Antimicrobial Chemotherapy


Failure of therapy: Case 1

Amoxycillin resistance of the isolate
Information on ampicillin
susceptibility testing

AC is an 8 year old boy who was taken by his mother to their General Practitioner because he had developed a large carbuncle in the nape of his neck. This was causing the lad considerable discomfort, and his GP decided that the best course of action was to prescribe amoxycillin for the child. The GP arranged for the Practice Nurse to take a swab from the boy's lesion, and had it sent to the local hospital for culture and sensitivity testing. They isolated a pure growth of Staphylococcus aureus.

Despite taking the full course of antibiotic as recommended, the carbuncle did not get any better. If anything it seemed to the boy's distressed mother that it actually grew larger. Additionally, the lad developed a mild diarrhoea. Dissatisfied with his son's condition, his father took him to see another doctor in the Practice. Since the second GP had access to the lab report, the boy's prescription was changed to erythromycin syrup, and he also had his lesion drained. This led to a rapid resolution of the problem.

 

 

Was the use of a broad-spectrum agent as the first line of therapy appropriate in this case?

 

Why was amoxycillin an inappropriate choice of therapy?

 

What are the ways in which bacteria can resist the action of b-lactams?

 


Failure of therapy: Case 2

Trimethoprim susceptibility of the isolate
Information on trimethoprim susceptibility testing

CS was troubled with regular bouts of cystitis. At the start of her latest bout, C consulted her General Practitioner, who requested that she supply a urine sample for microbiological investigation. The cause of her problem turned out to be a coliform that was sensitive to all antibacterials tested except for ampicillin. C had been given a prescription for trimethoprim but she remembered that she had a couple of trimethoprim tablets left over from a previous episode, which had cleared up before she had finished her course of treatment. She used up her old tablets before starting on her new prescription.

Two days later, C experienced a severe worsening of her symptoms. She developed a pain in her loin and became pyrexial. She noticed also that her breathing rate had increased, along with an alarming increase in her pulse. She contacted her GP, requesting a domicilliary visit, explaining that she felt too unwell to visit the health centre. On examination, her GP noted that C's blood pressure was low and he arranged for her to be admitted to her local hospital. On admission, a urine sample was sent to the Microbiology Laboratory for analysis, as was a set of three blood cultures. The urine was sterile upon culture but all blood culture bottles yielded Escherichia coli, sensitive to all antibiotics tested other than ampicillin. Further clinical tests revealed that C was suffering from septicaemia as a complication of pyelonephritis.

 

 

Why was the urine sample taken in hospital sterile, despite C having pyelonephritis?

 

Was trimethoprim a suitable antibiotic with which to treat C's urinary tract infection?

 

Would trimethoprim remain the drug of choice for septicaemia?

 

What is the mode of action of trimethoprim, and does this have a bearing on this case?


Meticillin-resistant Staphylococcus aureus

Susceptibility testing of meticillin-resistant Staph. aureus
Information on MRSA

Nurse E was a student attached to the Surgical Unit of a District General Hospital. Shortly after she was posted to the Unit, an increased number of patients were found to be suffering from post-operative wound infections. Analysis of the culture reports indicated that most cases were caused by meticillin-resistant Staphylococcus aureus.

Because of the increased incidence of wound infections, and because they were caused by MRSA's, the hospital Infection Control Team initiated an investigation. Sub-typing showed that all of the MRSA's were clonal, that is they all belonged to the same strain, as far as could be determined with the techniques available. Despite initiating a surveillance programme on the Unit, at first no source could be found for the MRSA's .

A monitoring programme to check the efficacy of hand-washing was then initiated. After each time that they washed their hands, staff on the Unit were requested to make fingertip impressions on mannitol salt agar, a medium selective for staphylococci. No MRSAs were isolated for five days, during which MRSA wound infections continued on the Unit. Then, when collecting the impression plates one afternoon, one of the Hospital Infection Control Team observed that after she had made her fingertip impression, Nurse E rubbed her hands with a moisturising cream, she said it was "...because of the roughening of my skin". She suffered from intermittent bouts of eczema, and had just recovered from an episode before starting on the surgical Unit.

The Infection Control Officer asked if she could sample the hand cream, and it yielded a culture of MRSA, indistinguishable from the clone that was isolated from patients on the Unit. Use of the moisturising cream on the Unit was banned, and all the staff were required to wash their hands using alcohol-based chlorhexidine. Monitoring of handwashing with fingertip impression plates continued for a week, but following the introduction of control measures, no further cases of MRSA wound infection were seen on the Unit.

 

 

What was the source of the MRSA?

 

Is it probable that the strain of MRSA isolated in this incident was merely colonising Nurse E and yet was seemingly causing wound infections in the surgical patients?

 

What was the mode of spread of infection in this incident?

 

 


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Page edited April 2006


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