Arizona hinshawii Infections New Cases, Antimicrobial Sensitivities, and Literature Review RUDOLPH H. JOHNSON, M.D.; LARRY I. LUTWICK, M.D.; GERALDINE A. HUNTLEY, B.S.; and KENNETH L. VOSTI, M.D.; Stanford, California

Although disease caused by Arizona hinshawii is known to resemble the spectrum of clinical syndromes seen with Salmonelia infections, little is known of their sensitivity to antimicrobials. We present three cases that are illustrative of Arizona sepsis, localized infection, or both; review the literature; and report sensitivities to 12 antimicrobials for 32 human and animal isolates of Arizona hinshawii from various geographic areas. With the exception of erythromycin and streptomycin, most strains were sensitive to many of the commonly used antibiotics. As with Salmonella infections, ampicillin or chloramphenicol appear to be the initial antimicrobial agents of choice for severe infections with A. hinshawii. Definitive antimicrobial therapy must be individualized on the basis of sensitivity testing and with regard to host factors.

DISEASE IN MAN caused by strains of the genus Arizona (1) is indistinguishable from the spectrum of syndromes seen with Salmonella infections (2, 3). Patients with Arizona infections may present with gastroenteritis (4-6), enteric fever (6), septicemia ( 7 ) , localized infection, or a combination of these (1, 6-13). The ingestion of contaminated dairy products and food handlers who carry Arizona in their feces have each been implicated in outbreaks (4, 6, 7 ) . Cases are also known (14) that lack an epidemiologic relation to ingestion of dairy products or contact with reptiles, which also may serve as a reservoir for infection. We recently saw three patients with Arizona hinshawii infections. The infrequency of such cases and the scarcity of published information on antimicrobial sensitivity patterns of strains of A. hinshawii isolated from animal and human sources stimulated the present study. Three case reports, sensitivity to 12 antimicrobial agents of 32 strains of A. hinshawii obtained from various sources, and a review of the literature form the basis of this report. Case Reports CASE 1

A 29-year-old Mexican-American man with Hodgkin's • From the Stanford University Medical Center, Stanford, California; and the Enteric Section, Center for Disease Control, Public Health Service, U.S. Department of Health, Education, and Welfare, Atlanta, Georgia. Annals of Internal Medicine 85:587-592, 1976

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disease visited Mexico and consumed unpasteurized milk on several occasions. On 2 May 1975, he was admitted to the hospital in a cachectic state. Physical findings were unremarkable except for a temperature of 40.1 °C and an enlarged, tender liver. Culture of specimens of urine, stool, and blood obtained at admission grew A. hinshawii. A liver scan showed hepatomegaly without focal defects. Liver disease was later clinically attributed to Hodgkin's disease. Chest X rays remained normal. Initial antimicrobial therapy consisted of cefazolin and gentamicin; however, the patient continued to have positive blood cultures and fever. Subsequently the therapy was changed to ampicillin. Serum bactericidal levels were 1:4 on cefazolin and gentamicin, and 1:64 on ampicillin. Minimal inhibitory concentrations and minimal bactericidal concentrations (MIC/MBC) of the blood isolate of A. hinshawii were as follows: cephalothin, 3.13/25; gentamicin, 0.78/6.25; chloramphenicol, 3.13/50; and ampicillin, 0.78/0.78jtig per ml. He received intravenous (i.v.) ampicillin for 4 weeks and became afebrile during treatment. Post-treatment cultures of blood and stools were negative. He subsequently was readmitted for evaluation of fever, chills, weight loss, and malaise but became afebrile without specific therapy. He was readmitted later in clinical shock. Blood cultures subsequently grew out A. hinshawii, sensitive to ampicillin. He received i.v. ampicillin for 10 days and became afebrile, with negative blood cultures. He was discharged on oral amoxicillin. However, he was admitted again for evaluation of shaking chills, fever, thrombocytopenia, and lethargy. Subsequently, he developed profound leukopenia and died. Postmortem examination was refused. Multiple blood and urine cultures were sterile during this final hospitalization. Comments: This patients' case with a complex debilitating underlying disease, represents either reinfection or failure of adequate serum bactericidal levels of ampicillin to eradicate Arizona, with subsequent relapse from an undefined focus. CASE 2

A 54-year-old white man received a cardiac transplant and was placed on immunosuppressive therapy. He was subsequently admitted for intermittent fever and weakness with 10 days' history of abdominal tenderness and diarrhea. Previously, stool cultures grew only normal flora. The patient was cushingoid and tachypneic with right posterior basilar rales, S3 and S4 gallops, diffuse abdominal tenderness, and prominent pedal edema. Chest X ray showed cardiomegaly and prominent vascular markings in the upper lung fields. The leukocyte count was 5700/mm3 (67% polymorphonuclear leukocyte and 7% bands). An endomyocardial biopsy showed acute rejection. The patient improved with immunosuppressive medications, but fever up to 38.5 °C recurred with associated dyspnea and cough. Chest X ray showed a new left retrocardiac density, 587

Figure 1 Cumulative percentages of 32 strains of Arizona hinshawii inhibited by 12 antibiotics (agar plate dilution method [17]). AMP = ampicillin, TOBRA — tobramycin, GENTA = gentamicin, CARB = carbenicillin, KEF = cephalothin, PEN-G = penicillin G, TETRA = tetracycline, CHLORO = chloramphenicol, KANA = kanamycin, COL = colistin, SM = streptomycin, ERYTHRO = erythromycin.

an increasing infiltrate with air bronchograms at the left base, and spotty infiltrates in the right lower lobe. The leukocyte count was 2100/mm3. A transtracheal aspirate showed moderate numbers of polymorphonuclear leukocytes with Gram-positive cocci and Gram-negative rods. The transtracheal aspirate grew moderate numbers of Streptococcus pneumoniae and Candida albicans and small numbers of Escherichia coli and Enterobacter species. Propionibacterium acnes and Peptococcus species grew anaerobically. A stool culture subsequently grew normal flora plus moderate numbers of C. albicans and A. hinshawii; the latter was sensitive to ampicillin, cephalothin, tetracycline, kanamycin, and gentamicin. A blood culture grew S. pneumoniae and A. hinshawii. The patient's condition deteriorated rapidly and he died. Autopsy showed bilateral necrotizing bacterial pneumonitis and cytomegalovirus inclusions in the lung, adrenal glands, and lymph nodes. Esophageal candidiasis and focal hemorrhages in the mucosa of the rest of the gastrointestinal tract were present. The A. hinshawii blood isolate was sensitive to ampicillin, carbenicillin, cephalothin, tetracycline, chloramphenicol, gentamicin, kanamycin, streptomycin, and colistin. Comments: This patient's case represents an immunosuppressed host who died of multiple infections, including pneumonia and bacteremia with S. pneumoniae, disseminated cytomegalovirus infection, and enteric infection and bacteremia with A. hinshawii.

count was 6700/mm3 (69% polymorphonuclear leukocytes and 12% bands). A Gram stain of sputum showed many polymorphonuclear leukocytes and Gram-positive cocci, and a few Gram-negative rods and cocci. Treatment with i.v. penicillin G. was started. Sputum culture grew many coagulase-positive Staphylococcus aureus, moderate Hemophilus species, and A. hinshawii. A stool culture also grew A. hinshawii. Because of continued fever and lack of clinical improvement, the patient's therapy was changed to i.v. cephalothin. Repeat chest X ray showed a small pleural effusion and the previously noted infiltrate. A diagnostic thoracentesis obtained straw-colored cloudy fluid that had a leukocyte count of 8900/mm3 (16% polymorphonuclear leukocytes and 84% mononuclears). Numerous blood cultures were sterile but the pleural effusion and a transtracheal aspirate both grew A. hinshawii. Treatment with i.v. ampicillin was begun, which resulted in prompt resolution of fever. Therapy was continued for 6 days. Stool and sputum cultures contained no A. hinshawii after therapy. She was subsequently lost to follow-up. Arizona hinshawii isolated from the pleural effusion and transtracheal aspirate were sensitive to ampicillin, tetracycline, chloramphenicol, cephalothin, gentamicin, carbenicillin, and kanamycin. Comment: Although A. hinshawii was cultured initially from the sputum, it was not thought to be involved in the pneumonic process until it was isolated from pleural fluid and a transtracheal aspirate.

CASE 3

A 54-year-old mentally retarded white woman was admitted because of pleuritic chest pain and a pulmonary infiltrate. She lived in a custodial facility and was said to have been a Salmonella stool carrier in the past. Physical examination showed a thin and agitated patient with a temperature of 38.3 °C. Rales were heard over the right anterior chest. Chest X ray showed a right middle-lobe infiltrate. The leukocyte 588

Materials and Methods ORGANISMS

Thirty-two strains of Arizona hinshawii obtained from human and animal sources were acquired during a 2-year period by the Enteric Section at the Center for Disease Control, Atlanta, Georgia, by referral from various geographic areas. They were characterized as A. hinshawii by the criteria of Edwards

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and Ewing (15), and were considered representative of all submitted human and animal isolates.

Table 1. Antimicrobial C)isc Sensitiviity Data* for 32 Arfzona hinshawii Strains

ANTIMICROBIAL SENSITIVITY TESTING

Number of Strains

Antibiotic

The Bauer-Kirby disc method (16) was used to measure zone sizes with various antimicrobials. All isolates were tested for minimum inhibitory concentration (MIC) by an agar plate dilution technique (17), using a Steers replicator (18). Selected strains were tested for MIC and the minimum bactericidal concentration (MBC) by the broth tube dilution method (17). DISC TEST

Microbial susceptibility test discs (BBL/Sensi-Disc) of colistin, nalidixic acid, sulfadiazine, gentamicin, streptomycin, kanamycin, tetracyline, chloramphenicol, penicillin G, ampicillin, cephalothin, and a combination disc containing trimethoprim and sulfamethoxazole were used. Zone sizes were interpreted as recommended by the manufacturer (Becton, Dickinson and Company; Cockeysville, Maryland).

Resistant

Intermediate

Sensitive

0 0 0 0 7 0 1 0 0 0

0 0 8 0 9 0 0 0 30 0

32 32 24 32 16 32 31 32 2 32

0 0

0 0

32 32

Colistin Nalidixic Acid Sulfadiazine Gentamicin Streptomycin Kanamycin Tetracycline Chloramphenicol Penicillin G Ampicillin Sulfamethoxazole and trimethoprim Cephalothin * Bauer-Kirby method (16).

AGAR PLATE DILUTION TEST

AGAR PLATE DILUTION SENSITIVITIES

Ampicillin, carbenicillin, penicillin G, cephalothin, chloramphenicol, erythromycin, tetracycline, streptomycin, kanamycin, gentamicin, tobramycin and colistin were tested. Staphylococcus aureus (derived from ATCC #25923) and E. coli (derived from ATCC #25922) with known MICs were used for quality controls. BROTH TUBE DILUTION TEST

Two human isolates (1727/75 and 1588/75) were tested with chloramphenicol, tetracycline, cephalothin, gentamicin, and tobramycin. Nine human isolates were tested with ampicillin.

Cumulative percentages of A. hinshawii inhibited by 12 antibiotics are shown in Figure 1. The organism was effectively inhibited by ampicillin, tobramycin, gentamicin, tetracycline, carbenicillin, cephalothin, chloramphenicol, and kanamycin. Some strains (19/32) were resistant to streptomycin (MIC > 20/Ag/ml), and all 32 strains were resistant to penicillin G (MCIs to both antibiotics > 20/Ag/ strain was resistant to tetracycline and another was resistant to penicillin G (MCIs to both antibiotics > 20/xg/ ml). BROTH TUBE DILUTION SENSITIVITIES

Results BAUER-KIRBY DISC SENSITIVITIES

Sensitivities for all 32 strains and each antibiotic are shown in Table 1. Seven strains were resistant to streptomycin and one strain was resistant to tetracycline. The remaining strains were sensitive or intermediate-sensitive.

The MICs and MBCs against chloramphenicol, tetracycline, cephalothin, gentamicin, and tobramycin are shown in Table 2 (upper panel). These antibiotics effectively inhibited the two strains of A. hinshawii tested. However, clinically achievable bactericidal activity against these two strains was not demonstrable except for genta-

Table 2. Minimal Inhibitory Concentration (MIC) and Minimal Bactericidal Concentration (MBC) for Nine Human Isolates of Arizona binshawii against Six Antibiotics Strain

Source

Antibiotic

MIC

1727/75

Male: immunosuppressed with septic arthritis (joint fluid)

1588/75

Male: colitis (stool)

1320/75 1349/75 969/75 137/75 3593/74 1835/75 2347/75

Female: fatalf Male: nausea, vomiting, diarrhea, abdominal painf Female: acute peritonitis, fever, diarrhea, pneumoniat Male: osteomyelitis and left-knee woundf Female: (blood) Male: (blood) Female: myeloid leukemia with snake bite (wound)

Chloramphenicol Tetracycline Cephalothin Gentamicin Tobramycin Ampicillin Chloramphenicol Tetracycline Cephalothin Gentamicin Tobramycin Ampicillin Ampicillin Ampicillin Ampicillin Ampicillin Ampicillin Ampicillin Ampicillin

3.13 1.56 1.56 100 >100 100 3.13 25 50 50 25 50 50 50 50 25

* Broth tube dilution method. t Exact site of culture unspecified. Johnson etal. • Arizona hinshawii Infections

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micin with strain 1588/75. The MICs and MBCs against ampicillin are also shown in Table 2 (lower panel). The nine human isolates were uniformly inhibited by ampicillin (MIC 0.78 to 1.56 /xg/ml); however, clinically achievable bactericidal activity (MBC 0.78/xg/ml) was shown only for strain 1727/75. The remaining eight strains had MBCs of 25 or 50/i.g/mL COMPARISON SENSITIVITY TESTS

The MICs obtained by agar plate dilution and by broth tube dilution methods for the Arizona strains and for the quality control strains of Staph, aureus and E. coli were comparable. For streptomycin and tetracycline, strains resistant or intermediate by disc were resistant by plate and tube dilution techniques. For penicillin G, strains that were intermediate or sensitive by disc were sensitive by the agar plate dilution method. With the other antibiotics, there was excellent correlation between disc, agar plate, and broth tube dilution methods for all the strains of A. hinshawii examined. Discussion

Arizona (15) is composed of a group of Enterobacteriaceae that resembles Salmonella serologically and biochemically. Like Salmonella, Arizona possesses H and O antigens and is H2S-positive. Arizona differs from Salmonella in that the former liquefies gelatin, ferments lactose (rapidly or delayed), usually ferments malonate,

and does not ferment tartrate or dulcitol. Members of genus Arizona are known to be pathogenic for snakes, turkeys, chickens, and man. Poultry diseases are spread by eggs and egg products (19), resulting in septicemia and diarrhea in birds. Sharma, Kaura, and Singh (20) emphasized that snakes and rats have a high Arizona carrier rate and are a potential reservoir for human infection. Iveson, Mackay-Scollay, and Bamford (21) stressed the importance of reptiles as a natural reservoir for Salmonella and Arizona strains in Australia. The true natural reservoir may actually be more extensive, as others (6, 22) report that strains of Arizona have been isolated from many other animal sources. Localized human infections with Arizona have been described in many sites (1, 6-13) and are believed to occur more frequently with Arizona than with Salmonella infections ( 6 ) . This may be due either to truly increased invasiveness of Arizona for man or to the possibility that many strains of Arizona may be overlooked in feces because pathogenic lactose-fermenters are frequently not recognized ( 1 , 5 , 6 ) . However, in diagnostic laboratories where all H2S-positive colonies are fully characterized Arizona should not be missed in feces ( 5 ) . Our case reports show severe disease with sepsis or localized infection with A. hinshawii. These and nine additional well-described, previously reported cases of infection with A. hinshawii are summarized in Table 3 (1, 5, 8-13).

Table 3. Summary of 12 Clearly Descxibed Infections Caused by Arizona hinshawi / Case 1

Age, Race, Sex

Underlying Disease

29 yrs, Hodgkin's Mexicandisease. American, male.

2

54 yrs, white male.

Cardiac transplant, January 1970.

3

54 yrs, white, female.

Mental retardation.

4

52 yrs, black, female.

SLE*., Diabetes mellitus

Reported Syndrome Enteric fever, May 1975. Septicemia, August 1975. Enteric fever.

Antimicrobial Therapy Cefazolin, gentamicin; ampicillin. Ampicillin.

Nafcillin, cephalothin, gentamicin, clindamycin, pentamidine. Localized infection: Penicillin G. right middle lobe > Cephalothin. pneumonia and Ampicillin. pleural effusion.

Localized infections: Cephaloridine, urinary tract. colistimethate. Arthritis left knee. Ampicillin, cephalothin.

Left tibial abscess. Chloramphenicol. Arthritis right knee. Chloramphenicol, ampicillin, cephaloridine. 590

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Outcome Infection cleared.

Comment

Reference

See text.

This report.

See text.

This report.

Infection cleared. Death.

Failed to respond. See text. Failed to respond. Fever promptly resolved; chest X ray showed some resolution. Patient lost to follow-up. All infection Infection developed cleared, normal while patient on range of motion prednisone 40 mg/day both knee joints; no X-ray evidence Serum bactericidal test on ampicillin: of osteomyelitis. 1:8, static; undiluted to 1:2, cidal. Blood cultures negative.

This report.

(1)

Table 2. (Continued) Case 5

Age, Race, Sex 21 yrs, white, male.

Underlying Disease None.

Reported Syndrome Gastroenteritis.

Antimicrobial Therapy Ampicillin.

Chloramphenicol.

6

87 yrs, white, male.

Possible diabetes mellitus.

Localized infection: 12-cm multiloculated hepatic abscess.

Penicillin, streptomycin.

7

63 yrs, white, female.

Localized infection: chronic osteomyelitis left femur with septic arthritis knee.

Tetracycline.

8

23 yrs, black, female.

S/P splenectomy for acute thrombocytopenic purpura, at age 52 SLE.*

Sickle cell trait.

Localized infection: Ampicillin. 1 left tibial abscess, February 1973. Cephalothin, cephalexin. Cephalothin, cephalexin. septic arthritis right knee and right elbow, December 1973.

9

10

2 yrs, black, male.

Letterer-Siwe disease.

Septicemia, multiple bone lesions.

Chloramphenicol, tetracycline.

2} yrs, black, female.

Sickle cell anemia.

Septicemia, multiple bone lesions.

Ampicillin, gentamicin.

Alcoholism.

Gastroenteritis, enteric fever, September 1973. Localized infection: spinal osteomyelitis, August 1974.

Ampicillin. Ampicillin and extensive surgical debridement.

Localized infection: otitis media.

Given but not specified.

11 52>yrs, black, male.

12

Ampicillin.

1 yrs, black, female.

Sickle cell anemia.

Outcome

Comment

Reference

Contact with dog "(5) with diarrhea 1 week before admission. Fever remitted; Arizona resistant to ampicillin, other symptoms sensitive to resolved. chloramphenicol. Died 4 days after No clinical or (8) admission. autopsy evidence to explain development of liver disease. Required extensive Multiple cultures of (8) curettage of bone; curetted material fever subsided grew Arizona after 3 weeks; while patient on final outcome not therapy. detailed. Continued febrile.

Initially resolved but recurred, requiring surgical drainage. Reappeared and drained through cutaneous sinus. Required surgical decompression, drainage and excision. Promptly became afebrile; full return elbow function; mild residual flexion deformity of knee persisted. Recovered.

Recovered with normal gait and full use of all extremities. Developed low-back pain 6 weeks after therapy. Ambulatory 8 months after therapy discontinued. Became afebrile on 33rd. hospital day.

Developed while patient on prednisone, 10 mg/day.

(9)

Developed while patient on prednisone, 60 mg/day, for exacerbation of SLE*. Author attributed etiologic role in Letterer-Siwe disease to Arizona. Pretreatment, stool, blood, bone aspirate grew Arizona. Spinal osteomyelitis developed 11 months after episode of gastroenteritis and enteric fever treated with ampicillin 8 g/day for 14 days. Patient developed right otitis while on therapy for left otitis. Had evidence of pulmonary consolidation.

(10)

(ID

(12)

(13)

* SLE = systemic lupus erythematosus.

Previously published results of antimicrobial sensitivities of A. hinshawii are limited to four reports. First, Guckian, Byers, and Perry (1) reported a single infecting strain

that was sensitive to ampicillin (MIC 0.78/xg/rnl), cephalothin (MIC 3.1/xg/ml), and cephaloridine (MIC 6.25/xg/ml); MICs for chloramphenicol, tetracycline, Johnson et al. • Arizona hinshawii Infections

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streptomycin, and kanamycin were 3.1, 3.1, 6.25, and 12.5 /xg/ml, respectively. Second, six patients were reported briefly by Murray and associates ( 1 4 ) . Three of the isolates were susceptible to cephalothin (MIC ^ = 1 0 /xg/ ml), ampicillin (MIC < 10 /xg/ml), tetracycline (MIC ^ 5 /xg/ml), kanamycin (MIC — 5 /xg/ml), chloramphenicol (MIC ^ 1 0 /xg/ml), and gentamicin (MIC ±=3 /xg/ml), but the other three were sensitive to gentamicin and resistant to cephalothin (MIC > 20 /xg/ml), ampicillin (MIC > 20 /xg/ml), tetracycline (MIC > 5 /xg/ml), and chloramphenicol (MIC > 20 /xg/ml). Third, the single strain described by Andrews (5) was sensitive to chloramphenicol, colistin, and streptomycin; resistant to ampicillin, cephalothin, kanamycin, neomycin, penicillin, and tetracycline. Fourth, Fisher (10) reported the single infecting strain to be sensitive to streptomycin, chloramphenicol, and tetracycline, but resistant to penicillin. However, the techniques used for sensitivity testing were not well described in any of these reports. Our results of testing by disc, agar plate dilution, and broth tube dilution techniques indicate that many of the commonly used antibiotics, except erythromycin and streptomycin, may be useful in the treatment of Arizona infections. However, only ampicillin appears bactericidal at a level that occasionally can be achieved in serum. Initial therapeutic failures in our Cases 1 and 3 before ampicillin was begun may possibly be related to failure to achieve satisfactory serum bactericidal levels of the other antibiotics. Published case reports (Table 3) and our data suggest that host factors (for example, site of infection, the nature of underlying disease, the adequacy of drainage of abscess material) and properties of individual antimicrobial agents (for example, antimicrobial penetration to the site of infection, bacteriostatic versus bactericidal activity) each may be important in determining the final outcome of infections with A. hinshawii. As with nontyphoid Salmonella infections (23), ampicillin would appear to represent the initial drug of choice for severe infections, based on our sensitivity testing and on the in-vivo effectiveness shown in published case reports (Table 3 ) . In the penicillin-allergic individual, chloramphenicol would be an appropriate initial alternative to ampicillin, based on its demonstrable in-vivo effectiveness in published case reports (Table 3 ) . Because these infections may occur in compromised patients who have multiple infecting organisms, therapy must be individualized on the basis of the organisms identified and the results of antimicrobial sensitivity testing. ACKNOWLEDGMENTS: The authors thank Ms. Isabelle Smith for secretarial assistance and Ms. Helen K. Okuda for technical assistance. Don J. Brenner, Ph.D., Chief, Enteric Section at the Center for Disease Control, Atlanta, thoughtfully reviewed the manuscript. Grant support: Dr. Johnson was supported by an Advanced Research Fellowship from the Bay Area Heart Research Committee, San Francisco, California. Dr. Lutwick was supported by a Research Fellowship from the National Institutes of Health (#5-F22-CA0168002). The use of trade names is for identification only and does not constitute endorsement by the Public Health Service or by the U.S.

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Department of Health, Education, and Welfare. Received 3 March 1976; revision accepted 9 July 1976. • Requests for reprints should be addressed to Rudolph H. Johnson, M.D.; Section of Infectious Diseases, Medical Service, Veterans Administration Hospital; 1030 Jefferson Avenue; Memphis, TN 38104. References 1. GUCKIAN JC, BYERS EH, PERRY JE: Arizona infection of man:

report of a case and review of the literature. Arch Intern Med 119:170-175, 1967 2. STUART BM, PULLEN RL: Typhoid: clinical analysis of three hundred and sixty cases. Arch Intern Med 78:629-661, 1946 3. BLACK PH, KUNZ LJ, SWARTZ MN: Salmonellosis—a review of

some unusual aspects. N Engl J Med 262:811-817, 864-870, 921-927, 1960 4. MURPHY WJ, MORRIS JF: TWO outbreaks of gastroenteritis ap-

parently caused by a paracolon of the Arizona group. J Infect Dis 86:255-259, 1950 5. ANDREWS MD: Arizona group gastroenteritis. J Okla State Med Assoc 63:421-425, 1970 6. EDWARDS PR, FIFE MA, RAMSEY CH: Studies on the Arizona

group of Enterobacteriaceae. Bacteriol Rev 23:155-174, 1959 7. EDWARDS PR, MCWHORTER AC, FIFE MA: The occurrence of

bacteria of the Arizona group in man. Can J Microbiol 2:281287, 1956 8. KRAG D, SHEAN DB: Serious human infections due to bacilli of the Arizona group. Calif Med 90(3) :230-233, 1959 9. SMILACK JD, GOLDBERG MA: Bone and joint infection with Arizona hinshawii: report of a case and a review of the literature. Am J Med Sci 270:503-507, 1975 10. FISHER RH: Multiple lesions of bone in Letterer-Siwe disease: report of a case with culture of paracolon Arizona bacilli from bone lesions and blood, followed by response to therapy. J Bone Joint Surg [Am] 35A:445-464, 1953 11. HRUBY MA, HONIG GR, LOLEKHA S, et al: Arizona hinshawii

osteomyelitis in sickle cell anemia. Am J Dis Child 125:867868, 1973 12. KEREN DF, RAWLINGS W, MURRAY HW, et al: Arizona hin-

shawii osteomyelitis with antecedent enteric fever and sepsis: case report with a review of the literature. Am J Med 60:577582,1976 13. BUTT E, MORRIS JF: Arizona paracolon recovered from middle ear discharge. J Infect Dis 91:283-284, 1952 14. MURRAY PR, WASHINGTON J A, RHODES KH, et al: The clinical

manifestations and antimicrobial susceptibilities of six Arizona hinshawii isolates (abstract no. 339). Presented at the Fifteenth Interscience Conference on Antimicrobial Agents and Chemotherapy, American Society for Microbiology, Washington, D.C., 1975 15. EDWARDS PR, EWING WH: The genus Arizona, in Identification of Enterobacteriaceae, 3rd ed. Minneapolis, Minnesota, Burgess Publishing Co., 1972, pp. 259-275 16. BAUER AW, KIRBY WMM, SHERRIS JC, et al: Antibiotic sus-

ceptibility testing by a standardized single disk method. Am J Clin Pathol 45:493-496, 1966 17. BAILEY WR, SCOTT EG: Determination of susceptibility of bacteria to antimicrobial agents, in Diagnostic Microbiology: A Textbook for the Isolation and Identification of Pathogenic Microorganisms, 4th ed. St. Louis, Missouri, C. V. Mosby Co., 1974, pp. 313-329 18. STEERS E, FOLTZ EL, GRAVES BS: An inocula replicating ap-

paratus for routine testing of bacterial susceptibility to antibiotics. Antibiot Chemother 9:307-311, 1959 19. KUMAR MC, NIVAS SC, BAHL AK, et al: Studies on natural

infection and egg transmission of Arizona hinshawii 7:1, 7,8 in turkeys. Avian Dis 18:416-426, 1974 20. SHARMA VK, KAURA YK, SINGH IP: Arizona infection in snakes,

rats, and man. Indian J Med Res 58:409-412, 1970 21. IVESON JB, MACKAY-SCOLLAY EM, BAMFORD V: Salmonella and

Arizona in reptiles and man in Western Australia. J Hyg (Camb) 67:135-145, 1969 22. EDWARDS PR, MCWHORTER AC, FIFE MA: The Arizona group

of Enterobacteriaceae in animals and man: occurrence and distribution. Bull WHO 14:511-528, 1956 23. ROBERTSON RP, WAHAB MFA,

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chloramphenicol and ampicillin in Salmonella enteric fever. N Engl J Med 278:171-176, 1968

Arizona hinshawii infections. New cases, antimicrobial sensitivities, and literature review.

Arizona hinshawii Infections New Cases, Antimicrobial Sensitivities, and Literature Review RUDOLPH H. JOHNSON, M.D.; LARRY I. LUTWICK, M.D.; GERALDINE...
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