Scandinavian Journal of Infectious Diseases
ISSN: 0036-5548 (Print) 1651-1980 (Online) Journal homepage: http://www.tandfonline.com/loi/infd19
Meningitis and Bacteremia Caused by Pasteurella Ureae: Report of a Case following Intracranial Surgery Frank Bia, Robert Marier, F. Collins William Jr & Alexander Von Graevenitz To cite this article: Frank Bia, Robert Marier, F. Collins William Jr & Alexander Von Graevenitz (1978) Meningitis and Bacteremia Caused by Pasteurella Ureae: Report of a Case following Intracranial Surgery, Scandinavian Journal of Infectious Diseases, 10:3, 251-253, DOI: 10.3109/ inf.1978.10.issue-3.18 To link to this article: http://dx.doi.org/10.3109/inf.1978.10.issue-3.18
Published online: 02 Jan 2015.
Submit your article to this journal
View related articles
Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=infd19 Download by: [University of California, San Diego]
Date: 04 April 2016, At: 08:31
Scand J Infect Dis 10: 251-253, 1978
Case Report
.
Meningitis and Bacteremia Caused by Pasteurella ureae Report of a Case Following lntracranial Surgery FRANK BIA,’ ROBERT MARIER,’ WILLIAM F. COLLINS JRZ and ALEXANDER VON GRAEVENITZ3
Downloaded by [University of California, San Diego] at 08:31 04 April 2016
From the ‘Infectious Disease Section, Department of Internal Medicine, the =Departmentof Neurosurgery and the 3Department of Laboratory Medicine, Yale University School of Medicine and the Yale-New Haven Hospital, New Haven, Connecticut, USA
ABSTRACT. An otherwise healthy 53-year-old woman underwent intracranial surgery for trigeminal neuralgia. One week later she developed meningitis and bacteremia caused by Pasteurella ureae and was treated successfully with antimicrobials. This organism is known to colonize the respiratory tract in certain individuals and is an extremely rare cause of meningitis or bacteremia. This is the first reported case of bacteremia in an adult.
INTRODUCTION
CASE REPORT
Pasteurella ureae was first described in 1960 as a variant of P. haemolytica (9,but is now accepted as a separate species (10). The organism has been isolated from sputa of patients with pneumonia (9), chronic bronchitis and bronchiectasis (7, 8), and from the respiratory tract of healthy individuals (7). It has also been isolated from patients with rhinitis and sinusitis, in the latter case in pure culture (6,8). An animal host is not known. Meningitis due to P. ureae has been reported twice (11, 12). In one patient, an alcoholic, it followed a cranial fracture; antibiotic treatment with parenteral penicillin, chloramphenicol, and sulfadiazine for 3 weeks was successful (12). In the other patient, whose only preexisting condition was a “slight cold”, the infection was fatal in spite of antimicrobial therapy (1 1). In neither patient were blood culture results reported. There is one report of frank septicemia extant in the literature (4). The patient, a 24-year-old “dystrophic and anemic” child from Kinshasa, died. The identity of another isolate from a patient with endocarditis is not quite clear (3). Of the few reactions reported, only the negative indole and xylose tests would favor P. ureae, whereas the results of lactose (positive) and mannitol (negative) fermentation tests would favor P. haemolytica. We report here a case of meningitis and bacteremia due to P. ureae following a neurosurgical procedure.
A 53-year-old Cuban woman was admitted to Yale-New Haven Hospital in September 1976 with a chief complaint of left facial pain present for 18 months. The patient, a widow, entered the US in 1968. She smoked a pack of cigarettes per day for over 30 years, denied a history of either chronic bronchitis or sinusitis, and kept a dog at home. In March 1975, she developed left facial pain diagnosed as trigeminal neuralgia. Increasing pain and failure to respond to increasing dosages of diphenylhydantoin or carbamazepine lead to further evaluation in June 1976. No dental pathology was demonstrated. Skull films, sinus films, brain scan and computerized tomographic brain study were normal. Lumbar puncture (LP) was not performed. In August 1976, an unsuccessful attempt at percutaneous alcohol nerve block of the maxillary division of the 5th cranial nerve was made. This prompted the current admission for neurosurgical decompression of that nerve. On admission, vital signs were normal. The body weight was 64 kg. She was alert and oriented without meningismus. Hyperalgesia to pin prick was present on testing the 2nd and 3rd divisions of the left trigeminal nerve and an infraorbital “trigger zone” was present. Admission laboratory data were unremarkable. On September 9, 1976 a neurovascular decompression was performed via the left occipital bone and dura which involved opening the mastoid air cells. During the procedure a ring of venous structures was freed from the trigeminal nerve and a teflon pattie was left adjacent to it. The wound was closed with interrupted silk sutures. Postoperative course was unremarkable until September 16, when she developed nausea and vomiting, followed by fever to 39.4”C (103’F) and a leukocytosis of 17000 cellslpl, with a leftward shift. Chest film showed no infiltrates. L P was performed and the patient was immediately given 2 g of intravenous oxacillin. Subsequently, blood cultures were drawn. Both Gram stain of spinal fluid (CSF, described below) and results of Scnnd J Infecr Dis 10
252
F . Bin et al.
Table I . Lumbar puncture and spinalfluid analysis sl. xan.=slight xanthochromia
Date, Sept.
Downloaded by [University of California, San Diego] at 08:31 04 April 2016
18a.m. Appearance Opening pressure (mmH,O) Closing pressure (mmH,O) Protein (mg/dl) Glucose (mg/dl) Red cells per p1 Nucleated cells per pl Lymphocytes, % Granulocytes, % Monocytes, % Other, % Spinal fluid culture
18p.m.
Turbid 4049 77 84 78 < 10 94 210 3 675 2 700 6 3 92 96 2 1
+
20
32
sl. xan. 172 I30 50 36 ..
21 497 23 75 1 1
-
22
-
0 200 59 36 5
-
24
26
30
sl. xan. 64 34 I 101
90 7 2 2
50 33 13 Ill 85 3 12
54 41 6 94 95 I 4
LP were reviewed by one of us (F. B.). Results of LPs (Table I) demonstrate initial polymorphonuclear leukocyte response, depressed CSF glucose concentration and mild protein elevation gradually resolving under therapy. Therapy consisted of the following: oxacillin was discontinued and intravenous chloramphenicol (1 g every 4 h), plus gentamicin (70 mg i.v. every 8 h) were administered for 3 days, with intrathecal gentamicin (4 mg daily) for 2 days. Intravenous ampicillin (2 g every 4 h) was begun on September 20, but when the identity and sensitivities of the isolate were known on September 21, a 12-day course of intravenous aqueous penicillin G, 12 million units per day, was administered until October 2. Her course was one of rapid clinical improvement, evident within 24 h after starting therapy. Six months later, residual air conduction deficit in the left ear and slightly unsteady gait were slowly improving. Nasal and pharyngeal cultures were repeated at that time.
(strongly positive), nitrate reduction, and oxidase. Negative reactions were recorded for motility, fermentation of lactose and xylose, formation of indole; the methyl red and Voges Proskauer reactions, citrate utilization, gelatin liquefaction, phenylalanine deaminase, esculin hydrolysis, lysine and ornithine decarboxylase, arginine dihydrolase, beta-galactosidase, catalase, deoxyribonuclease, hydrogen sulfide production (TSI), and growth at 42°C and on SS agar. In the Kirby-Bauer sensitivity test, the strain was sensitive to ampicillin, carbenicillin, cephalothin, chloramphenicol, colymycin, nitrofurantoin, gentamicin, kanamycin, tobramycin, tetracycline, and penicillin. It was intermediately sensitive to oxacillin and resistant to vancomycin. These typical characteristics led to the diagnosis of P. ureae. Catalasenegative strains of this species have been described before ( 13).
Bacteriology A Gram stain of the CSF sediment showed small gram-negative rods, cocci and coccobacillary forms. They grew overnight on sheep blood agar but not on MacConkey Agar (Baltimore Biological Laboratories, Cockeysville, Md). Colonies on blood agar were about 1 mm in diameter, circular, low convex and translucent after 24 h of growth at 37°C. There was greening beneath them. The blood cultures became turbid 4 days after inoculation and grew the same organism both in Trypticase Soy Broth (Baltimore Biological Laboratories) and Thioglycollate Medium without Indicator 135-C (Baltimore Biological Laboratories), both supplemented with 0.03 % sodium polyanethol sulfonate (Analabs, North Haven, Connecticut). Subcultures after 24 h growth had been negative. Microscopically, small gram-negative rods were seen on smears from blood agar colonies and from blood culture media. There were a few elongated forms as well. Positive reactions were obtained for: acid formation on the slant and in the butt of Triple Sugar Iron Agar (TSI, Baltimore Biological Laboratories), fermentation of glucose (without gas), sucrose, maltose, and mannitol; urease
DISCUSSION The occurrence of meningitis caused by members of the genus Pasteurella is well documented (1, 2, 14). Two cases due to P. ureae have also been described (1 1, 12). We describe a case of meningitis due to P. ureae after a neurosurgical procedure resulting in bacteremia in a previously healthy adult. Judging from the earlier literature, a colonized respiratory tract in either the patient or the members of the operating team could have served as a source of the organism. However, our patient’s nasal and ear canal cultures at the time of bacteremia were negative for P. ureae as were nasal and pharyngeal cultures 6 months later. The operating team was not cultured. Fever, vomiting, meningismus and leukocytosis were evident during the episode of bacteremia and appeared to be clearing within 24 h of beginning
Downloaded by [University of California, San Diego] at 08:31 04 April 2016
Pasteurella meningitis
appropriate antibiotic therapy. The positive blood cultures were, however, obtained within 30 min of an intravenous dose of oxacillin, to which the organism was only intermediately, sensitive. Intitial therapy in this case was directed at treatment of meningitis caused by either gram-negative rods, gram-negative cocci or coccobacillary bacteria because of the variable appearance of the organism on the initial Gram stain of the CSF sediment. Intravenous chloramphenicol was chosen to cover Neisseria, Haemophilus, and Enterobacteriaceae species; intravenous and intrathecal gentamicin was added to cover Pseudomonas aeruginosa and Acinetobacter calcoaceticus var. anitratus (formerly Herellea vaginicola). Therapy was ultimately narrowed to intravenous penicillin when the organism was identified as P. ureae, sensitive to penicillin. P. ureae may be part of the colonizing flora in the upper or lower respiratory tract in patients with chronic bronchitis, bronchiectasis or sinusitis. As such it can be considered a potential cause of gram-negative meningitis or bacteremia under conditions permitting its spread. In this instance, the response to therapy appeared quickly and the patient suffered no permanent neurological sequelae attributable to this episode. ACKNOWLEDGEMENT The authors thank Ms Arline Strouse for her technical assistance in the preparation of this report.
REFERENCES 1. Controni, G. &Jones, R. S.: Pasteurella meningitis. A
2. 3. 4.
5.
6. 7.
review of the literature. Am J Med Techno1 33: 379, 1967. Cooper, A., Martin, R. & Tibbles, J. A. R.: Pasteurella meningitis. Neurology (Minneap) 23: 1097, 1973. Doty, G. L., Loomus, G. N. & Wolf, P. L.: Pasteurella endocarditis. N Engl J Med 268: 830, 1968. Gatti, F., Seynhaeve, V. & Weaver, R.: Premitre description d’un cas de s e p t i c h i e humaine due 9 Pasteurella ureae. Ann SOCBelg Med Trop 48: 463, 1963. Henriksen, S. D. & Jyssum, K.: A new variety of Pasteurella haemolytica from the human respiratory tract. Acta Pathol Microbiol Scand 50: 443, 1960. -A study of some Pasteurella strains from the human respiratory tract. Acta Pathol Microbiol Scand 51: 354, 1961. Jones, D. M. & O’Connor, P. M.: Pasteurella haemolytica var. ureae from human sputum. J Clin Pathol 15: 247, 1962.
253
8. Omland, T. & Henriksen, S. D.: Two new strains of Pasteurella haemolytica var. ureae isolated from the respiratory tract. Acta Pathol Microbiol Scand 53: 117, 1961. 9. Starkebaum, G. A. & Plorde, J. J.: Pasteurella pneumonia: Report of a case and review of the literature. J Clin Microbiol5: 332, 1977. 10. Smith, J. E.: Pasteurella. In: Bergey’s manual of determinative bacteriology, 8th ed., p. 373. Williams and Wilkins Co., Baltimore 1974. 11. Thibault, P., Robin, L. A., Magard, H. & Second, L.: MCningite foudroyante 9 Pasteurella haemolytica var. ureae. Presse Med 75: 345, 1967. 2. Wang, W. L. L. & Haiby, G.: Meningitis caused by Pasteurella ureae. Am J Clin Pathol45: 562, 1966. 3. Weaver, R. E., Tatum, H. W. & Hollis, D. G.: The identification of unusual pathogenic gram negative bacteria. Center for Disease Control, Atlanta 1972. 4. Zeller, W. W. & Lepper, M. H.: Meningitis due to Pasteurella other than Pasteurella tularensis and Pasteurella pestis. Am J Med 15: 701, 1950. Address for reprints: F. Bia, M.D., Infectious Disease Section, Yale University School of Medicine, LCI-208,333 Cedar Street, New Haven, Conn., 06510, USA
ISSN: 0036-5548 (Print) 1651-1980 (Online) Journal homepage: http://www.tandfonline.com/loi/infd19
Meningitis and Bacteremia Caused by Pasteurella Ureae: Report of a Case following Intracranial Surgery Frank Bia, Robert Marier, F. Collins William Jr & Alexander Von Graevenitz To cite this article: Frank Bia, Robert Marier, F. Collins William Jr & Alexander Von Graevenitz (1978) Meningitis and Bacteremia Caused by Pasteurella Ureae: Report of a Case following Intracranial Surgery, Scandinavian Journal of Infectious Diseases, 10:3, 251-253, DOI: 10.3109/ inf.1978.10.issue-3.18 To link to this article: http://dx.doi.org/10.3109/inf.1978.10.issue-3.18
Published online: 02 Jan 2015.
Submit your article to this journal
View related articles
Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=infd19 Download by: [University of California, San Diego]
Date: 04 April 2016, At: 08:31
Scand J Infect Dis 10: 251-253, 1978
Case Report
.
Meningitis and Bacteremia Caused by Pasteurella ureae Report of a Case Following lntracranial Surgery FRANK BIA,’ ROBERT MARIER,’ WILLIAM F. COLLINS JRZ and ALEXANDER VON GRAEVENITZ3
Downloaded by [University of California, San Diego] at 08:31 04 April 2016
From the ‘Infectious Disease Section, Department of Internal Medicine, the =Departmentof Neurosurgery and the 3Department of Laboratory Medicine, Yale University School of Medicine and the Yale-New Haven Hospital, New Haven, Connecticut, USA
ABSTRACT. An otherwise healthy 53-year-old woman underwent intracranial surgery for trigeminal neuralgia. One week later she developed meningitis and bacteremia caused by Pasteurella ureae and was treated successfully with antimicrobials. This organism is known to colonize the respiratory tract in certain individuals and is an extremely rare cause of meningitis or bacteremia. This is the first reported case of bacteremia in an adult.
INTRODUCTION
CASE REPORT
Pasteurella ureae was first described in 1960 as a variant of P. haemolytica (9,but is now accepted as a separate species (10). The organism has been isolated from sputa of patients with pneumonia (9), chronic bronchitis and bronchiectasis (7, 8), and from the respiratory tract of healthy individuals (7). It has also been isolated from patients with rhinitis and sinusitis, in the latter case in pure culture (6,8). An animal host is not known. Meningitis due to P. ureae has been reported twice (11, 12). In one patient, an alcoholic, it followed a cranial fracture; antibiotic treatment with parenteral penicillin, chloramphenicol, and sulfadiazine for 3 weeks was successful (12). In the other patient, whose only preexisting condition was a “slight cold”, the infection was fatal in spite of antimicrobial therapy (1 1). In neither patient were blood culture results reported. There is one report of frank septicemia extant in the literature (4). The patient, a 24-year-old “dystrophic and anemic” child from Kinshasa, died. The identity of another isolate from a patient with endocarditis is not quite clear (3). Of the few reactions reported, only the negative indole and xylose tests would favor P. ureae, whereas the results of lactose (positive) and mannitol (negative) fermentation tests would favor P. haemolytica. We report here a case of meningitis and bacteremia due to P. ureae following a neurosurgical procedure.
A 53-year-old Cuban woman was admitted to Yale-New Haven Hospital in September 1976 with a chief complaint of left facial pain present for 18 months. The patient, a widow, entered the US in 1968. She smoked a pack of cigarettes per day for over 30 years, denied a history of either chronic bronchitis or sinusitis, and kept a dog at home. In March 1975, she developed left facial pain diagnosed as trigeminal neuralgia. Increasing pain and failure to respond to increasing dosages of diphenylhydantoin or carbamazepine lead to further evaluation in June 1976. No dental pathology was demonstrated. Skull films, sinus films, brain scan and computerized tomographic brain study were normal. Lumbar puncture (LP) was not performed. In August 1976, an unsuccessful attempt at percutaneous alcohol nerve block of the maxillary division of the 5th cranial nerve was made. This prompted the current admission for neurosurgical decompression of that nerve. On admission, vital signs were normal. The body weight was 64 kg. She was alert and oriented without meningismus. Hyperalgesia to pin prick was present on testing the 2nd and 3rd divisions of the left trigeminal nerve and an infraorbital “trigger zone” was present. Admission laboratory data were unremarkable. On September 9, 1976 a neurovascular decompression was performed via the left occipital bone and dura which involved opening the mastoid air cells. During the procedure a ring of venous structures was freed from the trigeminal nerve and a teflon pattie was left adjacent to it. The wound was closed with interrupted silk sutures. Postoperative course was unremarkable until September 16, when she developed nausea and vomiting, followed by fever to 39.4”C (103’F) and a leukocytosis of 17000 cellslpl, with a leftward shift. Chest film showed no infiltrates. L P was performed and the patient was immediately given 2 g of intravenous oxacillin. Subsequently, blood cultures were drawn. Both Gram stain of spinal fluid (CSF, described below) and results of Scnnd J Infecr Dis 10
252
F . Bin et al.
Table I . Lumbar puncture and spinalfluid analysis sl. xan.=slight xanthochromia
Date, Sept.
Downloaded by [University of California, San Diego] at 08:31 04 April 2016
18a.m. Appearance Opening pressure (mmH,O) Closing pressure (mmH,O) Protein (mg/dl) Glucose (mg/dl) Red cells per p1 Nucleated cells per pl Lymphocytes, % Granulocytes, % Monocytes, % Other, % Spinal fluid culture
18p.m.
Turbid 4049 77 84 78 < 10 94 210 3 675 2 700 6 3 92 96 2 1
+
20
32
sl. xan. 172 I30 50 36 ..
21 497 23 75 1 1
-
22
-
0 200 59 36 5
-
24
26
30
sl. xan. 64 34 I 101
90 7 2 2
50 33 13 Ill 85 3 12
54 41 6 94 95 I 4
LP were reviewed by one of us (F. B.). Results of LPs (Table I) demonstrate initial polymorphonuclear leukocyte response, depressed CSF glucose concentration and mild protein elevation gradually resolving under therapy. Therapy consisted of the following: oxacillin was discontinued and intravenous chloramphenicol (1 g every 4 h), plus gentamicin (70 mg i.v. every 8 h) were administered for 3 days, with intrathecal gentamicin (4 mg daily) for 2 days. Intravenous ampicillin (2 g every 4 h) was begun on September 20, but when the identity and sensitivities of the isolate were known on September 21, a 12-day course of intravenous aqueous penicillin G, 12 million units per day, was administered until October 2. Her course was one of rapid clinical improvement, evident within 24 h after starting therapy. Six months later, residual air conduction deficit in the left ear and slightly unsteady gait were slowly improving. Nasal and pharyngeal cultures were repeated at that time.
(strongly positive), nitrate reduction, and oxidase. Negative reactions were recorded for motility, fermentation of lactose and xylose, formation of indole; the methyl red and Voges Proskauer reactions, citrate utilization, gelatin liquefaction, phenylalanine deaminase, esculin hydrolysis, lysine and ornithine decarboxylase, arginine dihydrolase, beta-galactosidase, catalase, deoxyribonuclease, hydrogen sulfide production (TSI), and growth at 42°C and on SS agar. In the Kirby-Bauer sensitivity test, the strain was sensitive to ampicillin, carbenicillin, cephalothin, chloramphenicol, colymycin, nitrofurantoin, gentamicin, kanamycin, tobramycin, tetracycline, and penicillin. It was intermediately sensitive to oxacillin and resistant to vancomycin. These typical characteristics led to the diagnosis of P. ureae. Catalasenegative strains of this species have been described before ( 13).
Bacteriology A Gram stain of the CSF sediment showed small gram-negative rods, cocci and coccobacillary forms. They grew overnight on sheep blood agar but not on MacConkey Agar (Baltimore Biological Laboratories, Cockeysville, Md). Colonies on blood agar were about 1 mm in diameter, circular, low convex and translucent after 24 h of growth at 37°C. There was greening beneath them. The blood cultures became turbid 4 days after inoculation and grew the same organism both in Trypticase Soy Broth (Baltimore Biological Laboratories) and Thioglycollate Medium without Indicator 135-C (Baltimore Biological Laboratories), both supplemented with 0.03 % sodium polyanethol sulfonate (Analabs, North Haven, Connecticut). Subcultures after 24 h growth had been negative. Microscopically, small gram-negative rods were seen on smears from blood agar colonies and from blood culture media. There were a few elongated forms as well. Positive reactions were obtained for: acid formation on the slant and in the butt of Triple Sugar Iron Agar (TSI, Baltimore Biological Laboratories), fermentation of glucose (without gas), sucrose, maltose, and mannitol; urease
DISCUSSION The occurrence of meningitis caused by members of the genus Pasteurella is well documented (1, 2, 14). Two cases due to P. ureae have also been described (1 1, 12). We describe a case of meningitis due to P. ureae after a neurosurgical procedure resulting in bacteremia in a previously healthy adult. Judging from the earlier literature, a colonized respiratory tract in either the patient or the members of the operating team could have served as a source of the organism. However, our patient’s nasal and ear canal cultures at the time of bacteremia were negative for P. ureae as were nasal and pharyngeal cultures 6 months later. The operating team was not cultured. Fever, vomiting, meningismus and leukocytosis were evident during the episode of bacteremia and appeared to be clearing within 24 h of beginning
Downloaded by [University of California, San Diego] at 08:31 04 April 2016
Pasteurella meningitis
appropriate antibiotic therapy. The positive blood cultures were, however, obtained within 30 min of an intravenous dose of oxacillin, to which the organism was only intermediately, sensitive. Intitial therapy in this case was directed at treatment of meningitis caused by either gram-negative rods, gram-negative cocci or coccobacillary bacteria because of the variable appearance of the organism on the initial Gram stain of the CSF sediment. Intravenous chloramphenicol was chosen to cover Neisseria, Haemophilus, and Enterobacteriaceae species; intravenous and intrathecal gentamicin was added to cover Pseudomonas aeruginosa and Acinetobacter calcoaceticus var. anitratus (formerly Herellea vaginicola). Therapy was ultimately narrowed to intravenous penicillin when the organism was identified as P. ureae, sensitive to penicillin. P. ureae may be part of the colonizing flora in the upper or lower respiratory tract in patients with chronic bronchitis, bronchiectasis or sinusitis. As such it can be considered a potential cause of gram-negative meningitis or bacteremia under conditions permitting its spread. In this instance, the response to therapy appeared quickly and the patient suffered no permanent neurological sequelae attributable to this episode. ACKNOWLEDGEMENT The authors thank Ms Arline Strouse for her technical assistance in the preparation of this report.
REFERENCES 1. Controni, G. &Jones, R. S.: Pasteurella meningitis. A
2. 3. 4.
5.
6. 7.
review of the literature. Am J Med Techno1 33: 379, 1967. Cooper, A., Martin, R. & Tibbles, J. A. R.: Pasteurella meningitis. Neurology (Minneap) 23: 1097, 1973. Doty, G. L., Loomus, G. N. & Wolf, P. L.: Pasteurella endocarditis. N Engl J Med 268: 830, 1968. Gatti, F., Seynhaeve, V. & Weaver, R.: Premitre description d’un cas de s e p t i c h i e humaine due 9 Pasteurella ureae. Ann SOCBelg Med Trop 48: 463, 1963. Henriksen, S. D. & Jyssum, K.: A new variety of Pasteurella haemolytica from the human respiratory tract. Acta Pathol Microbiol Scand 50: 443, 1960. -A study of some Pasteurella strains from the human respiratory tract. Acta Pathol Microbiol Scand 51: 354, 1961. Jones, D. M. & O’Connor, P. M.: Pasteurella haemolytica var. ureae from human sputum. J Clin Pathol 15: 247, 1962.
253
8. Omland, T. & Henriksen, S. D.: Two new strains of Pasteurella haemolytica var. ureae isolated from the respiratory tract. Acta Pathol Microbiol Scand 53: 117, 1961. 9. Starkebaum, G. A. & Plorde, J. J.: Pasteurella pneumonia: Report of a case and review of the literature. J Clin Microbiol5: 332, 1977. 10. Smith, J. E.: Pasteurella. In: Bergey’s manual of determinative bacteriology, 8th ed., p. 373. Williams and Wilkins Co., Baltimore 1974. 11. Thibault, P., Robin, L. A., Magard, H. & Second, L.: MCningite foudroyante 9 Pasteurella haemolytica var. ureae. Presse Med 75: 345, 1967. 2. Wang, W. L. L. & Haiby, G.: Meningitis caused by Pasteurella ureae. Am J Clin Pathol45: 562, 1966. 3. Weaver, R. E., Tatum, H. W. & Hollis, D. G.: The identification of unusual pathogenic gram negative bacteria. Center for Disease Control, Atlanta 1972. 4. Zeller, W. W. & Lepper, M. H.: Meningitis due to Pasteurella other than Pasteurella tularensis and Pasteurella pestis. Am J Med 15: 701, 1950. Address for reprints: F. Bia, M.D., Infectious Disease Section, Yale University School of Medicine, LCI-208,333 Cedar Street, New Haven, Conn., 06510, USA
