Urinary Tract Infection

( UTI )
Introduction
 Introduction
 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
attach
- immune defences (humoral and cellular) play little role
here,
 Introduction
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
population.
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
 Introduction
 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, prostat and
urethra

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

 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
kidney
 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 lactobacilli
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
deterrend to infection than the male urethra
 Pathogenesis of UTI
Factors predisposing to infection
A. Mechanical Factors (continued ….)
- sexual intercouse facilitates the movement of
m.o. up the urethra, particularly women
- in women – preceeding bacterial colonization
of the peri-urethral area of the vagina –
important; in male, UTI more common in the
uncircumcised – colonization of the
inside of the prepuse and urethra with fecal m.o.
 Pathogenesis of UTI
B. Obstruction to complete bladder emptying
- Pregnancy, prostatic hypertrophy, renal calculi,
tumors 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 occur
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
 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 polysacharide (K) antigen – resist host
defences by inhibiting phagocytosis - pyelonephritis
3. Hemolysin – act as membrane damaging toxin
4. Produce Urease (Proteus spp) – ability causes pyelonephritis
 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
bacteria

 The role of humoral immunity – is poorly

understood

 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
AB
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
urinaria
Defence Mechanism of Urinary Tract
3. Faktor Mukosa
- Mukosa vesika urinaria t.d sel epitel lebih dari satu
lapisan
- 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
m.o.
- 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
bags
 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
berbeda
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

1. Antibiotika harus sesuai dengan uji

kepekaan

2. Stop kateterisasi atau ganti dgn balon

kateter atau drainase supra pubik

3. Atasi dulu gangguan struktur dan

neurological
 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
anus

B. Faktor patogenisitas

1. M.o. segera menempel pd mukosa via villi shg menimbulkan

kerusakan
2. LPS, menginduksi reaksi radang
3. Faktor host, termasuk obstruksi, hub. seks, kateter,
 M.O. Penyebab ISK (lanjutan)

1. Escherichia coli (lanjutan)

C. Gejala Klinik
1. Sistitis : sering b.a.k. dan nyeri, hematuri dan
urgency
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 (lanjutan)
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, kultur
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 (lanjutan)
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 (lanjutan)
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
Terima kasih