Infective endocarditis for urse student.pptx

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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.

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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 en docarditis 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 10 9 to 10 10 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 RFT

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.

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49. Classification of UTI 49 Epidemiologically as: Catheter-associated (or nosocomial ) infections 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 (>10 5 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 infections.

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/mm 3 )   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 10 5 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 >10 5 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 incidence of infection over the first 4 to 7 days.

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 (6 to 12 weeks).

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 OR Nitrofurantoin , 50 to 100mg, P.O, once daily or postcoita ;