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Pasteurella multocida meningitis in an infant with recovery
Volume 86 Number 1
sponse of cortisol to ACTH, and failure to observe a normal diurnal variation. While the normal AM plasma values of cortisol and the lack of suppression following administration of 1.0 mg dexamethasone/100 lb body weight/day are not clearly indicative of Cushing's syndrome, these findings have been described previously in other patients with Cushing's syndrome) 3 These values and the normal histology of the adrenal gland suggest that the h y p e r p r o d u c t i o n was mild. A n o r m a l growth h o r m o n e r e s p o n s e to arginine a n d i n s u l i n tolerance tests has also been described in patients with Cushing's syndrome, ll The course of this patient's disease can be contrasted with that of most other patients with Cushing's syndrome. All 13 patients in a report from the Mayo Clinic 1 had truncal obesity, moonface, and a buffalo hump, 11 had hirsutism and acne, ten were hypertensive, and five had premature appearance of public and axillary hair. Eleven of the patients were short. All of these patients tested had a diabetic response to a glucose tolerance test. Hence, in contrast with the typical presentation of Cushing's syndrome in childhood with abnormal fat distribution, hirsutism, acne, as well as short stature, our patient illustrates that Cushing's syndrome can be a subtle entity and should be considered in the differential diagnosis of growth failure in short children even if there are no other obvious symptoms of the syndrome. Urinary determinations of 17-OHCS, in mg/m2/24 hr are, therefore, indicated as part of the evaluation of short Children.
Pasteurella multocida meningitis in an infant with recovery Joseph P. Repice, M.D., and Erwin Neter, M.D.,* Buffalo, N. Y.
EARLY DIAGNOSIS and selection of optimal therapy may be difficult in rare infections, in part because iniFrom the Department of Pediatrics, State University of New York at Buffalo, and the Children "sHospital of Buffalo. *Reprint address: Children's Hospital of Btiffalo, 219Bryant St., Btlff'alo, N. Y. 14222.
Brief clinical and laboratory observations
91
REFERENCES
1. McArthur RG, Clouter MD, Hayles AB, and Sprague RG: Cushing's disease in children, Mayo Clin Proc 47:318, 1972. 2. Schletter FE, Clift GV, Meyer R, and Streeter DHP: Cushing's syndrome in childhood: Report of two cases with bilateral adrenocortical hyperplasia, showing distinctive clinical features, J Clin Endocrinol Metab 27:22, 1967. 3. KiUingerDW, Hudson RW, and Volpe R: Cushing's syndrome in childhood, Can Med Assoc J 106:131, 1972. 4. Tanner JM: Growth at adolescence, ed. 2, Oxford, 1962, Blackwell Scientific Publications, pp 32-33. 5. Greulich WW, and Pyle SI: Radiographic atlas of skeletal development of the hand and wrist, ed. 2, Stanford, Calif., 1959, Stanford University Press. 6. Nelson DH, and Samuels LT: A method for the determination of 17-hydroxycorticosteroids in blood: 17-hydroxycorticosterone in peripheral circulation, J Clin Endocrinol Metab 12:519, 1952. 7. Glenn EM, and Nelson DH: Chemical method for the determination of 17-hydroxycorticosteroids and 17ketosteroids in urine following hydrolysis with /3glucuronidase, J Clin Endocrinol Metab 13:911, 1953. 8. Jensen CC: Quantitative determination of dehydroepiandrosterone: determination in urinary extracts, Acta Endocrinol 4:374, 1950. 9. Kenny FM, Malvaux P, and Migeon CJ: Cortisol production rate in newborn babies, older infants, and children, Pediatrics 31:360, 1963. 10. Marie J, Leveque B, de Gennes JL, Rappaport R, and Desbois RR: Les troubles de la croissance staturale dans l'hypercorticisme spontane acquis de l'enfance, Ann Pediatr (Paris) 13:91, 1966. 11. Strickland AL, Underwood LE, Voina SJ, French FS, and Van Wyk J J: Growth retardation in Cushing's syndrome, Am J Dis Child 123:207, 1972.
tially the causative agent may not be considered in the differential diagnosis, and, in part, because adequate n u m b e r s of cases are not available for evaluating varied treatments. As an example of this group of rare infections we report a one-month-old infant who, without a n i m a l bite but after c o n t a c t with cats, developed Pasteurella multocida meningitis and recovered following antibiotic therapy. Abbreviations used WBC: white blood cells CSF: cerebrospinal fluid CASE R E P O R T
Clinical observations. B. P. (BCH No. 04-54-60) was admitted to Buffalo Children's Hospital at one month of age because of seizures and fever. The family history was unremarkable ex-
92
Brief clinical and laboratory observations
cept for close association of the family members with cats, involving cleaning their litter and even sleeping with them. Physical examination of the patient revealed the following: temperature, 37~ pulse, 122/min; respiratory rate, 26/min (crying); blood pressure, 110/70 (crying); height, 57.5 cm; weight, 3.76 kg; and head circumference, 36.5 cm. He was well developed, well nourished, but quite irritable when picked up. There was intermittent right-sided, tonic-clonic seizure activity on initial examination; Chvostek's sign was negative. White blood cell count was 10,700/ram 3 with 5% metamyelocytes, 17% bands, 20% polymorphonuclear leukocytes, 53% lymphocytes, and 5% monocytes; the number of platelets was adequate. Serum concentrations of chloride, sodium, potassium, calcium, and blood urea nitrogen were all normal, as was the urinalysis. The cerebrospinal fluid contained 6,592 WBC/mm3; with 60% polymorphonuclear leukocytes and 40% lymphocytes. Microscopic examination revealed pleomorphic, gram-negative bacteria. The concentration of glucose in CSF was 1 mg/dl and concentration of blood glucose 61 mg/dl; CSF concentration of protein was 315 mg/dl. Spinal fluid culture as well as two blood cultures were positive for a coccobacillus, later indentified as P. multocida. Stool and nasopharyngeal cultures grew normal flora, but P. multocida was recovered from a throat culture. Treatment was begun with ampicillin 200 mg/kg/day intravenously and kanamycin 15 mg/kg/day intramuscularly. In view of the fact that the strain of P. rnultocida was resistant in vitro to kanamycin and sensitive to cephalothin, the former drug was discontinued and replaced by sodium cephalothin, 200 mg/kg/day intravenously. The patient received this therapy for 10 days, during which time he became afebrile. Spinal fluid on the fourth hospital day contained 600 WBC/ mm 3, 227 mg/dl of protein and 30 mg/dl of glucose (concentration of blood glucose 70 mg/dl). Culture was sterile. On the twelfth hospital day cerebrospinal fluid contained 70 WBC/ mm 3, 196 mg/dl of protein, and 32 mg/dl of glucose (concentration of blood glucose 71 mg/dl). No organisms were recovered on culture. Electroencephalogram revealed a normal sleeping record. Diffuse, heavy uptake of isotope over the left frontoparietal area, extending into the temporal area, was noted on brain scan. The subdural space was tapped on the thirteenth hospital day, yielding 8 ml of sterile, xanthochromic fluid with concentrations of protein of 3,632 mg/dl and glucose of 68 mg/dl. Cerebrospinal fluid on the thirtieth hospital day, prior to the discharge of the patient, contained 10 lymphocytes/mm3 with concentrations of 111 mg/dl and glucose 35 mg/dl (blood glucose of 73 mg/dl). Neurologic examination was negative four months after onset of the disease. Bacteriologic and immunologic observations. Microscopic examination of the spinal fluid obtained on admission revealed the presence of pleomorphic, gram-negative bacteria, resembling Haemophilus influenzae. The culture, after overnight incubation (at 37~ and under 5% CO2) had good growth on both blood and chocolate agar, thus rendering this diagnosis untenable. Identification of P. multocida was based on the following
The Journal of Pediatrics January 1975
findings: growth on nutrient agar but not on MacConkey agar; indol and acid production without gas from glucose and maltose; nitrate reduction; and positive catalase reaction. The diagnosis was confirmed by Dr. John Timoney, Cornell University, Ithaca, N. Y., and by the New York State Department of Health, Albany, N. Y. The strain was studied further by Dr. G. R. Carter, Michigan State University, East Lansing, Mich., who found that it was pathogenic for mice and yet did not produce a capsule. The latter feature made capsular typing impossible. The antibiogram indicated sensitivity of the strain to penicillin, ampicillin, cephalothin, tetracycline, and resistance to gentamicin and kanamycin. It was this latter finding that led to changes in chemotherapy. Study of the immune response of the pa[ient by means of the passive hemagglutination test failed to reveal the production of specific antibodies during the recovery period, an observation that was confirmed by Dr. Carter using the bacterial agglutination procedure. DISCUSSION Diagnosis and m a n a g e m e n t o f u n u s u a l i n f e c t i o n s present certain difficulties, in part, because of unfamiliarity with the disease by physicians and laboratorians alike, and, in part, because definitive information of optimal therapy often is not available. Among s u c h i n f e c t i o n s is P. multocida m e n i n g i t i s . In 1950, Zeller and Lepper 1 summarized the available information indicating that only eight cases had been reported between 1925 and 1944 and described two additional cases of their own. More recently, Controni and Jones 2 extended this review to 1964 and added four additional cases. Of the 14 cases only three were children and two of the three, infants. Both infants died. Since then, another fatal case of P. multocida meningitis, developing during the first week of life, was reported by Bates and associates) To the best of our knowledge, the present case represents the first observation of P. multocida meningitis in the newborn period followed by recovery. Difficulty in the diagnosis of P. multocida as cause of meningitis is due to the fact that, as observed in the present case, the microscopic finding of pleomorphic, gram-negative coccobacilli suggests the diagnosis of the far more frequently encountered H. influenzae. In all likelihood, recovery can be ascribed to ampicillin therapy. Needless to say, definitive information on optimal therapy cannot be obtained from observation of single cases. Meningitis represents but a minority of human infections caused by P. multocida, a m i c r o o r g a n i s m frequently found in animals, which serve as source o f h u m a n infection. It is now generally agreed that wound infections from P. multocida in man are quite common, particularly after contact with animals such as cats. 4"6 Many such cases, undoubtedly, remain unrecognized because appropriate bacteriologic examination is not
Volume 86 Number 1
B r i e f cfinical and laboratory observations
carried out. In all likelihood, the infection in the p r e s e n t case originated f r o m cats, a l t h o u g h bacteriologic p r o o f of this a s s u m p t i o n was not obtained. Since P. multocida was isolated from the throat o f the patient, it can b e a s s u m e d that the respiratory tract served as the portal o f e n t r y of the m i c r o o r g a n i s m leading to h e m a t o g e n o u s spread and meningitis. Finally, it is of interest to n o t e that P. multocida may cause meningitis in animals s u c h as the dog. 7 The authors wish to thank Dr. John Timoney, Cornell University, Ithaca, N. Y.; and Dr. G. R. Carter, Michigan State University, East Lansing, Mich., for their study of the P. multocida strain and of the antibody response of the patient.
93
2. Controni G, and Jones RS: Pasteurella meningitis. A review of the literature, Am J Med Technot 33:379, 1967. 3. Bates HA, Controni G, Elliot N, and Eitzman DV: Septicemia and meningitis in a newborn due to PasteureUa multocida, Clin Pediatr 4:668, 1965. 4. Holloway WJ, Scott EG, and Adams YB: Pasteurelta multocida infection in man. Report of 21 cases, Am J Clin Pathol 51:705, 1969. 5. Hubbert WT, and Rosen MN: II. Pasteurella multocida infection in man unrelated to animal bite, Am J Public Health 60:1109, 1970. 6. Tindall JP, and Harrison CM: Pasteurella multocida infections following animal injuries, especially cat bites, Arch Dermatol 105:412, 1972. 7. Rogers RJ, and Elder JK: Purulent leptomeningitis in a dog associated with an aerogenic Pasteurella multocida. Aust Vet J 43:81, 1967.
REFERENCES
1.
Zeller WW, and Lepper MH: Meningitis due to Pasteurella other than Pasteurella tularensis and Pasteurella pestis, Am J Med 9:701, 1950.
Pulmonary involvement in infectious mononucleos& Daniel R. Fermaglieh, M.D., Lieutenant Commander, MC, USN, Portsmouth, Va.
R E C E N T L Y , we o b s e r v e d a 3 1/2-year-old girl with t h e hematologic and serologic criteria o f infectious m o n o nucleosis; the m a i n clinical feature was viral p n e u m o nia complicated by a s u p e r i m p o s e d bacterial infection and bilateral pleural effusions. T h e p u l m o n a r y s y m p t o m s d o m i n a t e d the presentation and the entire clinical course. CASE REPORT
A 3 1/2-year-old Caucasian girl was Seen 14 days prior to admission with bronchitis and was treated with penicillin and glyceryl guaiacolate. She developed an immediate urticarial pruritic rash and penicillin therapy was discontinued. At 3 days prior to admission, a radiograph of the chest was interpreted as bilateral lower lobe interstitial pneumonia. Physical examination revealed a mild pharyngitis without From the Department o f Pediatrics, Portsmouth Naval Hospital. The views expressed herein are those of the author and do not necessarily reflect to views o f the U.S. Navy. Reprint address:Divisionof Endocrinology, Departmentof Medicine, Children'sHospital Medical Center, 300 Longwood Ave., Boston, Mass. 02115.
exudate, no lymphadenopathy, a palpable spleen tip, and swollen eyelids (Hoagland's sign). Laboratory data included a hemoglobin concentration of 10.8 gm/dl and white blood cell count of 20,750/mm 3, with 42% polymorphonuclear forms, 4% stabs, 4% monocytes, and 50% lymphocytes. Ninety-seven percent of the lymphocytes were "atypical," consistent with Downey cells. A "mono spot test" (repeated twice) was markedly positive. A culture of sputum yielded a few colonies of alpha streptococci, gamma hemolytic streptococci, and Neisseria catarrhalis. I
Abbreviation used EBV: Epstein,Barr virus
The patient was treated with erythromycin, 200 mg four times a day, but the clinical course continued unchanged until the day of admission, when she developed moderate respiratory distress. At this time, physical examination revealed a pale girl with a respiratory rate of 64/min, heart rate 144/min, and temperature of 103.8 ~ F. There were intercostal retractions and inspiratory rhonchi and rales were heard over all lung fields. A tracheal aspirate on admission yielded a few colonies of Diploeoccus pneumoniae and Neisseria catarrhal& Two subsequent tracheal aspirates yielded heavy growths of Haemophilus influenzae. The interstitial pneumonia progressed radiographically with the appearance of small bilateral pleural effusions four days after admission (Figs. 1 and 2). On admission the white blood cell count was 15,200 mm 3, with 3~% lymphocytes. Thirty percent of these were "atypical" compatible with Downey cells. A third "mono spot test" was markedly positive. Acutely, the differential heterophile antibody titer was 1:14 and 19 days later increased to t:224. Anti-
sponse of cortisol to ACTH, and failure to observe a normal diurnal variation. While the normal AM plasma values of cortisol and the lack of suppression following administration of 1.0 mg dexamethasone/100 lb body weight/day are not clearly indicative of Cushing's syndrome, these findings have been described previously in other patients with Cushing's syndrome) 3 These values and the normal histology of the adrenal gland suggest that the h y p e r p r o d u c t i o n was mild. A n o r m a l growth h o r m o n e r e s p o n s e to arginine a n d i n s u l i n tolerance tests has also been described in patients with Cushing's syndrome, ll The course of this patient's disease can be contrasted with that of most other patients with Cushing's syndrome. All 13 patients in a report from the Mayo Clinic 1 had truncal obesity, moonface, and a buffalo hump, 11 had hirsutism and acne, ten were hypertensive, and five had premature appearance of public and axillary hair. Eleven of the patients were short. All of these patients tested had a diabetic response to a glucose tolerance test. Hence, in contrast with the typical presentation of Cushing's syndrome in childhood with abnormal fat distribution, hirsutism, acne, as well as short stature, our patient illustrates that Cushing's syndrome can be a subtle entity and should be considered in the differential diagnosis of growth failure in short children even if there are no other obvious symptoms of the syndrome. Urinary determinations of 17-OHCS, in mg/m2/24 hr are, therefore, indicated as part of the evaluation of short Children.
Pasteurella multocida meningitis in an infant with recovery Joseph P. Repice, M.D., and Erwin Neter, M.D.,* Buffalo, N. Y.
EARLY DIAGNOSIS and selection of optimal therapy may be difficult in rare infections, in part because iniFrom the Department of Pediatrics, State University of New York at Buffalo, and the Children "sHospital of Buffalo. *Reprint address: Children's Hospital of Btiffalo, 219Bryant St., Btlff'alo, N. Y. 14222.
Brief clinical and laboratory observations
91
REFERENCES
1. McArthur RG, Clouter MD, Hayles AB, and Sprague RG: Cushing's disease in children, Mayo Clin Proc 47:318, 1972. 2. Schletter FE, Clift GV, Meyer R, and Streeter DHP: Cushing's syndrome in childhood: Report of two cases with bilateral adrenocortical hyperplasia, showing distinctive clinical features, J Clin Endocrinol Metab 27:22, 1967. 3. KiUingerDW, Hudson RW, and Volpe R: Cushing's syndrome in childhood, Can Med Assoc J 106:131, 1972. 4. Tanner JM: Growth at adolescence, ed. 2, Oxford, 1962, Blackwell Scientific Publications, pp 32-33. 5. Greulich WW, and Pyle SI: Radiographic atlas of skeletal development of the hand and wrist, ed. 2, Stanford, Calif., 1959, Stanford University Press. 6. Nelson DH, and Samuels LT: A method for the determination of 17-hydroxycorticosteroids in blood: 17-hydroxycorticosterone in peripheral circulation, J Clin Endocrinol Metab 12:519, 1952. 7. Glenn EM, and Nelson DH: Chemical method for the determination of 17-hydroxycorticosteroids and 17ketosteroids in urine following hydrolysis with /3glucuronidase, J Clin Endocrinol Metab 13:911, 1953. 8. Jensen CC: Quantitative determination of dehydroepiandrosterone: determination in urinary extracts, Acta Endocrinol 4:374, 1950. 9. Kenny FM, Malvaux P, and Migeon CJ: Cortisol production rate in newborn babies, older infants, and children, Pediatrics 31:360, 1963. 10. Marie J, Leveque B, de Gennes JL, Rappaport R, and Desbois RR: Les troubles de la croissance staturale dans l'hypercorticisme spontane acquis de l'enfance, Ann Pediatr (Paris) 13:91, 1966. 11. Strickland AL, Underwood LE, Voina SJ, French FS, and Van Wyk J J: Growth retardation in Cushing's syndrome, Am J Dis Child 123:207, 1972.
tially the causative agent may not be considered in the differential diagnosis, and, in part, because adequate n u m b e r s of cases are not available for evaluating varied treatments. As an example of this group of rare infections we report a one-month-old infant who, without a n i m a l bite but after c o n t a c t with cats, developed Pasteurella multocida meningitis and recovered following antibiotic therapy. Abbreviations used WBC: white blood cells CSF: cerebrospinal fluid CASE R E P O R T
Clinical observations. B. P. (BCH No. 04-54-60) was admitted to Buffalo Children's Hospital at one month of age because of seizures and fever. The family history was unremarkable ex-
92
Brief clinical and laboratory observations
cept for close association of the family members with cats, involving cleaning their litter and even sleeping with them. Physical examination of the patient revealed the following: temperature, 37~ pulse, 122/min; respiratory rate, 26/min (crying); blood pressure, 110/70 (crying); height, 57.5 cm; weight, 3.76 kg; and head circumference, 36.5 cm. He was well developed, well nourished, but quite irritable when picked up. There was intermittent right-sided, tonic-clonic seizure activity on initial examination; Chvostek's sign was negative. White blood cell count was 10,700/ram 3 with 5% metamyelocytes, 17% bands, 20% polymorphonuclear leukocytes, 53% lymphocytes, and 5% monocytes; the number of platelets was adequate. Serum concentrations of chloride, sodium, potassium, calcium, and blood urea nitrogen were all normal, as was the urinalysis. The cerebrospinal fluid contained 6,592 WBC/mm3; with 60% polymorphonuclear leukocytes and 40% lymphocytes. Microscopic examination revealed pleomorphic, gram-negative bacteria. The concentration of glucose in CSF was 1 mg/dl and concentration of blood glucose 61 mg/dl; CSF concentration of protein was 315 mg/dl. Spinal fluid culture as well as two blood cultures were positive for a coccobacillus, later indentified as P. multocida. Stool and nasopharyngeal cultures grew normal flora, but P. multocida was recovered from a throat culture. Treatment was begun with ampicillin 200 mg/kg/day intravenously and kanamycin 15 mg/kg/day intramuscularly. In view of the fact that the strain of P. rnultocida was resistant in vitro to kanamycin and sensitive to cephalothin, the former drug was discontinued and replaced by sodium cephalothin, 200 mg/kg/day intravenously. The patient received this therapy for 10 days, during which time he became afebrile. Spinal fluid on the fourth hospital day contained 600 WBC/ mm 3, 227 mg/dl of protein and 30 mg/dl of glucose (concentration of blood glucose 70 mg/dl). Culture was sterile. On the twelfth hospital day cerebrospinal fluid contained 70 WBC/ mm 3, 196 mg/dl of protein, and 32 mg/dl of glucose (concentration of blood glucose 71 mg/dl). No organisms were recovered on culture. Electroencephalogram revealed a normal sleeping record. Diffuse, heavy uptake of isotope over the left frontoparietal area, extending into the temporal area, was noted on brain scan. The subdural space was tapped on the thirteenth hospital day, yielding 8 ml of sterile, xanthochromic fluid with concentrations of protein of 3,632 mg/dl and glucose of 68 mg/dl. Cerebrospinal fluid on the thirtieth hospital day, prior to the discharge of the patient, contained 10 lymphocytes/mm3 with concentrations of 111 mg/dl and glucose 35 mg/dl (blood glucose of 73 mg/dl). Neurologic examination was negative four months after onset of the disease. Bacteriologic and immunologic observations. Microscopic examination of the spinal fluid obtained on admission revealed the presence of pleomorphic, gram-negative bacteria, resembling Haemophilus influenzae. The culture, after overnight incubation (at 37~ and under 5% CO2) had good growth on both blood and chocolate agar, thus rendering this diagnosis untenable. Identification of P. multocida was based on the following
The Journal of Pediatrics January 1975
findings: growth on nutrient agar but not on MacConkey agar; indol and acid production without gas from glucose and maltose; nitrate reduction; and positive catalase reaction. The diagnosis was confirmed by Dr. John Timoney, Cornell University, Ithaca, N. Y., and by the New York State Department of Health, Albany, N. Y. The strain was studied further by Dr. G. R. Carter, Michigan State University, East Lansing, Mich., who found that it was pathogenic for mice and yet did not produce a capsule. The latter feature made capsular typing impossible. The antibiogram indicated sensitivity of the strain to penicillin, ampicillin, cephalothin, tetracycline, and resistance to gentamicin and kanamycin. It was this latter finding that led to changes in chemotherapy. Study of the immune response of the pa[ient by means of the passive hemagglutination test failed to reveal the production of specific antibodies during the recovery period, an observation that was confirmed by Dr. Carter using the bacterial agglutination procedure. DISCUSSION Diagnosis and m a n a g e m e n t o f u n u s u a l i n f e c t i o n s present certain difficulties, in part, because of unfamiliarity with the disease by physicians and laboratorians alike, and, in part, because definitive information of optimal therapy often is not available. Among s u c h i n f e c t i o n s is P. multocida m e n i n g i t i s . In 1950, Zeller and Lepper 1 summarized the available information indicating that only eight cases had been reported between 1925 and 1944 and described two additional cases of their own. More recently, Controni and Jones 2 extended this review to 1964 and added four additional cases. Of the 14 cases only three were children and two of the three, infants. Both infants died. Since then, another fatal case of P. multocida meningitis, developing during the first week of life, was reported by Bates and associates) To the best of our knowledge, the present case represents the first observation of P. multocida meningitis in the newborn period followed by recovery. Difficulty in the diagnosis of P. multocida as cause of meningitis is due to the fact that, as observed in the present case, the microscopic finding of pleomorphic, gram-negative coccobacilli suggests the diagnosis of the far more frequently encountered H. influenzae. In all likelihood, recovery can be ascribed to ampicillin therapy. Needless to say, definitive information on optimal therapy cannot be obtained from observation of single cases. Meningitis represents but a minority of human infections caused by P. multocida, a m i c r o o r g a n i s m frequently found in animals, which serve as source o f h u m a n infection. It is now generally agreed that wound infections from P. multocida in man are quite common, particularly after contact with animals such as cats. 4"6 Many such cases, undoubtedly, remain unrecognized because appropriate bacteriologic examination is not
Volume 86 Number 1
B r i e f cfinical and laboratory observations
carried out. In all likelihood, the infection in the p r e s e n t case originated f r o m cats, a l t h o u g h bacteriologic p r o o f of this a s s u m p t i o n was not obtained. Since P. multocida was isolated from the throat o f the patient, it can b e a s s u m e d that the respiratory tract served as the portal o f e n t r y of the m i c r o o r g a n i s m leading to h e m a t o g e n o u s spread and meningitis. Finally, it is of interest to n o t e that P. multocida may cause meningitis in animals s u c h as the dog. 7 The authors wish to thank Dr. John Timoney, Cornell University, Ithaca, N. Y.; and Dr. G. R. Carter, Michigan State University, East Lansing, Mich., for their study of the P. multocida strain and of the antibody response of the patient.
93
2. Controni G, and Jones RS: Pasteurella meningitis. A review of the literature, Am J Med Technot 33:379, 1967. 3. Bates HA, Controni G, Elliot N, and Eitzman DV: Septicemia and meningitis in a newborn due to PasteureUa multocida, Clin Pediatr 4:668, 1965. 4. Holloway WJ, Scott EG, and Adams YB: Pasteurelta multocida infection in man. Report of 21 cases, Am J Clin Pathol 51:705, 1969. 5. Hubbert WT, and Rosen MN: II. Pasteurella multocida infection in man unrelated to animal bite, Am J Public Health 60:1109, 1970. 6. Tindall JP, and Harrison CM: Pasteurella multocida infections following animal injuries, especially cat bites, Arch Dermatol 105:412, 1972. 7. Rogers RJ, and Elder JK: Purulent leptomeningitis in a dog associated with an aerogenic Pasteurella multocida. Aust Vet J 43:81, 1967.
REFERENCES
1.
Zeller WW, and Lepper MH: Meningitis due to Pasteurella other than Pasteurella tularensis and Pasteurella pestis, Am J Med 9:701, 1950.
Pulmonary involvement in infectious mononucleos& Daniel R. Fermaglieh, M.D., Lieutenant Commander, MC, USN, Portsmouth, Va.
R E C E N T L Y , we o b s e r v e d a 3 1/2-year-old girl with t h e hematologic and serologic criteria o f infectious m o n o nucleosis; the m a i n clinical feature was viral p n e u m o nia complicated by a s u p e r i m p o s e d bacterial infection and bilateral pleural effusions. T h e p u l m o n a r y s y m p t o m s d o m i n a t e d the presentation and the entire clinical course. CASE REPORT
A 3 1/2-year-old Caucasian girl was Seen 14 days prior to admission with bronchitis and was treated with penicillin and glyceryl guaiacolate. She developed an immediate urticarial pruritic rash and penicillin therapy was discontinued. At 3 days prior to admission, a radiograph of the chest was interpreted as bilateral lower lobe interstitial pneumonia. Physical examination revealed a mild pharyngitis without From the Department o f Pediatrics, Portsmouth Naval Hospital. The views expressed herein are those of the author and do not necessarily reflect to views o f the U.S. Navy. Reprint address:Divisionof Endocrinology, Departmentof Medicine, Children'sHospital Medical Center, 300 Longwood Ave., Boston, Mass. 02115.
exudate, no lymphadenopathy, a palpable spleen tip, and swollen eyelids (Hoagland's sign). Laboratory data included a hemoglobin concentration of 10.8 gm/dl and white blood cell count of 20,750/mm 3, with 42% polymorphonuclear forms, 4% stabs, 4% monocytes, and 50% lymphocytes. Ninety-seven percent of the lymphocytes were "atypical," consistent with Downey cells. A "mono spot test" (repeated twice) was markedly positive. A culture of sputum yielded a few colonies of alpha streptococci, gamma hemolytic streptococci, and Neisseria catarrhalis. I
Abbreviation used EBV: Epstein,Barr virus
The patient was treated with erythromycin, 200 mg four times a day, but the clinical course continued unchanged until the day of admission, when she developed moderate respiratory distress. At this time, physical examination revealed a pale girl with a respiratory rate of 64/min, heart rate 144/min, and temperature of 103.8 ~ F. There were intercostal retractions and inspiratory rhonchi and rales were heard over all lung fields. A tracheal aspirate on admission yielded a few colonies of Diploeoccus pneumoniae and Neisseria catarrhal& Two subsequent tracheal aspirates yielded heavy growths of Haemophilus influenzae. The interstitial pneumonia progressed radiographically with the appearance of small bilateral pleural effusions four days after admission (Figs. 1 and 2). On admission the white blood cell count was 15,200 mm 3, with 3~% lymphocytes. Thirty percent of these were "atypical" compatible with Downey cells. A third "mono spot test" was markedly positive. Acutely, the differential heterophile antibody titer was 1:14 and 19 days later increased to t:224. Anti-