Pneumococcal Cellulitis - Abstracts

Bacteremic pneumococcal cellulitis compared with bacteremic cellulitis caused by Staphylococcus aureus and Streptococcus pyogenes.

Capdevila O, Grau I, Vadillo M, Cisnal M, Pallares R.

Clinical Research Unit, Hospital de Bellvitge and University of Barcelona, Feixa Llarga s/n, 08907 L' Hospitalet, Barcelona, Spain.

In order to better characterize bacteremic cellulitis caused by Streptococcus pneumoniae, a review was conducted of 10 cases of bacteremic pneumococcal cellulitis, which represented 0.9% of all cases of pneumococcal bacteremia (n=1,076) and 3.2% of all cases of community-acquired bacteremic cellulitis (n=312) that occurred in the Hospital de Bellvitge, Barcelona, from 1984 to 2001. In addition to these 10 cases, 28 cases of bacteremic pneumococcal cellulitis from the literature (Medline 1975-2001) were reviewed.

Pneumococcal cellulitis of the face, neck, and trunk was observed more frequently in patients with systemic lupus erythematosus and hematologic disorders, while pneumococcal cellulitis of the limbs was more common in patients with diabetes, alcoholism, and parenteral drug use. In the Hospital de Bellvitge group, bacteremic cellulitis due to Streptococcus pneumoniae was more frequently associated with severe underlying diseases than that due to Staphylococcus aureus or Streptococcus pyogenes (100%, 57%, and 72%, respectively;P=0.01).

A concomitant extracutaneous focus of infection (e.g., respiratory tract infection) suggesting hematogenous spread with metastatic cellulitis was more frequent in patients with pneumococcal cellulitis, while a local cutaneous entry of microorganisms was feasible in most patients with Staphylococcus aureus or Streptococcus pyogenes cellulitis. The 30-day mortality was 10% in patients with pneumococcal cellulitis, 13% in patients with Staphylococcus aureus cellulitis, and 23% in patients with Streptococcus pyogenes cellulitis (P=0.3). Thus, bacteremic pneumococcal cellulitis is an unusual manifestation of pneumococcal disease and occurs mainly in patients with severe underlying diseases. In most cases, pneumococcal cellulitis has a different pathophysiologic mechanism than cellulitis caused by Staphylococcus aureus or Streptococcus pyogenes.

PMID: 12783279

[PubMed - indexed for MEDLINE]

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Clinical syndromes associated with adult pneumococcal cellulitis.

Parada JP, Maslow JN.Department of Medicine, Stricht School of Medicine, Loyola University, Maywood, IL, USA.

Streptococcus pneumoniae is an uncommonly recognized etiology of cellulitis in adults. A review of the literature uncovered 30 cases of pneumococcal skin infection in adults. Typically, all patients with pneumococcal cellulitis had an underlying chronic illness, or were immunocompromised by drug or alcohol abuse. Pneumococcal cellulitis presents as two distinctive clinical syndromes: one with extremity involvement in individuals with diabetes and substance abuse; and a second involving the head, neck and upper torso in individuals with systemic lupus erythematosis, nephrotic syndrome and hematologic disorders. For each there are statistically significant associations between the location of pneumococcal cellulitis and underlying clinical disorders. In contrast to other common bacterial etiologies, pneumococcal cellulitis is frequently associated with blood stream invasion, tissue necrosis and suppurative complications. Patients often require surgical interventions and prolonged hospitalizations. A high degree of suspicion and early aggressive management is needed for those presenting with cellulitis characterized by bullae and violaceous color.

Pub Med

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Pneumococcal Cellulitis

Case Based Pediatrics For Medical Students and Residents

Department of Pediatrics, University of Hawaii John A. Burns School of Medicine.

A 2-year-old male presents to the emergency department with a chief complaint of left thigh swelling, fever, irritability, and unwillingness to stand upright for the last 2 days. He has been scratching at mosquito bites that he had gotten while weekend camping about 1 week ago.
Exam: VS T 39.5, P 110, R 26, BP 120/70. Growth parameters are normal for age. He is fussy, somewhat distractible, but clearly uncomfortable. He is continuously scratching at a left upper inner thigh lesion measuring 6 x 3 cm. The skin over the area is indurated, erythematous and tense, and tender. No fluctuance or wound drainage is noted. There is no joint involvement. Some tender lymph nodes are palpable in the left inguinal region.

He is prescribed cephalexin and anti-pyretics. In follow-up the next day, the erythematous region is slightly darker (a shift from red toward a shade of purple). Tiny blisters are also noted over the area. These changes are expected and treatment is continued. On follow-up day 2, the fever has resolved and the cellulitis appears to be clearly improving. His parents are instructed to finish the course of antibiotics. He is next seen in follow-up 7 days later, at which time, his cellulitis is resolved.

The basic response to infection is fever. The local, dermatological acute inflammatory reaction of cellulitis stems specifically from granulocytic infiltrations, hyperemia, and capillary leakage. This is the basis for the skin disruption inherent in cellulitis. The patient may guard the tender area. If the cellulitic area overlies a mobile area such as a joint, the patient may display resistance or anxiety with limb movement, either passive or active.

The specific visual characteristics (appearance) of the cellulitic region can provide important clues as to the organism(s) involved, with implications for treatment and prognosis. Clinical presentation, treatment, and prognosis differ depending on the causative organism and the location of the cellulitis. The remainder of this chapter will be stratified by these factors.

Group A strep cellulitis

Generally, cellulitis suggests the presence of a skin infection due to group A beta-hemolytic streptococci (GABHS, also known as Strep pyogenes). GABHS cellulitis is a painful, erythematous, indurated infection of the skin and subcutaneous tissues. It is classically described as large lesions, erythroderma in color (magenta), slightly raised at the border, with a small, central open skin lesion (frequently an insect bite). It is common for varicella lesions to become secondarily infection with GABHS. GABHS cellulitis may present with scarlet fever.

Abscess formation beneath the cellulitis is very uncommon. GABHS is penicillin and cephalosporin sensitive.

Staph aureus cellulitis

Staph aureus is commonly cultured from impetigo lesions, albeit usually as a secondary pathogen, along with GABHS. Some of these lesions develop into cellulitis, which may be primarily caused by GABHS or alternatively, caused primarily by Staph aureus. Staph aureus cellulitis is typically smaller (than the larger GABHS cellulitis) and is frequently associated with an abscess or pustule. In many of these cases, the abscess is the major problem (i.e., incision and drainage is required), as opposed to the cellulitis which is relatively less of a problem.

H. flu type b cellulitis

H. influenzae type b (Hib) used to account for in 5-14% of the cellulitis cases in young children. More than 85% of children with H. influenzae type b cellulitis are 2 years of age or younger. Hib is a particularly virulent organism which is frequently associated with sepsis. A common location for Hib cellulitis was the periorbital and buccal region. Cellulitis is a complication of H. influenzae septic arthritis 10-30% of cases. Fortunately, there has been a substantial decline in the incidence of invasive infection caused by Hib with the practice of routine immunization of infants against this organism, to the point where Hib infection is almost non-existent. Hib is covered by high generation cephalosporins (e.g., ceftriaxone) and by broad spectrum oral drugs such as amoxicillin-clavulanate and cefuroxime.

Pasteurella/animal bite cellulitis

Cellulitis and lymphangitis typically appears 24-36 hours after mammalian bite injuries. The etiologies of infections following mammalian bites are polymicrobial and consist of mixed anaerobic and aerobic bacteria. In one study, an average of three different bacterial species was isolated from infected dog bites while a mean of five different species was recovered from infected human bites. Because of the numerous bacterial species in mammalian oral cavities and on the victim's skin, contamination of bite injuries is universal. Pasteurella multocida is sensitive to penicillins, but it is less sensitive to cephalosporins. Amoxicillin-clavulanate is generally used for animal bites to cover Pasteurella, staph aureus and anaerobes.

Orbital and periorbital cellulitis

Periorbital (preseptal) cellulitis involves inflammation of the lids and periorbital tissues without signs of true orbital involvement, such as proptosis or limitation of eye movement. It presents as a red and swollen infection limited to the superficial tissue layers anterior to the orbital septum. History usually yields an antecedent respiratory infection or bacteremia. Historically, H. influenzae type b was an important cause, and presented with fever, edema, tenderness, warmth of the lid, and, occasionally, purple discoloration (violaceous hue). However, streptococcal organisms are the most common cause of bacteremia associated with periorbital cellulitis in the post Hib-vaccinated era (9). S. pneumonia, Staphylococcus aureus, and group A beta-hemolytic streptococci cause clinically indistinguishable preseptal cellulitis (2). The latter two pathogens are more likely when fever is absent and with an interruption of the integument (e.g., an insect bite) (1).

Distinguishing periorbital from orbital cellulitis can be difficult. If proptosis, extraocular movement dysfunction, or visual deficits are clearly present, then orbital cellulitis is likely. However, in the absence of these findings, the diagnosis is unclear. In periorbital cellulitis, the lid swelling may be so severe, that it is not possible to tell if proptosis is present. A CT scan of the orbits will reliably distinguish periorbital from orbital cellulitis. Since the difference between the two can be important, a CT scan of the orbits has become routine in the evaluation of most patients with severe periorbital cellulitis and/or suspected orbital cellulitis.

Orbital cellulitis refers to a condition involving not only edema of the conjunctiva (chemosis), and inflammation and swelling of the eyelids, but also involvement of the tissues of the orbit, with subsequent proptosis (limitation of movement of the eye). In general, orbital cellulitis may follow direct infection of the orbit from a wound, metastatic deposition of organisms during bacteremia, or direct extension or venous spread of infection from contiguous sites such as the lids, conjunctiva, globe, lacrimal gland, nasolacrimal sac, or paranasal sinuses. The most common cause of orbital cellulitis in children is paranasal sinusitis, with the most frequent pathogenic organisms being Haemophilus influenzae, Staphylococcus aureus, group A beta-hemolytic streptococci, and Streptococcus pneumonia. Orbital cellulitis must be recognized promptly and treated aggressively. Hospitalization and systemic antibiotic therapy are usually indicated. In some cases surgical intervention is necessary to drain infected sinuses, or a subperiosteal or orbital abscess. Intravenous treatment for 10 to 14 days is highly recommended, along with repeated eye exams (visual acuity, pupillary reactivity, extraocular movements, and visual fields) to evaluate possible progression of infection and/or involvement of the optic nerve (10). As a worst case scenario, orbital cellulitis can lead to the complication of brain abscess, especially in the frontal lobe.

Finally, orbital cellulitis is an infrequent presenting sign of retinoblastoma. The severe clinical implications of retinoblastoma (enucleation may be inevitable) warrants vigilance for a white pupillary reflex (leukocoria, the reflection of light off the white tumor), pseudohypopyon (tumor cells layered inferiorly in front of the iris caused by tumor seeding in the anterior chamber of the eye), and hyphema (blood layered in the anterior chamber) secondary to iris neovascularization or vitreous hemorrhage.

Erysipelas

Erysipelas is an acute, well-demarcated aggressive infection of the skin with lymphangitis involving the face (associated with pharyngitis) and extremities (wounds). The skin is erythematous and indurated. The advancing margins of the lesions have raised, firm borders. The skin lesion usually is associated with fever, vomiting, and irritability. In some cases, streptococci break through the lymphatic barrier (lymphangitis), and subcutaneous abscesses, bacteremia, and metastatic foci of infection are observed. Bacteremia and death have been associated with streptococcal cellulitis, and progression may be so rapid that there may be no response to treatment with penicillin. The popular press has termed severe cases of GABHS cellulitis (necrotizing fasciitis) as "flesh eating bacteria".

Lymphangitis

Lymphangitis is an inflammation of the lymphatics draining an area of infection (i.e., a cellulitis site). On exam, tender red streaks extend proximally from the infected site. S. aureus and group A strep are the most frequent pathogens. A history of impetigo is also suggestive of cellulitis, in that, cellulitis has been reported in approximately 10% of patients with nonbullous impetigo but rarely follows the bullous form. There is no correlation between the number of lesions and clinical involvement of the lymphatics or development of cellulitis in association with streptococcal impetigo. The history is consistent with pruritic lesions subject to frequent scratching and secondary infection (including insect bites, pediculosis and scabies). This is followed by the development of a vesicle or vesiculopustule with an erythematous base that erodes through the epidermis into the dermis to form an ulcer with elevated margins. A dry crust that contributes to the persistence of the infection obscures the ulcer. Lesions may be spread by autoinoculation, may be as large as 4 cm, and occur most frequently on the legs or pruritic areas within reach.

Risk of osteomyelitis and septic arthritis

Although the risk of osteomyelitis and septic arthritis is fairly rare unless a penetrating wound is present, the relationship between osteomyelitis and cellulitis deserves special attention, in that a progression to osteomyelitis from cellulitis mandates a far more aggressive and prolonged antibiotic course, not to mention possible orthopedic surgical debridement. Thus, when a diagnosis of cellulitis is made, the comorbid presence of osteomyelitis must also be strongly considered especially when corroborated by a history of a penetrating wound. At the very least, cellulitis accompanied by point tenderness or joint pain is highly suggestive of osteomyelitis. Attempts at diagnosis are complicated by the fact that cellulitis of structures in proximity to bone can mimic osteomyelitis.

To effectively discern cellulitis with possible underlying osteomyelitis, combining technetium bone scanning with other radionuclide scanning techniques or MRI scanning may be useful. In a three phase bone scan, focal increased uptake in the initial phase, with subsequent decline in the later phases (especially the bone phase), is suggestive of cellulitis without osteomyelitis. In osteomyelitis, localized uptake is seen in all three phases, especially in the bone phase.
If the history, physical exam, or radiological studies suggest deep cellulitis near a joint, the level of suspicion is raised with regard to an infection in the respective joint, not to mention osteomyelitis, synovitis, septic bursitis and pyomyositis in nearby muscles. Deep cellulitis is also consistent with psoas or retroperitoneal abscesses. Cellulitis overlying a joint can interfere with studies crucial to the diagnosis of septic arthritis. If a cellulitic area is traversed during arthrocentesis for a workup for septic arthritis, the results can be confounded if organisms are introduced into a previously sterile uninvolved joint.

Cellulitis and immunodeficiency

The presence of cellulitis in the face of concomitant immunodeficiency requires inpatient treatment. Deficient expression of leukocyte adherence glycoproteins can present as cellulitis or small (<1>

Defects in the normal host response may be reflected in study findings that are disproportionately severe when compared to relatively benign findings on the physical exam. For example, deep cellulitis may be quite impressive on a CT of a neutropenic patient who has only mild superficial swelling or erythema. Indeed, surface pus formation is unusual at sites of even severe cellulitis in such patients.

Cellulitis in children with burns illustrates not only the acute effects of interrupted skin and mucous membrane barriers, presence of necrotic tissue, long-term administration of antibiotics and prolonged intravenous or urinary catheterization, but also the concomitant abnormal immune response to infection, including neutrophil dysfunction. The resulting neutrophil chemotactic defect, combined with an associated hypogammaglobulinemia is a perfect scenario for cellulitis with Pseudomonas aeruginosa being the most common organism.

In the neonatal period, cellulitis can be a manifestation of invasive infection, as is bacteremia with a septic-like clinical picture, pneumonia, respiratory distress syndrome with shock, conjunctivitis, scalp abscess, or meningitis. Cellulitis may be the presenting sign of immunodeficiency in an infant. Cellulitis, delayed separation of the umbilical cord and gingivitis is consistent with an infant with leukocyte adhesion deficiency. Cellulitis of the labia majora, pyogenic skin infections, oral ulcerations, or abscesses has been the presenting manifestations of autoimmune neutropenia of infancy.

Cellulitis of the perirectal area, sites of iatrogenic puncture (central venous catheter insertion, venipuncture, lumbar puncture, and bone marrow biopsy), or abrasions is a setup for gram negative dissemination. In the context of vaginitis, beta-hemolytic streptococcus is a common cause in prepubertal girls and may present with perianal cellulitis with local itching, pain, blood-streaked stools, erythema, and proctitis (3).

Rarely, cellulitis or skin discoloration overlying a fluctuant mass might be the presenting finding in tuberculosis of the superficial lymph nodes, often referred to as scrofula, the most common form of extrapulmonary tuberculosis in children. The tonsillar, anterior cervical, submandibular, and supraclavicular nodes become involved secondary to extension of a primary lesion of the upper lung fields or abdomen. The nodes usually enlarge gradually in the early stages of lymph node disease. They are firm (but not hard), discrete, and nontender. The nodes often feel fixed to underlying or overlying tissue. Disease is most often unilateral, but bilateral involvement may occur because of the crossover drainage patterns of lymphatic vessels in the chest and lower neck.

Cellulitis of the sublingual and submandibular spaces (Ludwig angina) tends to spread rapidly without lymph node involvement or abscess formation. It is an acute, life-threatening entity that may require tracheostomy in the event of respiratory obstruction.

Cellulitis of the auricle and external auditory canal is usually caused by S. pyogenes (GABHS) or occasionally by S. aureus. The skin is red, hot, and indurated, without a sharply defined border. Fever may be present with little or no exudate in the canal.

Cellulitis can be a complication of hidradenitis suppurativa, a chronic, inflammatory, suppurative disorder of the apocrine glands in the axillae or anogenital area, and occasionally, the scalp, posterior aspect of the ears, female breasts, and around the umbilicus. Cellulitis of the lateral nail fold can occur as spicules that have separated from the nail plate, penetrate the soft tissue. Predisposing factors include compression of the side of the toe from poorly fitting shoes, particularly if the great toes are abnormally long and the lateral nail folds are prominent, and improper cutting of the nail in a curvilinear manner rather than straight across. Oral antibiotics are necessary to treat cellulitis of the lateral nail fold.

Lab tests are generally not very helpful in cellulitis. A CBC might help to assess infection severity. A blood culture may be indicated if bacteremia or sepsis is suspected. A gram stain of a leading edge aspirate is done by injecting a small amount of non-bacteristatic saline into the leading edge of the cellulitis, then aspirating back the saline. Leading edge cultures have a low yield and they are usually not obtained. Since introduction of the Hib vaccine, the most common organisms are streptococci. In a series of 243 children admitted with cellulitis, Sadow and Chamberlain (1998) contend that, given a treatment threshold based on a band-to-neutrophil ratio of 0.20 on a CBC differential, routine cultures contribute little to the decision to treat (7). Most cases of early or mild cellulitis, especially those without fever, do not require laboratory testing. Empiric antibiotic treatment is successful in most instances.

Antibiotic treatment is targeted mainly against the usual pathogen, group A strep. Staph aureus is uncommon (unless an abscess is present), but difficult to exclude without a leading edge aspirate culture. GABHS is sensitive to penicillin and cephalosporins. Staph aureus used to be sensitive to anti-Staph aureus penicillins (cloxacillin, dicloxacillin, methicillin, oxacillin, nafcillin) and cephalosporins. However, currently, 25% of Staph aureus are resistant (i.e., methicillin and cephalosporin resistant). If GABHS is very likely, then utilizing a cephalosporin or penicillin is acceptable. However, if Staph aureus is suspected, then there is a 25% failure rate for cephalosporins and anti-Staph aureus penicillins. There is less Staph aureus resistance to clindamycin (also covers GABHS) and trimethoprim-sulfamethoxazole (does not cover GABHS as well). Thus, clindamycin is generally indicated if Staph aureus is suspected. Vancomycin and aminoglycosides are parenteral and can only be used for inpatient treatment of staph aureus. Erythromycin has been used in the past, but GABHS and Staph aureus have high resistance rates to erythromycin. If a satisfactory clinical response is not achieved within 7 days, a culture and sensitivity should be taken of a leading edge aspirate. If a resistant organism is detected, an appropriate antibiotic should be given for an additional 7 days.

Young children (<36>

Finally, aggressive attempts to restore skin integrity should be initiated. The skin should be gently moistened and cleansed. Impetiginous crusts should be softened with warm compresses and removed with an antibacterial soap. Application of an emollient provides lubrication and decreases discomfort. Topical antibiotics are unnecessary once systemic intervention is started.

Pneumococcal Cellulitis

Eosinophilic cellulitis and dermographism

Nathalie Q Nguyen MD and Linglei Ma MD PhD
Dermatology Online Journal 11 (4): 7 Department of Dermatology,
New York University School of Medicine

Abstract

A 26-year-old man presented with a history of intermittent erythematous plaques on his hands and legs. A peripheral blood eosinophilia was noted. Histopathologic examination showed numerous eosinophils and characteristic flame figures. The clinical presentation and histopathologic alterations are consistent with the diagnosis of Wells' syndrome, which is also known as eosinophilic cellulitis. Wells' syndrome is a rare condition of unclear etiology. We discuss its diagnosis and possible association with other conditions that manifest peripheral eosinophilia.

A 26-year-old man presented to the Charles C. Harris Skin and Cancer Pavilion with an eruption on his hands that had been recurring for 4 years. During the summer months, he noted the appearance of tender, red plaques and nodules on his palms, which spontaneously resolved. Over the past year, the red plaques and nodules recurred on his palms, and he noticed new lesions on his thighs. At one point, blisters developed on one of the red plaques on his left hand. The patient was treated with doxycycline, dicloxacillin, and clarithromycin, which failed to improve his symptoms. The patient has received several courses of prednisone, with clearance of his eruptions. He denies fevers, chills, malaise, or weight loss. Past medical history includes allergic rhinitis, eczema, and asthma.

Multiple, erythematous plaques were present on the palms and dorsal aspects of the hands. There were several, well-circumscribed, hyperpigmented macules. On the anterior thighs were multiple, circinate, erythematous plaques. A brisk, mechanical stroke elicited a linear wheal.

A complete blood count showed 16.7 percent eosinophils, with an absolute eosinophil count of 1653 cells/mcL. Basic metabolic panel, liver function tests, thyroid function tests, and serum protein electrophoresis were normal.

Histopathology reveals a superficial and deep, perivascular and interstitial, mixed-cell infiltrate of lymphocytes with innumerable eosinophils, which extends into the subcutaneous adipose tissue. Among dermal collagen bundles, there are collections of eosinophils with eosinophilic granules (flame figures).

Comment

Wells' syndrome was first described in 1971 and later renamed eosinophilic cellulitis [1]. Typical lesions present as single or multiple, erythematous patches and plaques that clinically resemble acute cellulitis. However, the plaques fail to resolve with antibiotic therapy. Acute, erythematous and edematous plaques extend peripherally. The intensity and rapidity of progression mimics that of an acute cellulitis. However, lesions are often cool to the touch. Most patients experience mild burning and itching. Although erythematous, edematous plaques are the most common presentation, nodules, bullae, or a papulonodular eruption may occur [2, 3, 4]. Within a few days, the inflammation subsides, and the erythema is replaced with a gray-blue hue.

The diagnosis of eosinophilic cellulitis is based on clinical and histopathologic features. In addition to the cutaneous manifestations, patients also present with peripheral blood eosinophilia. Histopathologic examination shows a dense infiltrate of eosinophils with degranulation. In older lesions, the granular material aggregates focally around collagen fibers to form the characteristic flame figures [5]. These eosinophilic bodies are not pathognomonic for eosinophilic cellulitis and have been described in other inflammatory conditions, such as eczema, prurigo, herpes gestationis, scabies, and bullous pemphigoid [6].

Eosinophilic cellulitis has been proposed to be in the same spectrum of diseases as other disorders with peripheral eosinophilia, such as idiopathic hypereosinophilic syndrome (HES) and Churg-Strauss syndrome [7]. However, patients with eosinophilic cellulitis rarely show systemic symptoms unlike patients with HES, who present with pulmonary, gastrointestinal, or neurologic symptoms. Cutaneous involvement is found in approximately 50 percent of HES patients, and it has been postulated that perhaps eosinophilic cellulitis may be a cutaneous manifestation of HES rather than a separate entity [7, 8]. Wells' syndrome has also been reported to be precipitated by arthropod bites, fungal infections, medications, and parasites.
Treatment options include antihistamines, prednisone, and cyclosporine. Anecdotal use of griseofluvin, minocycline, and dapsone has been reported [4].

References1.

Wells GC, Smith NP. Eosinophilic cellulitis. Br J Dermatol 1979;100:1012.
Ghislain PD, Van Eeckhout P. Eosinophilic cellulits of papulonodular presentation (Wells' syndrome). Eur Acad Dermatol Venereol 2005;19:2263.
Holme SA, McHenry P. Nodular presentation of eosinophilic cellulitis (Wells' syndrome). Clin Exp Dermatol 2001;26:6774.
Ling TC, et al. Two cases of bullous eosinophilic cellulitis. Br J Dermatol 2002; 146:1605.
Abell E. Inflammatory diseases of the epidermal appendages and of cartilage. In Elder D, et al, eds. Lever's Histopathology. 8th ed. Philadelphia: Lippincott Williams & Wilkins;1997;18:409.6. Ferreli C, et al. Eosinophilic cellulits (Wells' syndrome): a new case description. J Eur Acad Dermatol Venereol 1999;13:417.
Fujii K, et al. Eosinophilic cellulitis as a cutaneous manifestation of idiopathic hypereosinophilic syndrome. J Am Acad Dermatol 2003;49:11748.
Weller PF, Bubley GJ. The idiopathic hypereosinophilic syndrome. Blood 1994; 83: 2759

© 2005 Dermatology Online Journal

Cellulitis-like fixed drug eruption attributed to paracetamol (acetaminophen)

M Mukhyaprana Prabhu MD, Smitha Prabhu MD DVD, Pranay Mishra, and Subeesh Palaian

Dermatology Online Journal 11 (3): 24

Department of Dermatology and Venereology, Manipal College of Medical sciences, Manipal Teaching Hospital, Pokhara, Nepal. drprabhu@fewanet.com.np

Abstract

Paracetamol (acetaminophen) is a widely used analgesic-antipyretic with consistent safety profile and very low incidence of side effects. We report a case of biopsy-confirmed fixed drug eruption associated with paracetamol and presenting like cellulitis.

Introduction

Paracetamol is a widely used analgesic-antipyretic with consistent safety profile and very low incidence of side effects [1, 2]. We report a case of biopsy-confirmed fixed drug eruption (FDE) associated with paracetamol and presenting like cellulitis.

Clinical synopsis

A 65-year-old Nepalese woman was admitted with a high-grade fever (103° F), chills, and rigors. Clinical examination, including neurological examination, was normal. Routine investigations revealed urinary tract infection (routine urine microscopy showed 4-6 white blood cells cells per high power field). The patient was started on intravenous ceftriaxone (2 g daily) pending culture. Paracetamol (500 mg) was given twice; the fever subsided, but simultaneously a painful erythematous rash appeared on the left shin. There was an edematous, erythematous, shiny, tender, indurated plaque with definite upper border, measuring approximately 15 × 7 cm, which mimicked cellulitis (Fig. 1). Blood culture was negative for bacterial growth. Meanwhile, the patient gave history of similar reactions at the same site, occurring five times in the past 5 years, whenever she took parcetamol. In view of this, possibility of cellulitis-like fixed-drug eruption was considered. Paracetamol was stopped. Within 48 hours the rash subsided completely.

In view of the strong history linking paracetamol with this unusual reaction, we conducted an oral rechallenge test with paracetamol. After 24 hours of disappearance of the rash, and after obtaining informed consent, the patient was given 125 mg, 250 mg and 500 mg of paracetamol at 6 hours apart. After the last dose, she complained of pruritus and burning sensation at the same site as the previous reaction, but no objective signs were noticed. Further challenge with 500 mg paracetamol was done after 6 hours, and the pruritus increased in intensity. Erythematous, edematous, tender, shiny infiltrated plaque with rise in temperature was noticed 3 hours later.

An incisional biopsy taken from the reaction site revealed changes consistent with fixed drug eruption rather than cellulitis. Histopathology of the affected area revealed a thinned epithelium lined with stratified squamous cells. The basal layer showed hydropic degeneration. The papillary dermis showed perivascular infiltration by lymphocytes and plasma cells. Pigment incontinence was seen in the upper dermis (Fig 3). Naranjo algorithm [3] for causality score done showed definitive association (score: 11/13).

Discussion

The characteristic presentation of FDE is the occurrence of lesions at the same site each time the offending drug is administered. Sites often affected include the lips, hands, legs, face, genitalia, and oral mucosa; the lesions may itch or burn [5]. Fixed-drug eruptions have been associated with phenolphthalein, sulfonamides, phenylbutazone, barbiturates, dapsone, chlordiazepoxide, indomethacin, quinine, salicylates and tetracyclines [4]. Paracetamol associated FDE is uncommon and occurs in less than 1.5 percent of all FDE [6]. Only a few case reports of fixed-drug eruption due to paracetamol have been published, the reactions presenting as maculopapular or erythematous discoid rashes [7, 8, 9, 10, 11].

Our patient developed fixed-drug rash clinically resembling cellulitis on paracetamol intake 5 times in the past. Allergy was confirmed by oral rechallenge and Naranjo causality assessment scale. Skin biopsy also confirmed the diagnosis of fixed drug eruption.

There is a reported case of paracetamol-induced vasculitis-like FDE [12]; however cellulitis-like reaction to paracetamol has not been reported previously.

Paracetamol is a widely used drug and it is considered to be very safe. However, practitioners should be aware that cutaneous side effects may occur.

References1.

Drugdex evaluations Acetaminophen. In: Thomson micromedex, Micromedex(R) Healthcare Series Vol. 121,1974 - 2004. 2.

Noel MV, Sushma M, Guido S. Cutaneous adverse drug reactions in hospitalized patients in a tertiary care center. Ind J Pharmacol 20004; 36:292-2953.

Naranjo CA, Busto U, Sellers EM et al. A method for estimating the probability of adverse drug reactions. Clin Pharmacol Ther. 1981; 30:239-245 4.

Lee A, Thomas SHL. Adverse drug reactions In: Walker R, Edwards C 'editors'. Clinical Pharmacy and Therapeutics. 3 rd edition. Philadelphia: Churchill Livingstone; 2003 ISBN 0-443-07138-1.5.

Stern RS, Chosidow OM, Wintroub BU. Cutaneous drug reactions Braulwald, Fauci, Kasper et al 'editor'. Harrison's Principles of Internal Medicine, 15th edition, New York; McGraw-Hill, Inc.; 2001 ISBN 0-07-007272-8. 6.

Ozkaya-Bayazit E, Bayazit H, Ozarmagan G. Drug related clinical pattern in fixed drug eruption. Eur J Dermatol 2000; 10(4):288-91.7.

Sehgal VN: Paracetamol-induced bilateral symmetric, multiple fixed drug eruption (MFDE) in a child. Pediatr Dermatol 1999; 16(2)165-166 8.

Cohen HA, Nussinovitch M, Frydman M. Fixed drug eruption caused by acetaminophen. Ann Pharmacother 1992; 26(12):1596-7 9.

Guin JD, Baker GF. Chronic fixed drug eruption caused by acetaminophen. Cutis 1988; 41 (2): 106-8 10. Galindo PA, Borja J, Feo F et al. Nonpigmented fixed drug eruption caused by paracetamol. Investig Allergo Clin Immunol 1999; 9(6):399-400.11.

Matheson I, Lunde PKM, Notarianni L. Infant rash caused by paracetamol in breast milk? (letter). Pediatrics 1985; 76:651-2 12. Harris A, Burge SM. Vasculitis in a fixed drug eruption due to paracetamol. Br J Dermatol 1995; 133(5):790-1.

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Preseptal cellulitis caused by Acinetobacter lwoffi

Preseptal cellulitis caused by Acinetobacter lwoffi

Mathews Divya, Mathews John P, Kwartz Jeff, Inkster Clare Department of Ophthalmology, Bolton Hospital NHS Trust, Bolton, United Kingdom

Correspondence Address: Mathews Divya Department of Ophthalmology, Bolton Hospital, NHS Trust, Minerva Road, Farnworth, Bolton, BL4 0JR United Kingdomdiv_doc@hotmail.com

Indian Journal of Opthalmology

Acinetobacter sp. are gram-negative bacteria that are commonly present in soil and water as free living saprophytes and are also isolated as commensals from the skin, throat and various secretions of healthy people. We treated a patient who had clinical signs of allergic conjunctivitis who was eventually found to have culture proven Acinetobacter calcoaceticus ar Lwoffi causing preseptal cellulitis.

A fifty-year old male Caucasian with no previous ocular history of infection, trauma, contact lens wear or medical problems was seen in the emergency clinic with a one-day history of painful swelling around the right eye. He gave no history of foreign body getting into the eye or any exposure to known allergens. On examination, he was afebrile. His visual acuity in each eye was 6/6. There was nontender periorbital oedema, conjunctival chemosis and papillary conjunctival reaction [Figure - 1]. There was no focus of infection in the adnexa of the right eye. The rest of the anterior segment was normal. Fundoscopy was normal and ocular motility was full. The left eye was unaffected. An initial diagnosis of allergic conjunctivitis was made and he was started on oral antihistamines and artificial tears. He showed no improvement during the next twenty-four hours during which time he developed conjunctival discharge. A conjunctival swab was taken from his right eye and chloramphenicol eye drops were applied simultaneously with the clinical diagnosis of bacterial conjunctivitis. On the third day, he presented with severe pain around the right periorbital region with no appreciable clinical improvement. Preauricular nodes on the right side were enlarged, but nontender. He was afebrile with vision of 6/6 in each eye and equally reactive pupils and full ocular movements. Microscopic examination showed no organism. Cultures on solid media including blood agar (aerobic) and chocolate agar (anaerobic) revealed 15-20 colonies of Acinetobacter calcoaceticus var Lwoffi, sensitive to g. amoxicillin and g.ofloxacillin and resistant to g.chloramphenicol. There were no other isolates from the swab. CT scan of the orbits showed soft tissue swelling in the right periorbital region consistent with preseptal cellulitis. The application of chloramphenicol eye drops was withdrawn and a combination of oral amoxicillin and clavulanic acid and ofloxacillin eye drops was administered. The infection resolved completely in two weeks.

Acinetobacter calcoaceticus var Lwoffi is a gram negative, non fermentative, aeroebic rod, ubiquitous in nature, a common part of human flora and an opportunistic pathogen.[1] A. calcoaceticus var Lwoffi isolated in the present case is an unusual case of preseptal cellulitis.

Fortunately, this patient recovered completely with no ocular or life-threatening complication with the appropriate medical therapy. A. calcoaceticus Lwoffi has been reported to cause trauma-induced endopthalmitis[2] and infectious crystalline keratopathy.[3]

To the best of our knowledge, this is the first case of preseptal cellulitis caused by A. calcoaceticus Lwoffi to be reported and should be considered as a causative agent in the differential diagnosis of preseptal cellulitis induced by gram negative organisms.

Cutaneous cryptococcosis cellulitis in a diabetic renal transplant recipient

R. K. Gupta1, Z. U. Khan2, M. R.N. Nampoory1, M. M. Mikhail1 and K. V. Johny3
1Mubarak Al-Kabeer Hospital, Ministry of Public Health, Kuwait 2,3Departments of Microbiology2 and Medicine3, Faculty of Medicine, Kuwait University, PO Box 24923, Safat, Kuwait 13110

Correspondence Z. U. Khan ziauddin@hsc.kuniv.edu.kw

Received June 25, 2003 Accepted January 5, 2004

A diabetic renal transplant recipient with cellulitis caused by Cryptococcus neoformans, serotype A, is described. The diagnosis was based on the demonstration of capsulated, budding yeast cells in the aspirated material and tissue from the cellulitic lesion and isolation of the aetiological agent in culture. The isolate formed well-developed capsules in the brain tissue of experimentally infected mice and produced cherry-brown colonies on niger seed medium. The patient's serum was positive for cryptococcal antigen (titre 1 : 4) with no other evidence of systemic infection. He was successfully treated with AmBisome, followed by fluconazole, resulting in the complete resolution of cellulitis and disappearance of the cryptococcal antigen. This report underscores the fact that patients with cutaneous cryptococcosis should be thoroughly evaluated, as it may be the first manifestation of a systemic disease. Prompt diagnosis and treatment are important to improve survival.

Abbreviations: BAL, bronchoalveolar lavage; PCC, primary cutaneous cryptococcosis.

Introduction

Cryptococcus neoformans is an encapsulated, basidiomycetous yeast that is present in the environment worldwide. It has been isolated from a large variety of natural substrates, especially soil contaminated with pigeon droppings (Khan et al., 1978; Li et al., 1993; Lopez-Martinez & Castanon-Olivares, 1995), decaying wood in tree trunk hollows (Lazera et al., 2000; Randhawa et al., 2003) and fruit and vegetables (Pal & Mehrotra, 1985; Lopez-Martinez & Castanon-Olivares, 1995). The main portal of entry is the respiratory tract, and lungs are the primary site of infection. In most instances, the infection is subclinical and self-limiting. However, the infection may be reactivated during immunosuppression of the host, particularly under the conditions of depressed T-cell-mediated immunity. The most important predisposing condition is AIDS (Pema et al., 1994; Mitchell & Perfect, 1995), but the disease can also occur in individuals receiving immunosuppressive therapy, such as patients with cancer, sarcoidosis, Hodgkin's lymphoma or those who have undergone organ transplantation (Mitchell & Perfect, 1995). Following haematogenous dissemination from the lungs, the central nervous system (CNS) and skin are the preferred sites of infection in about 6–15 % of patients (Powderly, 1993; Christianson et al., 2003). Primary cutaneous cryptococcosis (PCC) has also been reported in immunocompetent as well as immunocompromised individuals (Revenga et al., 2002; Neuville et al., 2003; Christianson et al., 2003).

Cryptococcosis from the Middle East has been sporadically reported (Abdel-Fattah et al., 1975; Al-Rasheed & Al-Fawaz, 1990; Sa'adah et al., 1995; Nampoory et al., 1996; Khan et al., 2003; Abdel-Salem, 2003). Of the three cases of cryptococcosis in renal transplant recipients from Kuwait reported previously, one had cutaneous lesions with CNS involvement, but chest X-rays were normal (Nampoory et al., 1996). In this communication, we describe a case of cutaneous cryptococcosis in a renal transplant recipient manifesting as cellulitis, which was the only sign of the disease when diagnosis was made.

Case Report

A 60-year-old Kuwaiti male underwent live-unrelated renal transplant in April 1988. Earlier, he had adult dominant polycystic kidney disease (ADPKD), which required pre-transplant bilateral nephrectomy. His post-transplant course was uncomplicated. He was maintained on triple immunosuppression comprising prednisolone, azathioprine and cyclosporine A with normal graft function. His serum creatinine levels were maintained between 110 and 120 µmol l–1. In 1992, he developed mild hypertension and diabetes mellitus that was adequately controlled by a calcium channel blocker and sulphonylurea derivatives. In May 2000, he developed a chest infection with bilateral pulmonary infiltrates caused by Haemophilus influenzae that was resolved completely by macrolides. Two years later, in February 2002, he presented with fever and features of cellulitis involving the calf region of the left leg (Fig. 1a). The examination revealed a tender, indurated, erythematous lesion, about 20 cm in diameter, with bullae formation. Clinically, he did not look toxic, and there was no evidence of lymphadenopathy or abdominal organomegaly. His lungs were clear and he showed no neurological deficit including meningeal signs. His total white blood cell count ranged between 6 and 8 x 109 l–1, platelet count was 160 x 109 l–1 and haemoglobin was 10.6 g dl–1. Blood coagulation profile, liver and renal function tests were within normal limits.

The summary of laboratory investigations is presented in Table 1. Since urine and blood cultures did not reveal any pathogen, he was empirically treated with parenteral third-generation cephalosporin, cloxacillin and clindamycin on the assumption that his cellulitis was probably of bacterial origin. However, no clinical improvement was observed with this therapeutic regimen. Subsequently, the infected area was debrided and the swab, tissue and aspirate were sent for microbiological examination. Direct microscopic examination of the aspirated material, swab smears and tissue showed poorly capsulated budding yeast cells and yielded C. neoformans in culture. The identity of the isolate was confirmed with the Vitek 2 yeast identification system, by the ability to produce brown colonies on niger seed agar at 28 °C, and by a mouse pathogenicity test which showed the formation of large capsulated yeast cells when examined 5 days post-intracerebral inoculation. His serum was positive for cryptococcal antigen (titre 1 : 4) by latex agglutination kit (Pastorex Crypto Plus; Bio-Rad). He was immediately given liposomal amphotericin B (AmBisome) at a dose of 3 mg kg–1 day–1. The isolate was susceptible to amphotericin B (0.016 µg ml–1) and fluconazole (2.0 µg ml–1) but resistant to flucytosine (> 16 µg ml–1) by E-test on RPMI agar (NCCLS, 1997). A week later, he developed bilateral chest infiltrates with drowsiness. A CT scan of his brain and cerebrospinal fluid (CSF) were normal. India ink examination of CSF was negative for C. neoformans and the pathogen did not grow in culture. The latex agglutination test for cryptococcal polysaccharides in CSF was also negative. However, his bronchoalveolar lavage (BAL) grew Pseudomonas aeruginosa. He was treated with meropenem, which resulted in complete resolution of the chest infiltrates. Since the patient responded to AmBisome, he continued to receive the drug for 21 days (total dose 4.8 g), followed by oral fluconazole (Diflucan) 200 mg daily for 4 months and then 100 mg daily for another 4 months. The patient's cellulitic lesion gradually resolved completely (Fig. 1b). When examined for the last time on 18 June 2003, he was afebrile and his renal and liver function parameters were within the normal range. He is being maintained on minimal triple immunosuppression regimen.

Discussion

Cutaneous cryptococcosis in most immunocompromised patients is a sign of disseminated disease (Thomas & Schwartz, 2001). However, critical analysis of the literature in two recent reviews (Neuville et al., 2003; Christianson et al., 2003) suggests that cutaneous cryptococcosis can also occur as a primary disease both in immunocompetent and immunocompromised individuals, where skin serves as the primary portal of entry. This observation is noteworthy since the existence of PCC as a distinct clinical entity has been controversial, despite some well-documented case reports (Goonetilleke et al., 1995; Hamann et al., 1997; Handa et al., 1998). C. neoformans has been shown to cause almost every type of cutaneous lesion. The lesions may occur as ulcers (Birkett & McMurray, 1976), pustules (Crounse & Lerner, 1958), granulomata (Crounse & Lerner, 1958; Rook & Woods, 1962), abscesses (Rook & Woods, 1962) and herpetiform or molluscum contagiosum-like lesions (Borton & Wintroub, 1984; Concus et al., 1988; Pema et al., 1994). Although a rarity, several cases of cellulitis have also been reported (Anderson et al., 1992; Gloster et al., 1994; Horrevorts et al., 1994), which appear to be mainly restricted to lower parts of the body, especially the legs (Horrevorts et al., 1994), as was seen in the present case. Based on the analysis of 28 cases of PCC, Neuville et al. (2003) proposed criteria for diagnosing this entity. According to these criteria, cutaneous lesions in secondary/disseminated disease are usually multiple and scattered, located both in clothed and exposed areas, whereas skin lesions characterizing PCC are solitary or confined to a limited area and located on unclothed areas. On the other hand, Christianson et al. (2003) reviewed 73 cases of PCC and drew a distinction in location of lesions between non-immunocompromised and immunocompromised individuals. Involvement of finger and facial sites was more commonly seen in non- immunocompromised hosts, whereas multiple sites of infection or infection localized to extremities of the lower body or to the trunk were seen more frequently in the immunocompromised patients.

Despite the asymptomatic nature of pulmonary cryptococcosis in most cases, symptoms are non-specific when manifested, and hence are not helpful in clinical diagnosis. Fever, dyspnoea, cough, chest pain or haemoptysis may be observed in about 18–54 % of patients (Campbell, 1996; Diamond, 1990). Since the organism has a preference to invade the CNS, meningitis or meningoencephalitis is often the first clinical evidence of infection. In severely immunocompromised patients, such as those with AIDS, meningeal signs may be subdued and inflammatory response in the CSF reduced, which may result in diagnostic delays. However, our patient had no pulmonary or meningeal signs or symptoms at the time of diagnosis of cutaneous cryptococcosis and culture of BAL and CSF were negative on repeated occasions (Table 1). Other preferred sites of C. neoformans infection include the urinary tract (prostate), bone and the skin. Some 20–30 % of transplant recipients may develop skin lesions weeks to months prior to development of CNS manifestations (Rubin, 1988). Our patient appears to fall into this category, since he had no CNS manifestations or positive CSF findings at the time of diagnosis, although he had a low cryptococcal antigen titre (1 : 4) in serum, which may be attributed either to an early stage of the disease or to the weakly capsulated nature of the strain, or both.

The dermatotropic characteristic of C. neoformans may vary depending upon the strain or serotype involved (Mitchell & Perfect, 1995; Dromer et al., 1996). Although our patient was infected with serotype A, it has been reported that serotype D has a greater propensity to cause skin lesions (Naka et al., 1995; Dromer et al., 1996). Besides dermatotropism, differences in temperature tolerance and geographical distribution between serotypes could be other factors (Chen et al., 2000; Martinez et al., 2001). In renal transplant recipients, infection due to C. neoformans occurs almost exclusively in the late post-transplant phase, from 4 months after transplantation and onwards. The incidence of the infection appears to vary between 0.8 and 5.8 % depending upon the type and intensity of immunosuppression used (Gallis et al., 1975, Nampoory et al., 1996; Husain et al., 2001). Our patient was on triple immunosuppression including prednisolone, and also had diabetes mellitus. Usage of corticosteroids has been found to be the most common risk factor in an analysis of 37 patients with PCC (Christianson et al., 2003). Recently, increased risk of dermatological presentation and decreased risk of CNS infection has been noted with the use of tacrolimus in solid organ transplant recipients (Husain et al., 2001). Cyclosporine A and tacrolimus have been shown to suppress the growth of C. neoformans in vitro by inhibiting the calcineurin pathway at 37 °C but not at 24 °C (Cruz et al., 2000). However, cyclosporine A fails to cross the blood–brain barrier effectively, while tacrolimus achieves a good CNS concentration. Thus, temperature-dependent inhibition of cryptococci by tacrolimus may prevent CNS infection, but allow the growth of the fungus at cooler body sites, such as the skin.

Regardless of the primary or secondary nature of cutaneous cryptococcosis, the most sensitive and specific approach for its diagnosis is microscopic examination and culture of a skin biopsy specimen or material aspirated from the skin lesion. Direct microscopic examination of the material in potassium hydroxide or India ink can reveal encapsulated yeast cells. Additional diagnostic evidence should be obtained to rule out systemic dissemination. This may include culture of sputum, BAL, CSF and urine (preferably after prostatic massage), as well as serological evidence for cryptococcal polysaccharide in serum and/or CSF specimens. Culture for C. neoformans should be positive in 3–7 days, colonies appearing as white to cream coloured with a mucoid consistency, but growth is inhibited by the presence of cycloheximide in the medium (Diamond, 1990). Being a basidiomycetous yeast, it is urease-positive. In addition, this yeast produces phenoloxidase, an enzyme that is associated with melanin synthesis, which turns the colour of the colonies brown on a medium containing a specific Dopa-like substrate, such as the one provided by niger seed medium. Capsular polysaccharide, urease and phenoloxidase are known virulence factors of C. neoformans and thus play an important role in the pathogenesis of the disease (Casadevall & Perfect, 1998).

Considering the asymptomatic nature of pulmonary cryptococcosis in the majority of cases, and the demonstration of a low antigen titre (1 : 4) in our patient, it may be inferred that he was probably in the early phase of a disseminated disease where the cutaneous lesion appeared as the first clinical manifestation. This observation is consistent with the prevailing view that all cases of cutaneous cryptococcosis in immunocompromised patients should be assumed to be due to disseminated infection until proved otherwise (Casadevall & Perfect, 1998). Such patients need aggressive antifungal chemotherapy. Our patient was given AmBisome for 3 weeks, followed by fluconazole. He responded to this therapy adequately, resulting in resolution of cellulitis and clearance of the cryptococcal antigen from the serum. Since the isolate was resistant to flucytosine and the patient had no meningeal involvement, this drug was not included in the treatment regimen. Primary resistance to flucytosine in clinical isolates of C. neoformans has been reported previously (Cuenca-Estrella et al., 2001; Kantarcioglu & Yucel, 2002).

Acknowledgements

The authors thank Rachel Chandy for excellent technical assistance.

References

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Journal of Microbiology

Cellulitis is NOT cellulite

CELLULITIS IS NOT CELLULITE

OK, so I am going to take a minute and express a pet peeve of mine.

In this blog world that I am new too, I found found there is an overwhelming amount of bad and/or fraudulent information.

Cellulitis is a serious, potentially life threatening bacterial infection. I have endured many massive infections throughout my life and have had complications and problems as a result. The infection can even lead to amputation of a limb, gangrene or death.

Cellulite is a fat condition and is totally unrelated.

As a person who has experienced cellulitis, I consider it fraud and internet abuse for these cellulite blogspots to spam the internet trying to capture readers by connecting the two words.

It is a shame they have such a lack of integrity.

Cellulitis in HIV Disease - Abstracts

Cellulitis and soft tissue infection in patients with HIV disease: epidemiological and microbiological features

[Article in Italian]

Manfredi R, Chiodo F.

Dipartimento di Medicina Clinica Specialistica e Sperimentale, Sezione di Malattie Infettive, Universit degli Studi di Bologna, Policlinico S. Orsola-Malpighi, Bologna.

In order to assess the epidemiological, microbiological, and clinical features of cellulitis and soft tissue infection occurring during the course of HIV disease, clinical and laboratory data of 2221 hospitalizations carried out since 1991 were retrospectively examined, and 67 bacteriologically-proven episodes of cellulitis-soft tissue infection were identified (3.02% of overall admissions). Among the 92 cultured pathogens, Staphylococcus aureus was the most frequent (46 cases), followed by Pseudomonas spp., Escherichia coli, and Streptococcus pyogenes; 38.1% of patients had a polymicrobial infection. i.v. drug use (p<.02) and the male gender (p<.05), were significantly associated with the occurrence of these complications, while a great variation in the severity of underlying immunodeficiency was shown. An elevated rate (83.6%) of episodes of cellulitis or soft tissue infection were community-acquired in origin; the comprehensive frequency of these episodes significantly dropped during the highly active antiretroviral therapy (HAART) era (p<.01). Limbs were involved in over 80% of episodes, and an hematogenous dissemination of bacterial infection (which occurred in 25.4% of cases), proved significantly related to a CD4+ lymphocyte count <100>

[PubMed - indexed for MEDLINE]

..........

Epidemiology and microbiology of cellulitis and bacterial soft tissue infection during HIV disease: a 10-year survey

Manfredi R, Calza L, Chiodo F.

Department of Clinical and Experimental Medicine, Division of Infectious Diseases, University of Bologna, S. Orsola Hospital, Bologna, Italy.

manfredi@med.unibo.it

BACKGROUND:

Cellulitis and soft tissue infection are underestimated complications of HIV disease.

PATIENTS AND METHODS:

Sixty-seven bacteriologically proven consecutive episodes were identified among 2221 HIV-infected patients hospitalized in a 10-year period, and assessed according to several epidemiological, microbiological and clinical variables.

RESULTS:

Staphylococcus aureus was the most frequently cultured pathogen (50% of 92 isolates), followed by Pseudomonas spp., Escherichia coli and Streptococcus pyogenes; a polymicrobial infection was present in 38.1% of episodes. Drug addiction (p <>

CONCLUSION:

Skin and soft tissue infections are continuing causes of morbidity in HIV-infected patients, even in the highly active antiretroviral therapy era.PMID: 11972714

[PubMed - indexed for MEDLINE]