zoonoses and its classification on basis of types

Nabeel805998 419 views 128 slides Apr 02, 2024
Slide 1
Slide 1 of 128
Slide 1
1
Slide 2
2
Slide 3
3
Slide 4
4
Slide 5
5
Slide 6
6
Slide 7
7
Slide 8
8
Slide 9
9
Slide 10
10
Slide 11
11
Slide 12
12
Slide 13
13
Slide 14
14
Slide 15
15
Slide 16
16
Slide 17
17
Slide 18
18
Slide 19
19
Slide 20
20
Slide 21
21
Slide 22
22
Slide 23
23
Slide 24
24
Slide 25
25
Slide 26
26
Slide 27
27
Slide 28
28
Slide 29
29
Slide 30
30
Slide 31
31
Slide 32
32
Slide 33
33
Slide 34
34
Slide 35
35
Slide 36
36
Slide 37
37
Slide 38
38
Slide 39
39
Slide 40
40
Slide 41
41
Slide 42
42
Slide 43
43
Slide 44
44
Slide 45
45
Slide 46
46
Slide 47
47
Slide 48
48
Slide 49
49
Slide 50
50
Slide 51
51
Slide 52
52
Slide 53
53
Slide 54
54
Slide 55
55
Slide 56
56
Slide 57
57
Slide 58
58
Slide 59
59
Slide 60
60
Slide 61
61
Slide 62
62
Slide 63
63
Slide 64
64
Slide 65
65
Slide 66
66
Slide 67
67
Slide 68
68
Slide 69
69
Slide 70
70
Slide 71
71
Slide 72
72
Slide 73
73
Slide 74
74
Slide 75
75
Slide 76
76
Slide 77
77
Slide 78
78
Slide 79
79
Slide 80
80
Slide 81
81
Slide 82
82
Slide 83
83
Slide 84
84
Slide 85
85
Slide 86
86
Slide 87
87
Slide 88
88
Slide 89
89
Slide 90
90
Slide 91
91
Slide 92
92
Slide 93
93
Slide 94
94
Slide 95
95
Slide 96
96
Slide 97
97
Slide 98
98
Slide 99
99
Slide 100
100
Slide 101
101
Slide 102
102
Slide 103
103
Slide 104
104
Slide 105
105
Slide 106
106
Slide 107
107
Slide 108
108
Slide 109
109
Slide 110
110
Slide 111
111
Slide 112
112
Slide 113
113
Slide 114
114
Slide 115
115
Slide 116
116
Slide 117
117
Slide 118
118
Slide 119
119
Slide 120
120
Slide 121
121
Slide 122
122
Slide 123
123
Slide 124
124
Slide 125
125
Slide 126
126
Slide 127
127
Slide 128
128

About This Presentation

This presentation contains a compression data on the Zoonosis, its types and classification. Along with it aslo contains data on bacterial and viral diseases that are zoonotic. There are terminologies related to epidemiology.


Slide Content

Zoonosis and its
classification
Dr.Sidra Saher
Dept: Epidemiology and Public Health

Zoonosis
Zoonosis (singular) / Zoonoses (plural)
Zoon = animals
Noses = diseases
Infections or agents that are naturally transmitted
Animals Humans
Diseases and infections which are naturally transmitted between vertebrate
animals and humans

Classification of zoonosis
Etiological agents
Transmission cycle
Reservoir hosts

Classification based on Etiological
agents.
Bacterial
Ex. Brucellosis, leptospirosis, listeriosis, TB
Viral
Ex. Rabies, Dengue
Rickettsial
Ex. Rocky mountain spotted fever
Mycotic / Fungal
Ex. Dermatophytosis

Parasitic
Protozoan
Ex. Toxoplasmosis, Babesiosis, African Trypanosomiasis
Trematode / Fluke
Ex. Fascioliasis
Cestodes / Tapeworms
Ex. Cysticercosis, Hydatidosis
Nematodes / Roundworms
Ex. Trichinellosis

Classification based on Transmission
Cycle
Direct zoonoses (Orthozoonoses).
Zoonotic diseases are perpetuated in nature by a single
vertebrate species
Transmission is either by direct or indirect contact
Ex. Anthrax, Rabies, Tuberculosis, Brucellosis

Cyclozoonoses.
Zoonotic diseases require two or more vertebrate hosts to complete
transmission cycle of an infectious agent
Subdivided into 2 subtypes
Obligatory cyclozoonoses(Euzoonoses) -human is must for completion
of Life Cycle Ex. .Taenia solium, Taenia saginata
Non-Obligatory cyclozoonoses-human is accidentally invovledin
completion of Life cycle Ex. Hydatid disease, Toxoplasmosis

Metazoonoses(Pherozoonoses).
Both vertebrate and invertebrate species are involved in the transmission
of an infectious agent.
In invertebrate hosts, infectious agent may multiply, develop or remain
dormant.
Ex. Yellow fever, plague.

Saprozoonoses.
Zoonotic diseases require a non-animate substance for completion of life
cycle in addition to vertebrate or invertebrate host.
An infectious agent may multiply, develop or propogatein an inanimate
site.
Ex. Fungal infections

Classification based on Reservoir hosts
Anthrapozoonoses
These are diseases of domestic and wild animals which occur in nature
independent of man. Human beings get infected from animals in
unusual circumstances, through occupational contact or food .
Ex. Leptospirosis, Rift valley fever, rabies.

Zooanthroponoses
These are diseases which normally pass from human to other vertebrate
animals. Ex. Tuberculosis (Human type).
Amphixenoses
The agent can pass from man to animal and animal to man. Ex.
Streptococcosis, non-host specific Salmonellosis, Staphylococcosis

Thanks

Zoonoses terminologies

Infection
Entry and development or multiplication of an infectious agent in the
body of the host. Ex. bacterial, viral, parasitic, fungal infections.
Infestation
Lodgementand development of arthropodesor endoparasites on or in
the body. Ex. Ticks, mites, lice.

Carrier
Infected person or animal which harbours a specific infectious agent in
absence of clinical symptoms and serves as potential source of infection for
others.
Asymptomatic carrier are those who become infected but show no signs
and symptoms.Ex. TB, HIV
Incubatory carrier arethose who can transmit the agent during the
incubation period before the clinical illness begins. Ex. Common cold virus,
Measles
Convalescent carrier are those who have recovered from illness but
remain capable of transmitting to others. Ex. Typhoid, diarrhoea patients

Disease
A condition of a body, organ or part in which its functions are impaired or
affected.
Iatrogenic (physician induced ) disease
Any untoward consequence of a preventive, diagnostic or therapeutic
procedures that cause impairment or disability resulting from professional
activity of a physician or health related personnel.

Communicable disease
A disease resulting from infection or infestation capable of being directly
or indirectly transmitted to a new host or from the environment through any
vehicle.
Contagious disease
A disease that is transmitted by direct contact between an infected host
and a susceptible host. Ex. Fungal infections
Nosocomial infection
An infection acquired or contracted in a hospital or other health care
facility.

Notifiable disease
Occurrence of a disease that requires immediate reporting to the higher
health authority to take necessary action for preventing further spread.
Host
Animal or man which affords lodgment or penetration of an infectious
agent under natural conditions.
Definite/Definitive host
Animal or man in which infectious agent attains its maturity.

Intermediate host
Host which provides a medium for larval or asexual or sexual phase of life
cycle of an infectious agent.
Non-obligatory host
Animal or man which may accidentally or occasionally provide
nourishment to an infectious agent.
Obligate host
Host which is essentially required for growth and multiplication of
infectious agent, in absence of which it may die.

Epidemiology
Study of distribution and determinants of disease occurrence in the
population.
Epizootic
Epidemic in animal population.
Epornithic
Epidemic in bird population.
Eradication
Total removal or elimination of a disease or a etiological agent from a
region.

Exzootic
A disease that has been eliminated or stamped out from a country.
Antigenic shift
A sudden, major change in the antigenic structure of a virus, usually the result of genetic
mutation.
Phenotypic expression is altered
Results in pandemic
Ex. Influenza A virus
Antigenic drift
A gradual relatively minor change in the antigenicity of a strain periodically
Phenotypic expression is unaltered
Results in epidemics
Ex. Influenza B, C virus

Endemic
The constant presence of a disease or an infectious agent within a
geographical area without importation from outside.
Sporadic
Incidence at intervals of single or scattered cases of a disease.
Epidemic
Occurrence of a disease in a community clearly in excess of normal
expectation for that population based on past experience.

Pandemic
Diseases spread over wide geographical areas involving several species,
countries, and continents.
Prevalence
Total number of cases both old and new at a given time in a population.
Incidence
Frequency of occurrence of new cases of a particular disease in a
population.

Source
Any living or non-living object from which an infectious agent passes to a
susceptible host.
Reservoir
An animate or inanimate object on or in which an infectious agent usually
lives, multiplies and survives in such a manner that it can be transmitted to a
susceptible host.
Vector
An invertebrate host or arthropod transmits the infection by biting or by
depositing infective material on the skin or on food or other objects.

Vehicle
A non-living substance through which an infectious agent passes from the
source to the susceptible host.
Prevention
Measures to protect man or animal from disease.
Control
Measures to reduce incidence or prevalence of disease or infection in
man or animal.

Quarantine
Restraint placed upon the movement of man, animals, plants or goods
which are suspected of being carrier or vehicles of infection or of having been
exposed to infection.
Surveillance
Exercise of continuous scrutiny or watchfulness over the distribution and
spread of infections and related factors for effective control.

Transmission of zoonoses
Transmission cycles
Sylvatic cycle
propagates among wild animals, hunters and forest rangers or domestic
animals e.g. Monkey pox
Synanthropic cycle.
The pathogens occur and propagate in domestic animals via synanthropic
animals like rodents, birds and lizards
Man is often exposed to zoonotic diseases propagating in the synanthropic
cycle. e.g. Plague
Human cycle.
man to man cycle and can also pass from man to animals e.g. Human
tuberculosis

Modes of transmission
Direct
Direct contact. -direct contact between the source of infection and the
susceptible host. e.g. Leptospirosis, Pox, Dermatophytosis. Droplet infection:
sneezing, coughing or talking. e.g. Tuberculosis, common cold.
Contact with soil. e.g. Hookworm infection, tetanus.
Bite of an animal. e.g. Rabies.
Transplacental / vertical transmissionfrom mother to offspring. e.g.
Toxoplasmosis, Salmonella

Indirect
Vector-borne transmission.
Mechanical transmission. -infectious agent is mechanically transmitted -
no development or multiplication of an infectious agent on or within the
vector. e.g. Amoebiasis, Cholera.
Biological transmission. -infectious agent undergoes growth and
multiplication in vector

Biological transmission
Propagative type
The agent merely multiplies in the vector, but does grow. e.g. Plague
bacilli in rat fleas.
Cyclo-propagative type. The agent undergoes both growth and
multiplication in the vector. e.g. Malaria parasites in mosquitoes.
Cyclo-developmental type. The agent undergoes only development but
no multiplication. e.g. Microfilaria in mosquitoes.
Transovarian type. The agent is transmitted from one generation to other.
e.g. Tick borne encephalitis

Vehicle-borne transmission.
Transmission of an infectious agent through either water, food, blood,
serum and other biological products such as tissues and organs. -
Transmitted mechanically or biologically e.g.
Water -Hepatitis A virus,
Meat -Salmonellosis , Trichinella spiralis,
Milk -Tuberculosis, brucellosis,
Fish -Vibrio parahaemolyticus,
Blood -Hepatitis B virus,
Organ -Cytomegalovirus in kidney transplants

Air borne transmission
Droplet nuclei. -minute particles formed either by evaporation of cough or
in laboratory, slaughterhouse or autopsy room. -remain air borne for long
period of time and may be disseminated by air currents to different places.
e.g. Tuberculosis, Q-fever.
Dust. -larger droplets which are expelled during talking, coughing or
sneezing -settle down along with dust and cause air-borne transmission.
e.g. Streptococcal infection, fungal spores.

Fomite-borne infections.
Fomites include soil, clothes, towels, cups, glasses, spoons, door handles,
etc. e.g. typhoid fever, skin infections.
Unclean hands and fingers.
Most common mode of transmission e.g. Staphylococcosisand
streptococcosis, Salmonellosis, Colibacillosis.

BacterialZoonoses
Dr.MuhammadRizwan
Assistant Professor
Department of Clinical Sciences

Campylobacterioses
Etiology:
Campylobacterspp.C.jejuni,C.coli,C.lari,C.upsaliensis,
andC.hyointestinalis
Occurrence:
WorldwideandareinmanyEuropeancountries.
Thenaturalhabitatofthezoonoticspeciesisthe
gastrointestinaltractofvariousanimals.
minimalinfectivedoseisapproximately500bacteria
Transmission:
Ingestionofcontaminatedfood
contaminateddrinkingorsurfacewater
contactwithanimalexcreta
directlyfromhumantohuman

ClinicalManifestation:Inhuman
acuteenteritis,diarrhea,feverupto40°C,chills,
headache,muscleaches,nausea
Inanimalscausediarrhea,Mastitis,hepatitis,infertility
andabortion.
Diagnosis:
byculturefromstool,milk,bloodormaterialfrom
abortion.
PCRmethods
Resultsofserologicaltestshavenotbeensatisfactoryas
thereareover50differentserovarsofC.jejuni.
DifferentialDiagnosis:
Salmonella,Shigella,YersiniaandClostridium

Therapy:
Replacementoffluidandelectrolytesisofprime
importance
Antibioticse.gciprofloxacin,gentamicin
Prophylaxis:
Foodhygiene,cook thefood
Avoidanceofunpasteurizedmilk
properhygieneofdrinkingwater
immediatehandwashingwithsoapanddisinfectionafter
contactwithhumansoranimals

Glanders
Etiology:
Malleus(glanders,farcy)iscausedbyBurkholderiamallei,
characterizedbypustularskinlesion,multipleabscesses,necrosesin
respiratorytract,pneumonia,andsepsis.
Gramnegativerod
Occurrence:
Horses,donkeys,andmulesaretheanimalsmostsusceptibletoB.
mallei
thediseaseisstillseen inMongolia,China,India,Pakistan,Indonesia,
thePhilippineIraq,Iranetc.
Riskgroupsareveterinarian,horsedealers,riders,farmers,knackers
Potentialpathogenforbiologicalwarfare-specialBSLlevel
Publichealthprogramshaveeliminatedglandersinmanycountries

Transmission:
contactwithinfectedanimals,nasalsecretion,pus,
Canpenetratemucusmembraneorminuteskinlesions
Indirectlythroughfomites,suchasfood,litteretc.
Airbornetransmission
human-to-humantransmissionisrare
ClinicalManifestations
Incubationperiod1-5daysbutmaybecomechronic
high fever, chills, regionallymphadenitis pustules and
nodulesonskin,nose,lung,andotherorgans
Diagnosis:
Culturebypustules,pus,sputumandnasaldischarge
PCR
CFtestandELISA

DifferentialDiagnosis:
Melioidosis,Tuberculosis,Anthrax,Erysipelas,Smallpox,and
Syphilis
Therapy:
Replacementoffluidandelectrolytesisofprimeimportance
Antibioticse.gdoxycyclineortrimethoprimsulfamethoxazole
Treatmentofdiseasedorpossiblyinfectedanimalsisprohibited
inmanycountries
Prophylaxis:
Novaccinesorantisera
Fomiteshavetobedestroyedorthoroughlycleanedand
disinfected.
banonimportanimalsfromendemicareas
Nocontactwithinfectedanimals.

Leptospiroses
Leptospirosesareactutesystemicinfectionsofhumanandanimals
causedbyvariousserovarsofLeptospirainterrogans.
Etiology:
Leptospiraebacteriae.gL.canicola,L.hardjo,L.ictero-haemorrhagiae,L..Pomona
Leptospiraesaremotile,gram-negativespiral-shapedbacteriawithterminalhooks.
Occurrence:
widespectrumofhostsofincludinghumansand>180animalsspecises
Worldwideoccurrence
peakcasesinsummerandfall
Atriskareagriculturalworkers,vets,breeders,abbatoirworkers,butchers,cooks,
dogsowners,sewageworkers.
Transmission:
Portalofentryinhumansisusuallyskinlesionsfromprofessionalexposure,
mucusmembranes
Infectedanimalsexcretee.gurine,amnioticfluid,andmaterialsfromabortion
contaminated(e.g.,canal)water
Infectionviacontaminatedfoodstuffsisrare

⚫Clinical Manifestations:inhuman
fever ,chill anemia, bloody urine, hemorrhages, vomiting,
convulsions,nephritis,andhepatitiswithjaundice
nonproductivecough
Inanimalscausesagalactia,stillbirths,abortion,neonatal
weakness,infertility,equineuveitisandsameclinicalsignsasin
human
Incubationperiod5-14 days(range2-26 days)
Diagnosis:
History
Culturebysample
Microagglutinationtest
ELISA,PCR
⚫DifferentialDiagnosis:
influenza,rheumaticfever,streptococcaltonsillitis,and,
,malaria,dengue

Therapy:
Antibioticse.gceftriaxone,doxycycline
renalfailure,dialysisisdone
Diseasedanimalsaretreatedwithtetracyclineor
streptomycin.
Prophylaxis:
ratandmousecontrol
Vaccinationinanimals
Barefootwalkingandswimminginstagnantwaters
shouldbeavoidedinendemicareas
personalprotectionmeasurements

Listeriosis
Listeriosisisadiseaseofanimalsandhumans,usually
foodborneinhumans
Etiology:
Listeriamonocytogenes
Occurrence:
Listeriosisoccursworldwideinhumansandanimals.
Peakincidenceinhumanshown insummerandfallthaninwinter
inanimals,thereisapeakbetweenFebruaryandApril.
Transmission:
consumptionofcontaminatedfoodstuffs
Inhalation
Contactwithinfectedanimalsandsilage
conjunctivaeofcontacts

ClinicalManifestations:
Incubationperiodmayrangesfrom1-4weeks
Inhumanabortion,fever,encephalitis,Papulousand
pustulousskinlesionLiverabscesses,arthritisand
swellingoftheregionallymphnodes
InanimalscausesCerebrallisteriosis,prematuredelivery,
abortion,mastitis,gastroenteritis,andocularinfection
Diagnosis:
History
Culturebyblood,CSF,fecesorplacentaetc.
PCR
DifferentialDiagnosis:
Enteroviruses,staphylococci,Candida,and
cercariae,Haemophilusinfluenzae

Therapy:
antibioticsAmpicillinplusgentamicin
Replacementoffluidandelectrolytesisofprime
importance
Prophylaxis:
Generalhygienicmeasures
washingofrawvegetables
Avoidancefrominfectedsilage
Pregnantwomenandimmunocompromisedindividuals
shouldavoidcontactwithinfectedmaterial,rawfood
andvegetables,undercookedmeat,cheeses

plague
Oneoftheoldestandmostdangerouszoonoses,most
virulent,potentiallylethal.Threeclinicalforms,:bubonic,
septicemic,andpneumonicplague
Etiology:
Yersiniapestisbelongto Enterobacteriaceae.
Occurrence:
mainreservoirsarerats,groundandrocksquirrels
PresentinAsia,AfricaandU.S
EuropeandAustraliaarefreeofplagueatpresent.
Transmission:
thebiteoftheratflea
Human-to-humantransmission
Throughskinwoundorinhalation

ClinicalManifestations:
lymphadenopathy (bubo), hepatosplenomegaly, renal
failure,disseminatedintravascularcoagulation,cough,and
bloodyorpurulentpustules,carbunclesonskin
Diagnosis:
History
Culture
IF,CF
PCR
⚫DifferentialDiagnosis:
malaria,typhus,toxoplasmosis,brucellosis,catscratch
disease,typhoid,lymphnodetuberculosis

Therapy:
Theantibioticsofchoicearestreptomycin(2×1
g/dayi.m.)orgentamicin5mg/kg/dayin3doses
i.m.ori.v.
Prophylaxis:
Ratandinsectcontrolisimportantinurbanareas
dogandcatspopulationcontrol
Officialsurveillanceshouldbedone
novaccation

Mycobacterium
Etiology:
MycobacteriumTuberculosis,MycobacteriumBovis
Occurrence:
Worldwideinpeopleandinwildanddomesticatedmammals
Transmission:
Aerogenicroute
Oralroute
Directinjurytotheskinandmucousmembranes.
ClinicalManifestations
Highandsustainedfever,Nightsweats,Drycough,Malaise,
Spleenomagally,

BoneandJointTuberculosis,CutaneousTB,andTBof
anotherorgansofbodyinhumanandanimal.
Diagnosis:
Culturebysample
Tuberculintest
SerologicalMethods
History
PCR
Radiograph,

Therapy:
Thecombinationof4drugs
Rifampin,Ethambutol.Pyrazinamide,Isoniazid
Prophylaxis:
M.BovisBCGVaccination
Nocontactwithinfectedpersonoranimal
Usemask

Enterohemorrhagic
Escherichiacoli(EHEC)Infections
Etiology:
Escherichiacolistrains
Occurrence:
presentinAmericas,Europe,Asia,andAfrica,witha
peak incidencebetweenJuneandSeptember.
cattle,sheep,andgoatsarecarriersandexcretethese
strains
Transmission:
fecal-oralroute.
directcontactwithinfectedanimals

ClinicalManifestations:
⚫severeabdominalpainaccompaniedbyinitiallynon
bloodywaterydiarrhea,nauseaandvomiting.
⚫Feverisrare.
Diagnosis:
History
Culture
enzymeimmunoassay(EIA)
PCR
DifferentialDiagnosis:
Entamoebahistolytica,intussusception,ulcerativecolitis,
andileus,

Therapy.
Fluidandelectrolytereplacement
Antimicrobialtreatment
Prophylaxis:
generalhygienicmeasures
handwashingwithwaterandsoapbeforemealsandafter
contactwithanimals
Rawvegetablesmustbepeeledorthoroughlywashed.
Usecookedfoodandcleanwater

thanks

Viral Zoonoses
Dr. Muhammad Rizwan
Assistant Professor
Department of Clinical Sciences,
BZU Multan

VIRAL ZOONOSES
PART I
ARTHROPOD BORNE
2

VIRAL ZOONOSES
ZOONOTIC VIRUSES
TRANSMISSIBLE FROM ANIMALS
ARTHROPODS
often via a blood sucking arthropod
VERTEBRATES
bites, body fluids, inhalation etc

transmission
arthropod vectors (blood sucking)
Many arboviral diseases world wide
(hundreds)
4

ARBOVIRUSES
5
FAMILY ENVELOPE
yes
yes
no
SYMMETRY
icosahedral
helical
icosahedral
GENOME
ssRNA (+ve)
ssRNA (-ve)
segmented
dsRNA,
segmented

6
PREVENTION
SURVEILLANCE
VECTOR CONTROL
REPELLENTS
CLOTHING
TIMING OF ACTIVITY (OR
CANCELLATION)
VACCINE

7
ARBOVIRAL DISEASE
MANY DIFFERENT ARBOVIRUSES
CAUSE DISEASE
OFTEN SUB-CLINICAL

8
ARBOVIRAL DISEASE
INITIAL VIRAL REPLICATION
endothelial cells
macrophages/monocyte lineage
INTERFERON (RNA VIRUSES)
headache, fever, myalgia
VIREMIA
spread to target tissues, depending on
tropism of virus

9
RECOVERY
INTERFERON
CELL-MEDIATED IMMUNITY
ANTIBODY MAY PLAY A ROLE IN
PREVENTING SPREAD DURING
VIREMIC PHASE

10
DIAGNOSIS
Immunological techniques
RT-PCR for viral RNA

11
ARBOVIRUSES –ENCEPHALITIS
FAMILY DISTRIBUTION
FLAVIVIRIDAE
West Nile virus encephalitis North America, parts of Europe, parts of Africa
St Louis encephalitis North America
TOGAVIRIDAE
Eastern equine encephalitis East US, Canada
Western equine encephalitis West US, Canada, Mexico, Brazil
BUNYAVIRIDAE
California serogroup (La Crosse etc)North America
JAPANESE ENCEPHALITIS

West Nile and
Eastern Equine Encephalitis
Carriers –horses, birds and other animals
Transmission –mosquito bite
Vector-mosquito
Reservoir: birds
human, horse
dead end hosts
Symptoms (horses) –neurologic problems
Symptoms (people)
90% do not become ill
Illness in the geriatric and immunocompromised
Fever, signs of meningitis (neck pain, headache, neurologic
problems)
Treatment-supportive
Prognosis –fatal in a small number of people
Prevention –mosquito control, vaccinate horses

13
WEST NILE VIRUS
http://www.cdc.gov/ncidod/dvbid/westnile/cycle.htm
flavivirus
More rarely:
Acute flaccid paralysis
West Nile polio-like
paralysis
poliomyelitis -
inflammation spinal
cord

1450
1999
51
2000
52
2001
53
2002
54
2003
1999
2000
2001
2002
2003
50
1999
51
2000
52
2001
53
2002
54
2003
1999
2000
2001
2002
2003 50
1999
51
2000
52
2001
53
2002
54
2003
1999
2000
2001
2002
2003
50
1999
51
2000
52
2001
53
2002
54
2003
1999
2000
2001
2002
2003 50
1999
51
2000
52
2001
53
2002
54
2003
1999
2000
2001
2002
2003
50
1999
51
2000
52
2001
53
2002
54
2003
1999
2000
2001
2002
2003 50
1999
51
2000
52
2001
53
2002
54
2003
1999
2000
2001
2002
2003
50
1999
51
2000
52
2001
53
2002
54
2003
1999
2000
2001
2002
2003 50
1999
51
2000
52
2001
53
2002
54
2003
1999
2000
2001
2002
2003
50
1999
51
2000
52
2001
53
2002
54
2003
1999
2000
2001
2002
2003
flavivirusWest Nile virus

15
West Nile Virus
For every ~150 people infected
~30 mild symptoms
mild fever, headache, body ache, maybe rash
may never see physician, even if do, may not be diagnosed
~1 severe illness
e.g. encephalitis, meningitis, high fever, stiff neck,
stupor, disorientation, coma, tremors, convulsions,
muscle weakness
frequency of flaccid paralysis unknown, but much less than
frequency of encephalitis
flavivirus

16
Case fatality ratio:
Seen in all age groups but higher in
the elderly
the majority of cases of neuroinvasive
diseases and fatalities are over 50 yrs age
Transplant recipients may be at higher
risk
increased incidence of clinical disease
increased risk of severe disease
WEST NILE VIRUS
flavivirus

17
WEST NILE VIRUS
flavivirus
transmission:
Mosquito (vast majority of cases)
Blood transfusion (blood supply is now screened)
Organ donation

18
WEST NILE VIRUS
flavivirus

19
EASTERN EQUINE ENCEPHALITIS
Reservoir: birds
Vector: mosquito
Sentinels
horse,quail, turkey
Under 15yrs, over 50yrs
at higher risk
CFR ~35%
~5 cases/year av.
horses and humans
dead end hosts
CDC
togavirus

20
ARBOVIRUSES –FEVER AND
HEMORRHAGIC FEVER
FAMILY
FLAVIVIRIDAE
Dengue
Yellow fever
REOVIRIDAE
Colorado tick fever
DISTRIBUTION
World wide,
especially tropics
Africa, S. and C. America
North America
MAIN DISEASES
fever, hemorrhagic fever
hemorrhagic fever
fever

21
DENGUE FEVER
jungle cycle (monkeys-mosquitoes)
urban cycle (man-mosquitoes)
rapidly increasing disease in tropics
approx. 100-200 cases/yr in US due to import
occasional indigenous transmission
50-100 million cases per year worldwide
~900,000 cases in Central and S. America in 2007
flavivirus

23
Patients being treated for Dengue fever in a hospital
flavivirus

25
DENGUE FEVER
Fever (overlaps with viremic phase)
headache
retro-orbital pain
myalgia, arthralgia
severe joint and muscle pain
‘breakbone fever’
sometimes rash
may look like flu, measles, rubella
more rarely encephalitis
flavivirus

26
DENGUE HEMORRHAGIC FEVER/DENGUE SHOCK
SYNDROME
hemorrhages
plasma leakage
hemoconcentration
hypotension
circulatory failure
shock
flavivirus

27
DHF -petechiae
CDC
flavivirus

28
Dengue hemorrhagic fever -pleural effusion
CDC
Vaughn DW et al. J Infect Dis 1997; 176:322-30.

29
DENGUE HEMORRHAGIC
FEVER
immunopathological
4 serotypes (1, 2, 3, 4)
increase in areas in which all 4 circulate has led to more
cases DHF fever
maternal antibody
flavivirus

30
DENGUE HEMORRHAGIC
FEVER
do not give aspirin, ibuprofen
because of anticoagulant affects
(acetaminophen OK)
children more severe disease
CFR depends on rapid response
can be as low as 1%
flavivirus

31
(Time Dec 2007)

32

33

34
CDC
YELLOW FEVER
jungle and urban cycles
hemorrhages
degeneration liver, kidney,
heart
CFR 50%
Vaccine (live attenuated)
important to consider in travel
to areas with yellow fever
egg grown
contraindicated in immune
suppression
flavivirus
last yellow fever epidemic in US -1905

35
VIRAL ZOONOSES
PART I I
VERTEBRATE VECTORS

Definition
Zoonesesarediseasesofvertebrateanimalsthatcanbe
transmittedtoman:eitherdirectlyorindirectlythroughaninsect
vector.
Whenaninsectvectorisinvolved,thediseaseisalsoknownas
anarboviraldisease.
However,notallarboviraldiseasesarezoonosis:wherethe
transmissioncycletakesplaceexclusivelybetweeninsectvector
andhumane.g.dengueandurbanyellowfever.
Examplesofviralzoonosesthatcanbetransmittedtoman
directlyincluderabies,hantaviruses,lassaandebolafevers.

Viral Zoonoses
Rabies
Monkeypox
Avian flu
Hantavirus
Lymphochoriomeningitis

38
RODENT BORNE
FAMILYENVELOPE
yes
yes
SYMMETRY
helical
helical
GENOME
ssRNA
ambi-sense
segmented
ssRNA (-ve)
segmentedHantavirus genus
of Bunyaviridae

39
CDC
rodent urine
contaminated materials (aerosols)
respiratory tract
ROUTE OF INFECTION

40
ARENAVIRUS-ASSOCIATED
HEMORRHAGIC FEVERS
Lassa fever, Bolivian, Argentine, Venezuelan,
Brazilian hemorrhagic fever
A few recent cases in California of deaths
thought to be associated with an arenavirus
(Whitewater Arroyo Virus)
dehydration, hemoconcentration,
hemorrhage, shock, cardiovascular collapse
CFR 5-35%
CDC

Arenaviruses
Enveloped ssRNA viruses
virions 80-150nm in diameter
genome consists of 2 pieces of
ambisense ssRNA.
7-8 nm spikes protrude from the
envelope.
host cell ribosomes are usually seen
inside the outer membrane but play
no part in replication.
Members of arenaviruses include
Lassa fever, Junin and Macupo
viruses.
Lassa fever virus particles budding
from the surface of an infected cell.
(Source: CDC)

Lassa Fever
FoundpredominantlyinWestAfrica,in
particularNigeria,SierraLeoneand
Liberia.
Thenaturalreservoirismultimammaterat
(Mastomys)
Manmaygetinfectedthroughcontactwith
infectedurineandfaeces.
Mantomantransmissioncanoccur
throughinfectedbodilyfluidsandLassa
feverhadcausedwell-documented
nosocomialoutbreaks.
Mastomys

Clinical Manifestations
Incubation period of 3-5 days.
Insidious onset of non-specific symptoms such as fever, malaise,
myalgia and a sore throat.
Typical patchy or ulcerative pharyngeal lesions may be seen.
Severe cases may develop the following:
Myocarditis
Pneumonia
Encephalopathy
Haemorrhagic manifestations
Shock
The reported mortality rate for hospitalized cases of Lassa fever is 25%.
It carries a higher mortality in pregnant women.

Laboratory Diagnosis
Lassa fever virus is a Group 4 Pathogen. Laboratory diagnosis should only
be carried out in specialized centers.
DetectionofVirusAntigen-thepresenceofviralantigeninseracanbe
detectedbyEIA.ThepresenceofviralantigenprecedesthatofIgM.
Serology-IgMisdetectedbyEIA.Usingacombinationofantigenand
IgMantibodytests,itwasshownthatvirtuallyallLassavirus
infectionscanbediagnosedearly.
VirusIsolation-virusmaybeculturedfromblood,urineandthroat
washings.Rarelycarriedoutbecauseofsafetyconcerns.
RT-PCR-beingusedexperimentally.

Management and Prevention
Goodsupportivecareisessential.
Ribavirin-hadbeenshowntobeeffectiveagainstLassafeverwitha2
to3folddecreaseinmortalityinhighriskLassafeverpatients.Must
begivenearlyintheillness.
Hyperimmuneserum-theeffectsofhyperimmuneserumisstill
uncertainalthoughdramaticresultshavebeenreportedinanecdotal
casereports.
PostexposureProphylaxis-Thereisnoestablishedsafeprophylaxis.
Variouscombinationsofhyperimmuneimmunoglobulinand/ororal
ribavirinmaybeused.
Thereisnovaccineavailable,preventionofthediseasedependson
rodentcontrol.

46
LYMPHOCYTIC CHORIOMENINGITIS
VIRUS
Arenavirus
5% wild mice infected, without obvious disease
can also get from pet rodents such as hamsters
often sub-clinical
clinical cases:
flu like symptoms, plus nausea, vomiting
may get meningitis, and/or encepalitis and/or myelitis
usually recover, may be sequelae
problems for fetus (1
st-
2
nd
trimester)
has been associated with deaths in transplant recipients

LYMPHOCYTIC CHORIOMENINGITIS
VIRUS

Lymphochoriomeningitis (LCMV)
Carriers
Rodents -including pocket pets such as hamsters.
Symptoms in people
Mostly a problem in geriatric and immunocompromised
people.
The early phase -flu-like symptoms
The late phase –neurologic problems like rabies and rarely
death

49
HANTAVIRUSES -all have rodent vector
NAME
Korean HFRS
HFRS
Hantavirus
pulmonary
syndrome (HPS)
TYPE OF DISEASE
hemorrhagic fever with
renal syndrome (HFRS)
hemorrhagic fever with
renal syndrome
hantavirus pulmonary
syndrome
OCCURRENCE
S.E.Asia
Europe, Asia
North and South
America
Rodent vector -limited number species per virus
BUNYAVIRIDAE

Hantaviruses
Forms a separate genus in the
Bunyavirus family.
Unlike under bunyaviridae, its
transmission does not involve an
arthropod vector.
Enveloped ssRNA virus.
Virions 98nm in diameter with a
characteristic square grid-like
structure.
Genome consists of three RNA
segments: L, M, and S.

History
HaemorrhagicFeverwithRenalSyndrome(HFRS:later
renamedhantavirusdisease)firstcametotheattentionofthe
WestduringtheKoreanwarwhenover3000UNtroopswere
afflicted.
Ittranspiredthatthediseasewasnotnewandhadbeen
describedbytheChinese1000yearsearlier.
In1974,thecausativeagentwasisolatedfromtheKorean
StrippedfieldmiceandwascalledHantaanvirus.
In1995,anewdiseaseentitycalledhantaviruspulmonary
syndromewasdescribedinthe“fourcorners”regionofthe
U.S.

Some Subtypes of hantaviruses
associated with human disease
Hantaan,Porrogiaandrelatedviruses-ThisgroupisfoundinChina,
EasternRussia,andsomepartsofS.Europe.Itisresponsibleforthe
severeclassicaltypeofhantavirusdisease.Itiscarriedbystrippedfield
mice.(Apodemusagrarius)
Seoultype-associatedwithmoderatehantavirusdisease.Itiscarriedby
ratsandhaveaworldwidedistribution.IthasbeenidentifiedinChina,
Japan,WesternRussia,USAandS.America.
Puumalatype-mainlyfoundinScandinaviancountries,France,UKand
theWesternRussia.Itiscarriedbybankvoles(Clethrionomysglareolus)
andcausesmildhantavirusdisease(nephropathiaepidemica).
SinNombre-foundinmanypartsoftheUS,CanadaandMexico.Carried
bytheDeerMouse(Peromyscusmaniculatus)andcauseshantavirus
pulmonarysyndrome.

Rodent Carriers of Hantaviruses
Stripped field mouse (Apodemus agrarius)
Bank vole (Clethrionomys glareolus)
Deer Mouse (Peromyscus maniculatus)
Rat (Rattus)

Clinical Features of Hantavirus Disease
ThemultisystempathologyofHVDischaracterizedbydamageto
capillariesandsmallvesselwalls,resultinginvasodilationand
congestionwithhemorrhages.
Classically,hantavirusdiseaseconsistsof5distinctphases.These
phasesmaybeblurredinmoderateormildcases.
Febrilephase-abruptonsetofasevereflu-likeillnesswitha
erythematousrashafteranincubationperiodof2-3days.
Hypotensivephase-beginsatday5ofillness
Oliguricphase-beginsatday9ofillness.Thepatientmaydevelopacute
renalfailureandshock.Haemorrhagesareusuallyconfinedtopetechiae.
Themajorityofdeathsoccurduringthehypotensiveandoliguricphases
Diureticphase-thisoccursbetweendays12-14.
Convalescentphase-thismayrequireupto4months.

Hantavirus Pulmonary Syndrome (HPS)
More than 250 cases of HPS have been reported throughout North
and South America with a mortality rate of 50%
In common with classical HVD, HPS has a similar febrile phase.
However, the damage to the capillaries occur predominantly in the
lungs rather than the kidney.
Shock and cardiac complications may lead to death.
The majority of HPS cases are caused by the Sin Nombre virus.
The other cases are associated with a variety of other hantaviruses
e.g. New York and Black Creek Canal viruses.

Diagnosis
Serologicaldiagnosis-avarietyoftestsincludingIF,HAI,SRH,ELISAs
havebeendevelopedforthediagnosisofHVDandHPS.
Directdetectionofantigen-thisappearstobemoresensitivethan
serologytestsintheearlydiagnosisofthedisease.Thevirusantigencan
bedemonstratedinthebloodorurine.
RT-PCR-foundtoofgreatuseindiagnosinghantaviruspulmonary
syndrome.
Virusisolation-isolationofthevirusfromurineissuccessfulearlyin
hantavirusdisease.Isolationofthevirusfromthebloodislessconsistent.
SinNombrevirushasneverbeenisolatedfrompatientswithHPS.
Immunohistochemistry-usefulindiagnosingHPS.

Treatment and Prevention
TreatmentofHVDandHPSdependsmainlyonsupportive
measures.
Ribavirin-reportedtobeusefulifgivenearlyinthecourseof
hantavirusdisease.Itsefficacyisuncertaininhantavirus
pulmonarysyndrome.
Vaccination-aninactivatedvaccineisbeingtriedoutinChina.
Othercandidatevaccinesarebeingprepared.
RodentControl-controlmeasuresshouldbeaimedatreducing
contactbetweenhumansandrodents.

58
HANTAVIRUS-ASSOCIATED
HEMORRHAGIC FEVERS
Korean hemorrhagic fever with renal
syndrome (CFR ~7%)
other HFRS viral diseases around the
world
HPS (CFR ~36%)
CDC
Hantavirus genus

59
VECTOR UNKNOWN
HEMORRHAGIC FEVERS DUE TO EBOLA,
MARBURG VIRUSES

60
VECTOR UNKNOWN
FAMILYENVELOPE
yes
SYMMETRY
helical
GENOME
ssRNA (-ve)
Filoviruses may be up to ~14,000 nm long (rhabdoviruses
have similar diameter but are only ~180 nm long)

61
EBOLA AND MARBURG VIRUSES
hemorrhagic fevers
case fatality rate can be as high as 60-90%
for certain strains
occur in Africa, natural reservoir and vector
unknown
infections seen in laboratory monkeys, but these
do not seem to be natural host
bats may be a natural host
high viremia -strict barrier nursing

Rabies Virus
member of the Lyassavirus of the Rhabdoviridae.
ssRNA enveloped virus, characteristic bullet-shaped appearance
with 6-7 nm spike projections.
virion 130-240nm * 80nm
-ve stranded RNA codes for 5 proteins; G, M, N, L, S
Exceedingly wide range of hosts.
There are 5 other members of Lyassavirus : Mokola, Lagosbat,
Duvenhage, EBL-1, and EBL-2.
Duvenhage and EBL-2 have been associated with human rabies.

Rabies Virus
Structure of rabies virus (Source: CDC)
Rabies virus particles

Epidemiology
Rabiesisazoonosiswhichisprevalentinwildlife.Themain
animalsinvolveddiffersfromcontinenttocontinent.
Europe fox, bats
Middle East wolf, dog
Asia dog
Africa dog, mongoose, antelope
N America foxes, skunks, raccoons,
insectivorous bats
S America dog, vampire bats

Pathogenesis
Thecommonestmodeoftransmissioninmanisbythebiteofa
rabidanimal,usuallyadog.RabiesisanacuteinfectionoftheCNS
whichisalmostinvariablyfatal.
Followinginoculation,thevirusreplicatesinthestriatedor
connectivetissueatthesiteofinoculationandenterstheperipheral
nervesthroughtheneuromuscularjunction.
ItthenspreadstotheCNSintheendoneuriumoftheSchwanncells.
Terminally,thereiswidespreadCNSinvolvementbutfewneurons
infectedwiththevirusshowstructuralabnormalities.Thenatureof
theprofounddisorderisstillnotunderstood.

Laboratory Diagnosis
Histopathology-Negribodiesarepathognomonicofrabies.However,
Negribodiesareonlypresentin71%ofcases.
Rapidvirusantigendetection-inrecentyears,virusantigendetection
byIFhadbecomewidelyused.Cornealimpressionsorneckskin
biopsyaretaken.TheDirectFluorescentAntibodytest(DFA)is
commonlyused.
Viruscultivation-Themostdefinitivemeansofdiagnosisisbyvirus
cultivationfromsalivaandinfectedtissue.Cellculturesmaybeused
ormorecommonly,thespecimenisinoculatedintracerebrallyinto
infantmice.Becauseofthedifficultiesinvolved,thisisrarelyoffered
bydiagnosticlaboratories.
Serology-circulatingantibodiesappearslowlyinthecourseof
infectionbuttheyareusuallypresentbythetimeofonsetofclinical
symptoms.

Negri Body in neuron cell
(source: CDC)
Positive DFA test (Source: CDC
Diagnosis of Rabies

Management and Prevention
Pre-exposureprophylaxis-Inactivatedrabiesvaccinemaybe
administeredtopersonsatincreasedriskofbeingexposedtorabiese.g.
vets,animalhandlers,laboratoryworkersetc.
Post-exposureprophylaxis-Incasesofanimalbites,dogsandcatsina
rabiesendemicareashouldbeheldfor10daysforobservation.Ifsigns
develop,theyshouldbekilledandtheirtissue.
Wildanimalsarenotobservedbutifcaptured,theanimalshouldbe
killedandexamined.Theessentialcomponentsofpostexposure
prophylaxisarethelocaltreatmentofwoundsandactiveandpassive
immunization.
Oncerabiesisestablished,thereisnothingmuchthatcouldbedone
exceptintensivesupportivecare.Todate,only2personswithproven
rabieshavesurvived.

Postexposure Prophylaxis
Woundtreatment-surgicaldebridementshouldbecarriedout.
Experimentally,theincidenceofrabiesinanimalscanbereducedby
localtreatmentalone.
Passiveimmunization-humanrabiesimmunoglobulinaroundthearea
ofthewound;tobesupplementedwithani.m.dosetoconfershort
termprotection.
Activeimmunization-thehumandiploidcellvaccineisthebest
preparationavailable.Thevaccineisusuallyadministeredintothe
deltoidregion,and5dosesareusuallygiven.
Thereisconvincingevidencethatcombinedtreatmentwithrabies
immunoglobulinandactiveimmunizationismuchmoreeffectivethan
activeimmunizationalone.Equinerabiesimmunoglobulin(ERIG)is
availableinmanycountriesandisconsiderablycheaperthanHRIG.

Rabies Vaccines
The vaccines which are available for humans are present are inactivated whole
virus vaccines.
NervousTissuePreparatione.g.SempleVaccine-associatedwiththerare
complicationofdemyelinatingallergicencephalitis.
DuckEmbryoVaccine-thisvaccinestrainisgrowninembryonatedduck
eggsThisvaccinehasalowerriskofallergicencephalitisbutisconsiderably
lessimmunogenic.
HumanDiploidCellVaccine(HDCV)-thisiscurrentlythebestvaccine
availablewithanefficacyrateofnearly100%andrarelyanyseverereactions.
Howeveritisveryexpensive.
OtherCellcultureVaccines-becauseoftheexpenseofHDCV,othercell
culturevaccinesarebeingdevelopedfordevelopingcountries.However
recentdatasuggeststhatamuchreduceddoseofHDCVgivenintradermally
maybejustbeeffective.

Control of Rabies
Urban-caninerabiesaccountsformorethan99%ofallhuman
rabies.Controlmeasuresagainstcaninerabiesinclude;
straydogcontrol.
Vaccinationofdogs
quarantineofimportedanimals
Wildlife-thisismuchmoredifficulttocontrolthancanine
rabies.However,thereareon-goingtrialsinEuropewherebait
containingrabiesvaccineisgiventofoxes.Successhadbeen
reportedinSwitzerland.