Volume 86 Number 1
manifested by a paroxysmal cough and radiographic changes compatible with an interstitial pneumonia. 3, 6 T h e p n e u m o n i a is generally u n c o m p l i c a t e d and resolves without antibiotic therapy. 5 The pulmonary pathology seen in infectious mononucleosis is similar to that of other viral pneumonias with mononuclear infiltration of the perivascular and peribronchial tissue as well as the intra-alveolar septa. 7 Custer and Smith 7 reported that a postmortem examination, in two of nine cases of fatal infectious mononucleosis, frank pneumonia consolidation was present with a polymorphonuclear exudate in one and a mononuclear exudate in the second. After i n v o l v em en t of the central nervous system, bacterial superinfection is the most c o m m o n cause o f death in infectious mononucleosis. 5 In our patient, two tracheal aspirates grew out heavy growths of Haemophilus influenzae which prompted the change of antibiotics (to chloramphenicol). Haemophilus influenza e is a comm o n secondary invader of other viral pneumonias. Baehner and Shuler 8 noted that about 7% of children with infectious mononucleosis had radiographic evidence of bronchopneumonia. Previously reported pulmonary manifestations of infectious mononucleosis in children have included interstitial pneumonia, 6, 8 hilar adenopathy, 6 superimposed bacterial pneumonia, 8 atelectasis, and pleuritic pain. Pleural effusion with infectious mononucleosis has been reported previously in adults 9, 10 but not in the pediatric age group. While
Multiple cerebral abscesses complicating hepatopulmonary ameb iasis Frank B. Hughes, M.D., Stephen T. Faehnle, M.D., and Jimmy L. Simon, M.D.,* Galveston, Texas
CEREBRAL AMEBIASIS is a rare and usually fatal complication of Entamoeba histolytica infections. This case report describes a child with proved hepatopulmonary a me bias i s w h o was f o u n d to h a v e t h r e e c e r e b r a l abscesses. A prolonged course of antiamebic therapy resulted in resolution of all lesions. From The Department of Pediatrics, The University of Texas Medical Branch. *Reprint address: Department of Pediatrics, BowmanGray School of Medicine, Winston-Salem, N.C. 27103.
Brief clinical and laboratory observations
95
pleural effusions in our patient may have been due to the secondary bacterial infection, prolonged presence (resolved after 3 months) would suggest a viral etiology. Antibodies (IFA) to Epstein-Barr virus were determined by using Jijoye cell line in the laboratory of Dr. Y. Hirshaut, Memorial Hospital, New York City. REFERENCES 1. Tischendorf P, et al: Development and persistence of immunity to Epstein-Barr virus in man, J Infect Dis 122:401, 1970. 2. Collins OD, and Louro JM: Incidence of positive slide agglutination tests for mononucleosis in children, J PEDIATR 73:745, 1968. 3. Rodstein M: A case of infectious mononucleosis with atypical pneumonia, Ann Intern Med 28:1177, 1948. 4. Evans AS, N i ed er m an J C , and McCollum RW: Seroepidemiologic studies of infectious mononucleosis with EB virus, N Eng! J Med 279:1121, 1968. 5. Evans AS: Complications of infectious mononucleosis: Recognition and management, Hosp Med 3:24, 1967. 6. Arendt J: The roentgenological aspects of infectious mononucleosis, Am J Roentgenol Radium Ther Nucl Med 64:950, 1950. 7. Custer RP, and Smith EB: The pathology of infectious mononucleosis, Blood 3:830, 1948. 8. Baehner RL, and Shuler SE: Infectious mononucleosis in childhood, Clin Pediatr 6:393, 1967. 9. Vander JB: Pleural effusion in infectious mononucleosis, Ann Intern Med 41:146, 1954. 10. Eaton OM, Little PF, and Silver HM: Infectious mononucleosis with pleural effusion, Arch Intern Med 115:87, 1965.
CASE R E P O R T A 3-year-old white boy from Houston, Texas, was seen eight weeks prior to admission for diarrhea. Stool culture showed normal flora. The diarrhea resolved in one week with no definitive treatment. One day prior to admission cough and abdominal pain developed. Physical examination at the time of hospital admission revealed a small child in moderate respiratory distress. Dullness to percussion and decreased breath sounds were noted over the right hemithorax. Abdominal tenderness and guarding over the right upper quadrant without hepatomegaly was found. Neurologic examination was normal. Chest roentgenogram revealed a larg e pleural effusion obscuring the right hemidiaphragm. Diagnostic thoracentesis yielded thick bloody fluid with marly neutrophils, but no bacteria. Intravenous nafcillin and chest tube drainage were begun. However, five days later the Patient was still febrile. Pleural cultures were negative as was a tubercu!in skin test. A second thoracentesis yielded a brown aspirate in which trophozoites of E. histolytica were demonstrated on wet mount
96
Brief clinical and laboratory observations
The Journal of Pediatrics January 1975
LLat
or liver abscess, and pulmonary involvement preceding central nervous system manifestations should strongly suggest the diagnosis of cerebral amebiasis. Serologic tests for amebiasis are positive in more than 95% of patients with liver abscess and in 85-90% of patients with invasive intestinal disease. 6 In the present case, identification of amebae in the lung, with a positive indirect hemagglutination titer for amebiasis, established the initial diagnosis. Fever and signs of central nervous system involvement led to the discovery of multiple intracerebral space-occupying lesions, presumably due to cerebral amebiasis. The course of cerebral amebiasis is rapid, steadily downhill, and nearly always fatal), 4 At least 97 cases of amebic brain abscess have been reported with only three survivors. 5, 7 In two of the three cases E. Histolytica was not f o u n d ; the third patient was treated surgically with no mention of medical therapy. Metronidazole is an effective agent for the treatment of amebic dysentery and hepatic amebiasis in adults and children. 6, 8
Fig. 1. and by trichrome stain. E. histolytica was not found in the patient's stools. A liver scan (99mTc sulfur colloid) revealed decreased uptake in the right posterolateral region of the liver compatible with an abscess. Chloroquine phosphate was begun orally and continued for 20 days with resolution of symptoms. Indirect hemagglutination titer for amebiasis was reported posRive (1:4096) by the Center for Disease Control, Atlanta, Georgia. The patient was discharged on the twenty-fifth hospital day on therapy with diiodohydroxyquin. Three days later he had a grand real seizure lasting approximately one hour. On readmission he was comatose and responded only to deep pain. Temperature was 39~ Bilateral sustained ankle clonus, hyperactive deep tendon reflexes, and bilateral Babinski signs were present. Skull roentgenograms were normal. Cerebrospinal fluid cell count was 4 white blood cells/mm 3. Twenty-four hours after admission a brief left focal seizure occurred; the temperature was 38~ On the third hospital day, asymetrical knee jerks and bilateral ankle clonus were noted; the temperature was 39.6~ Brain scanning (99mTc pertechnerate) revealed three abnormal areas--superficial right parietal, superficial left frontal, and deep left parietal--compatible with multiple abscesses (Fig. 1). At that time the presumptive diagnosis of amebic brain abscess was made. Following 24 hours of chloroquine phosphate therapy, the patient became afebrile. On the fifth day of chloroquine phosphate therapy, needle aspiration of the right parietal cerebral abscess yielded 2.25 ml of thick grayish brown material. No organisms were identified on wet mount. All cultures were negative, and microscopic findings were compatible with an acute brain abscess. The patient was treated with metronidazole for 21 days and chloroquine phosphate for 6 weeks. Two months after the completion of antiamebic therapy, the brain scan was essentially normal. The patient has remained in good health at follow up with the exception of one grand real seizure one month after completion of therapy. DISCUSSION Amebic brain abscess is uncommon, the incidence at 0 autoPsY ranging from 0.66-4.7% of patients with amebic liver abscess. 1,2 Cerebral amebiasis is particularly rare in children. The appearance of signs or symptoms indicating central nervous system involvement is abrupt; the course is often f u l m i n a n t 34 , and resembles that o f a pyogenic brain abscess. 5 The triad of dysentery, hepatitis,
SUMMARY A 3-year-old boy with hepatopulmonary amebiasis treated with chloroquine phosphate for 20 days subsequently was found to have three brain abscesses and r e s p o n d e d to p r o l o n g e d c o m b i n e d t h e r a p y with metronidazole and chloroquine phosphate. Cerebral amebiasis should be considered in any patient with amebic dysentery, hepatic abscess, or pulmonary i n v o l v e m e n t in w h o m signs or s y m p t o m s o f c e n t r a l n e r v o u s s y s t e m i n v o l v e m e n t appear. A prolonged course o f appropriate t h e r a p y with periodic brain scanning for evidence of i m p r o v e m e n t is suggested.
REFERENCES 1. Kern, BH, Gilmore, HR, and VanStone, WW: Fatal amebiasis: Report of 148 fatal cases from the Armed Forces Institute of Pathology, Ann Int Med 44:831, 1956. 2. Orbison, JA, Reeves, N, Leedham, CL, et al.: Amebic brain abscess, Medicine 30:247, 1951. 3. Halpert, B, and Ashley, JD: Amebic colitis complicated with abscess of the brain, Arch Pathol 38:112, 1944. 4. Stein, A, and Kazan, A: Brain abscess due to Entameba histolyfica, J Neuropathol Exp Neurol 1:32, 1942. 5. Collard, P, and Kendall, D: Cerebral amebiasis treated with emetine: Report of a case, Lancet 2:17, 1947. 6. Report of Committee on Infectious Disease: ed 17, Evanston, Ill., 1974, American Academy of Pediatrics, p 95. 7. Lombardo, L, Alanso, P, Arroyo, L, et al.: Cerebral amebiasis: Report of 17 cases, J Neurosurg 21:704, 1964. 8. Powell, SJ: New developments in the therapy of amebiasis, Gut 11:967, 1970.
manifested by a paroxysmal cough and radiographic changes compatible with an interstitial pneumonia. 3, 6 T h e p n e u m o n i a is generally u n c o m p l i c a t e d and resolves without antibiotic therapy. 5 The pulmonary pathology seen in infectious mononucleosis is similar to that of other viral pneumonias with mononuclear infiltration of the perivascular and peribronchial tissue as well as the intra-alveolar septa. 7 Custer and Smith 7 reported that a postmortem examination, in two of nine cases of fatal infectious mononucleosis, frank pneumonia consolidation was present with a polymorphonuclear exudate in one and a mononuclear exudate in the second. After i n v o l v em en t of the central nervous system, bacterial superinfection is the most c o m m o n cause o f death in infectious mononucleosis. 5 In our patient, two tracheal aspirates grew out heavy growths of Haemophilus influenzae which prompted the change of antibiotics (to chloramphenicol). Haemophilus influenza e is a comm o n secondary invader of other viral pneumonias. Baehner and Shuler 8 noted that about 7% of children with infectious mononucleosis had radiographic evidence of bronchopneumonia. Previously reported pulmonary manifestations of infectious mononucleosis in children have included interstitial pneumonia, 6, 8 hilar adenopathy, 6 superimposed bacterial pneumonia, 8 atelectasis, and pleuritic pain. Pleural effusion with infectious mononucleosis has been reported previously in adults 9, 10 but not in the pediatric age group. While
Multiple cerebral abscesses complicating hepatopulmonary ameb iasis Frank B. Hughes, M.D., Stephen T. Faehnle, M.D., and Jimmy L. Simon, M.D.,* Galveston, Texas
CEREBRAL AMEBIASIS is a rare and usually fatal complication of Entamoeba histolytica infections. This case report describes a child with proved hepatopulmonary a me bias i s w h o was f o u n d to h a v e t h r e e c e r e b r a l abscesses. A prolonged course of antiamebic therapy resulted in resolution of all lesions. From The Department of Pediatrics, The University of Texas Medical Branch. *Reprint address: Department of Pediatrics, BowmanGray School of Medicine, Winston-Salem, N.C. 27103.
Brief clinical and laboratory observations
95
pleural effusions in our patient may have been due to the secondary bacterial infection, prolonged presence (resolved after 3 months) would suggest a viral etiology. Antibodies (IFA) to Epstein-Barr virus were determined by using Jijoye cell line in the laboratory of Dr. Y. Hirshaut, Memorial Hospital, New York City. REFERENCES 1. Tischendorf P, et al: Development and persistence of immunity to Epstein-Barr virus in man, J Infect Dis 122:401, 1970. 2. Collins OD, and Louro JM: Incidence of positive slide agglutination tests for mononucleosis in children, J PEDIATR 73:745, 1968. 3. Rodstein M: A case of infectious mononucleosis with atypical pneumonia, Ann Intern Med 28:1177, 1948. 4. Evans AS, N i ed er m an J C , and McCollum RW: Seroepidemiologic studies of infectious mononucleosis with EB virus, N Eng! J Med 279:1121, 1968. 5. Evans AS: Complications of infectious mononucleosis: Recognition and management, Hosp Med 3:24, 1967. 6. Arendt J: The roentgenological aspects of infectious mononucleosis, Am J Roentgenol Radium Ther Nucl Med 64:950, 1950. 7. Custer RP, and Smith EB: The pathology of infectious mononucleosis, Blood 3:830, 1948. 8. Baehner RL, and Shuler SE: Infectious mononucleosis in childhood, Clin Pediatr 6:393, 1967. 9. Vander JB: Pleural effusion in infectious mononucleosis, Ann Intern Med 41:146, 1954. 10. Eaton OM, Little PF, and Silver HM: Infectious mononucleosis with pleural effusion, Arch Intern Med 115:87, 1965.
CASE R E P O R T A 3-year-old white boy from Houston, Texas, was seen eight weeks prior to admission for diarrhea. Stool culture showed normal flora. The diarrhea resolved in one week with no definitive treatment. One day prior to admission cough and abdominal pain developed. Physical examination at the time of hospital admission revealed a small child in moderate respiratory distress. Dullness to percussion and decreased breath sounds were noted over the right hemithorax. Abdominal tenderness and guarding over the right upper quadrant without hepatomegaly was found. Neurologic examination was normal. Chest roentgenogram revealed a larg e pleural effusion obscuring the right hemidiaphragm. Diagnostic thoracentesis yielded thick bloody fluid with marly neutrophils, but no bacteria. Intravenous nafcillin and chest tube drainage were begun. However, five days later the Patient was still febrile. Pleural cultures were negative as was a tubercu!in skin test. A second thoracentesis yielded a brown aspirate in which trophozoites of E. histolytica were demonstrated on wet mount
96
Brief clinical and laboratory observations
The Journal of Pediatrics January 1975
LLat
or liver abscess, and pulmonary involvement preceding central nervous system manifestations should strongly suggest the diagnosis of cerebral amebiasis. Serologic tests for amebiasis are positive in more than 95% of patients with liver abscess and in 85-90% of patients with invasive intestinal disease. 6 In the present case, identification of amebae in the lung, with a positive indirect hemagglutination titer for amebiasis, established the initial diagnosis. Fever and signs of central nervous system involvement led to the discovery of multiple intracerebral space-occupying lesions, presumably due to cerebral amebiasis. The course of cerebral amebiasis is rapid, steadily downhill, and nearly always fatal), 4 At least 97 cases of amebic brain abscess have been reported with only three survivors. 5, 7 In two of the three cases E. Histolytica was not f o u n d ; the third patient was treated surgically with no mention of medical therapy. Metronidazole is an effective agent for the treatment of amebic dysentery and hepatic amebiasis in adults and children. 6, 8
Fig. 1. and by trichrome stain. E. histolytica was not found in the patient's stools. A liver scan (99mTc sulfur colloid) revealed decreased uptake in the right posterolateral region of the liver compatible with an abscess. Chloroquine phosphate was begun orally and continued for 20 days with resolution of symptoms. Indirect hemagglutination titer for amebiasis was reported posRive (1:4096) by the Center for Disease Control, Atlanta, Georgia. The patient was discharged on the twenty-fifth hospital day on therapy with diiodohydroxyquin. Three days later he had a grand real seizure lasting approximately one hour. On readmission he was comatose and responded only to deep pain. Temperature was 39~ Bilateral sustained ankle clonus, hyperactive deep tendon reflexes, and bilateral Babinski signs were present. Skull roentgenograms were normal. Cerebrospinal fluid cell count was 4 white blood cells/mm 3. Twenty-four hours after admission a brief left focal seizure occurred; the temperature was 38~ On the third hospital day, asymetrical knee jerks and bilateral ankle clonus were noted; the temperature was 39.6~ Brain scanning (99mTc pertechnerate) revealed three abnormal areas--superficial right parietal, superficial left frontal, and deep left parietal--compatible with multiple abscesses (Fig. 1). At that time the presumptive diagnosis of amebic brain abscess was made. Following 24 hours of chloroquine phosphate therapy, the patient became afebrile. On the fifth day of chloroquine phosphate therapy, needle aspiration of the right parietal cerebral abscess yielded 2.25 ml of thick grayish brown material. No organisms were identified on wet mount. All cultures were negative, and microscopic findings were compatible with an acute brain abscess. The patient was treated with metronidazole for 21 days and chloroquine phosphate for 6 weeks. Two months after the completion of antiamebic therapy, the brain scan was essentially normal. The patient has remained in good health at follow up with the exception of one grand real seizure one month after completion of therapy. DISCUSSION Amebic brain abscess is uncommon, the incidence at 0 autoPsY ranging from 0.66-4.7% of patients with amebic liver abscess. 1,2 Cerebral amebiasis is particularly rare in children. The appearance of signs or symptoms indicating central nervous system involvement is abrupt; the course is often f u l m i n a n t 34 , and resembles that o f a pyogenic brain abscess. 5 The triad of dysentery, hepatitis,
SUMMARY A 3-year-old boy with hepatopulmonary amebiasis treated with chloroquine phosphate for 20 days subsequently was found to have three brain abscesses and r e s p o n d e d to p r o l o n g e d c o m b i n e d t h e r a p y with metronidazole and chloroquine phosphate. Cerebral amebiasis should be considered in any patient with amebic dysentery, hepatic abscess, or pulmonary i n v o l v e m e n t in w h o m signs or s y m p t o m s o f c e n t r a l n e r v o u s s y s t e m i n v o l v e m e n t appear. A prolonged course o f appropriate t h e r a p y with periodic brain scanning for evidence of i m p r o v e m e n t is suggested.
REFERENCES 1. Kern, BH, Gilmore, HR, and VanStone, WW: Fatal amebiasis: Report of 148 fatal cases from the Armed Forces Institute of Pathology, Ann Int Med 44:831, 1956. 2. Orbison, JA, Reeves, N, Leedham, CL, et al.: Amebic brain abscess, Medicine 30:247, 1951. 3. Halpert, B, and Ashley, JD: Amebic colitis complicated with abscess of the brain, Arch Pathol 38:112, 1944. 4. Stein, A, and Kazan, A: Brain abscess due to Entameba histolyfica, J Neuropathol Exp Neurol 1:32, 1942. 5. Collard, P, and Kendall, D: Cerebral amebiasis treated with emetine: Report of a case, Lancet 2:17, 1947. 6. Report of Committee on Infectious Disease: ed 17, Evanston, Ill., 1974, American Academy of Pediatrics, p 95. 7. Lombardo, L, Alanso, P, Arroyo, L, et al.: Cerebral amebiasis: Report of 17 cases, J Neurosurg 21:704, 1964. 8. Powell, SJ: New developments in the therapy of amebiasis, Gut 11:967, 1970.
