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TROPICAL INFECTIOUS

DISEASES – E.C. SPIROCHETES

Efrida Warganegara
SPIROCHETES - Overview
 SPIROCHETE – are long, slender, motile, flexible,
undulating, Gram-negtive bacilli that have
characteristic corkscrew or helical shape
 Depending on the species, they can be aerobic,
anaerobic, or facultative anaerobic. Some species are
free-living, and some are part of the normal flora of
human and animals.
 Individual cell too small to visualized by direct light
microscopy; can be seen with dark ground
illumination, or other Silver Impregnation or
immunofluoresencent staining.
SPIROCHETES – structural features
 Haveunique structure that is responsible for motility
 Spirochetes has a central protoplasmic cylinder bounded by a
plasma membrane and a typical gram-negative cell wall.
 Unlike other bacilli, this cylinder is enveloped by an outer sheat
composed of glycosaminoglycans.
 Between the cell wall and the outer sheath are located multiple
periplasmic flagella that do not protrude from the cell but are
oriented axially. Bundles of these endoflagella (axial fillament)
span the entire length of the cell and are anchored at both ends.
These axial periplasmic flagella rotate like the external flagella of
other motile bacteria, propelling the cell in a corkscrew-lika
manner
SPIROCHETES – structural features
 Spirochete that are important human patogen are
confined to three genera :
1) Treponema (T. pallidum - syphilis) STD; T.
pertenue –Yaws and T. carateum – pinta)
non-STD
2) Borrelia (B.burgdorferi - :Lyme disease;
B. recurrentis – Relapsing fever); and
3) Leptospira (L. interrogans – Leptospirosis)
 Transmission Spirochates : very susceptible to heat and
drying, so successfully transmission depends on very
close contact.
 Yaws and Pinta spread by direct contact from infected
skin lesions, no animal reservoir.
LEPTOSPIROSIS –
Leptospira interrogans

Efrida Warganegara
AETIOLOGY AND TRANSMISSION
 Leptospirosis are tightly coiled spirochaetes, 5-15
um long
 Active rotational movement and have 2 flagella
-like axial filaments
 Best seen by darkfield microscopy – because not
very well stained by dyes
 L. interrogans causes disease Leptospirosis, a
slender aerobic Gram negative spirochaetes with
question-mark like hooked ends. There are more
than 250 antigenic types of this species.
AETIOLOGY AND TRANSMISSION
 This spesies ingects mammals as rats, causing
chronic kidneys infection with excretion of
large numbers of bacteria in urine
 Bacteria are soon killed on drying, heating,
exposure to detergents or desinfectans
 They remain viable for several weeks in
stagnant alkaline water or wet soil.
 Human are infected by ingestion of or
exposure to contaminated water or food
AETIOLOGY AND TRANSMISSION

 Bacteria– by motility – enter through


breaks in skin or mucosae, so that infection
can be acquired by swimming, working or
playing in contaminatedwater

 Bacteria
are excreted in human urine but
person to person transmission is rare
LEPTOSPIROSIS – SIGN AND SYMPTOMS
 Leptospirosis is mainly a disease of animals, but
it can be passed to human.
 The causative bacterium enters the body
through a mucous membrane or wound and is
then carried to the urinary system by the blood
stream
 Leptospirosisinfections are often
asymptomatic, when sign and symptom do
occur, they begin after an incubation period
average 10 days (range 2 to 30 days)
LEPTOSPIROSIS – SIGN AND
SYMPTOMS
 Inmild cases, most common, symptom are
flulike, and include the sudden development of
headache, spiking fever, chills, muscle pain,
bloodshot eyes in the first (septicemia) phase,
then 1-3 days of improvement : heart, brain,
liver, and kidney damage in the second
(immune) phase
LEPTOSPIROSIS - PATHOGENESIS
 The bacteria penetrate mucous membranes or breaks
in the skin, multiply in the bloodstream, and are
carried to all parts of the body.
 Multiplication
in liver – hepatitis, jaudiceand
hemorrhage; in kidney – uremia and bacteriuria; in
CSF and humor aquos – aseptic meningitis; in eye –
conyuctival and scleral hemorrhage
 Septicemiaphase : severe pain with penetration of
body tissues, but little or no tissue damage.
LEPTOSPIROSIS - PATHOGENESIS
 Immune phase : damage to cells that line small
blood vessel and clotting of blood. Causes
severe damage to the liver, kidney, heart, brain,
and others organ
 The clinical picture depend to some extent on
the particular type of leptospire
 Weill’sDisease – severe form with
haemorrhagic complication and kidney and liver
failure – occurs in only 5-10% of patients ill
with leptospirosis
LEPTOSPIROSIS - EPIDEMIOLOGY
 Leptospirosis is a zoonosis and man is an un-
natural or ‘end’ host and does not transmit the
infection further.

 Worldwide distribution. Wide range of animal


hosts chronically excrete the bacteria in their
urine, causing contamination of natural waters
and soils. Organisms remain infectious under
warm, moist, neutral or alkaline conditions for
long periodes of time
DIAGNOSIS, TREATMENT AND
PREVENTION
 There is often a history of exposure
 Bactera can be isolated from blood, CSF, and
urine
 Rise in agglutination antibody can be
demonstrated
 Treatment : various antibacterial (Penicillin and
tetracyclin ) medications useful in treatment of
leptospirosis, but only if given early (a day or
two of onset of llness ) in the disease
DIAGNOSIS, TREATMENT AND
PREVENTION

 Measures for prevention include rodent


control, protective clothing and prophylactic
penicillin after cuts and abrasions in those at
risk
 Prevention : avoiding contact with animal
urine. Vaccine prevent disease in domestic
animals, may not urinary carriage.
Tetracycline antibiotics preventive in
epidemics. Doxycycline will prevent disease
in those exposed to infection
YAWS
– Treponema pertenue

Efrida Warganegara
YAWS – Treponema pertenue
 Yaws (frambesia tropica, polypapilloma tropicum) is
a tropical infection of the skin, bones and joints,
caused by T.pertenue
 Transmission : is spread by direct contact (non STD)
with the fluid from a lesion of an infected person.
 The disease is most common among children, who
spread it by playing together
 Sign and Symptom : disease begin with a round,
hard swelling of the skin, 2-5 cm in diameters. The
center may break open and form ulcer. This initial
skin lesion typically heals after 3-6 months.
YAWS – Treponema pertenue
 After week to years, joints and bones may become
painfull, fatique may develop, and new skin lesions may
appears. The skin of the palms of the hands and the
soles of the feet may thick and brek open. The bones
(nose) may become misshapen. After 5 years or more
large areas of skin death with subsequent scarring may
occur.
 Prevention : by curing those who have the disease
thereby decreasing the risk of transmission. Where the,
treating the entire community disease is effective.
Improving cleanliness and sanitation will also decrease
spread.
YAWS – Treponema pertenue

 Treatment is with antibiotics (azithromycin by


mouth; and benzathine penicillin by injection).
Withous treatment, physical deformites occurs in
10% of cases
 Epidemiology : about three quarters of people
affected are children under 15 years of age, with the
greatest incidence in children 6-1 years old.
Therefore,children are the main reservoir of infecton.
Because T.pertenue is temperatur and humidity
dependent, yaws is found in humid tropical region in
south america, Africa, Asia and Oceania
TREPONEMA PALLIDUM
 Dibahas pada penyakit akibat hubungan seksual
BACILLUS ANTHRACIS
A. KARAKTERISTIK UMUM
Ukuran : P : 3 – 5 um, L : 1 - 1,5 um
Koloni :
- Pd agar darah : putih abu-abu, bulat, permukaan
tdk rata, bentuk “medusa head”, ”ground
glass appereance”, non motile, non hemolisis.
- Pd agar tegak : mirip pohon cemara terbalik
Spora :
- endospora terletak ditengah & berbentuk elips
diantara basil yang bergerak,
- resisten thdp (perubahan lingkungan, pemanasan,
disenfektan kimia),
- hidup lama dlm tanah kering.
Vegetatif : di jaringan yg terinfeksi, rantai tampak lebih
pendek, simpai jelas, spora tdk terbentuk.
Zoonosis : dari hewan ternak ke manusia.
Hewan : sapi, kambing, domba, babi, kuda dsb.
Sumber penularan : feses, urine, saliva yg mengandung
spora Bacillus anthracis
Produk hewan yang terkontaminasi spora antrax baik itu
kulit, bulu, rambut, wool maupun tulang hanya dpt
disterilkan dngn autoclave.
B. PATOGENESIS
 Patogen utama genus bacillus
 Manusia terinfeksi dari hewan ternak
 Cara penularan:

 Luka pd kulit dan selaput lendir


Anthrax cutaneus
 Melalui gigitan vektor (nyamuk dan lalat)
Anthrax cutaneus
 Inhalasi pernafasan Pulmonary anthrax
 Konsumsi daging yg terkontaminasi
Anthrax gastrointestinal
Faktor virulensi
1. Exotoksin :
- kompleks protein – karbohidrat
atau protein saja
- dipengaruhi plasmid, kalau plasmid
hilang toxin tidak diproduksi
- terdiri dari:
- PA (antigen protektif),
- EF (faktor edema),
- LF (faktor letal).
Respon toxic yg sering ditemui :
edema kulit dan menimbulkan
kematian.
2. Simpai/Kapsul :
- mukoid,
- polipeptida (D-asam
glutamat),
- BM tinggi,
- antipagositik,
- tdk imunologik.
C. GEJALA KLINIS
Pada manusia kuman anthrax dapat
menyebabkan:
Anthrax cutaneus
 95% kasus anthrax di AS, inkubasi : 2 - 5
hr
 Disebut jg ”malignant pustule”
 Pd peternak dan pekerja di rumah
pemotongan hewan
Mekanisme :
- Spora masuk 12 – 36 jam germinasi di jaringan
pertumbuhan vegetatif menyebabkan
edema gelatinosa & kongesti papula erhytema
vesikel pustula ulkus nekrotik menyebar
ke KGB ke sirkulasi darah septikemik fatal

Erhytema papule setelah 7-10 hr akan membetuk


luka menghitam yang dikelilingi edema disebut
juga “Central Black Eschar”

Ditandai : edema, lymphangitis, lympadenopathy,


demam, malaise, sakit kepala, meningitis
Pulmonary anthrax
 5% kasus di AS, inkubasi : 6 minggu
 Disebut juga ”wool sorters disease”
 Infeksi terjadi karena inhalasi spora
ke organ pernapasan
 Mekanisme :

Inhalasi spora (dari debu, wool, bulu,


kulit) multiplikasi di paru-paru
ke KGB perdarahan & edema
Menyebabkan :
- mediastinitis hemoragik
- pneumoni hemoragik syok
- meningitis karena septikemia
(bakteriemia yg mencapai
selaput
otak
- sepsis kematian
- edema paru hemoragik
Anthrax gastrointestinal
 Jarang ditemukan
 Terutama infeksi usus halus karena
toxinnya yang membentuk gangren
 ditandai nyeri abdominal, vomitus,
disertai diare berdarah.
 disebabkan krn mengkonsumsi daging
hewan yg terinfeksi, juga karena adanya
hematogen dari pulmonary & cutaneus
anthrax
D. LABORATORIUM
 BP : cairan,pus dr lesi, darah, sputum
 Pewarnaan gram, tampak basil gram +, batang
besar, rantai panjang
 Pewarnaan fluorosensi umum digunakan pd sediaan
kering
 Biakan :
- Agar darah : koloni putih abu-abu, non-hemolitik,

tekstur kasar (ground glass appereance)


- Semi Solid : non motile
 BP disuntikkan intraperitoneal pd mencit / marmut,
yg berisi pus dari kuman menyebabkn mencit /
marmut akan mati
 Test serologi (ELISA) terdapat Ab anthrax pd serum
org yg imun
 Isolasi kultur pd medium bikarbonat untuk melihat
kapsul
 Test antitoksin anthrax positif
 B.anthracis sensitive penisilin
 B. anthracis akan lisis oleh γ-Bacteriophage
 Imunisasi anthrax berdasarkan percobaan
Louis Pasteur (1881). vaksinasinya
menggunakan basil hidup yg dilemahkan,
suspensi spora, antigen protektif dari filtrat
biakan.

E. PENGOBATAN

 Antibiotik : Penisilin (DOC), Streptomisin,


Tetrasiklin, Eritromisin, Klindamisin.
 Efektif sebelum terjadi bakteriemia, kurang
efektif bila toxinnya telah terbentuk.
F. PENCEGAHAN
 Kremasi dan mengubur bangkai hewan
 Vaksinasi hewan ternak
 Imunisasi orang yg beresiko terinfeksi krn
tempat dan pekerjaannya
 Dekontaminasi menggunakan autoclave
barang (sarung tangan / baju) yg digunakan
saat menangani hewan yg terinfeksi, juga
pd produk-produk hewan.
 Membatasi pergerakan hewan ternak.
TERIMA KASIH

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