Zoonosis tropis 2009

8/18/2019 Zoonosis tropis 2009

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ZOONOSESZOONOSES

dr. Muh. Nasrum Massi, Ph.D

Faculty of Medicine

Hasanuddin University


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Zoonoses

Transmission of the infectious agent

to humans from an ongoing reservoirlife cycle in animals, without the

permanent establishment of a new

life cycle in humansSpecies Jumping

The infectious agent derives from an

ancient reservoir life cycle in animals,but they have established a new life

cycle in humans that no longer

involves the animals


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Etiologic

Classifcation


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iral

!acterial

Parasitic

Mycotic


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Zoonoses" iral E#am$les

Colorado tick fever Japanese encephalitis

Ebola Monkeypox

Equine encephalitides(EE, EEE, !EE"

#ipah

$antaviruses %abies

$endra %ift !alley fever

$erpesvirus & est #ile virus

'nfluena )ello* fever


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Zoonoses" !acterialE#am$les

+nthrax lague

&rucellosis sittacosis

Campylobacteriosis - fever

Cat.scratch disease %elapsing fevers

/eptospirosis 0almonellosis/isteriosis Tularemia

/yme disease )ersiniosis


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Zoonoses" ParasiticE#am$les

PROTOZOAL !L"#$T#%

Trypanosomiasis &aylisascariasis

&abesiosis Cysticercosis

Cryptosporidiosis $ydatidosis

/eishmaniasis 0chistosome dermatitis

1iardiasis Trichinosis

Toxoplasmosis !isceral larva migransand toxocariasis


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Zoonoses" MycoticE#am$les

%s$er&illosis

!lastomycosis

'ry$tococcosis

Dermato$hytosis

Histo$lasmosisS$orotrichosis


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Zoonoses" %nimalS$ecies

2ogs 3 Cats

4 %abies

4 %ound*orm

4 %ing*orm

4 /yme 2isease (dogs only"

4 Cat 0cratch 2isease (cats only"

5ood +nimals 4 0almonella

4 E6coli

4 &rucellosis


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Zoonoses" %nimalS$ecies

&irds' 4 Psittacosis

4 (est $ile

4 %ryptococcus Reptiles) *ish) +

Amphibians 4 Salmonella

4 "ycobacterium (ild Animals

4 antavirus

4 Plague

4 Tularemia


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Routes o

TransmissionDirect( Dro$let or %erosol

( Oral

( 'ontact )ndirect

( Food*orne

( +ater*orne( Fomite

( ector*orne

( Environmental


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Diseases in Human


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Diseases Leptospirosis

Psittacosis

Anthrax Scrub typhus

Avian inuena

Rabies !SE "!ovine s$on&iform

ence$halo$athy-


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EP/OSP)0OS)S


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e$tos$irosis is an acute anthro$o1oonotic infection

)t occurs in tro$ical, su*tro$ical andtem$erate 1ones.

+eil Disease, Hemorrha&ic 2aundice, Mud Fever, S3ineherdDisease,'anicola Fever, sevenday

fever found commonly in 2a$an,'ane cutter4s disease in %ustralia,0ice 5eld e$tos$irosis in )ndonesia, Fort !ra&& fever in U.S.%ndamanhaemorrha&ic fever6%HF-

iN/0ODU'/)ON


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E$idemiolo&y

!ndemicLocations where the infection is

commonplace) caused by high rainfall) close

human contact with livestoc, or wild animals)

poor sanitation or wor,place e-posure .ricefarming) etc/0

1eneral

Locations where the infection is at the

international average of 2023 cases per422)222) and infection is usually the result of

accidental e-posure through wild rats)

livestoc, or direct contact with water through

leisure or occupation0


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/he reservoirs for Leptospira s$ecies include a 3ide ran&e of

3ild and domestic animals thatmay remain asym$tomatic

shedders for years.

Leptospira or&anisms e#creted inanimal urine, amniotic 7uid, or$lacental tissue are via*le in soil

or 3ater for 3ee8s to months.

Humans *ecome infected throu&h contact of mucosal surfaces ora*raded s8in 3ith contaminated

soil, 3ater, or animal tissues.


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People who are predisposed by

occupation include abattoir and sewerworkers, veterinarians, farmers, andmilitary personnel.

Recreational exposures and clusters of

disease have been associated withwading, swimming (especiallyswallowing water), or boating in

contaminated water,

particularlyduring flooding. Person-to-persontransmission is rare.


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Etiology

/eptospirosis is caused by spirochetes of

the genus Leptospira6

/eptospires are classified into a number of

species

defined by their degree of geneticrelatedness as determined by 2#+

reassociation6

There are 78 named pathogenic and

nonpathogenic species6 The genome sequence of Leptospira

interrogans serovar /ai has been

determined


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The genera Leptospira contains threespecies namely L interrogans) L

biflexa and L parv a0 4 The first includes 56 serogroups and

more than 532 serovars and is theprincipal cause of leptospirosis inhumans and animals0 most commonbeing L. canicola, L. hardjo and L.hebdomadis.

Two types of leptospirosis' 4 Anicteric leptospirosis or self7limited

illness .839 to :29 of the cases/ 4 #cteric leptospirosisor weil;s

syndrome .39 to 429 /


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#t is a thin spiral organism $%&mmx ' ( )$mm* +ith tightly set coils

#t is characterie, by very activemotility* by rotating "-spinning./

an, ben,ing% 0sually one or bothen,s o this single(cell organismare bent or hoo1e,

!ecause o their narro+ ,iameter*the leptospires are bestvisualie, by ,ar1(fel,illumination or phase contrastmicroscopy an, they ,o not stainrea,ily +ith aniline ,yes%

Leptospira interrogans


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A microscopic vie+ oLeptospira# bacteriastaine, apple green +ith auorescent ,ye "rom the

C2C3s Public 4ealth #mage


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Reservoirs

Wild and domestic animals rodents,

livestock (cattle, horses, sheep, goats,

swine), canines, and wild mammalsare the reservoir for leptospirosis.

Many animals have prolonged

leptospiruria without suffering fromthe disease themselves.


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Modes of Transmission

By direct or indirect contact of nasal, oral, oreye mucosal memranes or araded or

traumati!ed skin with urine or carcasses of

infected animals.

"rine# $ndirect e%posure through water, soil,or foods contaminated y urine from infected

animals is the most common route. &fter a

short period of circulating high levels of the

spirochete in their lood, animals shed the

spirochete in their urine, contaminating the

environment.

$nhalation of droplet aerosols of contaminated

fluids can occasionally occur


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$ncuation period

The incuation period is usually '

' days, ut usually (* + ' days)days.

-eriod of ommunicaility or $nfectious

-eriod /umans with leptospirosis usually

e%crete the organism in the urine for0 weeks and occasionally for

as long as 1 weeks.

-ersontoperson transmission isconsidered e%tremely rare.


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2irect &ssay

2emonstration of leptospires or

their products#

Microscopy 2arkfield microscopy

-hase contrast microscopy


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$ndirect &ssay


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2emonstration of a rise in antiody levelseither through M&T or 34$5& is essential

y repeating the sampling at least fourdays after taking the first sample.

$n hennai, the M&T test is availale at the6eterinary "niversity, Madhvaram, theM7R Medical "niversity, 7uindy and themicroiology department of the MadrasMedical ollege.

The $gM dip stick 34$5& is commerciallyavailale from 8rganon Teknika ($nfar

$ndia) and -an Bio (&ustralia). "sing thistest could help detect leptospirosis duringthe acute (early) phase of the illness.


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TREAT5E6T

Penicillin ' million units,aily #%7 "&$(&8 ,ays/

Amoxycillin* Erythromycin*9 2oxycycline

Patients +ith 5:;"5ulti

organ ailure/ to beobserve, an, treate, inintensive care unit


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-R3639T$89

3nvironmental Measures To prevent illness, prevent contamination of living, working

and recreational areas y urine of infected animals.

ontrol rodent populations in areas of human haitation.

2omestic animal owners should take necessary precautionsto minimi!e their animal:s potential contact with wildlife

( e.g., do not feed pets outside or allow animals to roam

unsupervised).

2o not allow animals to urinate in or near ponds or pools.

;eep animals away from gardens, playgrounds, sando%es,

and other places children may play.

&mong domesticated animals, vaccination of swine, cattle,

and dogs.


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Protected water supply to all0 Proper collection) transport) treatment

and secured disposal of garbage0


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Sinonym:fowl plague, fowl pest, peste aviaire, geflugelpest,

typhus exudatious gallinarium, Brunswick bird plague,Brunswick disease, fowl disease, fowl or bird grippe.

“ Suatu penyakit menular yg disebabkan oleh virusinfluenza subtipe !"#$ yg menyerang manusiadgn ge%ala demam & '(o), batuk, pilek, nyeri otot,nyeri tenggorokan dan pernah kontak dgn binatang tsbdlm * hr terakhir+


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amily: -rthomyxoviridae Btk filament virion diameter (./$0. nm uman !nfluen"a viruses# $,%,&

$vian !nfluen"a# limited to !nfluen"a $ viruses

INFLUENZA VIRUS


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1apat menyerang: / multiple species

2manusia, burung, kuda, babi, paus dll3

/ burung: vian influenza viruses

Beberapa subtipe menurut %enis !emaglutinin 2!3 dan

#euraminidase 2#3

$4 ! dan 5 #

6anusia: Subtipe !$#$, !0#0, !'#0

Burung: Semua subtipe

7aling virulen dibanding influenza B dan )

Virus Influenza A


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Avian Influenza A virus

"enginfe,si Tr0 Resp dan Tr0 1# burung' Biasanya tidak menyebabkan penyakit pada 8tik liar

Sering ter%adi genetik recombinant

6enyebabkan kesakitan dan kematian pada ternak

Avian influen?a virus ber,umpul @uga dalam feses

Bisa survive pd suhu rendah dan kelembaban rendahBisa hidup di air 9 hr 00o) a ' hr o)

6ati pd pemanasan "4o) ' %am a 4o) ' menit

1isinfeksi lingk sekitar diperlukan 2formalin a iodine3


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ward for influenza patients during $5$( pandemic


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)ontinues evolving of !"#$


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&linical 'pecimens for !nfluen"a

estingRespiratory

asal swap

asal wash

asal aspirate

asalpharyngeal swab *aintain &old &hain

'puta

hroat swab

racheal aspirate

+ther

'erum

Rectal swab

http#www.who.intcsrdiseaseavianinfluen"aguidlineshumanspecimensen


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aboratory precaution /0 esting

ighly pathogenic avian influen"a $ (/0) virus is classified as a selectagent and must be worked with under %iosafety level (%') 1 withenhancements conditions

&ontrolled access double door entry with change room and shower 2se of respirators 3econtamination of all wastes 'howering out of all personel 4ork with influen"a $ (/) suspected specimen must be separate from other

human influen"a $ (i.e., 0 or 1) virus work 3ue to the %' 1 5 re6uirements, respiratory virus cultures should not be

performed in most clinical laboratories and cultures should not be conducted

for patients suspected of having influen"a $ (/0) virus infection

http#www.who.int.csr.diseaseavianinfluen"aguidelineshandlingspecimens


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/0 3iagnosisRapid influen!a diagnostic tests

7 Results obtained within 0/-18 min

7 ot particularly sensitive

7 ot specific9 often miss avian :$; viruses

3etection of /=9 virus#

7 R-P&R in %'< conditions7 =iral isolation in %'1 enhanced lab conditions

> Results within =iral isolation the :gold standard;

3etection of antiody to /=9 virus

7 *icro-neutrali"ation assay using live /0 virus in %'1

enhanced lab conditions

7 &onfirm with 4estern %lot

7 'tandard influen"a ! antibody assay neither sensitive nor

specific9 produces false results

2iagnostics for $nfluen!a2iagnostics for $nfluen!a


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?merging !nfectious 3iseases,

08#@ Auly


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!nterpretation of Rapid est Results for

'uspected $vian !nfluen"a $ (/0)

egative result does not D o /0 infection#

> Calse negative (/0 detected by other tests)

> rue negative (no influen"a $ virus infection)Positive result does not D /0 infection#

Calse Positive

7 on-specific binding

7 !nfluen"a %

rue Positive (00, 0


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Molecular $dentification

of /=9

=iral R$ extraction

Reverse transcriptase of viral genome

$mplification of specific conserved region by

Polymerase &hain Reaction (P&R)

Eel-based detection of P&R amplicons

Real-time R-P&R (rR-P&R) Eene se6uencing

Phylogenetic mapping of viral isolates

$ t t ti f RT -R R lt$ t t ti f RT -R R lt


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he R-P&R assay result interpreted when# 7 he negative control reactions is negative

7 he positive control reaction is positive$ negative result is not necessarily definitive.

'uggests that influen"a virus genetic material

was absent from the sample tested

$ positive results based upon band side is

presumptive until proven by se6uencing

$nterpretation of RT-R Results#$nterpretation of RT-R Results#


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'ummary of aboratory

ests for !nfluen"a estingest arget 'pecimen 'ensitivity 'pecivicity ime

R-P&R R$ 'wabs,issue

55555 55555 F/ hr

=iralisolation

=irus 'wabs,issue

55555 55555 1-/ day

Rapid

est

$ntigen 'wabs 55 55 F0hr

! $ntibody 'era 555 5555 BG hr

*icro

ext

$ntibody 'era 5555 55555 @< hr


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gbr

7 'hipping permits are in order'hipping permits are in order

7 samples packed according tosamples packed according to

!nternational regulations!nternational regulations

7 =ials labeled=ials labeled

7 Hey of samples includedHey of samples included

7 racking information providedracking information provided

7 6uestionnaires have been filled in, list6uestionnaires have been filled in, list

of specimensof specimens

Time line for &nalysis and


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gbr

Time line for &nalysis and

Reporting /=9 ases

5ample ollection

5ample

5hipment

hrs

4aoratory

-rocessing>$nitial $2

'0 hrs

5hipment to W/8

Reference enter

'

weeks

haracteri!ation

Reporting

M8/,

W/8

Time 4apse#

' Weeks

'0 hrs


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hallenges in the 4aoratory

2iagnosis of /=9

?ducation of hospital and clinical staff &onsistent 6uality sampling

*aintaining sample cold chain &orrect keying of samples imely analysis of samples $ssay standardi"ation

3atabase maintenance &onfirmation of results ?ducation of health officialspublic


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P&R Materials re?uired

7 I!$amp =iral R$ *ini Hit or e6uivalent extraction kit7 I!$E? +ne'tep R-P&R kit

7 Rase inhibitor ($%!)


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;ips for cooking


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;ips for cookingpoultry

Separate raw food from cooked food


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!ovine s$on&iformence$halo$athy

:*ad &ow 3isease;


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Introduction

B53 is a fatal, neurodegerative disease in cattle,

that causes a spongy degeneration in the brain and

spinal and progressive degeneration of the nervous

system.

%'? has a long incubation period is about ervousness and aggression

> !ncoordination

> 3eath

o antemortem test


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!nfectious agent of %'? is believed to be a specifictype of misfolded protein called a prion

%ovine spongiform encephalopathy (%'?) is one ofseveral transmissible spongiform encephalopathies('?) diseases.

+r Prion diseases, which are progressive

neurological disorders thought to be caused byconversion of endogenous, host-encoded prion

protein (PrP) to an abnormal conformationdesignated PrPsc.

hose prion proteins carry the disease betweenindividuals and cause deterioration of the brain


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9:

+rigin of %'?

'till unclear, but $ppears to have originatedfrom scrapie, an endemic '? recogni"ed

since mid-0Gth

c.Rendered carcasses of livestock (includingsheep) fed to cattle as protein-richnutritional supplement

!n 0LG8, change in rendering processallowed etiologic agent to survive


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9;

&attle were infected through ingestion

&attle carcasses were recycled throughrendering plants, amplifying the cattle-adapted pathogen

Cirst verified case of %'? in the 2H in0LGM9 outbreak peaked in 0LL1

!n the end

> N 0G8,888 infected cattle > 'laughter of B./* cattle N18 months old

Eti l l f T i ibl S if


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Etiologycal of Transmissible Spongiform

Encephalopathies (TSEs)

$n unconventional virus

$ virino or OincompleteO viruscomposed of naked nucleic acid

protected by host proteins !nfectious fatal neurodegenerative

disorders

ransmissible agent unknown

*ost widely accepted theory is that'?s are caused by a modified form of

a normal cellular glycoprotein called a

prion protein

#ormal grey matter (co*"

!acuoliation of the

grey matter (co*"


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$ prion or abnormal proteinase resistant

protein, devoid of nucleic acid, capable of

causing a cell to produce more abnormal protein

Eenetic relationship to susceptibility

&ause no detectable immune or inflammatoryresponse in the host

ighly resistant to heat, ultraviolet light,

ioni"ing radiation, and common disinfectantsthat normally inactivate viruses or bacteria


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Prions

3efinition

Prions are single molecules containing

about


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?lectron *icroscopy of a Prion#

:ubulofilamentous particles


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'maller than most viral particles

!EK resistant to heat, 2= light,ioni"ing radiation, disinfectants

&auses no detectable immune or

inflammatory response

as not been observed microscopically

ittle is known about prion infectivity in

peripheral tissues.

Th N l i (P P )


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The Normal protein (PrP c )

is called PrP& (for cellular)

$ glycoprotein normally found at the cell surface

inserted in the plasma membrane has its secondary

structure dominated by alpha helices (probably 1of them)

?asily soluble

?asily digested by protease

?ncoded by a gene designated (in humans) PRP

located on our chromosome


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PrPSc

he abnormal, disease-producing protein

!s called PrP'c (for scrapie)

as the same amino acid se6uence as the normal

protein9 that is, their primary structures are

identical but

!ts secondary structure is dominated by beta

conformation !nsoluble in all but the strongest solvents


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ighly resistant to digestion by proteases

4hen PrP'c comes in contact with PrP&, it

converts the PrP& into more of itself (even in the

test tube).

hese molecules bind to each other formingaggregates.

!t is not yet clear if these aggregates are

themselves the cause of the cell damage or are

simply a side effect of the underlying disease process.

wo forms of prion# from PrPc to PrP'c


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wo forms of prion# from PrPc to PrP'c

The normal, membrane.associated protein (rc" can change its shape

to a harmful,disease.causing 3 highly aggregated form (r0c"6 Theconversion from rc to r0c then proceeds via a chain.reaction6 hen

enough r0c proteins have been made they form long filamentous

aggregates that gradually damage neuronal tissue6 The harmful r0c

form is very resistant to high temperatures, 9!.irradiation and strong

degradative enymes6

St t l Ch f i


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Structural Change of prion

protein

#ormal +bnormal


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ocali"ation of 3ifferent Prion 3iseases

#n fatal familial insomnia .**#/)

mutated prions accumulate in

the thalamus, *ith the result

that the patients are unable to

sleep6 #n %reut?feldt7Ja,ob disease

.%J


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Animal Transmissible Spongiform Encephalopathies

'crapie in 'heep and Eoatts

ransmissiblle *ink ?ncephallopatthy (*?) in

*ink &hroniic 4asttiing 3iisease (&43) in 3eer and

?llk

%oviine 'pongiiform ?ncephallopatthy (%'?) in

&attttlle,, &atts,, Hudu,, and yalla


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Process of Prion Hill in the %ody

Prion protein are found in all mammals. heirfunction is not fully understood but there are large

numbers of them in the brain, especially on the

surfaces of cell membranes.

$ccording to the prevailing theory, abnormally

folded prion proteins, make the normal proteins

refold into disease, causing shapes.

he normal proteins refold, taking on abnormalshapes.


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he newly refolded proteins interact with other

prion proteins, causing them to refold, too.

he altered proteins are resistant to breakdown

and may accumulate into pla6ues,

Prions on cell surfaces allow too much fluid to

enter cells, producing a spongey appearance

when cross-sections of brain tissue are

examined under a microscope.

*odels for prion disease process


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*odels for prion disease process

Prions in the body


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Prions in the body

hysical +ttributes of the affected brain:

4 Enlarged astrocytes. 0tar shaped

cells attached to blood vessels in

brain6

4 $oles *here neurons used to be6

4 +myloid laques.flo*er shaped

protein *axy buildup6

5ound in mainly in the brain, spinal cord and nervous tissue, *ith

increasing research discovering prions in glands and blood as *ell6

&0E &rain

0crapie &rain

Route of -rion


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&0E results *hen a

sufficient number of

nerve cells have

become damaged,

affecting the behaviorof the co*s

Route of -rion

$nfection


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ransmission

%'? can be transmitted from mother to fetus, as well as

from bull sperm to the female.

$lso contracted when infectious agent (prion) is ingested

in food.

&alves are fed a :baby formula; made from bovine blood

because it it much less expensive than milk, not to mention

the comparative resale values of the two li6uids


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%'? of &linical 'ymptoms

&hanges temperament (nevrousness or

aggression)

$bnormal posture !ncoordination and difficulty in rising

3ecreased milk production

oss of body conditioning

o change in appetite early in the disease


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3iagnosing %'?

&urrently the only sure way to diagnose %'? is to

look at the brain

> his means you have to kill the animal

'ectiions of the brain are prepared and examiined

under the microscope looking for the

characteriistiic :spongy; change

'pecial stains can also be used to identiify thefibrils formed by the abnormal prion protein


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&urrently there is no test that can be

performed on the live animal

*any researchers are trying to develop such

a test2sing laboratory tests, it is possible to

distinguish between the different forms of

'?

his means it is possible to distinguish %'?

from scrapie and from &43


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2iagnosis of microspoce

,r% 5uh% 6asrum 5assi*


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0a*ies0a*ies

Ph%2

+h t i 0 *i+h t i 0 *i


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0a*ies is a disease0a*ies is a disease

that a


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/he ra*ies virus can /he ra*ies virus can&et into your *ody&et into your *ody

and attac8 yourand attac8 yourcentral nervouscentral nervoussystemsystem

+atch as the ra*ies+atch as the ra*iesvirus from anvirus from ane#$osure on the le&e#$osure on the le&s$reads u$ the s$inals$reads u$ the s$inal

cord to the *rain andcord to the *rain andthrou&hout the restthrou&hout the restof the *odyof the *ody

)nterestin& facts a*out)nterestin& facts a*out


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)nterestin& facts a*out)nterestin& facts a*out

ra*iesra*ies

7;,


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'ommon'ommon

'arriers'arriershe raccoon is thehe raccoon is themost commonmost common

carrier B8.Mcarrier B8.M

'kunk


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=ind of animals &et ra*ies=ind of animals &et ra*ies

The rabies virus can infect allThe rabies virus can infect all

mammals .dogs) cats/0mammals .dogs) cats/0

"ammals are warmblooded"ammals are warmbloodedanimals that have hair andanimals that have hair and

mammary glands to producemammary glands to produce

milk for their babies6milk for their babies6 +nimals like frogs, birds, and +nimals like frogs, birds, and

snakes do not get rabies6snakes do not get rabies6

/ i i/ i i


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/ransmission /ransmission

The commonest *ay of rabies transmissionThe commonest *ay of rabies transmissionis by the bite of an infected mammalis by the bite of an infected mammal

&ites by rabid animals generally inoculate virus.&ites by rabid animals generally inoculate virus.

laden saliva through the skin into muscle andladen saliva through the skin into muscle and

subcutaneous tissuessubcutaneous tissues

%abies virus entry occurs through *ounds or%abies virus entry occurs through *ounds or

direct contact *ith mucosal surfaces6 Thedirect contact *ith mucosal surfaces6 The

virus cannot cross intact skinvirus cannot cross intact skin %abies can be transmitted by moisture%abies can be transmitted by moisture

droplets in the air (aerosol"droplets in the air (aerosol"

Rabies ife &ycleRabies ife &ycle


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Dunne ')DPDunne ')DP 2anuary ;>, ? 2anuary ;>, ?:

Rabies ife &ycleRabies ife &ycle

7irusinoculation

"bite/

Salivaryglan,

excretion


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RA!#ES L#;E C


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0a*ies iruses0a*ies iruses The family %habdoviridaeThe family %habdoviridae generagenera

LyssavirusLyssavirus

StructureStructure%abies virus is a rod. or bullet.shaped,%abies virus is a rod. or bullet.shaped,single.stranded, negative.sense,single.stranded, negative.sense,

unsegmented, enveloped %#+ virus6 Theunsegmented, enveloped %#+ virus6 The

virus genome encodes five proteinvirus genome encodes five protein

associated *ith either the ribonucleoproteinassociated *ith either the ribonucleoprotein

(%#" complex or the viral envelope(%#" complex or the viral envelope


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Phatogenesi


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%abies virus may enter the peripheral%abies virus may enter the peripheralnervous system directly, or may replicatenervous system directly, or may replicatein muscle tissue after entering the host,in muscle tissue after entering the host,remaining at or near the site ofremaining at or near the site of

introduction for most of the incubationintroduction for most of the incubationperiod6period6

The precise sites of viral sequestrationThe precise sites of viral sequestration

remain unkno*n, since neither antigenremain unkno*n, since neither antigennor virus can usually be found in anynor virus can usually be found in anyorgan during this phaseorgan during this phase

Phatogenesi

s

PATHOGENESISPATHOGENESIS


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PATHOGENESIS PATHOGENESIS

Live virus Live virus Epidermis, Mucus membrane Epidermis, Mucus membrane

Peripheral nerve Peripheral nerve

CNS ( ra! ma""er #CNS ( ra! ma""er #

O"her "issue (salivar! lands,$#O"her "issue (salivar! lands,$#

cen"ripe""all!

cen"ri%uall!


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Sym$toms in humansSym$toms in humans


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Sym$toms in humansSym$toms in humans

Sym$toms occur A: to B: days afterSym$toms occur A: to B: days afterthe *ite.the *ite.

Early sym$toms include fever,Early sym$toms include fever,

headache, sore throat and feelin& tired.headache, sore throat and feelin& tired.

)f the virus &ets to the *rain the $erson)f the virus &ets to the *rain the $erson3ith it mi&ht act nervous, confused,3ith it mi&ht act nervous, confused,

and u$set.and u$set.

Other sym$toms" $ain or tin&lin& in theOther sym$toms" $ain or tin&lin& in the

s$ot 3here the $erson 3as *itten,s$ot 3here the $erson 3as *itten,

hallucinations, hydro$ho*ia, andhallucinations, hydro$ho*ia, and

$aralysis.$aralysis.

5ive general stages of rabies are recognied5ive general stages of rabies are recognied


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in humansin humans::

776 'ncubation6 'ncubation

> Typically '@+A@ daysTypically '@+A@ days

> (0 days to C years)(0 days to C years)

> 2ose, location, variant, host factors2ose, location, variant, host factors

==00 rodrome phaserodrome phase (malaise, vomiting, sore throat,(malaise, vomiting, sore throat,paresthesia at site of bite"paresthesia at site of bite"

8686 +cute neurologic period : +cute neurologic period : sensory phasesensory phase

(ympathetic overactivity, salivation, perspiration,(ympathetic overactivity, salivation, perspiration,spasm of the throat muscle: hydrophobiaspasm of the throat muscle: hydrophobia

>6>6ComaComa (excitement", and(excitement", and

;6;6 aralytic or depressivearalytic or depressive ? death? death


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hy,rophobia excitement

&IAGNOSIS &IAGNOSIS


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74aoratory finding# ( 5< )4aoratory finding# ( 5< )73%clusion of other etiologies3%clusion of other etiologies

7-athology#-athology#


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&IAGNOSIS &IAGNOSIS


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7 Is'la"i'n '% virus (saliva,CS, brain # Is'la"i'n '% virus (saliva,CS, brain #

7 Ser'l'! Ser'l'!

7)iral A de"ec"i'n ( in%ec"ed "issue #)iral A de"ec"i'n ( in%ec"ed "issue #

7)iral &NA de"ec"i'n ( PC* #)iral &NA de"ec"i'n ( PC* #

Prevention Prevention


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Preventionevention1ive your household pets vaccinations1ive your household pets vaccinations

regularly6 't *ill prevent your pet fromregularly6 't *ill prevent your pet fromgetting rabies from *ild animals6getting rabies from *ild animals6

+void *ild animals acting abnormally6 +void *ild animals acting abnormally6

+nti.rabies shots can prevent the disease6 +nti.rabies shots can prevent the disease6 4 +t first, 7.8 shots of antibodies are given +t first, 7.8 shots of antibodies are given

around the bite6around the bite6

4 Then, five shots of vaccine are given in theThen, five shots of vaccine are given in thearm over 8< days6arm over 8< days6

4 %abies shots help your body make po*erful%abies shots help your body make po*erful

antibodies that kill the virusantibodies that kill the virus


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he +rganism $gent

/he Or&anism


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&

Psittacosis is "oonotic infection caused by

Chlamydophila psittaci

amily Chlamydiaceae

Chlamydophila psittaci, formerly named Chlamydia

psittaci

Eram negative

+bligate intracellular bacteria

$ir-born spread (birds faeces)

arget cells# macrophages, lung parenchyma

Structure C psittaci


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Structure C. psittaci

?nergy ($P) parasite bacteria with uni6e


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biphasic life cycle

he developmental cycle includes two formare ?lementary body (?%) and Reticulate body(R%)

he bacteria that causes endemic avianchlamydiosis, epi"ootic outbreaks inmammals, and respiratory psittacosis inhumans.

&hlamydiaceae are well adapted for survivaloutside of the host and for persistence in ahost.

&omparison of ?% and R%


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&omparison of ?% and R% ?lementary body (?%)

> he extracellular form survival

> !nfectious and toxic for mice

> !t is smaller than the reticulate body (?% si"e 8,1 N m)

> he ?% is relatively resistant to sonication and trypsin

> he permeability of the ?% is low

> he R$ # 3$ ratio of the ?% is

approximately 0 # 0 > !nduces endocytosis and metabolicaly inactive

Reticulate body (R%)


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Reticulate body (R%)

> he reticulate body is the intracellular form and

8,/ > 0,8 N m > he reticulate body is not infectious and not toxic

mice

> he reticulate body is sensitive to sonication > he R% is permeable to metabolites

> he R$ # 3$ ratio of the R% is approximately

1 # 0

> !nduces no endocytosis

> *etabolicaly active


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$n elementary body of Chlamydophila psittica sho!ing theouter membrane (+*) and the cytoplasmic membrane (&*)

$nd the absence of a peptidoglycan layer. he peptoglycan

layer is also absent in reticulate bodies

Replication of C psittasi


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Replication of C" psittasi

?lementary bodies attach to the microvilli ofsusceptible cells

he ?%s are internali"ed in cytoplasmic

phagosomes9 fusion with lysosomes andkilling does not occur with viable ?%s

?%s change into reticulate bodies (R%)

Reticulate bodies are metabolically active

4ife cycle and method of


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infection

hey are able to synthesi"e# 3$, R$,


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y y , ,Protein, &ellular components

7 $re energy parasites that use $P produced bythe host cell

7 he reticulate bodies then convert back to

elementary bodies and are released back intothe lung, often after causing the death of thehost cell. he ?%s are there after able to infectnew cells, either in the same organism or in a

new host

ew axonomic


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&lassification &hlamydiaceae

• GenusChlamydia−

C. trachomatis−C. muridarum

−C. suis

• GenusChlamydophila−C. psittaci

−C. abortus

−C. felis

−C. pecorum

−C. pneumoniae

−C. caviae


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'erovar of & psittaci


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'erovar of &. psittaci

!dentification of serovar may help to determine

the source of infection

Chlamydophila psittaci has eight known

serovars#

> six have been primarily isolated in birds and

two strains have been isolated in mammals.


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C" psittaci serovar $ is endemic among

psittacine birds and has caused sporadic"oonotic disease in humans, other mammals

and tortoises.

'erovar % is endemic among pigeons, has beenisolated from turkeys, and has also been

identified as the cause of abortion in a dairy

herd.


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'erovars & and 3 are occupational ha"ards for

slaughterhouse workers and for people incontact with birds.

'erovar ? isolates have been obtained from avariety of avian hosts worldwide and outbreak

in humans, a specific reservoir for serovar ?

has not been identified.

he C psittaci


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he C" psittaci

Resistant to drying

> Remains infectious for months

> Remains viable on surfaces for 'urvives in turkey carcass for N0

year.

http://www.usda.gov/oc/photo/78c0509.jpghttp://www.usda.gov/oc/photo/78c0509.jpg


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?pidemiology

?pidemiology


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?pidemiology

+ccurs worldwide as sporadic disease

here are /8-088 confirmed cases

per year

> 0-< deaths

> rue incidence unknown

ationally reportable in humans

Pet store employees, bird owners, poultry

processing plant workers

Populations at Risk


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Populations at Risk

ab workers

=eterinarians

$vian 6uarantine

workers

Qoo workers

Carmers

Pregnant women

%ird fanciers

(pigeon fanciers too)

%ird owners

Pet shop employees

Poultry slaughter and

processing workers

4ildlife rehab workers


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ransmission

Transmission to /umans


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%irds are the reservoirs of the disease and the infection

is usually transmitted to humans #

> !nhalation

7 3ried infective droppings

7 'ecretions or dust fromfeathers

> *outh-to-beak

> 3irect contact

7 andling plumage or tissues of infected birds > Person-to-person transmission

7 ot proven and venereal transmission reported


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3isease in umans

Psittacosis

/uman 2isease of


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-sittacosis !ncubation period# 0-B weeksRange

> !napparent infection

> 'ystemic infection with pneumonia

7 Pneumonia 18-M8 years of age

&ommon signs > abrupt onset

> Cever, chills, headache, malaise, myalgia,

sore throat, cough, dyspnea, splenomegaly,

rash

Clinical Signs


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Psittacosis (ornithosis) usually is an acute febrilerespiratory tract infection with systemic symptoms

and signs that often include fever, nonproductive

cough, headache, and malaise.

?xtensive interstitial pneumonia can occur with

radiographic changes characteristically more severe

than would be expected from physical examination

findings.

g

+fter several days of untreated illness,


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lethargy and sluggish speech may be seen

*ith coma or stupor6 May also see : 4 Endocarditis, placentitis, myocarditis,

hepatitis, arthritis6 @eratoconAunctivitis,

and encephalitis Myocarditis, Aaundice, 4 %espiratory failure, thrombocytopenia, and

fetal death have been reported respiratory

failure6

4 Epistaxis and mucocutaneous

manifestations frequently occur

4 +rthralgia rare


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45 year old male, rail station worker with Chlamydial pneumonia

2iagnosis


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2iagnosis

&onfirmed case > &linical signs 5 laboratory results

7 &ulture from respiratory secretions

7 B-fold rise in titer 7 $ reciprocal titer of 0M of !g* detected by *!C

(microimmunofluorescence

Probable case

> inked epidemiologically to confirmed case of

Psittacosis

> 'ingle titer ≥0#1<

reatment and Prognosis


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reatment and Prognosis

4ith treatment

> 0-/ case-fatality rate

> etracyclines are drug of choice

> Remission of symptoms

7 2sually in BG-@< hours

> Relapse possible

4ithout treatment

> *ay resolve in few weeks-months

> 08-B8 case-fatality rate


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3isease in $nimals

Avian Chlamydiosis (AC)


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$vian &hlamydiosis


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$vian &hlamydiosis

&arriers may appear healthy

> 'hed intermittently

'hedding activated by stress > 'hipping, breeding crowding,

chilling

'hedding greatest in young birds

$vian &hlamydiosis


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$vian &hlamydiosis

!ncubation period

> 1 days to several weeks

atent infection > common

*orbidity and mortality

> vary with species and serotype

&linical 'igns in Pet %irds


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Center for 5ood 0ecurity and ublic $ealth

'o*a 0tate 9niversity . =


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Center for 5ood 0ecurity and ublic $ealth

'o*a 0tate 9niversity . =</ppin urkey, 3uck Pigeon/pp > 3epression

> Ruffled feathers

> 4eakness > !nappetence

> asal discharge

> Respiratory distress

> Kellow-green diarrhea

> &onSunctivitis

> 3ecreased egg production

> $taxia-pigeons

> rembling-ducks


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3iagnosis

3iagnosis


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g

3iagnosis difficult

&ase definitions

> &onfirmed, probable, suspect

'ingle test may not be ade6uate

> &ombination testing recommended

Proper sample collection techni6ues critical for

accurate results

&onsult an experienced avian veterinarian

3iagnosis


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g

Pathologic diagnosis

&ulture

$ntibody tests

> &C, ?%$

$ntigen ests

?!'$, !C$, P&R R!*

reatment for Pet %irds

http://www.nirgal.net/graphics/petri_dish.jpghttp://virology-online.com/general/CFT.gif


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*ay be difficult

Catalities occur

'upervised by licensed veterinarian in consult

with avian specialist

$ll birds treated B/ days

?ven with treatment

> atent infections can remain

> 'hedding may occur


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Prevention and &ontrol

Prevention and &ontrol


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?ducate and protect those at risk

> &lothing, gloves, cap, ?P$ filters

> 4et carcass with water and detergent prior to necropsy

3isinfect

> 0#0888 6uaternary ammonium compounds

> 0 ysol

> @8 isopropyl alcohol > 0#088 bleach

dr. Muh. Nasrum Massi, Ph.D


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%N/H0%C

!ntroduction


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$ diseases caused by #acillus anthracis spores

uman "oonotic disease

> 'pores found in soil worldwide

> Primarily a disease of domesticated wild animals

7 'heep, goats, cattle, cows, horses, goats

7 *any large documented epi"ootics

> +ccasional human disease

7 ?pidemics have occurred but uncommon7 Rare in developed world

atural reservoir is soil

3oes not depend on an animal reservoir making it


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> 3oes not depend on an animal reservoir making ithard to eradicate

> &annot be regularly cultivated from soils wherethere is an absence of endemic anthrax

> +ccurs sporadically throughout 2'

> 'outh 3akota, $rkansas, exas, ouisiana,*ississippi, &alifornia recogni"ed endemic areas

$nthrax "ones

> 'oil rich in organic matter (p F M.8)

> 3ramatic changes in climate

E$idemiolo&y


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*ay be spread by streams, insects, wild animals, birds,contaminated wastes

$nimals infected by soilborne spores in food water or bitesfrom certain insects

umans can be infected when in contact with flesh, bones, hides,hair, excrement

> nonindustrial or industrial

> cutaneous inhalational most common

Risk of natural infection 0088,888

> +utbreaks occur in endemic areas after outbreaks in livestock

?pidemiology


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p gy

uman cases > historical risk factors

> $gricultural

7 ?xposure to livestock

> +ccupational

7 ?xposure to wool and hides

7 4oolsorterTs disease D inhalational anthrax

7Rarely laboratory-ac6uired

#acillus anthracis


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Eram 5 rod Cacultative anaerobe 0 - 0.


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'porulation re6uires

> Poor nutrient conditions > Presence of oxygen

'pores (dehydrated cells) > 'urvive for decades > aken up by host and

germinate

> ighly resistant to heat, cold,

chemical disinfectants, dry periods

ethal dose /.< million bp


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> $mes strain se6uenced

< plasmids > px80

7 0GB kbp

7 Pathogenicity island

> pV8<

7 L/.1 kbp7 &apsule

$nthrax receptor

> +ccurs N than ten thousendfold

on macrophage cell

> $R?*G gene7 &hromosome B

Patho&enesis


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he infectious dose of #" anthracis in humans by any route is not

precisely known.

> Rely on primate data

> *inimum infection dose of W0,888-G,888 spores

> 3/8 of G,888-08,888 spores forinhalation

=irulence depends on < factors

> &apsule

> 1 toxins

&apsule


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Elycocalyx

> 'ticky, gelatinous polymerexternal to cell wall

pV8< plasmid *ade up of 3-glutamic acid

on-toxic on its own +nly encapsulated #" anthracis

virulent *ost important role during

establishment of disease > Protects against phagocytosis lysis during vegetative state

/o#ins pV80 plasmid


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pV80 plasmid

$% model

> %inding

> $ctivating

Protective antigen (P$), edema factor (?C) lethal factor (C)

> *ake up /8 of proteins in theorganism

!ndividually non-toxic

> P$5C lethal activity

> ?C5P$ edema

> ?C5C inactive

> P$5C5?C edema necrosis9lethal

htt$"333.rcs*.or&$d*molecules$d*?>;.html

/o#in Protective antigen (P$, G1k3a) > Pag gene


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> %inds to receptor helps internali"e

other < proteins ?dema factor (?C, GL k3a)

> Cya gene

> $denylate cyclase

> $ffects all cells

ethal factor (C, G@ k3a)

> $ef gene

> *ore important virulence factor

> *etalloprotease

> &leaves mitogen activated proteinkinase kinsase (*$PHH)

> $ffects only macrophages

Mehanis! of Infetion

$ h b d


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$nthrax spores enter body

Eerminate multiple in lymph nodes P$, ?C, C excreted from bacteria P$ binds to ?*G. P$ nicked by protease furin

> eptamer forms ?C andor C binds &omplex internali"ed by endocytosis $cidification of endosome

C or ?C crosses into cytosol via P$ mediated ion-conductivechannels C cleaves *$PHH 0 < ?C stimulates c$*P

Pathway of &ellular $nthrax

$ttack


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$ttack

&linical !nformation


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!nfection

'ymptoms (0st and


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he estimated number of naturally occurring human cases of

anthrax in the world is


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here are two phases of symptom.

0) ?arly phase - *any symptoms can occur

within @ days of

infection


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Cever (temperature N 088 degrees C) &hills or night sweats eadache, cough, chest discomfort, sore throat Aoint stiffness, Soint pain, muscle aches 'hortness of breath ?nlarged lymph nodes, nausea, loss of appetite,

abdominal distress, vomiting, diarrhea *eningitis

-


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%reathing problems, pneumonia

'hock

'wollen lymph glands

Profuse sweating

&yanosis (skin turns blue)

3eath

hree clinical forms of$nthrax #


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&utaneous anthrax

> 3irect contact of spores on skin

> *ost common (L/)

> 'pores enter to skin through small lesions

!nhalation anthrax > 'pores are inhaled

> rare (F/)

> *ost likely encountered in bioterrorism event

Eastrointestinal (E!) anthrax > 'pores are ingested

> +ral-pharyngeal and abdominal

*ortality

> !nhalational GM-088 (despite treatment)


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( p )

7 ?ra of crude intensive supportive care

> &utaneous F/ (treated) > E! approaches 088

!ncubation Period > ime from exposure to symptoms

> =ery variable for inhalational

7


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ransmission > o human-to-human

> aturally occurring cases

7 'kin exposure7 !ngestion

7 $irborne

> %ioterrorism

7 $erosol (likely)7 'mall volume powder (possible)

7 Coodborne (unlikely)

ypes three of anthrax infection

occur in humans#


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0) &utaneous


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when the bacterium enters a cut or

scratch on the skin due to handlingof contaminated animal productsor infected animals.

*ay also be spread by bitinginsects that have fed on infectedhosts.

$fter the spore germinates in skintissues, toxin production initiallyresults in itchy bump that develops

into a vesicle and then painless black ulcer.

htt$"science.ho3stu


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he most common naturally occurring form ofanthrax.

2lcers are usually 0-1 cm in diameter.

!ncubation period#

> 2sually an immediate response up to 0 day

&ase fatality after < days of infection# > 2ntreated ( 4ith antimicrobial therapy (0)

&utaneous $nthrax


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C2C, Cutaneous +nthraxB!esicle 2evelopment

!nhalation $nthrax


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he infection begins with the

inhalation of the anthrax spore.

'pores need to be less than /microns (millionths of a meter) toreach the alveolus.

*acrophages lyse and destroysome of the spores.

'urvived spores are transported tolymph nodes.

$t least


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3isease immediately follows

germination.

'pores replicate in the lymph nodes.

he two lungs are separated by astructure called the mediastinum,

which contains the heart, trachea,esophagus, and blood vessels.

%acterial toxins released duringreplication result in mediastinalwidening and pleural effusions

(accumulation of fluid in the pleuralspace).

!nhalation $nthrax


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3eath usually results


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E! anthrax may follow afterthe consumption ofcontaminated, poorlycooked meat.

here are < different formsof E! anthrax#

0) +ral-pharyngeal


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+ral-pharyngeal form - results from the deposition and

germination of spores in the upper gastrointestinal tract.

ocal lumphadenopathy (an infection of the lymph

glands and lymph channels), edema, sepsis develop after

an oral or esophageal ulcer.

$bdominal form - develops from the deposition and

germination of spores in the lower gastrointestinal tract,

which results in a primary intestinal lesion.

'ymptoms such as abdominal pain and vomiting appearwithin a few days after ingestion.

E! !nfection


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E! anthrax cases are uncommon.

here have been reported outbreaks in Qimbabwe, $frica andnorthern hailand in the world.

E! anthrax has not been reported in the 2'.

!ncubation period#

> 0-@ days

&ase fatality at < days of infection#

> 2ntreated ( 4ith antimicrobial therapy (undefined) due to the rarity

Pathophysiology


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18=#-S8S Eram stain


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Eram stain

&ulture of #" anthracis from the blood, skin lesions,vesicular fluid, or respiratory secretions

V-ray and &omputed omography (&) scan

Rapid detection methods

- P&R for detection of nucleic acid

- ?!'$ assay for antigen detection

- +ther immunohistochemical and immunoflourescenceexaminations

- hese are available only at certain labs

Eram 'tain $nalysis


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2seful for cutaneous and

inhalation anthrax.

$ blood sample or skinlesion is taken from the patient and cultured for M to


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2seful for inhalation and E!

anthrax

&hest V-rays is advised as aninitial method of inhalationanthrax detection, but it issometimes not useful for patientswithout symptoms.

Cind a widened mediastinum and pleural effusion.

Picture shows widened

mediastinum caused by #"anthracis infection % resulting lessavailable space in lungs

'nhalation +nthrax, 'ntroduction, 2%, +rmed 5orces 'nstitute of athology

At day 4At day 4 At day 6At day 6

); scan


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2seful for inhalation and E! anthrax ?ven when V-rays are negative, & scans may provide more precise

information. &hest & (Right) shows the increase in the si"e of the pleural effusions

(accumulation of fluid in the pleural space).

'nhalation +nthrax, 'ntroduction, 2%, +rmed 5orces 'nstitute of athology

P&R $ssay

P&R is a target amplification method of nucleic acid based


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P&R is a target amplification method of nucleic acid based

%. anthracis detection.

2sed for the detection of anthrax toxin genes.

ex) rpo% gene - used as a specific chromosomal marker forR-P&R detection.

he rpo% gene was se6uenced from 1M %acillus strains

he assay was specific for 0BB %acillus anthracis strains from

different geographical locations.

Provided 088 sensitivity and specificity

P&R $ssay 3etection time#


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3etection time#

- P&R only takes several hours

ex) Rapid-cycle R-P&R can be finished within 0-< hours

&an start early treatment of $nthrax

here are many different types of P&R assays for the detection of $nthrax

such as multiplex P&R, enterobacterial repetitive intergenic consensus-P&R

(?R!&-P&R), and long-range repetitive element polymorphism-P&R.

Rapid diagnostic methods provide answers in minutes or hours instead of

days.

reatment

%efore 'topped for fear of geneticallyengineered resistant strains


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M8 day course of antibiotics

&iprofloxacin > fluoro6uinolone

> /88 mg tablet every 0 M-deoxy-tetracycline

> 088 mg tablet every 0 clindamycin

> rifampin

> chloramphenico

=accine %iohrax$nthrax vaccine absorbed


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%iohrax$nthrax vaccine absorbed

> *ade by %ioport > Route of exposure not important $dministered subcutaneously

> ./m at 8,


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Zoonosis tropis 2009

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