able hydridization assay uses a radioiodinated probe, which is not practical for use in the clinical laboratory (5). The colorimetric method, on the other hand, uses neutral red, which is both inexpensive and stable, and requires a spectrophotometer that is standard equipment in most laboratories. Nevertheless, the length of time required to isolate the virus, grow a stock, determine the titer and challenge dose, and then infect cells and perform the assay makes the current assays both cumbersome and slow. Unlike HSV, which is readily and rapidly propagated, CMV and VZV are slow to replicate, labile, and cell-associated, making laboratory manipulations more difficult. Antiviral assays for HIV have also been developed, but culture techniques are expensive, are not routinely performed outside of the research setting, and require biosafety level 3 practices. Thus HIV testing is likely to be confined to a few laboratories with expertise in retrovirus isolation. What does the future hold? Work is underway to minimize the development of resistance by more carefully defining the optimal dosing for both induction and maintenance therapy, and to design drug combination therapy for viruses similar to that used for bacteria and cancer. Nevertheless, the incidence of resistance to antiviral chemotherapy will most certainly increase. Clearly, more studies are needed to examine the correlation between in vitro and in vivo results if clinical decision making is to be predicated on laboratory testing. Tertiary care centers with large immunosup-
pressed populations and experienced viral diagnostic laboratories should be encouraged to screen isolates for antiviral drug resistance, starting with HSV. Collaboration between clinicians, the viral diagnostic laboratory, and a basic research laboratory is necessary to both establish and critically evaluate the methodology. Laying the proper groundwork now to standardize important variables and to establish the usefulness of antiviral susceptibility testing in patient management is essential before its widespread implementation can be recommended for the routine clinical laboratory.
8.
9.
10.
References 1. Barry, D. W. et al. 1985. Viral resistance, clinical experience. Scand. J. Infect. Dis. 47:155-164. 2. Belshe, R. B. et al. 1989. Resistance of influenza A virus to amantadine and rimantadine: Results of one decade of surveillance. J. Infect. Dis. 159:430435. 3. Chatis, P. A. et al. 1989. Successful treatment with foscarnet of an acyclovir-resistant mucocutaneous infection with herpes simplex virus in a patient with acquired immunodeficiency syndrome. N. Engl. J. Med. 320:297300. 4. Drew, W. L. and T. R. Matthews. 1989. Susceptibility testing of herpes virus. Clin. Lab. Med. 9:279-286. 5. Englund, J. A. et al. 1990. Herpes simplex virus resistant to acyclovir. A study in a tertiary care center. Am. Intern. Med. 112:416--422. 6. Erice, A. et al. 1989. Progressive disease due to ganciclovir-resistant cytomegalovirus in immunocompromised patients. N. Engl. J. Med. 320:289293. 7. Erlich, K. S. et al. 1989. Acyclovirresistant herpes simplex virus infec-
11.
12.
13.
14.
15.
16.
tions in patients with the acquired immunodeficiency syndrome. N. Engl. J. Med. 320:293-296. Honess, R. W. et al. 1984. Single mutations at many sites within the DNA polymerase locus of herpes simplex viruses can confer hypersensitivity to aphidicolin and resistance to phonsphonoacetic acid. J. Gen. Virol. 65:1-17. Jacobson, M. A. et al. 1990. Acyclovir-resistant varicella zoster virus infection after chronic oral acyclovir therapy in patients with the acquired immunodeficiency syndrome (AIDS). Ann. Intern. Med. 112:187-191. McLaren, C., M. N. Ellis, and G. A. Hunter, 1983. A colorimetric assay for the measurement of the sensitivity of herpes simplex viruses to antiviral agents. Antiviral Res. 3:223-224. Plotkin, S. A. et al. 1985. Sensitivity of clinical isolates of human cytomegalovirus to 9-(1,3-dihydroxy-2propoxymethyl) guanine. J. Infect. Dis. 152:833--834. Parris, D. S. and J. E. Harrington. 1982. Herpes simplex virus variants resistant to high concentrations of acyclovir exist in clinical isolates. Antimicrob. Agents Chemother. 22:71-7. Richman, D. D. 1990. Zidovudine resistance of human immunodeficiency virus. Rev. Infect. Dis. 12:$507-512. Sacks, S. L. et al. 1989. Progressive esophagitis from acyclovir-resistant herpes simplex. Clinical roles for DNA polymerase mutants and viral heterogeneity? Ann. Intern. Med. 111:893899. Straus, S. E. et al. 1984. Suppression of frequently recurring genital herpes: A placebo-controlled double-blind trial of oral acyclovir. N. Engl. J. Med. 310:1545-1550. Wahren, B. et al. 1983. A novel method for determining the sensitivity of herpes simplex virus to antiviral compounds. J. Virol. Meth. 6:141149.
Case Report
Listeria Brain Abscess Stanely S. Raphael, M.B., F.R.C.P.(C), F.R.C.Path. Shelley Sinclair, R.T.
Microbiology Hotel-Dieu of St. Joseph Hospital Windsor, Ontario, Canada This case is reported because it represents an unusual presentation of an uncommon infection and it illustrates a
Clinical Microbiology Newsletter 14:9,1992
differential diagnosis of an acute or subacute cerebral space-occupying lesion.
Case Report The patient was a 52-yr-old storeowner who had had a history of headaches with increasing malaise and lethargy for about 3 wk. Four wk before admission into the hospital, he had returned from a holiday in Mex-
© 1992 Elsevier Science Publishing Co., Inc.
ico. Increasing drowsiness and confusion brought him to the hospital. He recently had bright red blood in his stools (due to hemorrhoids) and had lost 25 lbs in the past year. His hemoglobin was 95 g/L. He had been healthy previously, apart from herpes zoster 2 yr before. Physical examination revealed some papilledema but no neck rigidity was noted. A C T scan showed a mass 4 cm in diameter sur-
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rounded by edema in the right frontal lobe. A diagnosis of cerebral tumor was made. Craniotomy was performed with excision of the mass, which on frozen section was found to be composed of acutely inflamed brain substance. A Gram-stained smear showed a few pus cells and occasional gram negative rods (in retrospect, probably dead Listeria organisms). Initial plating was made on sheep blood, chocolate, Mac Conkey, and CNA (colistin-nalidixic acid) blood agar media, as well as on Brucella agar and in pre-reduced cooked meat broth for anaerobic studies. Beta-hemolytic colonies consisting of grampositive rods were recovered on the sheep blood agar after 24 hr incubation at 35°C. The organism was identified as Listeria monocytogenes on the Vitek system using the Gram Positive Identification Card. Additional tests showed the typical tumbling motility, production of catalase, acid from rhamnose, negative H 2 S in TSI medium, and positive CAMP test with S. aureus. The organism was found to be moderately susceptible to ampicillin and penicillin, and susceptible to cotrimoxazole, tetracycline, amikacin, erythromycin, vancomycin, and chloramphenicol. It was resistant to methicillin and clindamycin. No blood or CSF cultures were taken at this time. A bone marrow examination showed
7% plasma cells with atypical forms and an IgM was elevated to 50 g/L (normal 0.6 to 2.5), while immunoelectrophoresis showed an IgM lambda monoclonal protein. He was treated initially with chloramphenicol, but after the culture results became available therapy was changed to penicillin. A diagnosis of plasma cell dyscrasia with relative immunodeficiency and Listeria brain abscess was made. Following surgical convalescence he was transferred to a tertiary care center for treatment of his plasma cell dyscrasia.
ria monocytogenes had been described until 1986 (5). Listeric infections are widespread in mammals and it would appear that sheep and cows are possibly responsible for the contamination of milk and its products as well as of vegetable foodstuffs. In ruminants as compared to humans, the more common type of central nervous system infection is encephalitis rather than meningitis, but in young animals before the rumen forms, septicemia occurs and encephalitis is not seen (6).
Discussion
References
Listeria infections occur in immuno-
compromised patients, in pregnant women and in neonates. Considerable interest has been aroused recently because of the relationship of such infections with food-borne vehicles. Cheese (1), coleslaw (2), and milk (3) have been cited in outbreaks of this disease. The presence of the bacteria in food may be more widespread than previously thought (4). In this case the source of infection is unknown and the case appears to be an isolated incident in an immunocompromised individual. The usual presentation of such infections in adults is as meningitis or septicemia; the incidence of brain abscess is much less. In the English-language literature only 14 cases of brain abscess due to Liste-
1. James, S. M., et al. 1985. Listeriosis outbreak associated with Mexican style cheese----California. MMWR. 34:357359. 2. Shlech, W. F., et al. 1983. Epidemic listeriosis--Evidence for transmission by food. New Engl. J. Med. 308:203206. 3. Flemming, D. W., et al. 1985. Pasteurized milk as a vehicle of infection in an outbreak of listeriosis. New Engl. J. Med. 312:404-407. 4. Kerr, K., S. F. Dealler, and R. W. Lacey. 1988. Listeria in cook-chilled food. Lancet. ii:37-38. 5. Dee, R. D., and B. Lorber. 1986. Brain abscess due to Listeria monocytogenes: Case report and literature review. Rev. Inf. Dis. 8:968-977. 6. Gray, M. L., and A. H. Killinger. 1966. Listeria monocytogenes and Listeric infections. Bacteriol. Rev. 30:309-382.
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Clinical Microbiology Newsletter 14:9,1992