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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Bartonella henselae –
Diagnosis
• Culture
+ Slo21gro2ing# lo2 sensitivity
• *istopathology
+ Aarthin1Starry silver stain
• >C)
• Serology + immunofluorescenceassays and enzyme
immunoassays
Bartonella henselae
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Bartonella henselae –
&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 +
Clinical 0anifestations
• ive categories
+ ?c%uired in immunocompetent patient
+ ?c%uired or reactivated in
immunodeficient patient
+ Ocular
+ @n pregnancy
+ Congenital
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&o!oplasmosis +
Clinical 0anifestations
• ?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 +
Clinical 0anifestations
• @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 +
Clinical 0anifestations
• 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
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