J Neurosurg 48:465-469, 1978
Anaerobic spinal epidural abscess Case report ISABEL C. GUERRERO, M.D., GAlL BARSKY SLAP, M.D., ROB ROy MACGBEcOn, M.D., PABLO LAWNEn, M.D., SEBASTIAN RUGGERI, M.D., AND THOMAS GENNARELLI~M.D.
Infectious Disease Section, University of Pennsylvania School of Medicine, and the Department of Neurosurgery, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania ~" An acute spinal epidural abscess is reported from which a pure growth of the anaerobe Fusobacterium necrophorum was isolated. The mode of infection and pathogen makes it unique. The literature concerning the bacteriology of epidural abscess and the implications of anaerobic epidural infection are discussed. KEY WORDS 9 Fusobacterium
9 spinal epidural abscess 9 anaerobic infection necrophorum 9 sinusitis
S
PINAL epidural abscess is a rare but well recognized disease entity, first defined in 17267 e Its incidence did not change significantly with the onset of the antibiotic era. In 1948, Heusner reported 20 cases in 19 years at the Boston City Hospital; 17 H u l m e and Dott found records of 19 cases in 20 years in Edinburgh; TM Dtls reported on 18 cases seen in 10 years in Hungary; 11 Altrocchi reported on eight cases seen between 1938 and 1962 at ColumbiaPresbyterian Medical Center; 8 and Hancock reported on 49 patients seen between 1945 and 1968 at the National Spinal Injury Center? e In the most recent study of spinal epidural abscess, Baker, et al., in 1975, reviewed 39 cases in 27 years at the Massachusetts General Hospital.' The clinical presentation and the importance of early surgical intervention have been stressed repeatedly in the literature. In contrast, the bacteriology of spinal epidural
J. Neurosurg. / Volume 48 / March, 1978
abscess has received little emphasis, perhaps as a result of the p r e p o n d e r a n c e o f Staphylococcus aureus in the reported cases. The review by Baker, et al., was the first study to note the changing microbiology of spinal epidural abscess.' A comparison of their 39 patients evaluated between 1947 and 1974 with Heusner's population of 20 from 1930 to 194817 revealed a decrease in the isolation of Staphylococcus aureus from 100% to 62% of those in whom an organism was isolated, and the appearance of G r a m negative organisms. In addition, isolation of anaerobic organisms from epidural infections was reported for the first time in three of their 39 patients. In this report, we describe a recent case of acute spinal epidural abscess from which a pure growth of the anaerobe Fusobacterium necrophorum was isolated. We review the literature on the bacteriology of epidural abscess and discuss the implications o f 465
I. C. Guerrero, et al.
FIG. 1. Gram-stained smear of the abscess material showing pleomorphic Gram-negative rods. X 1000.
anaerobic organisms as causative agents in this syndrome.
Case Report This 20-year-old man entered the hospital because of low-back pain and paralysis of the right leg. He was in excellent health until 4 weeks before admission when he developed sore throat and coryza which persisted for 3 days, and a dry cough which lasted 2 weeks. Thirteen days before admission he awoke with a diffuse throbbing headache and shaking chill, which resolved within 24 hours. He then felt well until 9 days before admission when he developed a purulent nasal discharge and throbbing left supraorbital pain. He was treated for an apparent sinusitis with ampicillin, 250 mg orally every 6 hours, and decongestants. Symptoms resolved within 24 hours and he discontinued the ampicillin after 4 days. Six days before admission he awoke with continuous, aching, localized right paraspinal low-back pain. The pain worsened over the following days, but remained localized to the right low back. On the morning of admission he experienced the sudden onset of right posterior thigh numbness. Paresthesias progressed over the next 2 hours to involve the entire right leg, groin, and buttock, associated with inability to void. Right leg weakness progressed within 5 hours to complete paralysis. The left leg remained normal. 466
Examination. On admission the oral temperature was 102 ~ F, pulse 90, and respirations 16. The blood pressure was 140/80 mm Hg. There was no sinus tenderness. The eyes, ears, and nasopharynx were normal. The neck was supple. The chest, cardiovascular, and abdominal examinations were normal. Palpation of the back revealed marked L4-5 paraspinal tenderness. Neurological examination showed loss of all sensory modalities of the right leg in the distribution of L4-$3, flaccid paralysis of the right leg and foot, decreased right patellar reflex, and absent Achilles reflexes bilaterally. The urine was normal. Hematocrit was 41%; the white blood cell count was 31,700, with 92% neutrophils. Chest and lumbosacral spine films were normal. A cisternal puncture yielded clear, colorless cerebrospinal fluid that contained six red blood cells, 49 neutrophils, 23 lymphocytes, and 32 monocytes/cu mm; the protein was 46 mg% and the glucose 78 rag%. A myelogram revealed an extradural block at the level of L3. A preoperative diagnosis of spinal epidural abscess was made. Operation. Emergency laminectomies of L3 to L-5 were performed. Five cc of nonodorous pus were drained from an abscess of the posterior epidural space that extended from L-3 to S-1. A Gram-stained smear of the abscess material revealed many pleomorphic Gram-negative rods (Fig. 1). Blood and abscess cultures grew Fusobacterium necrophorum. Postoperative Course. Postoperatively, the patient was treated with gentamicin, cephalothin, and nafcillin, pending culture results. Once the organism was identified, a 2-week course of antibiotic therapy was completed with aqueous penicillin G, 2 million units intravenously every 6 hours. The patient was transferred to the Physical Rehabilitation Center 17 days postoperatively. He was walking with the use of a cane, but was still unable to void spontaneously. A follow-up examination showed neurological improvement except for residual weakness and hypesthesia of the right foot.
Discussion Our patient's clinical presentation was typical for spinal epidural abscess, conformJ. Neurosurg. / Volume 48 / March, 1978
Anaerobic spinal epidural abscess ing to the four developmental phases of the syndrome described by Heusner: ~7 spinal ache, root pain, weakness, and paralysis. Baker, et al., 4 found that all of their 20 patients with acute spinal epidural abscess had back pain; 18 demonstrated local tenderness, 17 had root weakness, and 15 had progressed to paraparesis and paraplegia. The neurological symptomatology of epidural abscess is far more extensive than can be accounted for by mechanical effects of compression alone, which in this case was caused by a small abscess. Severe vascular impairment of the intrinsic circulation of the cord causing further ischemia and infarction of the neural tissue would explain the extensive neurological symptoms, and has been suggested by others as the possible pathophysiological mechanism in this syndrome. 4,7,~7 Although many reports consider the clinical presentation diagnostic,7,15,~7,28 it may prove difficult to differentiate epidural abscess from acute transverse myelitis? Incorrect diagnosis of transverse myelitis in a patient with an abscess may result in delay of surgical intervention, with consequent increased morbidity and mortality. The myelogram indicating extradural compression was helpful in reaching the correct diagnosis in the present case. The clinical history in our patient suggests that the mechanism of epidural infection was a hematogenous spread from an infected frontal sinus. A probable primary source was found in 75% of Heusner's series ~7and in 82% of that of Baker, et al., 4 with hematogenous spread implicated in 50% and 20%, respectively. Although in both studies skin infection was the most common site from which organisms spread hematogenously to the epidural space, Baker, et al., ~ noted several reports of urinary tract infection, respiratory infection, and dental abscesses preceding epidural abscess. A direct extension from a contiguous focus such as vertebral osteomyelitis, psoas abscess, or sacral decubitus ulcer may also result in an epidural space infection. Other possible factors predisposing to epidural abscess such as antecedent trauma, skin infection, osteomyelitis, diabetes mellitus, or intravenous drug abuse were not present in this case. Although our patient did not describe symptoms of chronic sinusitis, the history and bacteriology suggest that his acute sinusitis J. Neurosurg. / Volume 48 / March, 1978
was the primary focus of infection. Anaerobic organisms have been found frequently in upper respiratory tract infections. Gorbach and Bartlett, ~4 in their review of anaerobic infections, found that Fusobacterium and Peptostreptococcus were the anaerobes most commonly reported in upper respiratory tract infections. Several reports have shown that although anaerobes were important pathogens in chronic sinusitis, they were rarely found in acute sinusitis. Urdal and Berda124 recovered anaerobes from maxillary sinus aspirates in only one of 45 patients with acute sinusitis versus seven of 36 patients with chronic sinusitis. Frederick and Braude TM clearly established the pathogenic role of anaerobes in 43 of 83 patients (52%) undergoing surgical drainage for chronic sinusitis. The anaerobes most commonly seen were Fusobacterium, P e p t o s t r e p t o c o c c u s , and Bacteroides. The mode of infection and the infecting organism make this case unique. This is the first report in the English literature of isolation of Fusobacterium sp. from a spinal epidural abscess. Staphyloccoccus aureus was the pathogen most commonly reported in the series we reviewed (Table 1). In addition, Gram-negative organisms like E. coli and eseudomonas 4,7,9 were recovered in some cases. However, Baker, et al., 4 are the only authors to report isolation of anaerobes. Anaerobic organisms were isolated from three of the abscesses; one was a pure anaerobic streptococcal infection and the others were of mixed anaerobic and aerobic organisms, B a c t e r o i d e s melaninogenicus, Veillonella, and anaerobic streptococci in one, and anaerobic Propionibacterium with alphahemolytic streptococcus in the other. The organism from our case exhibited chromatographic and antibiotic sensitivity patterns characteristic of Fusobacterium sp.: it was sensitive to penicillin at 0.5 ~tg/ml, chloramphenicol at 0.03 #g/ml, clindamycin at 0.03 #g/ml, and cephalothin at 0.2 gg/ml. In vitro antimicrobial sensitivity studies by Martin, et al., have shown that Fusobacterium sp. are sensitive to penicillin G at 0.8 gg/ml, clindamycin and tetracycline at 1.6 ~g/ml, chloramphenicol at 6.2 #g/ml, cephalothin and lincomycin at 12.5 #g/ml, and gentamicin and kanamycin at 25 izg/ml.2~ The anaerobe was lipase-positive and hence was finally identified as F u s o b a c t e r i u m 467
I. C. Guerrero, et al. TABLE 1 Review o f organisms isolated in spinal epidural abscess*
Author, Yeart
Primary Focus
Organism
Dandy, 1926 skin infection (2) (2/3)
S. aureusr
Allen & skin infection (3) Kahn, 1932 (3/3)
S. aureus
Browder & URTI, tonsillitis (1) Meyers, URTI (1) 1937w (a:6/7) uterine infection (1) skin infection (1) pneumonia (1)
S. aureus S. aureus & non-
hemolytic strep.
S. aureus S. aureus Diplococcus lanceolatus dental abscess (1) S. aureus (b:51/76) skin infection (30) S. aureus skin infection (1) B. pyocyaneus URTI (2) S. aureus bronchitis (1) Diplococcus lanceolatus pneumonia (2) S. aureus trauma to spine (3) S. aureus oral infection (2) S. aureus cholecystitis (1) S. aureus endocarditis (1) S. aureus ear infection (1) S. aureus septicemia etiol? (4) S. aureus phlebitis (1) S. aureus tonsillitis S. aureus
Campbell, 1937 (6/8)
skin infection (2) skin infection (1) unknown cystitis (1) skin infection (!)
S. aureus S. aureus, P. aeruginosa S. aureus, P. aeruginosa S. aureus S. albus
Author, Yeart Hulme & Dott, 1954 (6/10)
Primary Focus
septic arthritis (1) skin infection (1) vertebral osteomyelitis (1) unknown (1)
? typhoid fever (1) unknown (1) Hutchinson, URTI (1) 1955 (1/1) Rushworth skin infection (1) & Martin, 1958 (1/1) Dds, 1960 skin infection (2) (5/8) lymphadenitis (1) unknown (1) Miller & trauma (1) Hesch, 1962 (1/1) Aieardi & unknown (1) Lepintre, 1967 (1/1) Baker, 1971 unknown (1) (1/1)
S. aureus
S. aureus
S. aureus
unspecified (1)
Streptococcus
E. eoli Pseudomonas aeruginosa D. p n e u m o n i a e S. albus, non-
nonhemolytic streptococci
unspecified (1) unspecified (1)
skin infection (1)
S. albus
unspecified (1) unspecified (1)
S. aureus S. aureus
S. aureus S. aureus S. aureus
unspecified (1)
1975 (34/39)
unspecified (21) unspecified (1)
mastoiditis (1)
S. aureus S. aureus S. aureus
S. aureus
S. aureus Streptococcus pyogenes Streptococcus
et al.,
Echols, 1941 (4/4)
skin infection (5) empyema sinus (1) pyelitis (1) vertebral osteomyelitis (7) unknown (1)
S. aureus
Baker,
unspecified (3) unspecified (1)
Heusner, 1948 09/20)
S. aureus S. aureus, S. recalls Bacillus coli S. aureus
S. aureus
S. aureus S. aureus & Pneumococcus S. aureus
S. aureus
S. aureus S. aureua
Hancock, unknown (1) 1973 (31/49)
Browder & skin infection (3) Meyers, acute URTI, 1941 pneumonia (2) (6/7) dental abscess (1)
Boharas & unknown (1) Koskoff, 1941 (1/1)
Organism
dental abscess (1)
(nonhemolytic) (anaerobic)
hemolytic streptococcus
S. aureus, S. p y o g e n e s
anaerobic propionibaeterium, alpha hemolytic streptococci B. melaninogenicus, Veillonella, anaerobic
streptococci
*Reports dated before 1937 are included in Browder's review unless specifically cited. URTI = upper respiratory tract infection. tNumbers in parentheses indicate bacteriologically confirmed cases/total cases reported. ~tOrganism cultured out from wound instead of abscess material w review of literature excluding Dandy's and Browder's own cases. 468
J. N e u r o s u r g . / V o l u m e 4 8 / M a r c h ,
1978
Anaerobic spinal epidural abscess necrophorum, the only lipase-positive Fusobacterium. Conclusions
Early diagnosis and therapy have always been emphasized for this potentially crippling but treatable disease. Unfortunately, correct diagnosis is often missed. Primary treatment consists o f i m m e d i a t e l a m i n e c t o m y for drainage of the epidural space. Antibiotic therapy is an essential adjunct and should be started during surgery. Gram-staining of the abscess material should be performed. A penicillinase-resistant penicillin is reasonable for initial therapy if there is nothing to suggest unusual bacteriology. In the presence of Gram-negative organisms, especially when associated with a consistent primary focus of infection, antibiotic coverage for both aerobic and anaerobic Gram-negative organisms should be initiated. Because the most common anaerobes are sensitive to penicillin (including those found by us and by Baker, et al.), the use o f penicillin is recommended. Baker, et al.,4 suggest parenteral therapy for 3 to 4 weeks; 6 to 8 weeks is suggested in the presence of vertebral osteomyelitis. However, our patient did well with a 2-week course of therapy. The literature provides little information regarding the duration of antibiotic therapy in spinal or epidural abscess or even whether its use is critical. In contrast, immediate surgical intervention before the onset of paralysis led to a favorable outcome in all series; hence the need for i m m e d i a t e diagnosis and surgical therapy is established as imperative. References
1. Aicardi J, Lepintre J: Spinal epidural abscess in a 1-month old child. Am J Dis Child 114: 665-667, 1967 2. Allen SS, Kahn EA: Acute pyogenic infection of the spinal epidural space. JAMA 98: 875-878, 1932 3. Altrocchi PH: Acute spinal epidural abscess vs acute transverse myelopathy. A plea for neurosurgical caution. Arch Neurnl 9:17-25, 1963 4. Baker AS, Ojemann RG, Swartz MN, et al: Spinal epidural abscess. N Engl J Mefl 293: 463--468, 1975 5. Baker C J, Primary spinal epidural abscess. Am J Dis Child 121:337-339, 1971 6. Boharas S, Koskoff YD: The early diagnosis of acute spinal epidural abscess. Report of an illustrative case. JAMA 117:1085-1088, 1941 J. Neurosurg. / Volume 48 / March, 1978
7. Browder J, Meyers R: Infections of the spinal epidural space: an aspect of vertebral osteomyelitis. Am J Surg 37:4-26, 1937 8. Browder J, Meyers R: Pyogenic infections of the spinal epidural space. Surgery 10:296-308, 1941 9. Campbell MM: Pyogenic infections within the vertebral canal. Bull Neural lnst NY 6:574-591, 1937 10. Dandy WE: Abscesses and inflammatory tumors in the spinal epidural space (so-called pachymeningitis externa). Arch Surg 13: 477-494, 1926 11. Dtls V: Spinal peripachymeningitis (epidural abscess). Report of 8 cases. J Neurosurg 17:972-983, 1960 12. Echols DH: Emergency laminectomy for acute epidural abscess of the spinal canal. Surgery 10:287-295, 1941 13. Frederick J, Braude AI: Anaerobic infection of the paranasal sinuses. N Engl J Med 290:135-137, 1974 14. Gorbach SL, Bartlett JG: Anaerobic infections. N Engl J Med 290:1177-1184, 1237-1245, 1289-1294, 1974 15. Grant FC: Epidural spinal abscess. JAMA 128:509-512, 1945 16. Hancock DO: A study of 49 patients with acute spinal extradural abscess. Paraplegia 10:285-288, 1973 17. Heusner AP: Nontuberculous spinal epidural infections. N Engl J Mcd 239:845-854, 1948 18. Hulme A, Dott NM: Spinal epidural abscess. Br Med J 1:64-68, 1954 19. Hutchinson FD: Non-tuberculous spinal epidural abscess. Can Med J 72:208-210, 1955 20. Martin WJ, Gardner M, Washington JA II: In vitro antimicrobial susceptibility of anaerobic bacteria isolated from clinical specimens. Antimicrob Agents Chemother 1:148-158, 1972 21. Miller WH, Hesch JA: Nontuberculous spinal epidural abscess. Report of a case in a 5-weekold infant. Am J Dis Child 104:269-275, 1962 22. Rushworth RG, Martin PB: Acute spinal epidural abscess; a case in an infant with recovery. Arch Dis Child 33:261-264, 1958 23. Sarrell WG, LaFia D J: Acute lumbar epidural abscess. Report of a case. N Engi J Med 250:318-320, 1954 24. Urdal K, Berdal P: The microbial flora in 91 cases of maxillary sinusitis. Aeta Otolaryngol 37:20-25, 1949
Address reprint requests to: Rob Roy MacGregor, M.D., 552 Johnson Pavilion, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104.
469
Anaerobic spinal epidural abscess Case report ISABEL C. GUERRERO, M.D., GAlL BARSKY SLAP, M.D., ROB ROy MACGBEcOn, M.D., PABLO LAWNEn, M.D., SEBASTIAN RUGGERI, M.D., AND THOMAS GENNARELLI~M.D.
Infectious Disease Section, University of Pennsylvania School of Medicine, and the Department of Neurosurgery, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania ~" An acute spinal epidural abscess is reported from which a pure growth of the anaerobe Fusobacterium necrophorum was isolated. The mode of infection and pathogen makes it unique. The literature concerning the bacteriology of epidural abscess and the implications of anaerobic epidural infection are discussed. KEY WORDS 9 Fusobacterium
9 spinal epidural abscess 9 anaerobic infection necrophorum 9 sinusitis
S
PINAL epidural abscess is a rare but well recognized disease entity, first defined in 17267 e Its incidence did not change significantly with the onset of the antibiotic era. In 1948, Heusner reported 20 cases in 19 years at the Boston City Hospital; 17 H u l m e and Dott found records of 19 cases in 20 years in Edinburgh; TM Dtls reported on 18 cases seen in 10 years in Hungary; 11 Altrocchi reported on eight cases seen between 1938 and 1962 at ColumbiaPresbyterian Medical Center; 8 and Hancock reported on 49 patients seen between 1945 and 1968 at the National Spinal Injury Center? e In the most recent study of spinal epidural abscess, Baker, et al., in 1975, reviewed 39 cases in 27 years at the Massachusetts General Hospital.' The clinical presentation and the importance of early surgical intervention have been stressed repeatedly in the literature. In contrast, the bacteriology of spinal epidural
J. Neurosurg. / Volume 48 / March, 1978
abscess has received little emphasis, perhaps as a result of the p r e p o n d e r a n c e o f Staphylococcus aureus in the reported cases. The review by Baker, et al., was the first study to note the changing microbiology of spinal epidural abscess.' A comparison of their 39 patients evaluated between 1947 and 1974 with Heusner's population of 20 from 1930 to 194817 revealed a decrease in the isolation of Staphylococcus aureus from 100% to 62% of those in whom an organism was isolated, and the appearance of G r a m negative organisms. In addition, isolation of anaerobic organisms from epidural infections was reported for the first time in three of their 39 patients. In this report, we describe a recent case of acute spinal epidural abscess from which a pure growth of the anaerobe Fusobacterium necrophorum was isolated. We review the literature on the bacteriology of epidural abscess and discuss the implications o f 465
I. C. Guerrero, et al.
FIG. 1. Gram-stained smear of the abscess material showing pleomorphic Gram-negative rods. X 1000.
anaerobic organisms as causative agents in this syndrome.
Case Report This 20-year-old man entered the hospital because of low-back pain and paralysis of the right leg. He was in excellent health until 4 weeks before admission when he developed sore throat and coryza which persisted for 3 days, and a dry cough which lasted 2 weeks. Thirteen days before admission he awoke with a diffuse throbbing headache and shaking chill, which resolved within 24 hours. He then felt well until 9 days before admission when he developed a purulent nasal discharge and throbbing left supraorbital pain. He was treated for an apparent sinusitis with ampicillin, 250 mg orally every 6 hours, and decongestants. Symptoms resolved within 24 hours and he discontinued the ampicillin after 4 days. Six days before admission he awoke with continuous, aching, localized right paraspinal low-back pain. The pain worsened over the following days, but remained localized to the right low back. On the morning of admission he experienced the sudden onset of right posterior thigh numbness. Paresthesias progressed over the next 2 hours to involve the entire right leg, groin, and buttock, associated with inability to void. Right leg weakness progressed within 5 hours to complete paralysis. The left leg remained normal. 466
Examination. On admission the oral temperature was 102 ~ F, pulse 90, and respirations 16. The blood pressure was 140/80 mm Hg. There was no sinus tenderness. The eyes, ears, and nasopharynx were normal. The neck was supple. The chest, cardiovascular, and abdominal examinations were normal. Palpation of the back revealed marked L4-5 paraspinal tenderness. Neurological examination showed loss of all sensory modalities of the right leg in the distribution of L4-$3, flaccid paralysis of the right leg and foot, decreased right patellar reflex, and absent Achilles reflexes bilaterally. The urine was normal. Hematocrit was 41%; the white blood cell count was 31,700, with 92% neutrophils. Chest and lumbosacral spine films were normal. A cisternal puncture yielded clear, colorless cerebrospinal fluid that contained six red blood cells, 49 neutrophils, 23 lymphocytes, and 32 monocytes/cu mm; the protein was 46 mg% and the glucose 78 rag%. A myelogram revealed an extradural block at the level of L3. A preoperative diagnosis of spinal epidural abscess was made. Operation. Emergency laminectomies of L3 to L-5 were performed. Five cc of nonodorous pus were drained from an abscess of the posterior epidural space that extended from L-3 to S-1. A Gram-stained smear of the abscess material revealed many pleomorphic Gram-negative rods (Fig. 1). Blood and abscess cultures grew Fusobacterium necrophorum. Postoperative Course. Postoperatively, the patient was treated with gentamicin, cephalothin, and nafcillin, pending culture results. Once the organism was identified, a 2-week course of antibiotic therapy was completed with aqueous penicillin G, 2 million units intravenously every 6 hours. The patient was transferred to the Physical Rehabilitation Center 17 days postoperatively. He was walking with the use of a cane, but was still unable to void spontaneously. A follow-up examination showed neurological improvement except for residual weakness and hypesthesia of the right foot.
Discussion Our patient's clinical presentation was typical for spinal epidural abscess, conformJ. Neurosurg. / Volume 48 / March, 1978
Anaerobic spinal epidural abscess ing to the four developmental phases of the syndrome described by Heusner: ~7 spinal ache, root pain, weakness, and paralysis. Baker, et al., 4 found that all of their 20 patients with acute spinal epidural abscess had back pain; 18 demonstrated local tenderness, 17 had root weakness, and 15 had progressed to paraparesis and paraplegia. The neurological symptomatology of epidural abscess is far more extensive than can be accounted for by mechanical effects of compression alone, which in this case was caused by a small abscess. Severe vascular impairment of the intrinsic circulation of the cord causing further ischemia and infarction of the neural tissue would explain the extensive neurological symptoms, and has been suggested by others as the possible pathophysiological mechanism in this syndrome. 4,7,~7 Although many reports consider the clinical presentation diagnostic,7,15,~7,28 it may prove difficult to differentiate epidural abscess from acute transverse myelitis? Incorrect diagnosis of transverse myelitis in a patient with an abscess may result in delay of surgical intervention, with consequent increased morbidity and mortality. The myelogram indicating extradural compression was helpful in reaching the correct diagnosis in the present case. The clinical history in our patient suggests that the mechanism of epidural infection was a hematogenous spread from an infected frontal sinus. A probable primary source was found in 75% of Heusner's series ~7and in 82% of that of Baker, et al., 4 with hematogenous spread implicated in 50% and 20%, respectively. Although in both studies skin infection was the most common site from which organisms spread hematogenously to the epidural space, Baker, et al., ~ noted several reports of urinary tract infection, respiratory infection, and dental abscesses preceding epidural abscess. A direct extension from a contiguous focus such as vertebral osteomyelitis, psoas abscess, or sacral decubitus ulcer may also result in an epidural space infection. Other possible factors predisposing to epidural abscess such as antecedent trauma, skin infection, osteomyelitis, diabetes mellitus, or intravenous drug abuse were not present in this case. Although our patient did not describe symptoms of chronic sinusitis, the history and bacteriology suggest that his acute sinusitis J. Neurosurg. / Volume 48 / March, 1978
was the primary focus of infection. Anaerobic organisms have been found frequently in upper respiratory tract infections. Gorbach and Bartlett, ~4 in their review of anaerobic infections, found that Fusobacterium and Peptostreptococcus were the anaerobes most commonly reported in upper respiratory tract infections. Several reports have shown that although anaerobes were important pathogens in chronic sinusitis, they were rarely found in acute sinusitis. Urdal and Berda124 recovered anaerobes from maxillary sinus aspirates in only one of 45 patients with acute sinusitis versus seven of 36 patients with chronic sinusitis. Frederick and Braude TM clearly established the pathogenic role of anaerobes in 43 of 83 patients (52%) undergoing surgical drainage for chronic sinusitis. The anaerobes most commonly seen were Fusobacterium, P e p t o s t r e p t o c o c c u s , and Bacteroides. The mode of infection and the infecting organism make this case unique. This is the first report in the English literature of isolation of Fusobacterium sp. from a spinal epidural abscess. Staphyloccoccus aureus was the pathogen most commonly reported in the series we reviewed (Table 1). In addition, Gram-negative organisms like E. coli and eseudomonas 4,7,9 were recovered in some cases. However, Baker, et al., 4 are the only authors to report isolation of anaerobes. Anaerobic organisms were isolated from three of the abscesses; one was a pure anaerobic streptococcal infection and the others were of mixed anaerobic and aerobic organisms, B a c t e r o i d e s melaninogenicus, Veillonella, and anaerobic streptococci in one, and anaerobic Propionibacterium with alphahemolytic streptococcus in the other. The organism from our case exhibited chromatographic and antibiotic sensitivity patterns characteristic of Fusobacterium sp.: it was sensitive to penicillin at 0.5 ~tg/ml, chloramphenicol at 0.03 #g/ml, clindamycin at 0.03 #g/ml, and cephalothin at 0.2 gg/ml. In vitro antimicrobial sensitivity studies by Martin, et al., have shown that Fusobacterium sp. are sensitive to penicillin G at 0.8 gg/ml, clindamycin and tetracycline at 1.6 ~g/ml, chloramphenicol at 6.2 #g/ml, cephalothin and lincomycin at 12.5 #g/ml, and gentamicin and kanamycin at 25 izg/ml.2~ The anaerobe was lipase-positive and hence was finally identified as F u s o b a c t e r i u m 467
I. C. Guerrero, et al. TABLE 1 Review o f organisms isolated in spinal epidural abscess*
Author, Yeart
Primary Focus
Organism
Dandy, 1926 skin infection (2) (2/3)
S. aureusr
Allen & skin infection (3) Kahn, 1932 (3/3)
S. aureus
Browder & URTI, tonsillitis (1) Meyers, URTI (1) 1937w (a:6/7) uterine infection (1) skin infection (1) pneumonia (1)
S. aureus S. aureus & non-
hemolytic strep.
S. aureus S. aureus Diplococcus lanceolatus dental abscess (1) S. aureus (b:51/76) skin infection (30) S. aureus skin infection (1) B. pyocyaneus URTI (2) S. aureus bronchitis (1) Diplococcus lanceolatus pneumonia (2) S. aureus trauma to spine (3) S. aureus oral infection (2) S. aureus cholecystitis (1) S. aureus endocarditis (1) S. aureus ear infection (1) S. aureus septicemia etiol? (4) S. aureus phlebitis (1) S. aureus tonsillitis S. aureus
Campbell, 1937 (6/8)
skin infection (2) skin infection (1) unknown cystitis (1) skin infection (!)
S. aureus S. aureus, P. aeruginosa S. aureus, P. aeruginosa S. aureus S. albus
Author, Yeart Hulme & Dott, 1954 (6/10)
Primary Focus
septic arthritis (1) skin infection (1) vertebral osteomyelitis (1) unknown (1)
? typhoid fever (1) unknown (1) Hutchinson, URTI (1) 1955 (1/1) Rushworth skin infection (1) & Martin, 1958 (1/1) Dds, 1960 skin infection (2) (5/8) lymphadenitis (1) unknown (1) Miller & trauma (1) Hesch, 1962 (1/1) Aieardi & unknown (1) Lepintre, 1967 (1/1) Baker, 1971 unknown (1) (1/1)
S. aureus
S. aureus
S. aureus
unspecified (1)
Streptococcus
E. eoli Pseudomonas aeruginosa D. p n e u m o n i a e S. albus, non-
nonhemolytic streptococci
unspecified (1) unspecified (1)
skin infection (1)
S. albus
unspecified (1) unspecified (1)
S. aureus S. aureus
S. aureus S. aureus S. aureus
unspecified (1)
1975 (34/39)
unspecified (21) unspecified (1)
mastoiditis (1)
S. aureus S. aureus S. aureus
S. aureus
S. aureus Streptococcus pyogenes Streptococcus
et al.,
Echols, 1941 (4/4)
skin infection (5) empyema sinus (1) pyelitis (1) vertebral osteomyelitis (7) unknown (1)
S. aureus
Baker,
unspecified (3) unspecified (1)
Heusner, 1948 09/20)
S. aureus S. aureus, S. recalls Bacillus coli S. aureus
S. aureus
S. aureus S. aureus & Pneumococcus S. aureus
S. aureus
S. aureus S. aureua
Hancock, unknown (1) 1973 (31/49)
Browder & skin infection (3) Meyers, acute URTI, 1941 pneumonia (2) (6/7) dental abscess (1)
Boharas & unknown (1) Koskoff, 1941 (1/1)
Organism
dental abscess (1)
(nonhemolytic) (anaerobic)
hemolytic streptococcus
S. aureus, S. p y o g e n e s
anaerobic propionibaeterium, alpha hemolytic streptococci B. melaninogenicus, Veillonella, anaerobic
streptococci
*Reports dated before 1937 are included in Browder's review unless specifically cited. URTI = upper respiratory tract infection. tNumbers in parentheses indicate bacteriologically confirmed cases/total cases reported. ~tOrganism cultured out from wound instead of abscess material w review of literature excluding Dandy's and Browder's own cases. 468
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1978
Anaerobic spinal epidural abscess necrophorum, the only lipase-positive Fusobacterium. Conclusions
Early diagnosis and therapy have always been emphasized for this potentially crippling but treatable disease. Unfortunately, correct diagnosis is often missed. Primary treatment consists o f i m m e d i a t e l a m i n e c t o m y for drainage of the epidural space. Antibiotic therapy is an essential adjunct and should be started during surgery. Gram-staining of the abscess material should be performed. A penicillinase-resistant penicillin is reasonable for initial therapy if there is nothing to suggest unusual bacteriology. In the presence of Gram-negative organisms, especially when associated with a consistent primary focus of infection, antibiotic coverage for both aerobic and anaerobic Gram-negative organisms should be initiated. Because the most common anaerobes are sensitive to penicillin (including those found by us and by Baker, et al.), the use o f penicillin is recommended. Baker, et al.,4 suggest parenteral therapy for 3 to 4 weeks; 6 to 8 weeks is suggested in the presence of vertebral osteomyelitis. However, our patient did well with a 2-week course of therapy. The literature provides little information regarding the duration of antibiotic therapy in spinal or epidural abscess or even whether its use is critical. In contrast, immediate surgical intervention before the onset of paralysis led to a favorable outcome in all series; hence the need for i m m e d i a t e diagnosis and surgical therapy is established as imperative. References
1. Aicardi J, Lepintre J: Spinal epidural abscess in a 1-month old child. Am J Dis Child 114: 665-667, 1967 2. Allen SS, Kahn EA: Acute pyogenic infection of the spinal epidural space. JAMA 98: 875-878, 1932 3. Altrocchi PH: Acute spinal epidural abscess vs acute transverse myelopathy. A plea for neurosurgical caution. Arch Neurnl 9:17-25, 1963 4. Baker AS, Ojemann RG, Swartz MN, et al: Spinal epidural abscess. N Engl J Mefl 293: 463--468, 1975 5. Baker C J, Primary spinal epidural abscess. Am J Dis Child 121:337-339, 1971 6. Boharas S, Koskoff YD: The early diagnosis of acute spinal epidural abscess. Report of an illustrative case. JAMA 117:1085-1088, 1941 J. Neurosurg. / Volume 48 / March, 1978
7. Browder J, Meyers R: Infections of the spinal epidural space: an aspect of vertebral osteomyelitis. Am J Surg 37:4-26, 1937 8. Browder J, Meyers R: Pyogenic infections of the spinal epidural space. Surgery 10:296-308, 1941 9. Campbell MM: Pyogenic infections within the vertebral canal. Bull Neural lnst NY 6:574-591, 1937 10. Dandy WE: Abscesses and inflammatory tumors in the spinal epidural space (so-called pachymeningitis externa). Arch Surg 13: 477-494, 1926 11. Dtls V: Spinal peripachymeningitis (epidural abscess). Report of 8 cases. J Neurosurg 17:972-983, 1960 12. Echols DH: Emergency laminectomy for acute epidural abscess of the spinal canal. Surgery 10:287-295, 1941 13. Frederick J, Braude AI: Anaerobic infection of the paranasal sinuses. N Engl J Med 290:135-137, 1974 14. Gorbach SL, Bartlett JG: Anaerobic infections. N Engl J Med 290:1177-1184, 1237-1245, 1289-1294, 1974 15. Grant FC: Epidural spinal abscess. JAMA 128:509-512, 1945 16. Hancock DO: A study of 49 patients with acute spinal extradural abscess. Paraplegia 10:285-288, 1973 17. Heusner AP: Nontuberculous spinal epidural infections. N Engl J Mcd 239:845-854, 1948 18. Hulme A, Dott NM: Spinal epidural abscess. Br Med J 1:64-68, 1954 19. Hutchinson FD: Non-tuberculous spinal epidural abscess. Can Med J 72:208-210, 1955 20. Martin WJ, Gardner M, Washington JA II: In vitro antimicrobial susceptibility of anaerobic bacteria isolated from clinical specimens. Antimicrob Agents Chemother 1:148-158, 1972 21. Miller WH, Hesch JA: Nontuberculous spinal epidural abscess. Report of a case in a 5-weekold infant. Am J Dis Child 104:269-275, 1962 22. Rushworth RG, Martin PB: Acute spinal epidural abscess; a case in an infant with recovery. Arch Dis Child 33:261-264, 1958 23. Sarrell WG, LaFia D J: Acute lumbar epidural abscess. Report of a case. N Engi J Med 250:318-320, 1954 24. Urdal K, Berdal P: The microbial flora in 91 cases of maxillary sinusitis. Aeta Otolaryngol 37:20-25, 1949
Address reprint requests to: Rob Roy MacGregor, M.D., 552 Johnson Pavilion, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104.
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