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Spinal epidural abscess caused by group G streptococci
SPINAL EPIDURALABSCESS CAUSEDBY GROUPG STREPTOCOCCI Group G streptococci were first recognized by Lancefield and Hare [l] more than 50 years ago. Since then, group G streptococci have been identified as part of the normal flora of the skin, pharynx, gastrointestinal tract, and vagina, and have been implicated as pathogens in valvular, skin, pharyngeal, pleuropulmonary, puerperal, peritoneal, rheumatologic, and other infections [2,3]. However, group G streptococci are infrequently associated with central nervous system infections in adults. A review of the English literature reveals reports of this organism in meningitis [4] and in brain abscesses and subdural empyema [5]. We add to the literature a spinal epidural abscess caused by group G streptococci that was associated with epidural catheter placement. A 35year-old woman who had an uneventful pregnancy was delivered at term of a normal infant. During the labor and delivery, the patient received spinal anesthesia via an epidural catheter. The patient’s past medical history was unremarkable. After discharge, the patient did well until approximately 36 to 48 hours postpartum, when she began to develop mid-thoracic back pain (greater on the left). She subsequently noted paresthesia8 of the medial thigh and plantar surface of the feet (also greater on the left). She presented to the emergency room when the above symptoms continued to worsen. She denied headaches, neck discomfort, photophobia, incontinence, fever, chills, or other symptoms. On physical examination, the patient appeared acutely ill with a temperature of 37.7OC. Her neck was supple, and there were no Kernig’s or Brudzinski’s signs.
There was mild tenderness to palpation over the mid-thoracic spine, but no erythema or flocculation was noted. A rectal examination revealed normal tone. Her motor examination demonstrated intact and symmetric findings. She had decreased sensation (to light touch) of the left great toe, but no other deficits. Her deep tendon reflexes were equal, and the plantars were down-going. Laboratory evaluation revealed a leukocyte count of 22,800/mm3, with 76% segmented forms and 8% bands. Emergent magnetic resonance imaging revealed a posterior mid-thoracic epidural collection consistent with an epidural abscess (Figure 1). She immediately underwent laminectomy, at which an epidural abscess was found and evacuated. Gram stain of the abscess revealed gram-positive cocci, and empiric treatment with oxacillin was begun. Her cerebrospinal fluid culture was negative. Culture of the abscess subsequently grew group G streptococci, and was sensitive to penicillin. Oxacillin therapy was discontinued and administration of intravenous penicillin G (24,000,OOO units/ day) was started. Her leukocyte count and temperature normalized, her back pain readily improve’d, and her paresthesias gradually resolved. She was discharged receiving intravenous penicillin G (with probenecid) to complete a 6-week course, and had total resolution of her symp-
Figure 1. Magnetic resonance imaging of the thoracic spine reveals a posterior epidural abscess extending from the T5 through T7 levels. There is associated narrowing of the adjacent subarachnoid space and compression of the spinal cord.
toms.
Acute spinal epidural abscesses are infrequent but well-recognized infections of the central nervous system. Since Dandy’s [6] review in 1926, much has been written about spinal epidural abscesses, and the importance of early recognition has been emphasized. A common basic clinical pattern has been described by Heusner [7]: the four phases are spinal ache (back pain and tenJuly 1991
The American
derness), root pain (pains radiating from the site, headache, neck stiffness, and reflex changes), weaknesses of voluntary muscles, sphincters, and sensibilities (motor and sensory deficits relating to the level of the infection), and paralyses (complete paralysis, frequently associated with sepsis and even death). However, nonspecific and variable symptoms often contribute to a lack of cliniJournal
of Medicine
Volume
91
89
BRIEF CLINICAL OBSERVATIONS
cal suspicion, and the diagnosis can be missed.Danner and Hartman [8] found that the correctdiagnosisof spinal epidural abscess was made initially in only 17.9% of cases.Fortunately, the history of a recent epidural catheter and the neurologicfindings in our patient suggestedthe possibility of an epidural process,and emergent diagnostic and therapeutic measureswere performed. The bacteriology of spinal epidural abscessesis somewhatvaried, with Staphylococcus aureus the most common pathogen isolated [9]. Although streptococci have been found, group G streptococci have not been reported. The most common sites of infection with group G streptococci are the skin and soft tissues [9]. During delivery, colonization of the skin and contamination by the vaginal flora with group G streptococci with introduction into the epidural spaceby the anesthesiacatheter is the probable sourceof infection in our patient. In general, spinal epidural abscessis a rare complication of spinal anesthesia [lo]. Of interest, there are also several reports of postpartum spinal epidural abscessnot related to epidural anesthesia [11,12]. Our case report describes a catheter-relatedgroup G streptococcalspinal epidural abscess,an associationnot previouslyreported in our review of the literature. More significantly, it underscores againthe importance of early diagnosisand treatment. Heusner [7] and others have shown that diagnosisand intervention in the earlier phasesof spinal epidural abscess lead to favorable outcomes,while those patients diagnosedin the later phasescan experience irreversible neurologic damageand evendeath. Furthermore, delays in diagnosis have preventedreduction in morbidity and mortality despite improvements in therapy over the de90
cades[7,8].The patient discussed here did well after presenting in phase 2 of Heusner’s classification becauseof prompt diagnosis and treatment. LINAS M. KLYGIS, M.D. BORIS E. REISBERG, M.D.
Northwestern Memorial Hospjtal Northwestern University M;fed;zE Chicago, Illinois 1. Lancefield RC, Hare R. The serological differentiation of pathogenic and nonpathogenic strains of hemolytic streptococci from parturient women. J Exp Med 1935; 61: 335-49. 2. Vartian C, Lerner PI. Shlaes DM, Gopalakrishna KV. Infections due to Lancefield group G streptococci. Medicine (Baltimore) 1985; 64: 75-88. 3. Duma RJ, Weinberg AN, Medrek TF, Kunz LJ. Streptococcal infections: a bacteriologicand clinical study of streptococcal bacteremia. Medicine (Baltimore) 1969; 48: 87-127. 4. Lam K, Bayer AS. Serious infections due to group G streptococci: report of 15 cases with in vitro-in viva correlations. Am J Med 1983; 75: 561-70. 5. Gossling J. Occurrence and pathogenicity of the Streptococcus millen’ group. Rev Infect Dis 1988; 10: 257-85. 6. Dandy WE. Abscesses and inflammatory tumors in the spinal epidural space (so-called pachymeningitis externa). Arch Surg 1926; 13: 477-94. 7. Heusner AP. Nontuberculous spinal epidural infections. N Engl J Med 1948; 239: 845-54. 8. Danner RL, Hartman BJ. Update of spinal epidural abscess: 35 cases and review of the literature. Rev Infect Dis 1987; 9: 265-74. S.Kaufman DM. Kaplan JG. Litman N. Infectious agents in spinal epidural abscesses. Neurology 1980; 30: 844-50. 10. North JB, Brophy BP. Epidural abscess: a hazard of spinal epidural anaesthesia. Aust NZ J Surg 1979: 49: 484-5. 11. Male CG, Martin R. Puerperal spinal epidural abscess. Lancet 1973; 1: 608-9. 12. Crawford JS. Pathology in the extradural space. Br J Anaesth 1975; 47: 412-5. Submitted
May 23, 1990, and accepted in revised form February 5, 1991
LOCALIZEDRHEUMATOID VASCULITISPRESENTINGAS ACUTE ALITHIASIC CHOLECYSTITIS Rheumatoid arthritis is occasionally complicatedby systemicnecrotizing vasculitis indistinguishable pathologically from the primary forms of polyarteritis nodosa (PAN) [l]. Although lo-
July 1991 The American Journal of Medicine
Volume 91
calizedforms are not uncommon, only one case of localized rheumatoid vasculitis of the gallbladder has been reported [2]. Our patient was a 69-year-old woman with a history of hypertension, atria1 fibrillation, and seropositive erosive rheumatoid arthritis with subcutaneousnodules since 11 years previously. She received nonsteroidal antiinflammatory drugs (NSAIDs), corticosteroids,and aurothiomalate, remaining in clinical and analytical remissionuntil 6 months ago,when shepresentedwith intense constitutional symptoms, anemia, and an increase in the erythrocyte sedimentation rate (ESR) with no arthritis. She was admitted to our hospital in a state of shock from a bleeding gastric ulcer, for which surgery was immediately performed. During the postoperativeperiod, she had supraventricular tachycardia, congestiveheart failure, and a high temperature.She was treated with antibiotics, but blood, urine, and intravenous catheter cultures performed previously were all negative.On the 10th postoperativeday, with the temperature still high, the patient developeddiffuse abdominal pain, and there wasa general overall worsening, hypotension, and oligoanuria.Echographyand abdominal computed tomography revealed a distended gallbladder with no calculi and two collections of liquid, one surrounding it and the other in the right ileac fossa.A culture on 15 mL of bile extracted from this latter site by needlepuncturewas negative. Cholecystectomy was carriedout, but the generalstate, anasarca, and fever persisted with no apparent septic focus. Laboratory studies showed the following values: leukocytosis 40 X log/L (granulocytes96.7%),hemoglobin 114g/L, platelets 525X log/L, reticulocytes 30 per 1,000, ESR 69 mm/hour, glucose 8.8
There was mild tenderness to palpation over the mid-thoracic spine, but no erythema or flocculation was noted. A rectal examination revealed normal tone. Her motor examination demonstrated intact and symmetric findings. She had decreased sensation (to light touch) of the left great toe, but no other deficits. Her deep tendon reflexes were equal, and the plantars were down-going. Laboratory evaluation revealed a leukocyte count of 22,800/mm3, with 76% segmented forms and 8% bands. Emergent magnetic resonance imaging revealed a posterior mid-thoracic epidural collection consistent with an epidural abscess (Figure 1). She immediately underwent laminectomy, at which an epidural abscess was found and evacuated. Gram stain of the abscess revealed gram-positive cocci, and empiric treatment with oxacillin was begun. Her cerebrospinal fluid culture was negative. Culture of the abscess subsequently grew group G streptococci, and was sensitive to penicillin. Oxacillin therapy was discontinued and administration of intravenous penicillin G (24,000,OOO units/ day) was started. Her leukocyte count and temperature normalized, her back pain readily improve’d, and her paresthesias gradually resolved. She was discharged receiving intravenous penicillin G (with probenecid) to complete a 6-week course, and had total resolution of her symp-
Figure 1. Magnetic resonance imaging of the thoracic spine reveals a posterior epidural abscess extending from the T5 through T7 levels. There is associated narrowing of the adjacent subarachnoid space and compression of the spinal cord.
toms.
Acute spinal epidural abscesses are infrequent but well-recognized infections of the central nervous system. Since Dandy’s [6] review in 1926, much has been written about spinal epidural abscesses, and the importance of early recognition has been emphasized. A common basic clinical pattern has been described by Heusner [7]: the four phases are spinal ache (back pain and tenJuly 1991
The American
derness), root pain (pains radiating from the site, headache, neck stiffness, and reflex changes), weaknesses of voluntary muscles, sphincters, and sensibilities (motor and sensory deficits relating to the level of the infection), and paralyses (complete paralysis, frequently associated with sepsis and even death). However, nonspecific and variable symptoms often contribute to a lack of cliniJournal
of Medicine
Volume
91
89
BRIEF CLINICAL OBSERVATIONS
cal suspicion, and the diagnosis can be missed.Danner and Hartman [8] found that the correctdiagnosisof spinal epidural abscess was made initially in only 17.9% of cases.Fortunately, the history of a recent epidural catheter and the neurologicfindings in our patient suggestedthe possibility of an epidural process,and emergent diagnostic and therapeutic measureswere performed. The bacteriology of spinal epidural abscessesis somewhatvaried, with Staphylococcus aureus the most common pathogen isolated [9]. Although streptococci have been found, group G streptococci have not been reported. The most common sites of infection with group G streptococci are the skin and soft tissues [9]. During delivery, colonization of the skin and contamination by the vaginal flora with group G streptococci with introduction into the epidural spaceby the anesthesiacatheter is the probable sourceof infection in our patient. In general, spinal epidural abscessis a rare complication of spinal anesthesia [lo]. Of interest, there are also several reports of postpartum spinal epidural abscessnot related to epidural anesthesia [11,12]. Our case report describes a catheter-relatedgroup G streptococcalspinal epidural abscess,an associationnot previouslyreported in our review of the literature. More significantly, it underscores againthe importance of early diagnosisand treatment. Heusner [7] and others have shown that diagnosisand intervention in the earlier phasesof spinal epidural abscess lead to favorable outcomes,while those patients diagnosedin the later phasescan experience irreversible neurologic damageand evendeath. Furthermore, delays in diagnosis have preventedreduction in morbidity and mortality despite improvements in therapy over the de90
cades[7,8].The patient discussed here did well after presenting in phase 2 of Heusner’s classification becauseof prompt diagnosis and treatment. LINAS M. KLYGIS, M.D. BORIS E. REISBERG, M.D.
Northwestern Memorial Hospjtal Northwestern University M;fed;zE Chicago, Illinois 1. Lancefield RC, Hare R. The serological differentiation of pathogenic and nonpathogenic strains of hemolytic streptococci from parturient women. J Exp Med 1935; 61: 335-49. 2. Vartian C, Lerner PI. Shlaes DM, Gopalakrishna KV. Infections due to Lancefield group G streptococci. Medicine (Baltimore) 1985; 64: 75-88. 3. Duma RJ, Weinberg AN, Medrek TF, Kunz LJ. Streptococcal infections: a bacteriologicand clinical study of streptococcal bacteremia. Medicine (Baltimore) 1969; 48: 87-127. 4. Lam K, Bayer AS. Serious infections due to group G streptococci: report of 15 cases with in vitro-in viva correlations. Am J Med 1983; 75: 561-70. 5. Gossling J. Occurrence and pathogenicity of the Streptococcus millen’ group. Rev Infect Dis 1988; 10: 257-85. 6. Dandy WE. Abscesses and inflammatory tumors in the spinal epidural space (so-called pachymeningitis externa). Arch Surg 1926; 13: 477-94. 7. Heusner AP. Nontuberculous spinal epidural infections. N Engl J Med 1948; 239: 845-54. 8. Danner RL, Hartman BJ. Update of spinal epidural abscess: 35 cases and review of the literature. Rev Infect Dis 1987; 9: 265-74. S.Kaufman DM. Kaplan JG. Litman N. Infectious agents in spinal epidural abscesses. Neurology 1980; 30: 844-50. 10. North JB, Brophy BP. Epidural abscess: a hazard of spinal epidural anaesthesia. Aust NZ J Surg 1979: 49: 484-5. 11. Male CG, Martin R. Puerperal spinal epidural abscess. Lancet 1973; 1: 608-9. 12. Crawford JS. Pathology in the extradural space. Br J Anaesth 1975; 47: 412-5. Submitted
May 23, 1990, and accepted in revised form February 5, 1991
LOCALIZEDRHEUMATOID VASCULITISPRESENTINGAS ACUTE ALITHIASIC CHOLECYSTITIS Rheumatoid arthritis is occasionally complicatedby systemicnecrotizing vasculitis indistinguishable pathologically from the primary forms of polyarteritis nodosa (PAN) [l]. Although lo-
July 1991 The American Journal of Medicine
Volume 91
calizedforms are not uncommon, only one case of localized rheumatoid vasculitis of the gallbladder has been reported [2]. Our patient was a 69-year-old woman with a history of hypertension, atria1 fibrillation, and seropositive erosive rheumatoid arthritis with subcutaneousnodules since 11 years previously. She received nonsteroidal antiinflammatory drugs (NSAIDs), corticosteroids,and aurothiomalate, remaining in clinical and analytical remissionuntil 6 months ago,when shepresentedwith intense constitutional symptoms, anemia, and an increase in the erythrocyte sedimentation rate (ESR) with no arthritis. She was admitted to our hospital in a state of shock from a bleeding gastric ulcer, for which surgery was immediately performed. During the postoperativeperiod, she had supraventricular tachycardia, congestiveheart failure, and a high temperature.She was treated with antibiotics, but blood, urine, and intravenous catheter cultures performed previously were all negative.On the 10th postoperativeday, with the temperature still high, the patient developeddiffuse abdominal pain, and there wasa general overall worsening, hypotension, and oligoanuria.Echographyand abdominal computed tomography revealed a distended gallbladder with no calculi and two collections of liquid, one surrounding it and the other in the right ileac fossa.A culture on 15 mL of bile extracted from this latter site by needlepuncturewas negative. Cholecystectomy was carriedout, but the generalstate, anasarca, and fever persisted with no apparent septic focus. Laboratory studies showed the following values: leukocytosis 40 X log/L (granulocytes96.7%),hemoglobin 114g/L, platelets 525X log/L, reticulocytes 30 per 1,000, ESR 69 mm/hour, glucose 8.8