Monday, November 19, 2012

Tuberculous cellulitis in a patient with chronic kidney disease and polymyalgia rheumatica.


Tuberculous cellulitis in a patient with chronic kidney disease and polymyalgia rheumatica.


Nov 2012

Source

Department of Internal Medicine, Mishuku Hospital, Japan.

Abstract


An 89-year-old man with advanced renal failure, polymyalgia rheumatica and a past history of tuberculosis was admitted with a high fever. Erythema and swelling appeared in the femoral region. Since the cellulitis failed to respond to antibiotic therapy, a skin biopsy was performed. The specimen showed the presence of epithelioid cell granuloma and panniculitis. Acid-fast organisms were found on Ziehl-Neelsen staining. A polymerase chain reaction test of tuberculosis was positive. Although a diagnosis of miliary tuberculosis was suggested, examinations of a bone marrow biopsy and fundoscopy revealed normal results. The patient's symptoms improved following treatment with isoniazid, rifampicin and ethambutol. This case represents an unusual presentation of tuberculous cellulitis in an immunocompromised patient.

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Thursday, September 20, 2012

Life-threatening Escherichia coli cellulitis in patients with haematological malignancies.


Life-threatening Escherichia coli cellulitis in patients with haematological malignancies.


Sept 2012

Source

1Service de Médecine Interne et Maladies Infectieuses, CHRU de Tours, France.

Abstract


Cellulitis due to Escherichia coli is rare and usually secondary to a cutaneous portal of entry. Skin and soft tissue infections (SSTI) secondary to E. coli bacteraemia have been reported exclusively in immunodeficient patients. Here, we report two cases of serious cellulitis secondary to E. coli bacteraemia in patients with haematological malignancies. Both isolated strains belonged to phylogenetic group B2 and harboured some of the main virulence factor genes commonly found in extra-intestinal pathogenic E. coli (ExPEC), including neuC, iro and fimH. Cellulitis due to E. coli seems to be linked to the immunocompromised status of patients rather than to a highly virulent clone. Nevertheless, some of the virulence factors appear to be important because both isolates belong to phylogenetic group B2. This aetiology should be considered in SSTI in patients with haematological malignancies.

Full Text Article

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Monday, October 08, 2007

Clinical Presentation of Cellulitis (erysipelas)

Clinical Presentation of Cellulitis (erysipelas)
Posted by EditorsChoice

Sunday, 07 October 2007


Diagnosis Hallmarks Distribution: no characteristic pattern Sudden onset of a large red plaque Pain and tenderness Rapid response to antibiotic therapy

Clinical Presentation

Cellulitis occurs as a tender, edematous, bright red plaque 5 to 20 cm in diameter. Generally, only a single lesion is present. A thin red line progressing proximally from the lesion (lymphangitis) is seen in about 20% of patients The initial lesion of cellulitis appears suddenly. Centrifugal growth of the lesion is rapid during the first 24 hours but occurs more slowly thereafter. Cellulitis is quite tender, but it is less painful than furunculosis, and fluctuant areas never develop. Fever, malaise, and regional lymphadenopathy may or may not be present.

Differentiation of cellulitis from an acute urticarial plaque such as occurs following bee stings is sometimes difficult, but the course of events over the succeeding 24 hours generally allows for appropriate identification.

The diagnosis of cellulitis is made on a clinical basis. It is theoretically possible to culture the lesion by way of injection, and subsequent aspiration, of sterile saline, but most clinicians do not find this helpful or necessary.

Course and Prognosis

Most instances of cellulitis resolve spontaneously over 10 to 20 days. Unfortunately, in debilitated or otherwise immunocompromised patients there may be progressive spread, and systemic infection may develop. The process is particularly troublesome when it occurs in patients taking systemic steroids, since not only is resistance reduced but the signs and symptoms of the infection may be greatly masked by the anti-inflammatory action of the steroids.

Special attention should be given to cellulitis of the central face, since, if it is left untreated, there is a significant risk of extension to the cavernous sinus.

Cellulitis is not usually recurrent. In patients with chronic lymphedema, however, there is a tendency both for the development of multiple lesions and for the occurrence of repeated episodes. The presence of hypesthesia, anesthesia, or blister formation (especially if the fluid is yellow or hemorrhagic) over an area of cellulitis should alert the clinician to the possible presence of underlying necrotizing fasciitis.

Pathogenesis

Cellulitis is a nonfollicular, mid to deep dermal infection caused by Staphylococcus aureus or Streptococcal pyogenes. Clinical signs indicating which of the two organisms is responsible are unreliable, but lymphangitis is more commonly found in staphylococcal infection. Fever, on the other hand, is more often seen in streptococcal infection. Trauma to the skin predisposes to the development of cellulitis, but occurrence ill the absence of trauma is common. Patients with chronic lymphedema seem particularly susceptible to the development of cellulitis.

Therapy

Systemic antibiotics, the treatment of furunculosis should be administered to all patients with cellulitis. It is not necessary to decide whether the problem is staphylococcal or streptococcal before initiating therapy, and in fact, culture is usually not possible even with saline injection and aspiration . Incision and irainage are never carried out. Hot packs or hot soaks are often recommended, but there is little evidence that this approach speeds resolution.

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