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Urinary Tract Infection

( UTI )



Urinary Tract : Urethra to calyces, is lined with a sheet of

epithelium that is continuous with that of the skin is
potential pathway for entry of m.o. from the outside

UTI is arise by :
- the ascent of bacteria following colonization of
periurethral area by fecal organism
- hematogenous infection of the kidney much rarer

The main defences against UTIs are :

- the flow of urine
- the sloughing of epithelial cell to with bacteria may be
- immune defences (humoral and cellular) play little role

The Urinary Tract is one of the most common sites of
bacterial infection, particularly in females (the
mayority of patients are women)
10-20% of women have UTI at some time in their life by the
age of 30 years and have recurrent infection

Majority of infection are acute and short lived

contributed to a significant amount of morbidity in
Severe infection result in loss of renal function and
serious longterm sequele
In female : a distinction is made between cystitis,
urethritis, vaginitis but GU tract is continum and
the symptom often overlap


All portions of the urinery tract may be affected, but the

most common UTIs are infection of the bladder (cyctitis)
and the kidney (pyelonephritis).

Infection of the urethra alone or urethritis, is discussed with

the STD

Prostatic infection is usually considered as separated from

UTI, although chronic bacterial prostatitis may lead to
recurrent UTI

Renal abscesses mau occur as a result of ascending UTI or

of bacteremia, and pyelonephritis may also result from
bacteremia, without other involvement of the urinary trac

Classification of UTI, according location :

1.Upper UTI pyelum to ureter
2.Lower UTI vesica urinaria,


Other Classification :
1. according symptom
- Symptomatic UTI
- Asymptomatic UTI
2. According structure
- Complicated UTI
- Uncomplicated UTI

prostat and

Normal Flora
The Renal, Ureter to Bladder are

normally steril
Commonly in women and man, there is

m.o. in distal urehtra (1/3 distal)

M.o. in distal urethra are same with

flora normal in skin and perineum or



Access of infectious agents into the urinary

tract is nearly always by accent from the
urethra (blood-borne infections relatively
infrequent source and may be result in renal

Most asecending UTIs are caused by enteric or

skin bacteria most frequent are fecal bacteria,
frequent chlamydiae and candida albicans, and
rarely by virus, protozoa or worm.

Acquition and Aetiology

A. Bacteial Infection

Usually acquired by ascending route from

urtethra to bladder and may proceed to
kidney with the renal tissue to be infected

Less commonly infection may result from

hematogenous spread of an organism to the

Occasionaly : bacteria infecting UT invade the

circulation to cause septicemia

Acquition and Aetiology

A. Bacteial Infection cont.

Ascending infection of UTI most commonlly caused by:

1. Gram negative rod : E. coli
2. Other members of Enterobacteriaceae :

a) Proteus mirabilis associated with urinay stone

(produce urease act to urea, produce ammonia
causes urine alkaline);
b) Klebsiella, Enterobacter, Serratia species and
Pseudomonas aeruginosa more frequently found
in hospital-acquired UTI, because their resistance to
antibiotica favour their selection in hospital patience

Acquition and Aetiology

A. Bacterial Infection cont.
3. Gram positive species :
a) Staphylococcus saprophyticus causing
infection in young, sexually active women
b) Staphylococcus epidermidis UTI in
hospitalized patient
c) Others, capnophilic (m.o. which grow
better in air enriched with CO2 ) :
corynebacterium and lactabacilli
d) rarely : obligate anaerob

Acquition and Aetiology

B. Viral Infection

Viral causes of UTI is rare, although certain virus may be

recovered from urine in the absence of UTI

E.g. a) Human polyoma virus JC and BK from respiratory

syst. to epithelial cell in kidney tubulus and ureter;
b) cytomegalo-virus;
c) adenovirus causes of haemorrhagic cystitis

C. Other type of infection

Non-bacterial causes of UTI include fungi Candida spp

and Histoplasma capsulatum

Pathogenesis of UTI
Factors predisposing to infection
A. Mechanical Factors

- anything that disrups normal urine flow or complete emptying

of the bladder or facilitates acces of m.o. to the bladder will
predispose to infection
- the shorter female urethra is a less effective deterent to
infection than the male urethra
- sexual intercouse facilitates the movement of m.o. up the
urethra, particularly women
- in women preceeding bacterial colonization of the periurethral area of the vagina important; in male, UTI
more common in the uncircumcised colonization of the

Pathogenesis of UTI
B. Obstruction to complete bladder emptying
- Pregnancy, prostatic hypertrophy, renal calculi,
tumours and strictures of any sort causes
obstruction UTI when residual urine more
than 2-3 ml, infection is more likely

- Loss of neurological control of the bladder and

sphincter resultant large residual volume
urine in the bladder functional obstruction
C. Vesicourethral reflux
- anatomical abnormalities of UT ascending UTI
kidney damage

Pathogenesis of UTI
D. Diabetic
- may suffer more severe UTI and when
diabetic neuropathy interference with normal
bladder function persistent UTI commonly
E. Catheterization
- is another major predisposing factor for UTI
- During insertion of catheter m.o. carried to
bladder via lumen or by tracking up between
the outside of catheter and urethral wall

Pathogenesis of UTI
Bacterial Virulence Factors

Most Urinary tract pathogens originate in the fecal flora but

only the aerobic and facultative species such as E. coli posses
the attributed required to colonize and infect the UT - Ability
to colonized the periurethral area:

1. Fimbrie (pili) adhere to urethral and bladder epithelium

2. Capsular acid ppolysacharide (K) antigen resist host
defences by inhibiting phagocytosis - pyelonephritis

3. Hemolysin act as membrane damaging toxin

4. Produce Urease (Proteus spp) ability causes

Pathogenesis of UTI
Host Defence mechanism Host Factor

pH, chemical content and flushing mechanism

normal urethral flora do not multiply readily in
urine, although urine is good cultur medium for

The role of humoral immunity is poorly


After infection of the kidney, IgG and secretory IgA

antibodies can be detected in urine, but protective
role of these antibodies unclear

Host Defence mechanism - Host factor

1. Complicated UTI - structure abnormalities :
a. stones - caused by Proteus sp. urea-splitting
m.o. raise the pH urine b. obstructions prostatic hypertrophy
c. catheters caused by Gram neg (Klebsiella,
Enterobacter, Acinetobacter, Serratia sp. or
Pseudomonas aeruginosa, relative resistant to
2. Uncomplicated UTI without anatomic
abnormalities caused by strain E.coli

Defence Mechanism of Urinary Tract

1. Faktor Urine :
- Urea conc. Tinggi dan osmolaritas
- pH urine yg rendah membunuh bakt.

2. Faktor Hidrokinetik
- Eksresi urine secara periodik

- Pengenceran sisa urin krn aliran dari ginjal

- Pengosongan sempurna urine pada vesika

Defence Mechanism of Urinary Tract

3. Faktor Mukosa
- Mukosa vesika urinaria t.d sel epitel lebih dari satu
- Mukosa sal. Kemih dan vesika urinaria ditutupi oleh
mukus mencegah penempelan
- Efek antribakteri dari sekret prostat
- Sekresi lokal IgA mencegah penempelan m.o. pada
uroepithelium dan mencegah toksin penetralisir dari
- Perioksidase pada lapisan mukosa efek bakterisidal

Clinical Features and Complication

1. Lower urinary Tract
Acute infection of lower urinary tract are characterized by a rapid onset of
dysuria (burning pain on passing urine); urgency (the urgent need to
pass urine) and frequency of micturition
Urine is cloudy, due to the presence of pus cell (pyuria) and bacteria
(bacteriuria), and many contain blood (haematuria). Patient with
genital tract infection (vaginal thrush or chlamydia urethritis) may
present with similar symptom

Pyuria in the absence of positive urine culture can be due to chlamydia,

tuberculosis or patient receiving antibacterial therapy for UTI
Recurrent infection they may be relaps (same m.o.) or re-infection
(different m.o.) can result in chronic inflamatory changes in the
bladder, prostate and periurethral gland

Clinical Features and Complication

2. Upper Urinary Tract
Patient with pyelonephritis, complain of lower tract
symptom and usually have a fever
Staphylococcus are a common cause and renal abscesses
are generally present
Recurrent episode of pyelonephritis result in loss of
function of renal tissues which may, in turn, cause
hypertension, itself a cause of renal damage.
Infection associated with stone formation can result in
obstrction of the renal tract and septicaemia

Laboratory Diagnosis of UTI

1. Sampel Urine :

- Urine midstream
- Aspirasi supra pubik
- Kateterisasi

2. Kultur
- Umumnya ISK ditandai dengan adanya bakteriuri

- Bakteriuri Infectif :
a. jumlah m.o. > 100.000 per ml urine
b. jumlah m.o. < 100.000 per ml urine dengan lekosituri
c. jumlah m.o. < 100.000 per ml urine, pada kultur kedua
didapatkan jenis m.o. yang sama
d. jumlah m.o. < 100.000 per ml urine, t.d. satu spesies m.o. dengan
gejala klinik yang significans

e. jumlah fungi > 1.000 per ml urine infeksi fungi

Prevention of UTI

Infection in catheterized patients is very common but

can be reduced by good catheter care procedure.

Whenever possible catheterization should be avoid or

kept to a minimum duration

Use intermittent, rather than continous, catheterization

when feasible

Insert catheter with good aseptic technique, use a

closed sterile drainage system

Use topical antiseptic around the meatus in women

Wash hands before and after inserting catheters and

collecting specimens, and after emptying drainage

Pengobatan ISK, perlu difikirkan :

1. Penyebab ISK : Bakteri Gram (-) batang usus
dan Enterokokus
2. Kegagalan terapi disebabkan oleh :
- Hipertropi prostat
- Disfungsi o.k. batu vesikaurinaria
- Gangguan neurologi
- Cateterisasi

Pengobatan ISK, perlu difikirkan :

3. Gangguan Respon Imun, karena :
a. Persistent m.o. tetap dlm urine dengan atau tanpa gejala,
diperkirakan : abses perinefrik, infeksi prostat, corpus alinum
b. Relaps infeksi berulang sesudah terapi berakhir
c. Reinfeksi umumnya infeksi disebabkan oleh spesies yg
d. Infeksi rekurent berfluktuasi

4. Sisi Infeksi :
a. ISK bag. Bawah : Antibiotika yg tepat, Dosis tunggal
b. ISK bag. Atas : Waktu lebih lama

Dalam Pengobatan ISK


Antibiotika harus sesuai dengan uji



Stop kateterisasi atau ganti dgn balon

kateter atau drainase supra pubik


Atasi dulu gangguan struktur dan


M.O. Penyebab ISK

1. Escherichia coli
A. Sifat Umum :
* Penyebab plg umum dari ISK
* terjadi setelah kontak daerah genital dengan feces
* Sering pd wanita o.k. urethra yg pendek dan dekatnya area

B. Faktor patogenisitas
1. M.o. segera menempel pd mukosa via villi shg menimbulkan
2. LPS, menginduksi reaksi radang

3. Faktor host, termasuk obstruksi, hub. seks, kateter,

M.O. Penyebab ISK


1. Escherichia coli (lanjutan)

C. Gejala Klinik
1. Sistitis : sering b.a.k. dan nyeri, hematuri dan
2. Piolonefritis (infeksi ginjal) o.k. ISK yang asenderens.
Khas : demam, nyeri dan panas pd pinggang, dan
mungkin menyebabkan shock endotoksin
3. Prostatitis dpt terjadi pada laki-laki tua
D. Pengobatan
1. Dengan antibiotik yang sesuai
2. Kebanyakan E.coli peka thdp penisilin, siproflaksin

M.O. Penyebab ISK


2. Staphylococcus saphrophyticus
A. Sifat Umum :

- Termasuk Staphylococcus, seluruhnya catalase (+), gram (+),

biasanya tersusun dlm sel tunggal, diplokokus, rantai pendek
dlm jaringan
- Non hemolitik, coagulase (+), resisten novobiosin,
pada agar darah


- Tidak mempunyai protein A

B. Faktor Patogenitas : m.o. menempel pada sel uroepithelial

C. Gejala Klinik : ISK terjadi pada wanita yg aktif kehidupan
seksnya (honeymoon cystitis)

M.O. Penyebab ISK


3. Proteus mirabilis
A. Sifat Umum :
- Bakteri gram (-), batang pendek, bergerak
- Menghasilkan pertumbuhan swarming yg khas pada
kultur pada agar darah
- bersifat opportunistik, transmisi mel. kateter
B. Faktor Patogenisitas :
- menghasilkan protease yg kuat yg dpt menghidrolisis urea
jadi amonia dan CO2
- Hasil dari batu & calculus menyebabkan obstruksi sal. kemih
C. Gejala Klinik : ISK terjadi baik pada masyarakat dan nosokomial

D. Pengobatan : Ampisilin, sefalosporin, m.o. resisten pd tetra

M.O. Penyebab ISK


4. Enterococcus faecalis
A. Sifat Umum :
- Dulu diklasifikasi sbg Group D Streptococcus
- Merupakan flora normal pada usus dan oral pada manusia
dan hewan
- bersifat B-hemolitik, paling sering adalah a atau Y hemolitik
- Dapat dibedakan mel. reaksi thdp antiserum, resistensi
bacitracin, tumbuh dlm 40% bile, pH 9.0 / sol. 6.5 % garam
B. Faktor Patogenisitas : belum diidentifikasi
- M.o. umumnya noninvasif, menyebabkan infeksi nosokomial
C. Gejala Klinik : ISK, Septikemia, berhub. dgn endocarditis
D. Pengobatan : Uji kepekaan antibiotik utk menentukan terapi yg
tepat, M.o. relatif resisten thdp banyak antibiotik, dihambat
tapi tidak dibunuh oleh penisilin