough and conjunctivits
• Koplik’s spots (red spots with a bluish white
centre on the buccal mucosa) may be present at
this stage.
• After 1-2 days the acute symptoms decline
• appearance of a wide spread maculopapular
rush
• The rush can be inhibited by local injections of
immune serum.
• Recovery is complete over the next 10-14 days.
Complications include
• a giant cell pneumonia, more common in adults,
• otitis media and a post–measles encephalitis.
• Measles encephalitis can cause severe and permanent mental
impairment in those it does not kill. It is rare but disastrous.
• Most cases of measles are diagnosed
clinically ,
• Diagnosis may be made by
immunofluorescence on exfoliated
respiratory cells taken from
nasopharyngeal secretions.
• Epidemiology
• Transmission is person to person,
• by respiratory droplets,conjunctivitis may also
be a source.
• The disease is ubiquitous through out the world
• In tropical areas children become infected under
the age of 1 year
• mortality rises as high as 42% in children under
4 years of age.
• a candidate for eradication
• Measles vaccine has been combined with those against mumps
and rubella to form MMR.
• the vaccine has to be given under 6 months to have any effect.
• A second dose at 12-13 months is necessary.
RESPIRATORY SYNCYTIAL VIRUS
Description
• RS virus is a single stranded negative sense virus
• molecular weight of about 5x106
• superficially resembles other paramyxoviruses,
• with a similar pleomorphic envelope.
• lacks haemoagglutinin, a
haemolysin,or a neurominidase.
• It has G glycoprotein which is a receptor
for cell attachment.
• There are fusion (F) ,
• Matrix (M),polymerase and nucleocapsid
proteins
• Clinical Features and Pathogenesis
• The most serious illness caused by RS virus is bronchiolitis in
young babies.
• In older children and adults, the virus causes minor infections.
Laboratory DX
• Immunoflurescence, enzyme immunoassay, or culture can
demonstrate in nasopharyngeal secretion.
• Control
• No satisfactory vaccine.
• Treatment
• The babies who are at high risk of congenital
heart or lung abnormalities are given tribavirin,
• others are managed by appropriate oxygen use,
physiotherapy,
• and tube feeding if the baby has difficulty in
suckling.
CORONAVIRUSES
Morphology and structure
• Pleomorphic, enveloped ,
• 75-160 nm in diameter,
• with surface projection or peplomers,
• single stranded positive sense viruses.
• Posses transmembrane protein(M) ,and nucleoprotein (N).
Human coronaviruses (HCV) is the only human species,
• human enteric coronavirus(HECV) is the second species.
Cultivation
• The traditional methods of cultivating HCV has been in fetal tracheal
organ culture.
• human diploid cells may be used for the isolation.
Replication
• Replicate in the cytoplasm within growth cycle of 10-12h.
• they do not bud from the plasma membrane but from the
endoplasmic reticulum into intracytoplasmic vesicle
• and leave the cell by fusion of these with the plasma
membrane.
• Viral infection may result in cell lysis
• Clinical features and pathogenesis
• it is estimated that up to 30% of common
cold are caused by coronaviruses.
• incubation period is from 2-4days.
• Reinfection commonly occurs
• LabDX
• No need for lab since infections are mild
• for research purpose .organ cuture,
• serology such as complement fixation and
neutralization,ELISA can be used
Epidemiology
• occur wherever in the world they have
been sought.
• Transmission is airborne route.
GASTROINTESTINAL DISEASES CAUSED BY
VIRUSES
ROTA VIRUS
Description
• Is a member of Reoviruses.
• Reoviruses are a diverse family of viruses infecting man and
other vertebrates, plants and insects.
• double stranded RNA that are divided into
11segments.
• double layered capsid, no envelope
• measures 60-80nm in diameter
ROTA VIRUS
• Replication
• Attachment is via a specific component of the capsid V4.
• Interaction leads to change in the capsid,
• is taken into the cell by endocytosis.
• The viral RNA does not leave the inner capsid but is
transcribed by a virion –associated RNA polymerase to
produce mRNA from each RNA segment.
• The mRNA are translated to produce the various viral proteins
but also acted as template for RNA replication.
• Replication takes place in the cytoplasm.
• Mature virions are associated with endoplasmic reticulum.
ROTA VIRUS
• Pathogenesis
• Rotaviruses replicate in the epithelial cells at the tip of
the villi of the small intestine.
• Virus replication takes place in the cell cytoplasm and
new virus is produced after 10-12 h.
• as a consequence of virus replication the cells are killed,
• The cellular damage is followed by maldigestion,and
malabsorption of nutrients,electrolytes
• The infection is followed by local humoral,and cell-
mediated immune response and is normally overcome
within a week.
ROTA VIRUS
• Clinical features
• The onset of symptoms is abrupt after a short incubation
period of 1-2 d.
• Diarrhoea and vomiting occur in the majority of infected
children and last for 2-6 d.
• The disease is especially grave and protracted in
immunodeficient children.
• If children are already malnourished rotavirus infection can
be life –threatening.
ROTA VIRUS
• Lab.DX
• Serological tests :agglutinationtests,ELISA, are most commonly used.
• Electron microscopy easily detect the characteristic virus particles.
• Epidemiology
• Rotavirus infections occur worldwide.
• Most infections occur in children under 2 years of age.
• Long lasting outbreaks may be maintained by the ability of the
virus to survive outside the body for some time.
ROTA VIRUS
Control
• Control is the same as for any infectious agent transmitted by
the faecal-oral route.
• Simple measures such as hand washing and disinfection of
contaminated surfaces are of paramount importance.
Treatment
• Consists of mainly oral,sometimes intravenous rehydration
with fluid of the appropriate electrolyte and glucose.
CALICIVIRUSES ‘SMALL ROUND STRUCTURED’
VIRUSES, ASTROVIRUSES AND PARVO-LIKE VIRUSES
• Human caliciviruses(HCVs),
• ‘small round structured’ viruses(SRSVs),
• astroviruses and parvo-like viruses
cause diarrhoeal disease in man and animals.
HCV SRSV Astrovirus Parvo-
like
virus
Nucleic acid ssRNA ssRNA ssRNA ssRNA
protein VP1 VP1 VP1,VP2,VP
3,Vp4
Molecular wt 65000 60000- 36000,34000,
70000 33000,32000
Diameter 28-35 30-38 28-30 20-30
(nm)
replication cytoplasm cytoplasm
Pathogenesis and Clinical features
• The incubation period for HCVs and SRSVs is
between 12 and 72h,
• and slightly longer, 3-4d, for astrovirus.
• 1 and 4d with excretion of detectable number of
particles for the same period.
• Replication occurs in the jejunum.
• The symptoms are similar for the three groups of
viruses
• Diarrhoea, headache, fever, aching limbs and malaise.
• LabDX
• Electron microscopy is the available diagnostic tool.
• Epidemiology
• HCV,SRSV,asteroviruses and parvo-like viruses have
worldwide distribution,
• outbreaks of HCV and astrovirus infection most
commonly involve infants, school children and the
elderly.
• Contaminated food or water is the source of infection.
• It is therefore important to recognize that a minor
contamination of hands,work surfaces taps, carpets, etc.,
can be a major source of infection.
HERPESVIRUSES
DESCRIPTION
• The genome is linear double stranded DNA
• Herpesviruses are negative staining icosahedral
• diameter of 100 nm,162
• consisting of hollow hexagonal and pentagonal
capsomers, enveloped,
• glycoprotein spikes projeting from the envelope.
• varying in length from 125 -240 kilobase pair (kbps).
HERPESVIRUSES
• The herpesviruses is a large family infecting many animal

species sharing a number of features:
• including their structures
• mode of replication
• capacity to establish life long latent infections
• Herpes simplex virus-1 (HSV-1)

• Varicella-zoster virus (VZV)
• Epstein-Barr virus (EBV)
• Cytomegalovirus (CMV)
• Human herpesvirus 6 (HHV6)
Human herpesviruses-
There are six human herpesviruses:
• Varicella-zoster vrus (VZV)
• Epstein-Barr virus (EBV)
• Cytomegalovirus (CMV)
• Human herpesvirus 6 (HHV6)
Replication
• After attachment to receptor,
• the envelope fuses with the cell membrane.
• The necleocapsids cross the cytoplasm to the
nuclear membrane.
• The replication of viral DNA and assembly of
capsids takes place within the nucleus.
• Viral glycoproteins are processed in the Golgi
complex and are incorporated into cell
membranes from which the viral envelope is
acquired.
1. HERPES SIMPLEX VIRUS (HSV)
• Is ubiquitous, infecting the majority of

the world’s population early in life and
persisting in latent form.
• The description already given above holds
true to HSV
• in contrast to other members of the group
HSV can be grown in cells from wide
variety of animals.
• The two types of HSV (HSV-1 and HSV-2) are generally
associated with different sites of infection in patients.
• Type 1 strains are associated primarily with the mouth, the eye
and the central nervous system
• while type2 strains are found most often the genital tract and
nearby sites of infection.
Pathogenesis
• Primary infection- The typical lesion produced by HSV
is the Vesicle,
• a ballooning degeneration of intra-epithelial epithelial
cells.
• The underlying layer of basal epithelium is usually
intact,vesicles only occasionally penetrate the sub-
epithelial layer.
• During the replication phase at the site of entry in the
epithelium,virus paricles enter through the sensory nerve
endings which penetrate to the parabasal layer of the
epithelium and are transported along the axon to the
nerve body in the sensory (dorsal root) ganglion by
retrograde axonal flow.
• Latent infection- latent infection of
sensory neurones is a feature of the
neurotropic herpesviruses (HSV) and VZV.
• In latency the viral DNA exists as free
circular episomes-perhaps about 20
copies per infected cell.
• Very few virus genes are expressed in
latent state.
•
• HSV-1 is regularly detected in the
trigeminal ganglion,
• it has also been found in other sensory
and autonomic gangelio (e.g.vagus).
• HSV-2 latency has been demonstrated in
the sacral ganglia.
• Reactivation and recrudescence
• Herpes DNA some way passes along the nerve
axon
• back to the nerve ending where infection of
epithelial cells may occur.
• Not all reactivation results in a visible lesion,
• there may be asymptomatic shedding of viruses
only detectable by culture.
• Depression of cell-mediated immunity
predisposes to herpes recurrence.
• Clinical features
• Classically the first infection presents as an
acute, febrile gingivostomatitis in preschool
children.
• Vesicular lesion which rapidly ulcerate can be
seen in the front of the mouth and the tongue.
The child is miserable for 7-10 days in untreated
case before the lesions heal. However, the
majority of primary infections go unrecognized.
Genital infection can be caused by both type 1
and 2 strains.
• Genital infection most often results from
intimate sexual contact.
• The lesions are vesicular at first but rapidly
ulcerate.
• Fever and malaise are accompanied by
regional lymphadenopathy, urethritis and
vaginal discharge.
• Laboratory
• Virus isolation of HSV from an infected patient is done in
culture of human diploid fibrbroblast cells.
• Growth is rapid and within 24h a cytopathic effect(CPE)
may be visible.
• Herpes virion may be demonstrated by electron
microscopy in vesicle fluid or tissue preparations.
• Complement fixation
• ELISA is much more sensitive and specific than
complement fixation tests
• Treatment
• Vidarabine and acyclovir have been proven effective
when used early enough in appropriate dosage
• Latency is not eradicated by these agents
• Acyclovir is the most widely used antiherpes treatment.
• Epidemiology
• HSV is probably transferred by direct contact.
• Many children especially in crowded conditions acquire
oral HSV-1 infections in the first year of life.
• Control
• Transmission of herpes siplex can be
reduced by allevating overcrowding,
practicing simple hygiene and education
regarding the infectious stages.Sexual
transmission may be significantly reduced
by the use of condoms.
• Control
• Transmission of herpes siplex can be
reduced by allevating overcrowding
• practicing simple hygiene and education
regarding the infectious stages.
• Sexual transmission may be significantly
reduced by the use of condoms.
2. VARICELLA-ZOSTER VIRUS (VZV)
Virus replication is identical to that of the herpes virus.

Infection with VZV presents in two forms.
• Varicella (chickenpox) is a generalized eruption .
• Zoster (shingles) – This is the manifestation of reactivated VZV infection
Pathogenesis
• Varicella-This is a disease predominantly of children,
characterized by a vascular skin eruption.
• Virus is thought to enter through the upper respiratory tract or
conjunctivae and multiply in local lymph tissue before
entering the blood and being distributed through out the body.
• The clearance of virus infected cell is dependent on functional
cell-mediated immune mechanisms.
• A person deficient in cellular immunity will have difficulty in
controlling infection.
Zoster-The pathogenesis is not so well established as that of HSV recurrence.
• The latent virus is found in neurones and satellite cells in sensory ganglia.
• The virus seems to reach the ganglion from periphery by
travelling up nerve axons, as HSV does,
• but there is also the possibility of some viruses enter ganglion
cells during viraemia.
• There is usually a latent period of several decades;
• a much shorter latent period is seen in immunocompromised
patients.
• More than one episode of zoster is uncommon in any
individual
Laboratory diagnosis
• Typical presentations of varicella or zoster seldom need
laboratory confirmation,
• however atypical presentations needs investigations.
• Direct examination of vesicle fluid by electron microscopy
• virus isolation in tissue culture,
• monoclonal antibody tests, complement fixation, are among
useful tests.
• Treatment
• Both acyclovir and vidarabine given intravenously
are effective in the treatment of varicella and zoster in
immunocompromised patients
• Treatment is given to
all high risk of complication group:
• Neonates(within3 weeks of life),
• Immunocompromised patients,
• Those with ophthalmic zoster,
• Healthy patients with variecella where there is
complicating factors such as smoking or pneumonia
Epidemiology
• The majority of children contact varicella between
the age of 4-10 years
• around 8%of young adults remain susceptible.
• Zoster is associated with decreased T cell function,
• and occurs increasingly in old age,
• the pre AIDS HIV infection, and after organ
transplantation and chemo-or radiotherapy for
lymphomas or leukaemia.
Control
• Passive immunization is partly protective when given within
72h of exposure.
• Live attenuated varicella vaccine has been in use in some
countries
• Immunization does not necessarily prevent latency developing
after exposure to another VZV strain.
EPSTEIN-BARR VIRUS (EBV)
Properties of the virus

• The characteristic morphology seen on microscopy placed
EBV with herpesvirus. EB virus is distinct from all other
human herpes viruses :
• cannot grow in human fibroblast or epithelial cell lines
• Its DNA genome contains about 172 kbp
• and has a guanine –plus cytosine content of 59%.
• target cell for EB virus is the B lymphocyte.
Infectious mononucleosis
• EB virus is transmitted by infected saliva .
• Infection starts in the oropharynx, then the virus infects B
lymphocytes which are transformed and proliferate.
• EB virus remains latent in lymphocytes
• These cells are rejected by activated T lymphocytes (Tc).
• This leads to appearance of atypical T lymphocytes in the
peripheral blood.
• The disease manifests by fever sore throat, enlarged lymph
nodes and spleen, rash may appear.
• It is self limited disease.
Diagnosis
• Serologogy:
• Paul- Bunnel test: detection of heterophile antibodies that
agglutinate sheep RBC’s. It is useful as an early diagnostic
test.
• Demonstration of EB virus-specific IgM by ELISA or by
immunofluorescence test with viral capsid antigen.
• Detection of EB virus in patient’s peripheral lymphocytes by
DNA hybridization is the most sensitive method.
• Haematology:
• Blood picture shows increased lymphocytic count
(25.00/cmm) with absolute lymphocytosis
• and the demonstration of atypical lymphocytes and
mononuclear cells
CYTOMEGALO VIRUS (CMV)
• Properties of the virus

• CMV is the largest member of the human
herpes viruses.
• It has DNA genomes (240kbp)
• It has a cell surface glycoprotein that acts
as an FC receptor that can specifically
bind the Fc portion of immunoglobulins.
• CMV is very species –specific and cell type
specific.
• Human virus is often isolated from epithelial
cells of the host.
• CMV produces a characteristic cythopathic
effect,
• Infection is normally, but not always,
symptomless.
• cytomegalovirus can infect the fetus during
maternal infection in pregnancy.
• Many affected cells become greatly enlarged .
• The virus is excreted in the urine ,saliva, semen, breast
milk and cervical secretions.
• Clinical findings
• There are two types of diseases due to CMV:
• Congenital :
• 1. Maternal infection is almost always symptomless.
• 2. The foetus can be damaged by infection in any of the
three trimesters of pregnancy.
• 3. Foetal infection can follow reactivation as well as
primary maternal infection.
•
some show neurological sequelae later in life, principally,
1. Deafness
2. Mental retardation
II. Postnatal
• Hepatitis – In young children ,CMV can rarely cause hepatitis
with enlargement of the liver and disturbances of liver
function. Jaundice may or may not be present.
• Infectious mononucleosis: In adults and in older children
,infection can give rise to infectious mononucleosis
• There is fever ,hepatitis, and lymphocytosis with atypical
lymphocytes in the peripheral blood
Infection in the immunocompromised:
• Disseminated infection is sometimes seen in immunodeficient
(AIDS)
• and organ transplant patients with massive lesions in lungs as
well other organs and tissues.
• In these patients infection may be due to reactivation of their
own latent virus.
Diagnosis
• Isolation of virus : Specimens from urine and throat swab are
inoculated on human embryo lung cell cultures.
• Characteristic CPE of foci of swollen cells take place 2 to 3
weeks to appear.
• The direct early antigen fluorescent foci test (DEAFF) is a
rapid method of detecting early virus growth in cell culture
• Serology: Immunofluorescence;
• ELISA test for IgM;
• Complement fixation test.
• Demonstration of typical intranuclear owels eye shape inclusions in
cells of urinary sediment or other tissues.
• Treatment
• -Gaciclovir which inhibit viral DNA synthesis gave a
promising results.
• -Foscarnet has been useful treatment of CMV retinitis in
AIDS patients.
• -CMV immune globulins decrease CMV infection in
transplant patients
• Vacines are under trial.
• Serology: Immunofluorescence;
• ELISA test for IgM;
• Complement fixation test.
• Demonstration of typical intranuclear owels eye shape inclusions in
cells of urinary sediment or other tissues.
• Treatment
• -Gaciclovir which inhibit viral DNA synthesis gave a
promising results.
• -Foscarnet has been useful treatment of CMV retinitis in
AIDS patients.
• -CMV immune globulins decrease CMV infection in
transplant patients
• Vacines are under trial.
INFECTION CAUSED BY SEXUALLY
TRANSMITTED VIRUSES
The most common sexually transmitted viruses are:
• Hepatitis
• Genital herpes
• Human papilloma virus
• Human immuno deficiency Virus
HEPATITIS VIRUSES
• Hepatitis A Virus (HAV) is an enterovirus type 72.

• It is now placed in a new genus in the picorna virus
family called Heparna virus.
• It is an + ss RNA
• Icosahedral virus,
• 27-30 nm in diameter,
• Naked capsid virus.
• Only one serotype is known i.e. has a single
immunological type.
• The virus is relatively heat resistant
• it withstands 60 0C for 1 hour.
• It is destroyed by boiling for five minutes.
• It is pathogenic to primates e.g.
man,chimpanzees.
• It has been recently cultivated on primary cell
lines of primate liver.
• Pathogenesis of HAV infection
• HAV undergoes primary replication in the
gastrointestinal tract ,leading to viremia that spread to
the liver,kidney and spleen.
• virus is shed in faeces and is present in the blood
through out the preecteric period.
• It may occur in sporadic or epidemic forms in
summer camps or schools. Life long immunity
follows infection.
• Increased level of liver enzymes
• Detection of the virus in stools by immunoelectron
microscopy early in the disease.
• Detection of anti HAV of the IgM type by RIA or ELISA is
diagnostic of recent infection.
Prophylaxis :
• Vaccine preparations are under trial
• Gamma globulin if givn early after exposure renders the
infection milder or subclinical.
HEPATITIS B VIRUS (HBV)
Morphologically three forms are known:

• a/ spherical particles: 22 nm in diameter
are the most common particles seen in
infected serum.
• b/ Filamentous forms 22 nm in diameter
and 50- 230 nm length
• c/ The Dane particles: The least common
of the three is the only one with complete
viral morphology.
• All the three structures contain HBV surface antigen (HBsAg)
• It is a complex, double layered, spherical particle, 42 nm in
diameter,22 nm core.
• It contains a partially ds circular DNA about 3600 nucleotides
in length
• The DNA is associated with a DNA polymerase
• Endogenous DNA polymerase is capable of filling the open
regions of each DNA strand.
• Replication in the hepatocytes has been observed after 2w of
infection.
• The virus is found in the blood urine, semen, feces and
nasopharyngeal secretions during the 2nd half of incubation
period (2-6m).
Replication
• Synthesis of DNA and assembly of virus core appears to occur
in the nucleus of infected cells.
• HBsAg is abundant in the cytoplasm of infected cells
Epidemiology:
• After exposure is a long incubation period 2-6 m.
• The virus is present in the blood and other body fluids e.g.
semen ,saliva, vaginal secretions and milk.
• The incidence of serum hepatitis increases with age.
Mode of transmission:
• Parenteral by blood and plasma transfusion or
by the prick of contaminated needles.
• Risk groups are medical personnel,drug
abusers,renal dialysispatients, and those
receiving transfusion repeatedly e.g.
haemophiliacs.
• Sexual contact as virus is found in semen and
vaginal secretion.
• Perinatal transmission to the new born from
mothers with hepatitis B
Outcome of infection
• Infection is more severe than in hepatitis A and may be
complicated by:
• Persistant HBV antigenaemia HBsAg carriers and 3-5%
of aduts and 10-15 % of children
• Fulminating hepatitis
• Chronic active hepatitis
• Cirrohosis
• Hepatocellular carcinoma
• There is a strong correlation between hepatocarcinoma
and prior infection with either HBV or HCV.
• Increased levels of liver enzymes
• Detection of hepatitis markers i.e. antigens and
antibodies in blood.
• Antigens:
• Hepatitis B surface antigen (HBs Ag) is detected during
the incubation period and during active disease. It may
remain for months or years in carriers.
• Hepatitis B core antigen (HBcAg) is not detectable in
serum but can be found in the nuclei of liver cells.
Prophylaxis
• Preexposure prophylaxis by active vaccination
• Plasma derived vaccine ( Hepatvax B) .
• This is prepared by purifying HBsAG from pooled
plasmas
• Recombinant hepatitis B vaccine is a more recent
vaccine .
• It is prepared by cloning HBsAg gene in yeast cells
where it is expressed .
• HBsAg produced is used for vaccination .
• The vaccine is given in 3 injections
• Vaccine is given to those at high risk
Post exposure prophylaxis:
• Persons exposed by prick of contaminated needle or infants to
HBsAg positive mothers should immediately receive both
hepatitis B specific immunoglobulin (HBIG) And hepatitis B
vaccine (active immunization) given simultaneously at
different sites.
Other control measures include
• Careful screening of blood and blood products is essential for
HBV control i.e.free of (HBsAg).
• Use of plastic disposable syringes and
• careful handling of all medical supplies that have had contact
with blood.
Hepatits C VIRUS ( HCB)
• This was previously known as non –A non B agent .

HCV is a 30-60 nm .
• Single stranded RNA virus.
• Classified as a togavirus.
• Mode of transmission is similar to HBV i.e. by
intravenous
• administration of infected blood or serum.
• It accounts for 90 % of transfusion associated
hepatitis.
• About 50% of HCV infections develop chronic
liver disease that passes to cirrhosis or
hepatocellular carcinoma.
• It is diagnosed by detection of antiHCV
antibodies in the body by ELISA which give
False positive results.
• A second generation test ‘’Recombinant base
immunosorbant assay, RIBA’’ is more specific
and is used for confirmation.
• Hpatitiis D Virus (HDV)
• It s an RNA virus 35nm in diameter in
blood
• Hepatitis –D virus is a defective virus that
replicate only in HBV-infected cells
• it acquires an HBs Ag coat.
• HBV provides a rescue function for HDB.
• It is mode of transmission is similar to HBV.
• The incubation period is 2-12 weeks.
• Delta hepatitis affects hepatitis B carrier receiving
repeated blood transfusions or pooled blood as well
as drug addicts.
• It participates in increasing the incidence of
complications leading to chronic active or
fulminating hepatitis.
• Infection with HDV is diagnosed by detection of
anti–HDV of the IgM type.
• Hepatitis E Virus (HEV)
• Another virus originally classified as non A
non B agent and is now known as HEV. It
is 32 nm RNA virus still being studied. It
infects by the feco-oral route. Epidemic
forms are reported. It causes high
mortality rate.
HUMAN IMMUNODEFICIENCY VIRUS
(HIV)
• Previously known as lymhadenopathy–associated
virus (LAV)
• Human T-cell leuemia virus (HTLV-III)
• Or AIDs-related retrovirus(ARV).
• HIV is a non oncogenic retrovirus and a member of
lentiviridae family.
• HIV is the aetiologic agent AIDS
• and AIDS related complex, first described in 1981.
• The disease is thought to have originated in central
Africa where monkeys may originally have harboured
the virus.
• single stranded RNA virus
• Contains reverse transcriptase enzyme (present in all
retroviruses
• The virion is a 100- 140 nm spherical particle with
with a cylindrical core
There is an outer glycoprotein envelope which undergoes
antigenic variation.
• The genes that code for the viral proteins are:-
• 1.gag- viral core proteins are P15,P17,P24,P55
• 2. env- envelope proteins are P41,P120,P160
• 3. pol- reverse transcriptase P53,P66
Two types of viruses are known : HIV-1 and HIV-2
They differ in the envelope .
• HIV-2 is prevalent in west Africa and much less
virulent.
Replication: HIV replicates in T-lymphocytes carrying
the CD4 antigen on their surface .
• Loss of immune function result from depletion of the
CD4 subset of T-cells .
• The CD4 molecule also is the receptor for virus
attachment.
• All CD4 cell types, including
• peripheral blood monocytes
• some tissues macrophages,
• skin langerhans cells and brain microglial cells,
are susceptible to HIV infection.
Disinfection and infection:
• HIV is inactivated by treatment with household
bleach, 50% ethanol ,
• 0.5% Lysol or 0.3% H2O2 ,extremes of pH .
• However the virus is protected in lyophilized blood
products and heating for 72 hrs at 68oC is needed for
complete inactivation.
• Pathogenesis
• HIV attack T4 helper cells.
• The CD4 molecules on these cells are the receptors for virus
glycoproteins (attachment site) .
• It is found that infected T4 cells express high level of HIV
envelope glycoprotein on their surface.
• This leads to fusion with neighbouring uninfected T4 cells.
• This is followed by lysis of large numbers of fused cells
• and rapid duplication of T4 helper cells leading to marked
suppression of the immune response.
Latency and Activation:
• The virus has the property of remaining latent in both
lymphocyte and monocytes .
• Hence clinical disease may appear 7 years after initial
infection.
• incubation period ranges from 5 -65 months
• when the latent virus is activated.
• Activation may be due to concomitant virus
infections by Epstein Barr virus , herpes simplex
virus ,hepatitis B virus or cytomegalo virus.
Mode of transmission:
• Sexual contact:
• Parental transfusion of infectious blood products or
by contaminated needles.
• Mother to foetus transplacental or during the perinatal
period.
• Clincal Manifestations :
• The incubation period varies from 6 months or
7 years . Infected neonates develop symptoms
by 2 years .
• AIDs related complex (ARC) may proceed
AIDs
• and is characterized by fatigue wasting ,fever ,
chronic diarrhoea,oral candidiasis and
lymphoadenopathy.
• In its blown picture AIDs manifests by :
• Infection with opportunistic organisms:
• protozoa- Pneumocystis carinii ,toxoplasma gondii .
• fungi- Candida albicans, Cryptococcus neoformans.
• Bacteria – M. avium, M.tuberculosis , Listeria
monocytogenes
• Laboratory Diagnosis:
• 1. Detection of HIV antibodies by ELISA –
• a positive test must be repeated and confirmed
by Western blot Western blot technique is more
specific test that detects antibodies against core
protein P24 or envelope glycoproteins gp41,
gp120, gp160.
• 2. Isolation of the virus from lymphocyte, bone
marrow or plasma on tissue culture.
• 3. Detection of HIV by PCR. One HIV
infected cell in a million can be detected.
Prevention and Control:
1. Vaccines against HIV :are under trial.
• Envelope glycoproteins, prepared by recombinant
technique, are used for vaccinations
• 2. Antiviral drugs
• azidothymidine (AZT) and dideoxyinosine(DDI).
• AZT inhibits the replication of HIV by inhibiting
viral reverse transcriptase and blocking proviral DNA
synthesis.
• DDI also inhibits HIV as AZT however, it is less
toxic.
3. control measures.
The most important are:
• Screening of donors for HIV antibodies
• Sex education
• Use of disposable syringes
• Care in handling blood or tissue specimens.

Microbial Structures and Functions Moicroorganisms

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What are the different types of microorganisms discussed in the passage?

What are the different types of microorganisms discussed in the passage?

What are the different shapes that bacteria can take?

What are the different shapes that bacteria can take?

1.

Microbial structures and Functions

Cell wall: The outer layer of cell envelope.

cell wall differs in gram positive and gram negative

Cell membrane/cytoplasmic membrane:

Cytoplasm: Is a colloidal system of organic and in organic

• Bacteria divide by binary fission.

• Lag phase-the initial period is the time required for

• Lag phase-the initial period is the time required for

• The principal constituent of bacterial cells is water,

classified nutrionally based on their energy requirements,

The influnce of free oxygen is related to the metabolic

• Fungi, algae and protozoa :

• Protozoa- Are unicellular eukaryotic microorganisms

• Genetics is the study of heredity.

• DNA is organized in all cells into structures referred

• microoganisms includes prokaryotes and (mainly

• bacteria multiply by binary fission ,so in

GENETIC RECOMBINATION & TRANSFER

• The phage synthesizes lysozyme, which breaks the cell wall

• Stage 2: The phage DNA now directs the bacterial cell to

• Parasitic organisms are those which live in /on a

Infection and Disease

Factors that govern disease production

• Virulence in the clinical sense is a

Toxin production – are bacterial products which have a direct

4. Extracellular enzymes: These are substances produced by

Host resistance factors (Immune system)

• 1/ innate immune system- acts as a first line

• 3. Normal bacterial flora present at the portal of entry.

• Naturally active immunity occurs following clinical

• 1. Bactercidal drugs are these which have a rapid

1. Active against gram positive organisms e.g.

1. Inhibition of cell wall synthesis –Some antibiotics

• e.g.ii/ Cephalosporins are produced by species of the

2. Inhibition of cytoplasmic membrane function

• e.g.ii/. Nystatin and amphotericin B which are

• E. g. i/ the aminoglycosides inhibit protein synthesis in

• iv. Erythromycin produced by Streptomyces

• 4. Inhibition of transcription and nucleic

• Chloroquine is an important antiprotozoan.

1.The organism produces enzymes that destroy the

3.The organism develops an altered receptor

• Non genetic drug resistance Metabolic inactivity –

1.Plasmid mediated resistance

2. Transposons (are DNA elements that jump from

3. chromosomal drug resistance. This develops as a

• 1. Development of drug resistance

Prolonged oral chemotherapy leading to suppression

• while waiting for the result of sensitivity

• N.gonorrheae is the cause of sexually

• Opthalmia neonatorum-Babies born to infected woman may

• Chlamydia trachomatis is the causative agent.

• Once chlamydiae cell have come into contact of the

• Trachoma has been known for thousands of years.