Mr. C, a 55-year-old cattle farmer from central Texas, came into our small, rural emergency department (ED) complaining of a pruritic rash and a weeping, tender blister on his right lower leg (Figure 1). The patient had daily contact with both dairy cattle and poultry and frequently worked in warm, wet conditions. He could not recall any recent trauma, bites, stings, or scratches to the area.
The lesion initially began as an erythematous, maculopapular rash that quickly spread from the patient’s mid-shin area both proximally and distally over the next few days. On about the third day, a “blister” formed, grew quickly in size, and began weeping bright yellow (almost fluorescent) fluid.
Mr. C’s past medical history was significant for hyperlipidemia and long-standing hypertension, treated with daily simvastatin and felodipine to good effect. While he did not smoke cigarettes, he occasionally chewed tobacco, and he drank moderate amounts of alcohol. A family medical history and review of symptoms were otherwise noncontributory.
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1. Physical examination
Mr. C was a well-developed, moderately obese, middle-aged man in no acute distress. His trousers were soiled and wet from the legs downward secondary to hosing out the milking barn before reporting to the ED. Vital signs were temperature 99.0° F, BP 132/74 mm Hg, and pulse 76 beats per minute.
Examination found an extensive, erythematous, maculopapular rash extending nearly the entire length and circumference of the lower portion of the patient’s right leg. An extremely bright yellow fluid-filled and partially draining bulla was present in the center of the lesion, which measured 8 cm ´ 2.5 cm. The fluid did not appear purulent and was not malodorous. The circumference of Mr. C’s right mid-calf was 48 cm, compared with 44 cm on the left. Capillary refill was normal, and distal pulses were present and symmetrical bilaterally.
2. Laboratory tests
Tests on the night of presentation included a complete blood count, blood and wound cultures, comprehensive metabolic panel, and routine urinalysis. The bulla was promptly drained and culture obtained. Gram-staining was not available in the ED at the time.
All the lab values were normal except for a WBC count of 14,500/µL with left shift.
3. Diagnosis
Mr. C was preliminarily diagnosed as having cellulitis with bulla of unknown etiology. The blood and wound cultures were still pending when the patient was subsequently admitted to the inpatient medicine ward. Multiple studies suggest that 28%-72% of all current skin infections and abscesses are attributable to methicillin-resistant Staphylococcus aureus (MRSA).1 Given the current practice environment, the patient was started empirically on IV vancomycin.
The next day, Gram’s stain revealed gram-negative rods, and the wound culture was returned as Pseudomonas aeruginosa.
Pseudomonas means “false unit.” The stem word mon was used early in the history of microbiology to refer to germs (e.g., kingdom Monera). The species name aeruginosa is a Latin word meaning “copper rust,”which also describes the blue-green bacterial pigment seen in laboratory cultures of P. aeruginosa. This pigment is a combination of two metabolites of P. aeruginosa—pyocyanin (blue) and pyoverdine (yellow), which impart the characteristic blue-green hue.2 In Mr. C’s case, however, the fluid was clear yellow.
A versatile, opportunistic, aerobic, gram-negative, rod bacterium, P. aeruginosa is commonly found in soil, marshes, wetlands, plants, and animal tissue. It thrives on wet skin and in nail beds.2 The organism mutates easily and can quickly develop antibiotic resistance. It also has a remarkable ability to cause disease in human beings by producing “a number of toxic proteins which not only cause extensive tissue damage but also interfere with the human immune system’s defense mechanisms. These proteins range from potent toxins that enter and kill host cells at or near the site of colonization to degradative enzymes that permanently disrupt the cell membranes and connective tissues in various organs.”1
Vancomycin was discontinued after Gram’s stain and culture and sensitivity results became available. Mr. C was subsequently switched to IV imipenem, which has a broad spectrum of activity against aerobic and anaerobic gram-positive as well as gram-negative bacteria—especially P. aeruginosa.
4. Discussion
At a time when increasing attention is being paid to MRSA, numerous age-old pathogens should also be considered. Antibiotic therapy should not routinely be started until the exact pathogen is confirmed by Gram’s stain and/or culture and sensitivity is obtained.
Pseudomonas aeruginosa remains as great a threat as ever. Many individuals are P. aeruginosa carriers, and the organism is commonly found on swabs obtained from hospitalized patients and caregivers. Infections often result in a high mortality among immunocompromised patients (e.g., those with HIV/AIDS or cystic fibrosis and those who have undergone organ transplant). Additionally, P. aeruginosa is one of the leading causes of nosocomial infections and still appears within the community with some frequency.
Mr. C likely contracted the pathogen somewhere on his farm via a small nick or scratch. The situation was exacerbated by the nature of his occupation and frequently wet skin and clothing. Left untreated, Mr. C’s P. aeruginosa infection may well have progressed to ecthyma gangrenosum (EG), which is usually associated with systemic infections in immunocompromised patients. The hallmark of EG is hemorrhagic pustules with surrounding erythema that develop into necrotic ulcers. In fact, it’s likely that our patient was close to having EG at the time of presentation. Luckily, the condition improved dramatically on IV imipenem over the next few days, and Mr. C was eventually released from the hospital and referred to his primary-care provider for follow-up.
Maj. Weaver is a physician assistant with the Department of Veterans Affairs in Temple, Tex. He is currently serving as an aeromedical physician assistant with the Army National Guard General Support Aviation Battalion in Balad, Iraq.
References
1. Moran GJ, Amii RN, Abrahamian FM, Talan DA. Methicillin-resistant Staphylococcus aureus in community-acquired skin infections. Emerg Infect Dis. 2005;11:928-930.
2. Wikipedia. Pseudomonas aeruginosa.
All electronic documents accessed October 12, 2008.
