Anaerobic bacteremia
Anaerobes accounted for 10% to 15% of episodes of bacteremia.1 In recent years the incidence was lowered to 5% or less. 2 This decline may be due to the extensive use of antimicrobial effective against anaerobes for prophylaxis and treatment.
Microbiology
About 75% of anaerobic bacteremia are due to gram-negative bacilli, mostly Bacteroides fragilis group. The other species include Peptostreptococcus spp., and Clostridium spp. (10% each), and Fusobacterium spp. (5%). Many of these infections are polymicrobial. 3,4 Propionibacterium acnes is often a contaminate of blood cultures. However, it can be recovered from the blood of patients with shunt or vascular catheter bacteremia.
Pathogenesis
Anaerobic bacteremia is almost invariably secondary to a focal primary infection where the strain of anaerobic organisms recovered depended to a large extent on the portal of entry and the underlying disease. 1,4
The gastrointestinal tract accounted for half of anaerobic bacteremias and that the female genital tract is source of 20%. The gastrointestinal tract is the principal source of B. fragilis group and clostridial bacteremias and the female genital tract is the principal source of Peptostreptococcus and Fusobacterium bacteremias. 1,4
The may origin of bacteremias due to B. fragilis group is the gastrointestinal tract , soft-tissue wound infections, female genitourinary tract, lung infections and malignancies (genitourinary,gynecological, acute leukemia, and gastrointestinal) .5
The ear, sinus, and oropharynx are the portals of entry for bacteremia with Peptostreptococcus sp. and Fusobacterium sp. This is not surprising since these organisms are part of the oral flora and are involved in local infections.
Predisposing factors
Predisposing factors to anaerobic bacteremia in adults include malignant neoplasms, hematologic disorders, transplantation of organs, recent GI or obstetric gynecologic s intestinal obstruction, diabetes mellitus, post-splenectomy, use of cytotoxic agents or corticosteroids, an undrained abscess, and use of prophylactic antimicrobial agents for bowel preparation prior to surgery.4
The predisposing conditions in children include: chronic debilitating disorders such as malignant neoplasms, hematologic abnormalities, immunodeficiencies, chronic renal insufficiency, or decubitus ulcers and carried a poor prognosis. 6
Anaerobic bcteremia in newborns is associated with prolonged labor, premature rupture of membranes, maternal amnionitis, prematurity, fetal distress, and respiratory difficulty. Bacteremia in newborns has also been attributed to Bacteroides species Clostridium spp. and F. nucleatum.
Dental or oral surgery can also predispose to anaerobic bacteremia in adults and children.1
Diagnosis & clinical features
The clinical features of anaerobic bacteremia are not much different from other types of bacteremia; however, a relatively longer period is generally needed before an etiologic diagnosis can be made. This can be a result of the longer time needed for growth and identification of anaerobic organisms.
Diagnosis should include detection of the primary infection. The clinical presentation of anaerobic bacteremia relates in part to the nature of the primary infection, which will typically include fever, chills, and leukocytosis. Anemia, shock, and intravascular coagulation also may be present. Bacteroides bacteremia generally is characterized by thrombophlebitis, metastatic infection, hyperbilirubinemia, and high mortality rate (up to 50%). Clostridium perfringens bacteremia may present with hemolytic anemia, hemoglobinemia, hemoglobinuria, disseminated intravascular coagulation, bleeding tendency, bronze color skin, hyperbilirubinemia, shock, oliguria, and anemia. Clostridial bacteria may, however, be transient and inconsequential. However, Clostridium septicum infection may be a marker for a silent colonic or rectal malignancy.7
Blood culture supporting the growth of anaerobic bacteria should be used routinely in all patients. Inadequate methodology can lead to missing cases of anaerobic bacteremia.
Institution of early and prolonged effective therapy is important. The primary source of infection, such as an abscess, should be drained. The
survival rate of anaerobic bacteremia was significantly worse in patients who
received inappropriate therapy compared with those underwent appropriate
therapy.(8)
When anaerobes resistant to penicillin, such as the B. fragilis group, are suspected or isolated, antimicrobials such as clindamycin, chloramphenicol, metronidazole, cefoxitin, a carbapenem, or the combination of a beta-lactamase inhibitor and a penicillin should be administered. Local surveillance of antimicrobial susceptibility patterns can provide guidelines as to the choice of the best antimicrobial agent. The development of resistance to all known agents by anaerobes, make the selection of reliable empirical therapy difficult. Many anaerobic species besides the B. fragilis group have developed beta-lactamase activity. Rarely, resistance to carbapenems, induced by metalloenzymes, and to metronidazole has been reported. Consequently, one is not able to predict the susceptibility of some anaerobic isolates. Performing susceptibility testing is of great importance in treating bacteremia due to anaerobes. In the case of polymicrobial bacteremia coverage is needed against all pathogens.
Organisms identical to those causing bacteremia often can be recovered from other infected sites. These extravascular sites may serve as a source of persistent bacteremia in some cases; however, most patients recover when prompt treatment with appropriate antimicrobials is instituted.
Preventing bacteremia associated with dental or oral surgery can be accomplished by prophylactic administration of penicillin alone or with or metronidazole or clindamycin.
Complications
Mortality remains high (15 to 35%). Risk factors for a fatal outcome include compromised status, advanced age, inadequate or no surgical therapy, and the presence of polymicrobial sepsis.
Certain other serious concomitant sites of infection can be present in patients with anaerobic bacteremia. Most of these sites serve as the source of the infection; however, others may represent a site of secondary hematogenous spread ( i.e. mycotic aneurysm ).
REFERENCES
1. Finegold, S.M.: Anaerobic bacteria in human disease. New York
2. Dorsher, C.W., Rosenblatt, J.E., Wilson
3.Brook, I. Martin WJ, Cherry JD, Sumaya CV.: Recovery of anaerobic bacteria from pediatric patients: a one-year experience. Am. J. Dis. Child. 133:1020-4, 1979.
4. Brook, I. : Anaerobic bacterial bacteremia: 12-year experience in two military hospitals. J. Infect. Dis. 160:1071–5, 1989.
5. Fainstein, V., Elting, L.S., Bodey, G.P.: Bacteremia caused by non-sporulating anaerobes in cancer patients. A 12-year experience. Medicine (Baltimore
6.Brook, I. Controni G, Rodriguez WJ, Martin WJ.: Anaerobic bacteremia in children. Am. J. Dis. Child. 134:1052-6, 1980.
7.Caya, J.G., Farmer SG, Ritch PS, et al.: Clostridial septicemia complicating the course of leukemia. Cancer 57: 2045-8, 1986.
8. Kim J, Lee Y, Park Y. et al. Anaerobic Bacteremia: Impact of Inappropriate Therapy on Mortality. Infect Chemother. 2016 ;48:91-8.
8. Kim J, Lee Y, Park Y. et al. Anaerobic Bacteremia: Impact of Inappropriate Therapy on Mortality. Infect Chemother. 2016 ;48:91-8.
Endocarditis
Endocarditis (E) due to anaerobic bacteria is a rare as 2% to 16% of all cases of infectious E involved anaerobes.1
Vegetative endocarditis
Microbiology
The predominant organism causing endocarditis are streptococci (mostly viridans streptococci and enterococci), Staphylococcus aureus, Staphylococcus epidermidis, enteric bacteria and fungi.2 No organisms are recovered in 5% to 10% of cases of endocarditis. Most of these cases involve patients who received prior antibiotic therapy, but occasionally E due to fastidious organisms such as anaerobic bacteria as well as to Haemophilus aphrophilus, Cardiobacterium hominis, Actinobacillus actinomycetem comitans, Eikenella corrodens, and Kingella kingae.
Most cases of anaerobic endocarditis are caused by anaerobic cocci, Propionibacterium acnes and Bacteroides fragilis.3,4 Predisposing factors and signs and symptoms of endocarditis caused by anaerobes are similar to those seen in endocarditis with facultatives with the following exceptions: there is a lower incidence of preexisting valvular heart disease, a higher incidence of thromboemboli events and a higher mortality rate with anaerobic endocarditis.
The increase in the number of reported cases of anaerobic endocarditis noted years may be explained by: the increased frequency of polymicrobial bacteremias, the increased use of prosthetic intravascular devices, and improvements in microbiological methods. Polymicrobial endocarditis is more common in addicts (2% to 9% of cases).1
Pathogenesis
Bacteremia can be induced after numerous procedures.5 The rate of bacteremia after these procedures is as follows: periodontal surgery (88%), tooth extraction (60%), tonsillectomy (35%), rigid bronchoscopy (15%), tracheal intubation (10%), urinary tract catheter insertion or removal (13%), upper endoscopy (4%), barium enema (10%), colonoscopy (6%), and cardiac catherization (2%).
Anaerobes that may be considered contaminants ( ie P. acnes, Lactobacillus, Eubacterium, Bifidobacterium or Veillonella spp. ) should be considered possible pathogens in patients with a vascular graft, a prosthetic heart valve, or an intravascular prosthesis.
The gastrointestinal tract is the most common source for B. fragilis group, the head and neck for Fusobacterium and Bacteroides species, and the head and neck or genitourinary tract for peptostreptococci.2 The most common gastrointestinal sources were peritonitis, cholecystitis, appendicitis1 and aortoduodenal fistula. Oropharyngeal sources include carious teeth, periodontal abscesses, and suppurative tonsillitis. The most common genitourinary tract source is the female pelvis.2
The valves involved in patients with anaerobic endocarditis are similar to that in those with endocarditis caused by aerobic organisms. The tricuspid valve is most often infected in anaerobic endocarditis among users of in intravenous drugs.
The presence of large vegetations with extensive valvular destruction and congestive heart failure is common in B. fragilis E (60% to 70%) and peripheral embolization is frequently seen (30%-54%) and may be related to the production of heparinase.1,6
Diagnosis
The course of anaerobic endocarditis is generally subacute. Patients may present with malaise, anorexia and weight loss, chest pain, arthralgia, fever, and worsening cardiac function. The subtle nature of symptoms may postpone the diagnosis for months. Endocarditis should be suspected in children with congenital heart disease with unexplained fatigue (or anemia) and fever that is not influenced by oral antibiotics, and in patients who have sudden onset of sepsis, or vascular lesions in soft tissues or mucous membranes.
Physical examination typically reveals enlargement of the spleen, changing heart murmur, petechiae and evidence of peripheral emboli or vasculitis, especially involving the mucous membranes.
Other findings are rare but specific: Osler nodes, Janeway lesions, Roth spots and splinter hemorrhages in the nail beds. Several care definitions and diagnostic criteria have been published.
Obtaining cultures for aerobic and anaerobic bacteria, using appropriate blood culture media is essential. More than a single blood culture should be obtained. If several cultures are obtained and only one is positive, the diagnosis is uncertain. Echocardiography and doppler echocardiography are important diagnostic tools.
Treatment
The treatment of endocarditis mandates the use of bactericidal antimicrobials such as metronidazole. However, metronidazole is ineffective against several Gram-positive anaerobic bacilli such as P. acnes and Peptostreptococci. Carbapenems are effective for most anaerobic pathogens of endocarditis, including B. fragilis group. Patients with endocarditis caused by penicillin-susceptible anaerobes such as Peptostreptococcus spp. should receive therapy with penicillin G or vancomycin, and those unable to receive penicillin should be treated with metronidazole or clindamycin if the organism is susceptible to these agents.
Presumptive antimicrobial therapy is based on the patient's age, pre-existing cardiac condition and other risk factors such as intravenous drug use, surgery, and previous episodes of bacteremia or endocarditis. If blood cultures are positive, antibiotic treatment is then based on the susceptibility test results. Therapy is given intravenously for 4 to 6 weeks. Individuals with prosthetic intravascular valves are treated for 6 weeks.
Surgical intervention may be indicated for abscess of the valve annulus or myocardium, two or more embolic events, rupture of valve leaflet or chordae, valvular insufficiency, deteriorating cardiac failure, and inability to sterilize the blood. Removal of prosthetic valves may be indicated if medical therapy fails.
Complications
Complications include valvular destruction, multiple mycotic aneurysms,38 aortic-ring abscess and aortitis, cardiogenic shock, dysrhythmias and septic shock.
The mortality rate is 21% to 43%. E by B. fragilis or Fusobacterium necrophorum is associated with the highest mortality-46% and 75%, respectively. F. necrophorum has been associated with acute endocarditis, rapid valve destruction, and death. Patients with endocarditis caused by Peptostreptococcus spp have a more favorable prognosis than those with endocarditis due to the B. fragilis group or Fusobacterium spp.
REFERENCES
1. Sapico FL
2. Delahaye F, Hoen B, McFadden E, et al. Treatment and prevention of infective endocarditis. Expert Opin Pharmacother. ;3:131-45, 2002.
3. Nord CE. Anaerobic bacteria in septicemia and endocarditis. Scandinavian Journal of Infectious Diseases.;Supplement 31:95–104, 1982.
4. Nastro LJ, Finegold SM. Endocarditis due to anaerobic gram-negative bacilli. Am. J. Med.;54:482–496,1973.
5. Durack DT. Prevention of infective endocarditis. N. Engl. J. Med.;332:38-44, 1995.
6. Baddour LM, Meyer J, Henry B. Polymicrobial infective endocarditis in the 1980's. Reviews of Infectious Diseases.;13:963–970, 1991.
Pericarditis
Pericarditis (P) is an inflammation of the pericardium and the proximal part of the great blood vessels. It can occur as a life-threatening, fulminant condition. In the acutely ill patient, prompt diagnosis is lifesaving because decreased stroke volume associated with a large effusion (cardiac tamponade) can compromise cardiac function, and cause death.
Fibrinous pericarditis
Microbiology
Infectious P can be purulent, “benign,” or granulomatous. Purulent P is caused by bacteria, benign P is due to viruses; and occurs in postpericardiotomy syndromes, hypersensitivity, or postinfectious and granulomatous P that is generally caused by Mycobacterium tuberculosis and fungi.1
The list of etiologic agents of infectious P include bacteria, viruses, fungi and other organisms (mycobacteria, fungi and protozoa).1 The bacteria include Staphylococcus aureus, Neisseria meningitidis, Streptococcus pyogenes, Streptococcus pneumoniae, Haemophilus influenzae, Escherichia coli, Klebsiella spp, Salmonella spp, Pseudomonas aeruginosa, Staphylococcus epidermidis, and anaerobic bacteria. The viruses include: Entero (Coxsackie A, B and Echo), Human immunodeficiency, Influenza, Mumps, Adeno, Hepatitis B, Epstein-Barr, Cytomegalo, and Measles virus. The fungi include: Histoplasma capsulatum, Coccidioides immitis, Blastomyces dermatitidis, and Aspergillus spp. Other organisms include: M. tuberculosis, Mycoplasma pneumoniae, Coxiella burnetti, and protozoa (Amoebas, and Toxoplasma gondii).
While S. aureus, S. pneumoniae, and S. pyogenes were the predominant isolates recovered before 1961,2 Gram-negative aerobic bacilli, fungi, and, rarely, anaerobic bacteria were recovered in studies performed later.1,2 These etiological changes relate to advances in medicine that include cardiac surgery, cancer chemotherapy, organ transplantation, and antimicrobial therapy.
The predominant recovered anaerobes are: Gram-negative bacilli (mostly Bacteroides fragilis group and Prevotella ), Peptostreptococcus , Clostridium, Fusobacterium, and Bifidobacterium spp. and Propionibacterium acnes. 1,3,4 Anaerobes predominated in those with mediastinitis that followed esophageal perforation, and orofacial and dental infections.
Pathogenesis
P often results from contiguous extension of pneumonia, empyema, myocarditis, suppurative mediastinal lymphadenitis, myocardial abscess, and infective endocarditis. P can also result from spread during bacteremia, especially due to S. aureus and H. influenzae.
Anaerobes can reach the pericardium in 4 mechanisms:1-4 (1) spread from a contiguous focus of infection, either de novo or after surgery or trauma (pleuropulmonary, esophageal fistula or perforation, and odontogenic); (2) spread from a focus of infection within the heart, most commonly from endocarditis; (3) hematogenous; and (4) direct inoculation as a result of a penetrating injury or cardiothoracic surgery.
Diagnosis
There are no differences in the clinical and diagnostic features between P due to anaerobes and the one due to aerobic and facultative bacteria. Diagnosis is based on history, physical examination, and imaging tests. The major manifestations are precordial pain ( can be referred to other areas ), exercise intolerance, fever, irritability and a grunting expiratory sound.5 Heart sounds are muffled, and tachycardia increases as the effusion increases. A pericardial friction rub may be heard that is most audible during deep inspiration and with the patient kneels or lean forward. Tamponade is manifest by tachycardia, peripheral vasoconstriction, reduced arterial pulse pressure, and pulsus paradoxus.
X-rays typically shows an increase in the size of the cardiac shadow, mostly in the absence of pulmonary congestion. EKG usually manifests generalized ST segment elevations without reciprocal ST-segment depression, except in leads V1 and aVR. Later this returns to baseline, and there is flattening or inversion of the T-waves. Low-voltage QRS complexes can be seen without the pathologic Q waves of myocardial infarction. T wave abnormalities can persist after recovery.
Ultrasound illustrates a sonolucent space between the two layers of pericardium. CT and MRI are helpful to define masses.
The etiology is best determined by pericardial fluid examination for cell count, morphology, glucose, and protein concentrations. Microbiological evaluation of the fluid includes Gram, acid-fast, and silver stains, culture for aerobic and anaerobic bacteria, viruses, mycobacteria, and fungi. Latex agglutination tests for bacterial antigens can facilitate diagnosis. Blood cultures can be positive in 40%–70% of instances. Complete identification and testing for antimicrobial susceptibility are essential for the management of infections caused by all bacteria.
Viral cultures from a site other than the pericardial fluid (i.e. stool, throat), and a rise in antibody titters to that virus can confirm the diagnosis. Serology is helpful for the diagnosis of rickettsiae and mycoplasma.
Management
The administration of proper antimicrobials is essential. Antimicrobiual agents that generally provide coverage for methicillin-susceptible S. aureus as well as for anaerobes include clindamycin, cefoxitin, carbapenems, and combinations of a penicillin (e.g., ticarcillin) and a beta-lactamase inhibitor. The last 3 choices also provide coverage for Enterobacteriaceae. However, agents that are effective against these organisms (e.g., aminoglycosides and quinolones) should be added in cases where the infections include these bacteria. A glycopeptide (e.g., vancomycin) or linezolid should be administered in cases in which methicillin-resistant S. aureus is present or suspected. Therapy should be administered for 3 to 4 weeks. Fungal infection is treated for several months with amphotericin - B.
Large effusions with impending or established tamponade require immediate drainage by pericardiocentesis or open drainage. In the presence of acute deterioration, ultrasound-guided pericardiocentesis provides instant relief. Pericardiectomy is more definitive and is mandated if the fluid is too thick to drain through a small tube, persists after pericardiocentesis, or in a chronic and constrictive process.
Small effusions of viral etiology are managed with bed rest, pain relief and clinical monitoring. Antiviral therapy may be given for the herpes family of viruses.
Complications
Constrictive pericarditis is prevented by drainage3 and its presence mandates surgical pericardial stripping. Mortality is high (up to 80%) in those who receive antibiotics only, and no drainage, and is reduced to 22% in those who also have surgical drainage.1
REFERENCES
1. Ilan Y, Oren R, Ben-Chetrit E. Acute pericarditis: etiology, treatment and prognosis. Jpn Heart J. 1991;32:315-321.
2. Boyle JD, Pearce ML, Guze LB. Purulent pericarditis: review of literature and report of eleven cases. Medicine. 1961;40:119-144.
3. Brook I, Frazier EH. Microbiology of acute purulent pericarditis. A 12-year experience in a military hospital. Arch Intern Med. 1996;156:1857-60.
4. Skiest DJ, Steiner D, Werner M, Gamer JG. Anaerobic pericarditis: case report and review. Clin Infect Dis. 1994;19:435-440.
5. Hancock EW.. Differential diagnosis of restrictive cardiomyopathy and constrictive pericarditis. Heart. 2001;86:343-9..