Infection Microbiology

Best notes for microbiology, Infection topic

1. Infection
CLASSIFICATION OF INFECTIONS
SOURCES OF INFECTION
METHODS OF TRANSMISSION OF INFECTION
FACTORS PREDISPOSING TO MICROBIAL
PATHOGENICITY
TYPES OF INFECTIOUS DISEASES
INTRODUCTION
lnfegion and immunit involve interaction between the
animal
bod (host) and the infecting
micr~r anism.
Based
on their relationship
totheir hosts: microorgan­
isms can be classified as saprophytes (from Greek
sapros decayed; and phyton plant) and
p31rasites.
Saprophytes are free-living microbes that subsist on
dead or decaying organic matter. They are found in soil
and water and play an important role in the degradation
of organic materials in nature. They are generally inca­
pable
of multiplying on living tissues and therefore are
of little relevance in infectious disease. Exceptionally,
however, some saprophytes like
B.subtilis may infect
devitalised hosts whose natural
-;sistance is greatly
reduced (opportunistic infection).
Parasites are microbes that can establish themselves and
multiply in hosts. arasitic microbes
ma be either
h­
ogens (from Greek pathos suffering, and gen produce,
t at
is, disease-producing) or commensals (from Latin
com with; and mensa table, that is
li~ng together).
Patho s are microorganisms that are capable of
producing disease in the host. Commensal microbes
live in complete harmony with the host without caus­
ing any damage to it.~ normal bacterial flora of the
body consist largely
of commensals. Many commensals
behave as facultative atho ens in that they can pro­
duce disease when the host resistance
is lo ered.
It
is necessary to distinguish between the terms
'infection' and 'infectious disease'.
The lodgement
and
multiplication of a parasite in or on the tissues of a
host constitutes
infection. It does not invariably result
in disease. In fact, disease
is but a rare consequence of
infection, which is a common natural event.
CLASSIFICATION OF INFECTIONS
Infections may be classified in
v~rious ways.
• Initial infection with a parasite in a host
is termed
primary infection.
• Subsequent infections by the same parasite in the
host are termed
re-infectio .
• When a new parasite sets up an infection in a
host whose resistance is lowered by a re-e · t­
ing infectious disease this
is termed secondar
infection.
• Focal infection
(more appropriately focal sepsis)
indicates a condition where,
dpe to infection or sep­
sis
at localised sites such as the a endix or tonsils,
generalised
e~s are roduced.
•
When in a patient already suffering from a disease a
new infection
is set up from another host or another
external
SQ!!!fe, it is termed l'ross-infection.
• Cross-infections occurring in hospitals are called
~ ctions (from Greek nosocomion or
hospital).
~he term iatrogenic infection refers to physician­
induced infections resulting from investigative,
therapeutic
or other procedures.
• Depending
on whether the source of infection
is within or outside the host's own body, infec­
tions are classified as
endogenous or exogenous,
respectively.
Based
on the clinical effects of infections, they may be
classified into different varieties.
• Inapparent infection is one where the clinical effects
are
not apparen t. The term subclinical infection is
often used as a synonym.
• Atypical infection is one in which the ty ical or
characteristic clinical manifestations
of the particu­
lar infectious disease are not present.

2. Part II IMMUNOLOGY
/Latent infection is one in which some parasites,
following infection, may remain in the tissues in a
latent or hidden form, proliferating and producing
clinical disease when the host resistance
is lowered.
SOURCES OF INFECTION
Humans: The commonest source of infection in
humans are humans themselves. The parasite may
originate from a patient or a carrier. A
carrier is a
person who harbours the pathogenic microorganism
without suffering any
ill effect because of it. Several
types of carriers have been identified. A
healthy c arrier
is one who harbours the pathogen but has never suf­
fered from the disease caused
by the pathogen, while
a
convalescent ca rrier is one who has recovered from
the disease and continues to harbour the pathogen
in his body. Depending on the duration
of carriage,
carriers are classified as temporary and chronic. The
tempora ry carrier state lasts less than six months,
while
chronic carrier stage may last for several years
and sometimes even for the rest of one's life. The term
contact carri er is applied to a person who acquires the
pathogen from a patient, while the term
paradoxical
carrier
refers to a carrier who acquires the pathogen
from another carrier.
Animals: Many pathogens are able to infect both
human beings and animals (
Fig. 8.1). Animals may,
therefore, act
as sources of human infection. In some
instances, the infection in animals may be asympto­
matic. Such animals serve to maintain the parasite
in
nature and act as the reservoir of human infections.
They are, therefore, called
reservo ir hosts. Infectious
diseases transmitted from animals to human beings are
called
zoonoses. Zoonotic diseases may be bacterial
(plague from rats), viral (rabies from dogs), protozoa!
(toxoplasmosis from cats), helminthic (hydatid disease
from dogs) or fungal (zoophilic dermatophytes from
cats and dogs).
Insects: Blood sucking insects may transmit pathogens
to human beings. The diseases so caused are called
arthropod-borne diseases. Insects such as mosquitoes,
ticks, mites,
flies, fleas and lice that transmit infections
are called
vectors. Transmission may be mechanical
(for example, transmission of dysentery or typhoid
bacilli
by the domestic fly). Such vectors are called
mechanical vector s. In other instances, the pathogen
multiplies in the body of the vector, often undergo­
ing part of its developmental cycle in it. Such vectors
are termed
biological vecto rs (for example, Aedes
aegypti mosquito in yellow fever, Anopheles mosquito
in malaria). Biological vectors transmit infection only
after the pathogen has multiplied in them sufficiently
or has undergone a developmental cycle. The interval
between the time
of entry of the pathogen into the
vector and the vector becoming infective is called the
extrinsic incubation period.
Besides acting as vectors, some insects may also act
as reservoir hosts (for example, ticks in relapsing fever
and spotted fever). Infection
is maintained in such
insects
by transovarial or transstadial passage.
Soil and wate r: Some pathogens can survive in the
soil for very long periods. Spores
of tetanus bacilli
may remain viable in the soil for several decades and
serve
as the source of infection. Fungi (Histoplasma
capsulat
um, Nocardia asteroides) and parasites such
DOMESTIC ANIMALS AND RODENTS
Cattle
tetanus*
anthrax
brucellosis
tuberculosis
Houseflies
typhoid fever
chole
ra
dysentery
Goat
brucellosis
Sheep
tetanus•
anthrax
I
INSECTS
Dogs
rabies
(Biological or mechanical vectors)
Body lice
typhus
relapsing fever
Mosquitoes
mala ria
dengue
yellow fever
Horse
tetanus*
glanders
Rat flea
plague
Rats
ratbite fever
Weil
's disease
Ticks
relapsing fever
Fig. 8.1 Possible sources of infection (*Tetanus bacilli occur in the feces of these animals)

3. as roundworm and hookworm survive in the soil and
cause human infection.
Water may act as the source of infection either due
to contamination with pathogenic microorganisms
(cholera vibrio, infective hepatitis virus) or due to the
presence of aquatic vectors (cyclops
in guineaworm
infection).
Food: Contaminated food may act as a source of
infection. The presence of pathogens in food may be
due to external contamination (food poisoning by sta­
phylococcus) or pre-existent infection in meat or other
animal products (salmonellosis).
METHODS OF TRANSMISSION
OF INFECTION
Contact: Infection may be acquired by contact, which
may be direct or indirect. Sexually transmitted diseases
such
as syphilis and gonorrhea illustrate spread by
direct contact. The term contagious disease had been
used for diseases transmitted
by direct contact, distinct
from
infectious disease, signifying all other modes
of transmission. This distinction is now not generally
employed. Indirect contact may be through the agency
of fomites, which are inanimate objects such as cloth­
ing, pencils or toys which may be contaminated
by
a pathogen from one person and act as a vehicle for
its transmission to another. Pencils shared
by school
children may act
as fomites in the transmission of
diphtheria, and face towels in trachoma.
Inhalation: Respiratory infections such as influenza
and tuberculosis are transmitted by inhalation of the
pathogen. Such microbes are shed
by the patients into
the environment, in secretions from the nose or throat
during sneezing, speaking or coughing. Large drops
of such secretions
fall to the ground and dry there.
Pathogens resistant to drying may remain viable in the
dust and act
as sources of infection. Small droplets,
under
0.1 mm in diameter, evaporate immediately to
become minute particles or
droplet nuclei (usually
1-10 µmin diameter) which remain suspended in the
air for long periods, acting as sources of infection.
Ingestion: Intestinal infections are generally acquired
by the ingestion
of food or drink contaminated by
pathogens. Infection transmitted by ingestion may be
waterborne (cholera), foodborne (food poisoning) or
hand borne (dysentery). The importance
of fingerborne
transmission
is being increasingly recognised, not only
Infection
in the case of pathogens entering through the mouth,
but also those that enter through the nose and eyes.
Inoculation: Pathogens, in some instances, may be
inoculated directly into the tissues
of the host. Tetanus
spores implanted
in deep wounds, rabies virus deposited
subcutaneously
by dog bite and arboviruses injected by
insect vectors are examples. Infection by inoculation
may be iatrogenic when unsterile syringes and surgical
equipment are employed. Hepatitis B and the human
immunodeficiency virus (HIV) may be transmitted
through transfusion of infected blood, or the use
of
contaminated syringes and needles, particularly among
addicts of injectable drugs.
Insects: Insects may act as mechanical or biological
· vectors of infectious diseases.
Congenital: Some pathogens are able to cross the pla­
cental barrier and infect the fetus in utero. This
is known
as
vertical transmission. This may result in abortion,
miscarriage or stillbirth.
Live infants may be born with
manifestations of a disease, as
in congenital syphilis.
Intrauterine infection with the rubella virus, especially
in the first trimester of pregnancy, may interfere with
organogenesis and lead to congenital malformations.
Such infections are known
as teratogenic infections.
Iatrogenic and laboratory infections:
Infection may
sometimes be transmitted during administration
of
injections, lumbar puncture and catheterisation, if
meticulous care in asepsis
is lacking. Modern methods
of treatment such
as exchange transfusion, dialysis
and organ transplant surgery have increased the possi­
bilities for iatrogenic infections. Laboratory personnel
handling infectious material are at risk and special care
should be taken to prevent laboratory infection.
The outcome of an infection
will depend on the
interaction between microbial factors which predispose
to pathogenicity and host factors which contribute to
resistance.
FACTORS PREDISPOSING TO MICROBIAL
PATHOGENICITY
The terms 'pathogenicity' and 'virulence' refer to the
ability of a microbe to rod
~ or tissue injury
but it
is
im2-ortant to make a distinction between..tfil._m.
Pathogenicity is generally employed to refer to the abil­
ity
of a microbial species to produce disease,
wlill.Llhe
term virulen5e is applied to the same property in~n
gf microorganism. Thus the species M.tuberculosis

4. Part II IMMUNOLOGY
or the polio virus is referred to as being pathogenic. in minute amounts and constitute som _Lof the most
The pathogenic species
M. tuberculos is and
thuolio poisonous substanc es lgiQ_wn. One mg of tetanus or
virus contain strains of varying degrees
of virulence botulinum toxin is sufficient to kill more than one
including those which are avirulent, such
as the vac-million guinea pig_s and it has been estimated that
cine strains. The virulence of a strain is not
co~nt 3 kg of bo_tuQr,µm,. toxin can kill all the inhabitants of
and may undergo spontaneous or induced variation. the ~d. ~nt of exotoxins with formaldehyde
Enhancement of virulence
is known
aijgi.Itation) and yields toxoids that are nontoxic but retain the ability
can be demonstrated
ex erimentally by serial
pa§age in to induce antibodies (antitoxins). They exhibits ecific
suscepg_ble Q.Q,St . eduction of viru ence is known as tissue affinities and pharmacological activities, each
attenuation and can be achieved by passage through '\...--toxin producing a typical effect which can_l>~ made
unfavourable ho~ts, rep~ated cultures in artificial me:dia, out b charac · ris ·c clinical rrianifestations ot_ auto sy
growth in high temperature or in the presence of weak appearan_£es. oxins are generally formed b Gram-
antisertics, desiccation or prolonged storage in culture. positive bacteria but may als~ rodu~y some
Virulence
is the sum total of several determinants, Gram-negative organisms such s 1 a's s
as detailed below. bacillus,_ vibrio cholera and epterotoxigenic
E.coli.
Adhesion: The initial event
in the pathogenesis of Endotoxinsareheatstablelipopolysaccharides,Q.,PS)
many infection~ is th~ attachment of the bacteria _!Q which form an inte ral art of the cell of &ram-
b9dy surfaces. This attachment is not a chfil!_ce ~t negative bacteria.\.Mir toxicity depends on the lipic;!.
but a specific_ re3:ction between ~urface receptors on component (lipid A). They are not secreted outside the
host ce)js and adhesive structures (ligands) on the sur-bacterial cell and are released only by the disintegration
fuce of bacteria. These adhesive structures are called of the cell wall. They cann-ffi be toxoided. They are poor
adhesiru. Adhesins may occur as o~ganised structures, antigens and their toxicity is not c_ompletely neutralised
such as fimbria.e or fibrilla.e and iii or as colonisa-b the homolo ous antibodies.\.'.fhey _are active only in
Jion factors. ~ seecific adhesin may. account for relatively large dose . do not exhibits ecific har-
the tissue tropisms and host specificity exhibited ~ macological activities. eqgotoxins, whether isolated
f!lany pathogens. Adhesins serve as virulence factors, from 2athogenic or nonpathogenic bacteria, produce
and loss
of adhesins often renders the strain avirulent. similar
effe~ts. Administration of small quantities of
~sins are usually made of protein and are antigenic endotoxin in susceptible animals ~auses an elevation
~re. Specific immunisation with adhesins has of body temperature manifested within 15 minutes and
been attempted as a method of
___2!:Qphylaxis in some lasting for several hours. The pyrogenic effect of fluids
infections, as for instance against
E.coli diarrhea in used for intravenous
administration is usually due to
c~nd piglets, and gonorrhea in human beings. the presence of endotoxins from contaminant bacteria.
f
Intravenous injections of large doses of endotoxin and
Invasiveness: This re ers to the ability of a pathogen 'I ___,
- massive ative se ticemias cause 'ellaotoxic
to spread in the host tissues after establishing infection. =.::-.~=._....~ ;:::..:-=-====.= ~
'-HNhl invasive athogens characteristically produce s?o~k mar~ed_ by r;ieucopen~a,
th
rombocytopenia,
spreading or generalised lesions (for example, ~-significa~t all
10
. s ure, e1rculatory collapse and
tococcal septicemia following wound infection), while ~ody diarrhea leading to death (Tables 8.1 and 8.2) •
\.--1-;;=ss invasive pathogens ✓.§;ause more localised lesions Plasmids: Genes coding for some virulence character-
(for example, staphylocd&al abscess). Some p_athogens; istics may be plasmid~amples of plasmidborne.
though capable of causing serious or even fatal d~s, virulence factors are ~urface antigens responsible fQ[_Qie
14.ck invasiveness altogether (for example, the t~s colonisation of intestinal mucosa by ~i and entero-
bacillus which remains confined to the site of entry and toxin production by
E.coli and S.aureus. Multiple drug
produces the disease
by elaborating a potent
toxijl). resistance (R) plasmids increase the severity of clinical
Toxigenicity: Bacteria produce two types of toxins-disease by their resistance to antibiotic therapy.
~ns and endotoxins. Bacteriophages: The classical example of phage-
E~otoxins are heat labile proteins which are secreted directed virulence is seen in~-In the diphthe-
by certain species of bacteria and 9iffuse readily into ria bacilli, the gene for toxin production is present in
the surrounding medium. They are highly potent beta or other tox+ corynephages.

5. Infection
Table
8.1 Distinguishing features of exotoxins and endotoxins
EHotoxlns Endotoxins
~teins
A eat la..b.i le
~tively secreted by cells; diffuse into surrounding
~m
~dily separable from cultures by ghysical m_g_ans
such a tration
'\..--1\Clion often enzymic
Specific pharmacological effect for each exotoxin
Specific tissue affinities
Active in
very minute doses
1ghly antigenic
Action s ecificall neutralised b antibod
Table 8.2 Biological activities
of endotoxins
Pyrogenicity Lethal action
Li
po polysaccharides
Heat
stable
Form art of cell wall; do not diffuse into surroundi ng medium
Obtaine~ only b cell ly,fil
No enzymic action
Effect nonspecific; action common to all endoto i s
No specific tissue affinity
tive onl
in ver lar e doses
Weakly antigenic
Neutralisation by antibody ineffective
Activation of complement
Leucocytosis
Macrophage inhibition
lntravascular coagulation
Inhibition of glucose and
glycogen synthesis
in the liver
Interferon release
Depression of blood pressure
Leucopenia
Stimulation of B lymphocytes
Induction of prostaglandin synthesis
Clotting of limulus lysate (lysate of amebocytes from horseshoe crab, Limulus polyphemus, used as a test for detection of endotoxins.)
Communicability: The ability of a parasite to spread
from one host to another
is
known· as communicabil­
ity. \.:ffiis property does not influence the production
of disease in an individual host but determines the
survival and distribution of a parasite in a community.
A correlation need not exist between virulence and
communicability. In fact, a highly virulent earasite mE
not exhibit a hi h de ree of communicabilit due to its
ra i
d! lethal effect on the
host.~eneral, infections
in which th e atho en is shed in sec~etions, a_s in respi­
ratory or intestinal diseases, ar~ hi hl communicable.
In some instances, as in h dro hobia, h.!!fil_an illfection
represents a c!ead--end, there being an interruption in
the spread
of the pathogen to other hosts.
Development
of epidemic and pandemic diseases
requires the pathogen strain to possess high degrees of
virulence and communicability.
Other bacterial products: Some bacterial products
other than toxins, though devoid
of intrinsic toxicity,
may contribute to virulence
by inhibiting the mecha­
nisms of
)il_ost resistance. Pat~nic staphylococci
produce
allt'hrombin-like enzyme coagulase
which,J2!-e­
vents p hagocY,t · b formin a fibrin barrier around
the bacteria and w.Jl]liog off the le§ion. 1 rinol sins
'
promote the s read of infections b breakin down
the
fibrin barrier in tissues. Hyaluronidases split
h
yaluronic acid which is a component of intercel-
lular connective tissue and
th~ilitate the spread
of i,,n,f ~~ce~cocidins damage
t fp6lyniH'rp'6ort\Tu'iear leucocytes. Many pathogens EE.9-
duce hemolysins capable of destroying erythrocytes
but their significa~ce in pathogenicity is not clearly
understood.
Bacterial appendages: Capsulated bacteria such as
pneumococci,
K.pneumoniae and H. infl.uenzae are not
readily phagocytosed. Some bacterial surface antigens
such as the
Vi antigen of S. Typhi and K antigens of
E.coli also help the bacteria to withstand phagocytosis
and the lytic activity of complements.
Biofilms: These are well-organised microcoloni es of
bacteria enclosed in self-produced extracellular poly­
mer matrices known as glycocalyx. They are separated
by water channels that remove water and deliver nutri­
ents. They may be classified as adherent, clinging and
submerged biofilms.
Biofilms are of two types: monomicrobial biofilms and
polymicrobial biofilms.
Pathogenesis: Free-floating bacteria come in contact
with medical devices and attach to them with pili.
They then aggregate, multiply and secrete exracellu­
lar polymers and are encased. Prevention
is by using
sonication, antibiotics, catheter lock solutions, catheter
flushing and removal of the catheter.

6. Part II IMMUNOLOGY
Infecting dos e: Success ful infections require that an
adequate number of bacteria should gain entry into the
host. The dosage may be estimated as the minimum
infecting dose (MID) or minimum lethal dose (MLD)
which are, respectively, the minimum number of bacte­
ria required to produce clinical evidence of infection or
death, respectively,
in a susceptible animal under stand­
ard conditions.
As animals exhibit considerable indi­
vidual variation in susceptibility, these doses are more
correctly estimated as statistical expressions, ID 50 and
LD 50,
as the dose required to infect or kill 50 per cent
of the animals tested under standard conditions.
Route of infection: Some bacteria, such as strep­
tococci, can initiate infection whatever be the mode
of entry. Others can survive and multiply only when
introduced by the optimal routes. Cholera vibrios are
infective orally but are unable to cause infection when
introduced subcutaneously. This difference
is probably
related to the modes by which different bacteria are
able to initiate tissue damage and establish themselves.
Bacteria also differ in their sites of election in the host
body after introduction into tissues. They also differ
in the ability to damage different organs in different
species of animals. Tubercle bacilli injected into rabbits
cause lesions mainly in the kidneys and infrequently
in
the liver and spleen, but in guinea pigs the lesions are
mainly in the liver and spleen, the kidneys being spared.
The reasons for such selective multiplication in tissues
are largely obscure, though they may be related to the
presence
in tissues of substances that may selectively
hinder or favour their multiplication.
TYPES OF INFECTIOUS DISEASES
Infectious diseases may be localised or generalised.
Localised infections may be superficial or deep-seated.
Generalised infection involves the spread
of the infecting
agent from the site of entry
by contiguity, through tis­
sue spaces or channels, along the lymphatics or through
the bloodstream. Circulation of bacteria in the blood
is
known as bacteremia. Transient bacteremia is a frequent
event even
in healthy individuals and may occur during
chewing, brushing of teeth or straining at stools. The
bacteria are immediately mopped up by phagocytic cells
and are unable to initiate infection. Bacteremia
of greater
severity and longer duration
is seen during generalised
infections as in typhoid fever.
Septicemia is the condition
where bacteria circulate and multiply in the blood, form
toxic products and cause high, swinging type of fever.
Pyemia is a condition where pyogenic bacteria produce
septicemia with multiple abscesses in the internal organs
such
as the spleen, liver and kidneys.
Depending
on their spread in the community, infec­
tious diseases may be classified into different types.
• An endemic disease is one which is constantly
present in a particular area. Typhoid fever is endemic
in most parts
of India.
• An epidemic disease is one that spreads rapidly,
involving many persons in an area at the same time.
Influenza causes annual winter epidemics
in ,cold
countries.
• A
pandemic is an epidemic that spreads through
many areas of the world involving very large numbers
of people within a short period. Influenza, cholera,
plague and enteroviral conjunctivitis are pandemic
diseases.
• Epidemics vary in the rapidity of spread. Waterborne
diseases such as cholera and hepatitis may cause
explosive outbreaks, while diseases which spread
by
person-to-person contact evolve more slowly. Such
creeping or smouldering epidemics, as that
of cer­
ebrospinal fever, are termed
prosodemic diseases.
RECAP
• Infection and immunity involve interaction between the animal body (host) and the infecting microor­
ganism. Parasites
are microbes that can establish themselves and multiply in hosts. Pathogens produce
disease in the host, commensals do not cause damage to the host, many commensals are facultative
pathogens they can produce disease when host resistance is lowered.

7. Infection
• Infections may be classified as primary infection, re-infection,
secondary infection, focal infection, cross­
infection,
endogenous infection and inapparent infection.
• Sources of infection:
❖ Humans constitute the commonest source of infection. The parasite may originate from a patient
or a carrier. A carrier may be a healthy carrier, convalescent carrier a contact carrier or a paradoxical
carrier. The carrier
state may be temporary or chronic. ❖ Animals may serve as sources of human infection since the pathogen may be capable of infecting
both humans and animals. Infectious
diseases transmitted from animals to humans are zoonoses, -:-Blood sucking insects (mosquitoes, ticks, mites, flies, fleas, lice) that transmit pathogens to humans
(arthropod-borne diseases) are called vectors.
-:-Some pathogens can survive in the soil for very long periods,
-:-The presence of pathogens in food may be due to external contamination or due to pre-existing
infection in
meat and other animal products (salmonellosis).
• Infection may be
transmitted by direct contact or through fomites, inhalation of droplets, ingestion of
food or drink
contaminated by pathogens, or directly inoculated into the tissues of the host.
• Pathogenicity is the ability of a microbial species to cause disease, while virulence is the same property
in a microbial strain. Virulence is
the sum total of several determinants, including: ❖ The ability of the organism to adhere to surface receptors, spread in the host tissues and produce
toxins,
presence of plasmid-borne or bacteriophage-borne genes, and ability of the organism to
spread from one host to another. ❖ Microbial products other than toxins, that contribute to virulence include coogulase, fibrinolysins,
hyaluronidase and leucocidins.
❖ Microbial appendages such as capsules and certain surface antigens help the bacteria resist phago­
cytosis and
the lytic activity of complement.
• Infectious
diseases may be localised or generalised.
-:-Bacteremia refers to circulation of bacteria in the blood
❖ Septicemia refers to the circulation and multiplication of bacteria in the blood with formation of toxic
products and production of high fever
❖ Pyemia refers to the septicemia produced by pyogenic bacteria, which is accompanied by formation of
multiple abscesses in internal organs
• Infectious diseases may be classified into different types
depending on their spread in the community as: -:-Endemic, epidemic, pandemic and prosodemic diseases
• Biofilms are well-organised microcolonies of bacteria enclosed in self-produced extracellular polymer
matrices known as glycocalyx.
1. Methods.of transmission of infecti on
2. Factors contributing to microbial pathogenicity
3. Differences between exotoxins
and endotoxins
1 . Bacterial virulence
2. Carrier
SHORT ANSWERS
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