INDIVIDUAL TASK

Learning Unit 1
Kucing Muntaber
BLOK 19 HEWAN KESAYANGAN 2

Compiled by :
Name
NIM
Group:

: Annisa Wening M. Putri

: 12/333996/KH/7453
:6

FACULTY OF VETERINARY MEDICINE

UNIVERSITY OF GADJAH MADA
YOGYAKARTA
2015
I.

LEARNING OBJECTIVE

1. Explain the Infectious Gastrointestinal Disease in Small Animals Caused by

Parasites.
A. Diagnosis
B. Treatment
C. Prevention
D. Pathogenesis
E. Clinical Sign
II.

DISCUSSION
1. Toxoplasmosis
A. Diagnosis

Figure 1. (left); Toxoplasma gondii in tachyzoites for, (right) oocyst of T.gondii

(source : web.uconn.edu)
The term toxoplasmosis is reserved to describe the clinical or
pathological disease caused by Toxoplasma gondii and T. gondii infection for
an asymptomatic primary infection or persistence of the parasite in tissues
(chronic or latent infection) (Montoya, 2002).
The diagnosis of toxoplasmosis is typically made by serologic testing.
A test that measures immunoglobulin G (IgG) is used to determine if a person
has been infected. If it is necessary to try to estimate the time of infection,
which is of particular importance for pregnant women, a test which measures
immunoglobulin M (IgM) is also used along with other tests such as an avidity
test. Diagnosis can be made by direct observation of the parasite in stained
tissue sections, cerebrospinal fluid (CSF), or other biopsy material. These
techniques are used less frequently because of the difficulty of obtaining these
specimens. Parasites can also be isolated from blood or other body fluids (for
example, CSF) but this process can be difficult and requires considerable time.

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Molecular techniques that can detect the parasite's DNA in the amniotic fluid
can be useful in cases of possible mother-to-child (congenital) transmission.
Ocular disease is diagnosed based on the appearance of the lesions in the eye,
symptoms, course of disease, and often serologic testing (Anonim, 2015).
When considering toxoplasmosis in the differential diagnosis of a patients
illness, it is important to keep in mind that emphasis should not be placed on
whether the patient has or has not been exposed to cats. Transmission of
parasites essentially occurs without knowledge of the patient and may be
unrelated to direct exposure to a cat (e.g., by ingestion of vegetables or water
contaminated with oocysts or ingestion of undercooked meat contaminated
with cysts). On the other hand, patients with an indoor cat that is fed only
cooked food is not at risk of acquiring the infection from that cat. Serologic
investigation of a cat to establish whether it is a potential source of the
infection should be discouraged; the prevalence of T. gondii antibodies among
cats in a given locale is usually similar to their prevalence in humans.
Seropositivity in the cat does not predict shedding of oocysts. The diagnosis of
T. gondii infection or toxoplasmosis may be established by serologic tests,
amplification of specific nucleic acid sequences (i.e., polymerase chain
reaction [PCR]), histologic demonstration of the parasite and/or its antigens
(i.e., immunoperoxidase stain), or by isolation of the organism. Other rarely
used methods include demonstration of antigenemia and antigen in serum and
body fluids, a toxoplasmin skin test, and antigen-specific lymphocyte
transformation (Montoya, 2002).
1) Serological Test
The use of serologic tests for demonstration of specific antibody to T.
gondii is the initial and primary method of diagnosis. Different serologic
tests often measure different antibodies that possess unique patterns of rise
and fall with time after infection. A panel of tests (the Toxoplasma
Serological Profile [TSP]) consisting of the Sabin-Feldman dye test (DT),
double sandwich IgM ELISA, IgA ELISA, IgE ELISA , and AC/ HS test
has been used successfully by our group to determine if serologic test
results are more likely consistent with infection acquired in the recent or
more distant past. The AC/HS test is interpreted as previously described by
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comparing IgG titers obtained with formalin-fixed tachyzoites (HS

antigen) with those obtained with acetone-fixed tachyzoites (AC antigen)
(Montoya, 2002).
Table 1. Serological test for the demonstration of Toxoplasma
gondii antibodies in cat based on Bowman (2002) :

Current interpretation of results in the TSP at the Toxoplasma Serology

Laboratory at the Palo Alto Medical Foundation Research Institute (TSLPAMFRI) is as follows: Sera that are positive in the DT, negative in the
IgM, IgA, and IgE ELISAs, and reveal a chronic pattern in the AC/HS test
are typically found in patients infected in the most distant past. The
combination of high titers in the DT, positive IgM, IgA, and IgE ELISAs,
and an acute pattern in the AC/HS test is highly suggestive of a recently
acquired infection. In contrast, the presence of positive DT and IgM
ELISA results but a negative, low-positive, or equivocal result in the IgA
and IgE ELISAs and an equivocal pattern in the AC/HS test is more
difficult to interpret. In the latter setting, a follow-up sample is usually
obtained, the 2 samples are run in parallel, and the serologic test titer
results are compared. If the titers obtained in the 2 samples do not change
significantly, the infection is most likely to have been acquired in the
distant past. In contrast, significant changes (rise or decline) detected in the
titers of the 2 samples are considered to be suggestive of a recently
acquired infection (Montoya, 2002).
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IgG antibodies usually appear within 12 weeks of acquisition of the

infection, peak within 12 months, decline at various rates, and usually
persist for life. An IgM test is still used by most laboratories to determine
if a patient has been infected recently or in the distant past, and because of
the hurdles posed in interpreting a positive IgM test result, confirmatory
testing should always be performed. In patients with recently acquired
primary infection, T. gondii specific IgM antibodies are detected initially,
and in most cases, these titers become negative within a few months.
However, in some patients, positive T. gondiispecific IgM titers can still
be observed during the chronic phase of infection. IgA antibodies. IgA
antibodies may be detected in sera of acutely infected adults and
congenitally infected infants by use of ELISA or ISAGA. As is true for
IgM antibodies to the parasite, IgA antibodies may persist for many
months or more than a year (Montoya, 2002).
2) PCR
PCR amplification for detection of T. gondii DNA in body fluids and
tissues has successfully been used to diagnose congenital, ocular, and
cerebral and disseminated toxoplasmosis also has enabled detection of T.
gondii DNA in brain tissue, cerebrospinal fluid (CSF), vitreous and
aqueous fluids, bronchoalveolar lavage (BAL) fluid, and blood in patients
with AIDS (Montoya, 2002).
3) Histological Diagnosis

Figure 2. (left) Pseudocyts in Liver, (right) Encysted parasite in skeletal

muscle showing internal bradyzoite nuclei separated by clear internal
septations. (Hematoxylin and Eosin stain; 100) (Makhija, 2012)
The immunoperoxidase technique, which uses antisera to T. gondii, has
proven both sensitive and specific: It has been used successfully to
demonstrate the presence of the parasite in the central nervous system
(CNS) of AIDS patients [27]. The immunoperoxidase method is applicable
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to unfixed or formalin- fixed paraffin-embedded tissue sections [27]. A

rapid, technically simple, and under-used method is the detection of T.
gondii in air-dried, Wright-Giemsastained slides of centrifuged (e.g.,
cytocentrifuge) sediment of CSF or of brain aspirate or in impression
smears of biopsy tissue (Montoya, 2002).

Figure 3. Light microscopy of feline enterocytes infected with

bradyzoites of T.gondii stained by Giemsa. (A) two hours of infection
(1:5 parasite/host cells ratio). The lytic cycle is induced with rossete
formation (arrowhead); (B) six hours of infection (1:10 parasite/host
cells ratio), showing cyst-like structures (arrowhead); (C) six hours of
infection (1:20 parasite/host cells ratio). Parasitophorus vacuole
containing syncytial-like forms (Bar = 20 ) (source :
microbewiki.kenyon.edu)

Figure 4. Toxoplasma gondii tachyzoites (horizontal arrow) and a cyst

(vertical arrow) in the pancreatic lymph node (immunohistochemical
staining) of the catin this report (source : www.jsava.co.za)
B. Treatment
Table 2. Treatment of Feline Toxoplasmosis based on Bowman (2002):

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C. Prevention
1) For Cats
a. Avoid feeding cats with skin/meat that rarely used to prevent the
oocyst transmition.
b. Keep the cat at home, prevent the access to hunt the other animals.
c. Vaccination, prevent the oocyst spreading.
2) For Human
a. Not eat the skin or meat that rarely consumed.
b. Wash the hand with soap after preparing the meat.
c. Using gloves while gardening or washing the hand after gardening.
d. Wash all fruit and vegetables before it consumed.
e. Change the litter box regularly, at least after 24 hours. Pregnant woman
and Immunosupressive individual are prohibited to change the litter
box due to the transmition.
(Bowman, 2002)
D. Pathogenesis
The development of Toxoplasma gondii through 2 cycles, asexual
cycle and sexual cycle. The sexual cycle (enteroephitelial) take place in the
definitive host, that is cats and other animals of a kind, while the asexual
cycle take place in the intermediate host (human, warm blooded animals,
aves). The asexual cycle start when cyst or infectif oocyst acidentally
swallowed by the definitive host ( Cat eat the mouse that already infected by
T.gondii first form or third form). The pre paten periode of the bradizoit form
(second form) is 3-10 days, meanwhile takizoit (first form) need 5-10 days and
in the third form to becoming the oocyst need 24 hours or more.
The sexual stadium start with the development of merozoit to form the
macrogamet and microgamert inside the intestinum epithelium, both gametes
get the fertilisation process, zigot formed, zigot become oocyst. The oocyst
enter the intestinal lumen and come out from the body by the feses. After 2-3
days on temperature 24C its become infectif or sporulated.

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Figure 5. Life Cycle of Toxoplasma gondi. The only known definitive hosts for
Toxoplasma gondii are members of family Felidae (domestic cats and their relatives)
(source : web.uconn.edu)
The cycle outside intestinal celluler is the next phase of lifecycle, take
place outside the intestinal tissue of the definitive host, especially in the
intermediate host and this cycle happen at the same time as the cycle that take
place inside the intestinal epithelium of final host. After the peroral infection,
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takizoit developt endodyogeni in some kind cells vacuole. Accumulated inside

the cells that containing eight tachyzoit or more, this situation call pseudocyst.
If the pseudocyst broken, tachyzoit will attack the other cells and spread in the
entire body through the blood circulation and lymp. Parasitemia may occur
several times until the plasma antibody formed because of immune system.
Tachyzoit will be destroyed except for the one which already developed into
bradyzoit inside tissue cyst. Tissue cyst found faster on the 8th day after the
host got the first infection, its able to survive as long as host still alive. If the
immune system decreased, then bradyzoit will be released and forming the
new tachyzoit, so the infection repeated and the accute infection happen
(Soulsby, 1982; Levine, 1995)
2. Helminthiasis
2.1. Ancylostomiasis
A. Diagnosis
Site of infection : small intestine
Hosts : Dog, Cat and Fox
Spesies : Ancylostoma caninum (dog and fox), A. tubaeforme (cat), A.
braziliense (dog and cat) (Urquhart et al., 1996).

Figure 6. Ancylostoma caninum, buccal teeth (source :

medicine.academic.ru)
This depends on the clinical signs and history supplemented by
haematological faecal examination. High faecal worm egg counts are
valuable confirmation of diagnosis, but it should he noted that suckled
pups may show severe clinical signs before eggs are detected in the
faeces. Also, a few hookworm eggs in the faeces, although confirmatory
evidence of infection, do not necessarily indicate that an ailing dog is
suffering from hookworm disease.

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Figure 7. Ancylostoma egg found in the faeces, Ancylostoma spp. eggs

are 55 to 75 m by 34 to 47 m (source
:studyblue.com;www.cal.upenn.edu)
B. Treatment
Affected dogs should be treated with an antlhelmintic, such as
mebendazole, febendazole and nitroscanate, all of which will kill both
adult and developing intestina stages; several of the avermectins have
similar activity. If the disease is severe, it is advisable to give parenteral
iron and to ensure that the dog has a protein-rich diet. Young pups may
require a blood transfusion (Urquhart et al., 1996).
C. Prevention
A system of regular anthelmintic therapy and hygiene should be
adopted. Weaned pups and adult dogs should he treated every three
months. Pregnant bitches should be dosed at least once during pregnancy
and the nursing litters dosed at least twice, at 1-2 weeks of age and again 2
weeks later with a drug specifically recommended for use in pups. This
will also help to control ascarid. The perinatal transfer of both
Ancylostoma and Toxocara larvae may be reduced by the oral
administration of fenbendazole daily from 3 weeks before to 2 days after
whelping. Kennel floors should be free of crevices and dry and the
bedding should be disposed of daily (Urquhart et al., 1996).
D. Pathogenesis
Infection is by skin penetration or by ingestion, both methods being
equally successful. In percutaneous infection, larvae migrate via the blood
stream to the lungs where they moult to L4, in the bronchi and trachea,
and are then swallowed and pass to the small intestine where the final
moult occurs. If infection is by ingestion the larvae may either penetrate
the buccal mucosa and undergo the pulmonary migration described above
or pass direct to the intestine and develop to patency. Whichever route is
taken the prepatent period is 14-21 days. The worms are prolific egg

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layers and an infected dog may pass millions of eggs daily for several
weeks. This is essentially that of an acute or chronic haemorrhagic
anaemia. The disease is most commonly seen in dogs under one year old
and young pups, infected by the transmammary route, are particularly
susceptible due to their low iron reserves. Blood loss starts about the
eighth day of infection when the immature adult has developed the
toothed buccal capsule which enables it to grasp plugs of mucosa
containing arterioles. Each worm removes about 0.1 ml 01 blood daily and
in heavy infections of several hundred worms, pups quickly become
profoundly anaemic. In lighter infections, common in older dogs, the
anaemia is not so severe, as the marrow response is able to compensate for
a variable period. Ultimately however, the dog may become iron deficient
and develop a microcytic hypochromic anaemia. In previously sensitized
dogs, skin reactions such as moist cezema and ulceration at the sites of
perculaneous infcction occur especially affecting the interdigital skin
(Urquhart et al., 1996).
E. Clinical Sign
In acute infections, there is anaemia and lassitude and occasionally
respiratory embarrassment. In suckled pups the anaemia is oItcn severe
and is accompanied by diarrhoea which may contain blood and mucus.
Respiratory signs may be due to larval damage in the lungs or to the
anoxic effects of anaemia. In more chronic infections, the animal is
usually underweight, the coat is poor, and there is loss of appetite and
perhaps pica. Inconsistently there are signs of respiratory embarrassment,
skin lesions and lameness (Urquhart et al., 1996).
2.2. Dipylidiasis
A. Diagnosis
Hosts: Dog and cat; rarely man
Intermediate hosts: Fleas (Cfenocephalides canis, C . felis and Pulex
irritans) and lice (Trichodectes canis).
Site: Small intestine; cysticercoid in fleas and lice
Species: Dipylidium caninum

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Figure 8. Dipylidium caninum and the egg(Urquhart et al., 1996).

Often the first indication of infection is the presence uf a segment on
the coat around the perineum. If the segment is freshly passed, preliminary
identification may be made on the elongate shape, and the double genital
organs which may be seen with a hand lens. If it is dried and distorted it
will be necessary to break it up with mounted needles in water, where the
egg packets are easily seen under the microscope, thus differentiatine lhe
segment from that of Taenia spp. Which contains only numerous single
onchospheres (Urquhart et al., 1996).
B. Treatment and Control
In Dipylidilum infection, treatment and control must be instituted
together, for it is clearly of no value to eliminate the adult tapeworm while
leaving a reservoir in the animal's ectoparasites. Hence, administration of
anthelmintics

such

as

nitroscanate

and praziquantel

should be

accompanied by the use of insecticides. It is also imperative that thc

animal's bedding and customary resting places should receive attenlion
with insecticides to eliminate the immature stages of the flea, which are
many times more numerous than the adult parasites feeding on the dog or
cat (Urquhart et al., 1996).
C. Pathogenesis and Clinical Sign
The newly passed segments are active, and can crawl about on the tail
region of the animal. The onchospheres are contained in egg packets or
capsules, each with about 20 eggs, and these are either expelled by the
active segment or released by its disintegration. After ingestion by the
intermediate host, the onchospheres travel to the abdominal cavity where
they develop into cysticercoids. All stages of the biting louse can ingest
onchospheres, but the adult flea, with its mouthparts adapted for piercing,
cannot do so, and infection is only acquired during the larval stage which
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has chewing mouthparts. Development in the louse, which is permanently

parasitic and therefore enjoys a warm habitat, takes about 30 days, but in
the flea larva and the developing adult in the cocoon, both of which are on
the ground, development may extend over several months. The final host
is infected by ingestion of the flea or louse containing the cysticercoids
and development tu patency, when the first gravid segments are shed,
takes about three weeks (Urquhart et al., 1996).
The adult is non-pathogenic and several hundreds can be tolerated
without clinical effect. They shed segments, which, as they crawl actively
from the anus, may cause some discomfort, and a useful sign of infection
is excessive grooming of the perineum. It has been suggested that infected
dogs form the habit of rubbing the anus along the floor, but impacted anal
glands are a more common cause of this behaviour (Urquhart et al., 1996).
2.3. Ascariasis
A. Diagnosis

Figure 9. (left) Ovum of Toxocara cati (90 x 75 ) and and ovum of

Ancylostoma caninum, (right) Toxocara cati (source : repository.unhas.ac.id)
The subglobular eggs, with thick, pitted shells, are easily recognized in
faeces . Only a tentative diagnosis is possible during the pulmonary phase
of heavy infections when the larvae are migrating, and is based on the
simultaneous appearance of pneumonic signs in a litter, often within two
weeks of birth. The egg production of the worms is so high that there is no
need to use flotation methods, and they are readily found in simple faecal
smears to which a drop of water has been added (Urquhart et al., 1996).

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Figure 10. Differentiation of Toxocara cati and Toxoascaris leonina

may be made on the shape of the cervical alae (Urquhart et al., 1996).
B. Treatment
The adult worms are easily removed by anthelmintic treatment. The
most popular drug used has been piperazine, although this is being
superseded by the benzimidazoles, fenbendazole and mebendazole and by
nitroscanate. A simple and frequently recommended regime for control of
toxocarosis in young dogs is as follows. All pups should be dosed at 2
weeks of age, and again 2-3 weeks later, to eliminate prenatally acquired
infection. It is also recommended that the bitch should be treated at the
same time as the pups. A further dose should be given to the pups at two
months old, to eliminate any infection acquired from the milk of the dam
or from any increase in faecal egg output by the dam in the weeks
following whelping. Newly purchased pups should be dosed twice at an
interval of 14 days. Since there are likely to be a few worms present, even
in adult dogs, in spite of the diversion of the majority of larvae to the
somatic tissues, it is recommended that adult dogs should be treated every
3-6 months throughout their lives (Urquhart et al., 1996).
C. Prevention
Since infection acquired during suckling, complete control would be
based on removal of kittens from the dam and artificial rearing. In most
cases, adequate control is achieved by early and repeatcd administration
of anthelmintics to kittcns along the lines recommended for T. canis in
pups. T.cati has been reported as a rare cause of visceral larva migrans in
man (Urquhart et al., 1996).
D. Pathogenesis
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Like T. canis, the lile cycle of T. cati is migratory when infection

occurs by ingestion of the L2, in the egg and non-migratory after
transmammary infection with L3, or after ingestion of a paratenic host.
However, unlike T. canis prenatal infection does not occur. The prepatent
period from egg infection is about eight weeks (Urquhart et al., 1996).
Because the majority of infections are acquired either in the milk of the
dam or by ingestion of paratenic hosts, there is no migratory phase and
any changes are usually confined to the intestine, showing as pot-belly,
diarrhoea, poor coat and failure to thrive (Urquhart et al., 1996).
E. Clinical Sign
In mild to moderate infections, there are no clinical signs during the
pulmonary phase of larval migration. The adults in the intestine may
cause pot-belly, with failure to thrive, and occasional diarrhoea. Entire
worms are sometimes vomited or passed in the faeces. The signs in
heavy infections during larval migration result from pulmonary damage
and include coughing, increased respiratory rate, and a frothy nasal
discharge. Most fatalitics from T. canis infection occur during the
pulmonary phase, and pups which have been heavily infected
transplacentally may die within a few days of birth. Nervous convulsions
have been attributed by some clinicians to toxocarosis,but there is still
some disagreement on whether the parasite can he implicated as a cause
of these signs (Urquhart et al., 1996).
BIBLIOGRAPHY
Anonim.2015.Parasites-Toxoplasmosis(Toxoplasma Infection).source : http://www.
cdc.gov/parasites/toxoplasmosis/diagnosis.html [27 August 2015]
Bowman, D.D., Hendrix, M.C., Lindsay, S.D., and Barr, C.S. 2002. Feline Clinical
Parasitology.Iowa: Blackwell Science Comp.
Levine., N.D. 1995. Protozoologi Veteriner. Gadjah Mada University Press, Yogyakarta.
Makhija, M.2012. Histological identification of muscular sarcocystis: A report of two
cases.Indian journal of Pathology and Microbiology
Montoya, J.G.2002.Laboratory Diagnosis of Toxoplasma gondii Infection and
Toxoplasmosis.JID Oxford Journal page :185
Soulsby, E. J. L.1982. Soulbey'sHelminths, Arthropods and Protozoa of Domestic
Animals, 7th ed.
Urquhart, G. M., Armour, J., Duncan, J. L., Dunn, A. M. & Jennings, F.
W.1996.Veterinary parasitology,2nd ed. Blackwell Science.

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Penentuan diagnosa didasarkan pada pemeriksaan serologik, dengan mengukur titer antibodi dari 2 spesime serum
yang diambil dengan jarak 2-3 minggu. Kenaikan yang mencolok, 4 kali atau lebih, menunjukkan adanya infeksi
aktif. Juga pengukuran IgM dalam uji imunoflouresens bila titernya tinggi (1:80) membuktikan adanya infeksi
aktif. Uji serologi lain yang dapat dilakukan meliputi uji aglutinasi dan uji komplemen, dan uji polimerase chai
reaction (PCR) dari cairan sumsum tulang.
Waktu dan Tempat Penelitian Penelitian dilakukan pada bulan Agustus 2014. Tempat
pengambilan feses, pengamatan dan pengambilan data pasien anjing penderita diare
dilakukan di Klinik Hewan Makassar. Pemeriksaan feses dilakukan di Laboratorium
Parasitologi Bagian Helmintologi Balai Besar Veteriner Maros. 3.2 Materi Penelitian 3.2.1
Bahan Bahan yang akan digunakan dalam penelitian ini adalah feses 2 gram, kapas, dan
formalin 10%, air, Gula atau garam jenuh, larutan Lugols Iodine atau Methylene Blue. 3.2.2
Alat Alat-alat yang digunakan dalam penelitian ini adalah kantong plastik, coolbox,
refrigerator, timbangan, object glass, cover glass, mikroskop, sentrifus, tabung plastik
sentrifus bertutup yang mempunyai skala ukuran volume 30 ml, saringan teh, pengaduk,
gelas ukur, pipet Pastuer, dan sendok pengaduk. 3.3 Metode Pengambilan Sampel
Pengambilan sampel feses dilakukan berdasarkan anjing penderita diare yang ada di Klinik
Hewan Makassar. Selanjutnya dilakukan identifikasi berdasarkan kriteria jenis diare,
kemudian dilakukan pemeriksaan laboratorium. Kriteria pengambilan sampel didasarkan
pada jenis feses anjing yang mengalami perubahan. Perubahan tersebut mencakup
beberapa hal, diantaranya : Frekuensi defekasi dalam sehari Volume feses Konsistensi
feses

warna feses

Bau feses

Material ikutan pada feses: darah, lendir, busa,

reruntuhan jaringan maupun cacing dewasa. Kriteria pengambilan sampel secara lebih
spesifik dipaparkan lebih jelas pada Lampiran 1. Pasien yang diambil sampel fesesnya
dilakukan pencatatan terhadap riwayat pembe

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Metode yang digunakan untuk penelitian ini adalah metode pemeriksaan klinis dan
laboratoris secara mikroskopis. Pada pemeriksaan laboratoris dilakukan metode apung dan
metode sedimentasi. Metode apung merupakan metode umum yang digunakan untuk
pemeriksaan parasit cacing dalam feses. Metode ini membutuhkan sentrifus dalam
prosedurnya. Sedangkan Metode sedimentasi mempunyai prinsip pemeriksaan yaitu
sampel diendapkan melalui proses sentrifugasi kemudian diperiksa dibawah mikroskop
dengan pembesaran 10x10. Metode sedimentasi ini juga membutuhkan alat sentrifus
untuk mengendapkan telur cacing ke dasar tabung maupun partikelpartikel lainnya yang
terdapat dalam sampel feses.

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www.capcvet.org

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This species has the most complex life cycle in the superfamily, with four
possible modes of infection. The basic form is typically ascaridoid, the
egg containing the L, being infective, at optimal tempcratures, four weeks
after being passed. After ingestion, and hatching in the small intestine, the
L, travel by the bloodstream via the liver to the lungs, where the second
moult occurs, the L, returning via the trachea to the intestine where the
final two moults take place

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