Printer Friendly

Why did our reporting trends suddenly change? What a microbiology lab learned about resistance and about a jump in recovery of one pathogen had a major impact on antibiotic therapy.

Amarked increase in antibiotic resistance by several organisms and a surge in recovery of one pathogen posed microbiology puzzles at our 212-bed hospital. It was important to find out why these new trends had developed in order to help clinicians plan a better course of antibiotic therapy.

The matter of resistance surfaced two years ago. One of the functions of the microbiology department, in conjunction with the infection control committee, is to monitor susceptibility trends for the hospital. From January to June 1983, I noticed frequent significant departures from the normal susceptibility patterns for Proteus mirabilis and some Enterobacteriaceae--changes serious enough to warrant investigation and action.

Proteus mirabilis seemed the best choice to focus on in a study because we isolated it more often than the other organisms in question. I looked at its susceptibilities to four antibiotics--ampicillin, cephalothin, cefamandole, and cefoxitin--in January-June 1981, 1982, and 1983.

During the first two years, P. mirabilis susceptibilities were stable at 90 to 99 per cent. In the first half of 1983, they plunged to a range of 30 to 66 per cent. The precipitous decline raised two questions: Was this trend manifesting itself in other hospitals, or was it confined to our institution? What happened in 1982 at our hospital to cause the increased antibiotic resistance we were finding in 1983?

To answer the first question, I enlisted the aid of detail representatives from two pharmaceutical manufacturers. On their calls to other hospitals in southwest Florida, they solicited susceptibility data for P. mirabilis over the time frame of our study. Not all laboratories kept good records on clinical isolates, but the representatives nonetheless brought usable data from several large institutions.

A comparison of our experience with that of the other hospitals was alarming. No other hospital recorded a substantial change in Proteus susceptibilities in January-June 1983. Their percentages closely mirrored 1981 and 1982 averages. That meant the problem was internal.

The second question had to be addressed. What change might have occurred in 1982 to lead to greater antibiotic resistance the following year? We soon had an answer.

Examination of pharmacy reports revealed that at least 50 per cent of the antibiotic therapy administered in the hospital during 1982 involved use of the new expanded-spectrum cephalosporins. A literature search linked this evidence to the problem we were investigating. Although early studies of these antibiotics had been promising, one disturbing observation was a rapid development of bacterial resistance.

I presented the findings to our hospital's infection control committee in November 1983. The committee granted my request to study antibiotic therapy records of patients with multiple admissions and P. mirabilis infections.

First I listed all patients whose microbiology records showed P. mirabilis infections between March and December 1983. Then I went through medical records and eliminated all the patients who had only a single admission. For the rest, I could review therapy over the entire calendar year.

Twenty-four patients had more than one admission and a Proteus infection during their last admission. Only three had Proteus infections conforming to expected susceptibility patterns from the first to the final admission, and none had been treated with expanded-spectrum antibiotics.

The other 21 patients had resistant Proteus infections at last admission. Expanded-spectrum cephalosporins had been part of the drug regimen for 17. I found nothing that might have induced resistance in the remaining four patients.

All of the cases studied were enlightening--and some proved frightening. One patient was treated with a second-generation cephalosporin for ocular and urinary tract infections caused by a tetracycline-resistant P. mirabilis. Susceptibility testing showed no other resistance at the time. But when the patient was readmitted the next month with a urinary tract infection and septicemia caused by Proteus of the same biotype, the organism was resistant to ampicillin and the first-, second-, and third-generation cephalosporins tested.

Several other patients were admitted with Proteus urinary tract infections that responded to a second-generation cephalosporin. They were readmitted in less than a month with the same infections, however, and the pathogen was now resistant to ampicillin and first-, second-, and third-generation cephalosporins. In a number of cases, Proteus susceptibility patterns changed midway through second-generation cephalosporin therapy.

What about the four cases with unexplained resistance? Three patients had been admitted to other, distant hospitals before ours, and I had no access to antibiotic therapy records at those institutions.

The fourt patient had been admitted to our hospital three times. In each instance there had been a urinary tract infection. During the third admission, for fracture therapy, the patient had a series of infections, and resistant Proteus was the last of several pathogens identified--but expanded-spectrum antibiotics had not been previously used. Although I couldn't account for the low susceptibility in these cases, it's possible that some were nosocomial infections from already resistant Proteus.

Once infection control committee members saw the data, they asked me to make a presentation to the next meeting of the medical care evaluation committee, in February 1984. That committee agreed with infection control that clinicians should be told what was happening.

So in March, I took the data to the medical staff's general meeting. I stated the case succinctly: First, Proteus resistance at our hospital was increasing, and we had reason to implicate expanded-spectrum antibiotic use, which could confer cross-resistance to other drugs, particularly those of the same class. Second, physicians should study the change in resistance carefuly and then weigh potential advantages of these antibiotics against a new and serious problem. And third, what we uncovered might be occurring with other organisms.

The medical staff asked for more Proteus data--specifically from January to June 1984. Figure I shows the information I furnished them. There was a clear shift in minimum inhibitory concentrations from intermediate to resistant and from susceptible to intermediate between 1983 and the first six months of 1984.

That apparently convinced the medical staff. Prescriptions for third-generation cephalosporins dropped considerably in mid-1984, compared with a year earlier. This was also due to a program we instituted that educates clinicians on antibiotic costs, described in the October 1984 issue of MLO ("A Lab-Pharmacy Push to Cut Drug Therapy Costs"). Many physicians still prescribe second-generation cephalosporins, but some are returning to first-generation drugs.

In general, we must remember that pharmaceutical manufacturers' data reflect susceptibilities obtained largely through in vitro tests. In our area, which has a large retirement community, the median age of residents is 72. That means many multiple admissions for chronic or recurrent illness, and a good opportunity to study shifting in vivo susceptibilities in the same patients.

Uncovering a new resistance trend spells more effective therapy. It results in more cost-effective therapy, too, because over the long term, runaway resistance prompts development of costlier antibiotics. Since drugs in longstanding use are generally less expensive, therapy costs are held down when clinicians have good reason to keep using them.

We are currently looking at susceptibility patterns for other organisms. It's too early to be definitive, but signs point to decreasing susceptibility among other organisms, including some of the Enterobacteriaceae. We also want to see if reduced use of the expanded-spectrum antibiotics will curb the increase in resistant Proteus.

Let's turn now to out second puzzle. Why did our recovery of Group D Streptococcus isolates more than double in 1983, making this pathogen one of the most commonly encountered at the hospital?

As in the case of our Proteus investigation, the answer lay in discovering what had changed to being about the new trend. In February 1983, the microbiology laboratory installed a susceptibility testing instrument with four-hour turnaround time. This promised significant time savings, but it meant that we had to review our isolation methods. It was quickly apparent that in the case of Streptococcus speciation, traditional plating procedures would hold back our new acquisition from maximum efficiency.

No longer could we wait for visible strep colonies on primary culture before carrying out a bile esculin azide test for pure culture. That took an extra day. So to make use of the instrument's four-hour capability, we began using bile esculin azide as one of the primary plates for inoculating urinary, genital, wound, and surgical cultures, where group D strep is commonly found.

The extra plating gave us quick identification of group D, but it also increased the number of these isolates dramatically. We were soon reporting streptococcal infections that would have remained hidden on other primary plates because of overgrowth by gram-negative rods and other gram-positive organisms. After a few months we concluded that without aggressive pursuit this pathogen easily escaped detection.

This discovery had significant implications. Group D strep is frequently resistant to antibiotic therapy aimed at organisms that crowd it out in culture. Incomplete response by patients to indicated drug therapy may correlate with our failure to identify group D strep with the other pathogens.

Month-by-month comparison of 1982 and 1983 group D strep isolation data shows how many more infections we began picking up (Figure II). In the year before primary bile esculin azide plating, 137 clinical isolates represented 5.3 per cent of the pathogens reported. Afterward, the number jumped to 294, or 11.2 per cent of all pathogens.

Group D strep recovery changed only marginally in specimens from genital and surgical cultures. The rate moe than doubled in wound and urinary cultures, however.

In both culture types, the organism was one of at least two infecting agents and was usually not readily visible (except on the bile esculin azide plates) because of faster grouwth, greater numbers, spreading, or mucoid appearance of other pathogens.

What percentage of pathogens isolated in other labs are group D strep? If the rate is low, a more persistent pursuit may reveal that the organism is present more often than suspected. I don't believe that rising prevalence accounts for our findings.

If clinicians are able to take group D strep's role in infection into account whan culture reports are issued, they can choose the best course of therapy from the start. Faster patient recovery and discharge may result.

The added plating also saves us time and work, as first intended. We recover group D strep in pure form and in sufficient numbers to work directly with the isolate. Susceptibilities are charted four hours after we examine morning plates. At 24 cents each (using about 150 plates a month that require strep speciation), the plates don't add much to our costs; we would need many of them for secondary isolation, anyway.

The new protocol also brings us closer to an ideal: to diligently pursue and report every potential pathogen in a specimen. Patients then get better care and clinicians learn to trust the laboratory team more.
COPYRIGHT 1985 Nelson Publishing
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 1985 Gale, Cengage Learning. All rights reserved.

Article Details
Printer friendly Cite/link Email Feedback
Author:Rydzewski, M. Marcia
Publication:Medical Laboratory Observer
Date:Feb 1, 1985
Words:1774
Previous Article:Why I spent time as a hospital volunteer; when this education coordinator became a hospital volunteer, she found not only satisfaction in the work...
Next Article:A backup plan for computer failure.
Topics:


Related Articles
Super-bugs arrive.
Antibiotic Resistance in Escherichia coli from Nigerian Students, 1986-1998.
Bacterial Resistance to Antimicrobial Agents: Selected Problems in France, 1996 to 1998.
Surveillance for antimicrobial resistance in Croatia. (Synopsis).
Comparative antibiotic resistance of diarrheal pathogens from Vietnam and Thailand, 1996-1999. (Research).
Trends in fluoroquinolone (ciprofloxacin) resistance in Enterobacteriaceae from bacteremias, England and Wales, 1990-1999. (Research).
Using hospital antibiogram data to assess regional pneumococcal resistance to antibiotics. (Research).
Crisis: antimicrobial agent resistance.
Bacterial resistance: how to detect three types.
Antimicrobial resistance determinants and future control.

Terms of use | Copyright © 2016 Farlex, Inc. | Feedback | For webmasters