Diagnosis: Pseudomonas aeruginosa sepsis

ARTICLE

A 62-year-old woman affected by end-stage renal disease secondary to Waldenstrom's disease was admitted to place a central venous catheter for hemodialysis purposes. During the admission, she gradually developed a number of necrotic ulcerative and fluctuant nodular skin lesions on the submammary flexures, groins and limbs accompanied by high fever and chills (Fig.1). Yellow-green purulent material could be drained from the site of introduction of the jugular catheter. Skin biopsies were taken from the edge of an inguinal necrotic-ulcerative lesion and from a fluctuant nodular lesion of the thigh, where pus was drained and cultured (Figs. 2 and 3).

Diagnosis: Pseudomonas aeruginosa sepsis

Microscopic and laboratory findings and clinical course

Histological examination showed extensive epidermal necrosis and ulceration above hemorrhagic infarction of the entire dermis with an inflammatory infiltrate mainly consisting of plasma cells and neutrophils (Fig.2). Vasculitis without intimal damage was present (Fig.3). Pseudomonas aeruginosa was isolated from the blood as well as from the pus of the patient. Despite antibiotic treatment (piperacillin and amikacin) and general support measures, the patient rapidly deteriorated and died seven days later.

Discussion

Pseudomonas aeruginosa (PA) is a gram negative bacteria, first isolated by Gesard in 1882, which is a common cause of septicemia in compromised hospitalized hosts. Predisposing factors include burns, chronic pulmonary diseases, urethral and venous catheters, history of antibiotic therapy, treatment with corticosteroids or antitumoral agents. Skin lesions may be found in 1.3-13% of the cases during PA septicemia, often as a presenting sign of disseminated infection. The most typical dermatologic manifestation is ecthyma gangrenosum, first described by Becker in 1897, consisting of round, indurated and ulcerated lesions with central necrotic eschar and surrounding erythema, frequently localized in the anogenital or axillary regions [1]. Nonetheless, a wide spectrum of skin lesions can be found: gangrenous cellulitis, hemorrhagic vescicles and bullae, typhoid fever-like maculo-papular rash, petechial and ecchymotic purpura, subcutaneous nodular cellulitis [2]. Sometimes fluorescence, demonstrated using a Wood's lamp, may help to support the diagnosis. Characteristically, aspirated material from skin lesions shows numerous micro-organisms and a few leukocytes; cultures from cutaneous lesions and blood are usually positive. The histopathologic picture of skin lesions during PA sepsis is typically a necrotizing vasculitis of venules and arterioles without intimal damage [3].

Other findings include: hemorrhage, occasional thrombosis of dermal vessels, scarce inflammatory infiltrate or septal and lobular neutrophilic panniculitis [4]. Experimentally induced disease in the rat and rabbit models suggests that PA lesions are initiated at the capillary level, with transmural centripetal arterial or venous infiltration rather than direct hematogenous intimal invasion. Tissue necrosis and hemorrhage would then be the result of bacterial injury and toxin release rather than of vascular obstruction [5]. The high mortality rate (over 80%) recorded during PA sepsis is due to the initial poor general conditions of the immunocompromised patients and to the multiorgan spread of the bacteria [6]. Differential diagnosis includes cryoglobulinemia, adverse drug reaction, necrotizing vasculitis and various nodular subcutaneous diseases (Staphylococcus aureus sepsis, bacillary angiomatosis, mycobacterial infection, acanthamebiasis, protothecosis, Kaposi's sarcoma, deep mycosis). When PA sepsis is strongly suspected, especially in immunocompromised patients, it is necessary to start an antibiotic treatment with a combination of aminoglycoside (tobramycin, amikacin or gentamycin) plus a third generation cephalosporin (ceftazidime) or a fluoroquinolone (ciprofloxacin or ofloxacin). Conversely, antibioprophylaxis is ineffective and must be avoided [7, 8]. Incision and drainage of subcutaneous abcesses are required if skin lesions are persistent with a toxic state, in spite of an antibiotic treatment [9]. Recently, granulocyte-macrophage colony-stimulating factor has been successfully used in the management of severe ecthyma gangrenosum related to myelodysplastic syndrome [10].

References

1. Barker LF. The clinical symptoms, bacteriologic findings and postmortem appearances in cases of infection of human beings with Bacillus pyocyaneous. JAMA 1897; 29: 213-6.

2. Bagel J, Grossman ME. Subcutaneous nodules in Pseudomonas sepsis. Am J Med 1986; 80: 528-9.

3. Dorff GJ, Geimer NF, Rosenthal DR, et al. Pseudomonas septicemia. Illustrated evolution of its skin lesion. Arch Intern Med 1971; 128: 591-5.

4. Greene SL, Su WP, Muller SA. Ecthyma gangrenosum: report of clinical, histopathologic and bacteriologic aspects of eight cases. J Am Acad Dermatol 1984; 11: 781-7.

5. Teplitz C. Pathogenesis of Pseudomonas vasculitis in septic lesions. Arch Pathol 1965; 80: 297-307.

6. El Baze P, Lacour JP, Ortonne JP. Le Pseudomonas aeruginosa en dermatologie. Ann Dermatol Venereol 1985; 112: 925-34.

7. Silvestre JF, Betlloch MI. Cutaneous manifestations due to Pseudomonas infection. Int J Dermatol 1999; 38: 419-31.

8. Greene SL, Su WP, Muller SA. Pseudomonas aeruginosa infections of the skin. Am Fam Physician 1984; 29: 193-200.

9. Reed RK, Larter WE, Sieber OF, et al. Peripheral nodular lesions in Pseudomonas sepsis: the importance of incision and drainage. J Pediatr 1976; 88: 977-9.

10. Bechérel PA, Chosidow O, Berger E, et al. Granulocyte-macrofage colony-stimulating factor in the management of severe ecthyma gangrenosum related to myelodysplastic syndrome. Arch Dermatol 1995; 131: 892-4.

Article accepted on 29/1/02