infectious diseasesaetiology pathogenesis &consequences by dr.t.v.rao md

8/20/2019 INFECTIOUS DISEASES AETIOLOGY PATHOGENESIS & CONSEQUENCES by Dr.T.V.Rao MD

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INFECTIOUS DISEASESAETIOLOGY PATHOGENESIS &

CONSEQUENCES

Dr.T.V.Rao MD


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in·fe·!ion"i!ionar# $ean%

• a. Invasion by and multiplication ofpathogenic microorganisms in abodily part or tissue, which may

produce subsequent tissue injury andprogress to overt disease through avariety of cellular or toxic

mechanisms.• b. The pathological state resulting

from having been infected.

Dr.T.V.ao !D "


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Deni!ion%

• Di%ea%e an" Infe!io'% Di%ea%e –Di%ea%e

•#ny deviation from a condition of

good health and well$being –Infe!io'% Di%ea%e

•# disease condition caused by the

presence or growth of infectiousmicroorganisms or parasites

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Deni!ion%• Pa!(o)enii!# an" Vir'*ene

– Pa!(o)enii!#

• The ability of a microbe to cause disease

• This term is often used to describe orcompare species

– Vir'*ene

• The degree of pathogenicity in a

microorganism• This term is often used to describe orcompare strains within a species

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Prini+*e% of Infe!ion

• Un"er%!an"in) !(e ,a%i+rini+*e% of infe!ion i%

e%%en!ia* for an# (ea*!(are -orer in an# e*"of (ea*!( are.

/.Di%ea%e !ran%$i%%ion

0.Pre1en!ion of "i%ea%e

!ran%$i%%ion


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Na!'re of Miroor)ani%$%

• Miroor)ani%$% 2$iro,e%3are %$a**4 *i1in) or)ani%$%

!(a! are no! 1i%i,*e !o !(enae" e#e.

• Pa!(o)en% 2)er$%3 are$iroor)ani%$% !(a! a'%e"i%ea%e.

•Non5+a!(o)en% are


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in1a%ion of a (o%!or)ani%$7% ,o"i*#!i%%'e% ,#"i%ea%e5a'%in)

or)ani%$%4 !(eir$'*!i+*ia!ion4an" !(e rea!ionof (o%! !i%%'e% !o

!(e%e or)ani%$%an" !(e !o8in%!(e# +ro"'e.Infe!ion% are

a'%e" ,#$iroor)ani%$%%'( a% 1ir'%e%4+rion%4 ,a!eria4an" Viroi"%4 an"

*ar)er or)ani%$%

Infe!ion $ean%

Dr.T.V.ao !D 7


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9(a! i% an Infe!ion:

# harmful invasion and spread of foreignspecies, or pathogen, in a host. – VI%&

• S$a** +o84 $ea%*e%4 in;'en


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COURSE OF INFECTIOUSDISEASE%• -xposure0Invasion

of 1ost

• Incubation $$ period

of time betweenexposure and onsetof symptoms $$e.g., interval

between 1IVinfection anddevelopment of#ID& can be as

long as 23$24Dr.T.V.ao !D 5


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Na!'re of Miroor)ani%$%

• &aprophy

tes

• 'arasites

• 'athogen

s


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Ca'%a!i1e A)en!% e=e!in)('$an%

>a!eria

Vir'%e%F'n)i

Pro!o<

oaHe*$in

!(%

Prion%Dr.T.V.ao !D 11


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• Streptococci (chains)• Staphylococci (clusters)

• Diplococci (pairs)

• Micrococci (tiny)• Flagellated forms (tails)

• Bacilli (rod-shaped)

• Vibrios• Spirilla (spiral)

• Spirochetes (comma)

Types of Bacteria


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• F'n)i – A +*an!*ie or)ani%$ !(a!

*i1e% on "ea" or)ani

$a!!er. – Yea%!% an" $o*"% an ,e+a!(o)eni.

– Ca'%e on"i!ion% %'( a%

rin)-or$4 a!(*e!e?% foo!4#ea%! infe!ion%4 an"!(r'%(.

– An!i,io!i% "o no! i**

f'n)i. An!if'n)a*$e"ia!ion% are a1ai*a,*e4

T#+e% of Miroor)ani%$%


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T#+e% of Miroor)ani%$%

• Pro!o


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• Vir'%e% – S$a**e%! of a** $iroor)ani%$% @ 1i%i,*e

on*# '%in) an e*e!ron $iro%o+e.

– Canno! re+ro"'e 'n*e%% !(e# arein%i"e ano!(er *i1in) e**.

– S+rea" ,# on!a! -i!( ,*oo" an" o!(er,o"# ;'i"%.

– Di'*! !o "e%!ro#. No! a=e!e" ,#an!i,io!i%.

– A%%oia!e" -i!( "i%ea%e% %'( a% !(e

o$$on o*"4 (ien +o84 (er+e%4(e+a!i!i% >4 $ea%*e%4 -ar!%4 +o*io4

T#+e% of

Miroor)ani%$%


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C*a%%ia!ion of Infe!ion%

• Pri$ar# Infe!ionReinfe!ion

• Seon"ar# Infe!ion4• Foa* infe!ion4

• Cro%% infe!ion4

• No%oo$ia* infe!ion%

• Ia!ro)eni infe!ion


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So're of Infe!ion%

•-ndogenousinfection

•-xogenousinfections


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C*inia* Pre%en!a!ion%

• In a++aren! infe!ion%',*inia* Infe!ion

• In a++aren! infe!ion4

•A!#+ia* infe!ion%

•La!en! infe!ion%


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So're of Infe!ion

• 1umans from patient or carrier

• # healthy carrier

• *onvalescent carrier• Temporary carrier

• *ontact carrier

• 'aradoxical carrier


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So're of Infe!ion%

• #nimals

• Insects vectors

• !echanicalvector

• iological vector

• &oil and water• ood


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MODES OF COMMUNICA>LEDISEASE TRANSMISSION

• Dire!Tran%$i%%i

on• In"ire!

Tran%$i%%ion

Dr.T.V.ao !D "2


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Mo"e% of Tran%$i%%ion

• Direct contact

• Indirect

contact• Droplet

transmission

• 1ands• Vector$borne

• )osocomialDr.T.V.ao !D ""


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Transmission of Pathogens

•Direct contact

•Indirect contacts• Air• Objects

•Vectors


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Mo"e% of Tran%$i%%ion

Directtransmission

Indirect transmission

Direct contact Airborne

Droplet spread Vehicle borne

Vector borne


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DIRECT TRANSMISSION

• Immediate transfer of the disease agent bydirect contact between the infected and thesusceptible individuals

• (ccurs through such acts as touching, biting,6issing, sexual intercourse, or by directprojection 7droplet spread8 by coughing orsnee9ing within a distance of one meter

• -xamples of diseases for which transmissionis usually direct are #ID&, syphilis,gonorrhea, and the common cold

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INDIRECT TRANSMISSION

• !ay be one of three types: air$borne, vehicle$borne, or vector$borne

• Air-borne transmission $$ transmission of

microbial aerosols to a suitable port of entry,usually the respiratory tract

– !icrobial aerosols are suspensions of dustor droplet nuclei made up wholly or in part

by microorganisms $$ may be suspendedand infective for long periods of time

– -xamples of air$borne diseases include

tuberculosis, in;uen9a, 1istoplasmosis, andDr.T.V.ao !D "=


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INDIRECT TRANSMISSION2on!?".3• Vehicle-borne transmission --

contaminated materials or objects 7fomites8serve as vehicles, nonliving objects by whichcommunicable agents are transferred to a

susceptible host – The agent may or may not have multiplied

or developed on the vehicle

–-xamples of vehicles include toys,hand6erchiefs, soiled clothes, bedding, foodservice utensils, and surgical instruments

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INDIRECT TRANSMISSION2on!?".3

• #lso considered vehicles are water,mil6, food 7e.g., common vehicles8,or biological products such as blood,

serum, plasma, organs and tissues• #lmost any disease can be

transmitted by vehicles, including

those for which the primary mode oftransmission is direct, such asdysentery and hepatitis


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Ca'%in) an Infe!ion

• En"o)eno'% @ "i%ea%e ori)ina!e%-i!(in !(e ,o"#. E8B $e!a,o*i"i%or"er%4 on)eni!a* a,nor$a*i!ie%4

!'$or%.• E8o)eno'% @ "i%ea%e ori)ina!e% o'!%i"e

!(e ,o"#. E8B (e$ia* a)en!%4e*e!ria* %(o4 !ra'$a.

• No%oo$ia* @ a'ire" ,# an in"i1i"'a*in a (ea*!( are fai*i!# 2-orer% !o+a!ien!3. – Man# are an!i,io!i re%i%!an!4 *ife5

!(rea!enin).• @ ?


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Signs & Symptoms of nfection

• Redness

• Swelling

• Tenderness• Warmth

• Drainage

• Red streaks leading away fromwound

Dr.T.V.ao !D 30


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De1e*o+$en! of Infe!ionBC*inia* Si)n% an" S#$+!o$%

• Loa* %i)n% – In;ammation

– 'urulent exudate if bacterial infection?

serous exudate if viral – Tissue necrosis

–


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Genera*i


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Genera*i


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Fa!or% +re"i%+o%in)+a!(o)enii!#

• 'athogenicitymeans ability ofthe microbe to

produce diseaseor tissue injury

• Virulence

• !ay undergovariation

i * "


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Vir'*ene an"Pa!(o)enii!#• Pa!(o)enii!#B capacity of

microbes to cause disease

• Vir'*eneB degree of pathogenicityof speciBc microbe – >a%e" onB

• Invasive qualities

• Toxic qualities• 'resence of pili or Bmbriae for adhesion

• #bility to avoid host defenses 7mutate8

Dr.T.V.ao !D A4

Vi * F "


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Vir'*ene Fa!or% an"To8in%

• &tate of the 1ostImmune &ystem

• )umber of

'athogenic *ellsencountered bythe 1ost

–Infe!io'% Do%e

Dr.T.V.ao !D A=

Vir'*ene Fa!or%


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Vir'*ene Fa!or%an" To8in%

• En


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• #dhesion actors – -xamples:

• 'rotein #

7Staphylococcus aureus8

• 'rotein !7Streptococcus

pyogenes8

Dr.T.V.ao !D A


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Vir'*ene Fa!or%

• Virulence factors help bacteria to 728invade the host, 7"8 cause disease,and 7A8 evade host defences. The

following are types of virulencefactors:

• #dherence actors: !any pathogenic

bacteria coloni9e mucosal sites byusing pili 7Bmbriae8 to adhere to cells.

Vi * F !


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Vir'*ene Fa!or%

• In1a%ion Fa!or%: &urfacecomponents that allow the bacteriumto invade host cells can be encoded

on plasmids, but more often are onthe chromosome.

• Ca+%'*e%B !any bacteria are

surrounded by capsules that protectthem from opsonisation andphagocytosis

Vir'*ene Fa!or%


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• E8o!o8in% – # type of bacterial toxin with the

following properties:• !ay be produced by either gram$positive or

gram$negative bacteria

• Is secreted by the bacteria

• The action of the exotoxin does notnecessarily require the presence of the

bacteria in the host• !ost exotoxins are peptide or protein

• !ost exotoxins are heat sensitive 7exception:enterotoxin of Staphylococcus aureus8

Dr.T.V.ao !D C2

Vir'*ene Fa!or%


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• E8o!o8in% 2on!.3 – *lasses of exotoxins: )eurotoxic,

cytotoxic, or enterotoxic exotoxins

• )eurotoxins: Interfere with propersynaptic transmissions in neurons

• *ytotoxins: Inhibit speciBc cellularactivities, such as protein synthesis

• -nterotoxins: Interfere with waterreabsorption in the large intestine? irritatethe lining of the gastrointestinal tract

Dr.T.V.ao !D C"

Vir'*ene Fa!or% an"


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• En"o!o8in% – # type of bacterial toxin having the

following properties:• 'roduced only by gram$negative bacteria• -ndotoxins are a component of the gram$

negative cell wall

• The action of endotoxin requires thepresence of the bacteria in the host. Theendotoxin may be released from the cellwall as the cells die and disintegrate

Dr.T.V.ao !D CA

Vi * F ! "


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• En"o!o8in% 2on!.3• -ndotoxin is

composed of


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En"o!o8in%

• -ndotoxins: Thelipopolysaccharide

endotoxins on /ram$negativebacteria cause fever,changes in blood pressure,

in;ammation, lethal shoc6,and many other toxic events.

M ( i f E " ! i


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Me(ani%$ of En"o!o8ina!i1i!#


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E8o!o8in%• -xotoxins: -xotoxins includeseveral types of protein toxins

and en9ymes produced and0orsecreted from pathogenicbacteria. !ajor categories

include cytotoxins,neurotoxins, and enterotoxins.


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E8o!o8in%• -xotoxins, unli6e the lipopolysaccharide

endotoxin, are protein toxins released from viablebacteria. They form a class of poisons that isamong the most potent, per unit weight, of all

toxic substances. !ost of the higher molecular$si9ed exotoxin proteins are heat labile? however,numerous low molecular$si9ed exotoxins areheat$stable peptides. %nli6e endotoxin, which is a

structural component of all /ram$negative cells,exotoxins are produced by some members ofboth /ram$positive and /ram$negative genera.


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E8o!o8in%• The functions of these exotoxins for the

bacteria are usually un6nown, and thegenes for most can be deleted with no

noticeable e@ect on bacterial growth. Incontrast to the extensive systemic andimmune$system e@ects of endotoxin onthe host, the site of action of most

exotoxins is more locali9ed and isconBned to particular cell types or cellreceptors.


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E8o!o8in%• Tetanus toxin, for example, a@ects

only intern uncial neurons. Ingeneral, exotoxins are excellent

antigens that elicit speciBcantibodies called antitoxins. )ot allantibodies to exotoxins are

protective, but some react withimportant binding sites or en9ymaticsites on the exotoxin, resulting in

complete inhibition of the toxic


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E8o!o8in%• -ndotoxin is comprised of toxic

lipopolysaccharide components of theouter membrane of /ram$negative

bacteria 7see *h. "8. -ndotoxin exertsprofound biologic e@ects on the host andmay be lethal. ecause it is omnipresentin the environment, endotoxin must be

removed from all medical suppliesdestined for injection or use duringsurgical procedures.


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E8o!o8in%• The term endotoxin was coined in 25A by

'fei@er to distinguish the class of toxicsubstances released after lysis of bacteriafrom the toxic substances 7exotoxins8 secretedby bacteria. ew, if any, other microbialproducts have been as extensively studied asbacterial endotoxins. 'erhaps it is appropriatethat a molecule with such important biologic

e@ects on the host, and one produced by somany bacterial pathogens, should be thesubject of intense investigation.


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(ther actors• 'lasmids

• acteriopha

ges

• *ompatibilit

y


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O!(er >a!eria* fa!or%

• *oagulase

• ibrinolysin

• 1yaluronidase


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Bacterial Appendages

• ioBlms

• ree ;oating bacteria come in

contact with medical devicesand attach to them with pili


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Infe!in) Do%e

•!inimum

infective dose

•!inimal lethaldose


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T#+e% of Infe!io'% "i%ea%e%

•acteraemia

•&epticaemia

•'yemia


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O!(er !#+e%

•-ndemic disease

•-pidemic disease•'andemic disease


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Hospital acquired infections

• Infection which wasneither present norincubating at the time ofadmission

• Includes infection whichonly becomes apparentafter discharge fromhospital but which wasacquired during

hospitalisation (Rcn, 1995)• Also called nosocomial

infection

Dr.T.V.ao !D =3

>a%i %!e+% in Pre1en!ion of


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>a%i %!e+% in Pre1en!ion ofInfe!ion

• There are possibletreatment andprevention to stop

the infection cycle. This is throughadequate hygiene,sanitary

environmentmaintenance andhealth education.

Dr.T.V.ao !D =2

An!i$iro,ia* a)en!% In


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An!i$iro,ia* a)en!% InInfe!ion

• #nti$infective drugs such as antibiotics,antiviral, antifungal and ant tubercular drugssuppress infection. It can be administered bymouth, topically or intravenously dependingon the infection extent and severity.&ometimes, if drug resistance is 6nown,multiple drugs are used to stop drug

resistance and increase drug e@ectiveness.#ntibiotics only wor6 for bacterial infectionand have no e@ect on viral ones.

Dr.T.V.ao !D ="

INSPITE OF MANY ADVANCES THERE IS NO


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INSPITE OF MANY ADVANCES THERE IS NOSTEP GREATER THAN HAND 9ASHING IN

CONTROL OF INFECTIOUS DISEASES


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• Pro)ra$ Crea!e" ,# Dr.T.V.RaoMD for Me"ia* an" Para$e"ia*

Profe%%iona* for G*o,a* e"'a!ionon Infe!io'% Di%ea%e%

• -mail

• "o!or!1rao)$ai*.o$

infectious diseasesaetiology pathogenesis &consequences by dr.t.v.rao md

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