Infective endocarditis is an inflammation of the endocardium, often categorized as acute or subacute based on severity and onset. Key risk factors include previous endocarditis, prosthetic valves, and congenital heart disease, with Streptococci and Staphylococci being the main etiologic agents. Clinical presentation can include peripheral manifestations such as Osler nodes and Janeway lesions, while treatment focuses on antibiotic therapy and potential surgical interventions.

1. Infective
endocarditis
1

2. Objective
2
 Definition and types of endocarditic
 Anatomy of Heart
 Risk factors
 Etiology
 Phatophysiology
 Clinical presentation
 Factors associated with increased mortality include
 Treatment
 Goal of therapy
 Antibiotic selection
 Two weeks and four weeks antibiotic treatment.

3. 3

4. Introduction
 Endocarditis is an inflammation of the
endocardium, the membrane lining the chambers
of the heart and covering the cusps of the heart
valves.
 Endocarditis is often referred to as acute and
subacute depending on the pace and severity of
the clinical presentation.
4

5. Introduction
5
 Acute endocarditis
 fulminating form
 involves the aortic valve
 is associated with high fevers and systemic
toxicity
 caused by virulent bacteria, such as
Staphylococcus aureus
 if untreated, death may occur within days to
weeks

6. Introduction
 Subacute
 is more indolent
 involve the mitral valve
 caused by less-invasive organisms, such as
viridans streptococci
 usually occurring in preexisting valvular heart
disease
6

7. Predisposing risk factors
 Presence of a prosthetic valve (highest risk)
 Previous endocarditis (highest risk)
 Congenital heart disease
 Chronic intravenous access
 Diabetes mellitus
 Healthcare-related exposure
 Acquired valvular dysfunction (e.g., rheumatic heart
disease)
 Hypertrophic cardiomyopathy
 Mitral valve prolapse with regurgitation
 IVDA
7

8. Etiology
 Three groups of organisms result in a majority of
cases: streptococci, staphylococci, and
enterococci
8

9. Pathophysiology
 The development of infective endocarditis via
hematogenous spread, the most common route,
requires the sequential occurrence of several
factors.
 The endothelial surface of the heart is damaged.
 This injury occurs with turbulent blood flow associated
with the valvular lesions previously described.
 Platelet and fibrin deposition occurs on the abnormal
epithelial surface.
 These platelet-fibrin deposits are referred to as
nonbacterial thrombotic endocarditis.
9

10. Pathophysiology
 Bacteremia gives organisms access to and
results in colonization of the endocardial surface.
 Bacteremia is the result of trauma to a mucosal
surface with a high concentration of resident bacteria,
such as the oral cavity and gastrointestinal tract.
 After colonization of the endothelial surface, a
"vegetation" of fibrin, platelets, and bacteria
forms. The protective cover of fibrin and platelets
allows unimpeded bacterial growth to
concentrations as high as 109 to 1010 organisms
per gram of tissue.
10

11. Pathophysiology
 The vegetations seen in infective endocarditis
may be single or multiple and vary in size from a
few millimeters to centimeters.
 Bacteria within the vegetation grow slowly and
are protected from antibiotics and host defenses.
 The adverse effects of infective endocarditis and
the resulting lesions can be far-reaching and
include
(a) local perivalvular damage
(b) embolization of septic fragments with potential
hematogenous seeding of remote sites
(c) formation of antibody complexes
11

12. Clinical Presentation
12

13. Peripheral manifestations
 Osler nodes:
 Purplish or erythematous subcutaneous papules or
nodules on the pads of the fingers and toes.
 These lesions are 2 to 15 mm in size and are painful
and tender.
 These nodes are not specific for infective endocarditis
and may be the result of embolism, immunologic
phenomena, or both.
 Janeway lesions:
 Hemorrhagic, painless plaques on the palms of the
hands or soles of the feet.
 These lesions are believed to be embolic in origin.
13

14. 14
 Janeway Lesions
Janeway lesions
Osler’s
Nodes

15. Peripheral manifestations
 Splinter hemorrhages:
 Thin, linear hemorrhages found under the nail beds of the
fingers or toes.
 These lesions are not specific for infective endocarditis and
more commonly are the result of traumatic injuries.
 Distal lesions are more likely the result of trauma, whereas
proximal lesions tend to be associated with infective
endocarditis.
 Petechiae:
 Small (usually 1 to 2 mm in diameter), erythematous,
painless, hemorrhagic lesions.
 These lesions appear anywhere on the skin but more
frequently on the anterior trunk, buccal mucosa and palate,
and conjunctivae.
 Petechiae are nonblanching and resolve after a few days.
15

16. 16
Splinter hemorrhages
Petechiae:

17. Peripheral manifestations
 Clubbing of the fingers:
 Proliferative changes in the soft tissues about
the terminal phalanges observed in long-
standing endocarditis.
 Roth spots:
 Retinal infarct with central pallor and
surrounding hemorrhage.
17

18. Peripheral manifestations
18
 Emboli:
 Embolic phenomena occur in up to one-third
of cases and may result in significant
complications.
 Left-sided endocarditis can result in renal
artery emboli causing flank pain with
hematuria, splenic artery emboli causing
abdominal pain, and cerebral emboli, which
may result in hemiplegia or alteration in
mental status.
 Right-sided endocarditis may result in
pulmonary emboli, causing pleuritic pain with
hemoptysis.

19. Investigations
19
 CBC, ESR or CRP, Rheumatoid factor
 Urine examination (for microscopic hematuria and
proteinuria)
 Blood culture-three blood culture sets (each with two
bottles), separated from one another by at least 1hr,
should be obtained from different venipuncture sites
over 24h.
 If the cultures remain negative after 48–72 hours
and empiric antibiotic are not started, two or
three additional blood culture sets should be
obtained
 Echocardiography

20. Prognosis
 Factors associated with increased mortality
include
(a) heart failure
(b) increasing age
(c) endocarditis caused by resistant organisms
such as fungi or gram-negative bacteria
(d) left-sided endocarditis caused by S. aureus
(e) paravalvular complications
(f) healthcare-acquired infection
(g) PVE (prosthetic valve endocarditis)
20

21. Treatment
 Desired Outcomes
 The desired outcomes for treatment and prophylaxis of
infective endocarditis are to:
 Relieve the signs and symptoms of the disease
 Decrease morbidity and mortality
 Eradicate the causative organism with minimal drug
exposure
 Provide cost-effective antimicrobial therapy
determined by the likely or identified pathogen, drug
susceptibilities, hepatic and renal function, drug
allergies, and anticipated drug toxicities.
 Prevent infective endocarditis from occurring or
recurring in high-risk patients with appropriate
prophylactic antimicrobials.
21

22. General Approach to Treatment
 The most important approach in the treatment of
infective endocarditis is
 isolation of the infecting pathogen and
determination of antimicrobial susceptibilities
 followed by high-dose, parenteral, bactericidal
antibiotics for an extended period.
22

23. Nonpharmacologic Therapy
 Surgery
 valvectomy and valve replacement
23

24. Pharmacologic Therapy
 Streptococcal endocarditis
Therapy of Native Valve Endocarditis Caused by Highly Penicillin-
Susceptible Viridans Group Streptococci and Streptococcus bovis
24

25. Streptococcal endocarditis
 The following conditions should all be present
to consider a 2-week treatment regimen:
✓ The isolate is penicillin sensitive (MIC less than
or equal to 0.1 mcg/mL).
✓ There are no cardiovascular risk factors such as
heart failure, aortic insufficiency, or conduction
abnormalities.
✓ No evidence of thrombotic disease.
✓ Native valve infection.
✓ No vegetation greater than 5 mm diameter.
✓ Clinical response is evident within 7 days.
25

26. Streptococcal endocarditis
Therapy for Endocarditis of Prosthetic Valves or Other Prosthetic
Material Caused by Viridans Group Streptococci and Streptococcus
bovis
26

27. Staphylococcal endocarditis
 S. aureus has become more prevalent as a
cause of endocarditis because of increased IV
drug abuse, frequent use of peripheral and
central venous catheters, and valve-
replacement surgery.
 Coagulase-negative staphylococci (CNST,
usually S. epidermidis) are prominent causes of
PVE.
27

28. Staphylococcal endocarditis
Therapy for Endocarditis Caused by Staphylococci in the Absence
of Prosthetic Materials
28

29. Staphylococcal endocarditis
Therapy for Prosthetic Valve Endocarditis Caused by
Staphylococci
29

30. Enterococcal endocarditis
 Enterococci cause 5% to 18% of endocarditis
cases and are noteworthy for the following
reasons:
(1) no single antibiotic is bactericidal
(2) MICs to penicillin are relatively high (1 to 25
mcg/mL)
(3) they are intrinsically resistant to all cephalosporins
and relatively resistant to aminoglycosides (i.e., “low-
level” aminoglycoside resistance)
(4) combinations of a cell wall– active agent, such as a
penicillin or vancomycin, plus an aminoglycoside are
necessary for killing.
(5) resistance to all available drugs is increasing.
30

31. Enterococcal endocarditis
 In addition to isolates with high-level
aminoglycoside resistance, β-lactamase-
producing enterococci (especially Enterococcus
faecium) are increasingly reported.
 If these organisms are discovered, use of
vancomycin or ampicillin-sulbactam in
combination with gentamicin should be
considered.
 Vancomycin-resistant enterococci, particularly
E. faecium, are becoming more common.
31

32. Enterococcal endocarditis
Therapy for Native Valve or Prosthetic Valve Enterococcal
Endocarditis Caused by Strains Susceptible to Penicillin,
Gentamicin, and Vancomycin
32

33. Empiric treatment of “community
acquired” Native Valve SBE (STG -
2014)
33

34. Empiric treatment of health care–
associated and IV medicine users
endocarditis (STG - 2014)
34

35. Organism specific antibiotic
therapy (STG - 2014)
35
 A. Penicillin susceptible and relatively penicillin
resistant streptococci
 Treat with the emperic treatment regimen for
“community acquired” Native Valve SBE (see
table)
 B. Moderately penicillin-resistant streptococci
and nutritionally variant organisms
 Treat with the empiric regimen for“community
acquired” Native Valve SBE (see table) with
the following modifications:

36. Organism specific antibiotic
therapy (STG - 2014)
36
Prolong the duration crystalline penicillin G to 6
wks and increase dose to 4-5million U, Q4hr
Prolong the duration of ceftriaxone to 6 weeks
Prolong the duration of gentamicin for 6 weeks
with close renal monitoring
Vancomycin based regimen (if available and
affordable) is preferable

37. Methicillin–suceptible Staphylococcal
endocarditis with out prosthetic material
(STG - 2014)
37
Methicillin–Resistant Staphylococcal endocarditis with
out prosthetic material

38. Enterococcal Infective
Endocarditis (STG - 2014)
38

39. Evaluation of Therapeutic
Outcomes
 Signs and Symptoms
 Fever usually subsides within 1 week of initiating therapy
 Persistence of fever may indicate ineffective
antimicrobial therapy, emboli, infections of intravascular
catheters, or drug reactions
 For some patients, low-grade fever may persist even
with appropriate antimicrobial therapy.
 Blood Cultures
 Blood cultures should be negative within a few days
 Blood cultures should be rechecked until negative after
the initiation of therapy.
 Additional blood cultures should be rechecked after
successful treatment , once or twice within the 8 weeks
after treatment to ensure cure.
39

40. Evaluation of Therapeutic
Outcomes
 Microbiologic Tests
 For all isolates from blood cultures, MICs should
be determined
 Serum Drug Concentrations
 aminoglycosides (except streptomycin) and
vancomycin
40

41. Prevention
Cardiac Conditions Associated with the Highest Risk of Adverse Outcome
from Endocarditis for Which Prophylaxis with Dental Procedures Is
Recommended
41

42. Prevention
 Antimicrobial prophylaxis is used to prevent IE
in patients believed to be at high risk.
Antibiotic Regimens for a Dental Procedure
42

43. 43
Urinary Tract Infections
and
Prostatitis

44. Introduction
44
 A UTI is defined as the presence of microorganisms in
the urinary tract that cannot be accounted for by
contamination.
 Infections of the urinary tract represent a wide variety
of syndromes, including urethritis, cystitis, prostatitis,
and pyelonephritis.
 Urinary tract infections (UTIs) are the most commonly
occurring bacterial infections, especially in females of
child-bearing age.
 The female urethra is relatively short and allows
bacteria easy access to the bladder.
 In contrast, males are partly protected because the
urethra is longer and antimicrobial substances are
secreted by the prostate.

45. Introduction
45
 Urinary tract infections again become a
problem for males after the age of 50, when
prostatic obstruction, urethral instrumentation,
and surgery influence the infection rate.
 Infection in younger men is rare and requires
careful evaluation for urinary tract pathology

46. Introduction
46
 Classification of UTI
 Anatomical classification
 Lower tract infections cystitis (bladder), urethritis,
prostatitis
 Upper tract infection pyelonephritis
 Complications
 Uncomplicated infections occur in individuals who
lack structural or functional abnormalities of the
urinary tract that interfere with the normal flow of
urine or voiding mechanism

47. Introduction
47
 Complicated UTIs are the result of a
predisposing lesion of the urinary tract, such as
a congenital abnormality or distortion of the
urinary tract, a stone, indwelling catheter,
prostatic hypertrophy, obstruction, or neurologic
deficit that interferes with the normal flow of
urine and urinary tract defenses.

48. 48

49. Classification of UTI
49
Epidemiologically as:
1. Catheter-associated (or nosocomial) infections
2. Non-catheter-associated (or community-
acquired) infections

50. Classification of UTI
50
 Recurrent UTIs in healthy nonpregnant women—three
or more UTIs occurring within 1 year—are a common
problem.
 characterized by multiple symptomatic infections with
asymptomatic periods occurring between each episode
 may be either reinfections or relapses
 Asymptomatic bacteriuria is a common finding (>105
bacteria/mL of urine) -very common in elderly women and
men
 Symptomatic abacteriuria or acute urethral syndrome
consists of symptoms of frequency and dysuria in the
absence of significant bacteriuria.
 This syndrome is commonly associated with Chlamydia

51. Epidemiology
51
 The prevalence of UTIs varies with age and
gender.
 In newborns and infants up to 6 months of age
 the prevalence of abacteriuria is approximately
1%
 more common in boys
 associated with structural or functional
abnormalities of the urinary tract
 also have been correlated with noncircumcision.

52. Epidemiology
52
 Between the ages of 1 and 6 years
 UTIs occur more frequently in females
 Infections occurring in preschool boys usually are
associated with congenital abnormalities of the
urinary tract
 often are symptomatic
 the majority of renal damage associated with UTI
develops

53. Epidemiology
53
 Through grade school and before puberty
 the prevalence of UTI is approximately 1%
 increases dramatically to 1% to 4% after puberty in
nonpregnant females primarily as a result of sexual activity
 In the elderly, the ratio of bacteriuria in women and
men is dramatically altered and is approximately equal
in persons older than age 65 years.
 obstruction from prostatic hypertrophy in males
 poor bladder emptying as a result of prolapse in females
 fecal incontinence in demented patients
 neuromuscular disease including strokes
 increased urinary instrumentation (catheterization)

54. Etiology
54
 Uncomplicated UTIs
 Escherichia coli, which accounts for 80% to 90%
of community-acquired infections
 Staphylococcus saprophyticus
 Klebsiella pneumoniae
 Proteus spp.
 Pseudomonas aeruginosa
 Enterococcus spp.

55. Etiology
55
 Complicated UTI
 E. coli accounts for less than 50% of infections.
 Proteus spp.
 K. pneumoniae, Enterobacter spp.
 P. aeruginosa
 Staphylococci
 enterococci

56. Etiology
56
 Community-Acquired Infections
 Most UTI are caused by gram-negative aerobic
bacilli from the intestinal tract.
 Escherichia coli cause 75% to 90%
 Coagulase negative staphylococci (i.e.,
Staphylococcus saprophyticus) account for another
5% to 20% of UTI in younger women.
 Other Enterobacteriaceae (Proteus mirabilis,
Klebsiella) and Enterococcus faecalis also are
common pathogens.
 Uncomplicated infections are nearly always caused
by only a single organism.

57. Etiology
57
 Hospital-Acquired Infections
 Up to 10% of hospitalized patients develop
Urinary tract infections
 E. coli remains the most common pathogen (5%
to 20%)
 Pseudomonas aeruginosa, Proteus, Enterobacter,
Serratia, and Acinetobacter (up to 25%)
 Enterococcus (25%)
 UTI caused by Staphylococcus aureus are
usually the result of hematogenous spread
 Candida albicans (20% to 30% of cases)

58. Pathophysiology
58
 The usual pathway for the spread of bacteria to the
urinary tract is the ascending route.
 A UTI usually begins with heavy and persistent
colonization of the introitus (i.e., vaginal vestibule
and urethral mucosa) with intestinal bacteria,
especially in women with recurrent UTI.
 Once introital colonization has occurred,
colonization of the urethra leads to retrograde
infection of the bladder.

59. Pathophysiology
59
 The bladder has additional defense
mechanisms that prevent spread of the
infection after urethral colonization occurs.
 Urination washes bacteria out of the bladder
and is effective if urine flows freely and the
bladder is emptied completely.
 Substances in the urine, including organic
acids (which contribute to a low pH) and urea
(which contributes to a high osmolality), are
antibacterial.

60. Pathophysiology
60
 The bladder mucosa (glycosaminoglycan) also has
antibacterial properties.
 Lastly, other substances, including IgA and
glycoproteins (e.g., Tamm-Horsfall protein), are
actively secreted into the urine and act to prevent
adherence of bacteria to uroendothelial Cells.
 The presence of Lactobacillus in the vaginal
flora and circulating estrogen levels also
prevent UTI.
 Focal renal involvement may result from the
spread of bacteria via the ureters and may be
facilitated by vesicoureteral reflux or decreased
ureteral peristalsis.

61. Pathophysiology
61
 Reflux can be produced by cystitis alone or by
anatomic defects.
 Ureteral peristalsis is decreased by pregnancy,
ureteral obstruction, or gram-negative bacterial
endotoxins.

62. Predisposing Factors
62
 Extremes of age
 Female gender
 Sexual activity
 Use of contraception
 Pregnancy
 Instrumentation
 Urinary tract obstruction
 Neurologic dysfunction
 Renal disease
 Previous antimicrobial use

63. Clinical Presentation
63
 Signs and symptoms
 Lower UTI: dysuria, urgency, frequency, nocturia,
suprapubic heaviness, Gross hematuria
 Upper UTI: flank pain, fever, nausea, vomiting,
malaise
 Physical examination
 Upper UTI: costo vertebral angle tenderness
 Laboratory tests
 Bacteriuria
 Pyuria (white blood cell count >10/mm3)
 Nitrite-positive urine (with nitrite reducers)
 Leukocyte esterase-positive urine
 Antibody-coated bacteria (upper UTI)

64. Clinical Presentation
64
 Urine culture – indicated in complicated UTIs,
recurrent UTI, Pyelonephritis and urosepsis.
Significant bacteriuria is defined as the presencr
of 105 bacteria /ml (CFU) of urine in clean catch
specimen. In women with symptomatic UTI
alower bacterial count should be used as 1/3 of
symptomatic women have CFU counts
below105 bacteria /ml. (e.g. 100 CFU/ml will
have higher positive predictive value)

65. Treatment
65
 Desired Outcome
 The goals of UTI treatments are
(a) to eradicate the invading organism(s)
(b) to prevent or to treat systemic consequences of
infection
(c) to prevent the recurrence of infection

66. General principles
66
 The management of a patient with a UTI
includes initial evaluation, selection of an
antibacterial agent and duration of therapy,
and follow-up evaluation.
 The initial selection of an antimicrobial agent
for the treatment of UTI is primarily based on
the severity of the presenting signs and
symptoms, the site of infection, and whether
the infection is determined to be complicated
or uncomplicated.

67. Pharmacologic treatment
67
 The therapeutic management of UTIs is best
accomplished by first categorizing the type of
infection: acute uncomplicated cystitis,
symptomatic abacteriuria, asymptomatic
bacteriuria, complicated UTIs, recurrent infections,
or prostatitis.

68. Acute Uncomplicated Cystitis
68
 the most common form of UTI
 typically occur in women of childbearing age
 often are related to sexual activity
 associated with dysuria, frequency, urgency,
and suprapubic discomfort
 goal of treatment for uncomplicated cystitis is
 to eradicate the causative organism
 to reduce the incidence of recurrence caused by
relapse or reinfection

69. Acute Uncomplicated Cystitis
69
 Short-course therapy is the treatment of choice
for uncomplicated lower UTIs
 Three-day courses of trimethoprim-
sulfamethoxazole or a fluoroquinolone (e.g.,
ciprofloxacin, levofloxacin, or norfloxacin)
 A 5-day course of nitrofurantoin
 Advantages of short-course therapy include
 increased compliance
 fewer side effects
 decreased cost
 less potential for the development of resistance.

70. Symptomatic Abacteriuria/acute
urethral syndrome
70
 represents a clinical syndrome in which females present
with dysuria and pyuria but the urine culture reveals less
than 105 bacteria/mL of urine.
 Causative agents : E. coli, Staphylococcus spp., or
Chlamydia trachomatis, Neisseria gonorrhoeae,
Gardnerella vaginalis
 Single-dose or short-course therapy with trimethoprim-
sulfamethoxazole
 If the patient reports recent sexual activity, therapy for C.
trachomatis should be considered.
 Chlamydial treatment should consist of 1 g
azithromycin or doxycycline 100 mg twice daily for 7
days.

71. Asymptomatic Bacteriuria
71
 the finding of two consecutive urine cultures with
>105 organisms/mL of the same organism in the
absence of urinary symptoms
 Most patients with asymptomatic bacteriuria are
elderly, Pregnant women and female.

72. Complicated Urinary Tract
Infections
72
 Acute Pyelonephritis
 Present with high-grade fever (>38.3°C [100.9°F]) and
severe flank pain
 Symptoms of nausea, vomiting, and dehydration may
require hospitalization.
 Gram stain of the urine should be performed, along with a
urinalysis, culture, and sensitivity tests.
 The goals of treatment include
 the achievement of therapeutic concentrations of an
antimicrobial agent in the bloodstream and urinary
 sufficient therapy to eradicate residual infection in the
tissues of the urinary tract.

73. Acute Pyelonephritis
73
 In the mildly to moderately symptomatic patient
in whom oral therapy is considered
 Agents such as trimethoprim-sulfamethoxazole and
the fluoroquinolones are the agents of choice.
 If a Gram stain reveals gram-positive cocci,
Enterococcus faecalis should be considered and
treatment directed against this potential pathogen
(ampicillin)

74. Acute Pyelonephritis
74
 In the seriously ill patient, parenteral therapy
should be administered initially.
 intravenous fluoroquinolone, an aminoglycoside
with or without ampicillin, and extended-spectrum
cephalosporins with or without an aminoglycoside
are the agents of choice
 Other options include aztreonam, the -lactamase
inhibitor combinations (e.g., ampicillin-sulbactam,
ticarcillin-clavulanate, and piperacillin-tazobactam),
carbapenems (e.g., imipenem, meropenem,
doripenem or ertapenem), or intravenous
trimethoprim-sulfamethoxazole.

75. Acute Pyelonephritis
75
 If the patient has been hospitalized within the
past 6 months, has a urinary catheter, or is a
nursing home resident, the possibility of P.
aeruginosa and enterococci, as well as multiple
resistant organisms, should be considered
 ceftazidime, ticarcillin-clavulanate, piperacillin,
aztreonam, meropenem, or imipenem in combination
with an aminoglycoside is recommended
 Ertapenem should not be used in this case owing to
its inactivity against enterococci and P. aeruginosa.

76. Acute Pyelonephritis
76
 Effective therapy should stabilize the patient within
12 to 24 hours.
 A significant reduction in urine bacterial
concentrations should occur in 48 hours.
 Usually by the third day of therapy the patient is
afebrile and significantly less symptomatic
 The patient has been afebrile for 24 hours,
parenteral therapy may be discontinued, and oral
therapy instituted to complete a 2-week course.
 Followup urine cultures should be obtained 2
weeks after completion of therapy to ensure a
satisfactory response and detect possible relapse

77. 77
 The conventional view is that therapy in males requires
prolonged treatment
 A urine culture should be obtained before treatment, because the
cause of infection in men is not as predictable as in women.
 Single-dose or short-course therapy is not recommended in
males.
 If gram-negative bacteria are presumed,
 trimethoprim–sulfamethoxazole or a fluoroquinolone is a
preferred agent.
 because these agents achieve high renal tissue, urine, and prostatic
concentrations.
 Initial therapy is for 10 to 14 days.
 For recurrent infections in males, cure rates are much higher
with a 6-week regimen of trimethoprim–sulfamethoxazole.
Urinary Tract Infections in Males

78. Recurrent Infections
78
 Recurrent episodes of UTI (reinfections and relapses)
account for a significant portion of all UTIs.
 These patients are most commonly women and can be
divided into two groups: those with fewer than two or three
episodes per year and those who develop more frequent
infections.
 In patients with infrequent infections (i.e., fewer than three
infections per year), each episode should be treated as a
separately occurring infection.
 Short-course therapy should be used in symptomatic female
patients with lower tract infection.
 In patients who have frequent symptomatic infections, long-
term prophylactic antimicrobial therapy may be instituted
 Therapy is generally given for 6 months, with urine cultures
followed periodically.

79. Recurrent Infections
79
 In women who experience symptomatic
reinfections in association with sexual activity,
voiding after intercourse may help prevent
infection.
 Also, self-administered, single-dose prophylactic
therapy with trimethoprim– sulfamethoxazole
taken after intercourse has been found to
significantly reduce the incidence of recurrent
infection in these patients.
 Women who relapse after short-course therapy
should receive a 2-week course of therapy.

80. Recurrent Infections
80
 In patients who relapse after 2 weeks, therapy
should be continued for another 2 to 4 weeks.
 If relapse occurs after 6 weeks of treatment,
urologic examination should be performed, and
therapy for 6 months or even longer may be
considered.

81. Urinary Tract Infection in
Pregnancy
81
 During pregnancy, significant physiologic changes
occur to the entire urinary tract that dramatically
alter the prevalence of UTIs and pyelonephritis.
 Severe dilation of the renal pelvis and ureters,
decreased ureteral peristalsis, and reduced bladder tone
occur during pregnancy.
 These changes result in urinary stasis and reduced
defenses against reflux of bacteria to the kidneys.
 In addition, increased urine content of amino acids,
vitamins, and nutrients encourages bacterial growth.
 All of these factors increase the incidence of
bacteriuria, resulting in symptomatic infections,
especially during the third trimester.

82. Urinary Tract Infection in
Pregnancy
82
 Asymptomatic bacteriuria occurs in 4% to 7% of pregnant
patients.
 Of these, 20% to 40% will develop acute symptomatic
pyelonephritis during pregnancy.
 If untreated, asymptomatic bacteriuria has the potential to
cause significant adverse effects, including prematurity, low
birth weight, and stillbirth.
 Treatment is recommended in order to avoid possible
complications during the pregnancy.
 Therapy should consist of an agent with a relatively low
adverse-effect potential (a sulfonamide, cephalexin,
amoxicillin, amoxicillin/clavulanate, nitrofurantoin)
administered for 7 days.

83. Urinary Tract Infection in
Pregnancy
83
 Tetracyclines should be avoided because of teratogenic
effects
 sulfonamides should not be administered during the
third trimester because of the possible development of
kernicterus and hyperbilirubinemia.
 Also, the fluoroquinolones should not be given because
of their potential to inhibit cartilage and bone
development in the newborn.
 A follow-up urine culture 1 to 2 weeks after completing
therapy and then monthly until gestation is complete is
recommended.

84. Catheterized Patients
84
 When bacteriuria occurs in the asymptomatic,
short-term catheterized patient (less than 30 days),
the use of systemic antibiotic therapy should be
withheld and the catheter removed as soon as
possible.
 If the patient becomes symptomatic, the catheter
should again be removed, and treatment as
described for complicated infections should be
started.
 The use of prophylactic systemic antibiotics in
patients with short-term catheterization reduces the

85. Catheterized Patients
85
 In long-term catheterized patients, however,
antibiotics only postpone the development of
bacteriuria and lead to emergence of resistant
organisms.

86. Prostatitis
86
 Bacterial prostatitis is an inflammation of the
prostate gland and surrounding tissue as a
result of infection.
 It is classified as
 Acute
 characterized by a sudden onset of fever,
tenderness, and urinary and constitutional
symptoms
 chronic.
 presents with few symptoms related to the prostate
but rather symptoms of urinating difficulty, low back
pain, perineal pressure, or a combination of these
 Prostatitis occurs rarely in young males, but it is
commonly associated with recurrent infections
in persons older than 30 years of age.

87. Etiology
87
 Gram-negative enteric organisms are the most
frequent pathogens in acute bacterial prostatitis.
 E. coli is the predominant organism, occurring in
75% of cases.
 Other gram-negative organisms frequently
isolated include K. pneumoniae, P. mirabilis, and
less frequently, P. aeruginosa, Enterobacter spp.,
and Serratia spp.
 Occasionally, cases of gonococcal and
staphylococcal prostatitis occur, but they are
infrequent.

88. Pathophysiology
88
 The possible routes of infection include ascending
infection of the urethra, reflux of infected urine into
prostatic ducts, invasion by rectal bacteria through
direct extension or lymphatic spread, and by
hematogenous spread.
 A number of physiologic factors are believed to
contribute to the development of prostatitis.
 altered prostate secretory functions
 Prostatic fluid obtained from normal males contains prostatic
antibacterial factor
 The pH of prostatic secretions in patients with
prostatitis is altered, become more alkaline (normal
PH 6.6 to 7.6).

89. Clinical Presentation
89
 Signs and symptoms
 Acute bacterial prostatitis: high fever, chills, malaise, myalgia, localized
pain (perineal, rectal, sacrococcygeal), frequency, urgency, dysuria,
nocturia, and retention
 Chronic bacterial prostatitis: voiding difficulties (frequency, urgency,
dysuria), low back pain, and perineal and suprapubic discomfort
 Physical examination
 Acute bacterial prostatitis: swollen, tender, tense, or
indurated gland
 Chronic bacterial prostatitis: boggy, indurated (enlarged)
prostate in most patients
 Laboratory tests
 Bacteriuria
 Bacteria in expressed prostatic secretions

90. Treatment
90
 Most patients can be managed with oral
antimicrobial agents, such as trimethoprim-
sulfamethoxazole and the fluoroquinolones (e.g.,
ciprofloxacin, levofloxacin)
 Other effective agents in this setting include
cephalosporins, and -lactam–-lactamase
combinations.
 The total course of antibiotic therapy should be 4
weeks in order to reduce the risk of development
of chronic prostatitis.
 Therapy may be prolonged with chronic prostatitis

91. Treatment
91
 Long-term suppressive therapy also may be
initiated for recurrent infections, such as three
times weekly ciprofloxacin, trimethoprim-
sulfamethoxazole regular-strength tablet daily,
or nitrofurantoin 100 mg daily.

92. Empirical Treatment of Urinary
Tract Infections and Prostatitis
92

93. A. Acute, Uncomplicated UTI in
women (STG - 2014)
93
 First line
 Ciprofloxacin, 500mg P.O., BID, for 3 days
 OR
 Norfloxacin, 400mg P.O.,BID, for 3 days.
 Alternatives
 Nitrofurantoin 50mg P.O., QID for 7 days
 OR
 Cefpodoxime proxetil 100mg P.O, BID for 3 days
 OR
 Cotrimoxazole (Trimethoprim-sulphamethoxazole)
160/800mg P.O, BID for 3 days

94. B. Acute uncomplicated
Pyelonephritis in non-pregnant
women: (STG - 2014)
94
 Mild and moderate acute uncomplicated
pyelonephritis (able to tolerate oral therapy
with no vomiting, no dehydration, no
evidence of sepsis):
 First line
 Ciprofloxacin, 500mg P.O., BID, oral for 7-10 days
 Alternatives
 Cotrimoxazole(Trimethoprim-sulphamethoxazole),
160/800mg P.O, BID for 14 days
 OR
 Cefpodoxime proxetil, 200mg P.O., BID for 10 days

95. Severe acute uncomplicated
pyelonephritis (STG - 2014)
95
 High fever, high white blood cell count,
vomiting, dehydration, or evidence of sepsis)
or
 Fails to improve during an initial outpatient
treatment period – intreavenous therapy
should be started and continued until the
patient improves (usually at 48–72 hours).
 On discharge oral therapy is continued to
complete 10-14 days course.
 Antibiotics should be started after urine culture
sample is collected.

96. Severe acute uncomplicated
pyelonephritis (STG - 2014)
96
 First line
 Ciprofloxacin, 400mg, I.V, BID till patient
improves and continue oral Ciprofloxacin
500mg, PO, BID to complete 10-14 days
course
 Alternatives
 Ceftriaxone, 2gm, I.V, daily or 1gm, I.V, BID till
patient improves and continue oral
Ciprofloxacin 500mg, PO, BID to complete 10-
14 days course.

97. Severe acute uncomplicated
pyelonephritis (STG - 2014)
97
 N.B.
 If no response in 48-72 hrs ultrsasound is
warranted therapy to evaluate for obstruction,
abscess, or other complications of
pyelonephritis.
 If no obstruction or complication is not found
gram positive organisms such as enterococci
and S. saprophyticus should be covered with
Penicillins and aminoglycoside combination

98. C. Complicated UTIs and UTI in
men (STG - 2014)
98
 Factors which suggest complicated UTI: The
presence of an indwelling catheter or the use of
intermittent bladder catheterization, obstructive
uropathy of any etiology, stones, vesicoureteric
reflux or other functional abnormalities, peri-and
postoperative UTI, CKD and transplantation,
diabetes mellitus and immunodeficiency states.
 First line and alternatives – similar to
uncomplicated UTIs but needs prolonged duration
and response should be closely followed as gram
postives could be the cause.

99. D. Recurrent UTI in women (STG
- 2014)
99
 Women with recurrent UTI who are sexually active
should be advised to void after each sexual
intercourse (postcoital voiding) and have liberal
fluid intake.
 Antibiotic prophylaxis is recommended for women
who experience two or more symptomatic UTIs
within six months or three or more over 12
months.
 The degree of discomfort experienced by the
woman needs to be considered in the decision.
 Recurrent pyelonephritis deserves prophylaxis.

100. D. Recurrent UTI in women (STG
- 2014)
100
 Any prophylaxis should be given after current
active infection is treated.
 Antibiotic regimens:
 Continuous: daily at night time
 Postcoital: Single dose after coitus
 Duration of antibiotics-for six months followed by
observation.
 If recurrent UTI comes again the prophylaxis
can be prolonged for 1-2years.

101. D. Recurrent UTI in women (STG
- 2014)
101
 Antibiotic choices:
 First line
 Cotrimoxazole, 240mg, P.O., daily OR 3x per week
OR postcoital
 Alternatives
 Cephalexin, 125 – 250mg, P.O., once daily or
postcoital
 OR Norfloxacin, 200mg, P.O., once daily or
postcoital
 OR Ciprofloxacin, 125mg, P.O., once daily or
postcoital