ZOONOSES

Prof.Dr.dr.Efrida Warganegara,M.Kes.,Sp.MK
 Zoonoses
 Zoonoses  where a non-human vertebratae
(non-human animal) host acts as the Reservoir
of infection and human are involved only
incidentally
 Zoonosis  A disease that occurs primarily in
animals and is secondarily transmitted to
human by arthropods
 There are two classes transmitted arthropods
(call vectors) : 1) Insecta (Flies, mosquitoes,
fleas, lice, tru bugs) and 2) Arachinida (ticks,
mites)
 Zoonoses
 Often more severe in human than in the typical
animal host because the infection in human is
accidental

 A successful pathogen needs only to overcome

the host defences, long enough to multiply, and
then exit the host.

 In fact, a pathogen that completely overwhelms

the host defences actually at a disadvantages,
because it will likely kill the host.
 Zoonoses
 If the host dies, the pathogen loses an
exclusive source of nutritions and perhaps the
opportunity to be transmitted

 Pathogen and their hosts generally evolve

over time to a state of balanced pathogenicity.

 The pathogen becomes less virulent while the

host becomes less susceptible (resistant)
 Diseases of Animal (Zoonoses) that are Transmissible to Humans
Disease Transmission to Human Animal Resrvoir
Bacterial
Salmonellosis Ingestion of contaminated food or water Dogs, cats, farm animal, poultry,
reptiles, rodents
Brucellosis Drinking raw milk or direct contact with animal Dogs, farm animal, rodent
Tularemia Ingestion of or contact with contminated meat and Rodents and Rabbits
arthropod vectors
Anthrax Contact with contaminated animal hides or product Farm animals
Leptospirosis Contact with contaminated water Dogs, cats, wild rodent, farm animal
Bubonic plaque Rat flea, but human-to-human transmission in Rodents, rats
pneumonic plaque
Rickettsial disease Ticks, fleas, mites Wild Rodents
Q Fever Ingestion of raw mlk, inhalation of contaminated Farm animal (cattle, sheeps, goats)
dust, or contact with contaminated animal
Cat-scratch Fever Scratch or bite of cat Cats
Viral
Rabies Bite of animal or contact with infectious saliva or Dogs, cats, Farm animal and wild-
tissue, inhalation of aerosol animal,
Equine Encephalitis Horses to mosquitoes to humans Horses, domestic pigeons
Parasitic (helminths)
Echinococcosis Ingestion of eggs deposited on raw fruit Foxes, dogs, cats is principle host,
Trichinosis Ingestion of contaminated meat, usually pork Pigs and bears most are important
reservoir
 Zoonoses
Penyakit2nya : (* dibahas disini)
1. Anthrax
2. Brucellosis ;
3. Plaque ;
4. Tularemia.
5. Leptospirosis
6. Rabies


The others disease  below Tabel

1. Anthrax
 Anthrax
* Etiology is Family : Bacillaceae,
Genus : Bacillus,
Spesies : B. anthracis
* General Characteristic :
- 3 – 5 μm in length and 1.0 – 1,5 μm in width, non –
motile, facultative anaerob
- Spores, located in the center of the cell
(endospore), is produced only when the cell are
cultivated outside animal host tissue
- Coloni on blood agar or other laboratory media
have a rought texture (ground-glass appearance)
and serrated edges
 Anthrax
General Characteristic : (continued)
- As the colonies age, the edges give the
undulating bands and is reffered to as “caput
medusae”
- When the bacillus is cultivated in the presence of
elevated CO2, coloni becomes mucoid due to
capsule formation : polypeptides; virulent
- The vegetative cells in clinical specimen
occurs as non-sporeforming cells in short
chains. In culture, long chains of endospore-
forming rods and resemble a jointed rod.
 Anthrax
Virulence Factor
 To be virulent B. anthracis  must produce a capsule and
a protein exotoxin (not stimulate protective antibody)
 Polypeptides capsule – enables m.o. to evade
phagocytosis
 The protein exotoxin is a complex three protein factor :
1) edema factor (EF);
2) protective antigen (PA); and
3) lethal factor (LF)
 Separately the toxins are non-toxic, but act in
combinations of two do produce two disticnt toxic
respons : Edema in skin and lethality
 Anthrax
Pathogenesis and Epidemiology
 Anthrax – primarily a disease of animal : sheep,
horses, cattle
 Spores in the soil and vegetative  are ingestion or
inhaled
 They gain entrance to the subcutaneous tissues
through abraded skin or mucosa
 Spores germinate in tissue – the vegetative produce
an exotoxin that, in combination with the capsule,
inhibits phagocytosis
 If bacilli reach lymph and bloodstream  fatal
 Anthrax
Clinical Manifestation :
 In human the disease is considered an occupational
disease.
1) Inhalation of anthrax spores can cause Wool
Sorters’s disease  Pulmonary anthrax
The inhaled spores settled in the respiratory tract
 producing local hemorrhaging and edema
2) Septicemia sometimes occurs, leading to
meningitis
3) in underdeveloped countries – contaminated
meats are sold  gastrointstinal anthrax
4) The most common form of the disease in humans 
cutaneus anthrax  “Malignant pustule”
 Anthrax
Clinical Manifestation (continued):
CUTANEUS ANTHRAX (“Malignant pustule”)
 Incubation periode : 2 - 5 hr, infect to person who
working in the farm and the others
 Spora enter the skin  12 – 36 jam germination in
tissue  vegetative  causes edema gelatinosa &
kongesti  papula erythema  vesikel  pustula 
necrotic ulcus  to lymph node  blood circulation 
fatal septicemia
 Erhytema papule, after 7-10 day will produce black
ulcer, it surrounded edema, its called “Central Black
Eschar”  Sign by : edema, lymphangitis, fever,
lympadenopathy, weakness, headache, meningitis
 Anthrax
Pulmonary anthrax
 Incubation periode : 6 weeks, its called ”wool
sorters disease”
 Infection because of the spora inhalated to
respiratory system
 Mechanism : Inhalation of spore (from dust, wool,
skin)  multiplication in lung  lymph node 
hemorrhage and edema
 Clinical Manifestation : mediastinitis hemoragik ,
pneumoni hemoragik syok, meningitis septicemia,
sepsis  death, hemorrhagic lung edema
 Anthrax
Gastrointestinal Anthrax
 Rare, primary infectie of intestine,
formation of gangrene
 Sign : Colic abdominal, vomitus, with
bloody diare.
 Can caused by consumption from the
infected meat from animal infection 
or by hematogen from pulmonary &
cutaneus anthrax
 Anthrax
Diagnostic Laboratory
 Specimen : exudate, pus, blood, sputum
 Gram staining : bacilli Gram (+), from clinical
specimen : non-sporeforming cells in short chain,
in cultur : long chains of endospore-forming rods
 Vegetative cells are easily stained with ordinary
laboratory dyes. The M’Fadyean stain is used to
detect capsule, but the latter can be detected by
fluoresence antibody as well
 Blood Agar : colony white grey, non-hemolitik,
appear like ground glass appereance). In Semi Solid
agar : non motile
 Anthrax
Some of recommended procedure for identification of
bacillus :
1. Culture specimen on sheep blood agar or selctive
medium when highly contaminated specimen
2. Culture (ad 1) in a bicarbonate- and serum- containing
medium in the presence of 5% carbondioxide 
determine the presence of the capsule
3. Determine the presence of toxin by using antitoxin 
positive reaction confirms B. anthracis
4. Determine the susceptibility to penicillin  B. anthracis
susceptible to penicillin,other bacilli are resistant
5. Determine the susceptibility to gamma phage  B.
anthracis sensitive
 Anthrax
Treatment and Prevention:
 Drug of choice : Penicillin, but streptomycin,
tetracyclin, erythromycin also effective
 Treatmen before appearance bacteriemia is
important because antibiotic not effective against
the toxin
 The most effective control program is vaccination of
cattle, cremation or burial with quicklime of infected
animal, and restricted movement of livestock,
Contol of disease in human, whose occupation may
be predisposing factor, is provided by immunization
with toxoid, and decontamination cloth and others
with autoclave
2. Brucellosis
 Brucellosis
 Brucellosis  often called Undulant Fever or Malta
Fever  are chronic disease in animal and human
 Etiology : Brucella sp. (discovered by Dr. David Bruce)
1. Brucella abortus – infect cattle
2. Brucella melitensis – ingect goats and sheeps
3. Brucella suis – infect pig/swine
4. Brucella canis – infect dog
 Brucella are facultative intracellular parasit, small,
Gram-negative rod /coccobacillary in shape, non-
motile, strict aerobic that require complex
nutritional media for cultivation
 Brucellosis
Sign and Symptom :
 Usually start gradually , sign & symptom
are vague
 Typically :mild fever, sweating, weakness,
aches and pain, enlarged lymph nodes,
and depression
 The recurrence of fevers over weeks or
months in some cases  undulant fever
 Brucellosis
Pathogenesis and Epidemiology :
 Brucella penetrate : mucous membrane GIT, ingestion of
unpasteurized milk, TR (droplet) or breaks in the skin 
and not persist long at the site of entry and  are
ingested by neutrophyl  are disseminated via the
lymphatic and settle in regional lymph node.
 The bacilli reproduce in neutrophyils and later lyse them.
 The released bacteria at this stage may be destroyed by
phagocytes, or they may overcome host defences
 If they overcome host defences, they can transport within
macrophage via the blood vessels to many areas in the
body.
 Brucellosis
Pathogenesis and Epidemiology (continued) :
 The bacilli localized in tissue (liver, bone, splein, or the heart,
kidneys, and other part of the body) where granulomas (similar
in TBC) are produce.
 Viable bacilli may persist for several month in the granulomas,
giving rise to accute or chronic symptom.
 For this reason the incubation period  may be very long
 The accute stage appears approximately one or two weeks
after infection  characterized fever and enlargement of the
lymph node, spleen, and liver. Body temperature during accute
phase 101-104o F and may continue for several weeks with
intermittent remission (undulant fever). About 80% recovery
spontaneously during the accute stage
 Brucellosis
Pathogenesis and Epidemiology (continued) :
 The chronic state is generally associated with the
hypersensitivity in which there are swelling of the joints
and persistence of a low-grade fever.
 Inflamation of spinal vertebrae (spondylitis) resulting in
severe back pain is a common complication of
brucellosis, particularly in older man
 The mortality rate is low and death is generally due to
endocarditis.
 Serious, rare complication is bone infection
(osteomyelitis)
 Brucellosis
Laboratory Diagnosis :
 Diagnosis is difficult because the disease is
commonly chronic and is accompanied by fever and
few symptoms.
 The m.o. are best recovered from the blood during
the fever stage. Blood culture often become
negative after the first few weeks of infection
because of the serum antibodies
 Culture and isolation can made from blood, abscess
and tissue samples. Cultured on tryptose agar or
brucella agar in 2-10% CO2
 Brucellosis
Laboratory Diagnosis (continued):
 Coloni (non-hemolytic) should be Gram stained 
Gram (-) coccobacilli, ferment lactose or glucose (-),
obligate aerob
 Are oxidase-positive are test for agglutination in
Brucella antiserum – these test define the genus
Brucella
 Brucelosis, is more commonly diagnosed
serologically, either by a four fold rise in serum
agglutination test titer over several weeks or a single
titer of at least 160 : 1 in a person with compatible
clinical manifestation
 Brucellosis
Treatment and Prevention:
 Because of the presence of brucella within host cells,
effective treatment is often difficult
 Brucellae are sussceptible to ampicillin, streptomycin,
and tetracyclin (first choice in treatment).
 Treatment is the best  during the accute stage of the
disease; During chronic sthage  unsatisfactory and
relapse are common; recommended WHO  include
six-week course of doxycycline and rifampin
 Prevention – Vaccination to cattle and for human
prevent from contact to sick animal
3. Tularemia
 TULAREMIA
 Tularemia is a disease of Rodent,
particularly rabbits (mayor reservoir of
infection), and is transmissible to humans
 The most important species that causes
Tularemia  Genus Francisella  species
Francisella tularensis (relates to Tulare
county California, where the disease was
first described)
 TULAREMIA
General Charcteristics :
 F. tularensis is a Gram (-), non-motile
bacillus that can produce a capsule in vivo
 F. tularensis species are facultative
intracelullar paracites, highly pleomorphic
in cultur and can resemble filamentous,
coccal, or bacillary form.
 Need cyctein or thioglycolate in medium for
maximum growth
 TULAREMIA
Sign and Symptom :
 Depend on how the agent enters the body through /by:
1) Direct contact with infected animals - minor cuts and
scratch in the skin
2) Handling or ingesting contaminated meat
3) bite of infected insect vectors arthropoda (ticks)
4) Inhalation of contaminated aerosol
 Typically, sign and symptom appear 2 to 5 days after the
person is bitten by an infected tick or insect or handles
an infected wild animal
 The characteristic sign is an ulcer that develops at the
site where the m.o. enters the body
 TULAREMIA
Sign and Symptom (continued):
 Regional lymph nodes enlarge, and fever, chills, and
achiness occur.
 Sign and symptom usually clear in 1 to 4 weeks, but
sometimes they last for months
 If the m.o. is inhaled or infect the lung from the blood
stream, pneumonia may occur.
 Sign and symptom include a dry cough and pain
beneath the sternum, a result of enlarged lymph node
 Tularemia pneumonia, although rare, is more serious
and has a mortality rate as high as 30% if untreat
 TULAREMIA
Pathogenesis and Epidemiology:
 The incubation periode is from 2 to 10 days and is coupled with
fever and headache
 F. tularensis enters through breaks in the skin or mucous
membranes and is carried to the regional lymph nodes, which
became large and terder.
 The nodes may become filled with pus and drain spontaneously
 The m.o. sread to other parts of the body (spleen, liver, lung) via
the lymphatics & blood vessels, where they produce granuloma
 F. tularensis is ingested by phagocytic cells and grow within
them
 Cell mediated immunity effectively rids the host of this infection
 Even without treatment, over 90% of infected people survive
 TULAREMIA
Pathogenesis and Epidemiology:
 Manifestasi tularemia (continued):
1) Ulceroglandular Tularemia – contact abraded skin
with infected animal tissue) –primary lesion : on
hand, arm,becomes ulcerated in 6 to 8 days.
During this period there will be fever and
involvement of local lymph node. The lesions
may be take 4 to 7 weeks to heal
2) Oculo-glandular Tularemia – accidental
contamination of the eye  which there is
ulceration of the conjuctiva
 TULAREMIA
Pathogenesis and Epidemiology:
Manifestasi tularemia (continued):
3) Pneumonic Tularemia – most severe form –
usually contracted through contaminated
aerosols. If left untreated, this clinical type of
tularemia can be fatal to 30% of the persons
infected
 Recovery from all three form of tularemia confers
permanent immunity
 TULAREMIA
Laboratory Diagnosis :
 The risk of infection by F.tularensis to
laboratory personel is very high
 Consequently, tularemia is diagnosed on the
basis of clinical finding, immunoserological
methods, and the patient’s history of recent
animal or tick exposure
 In addition, it is very difficult to isolate this
fastidious organism
 TULAREMIA
Laboratory Diagnosis (continued) :
 Culture : specimen from local lesion, regional
lymph node, sputum, or conjuctival scraping
can be perform using media rich in cystine.
 The most popular medium : blood-cystine-
dextrose agar
 Coloni appear about 3 to 5 days after
incubation of the specimen and are minute and
transparent
 TULAREMIA
Laboratory Diagnosis (continued) :
 Direct or indirect fluorescent antibody techniques
 best tools for rapid & specific identification of
bacilli in exudates, tissue section and so on
 Serodiagnosis  using an agglutination test on the
patient’s serum.
 The test result becomes positive about 10 to 14 dys
after infection
 The titers rises significantly at 3 weeks after
infection
 TULAREMIA
Treatment and Prevention :
 Streptomycin – most effective drug in the treament of
tularemia
 Chloramphenicol and tetracyclin  can use in treatment
 Relaps are more comon when tetracyclin and
chlaramphenicol are used because they fail to penetrate
the phagocytose, where the bacilli may be located
 If precautions are taken, labor. personels are at minimal
risk of incurring infection
 An attenuated vaccine is available for use by labor.
personels who are continually in contact with potentially
infected animal
4. Plaque
 Plaque (“Black Death”)
Causatic agent : Yersinia pestis
 Like other enterobacteriaceae  facultative anaerob, Gram
(-)rod, non-motile and grow best at 28oC, bipolar granule,
produce capsul in animal tissue
 M.O resemble a safety pin when stained with certain dyes
because the end of the bacterium stain more intensely than
the midldle
 Y.pestis harboured by rodent and transmitted to human by
insect vector e.g. rat flea
 Infection can also occur by direct contact infected animal
tissue. Insecticide have controlled the vectors responsible for
transmission
 Plaque (“Black Death”)
Pathogenesis :
 Rat flea pickup bacillus by bitting an infected rodent
 Y. pestis form biofilm in the digestive tract of infected
fleas, often blocking the tract  starves the flea  it
will try to feed again  causes bacteria regurgitated
into bite wound as the flea attempt to feed
 Even fleas that do not have an obstructed digestive
tract can transmit m.o. because they discharge
bacterial cells in the their saliva/feces, and these can
then be introduced into human tissue when a person
scratches the flea bite
 Plaque (“Black Death”)
Pathogenesis (continued) :
 From the site of flea bite – m.o. migrate to regional
lymph node (temporal, inguinal)  lymph node
enlargement  call Buboes  Bubonic Plaque
 M.o. are phagocytes by mononuclear cells and then
acquired antiphagocytic factor (include capsule as
well as Antigens V and W)  proliferate freely. If
proliferating in the lymph node enter the
circulation call septicemic plaque  they can infect
several different organ
 Plaque (“Black Death”)
Pathogenesis (continued) :
 Rare, bacilli infect the lung  pneumonic plaque 
producing massive hemorrhages  from the lung,
bacille can enter bloodstream
 Toxaemia caused by LPS Endotoxin of Y. pestis is the
principal causes of death
 Incubation periode Bubonic plaque : 2-6 days. Fever
and vomiting are frequent symptom of infection
 Inguinal and femoral nodes are enlarged in about
50% patient, axillary and cervical nodes less
frequently involved
 Plaque (“Black Death”)
Pathogenesis (continued) :
 Incubation periode Pneumonic plaque (aquired by
inhalation in respiration secretion from an infected patient
or animal) is 1-3 days
 Sputum becomes mucoid and profuse and may even be
bloody
 Untreated pneumonic palque result in death within 36m
to 48 hours
 A person with pneumonic plaque (10-12%) can
transmitted the disease to other in respiratory droplet.
M.O. acquired this way are already fully virulent and,
there fore, are especially dengerous
 Plaque (“Black Death”)
Epidemiology :
 Plaque is pimarily disease of rodent (endemic),
transmitted from animal to animal or animal to
human by infected fleas
 The main reservoir : rat, rabbit, dog and cat
 Species fleas able to transmit plaque, and the fleas
can remain infectious for a year or more
 Epidemic of pneumonic plaque in human are
caused by respiratory droplets by coughing
pneumonic plaque patient
 Plaque (“Black Death”)
Treatment and Prevention :
 Effective with Gentamicin, ciprofloxacin, or docycycline,
especially if given within 24 hours of the onset of sign and
symptoms
 Between 50-80% people with bubonic plaque die if not treated
 Mortality rate for untreat pneumonic plaque is almost 100%
 Plaque epidemic can be prevented by rat control and must be
combined with use insecticides
 There is no vaccine for plaque, but vaccine genetic engineering are
being evaluated.
 tetracyclin can be given as preventive for someone exposed to
plaque and useful controlling epidemic because its immediate
effect
Leptospirosis / Weil Disease
 Sole sources of infection are diseased rodent and
domestic animal (pigs)
 Classification : Family Leptospiraceae, species : L.biflexa
(apthogenic Leptospira) and L.interrogans (pathogenic).
 Kharacteristic : Spirochaetta- spiral rod (10-20 um long,
0,1-0,2 um thick), No flagella, their motile from rotating
motions of the cell corpus
 visualizatin : dark field or phase contract microscopic,
can be grown in invitro cultures in special cultures
medium.
 Most important serogroup is Icterohemorrhagiae
 Pathogenesis and Clinical picture
 Invade human through microinjuries in the skin or intact
conjuctival mucosa
 No sign of inflamation in evidence at the portal entry
 M.O. Spread to all parts of the body (including CNS) –
hematogenously
 Leptospirosis is actually a generalized vasculitis – m.o.
damage mainly the endothelial cell of the capillaries 
leading to greater permeability and hemorrhage and
interrupting O2 supply to the tissue.
 Milder course : Anicteric Leptospirosis; severe clinical
picture : Icteric Leptospirosis (Weil Disease)
 Pathogenesis and Clinical picture
 Both types Leptospirosis are characteristic :
fever with chills, headache, and myalgias that
set in after an incubation period of 7 – 12 days.
 Initial septic stage of the diasease last 3-7 days
(mild, aseptic meningitis) and then fpllowed by
the second (Immune stage), which last from 4-
30 days (hepatis and renal dysfunction,
extensive hemorrhaging, cardiovasculer
symptom)
Diagnosis,Therapy, Epidemioloy and Prevention

 Diagnosis : In Cultur from : Blood, LCS, Urine or

organ biopsies – incubated in special medium, 27-
3oc, 3-4 weeks.
 A microscopic cheeck (dark field) is carried out
every week to see if any leptospirae are
proliferating.
 Serologically : lysis-agglutination reaction with
specific test sera. For laboratorium diagnosis is an
antibody assay (AB produce after the first week of
the infection are detected in patient serum)
 Therapy, Epidemioloy and Prevention

 Therapy : the agent of choice is penicillin G

 Epidemiology : Zoonotic infection, the most important
source : Rodent and domestic animal
 The animal excrete the pathogen with urine  show little
resistance to drying out  infection only occur because
contact with a moist milieu contaminated with urine
 The person most at risk are Farmers, Butchers, Sewage
treatmen worker, and zoo staff.
 Prevention : mainly avoiding contact with material
containing the pathogen, control of Muridae rodent and
succesfful treatment of domestic livestock.
RHABDOVIRUS
Disease : Rabies  CNS inflammation
Spread by infected animal-bite.
Viral characteristic

A. Virus structure :
•Rhabdovirus : rode /round  75 X 180 nm.
•Glycoproteins cover p = 10 nm.
•Genome : single stranded RNA ; MW 4,6 X 106
•Have RNA polymerase
B. Reaction against physical & chemical substance :
- Resistant in t = 4C in several weeks.
- Inactivation by CO2.
- † : UV, in t 50C an hour, lipid solvent
(ether, 0,1% Sodium deoxycholic), trypsin,
detergent & extreme pH
C. Antigen characteristic:
Only 1 serotype but the strain can different,
based on :
- Species
- Geographic
- The differentiation on nucleoprotein &
glycoprotein
D. Animal susceptibility & Virus growing :
- Wide susceptibility host  all animal
poikilothermic & human could be infected.
- Virus : CNS, saliva, urine, lymph, milk & blood.

- Strain :
1. Long incubation period strain (21-60 days)
inclusion bodies in cytoplasm

2. Short incubation period strain (4-6 days) 

hasn’t inclusion bodies.
 CLINICAL APPEARANCE
 Rabies primary animal disease  human, through

1. Infected-animal bite
2. Contact with infected-salivary animal
 Incubation period 1- 6 weeks
The sign divided into 4 phases :
1. Prodormal phase: fever, malaise, anorexia, headache,
nausea & vomiting
2. Sensory phase : Lacrimation, hallucination, muscle rigidity.

3. Excitement phase : photophobia , sound, & water.

4. Paralytic phase : ascending muscle paralytic

 Laboratory Diagnosis
A. Microscopic:
• Immunofluorescensi : rabies hamster antisera
• Brain or cornea impression.
• Pathognomonic : negri bodies(+) in muscle /MS
B. Virus isolation:
• Infected tissue (saliva)  inoculate to mouse intra cerebral.
• (+) : Leg flaccid paralyzed, encephalytic & death.
• CNS’s mouse examination Negri bodies & rabies Ag
C. Serology :
- Ab test against rabies : IF, CF or Nt test.
- Ab : (+) in human / animal along sick.

D. Animal observation:
1. Suspected animal rabies  killed 
tissue examination.
2. Other animal rabies possibility  stalled
& observed about 10 days.
3. If sign (+)  killed & tissue exam.
Immunity & Preventing

Rabies preventing pathophysiology through vaccine:

1. Virus replication in muscle closed from inoculation
site  virus enough to cause infection of CNS.

2. Giving vaccine / immunogenic substance promptly 

depress virus replication & prohibit invasion to
CNS.

3. Action of passive ab :
a. inoculated infected virus & virus decrease
b. to give enough time to vaccine to stimulate
active AB production to prohibit virus entering
to CNS.
Vaccine type :

1. Human diploid cell vaccine(HDCV)

2. Rabies vaccine absorption (RVA)

3. Neural tissue vaccine (NTV)

4. Dock embryo vaccine (DEV)

5. Attenuated living vaccine

Terima Kasih