URINARY TRACT

INFECTIONS
By - ROLL NO 14,15,16.
OBJECTIVES
• Urinary Tract Infection (UTI)
• Etiological Agents of UTI
o Bacterial Infections
o Viral Infections
o Parasitic Infections
o Fungal Infections
• Catheter associated UTI
 URINARY TRACT INFECTION

Definition
• UTI is a disease caused by microbial invasion of the urinary tract.
• It can extend from the renal cortex to the urethral meatus.
• It is a leading cause of morbidity and healthcare expenditures in all
age groups.
Classification
Based on anatomical site:
• Lower UTI: Involves the urethra and bladder.
• Upper UTI: Involves the kidney and ureter.

Based on source of infection:

• Community-acquired UTI – Occurs outside healthcare settings.
• Healthcare-associated UTI – Includes Catheter-Associated UTI (CAUTI).
Normal Commensals of the Urinary Tract
• The urinary tract is sterile except for the distal urethra.
• Resident microbial flora includes:
• Lactobacilli
• Diphtheroids
• Coagulase-negative staphylococci
• Anaerobes
• Enterobacteriaceae
• Candida species (opportunistic pathogen).
• UTI occurs when pathogens invade the urinary tract.
• E.coli most common pathogen.
 Epidemiology of Urinary Tract
Infections (UTIs)
• UTIs are among the most common bacterial infections requiring
medical care.
• In community settings, they are the second most common infection
after respiratory tract infections.
• In hospital settings, they are the most common hospital-acquired
infections (HAIs), accounting for 35% of all HAIs.
Predisposing Factors
Prevalence:
• Approximately 10% of individuals develop UTI at some point in
their lives.

Gender:
• Predominantly affects females due to anatomical predisposition.
• 50% of women report at least one UTI episode in their lifetime.
• Increased risk in females due to:
• Short urethra, facilitating bacterial ascent.
• Close proximity of the urethral meatus to the anus, increasing bacterial
introduction.
Age:
• First year of life: UTI prevalence ~2% in both genders.
• Childhood (5–17 years): Incidence of bacteriuria ~1–3%.
• Adult life: Incidence 10–20% in females.
• Elderly males: Increased prevalence due to prostate enlargement, causing bladder
emptying issues.
• Reinfection risk: 50% of females aged 20–40 years experience recurrent infections within
one year.

Pregnancy:
• Anatomical and hormonal changes predispose to UTIs.
• Many pregnant females develop asymptomatic bacteriuria, which may lead to serious
infections in both mother and fetus.
Structural and Functional Abnormalities:

• Structural Obstructions: Urinary stasis increases infection risk.

• Examples: Urethral stricture, renal stones, prostate enlargement, tumors, renal
transplants.
• Functional Obstructions: Neurogenic bladder contributes to infection risk.
• Examples: Spinal cord injury, multiple sclerosis.

Bacterial Virulence Factors:

• Expression of pili facilitates bacterial adhesion to uroepithelium, enhancing
pathogenicity.
Vesicoureteral Reflux:
• Weakening of the vesicoureteric junction’s valve-like mechanism
allows retrograde urine flow into ureters and renal pelvis.

Genetic Factors:
• Genetically determined uroepithelial receptors may increase
bacterial adhesion, contributing to UTI susceptibility.

Urosepsis Risk:
• UTIs are a leading cause of Gram-negative sepsis (urosepsis).
• Hospitalized patients with urinary catheters account for ~50% of
nosocomial UTIs.
ETIOLOGY
• Escherichia coli (uropathogenic E. coli) is by far the most common cause of all forms
of UTIs (i.e. community acquired and healthcare-associated UTI and upper and
lower UTI); accounting for 70% of total cases.

o The endogenous flora such as gram-negative bacilli (e.g. E. coli, Klebsiella,

Proteus, etc.) and enterococci are the important agents
o In healthcare-associated UTIs, the agents are often multidrug resistant. In
addition to the members of Enterobacteriaceae, other organisms such as
staphylococci, Pseudomonas, Acinetobacter are also increasingly reported.
PATHOGENESIS
Routes of Infection
1.Ascending Route (Most common)
1. Enteric endogenous bacteria (e.g., E. coli, Klebsiella, Proteus, Enterococcus)
invade the urinary tract.
2. Facilitated by sexual intercourse, instrumentation (e.g., catheterization).
3. Colonization:
a. Adhesion to urethral epithelium is the first step.
b.Virulence factors (e.g., P fimbriae, mannose-resistant fimbriae in E. coli) aid adhesion.
PATHOGENESIS
4. Ascension:
a. Pathogen moves upward through the urethra to the bladder, causing
cystitis.
b.Bacterial toxins may inhibit peristalsis, leading to urinary stasis.
5. Further Ascension:
If vesicoureteral reflux occurs, bacteria ascend to the renal parenchyma,
leading to pyelonephritis.
6.Acute Tubular Injury:
Inflammatory cascade may cause tubular obstruction and damage, leading
to interstitial nephritis.
2. Descending Route (Hematogenous spread, ~5% of UTIs)
• Pathogens invade renal parenchyma via bloodstream (hematogenous
seeding).
• Occurs as a consequence of bacteremia.
• Common descending route pathogens:
• Staphylococcus aureus
• Salmonella
• Mycobacterium tuberculosis
• Leptospira
Host Defence Mechanisms
CLINICAL MANIFESTATIONS
1.UPPER UTI.
2. LOWER UTI.
 Lower UTI (Cystitis, Urethritis, Acute Upper UTI (Pyelonephritis,
Feature
Urethral Syndrome) Ureteritis, Renal Abscess)

Sites Involved Urethra, bladder Kidney, ureter, renal pelvis

Dysuria, urgency, frequency, Fever, flank pain, vomiting, systemic

Symptoms
suprapubic tenderness manifestations

Cloudy, foul-smelling, sometimes May show pyuria, hematuria, and

Urine Appearance
hematuria casts

Ascending (from bladder to kidney)

Route of Spread Ascending (from urethra to bladder)
or hematogenous
Occurrence More common Less common

Systemic Involvement Absent Present (fever, chills, malaise)

Can lead to renal scarring, abscess

Complications Rare, unless untreated
formation

E. coli, Staphylococcus aureus,

E. coli, Klebsiella, Proteus,
Common Pathogens Salmonella, Mycobacterium
Enterococcus
tuberculosis
 Laboratory Diagnosis of Urinary
Tract Infections (UTIs)
1.Specimen Collection
• Clean voided midstream urine – Most common method; requires
proper cleaning of urethral meatus or glans.
• Suprapubic aspiration – Ideal for infants or comatose patients;
directly aspirates urine from the bladder.
• Catheterized patients – Urine should be collected from the
catheter tube, not the uro bag.
2. Transport & Storage
• Immediate processing is preferred.
• If delayed >1–2 hours, store in refrigerator or add boric acid
(preserves sample for up to 24 hours).
3.Direct Examination
• Wet mount examination – Detects pus cells; >8 pus cells/mm³ is significant.
• Leukocyte esterase test – Rapid test detecting esterases from pus cells.
• Nitrate reduction test (Griess test) – Positive in nitrate-reducing bacteria (E.
coli).
• Gram staining – Limited reliability due to low bacterial count and rapid
deterioration of pus cells.
4.Culture & Identification
Culture media:
CLED agar(cysteine lactose electrolyte deficient agar)
MacConkey agar & Blood agar (alternative).

Kass Concept of Significant Bacteriuria:

≥10⁵ CFU/mL – Indicates infection.
10⁴–10⁵ CFU/mL – Doubtful significance; requires clinical correlation.
<10⁴ CFU/mL – Likely contamination, except in special cases (e.g.,
pyelonephritis, catheterized patients).
Quantitative Culture Methods:
Standardized loop technique (semi-quantitative).
Pour plate method (quantitative).

Colony Appearance:
Lactose fermenters (E. coli, Klebsiella) – Pink colonies on MacConkey agar,
yellow on CLED agar.
Non-lactose fermenters (Proteus, Pseudomonas, Acinetobacter) – Pale
colonies.

Identification Methods:
Automated systems – MALDI-TOF, VITEK.
Biochemical tests – Indole, citrate, urease, TSI reactions.
5.Antimicrobial Susceptibility Testing (AST)
• Essential for guiding treatment.
• Methods:
• Disk diffusion test (Mueller-Hinton agar).
• Automated MIC-based methods (e.g., VITEK).

6. Antibody-Coated Bacteria Test

• Differentiates upper vs. lower UTI using immunofluorescence.
• Upper UTI: Bacteria coated with specific antibodies (hematogenous
spread).
• Lower UTI: Bacteria not coated with antibodies.
TREATMENT
Preferred Antibiotics for UTIs:
• Quinolones (e.g., norfloxacin) – Effective against Gram-negative bacteria,
commonly used for uncomplicated UTIs.
• Nitrofurantoin – Preferred for lower UTIs (cystitis) due to its
concentration in urine.
• Cephalosporins – Broad-spectrum antibiotics used for both lower and
upper UTIs.
• Aminoglycosides – Used for severe infections, particularly pyelonephritis.
Treatment of Healthcare-Associated UTIs (Multidrug-Resistant
Pathogens):
• Carbapenems (e.g., meropenem) – Used for extended-
spectrum β-lactamase (ESBL)-producing bacteria.
• β-lactam/β-lactamase inhibitor combinations (e.g.,
piperacillin-tazobactam) – Effective against resistant Gram-
negative bacilli.
• Fosfomycin – Used for complicated UTIs, particularly in
multidrug-resistant infections.
ETIOLOGICAL AGENTS
OF UTI
BACTERIAL AGENTS
Enterobacteriaceae Causing Urinary Tract Infections (UTIs)
• Several members of the Enterobacteriaceae family can cause UTIs,
with Uropathogenic Escherichia coli (UPEC) being the most significant.
1. Uropathogenic Escherichia coli (UPEC)

• Most common UTI pathogen (70–75% of cases).

• Serotypes O1, O2, O4, O6, O7, and O75 are responsible for most
infections.
• Virulence factors:
• Cytotoxins: CNF-1 (Cytotoxic Necrotizing Factor 1) & SAT (Secreted
Autotransporter Toxin).
• Hemolysins: Promote tissue damage.
• Fimbriae: P fimbriae associated with lower UTIs.
• Capsular K antigen: Related to upper UTIs.
• E. coli also causes diarrhea, pyogenic infections, meningitis, etc.
2. Klebsiella pneumoniae
• Normally found in the intestines.
• Causes UTIs, neonatal meningitis, septicemia, abscesses, and wound
infections.

3. Enterobacter species
• Emerging nosocomial pathogens.
• Implicated in infected wounds, UTIs, and pneumonia.
5. Proteeae Infections

• Tribe Proteeae includes Proteus, Morganella, and Providencia.

• Common characteristic: Positive for phenylalanine deaminase (PPA)
test.
• Habitat: Commensals in the human intestine, but can cause
nosocomial infections such as UTIs and wound infections.
Proteus Species
• Notable for pleomorphism (varied sizes and shapes).
• Named after the Greek god Proteus, known for shape-shifting.

Antigenic Classification
• H antigen: Derived from the ability of flagellated Proteus strains to
grow as a thin film ("Hauch" – German for film of breath).
• O antigen: Associated with non-flagellated strains that do not form a
film ("Ohne Hauch" – without film of breath).
Pathogenesis
• Common species:
• Proteus mirabilis – Most frequently encountered.
• Proteus vulgaris – Less common but still clinically significant.
• Saprophytes:
• Found in decomposing organic matter, sewage, and soil.
• Commensals:
• Frequently present on moist areas of human and animal skin and intestines.
• Infections:
• Cause urinary tract infections (UTIs), wound infections, soft tissue infections, and
septicemia.
• Nosocomial outbreaks reported frequently.
• Renal Calculi (Struvite Stones):
• Proteus produces urease, breaking down urea into ammonia.
• Ammonia damages renal epithelium and alkalinizes urine, leading to phosphate
deposition and renal calculi formation.
Laboratory Diagnosis

• Pleomorphism: Proteus species are Gram-negative coccobacilli,

occasionally appearing bacillary or filamentous.
• Odor: Cultures produce a putrid fishy or seminal odor.
• Swarming: Proteus exhibits swarming motility on solid media like
blood agar:
• Continuous swarming: Uniform film covering the entire plate.
• Discontinuous swarming: Concentric circles around the inoculation site.
• Identification Methods:
• Automated systems (MALDI-TOF, VITEK).
• Conventional biochemical tests.
• Biochemical Characteristics:
• Catalase-positive, oxidase-negative.
• ICUT tests:
• Indole test: Positive for P. vulgaris, negative for P. mirabilis.
• Citrate test: Variably positive.
• Urease test: Positive.
• TSI test: Alkaline/acid reaction, variable gas production, H₂S present.
Morganella
• Species: Morganella morganii.
• Habitat: Found in human and animal feces.
• Infections: Rarely causes UTIs, pneumonia, wound infections.
• Most infections are nosocomial.

Providencia
• Species: P. rettgeri, P. stuartii, P. alcalifaciens, P. rustigianii, P.
heimbachae.
• Infections: Associated with nosocomial UTIs, wound infections,
burns.
Treatment of Proteeae Infections

• Multidrug Resistance (MDR):

• Resistant to many disinfectants.
• Intrinsic resistance to:
• Ampicillin, 1st & 2nd generation cephalosporins, nitrofurantoin, tetracyclines, tigecycline, polymyxins
(colistin & polymyxin B).
• Produces β-lactamases:
• Extended-spectrum β-lactamases (ESBL).
• AmpC β-lactamases → Resistance to most β-lactam drugs.
• Drug of Choice:
• Depends on antimicrobial susceptibility testing.
• Generally effective:
• Aminoglycosides.
• Fourth-generation cephalosporins (cefepime).
• Carbapenems.
• P. mirabilis is more susceptible to antibiotics than P. vulgaris
Non-fermenters Causing UTI
Non-fermenters such as Pseudomonas, Acinetobacter are important
cause of healthcare associated UTI.

They also cause skin and soft tissue infections and pneumonia.
Enterococcal Infections
• Enterococci are the most common gram-positive cocci to cause
UTI.

• They were initially grouped under group D Streptococcus, but

later have been reclassified as a separate genus Enterococcus.

• Based on the molecular structure,they are now placed under a

new family; Enterococcaceae.
 Virulence
factors
• Enterococci are part of normal flora of human intestine, biliary
tract and to lesser extent vagina and male urethra.
• At the same time, they are also becoming increasingly important
agents of human disease especially in hospitals, which is attributed
to their resistance to several antibiotics and also due to exhibiting a
number of virulence factors such as:
• Aggregation substances or pheromones: They help in clumping of
adjacent cells to facilitate plasmid exchange (transfers drug
resistance).
• Extracellular surface protein(ESP): It helps in adhesion to bladder
mucosa.
• Common group D lipoteichoic acid antigen: It induces cytokine
release such as tumour necrosis factor alpha.
• Clinical Manifestations -
• E.faecalis and E.faecium are the two species that are clinically
important.
• E.faecalis is the most common species isolated from clinical
specimens, whereas E.faecium is more drug resistant than
E.faecalis.
• Enterococci are one of the major healthcare-associated pathogens,
produce various infections such as:
• Urinary tract infections: Healthcare associated UTI (cystitis) is the
most common infection caused by enterococci; usually associated
with indwelling urinary catheterization, or instrumentation. Rarely
it may progress into pyelonephritis and perinephric abscesses.

• Chronic prostatitis: Enterococci can cause chronic prostatitis, when

urinary tract is manipulated surgically or endoscopically. As
antibiotics penetrate poorly into prostatic tissue, this can be a
source of recurrent enterococcal bacteremia.
MacConkey agar: It produces minute magenta pink
colonies.
Bile esculin hydrolysis test is positive.
They can grow in presence of extreme conditions such as-
6.5% NaCl, 40%bile, pH 9.6, 45°C and 10°C.
• E.faecalis and E.faecium can be differentiated by arabinose
fermentation test.
Accurate species identification can be made by automated
methods such as VITEK and MALDI-TOF.
• Bacteremia and left sided endocarditis involving mitral and
aortic valves(common in intravenous drug abusers).
• Intra-abdominal, pelvic and soft tissue infections, including
surgical site infections following intra abdominal surgeries.
• Neonatal infection: Such as sepsis (mostly late onset),
bacteremia, meningitis and pneumonia.
• Laboratory diagnosis-
• Specimen collection depends upon the site of infection.
• Urine, blood(collected in blood culture bottles), exudate, peritoneal
fluid,etc.are the useful specimens for culture.
• Enterococci show the following characteristics that help in their
identification:
They are gram-positive oval cocci arranged in pairs;at an angle to
each other (spectacle- shaped appearance).
Blood agar:It produces non-hemolytic translucent colonies.
Other Gram-positive cocci Causing UTI
• Staphylococcus aureus:S.aureus is an important cause of UTI.It
predominantly causes skin soft tissue infections.

• Staphylococcus saprophyticus: It causes UTI sexually active young

women.This is due to expression of a 160 kDa
hemagglutinin/adhesin protein that can adhere to uroepithelial
cells. It can be differentiated from other staphylococci in being
resistant to novobiocin disk(5 microgram).
• Streptococcus agalactiae: Group B Streptococcus (GBS) can
cause UTI- cystitis and asymptomatic bacteriuria. It usually
colonises in female genital tract; can cause more often
postpartum infection, neonatal sepsis, skin and soft tissue
infections.
Other bacterial infections of urinary
tract
• Renal Tuberculosis

• Genitourinary TB, which accounts for 10-15%of all extrapulmonary

tuberculosis, may involve any portion of the genitourinary tract.

• Upto 75% of patients have chest X-ray suggesting previous or

concomitant pulmonary Tuberculosis.

Symptoms: Urinary frequency, dysuria, nocturia, hematuria and

flank or abdominal pain are common presentations.
Urinalysis gives abnormal results in 90% of cases, revealing pyuria
and hematuria.
Sterile pyuria: Presence of pus cells in urine but negative routine
bacterial urine culture raises the suspicion of TB.
Urine culture for TB:Three consecutive early morning
urine specimens yield a definitive diagnosis in nearly 90%
of cases.Following centrifugation, the deposit is sent for
culture in MGIT(Mycobacteria Growth Indicator Tube) or
LJ(Lowenstein-Jensen) medium.
Radiology: Abdominal CT or MRI scan may show deformities,
obstructions, calcification and ureteral strictures.Severe ureteral
strictures may lead to hydronephrosis and renal damage.
Treatment: Genitourinary TB responds well to antitubercular
therapy.
• Post- streptococcal Glomerulonephritis (PSGN)
• PSGN is a non-suppurative sequela of group A streptococcal
infection.
• The antibodies developed against streptococcal antigens cross react
with glomerular basement membrane resulting in
Glomerulonephritis.
Seotypes involved: PSGN typically occurs following either
streptococcal pyoderma(usually by M serotypes-47,49,55,57,60) or
rarely following pharyngitis (caused by M serotypes 1-4,12,25)
PSGN due to impetigo develops 2-6 weeks after skin infection;
whereas it develops 1-3 weeks after streptococcal pharyngitis.
Pathology:PSGN results from the lodging of antigen antibody
complexes on the glomerular basement membrane (appears as
humps), followed by complement activation.Streptococcal pyogenic
exotoxin-B(SPE-B) may be the main nephritogenic antigen involved.
Clinical presentation: Urine retention and renal insufficiency occurs
that leads to edema, hypertension, hematuria, pyuria, proteinuria
and oliguria.
Diagnosis: Patients usually have elevated streptococcal anti-DNase
B antibodies (70%),compared to rise of antibodies titer more than
300-350 units/ml is diagnostic of PSGN and pyoderma.
Prognosis:PSGN usually occurs in children(2-14 years) and has a
good prognosis.
Apart from PSGN, another non-suppurative sequela is seen
following streptococcal sore throat called acute rheumatic fever.
 Perinephric and Renal Abscesses
• Perinephric and renal abscesses develop secondary to a urinary
tract infection rather than direct hematogenous spread.
• Infection ascends from the bladder (cystitis) to the kidney
(pyelonephritis), then ultimately proceeed to involve renal
parenchyma (medulla to cortex) to produce abscess. Areas of
abscess within the parenchyma may rupture into the perinephric
space.
• Pre-existing renal stones obstructing urinary flow is the major risk
factor associated with most of the cases.
• The common etiologies include uropathogenic organisms such as
E.coli,Proteus species and Klebsiella species.
• Treatment involves drainage of pus and antibiotic therapy directed at
the organism recovered.
 Viral Infections of Urinary System
• Viral Infections of urinary system is very rare.
• Only few viruses can infect urinary tract.
• BK Virus Infection
• BK Virus causes nephropathy in kidney transplant recipients.
• It can also cause hemorrhagic cystitis in haematopoietic stem cell
recepients.
• Infection in other individuals may occur,but almost always
asymptomatic.
Naming: BK Virus is named after the initials of the patient in whom
it was described first. It is a polyomavirus, possesses dsDNA.
Diagnosis: The diagnostic modalities include:
• Renal biopsy: Histologic examination of renal biopsy specimens
showing characteristic histopathologic changes ( inflammatory
infiltrates,fibrosis and tubular injury) plus positive
immunohistochemistry for BK Virus provides definite diagnosis.
• PCR: Identification of BK viremia (BK Virus DNA in blood) by PCR plus
features of nephropathy is also suggestive of the diagnosis.
• Asymptomatic BK Viruria(detection of BK Virus DNA in urine) is less
specific finding; may not be clinically significant.
Treatment:There is no specific treatment available.
• Cidofovir has been used for treatment of refractory cases.
• Adenovirus cystitis
• Adenovirus serotypes 11and 21 can cause acute hemorrhagic
cystitis in children, especially in boys.
• Certain viruses such as Cytomegalovirus and herpes simplex virus
(HSV) are excreted in urine, however they usually do not cause
urinary tract infections.
• Urinary retention may bfe seen in HSV infection secondary to
autonomic nervous system dysfunction.
 Parasitic Infections of Urinary
System
• Urinary Schistosomiasis (S.haematobium)
• Schistosoma haematobium is the causative agent of urinary
Schistosomiasis or Bilharziasis, named after its discoverer T.Bilharz in
1851.
• It is a good trematode (or fluke), resides in venous plexus of Urinary
bladder and ureter.
• The other two blood fluids Schistosoma mansoni and S.japonicum
reside in venous plexus of intestine and mesentery, produce
intestinal disease.
• Epidemiology
• World: S.haematobium infection is endemic in the African
continent (across Nile river valley), Middle East and the Indian
Ocean Islands.
• India: Schistosomiasis is extremely rare in India.An endemic focus
is present in Gimvi village of Ratnagiri district, Maharashtra.
• Life Cycle
• Humans are the definitive host and freshwater snails are
the intermediate host.
• Transmission:Man acquires infection by penetration of skin
by cercaria larvae(infective form) present in the
contaminated water.
• Development in man: The cercariae larva penetrate the
skin, travel via the dermalnveins to reach systemic
circulation and enter the portal system where they
develop into adult worms.
• Spread: Adult worms reach vesical plexus and undergo
fertilisation to produce eggs which are excreted in urine.
Eggs are the diagnostic form.
 Clinical manifestations
• Acute schistosomiasis presents as
cercarial dermatitis.
• Chronic schistosomiasis is due to the
deposition of eggs in the Urinary tract
to form egg granuloma.
• Urogenital disease: The eggs have
terminal spines which cause damage
to the bladder mucosa that leads to
dysuria and hematuria.
• Obstructive uropathies: Fibrosis may cause obstruction of the lower
end of the ureters that results in in hydroureter and hydronephrosis.
• Bladder carcinoma: The metaplastic changes in urinary mucosa may
lead to squamous cell carcinoma of the bladder.
• Involvement of other sites: Eggs may be carried by venous blood to
various parts of the body like spinal cord, liver, lungs or intestine and
produce similar granulomas.
•.
• Laboratory diagnosis
• Urine microscopy: Diagnosis if S.haematobium infection is
made by detection of oval and elongated, non-
operculated eggs of size 112-170*40-70 micrometre with
a terminal spine in the urine or rarely in feces or bladder
mucosal biopsy.
• Antibody detection: Useful for epidemiological purposes,
but not for the diagnosis as they cannot differentiate
between recent and past infection. Two assays are
available that detect serum antibodies against
S.haematobium adult worm microsomal antigen (HAMA).
- HAMA-FAST-ELISA: Falcon assay screening test ELISA
-HAMA-EITB: Enzyme linked immunotransfer blot.
• Antigen detection: Detection of circulating antigen indicates recent
infection and can be used for monitoring the treatment response.
Circulating cathodic antigen (CCA) and circulating anodic antigen
(CAA) can be detected in the serum and urine by ELISA or dipstick
assays.
• Prevention
• Preventive measures include:
• Proper disposal of human excreta and urine.
• Eradication of snails by using molluscicides such as metal salts(iron
or aluminium sulfate), metaldehyde, methiocarb and acetylcholine
esterase inhibitors.
• Treatment of infected persons.
• Dioctophyme renale infection
• Dioctophyme renale is commonly known as giant kidney worm
is a nematode of lower animals, human infection is extremely
rare (only 23 cases, 3 from India).
• Life cycle: Human gets infection from ingestion of fish infected
with larva of D.renale.Larva penetrate the intestine and reach
kidney (right kidney affected commonly) and transform into
adult worms. Adult worms are larger in size and can block the
kidney and ureter. Adult worms lay eggs that are passed in
urine.
• Clinical features: It includes hematuria and renal colic. Extensive
destruction of kidney parenchyma may occur.
• Laboratory diagnosis: Condition is diagnosed by demonstration of
characteristic eggs in urine. Eggs are oval-shaped, measures 60-80
micrometre size, contain an embryo surrounded by characteristic
thick sculptured or pitted egg shell.
• Treatment: No standard treatment is available.
• Prevention: Proper cooking of fish prior to consumption.
• Trichomonas vaginalis Urethritis
• T.vaginalis is a sexually- transmitted parasite that primarily
cause Urethritis.
• The trophozoites may be detected in urine sediment.
 Fungal Infections of Urinary
System
• Candiduria
• Isolation of Candida species in urine is a common finding which may
result from contamination during collection, bladder colonization or
upper UTI( due to hematogenous or ascending infection from
bladder).
• Treatment of candiduria in a asymptomatic patients is not
recommended but can be considered in the following situations:
• Symptomatic cystitis or pyelonephritis and patients at high risk for
disseminated disease.
• Neutropenic or immunosuppressed patients.
• Patients undergoing urologic manipulation
• If upper pole or bladder wall invasion or obstruction is associated
• Critically ill patients (have higher risk for invasive candidiasis)
• Low birth weight infants

Fluconazole(for 14 days) is the drug of choice, as it reaches high

levels in urine.
In case of fluconazole resistance, oral flucytosine and/or parenteral
amphotericin B can be considered.
CATHETER ASSOCIATED URINARY
TRACT INFECTION
(CAUTI)
ETIOLOGY
A broad range of bacteria can cause CAUTI, most of which are
multidrug resistant.
E. coli is the predominant agent
Gram-negative bacilli such as Klebsiella, Pseudomonas and
Acinetobacter
Gram-positive cocci such as Enterococcus
PATHOGENESIS
RISK FACTORS :-
1. Device-related: Long-term catheterization (for >30 days),
use of latex catheters has higher risk than silicone catheters
2. Patient-related: Female gender, old age [>50 years),
diabetes mellitus, poor personal hygiene etc.
3. Caregiver-related: Emergency catheter insertion, fallure in
adherence to aseptic technique both during insertion and
maintenance of catheter.
4. Extraluminal spread: This accounts for two-third of
cases:
• The source of the infection in catheterized patients
may include patients' endogenous flora, hands of
health care personnel, or inanimate objects
• If asepsis is not maintained at the time of insertion
or during maintenance of the catheter, there is
always a risk of extraluminal migration of bacteria
from one of these sources into the bladder
• When a urinary catheter is inserted, the
mechanism by which the urethral flora is constantly
flushed out is interrupted.
• This helps in extraluminal migration of urethral and
perineal flora into the bladder causing colonization
and subsequent infection.
5. Intraluminal spread: This accounts for one-third of
cases.
• If the drainage bag is open type or when the closed
drainage system is breached, there is a risk of reflux
of contaminated urine from the drainage bag.
Why Indwelling Catheter is a
Risk for UTI?
• The presence of an urinary catheter in the single
most important risk factor.
• The risk of developing CAUTI is directly proportional
to the duration of catheterization.
• Urethral pressure: An indwelling catheter exerts
lateral urethral pressure causing decreased mucosal
blood flow, urothelial mucosal disruption and
impaired mucin secretion; all together
predispose to infection
• Incomplete emptying: In catheterized patients,
bladder is often incompletely emptied because of
pressure differentials created by patient muvement
or catheter manipulation.
• A small amount of urine always pools around the
balioon which serves as a nidus for infection
LABORATORY DIAGNOSIS
SPECIMEN COLLECTION
• Urine for culture should be collected through the catheter port using
aseptic technique
• If a port is not present, by puncturing the catheter tubing with a
needle and syringe.
• Urine should never be collected from the urobag.
The clinical diagnosis of CAUTI is based on the
following three criteria:
1. Catheter criteria: Catheterized or history of recent
catheterization within 48 hours
2. Clinical criteria: Presence of at least one signs or
symptoms of UTI such as fever, suprapubic tenderness,
costovertebral angle pain, urinary urgency, frequency
or dysuria (pain during micturition)
3. Urine culture criteria: Presence of significant
bacteri-uria, defined as colony count exceeding:
• 210 CFU/mL: in symptomatic patients
• ≥105 CFU/mL: in asymptomatic patients.
TREATMENT
Management of CAUTI includes removal of catheter
and institution of appropriate antimicrobial therapy
based on the susceptibility pattern of the organism
isolated.
Treatment of asymptomatic bacteriuria is not
recommended except when:
• Bacteriuria persists for >48 hours after removal of
the catheter
• In pregnancy, as there is 20-30 fold increased risk of
developing pyelonephritis and risk of premature
delivery with low birth weight
• Prior to traumatic urological procedures such as
transurethral resection of prostate where mucosal
bleeding is anticipated which may cause bacteremia
PREVENTION OF CAUTI
• Insertion bundle
1. Catheter should be inserted only when appropriate indication is
present (e.g. acute urinary retention)
2. Only the sterile items are used for insertion of catheter
3. Catheter is inserted by non-touch technique with strict asepsis
4. Closed drainage system must be used

5. Catheter of appropriate size must be used

6. Catheter must be properly secured after

placement (by plaster-tube-plaster technique)
• Maintenance bundle
1. Daily catheter care (vaginal or meatal care) must
be given regularly and by strict aseptic measures
such as hand hygiene and single use gloves
2. Catheter is properly secured all the time
3. Drainage bag must be always above the floor and
below the bladder level
4. Closed drainage system is used all the time
5. While collection of urine from bag, the following
steps must be followed Hand hygiene, change of
gloves between patients; use of separate jug for each
bag, use of alcohol swabs for disinfection of outlet
6. Daily assessment of readiness for removal of
catheter must be documented
THANK YOU