ZOONOSES - JYew

8/17/2019 ZOONOSES - JYew

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ZOONOSES


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Definition

• Disease caused by pathogens naturallymaintained or residing in living animalsand not recognized as predictablyadapted to humans or responsible forinterhuman transmission on a regular

basis.• Causes illness in their natural hosts andare capable of infecting humans viacontact anthra!"# animal bites rabies"#ingestion salmonellosis"# inhalation

psittacosis"# and arthropodintermediates dengue fever"

• Some definitions$criteria re%uire avertebrate intermediate# other than

humans# in the natural cycle ofdistribution


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&opics

• 'eptospirosis

• (artonella henselae

• &o!oplasmosis• )abies

• *endra virus


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'eptospirosis +

,)at -rine ever/

• Zoonotic disease caused by spirochetesof the genus Leptospira

• 0any animal reservoirs 1 rodents are the

most important 2orld2ide• &ransmission by direct contact 2ith

animals# or indirect contact 2ith 2ater $soil contaminated by animal urine

• 3 Epidemiological patterns 2orld2ide4 + &emperate climates NZ"

+ &ropical 2et areas

+ -rban environment


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'eptospirosis +

• 0ost important occupationally1

ac%uired infection in Ne2 Zealand


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'eptospirosis +

• ,'eptospira/ derives from the

5ree6 leptos thin" and 'atin spira

coiled".

• &he cells have pointed ends# one

or both of 2hich is usually bent into

a characteristic hoo6.

• (ecause of their small diameter#

leptospires are best visualized by

dar6field microscopy


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'eptospirosis +

• 78 genomospecies9 :;


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'eptospirosis +

>athogenesis

• 'eptospires penetrate intact mucousmembranes or abraded s6in

• Enter bloodstream and rapidly carried to

all parts of the body• During 7st 2ee6 leptospires are readily

found in CS# but meningitis occurs later

due to host inflammatory response

• >rolonged e!cretion of leptospires in

urine

• Causes a systemic vasculitis


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'eptospirosis +

Clinical 0anifestations

• Subclinical infection

+ >robably common

• ?nicteric leptospirosis + *eadache# fever# chills# myalgia

+ 0eningitis

• @cteric leptospirosis AeilBssyndrome"

+ aundice# renal failure# haemorrhage


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(iphasic nature of leptospirosis and relevant investigations at different stages of disease. Specimens 7

and ; for serology are acute1phase specimens# 3 is a convalescent1phase sample that may facilitate

detection of a delayed immune response# and and are follo21up samples that can provide

epidemiologic information# such as the presumptive infecting serogroup. CS# cerebrospinal fluid.


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'eptospirosis +

'aboratory Diagnosis

• Serology

+ standard method

+ re%uires testing of acute and

convalescent serum samples

• Culture

+ technically demanding and slo2

• DN? detection by >C)

+ li6ely to become the preferred method


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'eptospirosis 1 &reatment

• ?ntibiotics penicillin# do!ycycline#others" reduce duration of illness#especially 2hen started early in the

illness• Supportive measures as needed

• >revention4 ?voidance measures

often difficult. (ut do!ycycline;


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Cat ?ssociated @nfectionsCat ?ssociated @nfections

• Bacterial infections

+ anthrax

+ cat scratch disease + Pasteurella maltocida

+ Capnocytophaga

+ leptospirosis

+ Rickettsia felis

• Fungal infections

+ ringworm

• Viral infections + rabies

• Parasitic infections

+ toxoplasmosis

+ cutaneous larva

migrans


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Bartonella henselae

• 5m1ve bacilli. @n tissue re%uires

silver impregnation techni%ues for

detection eg. Aarthin1Starry stain"

• Causes asymptomatic

intraerythrocytic bacteraemia in the

feline reservoir host

• Cat flea Ctenocephalides felis" are

primarily vectors for cat1to1cat

transmission


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Bartonella henselae –

Cat scratch disease

• >rimary cutaneous papule $ pustule atinoculation site 317< days after scratch $bite

• ollo2ed by ipsilateral lymphadenopathy71F 2ee6s later# lasting ;1 mths

•


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Bartonella henselae +

Cat scratch disease

• >arinaudBs oculaglandularsyndrome

• 5ranulomatous hepatitis

• >neumonitis

• Encephalitis

• Neuroretinitis• Endocarditis

B t ll h l


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Bartonella henselae +

(acillary angiomatosis

$ peliosis• Disorder of neovascularproliferation in s6in# lymph nodes#

liver# spleen# brain# lung# bone#

bo2el uterine cervi!

• Originally described in *@I

infection. Does also occur in other

immunocompromised# as 2ell asimmunocompetent hosts


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B t ll h l


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Diagnosis

• Culture

+ Slo21gro2ing# lo2 sensitivity

• *istopathology

+ Aarthin1Starry silver stain

• >C)

• Serology + immunofluorescenceassays and enzyme

immunoassays

Bartonella henselae


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&reatment

• &ypical CSD + ?zithromycin

• Neurologic CSD + Do!ycycline J

rifampicin

• (?$(> + erytrhomycin or

do!ycycline


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&o!oplasmosis

• Toxoplasma gondii + protozoan

parasite of felids# 2ith other 2arm1

blooded animals as intermediate

hosts

• E!ists in many forms 1 gametes#

oocysts# sporozoites# tachyzoites#

tissue cysts $ bradyzoites


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&o!oplasmosis


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&o!oplasmosis +

&ransmission K epidemiology

• Aorld2ide• Cats are po2erful amplifiers of infection#

as the se!ual cycle ta6es place in the

catsB small bo2el• @nfection in humans through

+ ingestion of ra2 $ undercoo6ed meat thatcontains tissue cysts#

+ 2ater or food contaminated 2ith oocysts + transplacentally from infection during

gestation

+ &ransfusion of infected blood cells ortransplantation of infected organ


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&o!oplasmosis +


• ive categories

+ ?c%uired in immunocompetent patient

+ ?c%uired or reactivated in

immunodeficient patient

+ Ocular

+ @n pregnancy

+ Congenital


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&o!oplasmosis +


• ?c%uired in immunocompetent hosts

+ Only 7


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&o!oplasmosis 1

@mmunodeficients hosts

• Solid organ transplants#haematopeitic stem cell transplants + Either ac%uired infection from the

transplant# or reactivation of latentinfection in the recipient

+ >ulmonary# myocardial# neurologicinvolvement

• *@I + )eactivation of latent infection

+ Encephalitis# pneumonitis#chorioretinitis


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Ocular to!oplasmosis in

immunocompetent hosts

• One of the most common causes of

uveitis.

• @f infection ac%uired in utero# tend to

present in ;nd K 3rd decades of life asrecurrences + bilateral disease# old

retinal scars# macular involvement#

severe disease

• @f ne2ly ac%uired infection# usually in th1

8th decades# unilateral involvement#

macula sparing# no old scars

&o!oplasmosis


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&o!oplasmosis +

in >regnancy

• 'argely asymptomatic for mother • &ransmission to fetus only 2ith

2omen 2ho ac%uire the infection

during gestation

• &ransmission ris6 increases as

gestation progresses

• Severity of infection in fetus

increases the earlier in gestation

transmission occurred


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Congenital to!oplasmosis

• Neonatal disease4 chorioretinitis#

blindness# epilepsy# retardation#

encephalitis# pneumonitis#

hydrocephalus# anemia# =aundice#rash# diarrhoea etc

• Subclinical

• )elapse $ se%uelae later in life


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&o!oplasmosis +

Diagnosis

• @solation of &o!oplasma gondii by

inoculating mice or tissue cell

cultures

• *istology $ microscopy CS#

amniotic fluid"

• >C)


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Serological Diagnosis

of Toxoplasmosis


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&o!oplasmosis +

&reatment

• 0ononucleosis syndrome inimmunocompetent individuals does notre%uire treatment

• @n immunodeficient hosts K ocularto!oplasmosis + )! pyrimethamine folicacid antagonist" J sulfadiazine J folinicacid

• @n pregnancy + spiramycin if diseaseearly in pregnancy9 other2ise if infectedafter 7L$< + pyrimethamine Jsulfadiazine J folinic acid


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)abies

• Neurotropic virus in the

)habdoviridae family# genus

'yssavirus

• M)abiesB + 'atin for MmadnessB#

MrabhasB + Sans6rit for MviolenceB#

MlyssaB + 5ree6 for madness

• (ullet1shaped virion containing

single# negatively stranded )N?


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)abies 1 Epidemiology

• Aorld2ide# e!cept for ?ntartica and a

fe2 island nations NZ# apan# &ai2an#

S2eden# Nor2ay# Spain# some

Carribean islands"• A*O estimates 3


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)abies 1 >athogenesis

• Centripetal spread of virus via peripheral

nerves to CNS

• >roliferation in CNS

• Cetrifugal spread via peripheral nervesto tissues

• Iiral shedding from sensory nerve

endings in oral mucosa result in highconcentration in saliva

• >robably causes neuronal dysfunction

rather than neuronal death

)abies +


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)abies +


• @ncubation from fe2 days to:7yrs. become ill 2ithin <days from e!posure

• &ypical viral prodrome# 2ithparaesthesias $ pain near e!posuresite

• ?cute neurologic syndrome 1urious encephalitic" vs. paralyticdumb" rabies. 'asts ;17 days

• Coma# then invariably death.

)abies +


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)abies +


• urious rabies Laralytic rabies L


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*ydrophobic spasm


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)abies 1 Diagnosis

• -sually clinically evident in the rightsetting

• Direct fluorescent antibody D?"

staining of s6in biopsy from nape ofnec6# above hairline

• )everse transcriptase1>C) to

detect rabies virus )N? from CSor saliva

• Serology +


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)abies 1 >revention

• >ree!posure prophyla!is +vaccination of animals# and ofpeople 2ith high ris6 of e!posure

eg. Iets"• >oste!posure treatment

+ Aoundcare4 soap# povidone1iodinevirucidal"

+ )@5 rabies immunoglobulin" +infiltrate around 2ound

+ )abies vaccine on day


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*endra virus

• pathogenic zoonotic paromy!ovirus

• single1stranded# )N? genome

• causes the formation of syncytia ininfected Iero cells

• named after the suburb inQueensland# ?ustralia 2here the 7st

outbrea6 occurred• flying fo!es are the probable

reservoirs. &hey have subclinicalinfection.

*endra virus +


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*endra virus epidemiology

Queensland"• 7 1 outbrea6 that 6illed 7horses and 7 human

• 7 + 7 human death. O2ned ;

horses that died the year before.

• ;


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*endra virus Clinicopathology

K &reatment• Self1limited influenza1li6e syndrome• @nterstitial pneumonia due to

necrotizing alveolitis 1 lung

congestion# edema# andhemorrhage

• ?septic meningitis and encephalitis

• Currently no specific treatment#although ribavirin has in vitroacitivity

Ni h i


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Nipah virus

• 7L174 7


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Thank You

Z


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Z

• Z

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