Sl
ls
Refer to: Bracis R, Seibers K, Julien RM: Meningitis caused by group II J following a dog bite. West J Med 131:438440, Nov 1979
Meningitis Caused by Group /I J Following a Dog Bite RAYMOND BRACIS, MD KATHY SEIBERS, MT ROBERT M. JULIEN, MD, PhD Portland, Oregon THE INCIDENCE of dog bites has been increasing in recent years.' While Pasteurella multocida is a well-known pathogen in such incidents, other organisms are also present in canine oral flora but their pathogenicity has not been well established.2-4 One of these organisms was first isolated from a canine nasal swab in 1972.4 It has since received the Center for Disease Control (CDC) alphanumeric designation group II J. We have recently seen a patient in whom meningitis following multiple dog bites developed and CDC group ii J was cultured from the spinal fluid.
Report of a Case A five-year-old girl was admitted to hospital because of fever, lethargy and headache. The patient had been well until three days before admission when a malamute dog bit her on the head and neck, and she sustained several lacerations. The patient's wounds had been cleaned in a local emergency department and she was treated with penicillin, 250 mg given four times a day. The girl vomited the first three doses of penicillin, but no subsequent vomiting occurred. On the day before the patient entered hospital she had a fever of 38.90C (1020F), was lethargic, complained of frontal headache and stiffness of the neck, and stated that it hurt to open her mouth. On initial physical examination, the patient was From Emanuel Hospital, Portland (Dr. Bracis), and the University of Oregon Health Sciences Center, Portland, Oregon (Ms.
Seibers and Dr. Julien). Submitted, revised, April 19, 1979. Reprint requests to: Raymond Bracis, MD, Emanuel Hospital, Department of Internal Medicine and Infectious Diseases, 2801 N Gantenbein, Portland, OR 97227.
438
NOVEMBER 1979 * 131
* 6
lethargic and appeared acutely ill. Temperature was 39.0°C (102.2°F), pulse was 128 per minute, respirations were 28 per minute, and blood pressure was 104/62 mm of mercury. Examination of the head showed multiple superficial scalp wounds with surrounding erythema, while ears, nose and mouth showed no abnormalities. Examination of the neck showed decreased range of motion and increased stiffness. No clinically significant adenopathy was noted. Lungs, heart and abdomen were normal. The Kernig sign was positive. Laboratory studies at admission gave the following values: normal electrolytes, blood urea nitrogen and glucose as well as normal hemoglobin and hematocrit. Leukocytes numbered 19,700 per cu mm with 82 percent neutrophils, 3 percent bands, 8 percent lymphocytes and 7 percent monocytes. Platelet count was 400,000 per cu mm and erythrocyte sedimentation rate was 28 mm per hour. Spinal fluid showed 50 erythrocytes and 1,108 leukocytes (100 percent neutrophils) per cu mm; glucose was 65 and protein 58 mg per dl. The Gram stain showed no organisms. Initial therapy included administration of nafcillin, 200 mg, penicillin, 200,000 units, and chloramphenicol, 100 mg per kg of body weight per day. By the second hospital day the patient was afebrile. Skull x-ray studies showed no abnormalities. Gram stain of colonies cultured from cerebral spinal fluid (csF) at 24 hours showed small, Gram-negative, bipolar staining rods. Blood cultures were negative. Administration of penicillin was increased to 250,000 units per kg of body weight per day. The patient's status was unchanged on the third hospital day. Organisms cultured from CSF were tentatively identified as a Pasteurella species. Preliminary sensitivity testing showed that the organism was sensitive to penicillin; therefore, nafcillin and chloramphenicol therapy was discontinued. On the fourth day, physical examination showed a more active patient, with persistent headache and stiffness. An additional bacteriologic study determined that the organism was not a Pasteurella species. On the sixth day, the cul-
CASE REPORTS
ture was identified as CDC group II J. Clinically the patient was substantially improved. Repeat spinal tap was done on the eighth day, and these findings were noted: five erythrocytes and five leukocytes (20 percent neutrophils and 80 percent lymphocytes) per cu mm. Glucose was 51 and protein 13 mg per dl. On the 14th day, administration of penicillin was discontinued. Five months after discharge the patient was asymptomatic except for continuous drainage from a wound above the right ear. At exploration, a tract, 5 mm in diameter, was noted extending through the skull and exposing the dura. Computerized axial tomography (CAT) showed no evidence of a brain abscess.
Bacteriologic Studies After overnight incubation (35°C, and under 3 percent carbon dioxide) the organism grew well on blood and chocolate agar but not on MacConkey agar. The initial Gram stain showed a pleomorphic, bipolar staining, Gram-negative rod ranging in length from 2 to 4 j.. Because of these characteristics, and the fact that catalase, oxidase and indole tests were positive, Pasteurella multocida was initially thought to be the responsible organism. However, a positive urease test and the lack of acid production from glucose made identification of P. multocida less likely. The culture was then identified by the CDC classification of miscellaneous Gram-negative bacteria as group II J.5 Initial disk susceptibility tests were done on Mueller-Hinton agar, and while the organism grew poorly, it appeared to be susceptible to penicillin. Group II i did not grow well in trypticase soy broth, Mueller-Hinton broth, brain-heart infusion or Columbia broth. A broth composed of one part Levinthal's medium (Prepared Media Lab, Tualatin, Oregon) and one part brain-heart infusion broth provided adequate growth for the organism.6 Broth dilution susceptibility tests were done using that medium. The minimal inhibitory concentration (MIC) of penicillin was 0.016 units per ml and the minimal bactericidal concentration (MBC) was 0.031 units per ml. Chloramphenicol had a MIC of 0.2 Mg per ml and a MBC of 1.6 ,4g per ml.
Discussion Because of the rising incidence of dog bites, physicians should better acquaint themselves with canine flora, especially where it differs from that
of humans. Dogs have a variety of unnamed species in their mouths. While some laboratories may identify them as Pasteurella-like, many of these isolates may actually fall into the CDC'S alphanumeric classification. In a recent survey of the oral and nasal flora of canines, group ii i was found in 90 percent of the dogs tested. Other organisms found in more than 50 percent of the animals included: EF-4, Pastuerella multocida and Staphylococcus aureus.4 To date, less than 100 isolates of group II J have been reported to the CDC (Robert Weaver, personal communication). An organism classified as Unidentified Species No. 5 was found less frequently. Butler and co-workers have reported a series of 17 patients with bacteremia from an unidentified Gram-negative rod.7 Most had suffered dog bites before their illnesses and four of these patients also had meningitis. Almost all the patients had a significant underlying disease. This unidentified Gram-negative rod had the same characteristics as Unidentified Species No. 5, noted in the survey of canine flora done by Bailie and
colleagues.4 If group ii i is so common in canine mouth flora, one may ask why more infections have not already been seen with this organism. It is possible that the organism has been either identified by microbiology laboratories as a Pasteurella species or has been considered a contaminant. While group ii i grew well on blood and chocolate agar, it did not grow on media routinely used for KirbyBauer agar diffusion susceptibility. The fact that group ii i is exquisitely sensitive to penicillin may mean that other unrecognized cases may have been treated by serendipity. Group ii i may be less virulent than other organisms found in canine mouth flora or, perhaps, a compromised host is necessary for it to be pathogenic.
Summary Infections secondary to relatively unusual pathogens, and resulting from animal bites appear to be on the rise. Awareness of these organisms by both microbiology laboratories and clinicians may lead to their increased recognition and identification. REFERENCES 1. Animal Bites in the United States. CDC Veterinary Public and Health Notes (November). US Dept of Health, Education Welfare, Center for Disease Control, Atlanta, Georgia, 1975 multocida 2. Holloway WJ, Scott EG, Adams YB: Pasteurella infection in man, report of 21 cases. Am J Clin Pathol 51:705708, 1969
THE WESTERN JOURNAL OF MEDICINE
439
CASE REPORTS 3. Saphir DA, Carter GR: Gingival flora of the dog with special references to bacteria associated with bites. J Clin Microbiol 3: 344-349, 1976 4. Bailie WE, Stowe EC, Schmitt AM: Aerobic bacterial flora of oral and nasal fluids of canines with reference to bacteria associated with bites. J Clin Microbiol 7:221-223, 1978 5. Tatum HW, Ewing WH, Weaver RE: Miscellaneous Gramnegative bacteria, In Lennette EH, Spaulding EH, Truant JP (Eds): Manual of Clinical Microbiology, 2nd Ed. Washington, DC, American Society for Microbiology, 1974, pp 270-294 6. Gordon RC, Thompson TR, Stevens LI, et al: In Vitro susceptibility of Haemophilus influenza to eight antibiotics. Antimicrob Ag Chemother 6:114-115, 1974 7. Butler TB, Weaver RE, Venkata Ramani TK, et al: Unidentified Gram-negative rod infection. Ann Intern Med 86:1-5, 1977
Refer to: Skory L, Shearn MA: Psoriatic arthritis induced by varicella. West J Med 131:440-441, Nov 1979
Psoriatic Arthritis Induced by Varicella LINDA SKORY, MD MARTIN A. SHEARN, MD Oakland, California THERE HAS BEEN increasing evidence in recent years to implicate viruses as etiologic factors in the pathogenesis of arthritic disorders.' Such entities accompanying infection with mumps, rubella and hepatitis B are well recognized, but a variety of other viruses such as rubeola, smallpox and the arboviruses may also induce articular disease.2 The pattern of joint disease produced by viral infection varies. Often, both small and weight-bearing joints are affected symmetrically, as in rubella arthritis.2 At the University of California Medical Center in San Francisco, we recently saw a patient with psoriasis and no previous arthritis in whom psoriatic arthritis involving the distal interphalangeal (DIP) joints developed after a varicella infection. With resolution of the infection, the arthritis cleared completely and the psoriasis was consid-
erably improved. Report of a Case A 22-year-old woman had a three-year history of psoriasis, which had flared severely four months before the present episode. Joint disease had not previously been noted. Two weeks before admission to hospital, typical lesions of varicella deFrom the Departments of Medicine, Kaiser-Permanente Medical Center, Oakland, California and the University of California Medical Center, San Francisco. Submitted April 23, 1979. Reprint requests: Martin A. Shearn, MD, Director of Medical Education, Kaiser-Permanente Medical Center, 280 W. MacArthur Blvd., Oakland, CA 94611.
440
NOVEMBER 1979 * 131 * 5
veloped; the patient said she had not had chickenpox in childhood. A week before admission, she noted psoriatic lesions at the site of each vesicle. At the same time, she had throbbing pain in all the DIP joints, associated with intense redness and swelling. Physical findings were confined to the skin, which bore hundreds of guttate plaques, and to the hands. The nails showed onycholysis and Beau lines consistent with a previous episode of severe psoriasis. All DIP joints of the hands were tender, swollen and erythematous. Findings on analysis of urine, hemogram and erythrocyte sedimentation rate, liver enzyme, uric acid, VDRL, antinuclear antibody and rheumatoid factor studies were all within normal limits. HLA (histocompatibility antigen) typing was not done, and x-ray films of the hands showed no bony abnormalities. Indomethacin, administered in a dosage of 25 mg three times a day, provided symptomatic relief; after nine days, the psoriatic arthritis had cleared completely with resolution of the varicella. Arthritis had not recurred after 11 months, when a follow-up examination was done.
Comment Arthropathy is a frequent manifestation of many common viral infections. Arthritis accompanying varicella is rare; in the few cases reported, monoarticular, large joint involvement occurred coincident with the development of the skin lesions.34 In our patient, the anatomic location and temporal sequence differed. The arthritis occurred a week after viral infection, and articular involvement was confined to the DIP joints, which is typical of psoriatic arthritis. In psoriasis, the joints may be affected in a variety of clinical patterns that include oligoarthritis, symmetric polyarthritis, ankylosing spondylitis, arthritis mutilans and classic psoriatic arthritis with predominant or exclusive involvement of the DIP joints.5'6 The classic form of psoriatic arthritis developed in our patient. The DIP joints, which appear to be predisposed to arthritis in some psoriatic patients, were affected following varicella. Although the psoriatic arthritis and the varicella infection might have been independent events, the temporal relationship and rapid resolution of arthritis after clearing of varicella suggest that the virus was an
ls
Refer to: Bracis R, Seibers K, Julien RM: Meningitis caused by group II J following a dog bite. West J Med 131:438440, Nov 1979
Meningitis Caused by Group /I J Following a Dog Bite RAYMOND BRACIS, MD KATHY SEIBERS, MT ROBERT M. JULIEN, MD, PhD Portland, Oregon THE INCIDENCE of dog bites has been increasing in recent years.' While Pasteurella multocida is a well-known pathogen in such incidents, other organisms are also present in canine oral flora but their pathogenicity has not been well established.2-4 One of these organisms was first isolated from a canine nasal swab in 1972.4 It has since received the Center for Disease Control (CDC) alphanumeric designation group II J. We have recently seen a patient in whom meningitis following multiple dog bites developed and CDC group ii J was cultured from the spinal fluid.
Report of a Case A five-year-old girl was admitted to hospital because of fever, lethargy and headache. The patient had been well until three days before admission when a malamute dog bit her on the head and neck, and she sustained several lacerations. The patient's wounds had been cleaned in a local emergency department and she was treated with penicillin, 250 mg given four times a day. The girl vomited the first three doses of penicillin, but no subsequent vomiting occurred. On the day before the patient entered hospital she had a fever of 38.90C (1020F), was lethargic, complained of frontal headache and stiffness of the neck, and stated that it hurt to open her mouth. On initial physical examination, the patient was From Emanuel Hospital, Portland (Dr. Bracis), and the University of Oregon Health Sciences Center, Portland, Oregon (Ms.
Seibers and Dr. Julien). Submitted, revised, April 19, 1979. Reprint requests to: Raymond Bracis, MD, Emanuel Hospital, Department of Internal Medicine and Infectious Diseases, 2801 N Gantenbein, Portland, OR 97227.
438
NOVEMBER 1979 * 131
* 6
lethargic and appeared acutely ill. Temperature was 39.0°C (102.2°F), pulse was 128 per minute, respirations were 28 per minute, and blood pressure was 104/62 mm of mercury. Examination of the head showed multiple superficial scalp wounds with surrounding erythema, while ears, nose and mouth showed no abnormalities. Examination of the neck showed decreased range of motion and increased stiffness. No clinically significant adenopathy was noted. Lungs, heart and abdomen were normal. The Kernig sign was positive. Laboratory studies at admission gave the following values: normal electrolytes, blood urea nitrogen and glucose as well as normal hemoglobin and hematocrit. Leukocytes numbered 19,700 per cu mm with 82 percent neutrophils, 3 percent bands, 8 percent lymphocytes and 7 percent monocytes. Platelet count was 400,000 per cu mm and erythrocyte sedimentation rate was 28 mm per hour. Spinal fluid showed 50 erythrocytes and 1,108 leukocytes (100 percent neutrophils) per cu mm; glucose was 65 and protein 58 mg per dl. The Gram stain showed no organisms. Initial therapy included administration of nafcillin, 200 mg, penicillin, 200,000 units, and chloramphenicol, 100 mg per kg of body weight per day. By the second hospital day the patient was afebrile. Skull x-ray studies showed no abnormalities. Gram stain of colonies cultured from cerebral spinal fluid (csF) at 24 hours showed small, Gram-negative, bipolar staining rods. Blood cultures were negative. Administration of penicillin was increased to 250,000 units per kg of body weight per day. The patient's status was unchanged on the third hospital day. Organisms cultured from CSF were tentatively identified as a Pasteurella species. Preliminary sensitivity testing showed that the organism was sensitive to penicillin; therefore, nafcillin and chloramphenicol therapy was discontinued. On the fourth day, physical examination showed a more active patient, with persistent headache and stiffness. An additional bacteriologic study determined that the organism was not a Pasteurella species. On the sixth day, the cul-
CASE REPORTS
ture was identified as CDC group II J. Clinically the patient was substantially improved. Repeat spinal tap was done on the eighth day, and these findings were noted: five erythrocytes and five leukocytes (20 percent neutrophils and 80 percent lymphocytes) per cu mm. Glucose was 51 and protein 13 mg per dl. On the 14th day, administration of penicillin was discontinued. Five months after discharge the patient was asymptomatic except for continuous drainage from a wound above the right ear. At exploration, a tract, 5 mm in diameter, was noted extending through the skull and exposing the dura. Computerized axial tomography (CAT) showed no evidence of a brain abscess.
Bacteriologic Studies After overnight incubation (35°C, and under 3 percent carbon dioxide) the organism grew well on blood and chocolate agar but not on MacConkey agar. The initial Gram stain showed a pleomorphic, bipolar staining, Gram-negative rod ranging in length from 2 to 4 j.. Because of these characteristics, and the fact that catalase, oxidase and indole tests were positive, Pasteurella multocida was initially thought to be the responsible organism. However, a positive urease test and the lack of acid production from glucose made identification of P. multocida less likely. The culture was then identified by the CDC classification of miscellaneous Gram-negative bacteria as group II J.5 Initial disk susceptibility tests were done on Mueller-Hinton agar, and while the organism grew poorly, it appeared to be susceptible to penicillin. Group II i did not grow well in trypticase soy broth, Mueller-Hinton broth, brain-heart infusion or Columbia broth. A broth composed of one part Levinthal's medium (Prepared Media Lab, Tualatin, Oregon) and one part brain-heart infusion broth provided adequate growth for the organism.6 Broth dilution susceptibility tests were done using that medium. The minimal inhibitory concentration (MIC) of penicillin was 0.016 units per ml and the minimal bactericidal concentration (MBC) was 0.031 units per ml. Chloramphenicol had a MIC of 0.2 Mg per ml and a MBC of 1.6 ,4g per ml.
Discussion Because of the rising incidence of dog bites, physicians should better acquaint themselves with canine flora, especially where it differs from that
of humans. Dogs have a variety of unnamed species in their mouths. While some laboratories may identify them as Pasteurella-like, many of these isolates may actually fall into the CDC'S alphanumeric classification. In a recent survey of the oral and nasal flora of canines, group ii i was found in 90 percent of the dogs tested. Other organisms found in more than 50 percent of the animals included: EF-4, Pastuerella multocida and Staphylococcus aureus.4 To date, less than 100 isolates of group II J have been reported to the CDC (Robert Weaver, personal communication). An organism classified as Unidentified Species No. 5 was found less frequently. Butler and co-workers have reported a series of 17 patients with bacteremia from an unidentified Gram-negative rod.7 Most had suffered dog bites before their illnesses and four of these patients also had meningitis. Almost all the patients had a significant underlying disease. This unidentified Gram-negative rod had the same characteristics as Unidentified Species No. 5, noted in the survey of canine flora done by Bailie and
colleagues.4 If group ii i is so common in canine mouth flora, one may ask why more infections have not already been seen with this organism. It is possible that the organism has been either identified by microbiology laboratories as a Pasteurella species or has been considered a contaminant. While group ii i grew well on blood and chocolate agar, it did not grow on media routinely used for KirbyBauer agar diffusion susceptibility. The fact that group ii i is exquisitely sensitive to penicillin may mean that other unrecognized cases may have been treated by serendipity. Group ii i may be less virulent than other organisms found in canine mouth flora or, perhaps, a compromised host is necessary for it to be pathogenic.
Summary Infections secondary to relatively unusual pathogens, and resulting from animal bites appear to be on the rise. Awareness of these organisms by both microbiology laboratories and clinicians may lead to their increased recognition and identification. REFERENCES 1. Animal Bites in the United States. CDC Veterinary Public and Health Notes (November). US Dept of Health, Education Welfare, Center for Disease Control, Atlanta, Georgia, 1975 multocida 2. Holloway WJ, Scott EG, Adams YB: Pasteurella infection in man, report of 21 cases. Am J Clin Pathol 51:705708, 1969
THE WESTERN JOURNAL OF MEDICINE
439
CASE REPORTS 3. Saphir DA, Carter GR: Gingival flora of the dog with special references to bacteria associated with bites. J Clin Microbiol 3: 344-349, 1976 4. Bailie WE, Stowe EC, Schmitt AM: Aerobic bacterial flora of oral and nasal fluids of canines with reference to bacteria associated with bites. J Clin Microbiol 7:221-223, 1978 5. Tatum HW, Ewing WH, Weaver RE: Miscellaneous Gramnegative bacteria, In Lennette EH, Spaulding EH, Truant JP (Eds): Manual of Clinical Microbiology, 2nd Ed. Washington, DC, American Society for Microbiology, 1974, pp 270-294 6. Gordon RC, Thompson TR, Stevens LI, et al: In Vitro susceptibility of Haemophilus influenza to eight antibiotics. Antimicrob Ag Chemother 6:114-115, 1974 7. Butler TB, Weaver RE, Venkata Ramani TK, et al: Unidentified Gram-negative rod infection. Ann Intern Med 86:1-5, 1977
Refer to: Skory L, Shearn MA: Psoriatic arthritis induced by varicella. West J Med 131:440-441, Nov 1979
Psoriatic Arthritis Induced by Varicella LINDA SKORY, MD MARTIN A. SHEARN, MD Oakland, California THERE HAS BEEN increasing evidence in recent years to implicate viruses as etiologic factors in the pathogenesis of arthritic disorders.' Such entities accompanying infection with mumps, rubella and hepatitis B are well recognized, but a variety of other viruses such as rubeola, smallpox and the arboviruses may also induce articular disease.2 The pattern of joint disease produced by viral infection varies. Often, both small and weight-bearing joints are affected symmetrically, as in rubella arthritis.2 At the University of California Medical Center in San Francisco, we recently saw a patient with psoriasis and no previous arthritis in whom psoriatic arthritis involving the distal interphalangeal (DIP) joints developed after a varicella infection. With resolution of the infection, the arthritis cleared completely and the psoriasis was consid-
erably improved. Report of a Case A 22-year-old woman had a three-year history of psoriasis, which had flared severely four months before the present episode. Joint disease had not previously been noted. Two weeks before admission to hospital, typical lesions of varicella deFrom the Departments of Medicine, Kaiser-Permanente Medical Center, Oakland, California and the University of California Medical Center, San Francisco. Submitted April 23, 1979. Reprint requests: Martin A. Shearn, MD, Director of Medical Education, Kaiser-Permanente Medical Center, 280 W. MacArthur Blvd., Oakland, CA 94611.
440
NOVEMBER 1979 * 131 * 5
veloped; the patient said she had not had chickenpox in childhood. A week before admission, she noted psoriatic lesions at the site of each vesicle. At the same time, she had throbbing pain in all the DIP joints, associated with intense redness and swelling. Physical findings were confined to the skin, which bore hundreds of guttate plaques, and to the hands. The nails showed onycholysis and Beau lines consistent with a previous episode of severe psoriasis. All DIP joints of the hands were tender, swollen and erythematous. Findings on analysis of urine, hemogram and erythrocyte sedimentation rate, liver enzyme, uric acid, VDRL, antinuclear antibody and rheumatoid factor studies were all within normal limits. HLA (histocompatibility antigen) typing was not done, and x-ray films of the hands showed no bony abnormalities. Indomethacin, administered in a dosage of 25 mg three times a day, provided symptomatic relief; after nine days, the psoriatic arthritis had cleared completely with resolution of the varicella. Arthritis had not recurred after 11 months, when a follow-up examination was done.
Comment Arthropathy is a frequent manifestation of many common viral infections. Arthritis accompanying varicella is rare; in the few cases reported, monoarticular, large joint involvement occurred coincident with the development of the skin lesions.34 In our patient, the anatomic location and temporal sequence differed. The arthritis occurred a week after viral infection, and articular involvement was confined to the DIP joints, which is typical of psoriatic arthritis. In psoriasis, the joints may be affected in a variety of clinical patterns that include oligoarthritis, symmetric polyarthritis, ankylosing spondylitis, arthritis mutilans and classic psoriatic arthritis with predominant or exclusive involvement of the DIP joints.5'6 The classic form of psoriatic arthritis developed in our patient. The DIP joints, which appear to be predisposed to arthritis in some psoriatic patients, were affected following varicella. Although the psoriatic arthritis and the varicella infection might have been independent events, the temporal relationship and rapid resolution of arthritis after clearing of varicella suggest that the virus was an
