Anaerobes have been involved in different types of urinary tract infection (UTI ). 1,2 These include acute and chronic urethritis, cystitis, para- or periurethral cellulitis or abscess, acute and chronic prostatitis, prostatic and scrotal abscesses, periprostatic phlegmon, ureteritis, periureteritis, pyelitis, pyelonephritis, renal abscess, scrotal gangrene, metastatic renal infection pyonephrosis, perinephric abscess, retroperitoneal abscess, and other infections. The clinical presentation and diagnosis of anaerobic infection are not different than those caused by aerobic and facultative bacteria.
Microbiology
The majority of UTI are due to Gram-negative aerobic or facultative bacilli, that include Escherichia, Klebsiella, , Pseudomonas, Serratia, Proteus, and Pseudomonas spp. The anaerobes implicated in UTI are Gram negative bacilli (including Bacteroides fragilis group and pigmented Prevotella and Porphyromonas spp.), Clostridium spp., anaerobic Gram-positive cocci, and Actinomyces spp. They are often isolated mixed with Enterobacteriaceae or streptococci. 1,2
URINARY TRACT INFECTION (UTI)
Pathogenesis
The patient's bacterial flora is usually the source of the UTI . Since anaerobes are the major component of the cervical and fecal flora, it is not surprising that they can cause UTI.
The usual route infection is through ascension of organisms from the external genitalia and the periurethral region rather than a hematogenous one, or by direct extension from adjacent organs. Anaerobes constitute 95% of the organisms of the female periurethral area.3 The colonization of the males urethra with anaerobes is related to sexual activity. The presence of anaerobes at these sites may explain their mode of infectivity. Patients with indwelling urethral catheters have a high incidence of anaerobes in the urine. 4
The low medullary blood flow, plasma skimming, and countercurrent flow all promote decreased oxygen supply to the medulla, assisting the growth of anaerobes. The oxygen tension of the urine is sharply decreased in the dehydrated patient, which predisposes to anaerobic UTI .
Diagnosis
Symptoms may be absent, especially in chronic infections. Signs include dull or sharp pain and tenderness in the kidney area or abdomen. Hypertension, anemia and chronic renal failure may occur in long-standing and severe cases. Leukocytosis ranges from 15,000 to 35,000/cu mm.
Urgency and dysuria are seen in cystitis and fever, chills, flank pain, nausea and vomiting, frequency, urgency, dysuria, and elevated sedimentation rate (>30 mm/hr) are typical for acute pyelonephritis.
At least two consecutive positive urine cultures are needed for diagnosis. Voided specimens are unreliable for diagnosis Suprapubic aspiration is the preferred method. It is recommended that appropriate cultures for anaerobes be obtained in symptomatic cases where routine cultures fail to yield bacterial growth, and gram stain shows bacteria in the urine sediment.
Management
Surgical repair of obstructive lesions is indicated. Administration of appropriate antibiotic therapy is required. A prolonged course of therapy (two to six months or longer) may be needed for recurrent infections.
Acute uncomplicated infection, which is often caused by enteric organisms such as E. coli, is generally treated by oral sulfonamides, trimethoprim-sulfamethoxazole, ampicillin, or a quinolone (in adults). At least 10 days of therapy is required for patients with pyelonephritis, reflux, or urinary tract abnormalities and for those who have not yet been evaluated radiographically. A shorter course (3 to 4 days) can be given for cystitis.
Isolation of anaerobes requires the administration of effective agents. Penicillin or cephalosporins can be used against most anaerobes; however, the recovery of penicillin-resistant anaerobes requires administration of clindamycin, ticarcillin, cefoxitin, metronidazole, a carbapenem or the combination of a penicillin plus a beta-lactamase inhibitor. Some of the newer quinolones have extended coverage against anaerobic bacteria (e.g. moxifloxacin).
Complications
Bacteremia can follow urologic procedures.4 Chronic renal disease can develop after repeated UTI in patients with obstructive uropathy, neurogenic bladder, structural renal disease, or diabetes. Untreated UTI can lead to renal abscess, pyelonephrosis, perinephric or retroperitoneal abscess.5
GENITOURINARY SUPPURATIVE INFECTIONS: PERINEPHRIC AND RENAL ABSCESSES
These abscesses are often misdiagnosed and consequently, mistreated or treated too late. 5-7 The newer imaging methods allow for an earlier diagnosis and a more accurate anatomical identification, enabling a less invasive therapeutic approach. 8
Microbiology
Suppurative genitourinary infections involve anaerobic bacteria in up to a quarter of cases. 8,9 The predominant anaerobes are Bacteroides spp. and anaerobic cocci. The predominate aerobes are S. aureus, Enterobacteriaceae (especially E. coli ), Pseudomonas sp., Enterococcus spp., coagulase-negative staphylococci, Streptococcus spp., Actinomyces spp., Fungi and Mycobacterium tuberculosis.5,6
Pathogenesis
Bacteria invasion of the perinephric space is through direct extension from an intrarenal abscess or by vesicoureteral reflux, urinary tract obstruction or surgery of the urinary tract or abdomen. S. aureus generally causes abscesses through hematogenous seeding.
Predisposing factors for anaerobic involvement are those that allow for their dissemination to the kidney and perinephric area from another site. These conditions include: obstruction leading to urinary extravasation, renal transplantation, colon perforation, a necrotic tumor. and seeding during anaerobic bacteremia from the upper respiratory tract or dental sites.5,6 The anaerobic organisms isolated from those abscesses are similar to these that colonize the mucos membranes of the site of origin. Anaerobes that originate from the oral cavity are recovered in abscesses associated with respiratory infections, whereas enteric anaerobes are present in abscesses of abdominal origin.
CT of renal abscess
Diagnosis
Symptoms are generally nonspecific lasting 1 to 3 weeks and include lethargy, decreased appetite, weight loss, nausea, and vomiting. Fever and unilateral pain in the flank or abdomen or tenderness in the costovertebral angle are often present. An abscess should be suspected in those with a predisposing condition, who fail to respond to therapy of pyelonephritis.
Laboratory findings include elevated white blood count, and erythocyte sedimentation rate. Microscopic pyuria or positive urine culture can be found in about half of the patients; and positive blood culture in a third.
An abscess should be aspirated for Gram stain and cultured for aerobic and anaerobic bacteria, fungi, and mycobacteria.
Ultrasonography and renal cortical scintigraphy may be diagnostic. Enhanced CT is the most reliable imaging.8
Management
Initial therapy includes parenteral administration of antibiotics. Percutaneous drainage, open surgical drainage, or nephectomy may be needed if this fails. Initial empiric antibiotic therapy should include agents effective against S. aureus, and Enterobacteriaceae. A pencillinase-resistant penicillin ( ie oxacillin), plus an fluoroquinolones or an aminoglycoside is an adequate combination.
Antimicrobials effective against of beta-lactamase producing anaerobes include metronidazole, chloramphenicol, clindamycin, a carbapenem , cefoxitin, and the combination of a penicillin and a beta-lactamase inhibitors.
Therapy should be adjusted according to the abscess culture results. Blood or urine culture results do not always correlate with recovery of isolates from an abscess.5
The length of therapy depends on the clinical response and whether percutaneous or surgical drainage is done. At least 14 days is appropriate in conjunction with abscess drainage in those with uncomplicated infection. Without drainage, 6 weeks or more may be needed.9 Therapeutic drainage is usually performed with ultrasonographic guidance.
Open drainage is generally performed when antimicrobials and percutaneous drainage fail. Nephrectomy is reserved to those with massive abscess where the involved kidney is unlikely to stay functional.
Complications
These include bacteremia, extension into the kidney or perinephric space, loss of renal function, and rupture into an adjacent space.
Anaerobes have been involved in different types of urinary tract infection (UTI ). 1,2 These include acute and chronic urethritis, cystitis, para- or periurethral cellulitis or abscess, acute and chronic prostatitis, prostatic and scrotal abscesses, periprostatic phlegmon, ureteritis, periureteritis, pyelitis, pyelonephritis, renal abscess, scrotal gangrene, metastatic renal infection pyonephrosis, perinephric abscess, retroperitoneal abscess, and other infections. The clinical presentation and diagnosis of anaerobic infection are not different than those caused by aerobic and facultative bacteria.
Microbiology
The majority of UTI are due to Gram-negative aerobic or facultative bacilli, that include Escherichia, Klebsiella, , Pseudomonas, Serratia, Proteus, and Pseudomonas spp. The anaerobes implicated in UTI are Gram negative bacilli (including Bacteroides fragilis group and pigmented Prevotella and Porphyromonas spp.), Clostridium spp., anaerobic Gram-positive cocci, and Actinomyces spp. They are often isolated mixed with Enterobacteriaceae or streptococci. 1,2
URINARY TRACT INFECTION (UTI)
Pathogenesis
The patient's bacterial flora is usually the source of the UTI . Since anaerobes are the major component of the cervical and fecal flora, it is not surprising that they can cause UTI.
The usual route infection is through ascension of organisms from the external genitalia and the periurethral region rather than a hematogenous one, or by direct extension from adjacent organs. Anaerobes constitute 95% of the organisms of the female periurethral area.3 The colonization of the males urethra with anaerobes is related to sexual activity. The presence of anaerobes at these sites may explain their mode of infectivity. Patients with indwelling urethral catheters have a high incidence of anaerobes in the urine. 4
The low medullary blood flow, plasma skimming, and countercurrent flow all promote decreased oxygen supply to the medulla, assisting the growth of anaerobes. The oxygen tension of the urine is sharply decreased in the dehydrated patient, which predisposes to anaerobic UTI .
Diagnosis
Symptoms may be absent, especially in chronic infections. Signs include dull or sharp pain and tenderness in the kidney area or abdomen. Hypertension, anemia and chronic renal failure may occur in long-standing and severe cases. Leukocytosis ranges from 15,000 to 35,000/cu mm.
Urgency and dysuria are seen in cystitis and fever, chills, flank pain, nausea and vomiting, frequency, urgency, dysuria, and elevated sedimentation rate (>30 mm/hr) are typical for acute pyelonephritis.
At least two consecutive positive urine cultures are needed for diagnosis. Voided specimens are unreliable for diagnosis Suprapubic aspiration is the preferred method. It is recommended that appropriate cultures for anaerobes be obtained in symptomatic cases where routine cultures fail to yield bacterial growth, and gram stain shows bacteria in the urine sediment.
Management
Surgical repair of obstructive lesions is indicated. Administration of appropriate antibiotic therapy is required. A prolonged course of therapy (two to six months or longer) may be needed for recurrent infections.
Acute uncomplicated infection, which is often caused by enteric organisms such as E. coli, is generally treated by oral sulfonamides, trimethoprim-sulfamethoxazole, ampicillin, or a quinolone (in adults). At least 10 days of therapy is required for patients with pyelonephritis, reflux, or urinary tract abnormalities and for those who have not yet been evaluated radiographically. A shorter course (3 to 4 days) can be given for cystitis.
Isolation of anaerobes requires the administration of effective agents. Penicillin or cephalosporins can be used against most anaerobes; however, the recovery of penicillin-resistant anaerobes requires administration of clindamycin, ticarcillin, cefoxitin, metronidazole, a carbapenem or the combination of a penicillin plus a beta-lactamase inhibitor. Some of the newer quinolones have extended coverage against anaerobic bacteria (e.g. moxifloxacin).
Complications
Bacteremia can follow urologic procedures.4 Chronic renal disease can develop after repeated UTI in patients with obstructive uropathy, neurogenic bladder, structural renal disease, or diabetes. Untreated UTI can lead to renal abscess, pyelonephrosis, perinephric or retroperitoneal abscess.5
GENITOURINARY SUPPURATIVE INFECTIONS: PERINEPHRIC AND RENAL ABSCESSES
These abscesses are often misdiagnosed and consequently, mistreated or treated too late. 5-7 The newer imaging methods allow for an earlier diagnosis and a more accurate anatomical identification, enabling a less invasive therapeutic approach. 8
Microbiology
Suppurative genitourinary infections involve anaerobic bacteria in up to a quarter of cases. 8,9 The predominant anaerobes are Bacteroides spp. and anaerobic cocci. The predominate aerobes are S. aureus, Enterobacteriaceae (especially E. coli ), Pseudomonas sp., Enterococcus spp., coagulase-negative staphylococci, Streptococcus spp., Actinomyces spp., Fungi and Mycobacterium tuberculosis.5,6
Pathogenesis
Bacteria invasion of the perinephric space is through direct extension from an intrarenal abscess or by vesicoureteral reflux, urinary tract obstruction or surgery of the urinary tract or abdomen. S. aureus generally causes abscesses through hematogenous seeding.
Predisposing factors for anaerobic involvement are those that allow for their dissemination to the kidney and perinephric area from another site. These conditions include: obstruction leading to urinary extravasation, renal transplantation, colon perforation, a necrotic tumor. and seeding during anaerobic bacteremia from the upper respiratory tract or dental sites.5,6 The anaerobic organisms isolated from those abscesses are similar to these that colonize the mucos membranes of the site of origin. Anaerobes that originate from the oral cavity are recovered in abscesses associated with respiratory infections, whereas enteric anaerobes are present in abscesses of abdominal origin.
CT of renal abscess
Diagnosis
Symptoms are generally nonspecific lasting 1 to 3 weeks and include lethargy, decreased appetite, weight loss, nausea, and vomiting. Fever and unilateral pain in the flank or abdomen or tenderness in the costovertebral angle are often present. An abscess should be suspected in those with a predisposing condition, who fail to respond to therapy of pyelonephritis.
Laboratory findings include elevated white blood count, and erythocyte sedimentation rate. Microscopic pyuria or positive urine culture can be found in about half of the patients; and positive blood culture in a third.
An abscess should be aspirated for Gram stain and cultured for aerobic and anaerobic bacteria, fungi, and mycobacteria.
Ultrasonography and renal cortical scintigraphy may be diagnostic. Enhanced CT is the most reliable imaging.8
Management
Initial therapy includes parenteral administration of antibiotics. Percutaneous drainage, open surgical drainage, or nephectomy may be needed if this fails. Initial empiric antibiotic therapy should include agents effective against S. aureus, and Enterobacteriaceae. A pencillinase-resistant penicillin ( ie oxacillin), plus an fluoroquinolones or an aminoglycoside is an adequate combination.
Antimicrobials effective against of beta-lactamase producing anaerobes include metronidazole, chloramphenicol, clindamycin, a carbapenem , cefoxitin, and the combination of a penicillin and a beta-lactamase inhibitors.
Therapy should be adjusted according to the abscess culture results. Blood or urine culture results do not always correlate with recovery of isolates from an abscess.5
The length of therapy depends on the clinical response and whether percutaneous or surgical drainage is done. At least 14 days is appropriate in conjunction with abscess drainage in those with uncomplicated infection. Without drainage, 6 weeks or more may be needed.9 Therapeutic drainage is usually performed with ultrasonographic guidance.
Open drainage is generally performed when antimicrobials and percutaneous drainage fail. Nephrectomy is reserved to those with massive abscess where the involved kidney is unlikely to stay functional.
Complications
These include bacteremia, extension into the kidney or perinephric space, loss of renal function, and rupture into an adjacent space.
REFERENCES
1. Finegold, S.M.: Anaerobic bacteria in human disease. New York : Academic Press, 1977.
2. Brook, I. : Urinary tract infection caused by anaerobic bacteria in children. Urology 16:596-8,1980.
3. . Bollgren, I. , Kallenius, G., Nord, C.E.: Periurethral anaerobic microflora of healthy girls. J. Clin. Microbiol. 10:419-24, 1979.
4. Sapico, F.L., Wideman, P.A., Finegold, S.M.: Aerobic and anaerobic bladder urine flora of patients with indwelling urethral catheters. Urology 7:382-4, 1976.
5. Brook, I. : Anaerobic bacteria in suppurative genitourinary infection, J Urol. 141:889-893, 1989.
6. Brook, I. : The role of anaerobic bacteria in perinephric and renal abscesses in children. Pediatrics. 93:261-264, 1994.
7. Yen DH, Hu SC , Tsai J, Kao WF, Chern CH, Wang LM, Lee CH. Renal abscess: early diagnosis and treatment. Am J Emerg Med ;17:192-7, 1999.
8. Kawashima A, Sandler CM, Ernst RD, Goldman SM, Raval B, Fishman EK. Renal inflammatory disease: the current role of CT. Crit Rev Diagn Imaging ;38:369-415, 1997.
9. Bartlett , G.J., Gorbach, S.L.: Anaerobic bacteria in suppurative infections of the male genitourinary system·J. Urol. 125:376-8, 1981.