urinary tract infections in pregnancy

1. Evaluation of Infection In
Pregnancy
KARKI, BIJAY KUMAR
MEDICAL LABORATORY STUDENT

2. • IN pregnant women, most infections are no more serious than
in non- pregnant women of similar age
 some infections can be transmitted to the fetus in utero or to the infant
during or immediately after delivery, with potentially serious sequale.
 Uncommonly, serious infectious illness in the mother can have non- specific
fetal or obstetric effects and lead to miscarriage, premature labour or fetal
death, these infections must be treated as any other serious illness.
 more common and a source of anxiety is mild illness or suggestive
laboratory findings in the absence of symptoms.
 Intra amniotic infection due to bacteria in the vaginal flora
not only initiate labor but can also cause infections such as
septicemias and meningitis in the new born.
Several host defense mechanisms operate against
ascending infections:
»Vaginal acidity
»Cervical mucus
»Intact membranes
»Antibacterial activity of amniotic fluid

3. • Organisms causing neonatal sepsis
Early onset sepsis ( 24 hours to 7 days postpartum):
Streptocococcus B- haemolyticus (GBS)
E. coli
Late onset sepsis ( later than 7 days postpartum):
Coagulase negative staphylococcus (CONS)
Streptococcus B- haemolyticus (GBS)
Staphylococcus aureus

4. Streptococcus B- haemolyticus of group B of lanncefield
(SGB) or streptococcus agalactiae
 The prevalence of SGB colonization among pregnant women
ranges from 10 to 30 %
 SGB disease can occur in three clinical forms:
 Early onset disease,, defined by the development of disease in newborn
infants up to the 7 th day of llife
 Late onset disease, charaterized by occurense between the 8 th day and
3rd month of life.
 Very late onset disease, occurring after the 3 rd month of life
 Prevention: SGB culture for women at between 35 and 37
weeks of gestation – antibiotic therapy if culture is positive

5. • Infection jeopardizing the fetus with no serious
maternal consequences.
o Cytomegalovirus
o Toxoplasmosis
o Parvovirus B19
Infections jeopardizing the fetus with possible
maternal complications
o Rubella
o Varicella
o Sexually transmitted infections
o malaria

6. cytomegalovirus
 Cytomegalovirus is the leading cause of congenital viral
infection
 Typical clinical syndromes : intrauterine growth restriction,
microcephaly, hepato splenomegaly, petechiae, jaundice,
thrombocytopenia, anemia, chorioretinitis
 Long term neurodevelopmental sequale include: mental
retardation, motor impairment, sensorineural hearing loss and/
or visual impairment
 Primary maternal CMV infection during gestation poses a 40 %
risk of intrauterine transmission

7. Toxoplasmosis
 Detection of T. gondii –specific IgM antibodies has been used
as an aid in determining the time of infection: a negative IgM
test result with a positive IgG result usually indicates infection at
least six months previously.
 When a pregnant women is found to be infected with T. gondii,
the next step is to determine whether the fetus is infected: PCR
testing of amniotic fluid is used to diagnose congenital
toxoplasmosis.

8. Parvovirus B19
• Most persons ( usually children: erythema infectiosum or fifth
disease) with parvovirus B19 infection are asymptomatic or
have mild, nonspecific, cold like symptoms.
• The virus is highly infectious and spreads mainly through
respiratory droplets.
• The infection can trigger an acute cessation of RBC production,
causing transient aplastic crisis, chronic red cell aplasia,
hydrops fetalis, or congenital anemia.
• Although the virus can be contracted in any trimester, the
second trimester seems to carry the highest risk of fetal loss

9.  To test a fetus for possible infection , a PCR is performed on
amniotic fluid.
 Fetal cord blood is not widely used because of the associated 1
% fetal loss rate, and also because the IgM does not often
appear in the fetal circulation until after 22 weeks gestation.
 Routine prenatal screening for parvovirus B19 is not advised. If
the fetus shows evidence of hydrops, the only treatment option
is intrauterine blood transfusion to correct the assosciated
anemia.

10. Rubella infection
 The earlier in gestation the maternal infection occurs,, the more
severe is the damage to the fetus.
 Maternal infection during the first 8 weeks after the last
menstrual period results in nearly all fetus becoming infected
and upto 100% of infected fetus developing congenital defects:
 Congenital heart diseases
 Congenital cataract
 Deafness
 Microcephaly
 Mental retardation
 The risk of fetal infection and the severity of congenital
abnormalities decreases after the 1st trimester, after 17 weeks
gestation, the risk of developing any defect is low

11. Varicella – zooster virus
 VZV is spread by respiratory transmission or direct contact with
infectious lesion.
 At any stage during pregnancy, severe maternal chickenpox
may cause intrauterine death.
 Varicella infection in the first and second trimesters may lead to
the congenital varicella syndrome
 The symptoms include:
 Skin lesion in dermatomal distribution
 Neurological defects
 Eye diseases
 Skeletal anomalies
 About 30% of infants born with these lesion die in the 1st
trimester of life

12. Pregnancy outcomes following maternal
sexually transmitted infections
 Neonatal herpes:
pulmonary diseases, seizures, fever, intracranial findings, a
high fatality rate
 Gonococcal infection:
preterm delivery, premature rupture of the membrane, LBW,
postpartum endometritis, gonococcal opthalmia neonaturum
 Chlamydia infection:
preterm delivery, LBW, infant pneumonia
 Trichomonas infection:
preterm delivery, LBW
 Bacterial vaginosis:
 Syphilis

13. Ureaplasma urealyticum
 Ureaplasmal colonization of the lower genital tract is not
assosciated with adverse pregnancy outcome.
 Ureaplasmal infection of the chorioamnion have been
implicated in :
o Infertility
o Spontaneous abortion
o Still birth
o Premature birth
o LBW
o Increased perinatal morbidity and mortality
 U. urealyticum is the single most common mos. Isolated from
the CNS and LRT of newborn infants

14. Malaria in pregnancy
• Women living in endemic areas are considered to have some
immunity and malarial infections are usually asymptomatic.
• The disease is almost always symptomatic, and potentially
lethal, in non immune patients particularly gravid females.
• Possible pregnancy complications.
 Preterm delivery
 IUGR
 Spontaneous abortion
 Still birth
 Postpartum haemorrhage
 Puerperal fever
 Maternal / fetal death

15. Screening of infections
 Universal screening of pregnant women should be
recommended for the following :
 Syphilis
 Chlamydia, ureaplasmal infection and gonorrhea or bacterial
vaginosis
SGB culture for women at between 35 and 37 weeks of gestation
HIV Testing
 history of genital and orolabial herpes simplex V virus infection
 rubella
 history of chickenpox vaccination
Routine screening for toxoplasmosis, cytomegalovirus or
parvovirus infection is not recommended.

16. CHANGES IN PREGNANCY
• Increased renal parenchymal volume due to intrarenal
fluid accumulation, hence…
• massive dilatation of renal calyces and ureter.
[approximately 90 % of pregnant women develop
ureteral dilatation, which will remain until delivery, and
up to 12th – 16th postpartum week.]
• By 2nd trimester, there is increased renal blood flow up
to 70-80 % and also GFR by 45-50%.

17. • Diagnosing intra amniotic infection
 intra amniotic infection is difficult to diagnose on the basis of any single criterion
and so diagnosis depends on a set of criteria, the most important clinically being
maternal fever and tachycardia and fetal tachycardia.
 Increased maternal leukocyte count , fetal biophysical profile examination using
ultrasound are also used in diagnosis.
 Detection and estimation of surrogate markers:
• C- reactive protein
• Cytokines
• Fetal fibronectin
 The infection may be polymicrobial, but collecting amniotic fluid samples without
contamination with normal vaginal flora is cumbersome and may require invasive
procedures.
 After membrane rupture many bacteria may enter the amniotic cavity without
having caused the rupture

18. UTI
• An urinary tract infection (UTI): Bacteriuria:
i] presence of at least 100,000 organisms/mL of urine in an
asymptomatic patient
ii] as more than 100 organisms/mL of urine with accompanying
pyuria (>7 WBCs/mL) in a symptomatic patient
can be lower/upper UTI
• Pregnant women are at increased risk for UTI's starting in
week 6 through week 24.

19. Essential Elements of Urine Cultures
• Pathophysiology of urinary tract infection
• Microbiology of urinary tract infection
• Clinical signs and symptoms of urinary tract infection
Technical variables in specimen collection and transport
• Interpretation of urine cultures
• Quality management

20. Pathophysiology of urinary tract infection
• Ascending route of infection most common
• Colonization of urethra and periurethral tissue by uropathogens
the initial event in urinary tract infection
• Urinary tract infection more common in women than men due to
short female urethra with distention and turbulent flow that
washes urethral organisms into the bladder during micturition
and in close proximity to perianal areas
• Hospital infection associated with lower urinary tract
instrumentation (catheterization, cystoscopy)
• Once in the bladder uropathogens multiply, then pass up the
ureters (especially if vesicoureteral reflux present) to the renal
pelvis and parenchyma
• Source of uropathogens: enteric bacteria

21. Pathophysiology of urinary tract infection
• Cystitis: localized infection of the bladder with superficial
neutrophilic inflammation of the mucosa (lower urinary tract
infection)
• Pyelonephritis: infection of the kidney with acute suppurative
inflammation of the pelvis, medullary and cortical tubules, and
corticomedullary intersititum (upper urinary tract infection)
• Urosepsis: bacteremia due to pyelonephritis
• Papillary necrosis: complication of pyelonephritis in diabetes and
urinary tract obstruction with coagulative necrosis of renal
pyramids and an intense inflammatory response between preserved
and necrotic tissue
• Sloughing of necrotic pyramids: complication of papillary necrosis
that can cause urinary tract obstruction (in some instances
sloughed portions voided and recovered in urine)
• Perinephric abscess: associated with obstruction of an infected
kidney with abscess formation in the pernephric space due to
extension of bacterial infection across the renal capsule

22. Pathophysiology contd……
• Uncomplicated urinary tract infection:
Bacterial or yeast infection in a structurally
and neurologically normal urinary tract
• Complicated urinary tract infection: Bacterial
or yeast infection in a urinary tract with
functional or structural abnormalities

23. Risk factors in complicated urinary tract infection
• Indwelling catheters
• Urinary calculi
• Neurogenic bladder
• Prostatic enlargement
• Uterine prolapse
• Urologic instrumentation or surgery
• Renal transplantation
• Diabetes mellitus

24. Bacterial virulence factors in urinary tract infection
• Escherichia coli strains expressing O-antigens O1, O2,
O4, O6, O7, O8, O75, O150, and O18ab cause high
proportion of infections
• Capsular K1, K5, and K12 antigens of E. coli associated
with clinical severity (antiphagocytic)
• P-fimbriae enhance mannose-resistant attachment of E.
coli to globoseries glycosphingolipid receptors (gal-gal)
of uroepithelial cells (P-fimbriated E. coli dominant as
cause of pyelonephritis and urosepsis)
• Type 1 fimbriae enhance mannose-susceptible
adherence of E. coli to uroepithelial cells (virtually all
cystitis-producing E. coli strains express type 1 fimbriae)
• Motile bacteria ascend the ureter against urine flow

25. Bacterial virulence factors in urinary tract infection
• Bacterial urease (Proteus, Corynebacterium urealyticum)
splits urinary urea with generation of ammonium ion that
alkalinizes urine with loss of acid pH as natural defense
barrier against infection, stone formation with ureteral
obstruction and survivial of bacteria deep within stones
resisting eradication by antibiotic, and alkaline-
encrusted cystitis
• Gram-negative endotoxin decreases ureteral peristalsis
• Hemolysin produced by many uropathogens damages
renal tubular epithelium and promotes invasive infection
• Aerobactin (a siderophore) present at increased
frequency in uropathogenic strains of E. coli promoting
intracellular iron accumulation for bacterial replication

26. Host protective factors in urinary tract infection
• Flushing mechanism of micturition a major protective
factor
• Low vaginal pH (3.5-4.5) (due to lactic acid produced by
action of Lactobacilli on glycogen of sloughed vaginal
epithelial cells) suppresses colonization by
uropathogens
• Normal acid pH of urine (4.6-6) anti-bacterial
• Urinary Tamm-Horsefall protein (secreted by ascending
loop of Henle) binds to mannose-sensitive fimbriae and
blocks E. coli attachment to uroepithelial cells
• Chemotactic interleukin-8 released upon bacterial
attachment to uroepithelial cells with recruitment of
phagocytic neutrophils and eradication of bacteriuria

27. Pathophysiology of urinary tract infection
• Hematogenous seeding of renal cortex less frequent
than ascending infection
• Kidney a common site of abscess formation in
Staphylococcus aureus bacteremia, less often in
candidemia, rarely with gram-negative bacteremia
• Hematogenous seeding of kidney also occurs with
Salmonella (typhoid) and Mycobacterium
tuberculosis
• Evidence for a role of periureteral and renal
lymphatics in urinary infection lacking

28. Common Uropathogens
• Escherichia coli
• Other Enterobacteriaceae (Klebsiella, Enterobacter,
Proteus, Citrobacter)
• Pseudomonas aeruginosa
• Enterococcus
• Staphylococcus saprophyticus
• Staphylococcus aureus1
• Streptococcus agalactiae (group B)2
• Candida
1Associated with staphylococcemia
2Denotes vaginal colonization in pregnant women

29. Uncommon Uropathogens
• Corynebacterium urealyticum1
• Haemophilus influenzae and H. parainfluenzae2
• Blastomyces dermatitidis3
• Neisseria gonorrhaeae4
• Mycobacterium tuberculosis5
1Colistin nalidixic acid (CNA) agar
2Chocolate agar
3Brain heart infusion, inhibitory mold, or Sabourad
dextrose agar
4Enhanced recovery with chocolate agar
5Lowenstein-Jensen medium, Middlebrook broth or
agar

30. Commensal Microflora of the Urethra
• Coagulase-negative staphylococci (except S.
saprophyticus)
• Viridans and non-hemolytic streptococci
• Lactobacilli
• Diphtheroids (Corynebacterium except C.
urealyticum)
• Saprophytic Neisseria
• Anaerobic bacteria

31. Common Risk Factors for Urinary Tract
Infection: Women
– Urinary tract obstruction (including calculi)
– Catheterization (straight, indwelling)
– Pregnancy
– Urologic instrumentation or surgery
– Neurogenic bladder
– Renal transplantation
– Sexual intercourse
– Estrogen deficiency (loss of vaginal lactobacilli)

32. Signs and Symptoms of Lower Urinary Tract Infection
• Inflammatory irritation of urethral and bladder
mucosa
• Frequent and painful urination of small volumes of
turbid urine
• Occasional suprapubic pain or sensation of
heaviness
• Fever generally absent

33. Signs and Symptoms of Upper Urinary Tract Infection
• Fever and chills (systemic reaction)
• Flank pain
• Lower urinary tract signs and symptoms (frequency,
urgency, and dysuria)

34. Asymptomatic Bacteriuria
• Presence of uropathogens by culture without signs
or symptoms of urinary tract infection
• Clinically significant (should be treated) with
preschool children (? vesicoureteral reflux,
congenital urinary tract anomaly), pregnant women,
and adults with obstructive uropathy
• Without clinical significance (should not be treated)
for adults in absence of urinary tract obstruction

35. Urinary Tract Specimens
• First-voided morning urine optimal (generally
bacteria have been proliferating in bladder urine for
several hours)
• Midstream urine specimens (initially voided urine
contains urethral commensals)
• Indwelling catheters (freshly placed, urine aspirated
by needle inserted into catheter) (Foley catheter tips
not acceptable)
• Straight catheter specimens
• Suprapubic aspirates (infants or children, recovery
of anaerobes)1
• Cystoscopic collection of urine
1Contamination-free specimen

36. Collection of Urine Specimens
• Urine collected in sterile specimen container must be
processed within 2 hours, or refrigerated and processed within
24 hours
• Urine collected in sterile specimen container with borate
preservative should be processed within 24 hours (no
refrigeration required)

37. Inoculation of Urine
• Inoculation of urine for quantitative culture (colony forming
units→cfu’s) performed with a calibrated 0.001 mL and 0.01 mL
plastic or wire loop
• Sheep blood agar (SBA) utilized for quantitative urine culture
• With 0.001 ml loop, 1 colony on SBA equivalent to 1,000 cfu’s per
mL of urine
• With 0.01 ml loop, 1 colony on SBA equivalent to 100 cfu’s per mL
of urine
• MacConkey agar utilized as selective differential agar for gram-
negative bacteria, colistin nalidixic acid agar as selective agar for
gram-positive bacteria, and chocolate agar for fastidious gram-
negative bacteria (Haemophilus)

38. Interpretation of Urine Cultures: General Guidelines
• A single species of Enterobacteriaceae recovered at
>105 cfu’s/mL urine: with patients symptomatic for
urinary tract infection, 95% probability of true
bacteriuria
• A single species of Enterobacteriaceae recovered at
104-105 cfu’s/mL urine: with patients symptomatic for
urinary tract infection, 33% probability of true
bacteriuira
• Gram-positive, fungal, and fastidious uropathogens
often present in lower numbers (104-105 cfu’s/mL urine)
• Urethral commensals recovered at <104 cfu’s/mL urine

39. Cumitech Guidelines for Inoculation of Urine Cultures1
• Routine: uncomplicated urinary tract infection in
ambulatory outpatients (0.001 mL loop, SBA, MAC; 24
hr incubation)
• Surveillance: neurogenic bladder, indwelling catheter,
geriatric patents (0.001 mL loop, SBA, MAC, CNA; 24 hr
incubation)
• Special: suprapubic aspirates or straight catheter
specimens where previous cultures negative,
unresponsive to therapy, or possibility of unusual
urinary tract pathogen (0.001 and 0.01 mL loop, BA,
MAC, CHOC; minimum 48 hr incubation)
1Clarridge, Johnson, Pezzlo, and Weissfeld, ASM Cumitech 2B, November 1998.

40. Cumitech Guidelines for Interpretation of Routine
Urine Cultures1
• One isolate at >104: Full ID and Susceptibility
• One or two gram-negative isolates at >105 and
other isolates at least 10X less: Full ID and
Susceptibility of gram-negative isolates
• Other patterns of isolates at >104:
Presumptive ID only
• Ignore mixed urethral flora at <104
1Clarridge, Johnson, Pezzlo, and Weissfeld, ASM Cumitech 2B, November
1998.

41. Cumitech Guidelines for Interpretation of
Surveillance Urine Cultures1
• One isolate at >104: Full ID and Susceptibility
• One gram-negative isolate at >105 with others at least
10X less: Full ID and Susceptibility
• Other patterns of isolates at >104: Presumptive ID only
• Ignore mixed urethral flora at <104
• One or two isolates at >102 to 105: Full ID and
Susceptibility
1Clarridge, Johnson, Pezzlo, and Weissfeld, Cumitech 2B, November 1998

42. ASM Manual Guidelines for Urine Culture Results
Likely to Be Significant1
• Midstream, female with cystitis, >102 with positive
urine leukocyte esterase
• Midstream, female with pyelonephritis, >105 with
positive urine leukocyte esterase
• Midstream, asymptomatic, >105 with negative urine
leukocyte esterase (usually)
• Midstream, male with UTI: >103 with leukocyte with
urine leukocyte esterase positive
• Straight catheter: >102 with urine leukocyte esterase
positive
• Indwelling catheter: >103 with urine leukocyte esterase
positive or negative
1 th

43. NMH Guidelines for Interpretation of Urine Cultures1
Urine leukocyte esterase positive
 One or two organisms at >103: Full ID and Susceptibility
 One organism at >104 with others (2 or more) at least 10X
less: Full ID and susceptibility of predominant organism
 Report all group B β-hemolytic streptococci for women <
50 years
1Modified from ASM Cumitech, ASM Manual, and CDC MMWR 2002;51 (RR-11):1-22

44. COMPLICATION
 UTIs are associated with risks to both the fetus
and the mother
* pyelonephritis
* preterm birth
* low birth weight
* increased perinatal mortality

45. Prevention
• Drink 6-8 glasses of water each day and eliminate
refined foods, fruit juices, caffeine, alcohol, and sugar.
• Take Vitamin C (250 to 500 mg), Beta-carotene (25,000
to 50,000 IU per day) and Zinc (30-50 mg per day) to
help fight infection.
• Develop a habit of urinating as soon as the need is felt
and empty your bladder completely when you urinate.
• Urinate before and after intercourse.
• Avoid intercourse while you are being treated for an UTI.

46. • After urinating, blot dry (do not rub), and keep your
genital area clean. Make sure you wipe from the
front toward the back.
• Avoid using strong soaps, douches, antiseptic
creams, feminine hygiene sprays, and powders.
• Avoid wearing tight-fitting pants.
• Don't soak in the bathtub longer than 30 minutes or
more than twice a day.

47. References
• Sobel and Kaye. Urinary Tract Infections. In
Mandell, Douglas, and Bennett’s Principles and
Practice of Infectious Diseases, 6th edition, Elsevier,
2005, pp. 975-905.
• Clarride, Johnson, Pezzlo, and Weissfeld.
Laboratory Diagnosis of Urinary Tract Infections.
Cumitech 2B, ASM Press, 1998, pp. 2-19.
• Thomson, Jr. and Miller. Specimen Collection,
Transport, and Processing: Bacteriology. In Manual
of Clinical Microbiology, 8th edition, ASM Press,
2003, pp. 286-330.
• Chapter 60. Infections of the Urinary Tract. In Bailey
& Scott’s Diagnostic Microbiology, 11th edition,
Mosby, pp. 927-938,

48. Thank You For Sincerely Paying Attention…