Disseminated cryptococcosis initially presenting as cellulitis in a rheumatoid arthritis patient

Disseminated cryptococcosis initially presenting as cellulitis in a rheumatoid arthritis patient

J Chin Med Assoc. 2007 Jun
Lu HC, Yang YY, Huang YL, Chen TL, Chuang CL, Lee FY, Lee SD.
Department of Gastroenterology, Taipei Veterans General Hospital, Taipei, Taiwan, R.O.C.

Key Words: cellulitis, Cryptococcus neoformans, rheumatoid arthritis

Infection with Cryptococcus neoformans often occurs in immunocompromised hosts. It is usually acquired by invasion of the respiratory tract, and then the organisms may spread hematogenously to other viscera, mainly the central nervous system. Although there are some reports of primary cutaneous cryptococcosis, cryptococcal skin disease is a rare feature of disseminated cryptococcosis, and has a poor outcome if unrecognized and untreated. We present a case of cryptococcal cellulitis in a patient with rheumatoid arthritis who was receiving long-term steroid treatment.

Reviewing the literature, this is the first report of rheumatoid arthritis with disseminated cryptococcosis initially presenting as cellulitis.

Elsevier

Microbiology of acute sinusitis of odontogenic origin presenting with periorbital cellulitis in children.

Microbiology of acute sinusitis of odontogenic origin presenting with periorbital cellulitis in children.

Ann Otol Rhinol Laryngol. 2007 May

Brook I.
Department of Pediatrics, Georgetown University School of Medicine, Washington, DC, USA.

OBJECTIVES: This study was undertaken to evaluate the aerobic and anaerobic microbiology of acute maxillary sinusitis of odontogenic origin presenting with periodontal infection in children.

METHODS: Aspirates of 18 acutely infected maxillary sinuses that were associated with odontogenic infection in children who presented with periorbital cellulitis were processed for aerobic and anaerobic bacteria.

RESULTS: A total of 54 isolates were recovered (3.0 per specimen): 13 aerobic and facultative (0.7 per specimen) and 41 anaerobic (2.3 per specimen). The number of isolates per specimen varied from 1 to 4. Aerobic and facultative organisms alone were recovered in 2 specimens (11%), anaerobes only in 7 (39%), and mixed aerobic and anaerobic bacteria in 9 (50%). The predominant aerobic and facultative organisms were alpha-hemolytic streptococci (4), microaerophilic streptococci (3), and Streptococcus pyogenes and Staphylococcus aureus (2 each). The predominant anaerobic bacteria were anaerobic gram-negative bacilli (17), Peptostreptococcus spp (11), Fusobacterium spp (8), and Propionibacterium acnes (2). Twelve beta-lactamase-producing bacteria were recovered from 9 specimens (50%).

CONCLUSIONS: This study demonstrates the unique aerobic and anaerobic microbiological features of acute maxillary sinusitis of odontogenic origin presenting with periorbital cellulitis in children.

PMID: 17561769 [PubMed - in process]

Bacteriology of chronic sinusitis and acute exacerbation of chronic sinusitis

Arch Otolaryngol Head Neck Surg. 2006 Oct

Brook I.
Department of Pediatrics, Georgetown University School of Medicine, Washington, DC 20016, USA. ib6@georgetown.edu

OBJECTIVE: To establish the microbiological characteristics of acute exacerbation of chronic sinusitis (AECS).

SETTING: Academic medical center.

PATIENTS: Thirty-two patients with chronic sinusitis and 30 patients with AECS.

MAIN OUTCOME MEASURE: The aerobic and anaerobic microbiology of maxillary AECS and chronic maxillary sinusitis.

RESULTS: A total of 81 isolates (33 aerobic and 48 anaerobic) were recovered from the 32 cases (2.5 per specimen) with chronic sinusitis. Aerobes alone were recovered in 8 specimens (25%), anaerobes only were isolated in 11 (34%), and mixed aerobes and anaerobes were recovered in 13 (41%). The predominant aerobic and facultative bacteria were Enterobacteriaceae and Staphylococcus aureus. The predominant anaerobic bacteria were Peptostreptococcus subspecies, Fusobacterium subspecies, anaerobic gram-negative bacilli, and Propionibacterium acnes.

Twenty-one beta-lactamase-producing bacteria were recovered from 17 specimens (53%). A total of 89 isolates (40 aerobic and facultatives, and 49 anaerobic) were recovered from the 30 patients (3.0 per specimen) with AECS. Aerobes were recovered in 8 instances (27%), anaerobes only in 11 (37%), and mixed aerobes and anaerobes were recovered in 11 (37%). The predominant aerobes were Streptococcus pneumoniae, Enterobacteriaceae, and S aureus. The predominant anaerobes were Peptostreptococcus subspecies, Fusobacterium subspecies, anaerobic gram-negative bacilli, and P acnes. Thirty-six beta-lactamase-producing bacteria were recovered from 28 specimens (53%).

CONCLUSIONS: This study demonstrates that the organisms isolated from patients with AECS were predominantly anaerobic and were similar to those generally recovered in patients with chronic sinusitis. However, aerobic bacteria that are usually found in acute infections (eg, S pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis) can also emerge in some of the episodes of AECS.

Journal of Otolaryngology

Occult subcutaneous panniculitis-like T-cell lymphoma with initial presentations of cellulitis-like skin lesion and fulminant hemophagocytosis.

Occult subcutaneous panniculitis-like T-cell lymphoma with initial presentations of cellulitis-like skin lesion and fulminant hemophagocytosis.

Tzeng HE, Teng CL, Yang Y, Young JH, Chou G.

Division of Hematology/Oncology, Taichung Veterans General Hospital, Taichung, Taiwan.

Hemophagocytic syndrome (HPS) may be primary or secondary to malignancies, infections, autoimmune diseases, or drugs. In most cases, HPS occurs at the same time as the diagnosis of underlying malignancy or when it relapses. In rare situations, the neoplastic disease can be occult, even for more than a decade. Were port the case of a 28-year-old woman admitted because of HPS. Treatment with etoposide for fulminant HPS was effective. Four months later, she was admitted again because of newly developed subcutaneous nodules and cellulitis-like skin lesions over her legs. Excisional biopsy of subcutaneous nodule showed subcutaneous panniculitis-like T-cell lymphoma. After etoposide, solumedrol, cytosine arabinoside, and cisplatin regimen chemotherapy, both skin lesions and subcutaneous nodules disappeared. In conclusion, for patients presenting with HPS and cellulitis-like skin lesions, occult lymphoma should be considered, which might not be diagnosed for months, even years. Adequate treatment, including steroid and chemotherapy against malignant lymphoma, should be started as soon as possible for patients with fulminant HPS because of its fatal course.

Elsevier Health Asia

Preseptal and orbital cellulitis: a 10-year review of hospitalized patients.

Preseptal and orbital cellulitis: a 10-year review of hospitalized patients.

J Chin Med Assoc. 2006 Sep

Liu IT, Kao SC, Wang AG, Tsai CC, Liang CK, Hsu WM.
Department of Ophthalmology, Taipei Veterans General Hospital and National Yang-Ming University School of Medicine, Taipei, Taiwan, ROC.

BACKGROUND: Preseptal and orbital cellulitis range in severity from minor to potentially severe complications. The purpose of this study is to describe the clinical features of patients with preseptal or orbital cellulitis in one medical center in Taiwan, and to assess the effectiveness of treatments and the complications.

METHODS: Patients admitted between 1996 and 2005 to Taipei Veterans General Hospital under the diagnosis of preseptal or orbital cellulitis were retrospectively reviewed. The demographics, administrative history, past history, clinical presentations, treatments, and complications were analyzed.

RESULTS: In total, 94 patients fulfilling the diagnostic criteria for preseptal or orbital cellulitis were identified (67 had preseptal cellulitis, 27 had orbital cellulitis). While paranasal sinus disease was the most common predisposing cause in orbital cases, skin lesions in children and dacryocystitis in adults were the most common in preseptal cases. Microbiologic investigations showed variable results, but the most common pathogen isolated was Staphylococcus aureus. Cultures from eye swabs and local abscesses gave the highest positive yield. Blood cultures were taken in some patients, but the positive rate was extremely low. Treatments included intravenous antibiotics alone, or intravenous antibiotics combined with surgical drainage. Only one case had permanent ocular motility impairment after removal of the orbital foreign body.

CONCLUSION: Despite the past history of potential morbidity and even mortality from orbital cellulitis, early diagnosis and prompt treatment with proper antibiotics and/or surgical intervention can achieve a good prognosis.

Elsevier

Acute bacterial skin infections and cellulitis

Acute bacterial skin infections and cellulitis
Curr Opin Infect Dis. 2007 Apr
Gabillot-Carré M, Roujeau JC.
Hopital Henri Mondor, Créteil, France.

PURPOSE OF REVIEW: Acute bacterial skin infections are very common, with various presentations and severity. This review focuses on deep skin infections. We separate acute nonnecrotizing infections of the hypodermis (erysipelas), forms with abscesses or exudates and necrotizing fasciitis. These three types actually differ in risk factors, bacteriology, treatment and prognosis.

RECENT FINDINGS: Leg erysipelas/cellulitis occurs in more than one person/1000/year. It remains mainly due to streptococci. Foot intertrigo is an important risk factor. Necrotizing fasciitis is much rarer and usually occurs in patients with chronic diseases. Staphylococci, especially community-acquired methicillin-resistant strains in some areas, play a growing role in the intermediate form of cellulitis with abscesses and exudates. For erysipelas or noncomplicated cellulitis, antibiotic treatment at home, when feasible, is much less expensive and as effective as hospital treatment. Intermediate cases with collections and exudates often require surgical drainage. For necrotizing fasciitis early surgery remains essential in order to decrease the mortality rate.

SUMMARY: Antibiotic treatment of deep skin infections must be active on streptococci; the choice of a larger spectrum of activity depends on clinical presentation, risk factors and the burden of methicillin-resistant staphylococci in the environment.

Lippincott, Williams & Wilkins

Sweet's syndrome associated with cellulitis

Sweet's syndrome associated with cellulitis

Australasian Journal of Dermatology

May 2007

Hope Dinh, Anand Murugasu and Douglas Gin
Departments of 1Dermatology and 2Anatomical Pathology, The Alfred Hospital, Prahran, Victoria, Australia

Dr Hope Dinh, Department of Dermatology, The Alfred Hospital, Prahran, Vic. 3181, Australia. Email: hopevudinh@yahoo.com

A 38-year-old woman developed an acute, painful cutaneous eruption on her lower legs, neck, chest and fingers while receiving a number of oral and intravenous antibiotics for left leg cellulitis caused by trauma. Clinically and histopathologically, she was diagnosed with Sweet's syndrome with typical pseudovesicular skin changes in conjunction with erythema nodosum-like lesions on her lower legs. She responded quickly to oral prednisolone. We propose Staphylococcal cellulitis as a cause of Sweet's syndrome.

Blackwell Synergy

Sweet's Syndrome

Sweet's syndrome, or acute febrile neutrophilic dermatosis, is a condition characterized by the sudden onset of fever, leukocytosis, and tender, erythematous, well-demarcated papules and plaques which show dense neutrophilic infiltrates on histologic exam ination. Although it may occur in the absence of other known disease, Sweet's syndrome is often associated with hematologic disease (including leukemia), and immunologic disease (rheumatoid arthritis, inflammatory bowel disease). Treatment with systemic corticosteroids is usually successful.

Sweet's syndrome, which was described by R.D.Sweet in 1964, is characterized by the sudden onset of fever, leukocytosis, and cutaneous eruption. The eruption consists of tender,erythematous, well-demarcated papules and plaques which show dense neutrophilic infiltrates microscopically. The lesions may appear anywhere, but favor the upper body including the face. [1] The individual lesions are often described as pseudovesicular or pseudopustular, but may be frankly pustular, bullous, or ulcerative. Oral and eye involvement (conjunctivitis or episcleritis) have been frequently reported. Arthralgias or arthritis are present in 33-62 percent. [2] Alveolitis, sterile osteomeyelitis, renal, hepatic, and central nervous system involvement have been reported.[3] The condition is more common in women and the mean age of onset is the mid to late fifties. Sweet's syndrome may last from one week to more than four years. Recurrance is common (25-37%).
Clinical Presentations

Clinical findings of Sweet's syndrome
Skin
Other Organs
Sudden/often recurrant(25-35%)
Well-demarcated, tender,erythematous,papules and/or plaques
Favors face,upper body,but may be located anywhere
Pseudovesicular,pseudopustularvesicles,pustules,bullae
Oral mucosa
Arthralgia/arthritis (33-62%)
Eye(conjunctivitis/episcleritis)
Lungs(alveolitis)
Kidney
Liver
Bone(sterile osteomyelitis)
Central Nervous System

Histopathology

A dense, perivascular, neutrophilic infiltrate is the hallmark of Sweet's syndrome.[4] Leukocytoclasis may be seen. Mononuclear cells and occasional eosinophils may be interspersed. The inflammatory cells form a band-like infiltrate in the papillary dermis. Dermal edema may be seen which may eventuate in subepidermal bulla formation. In neutropenic states the infiltrates may be less neutrophilic.

Histology

Dense perivascular,neutrophilic infiltrateLeukocytoclasia may be presentOccasionally interspersed with monos/eosBandlike papillary dermal infiltrateDermal edema may eventuate in bulla

Etiology/Pathogenesis

The etiology of Sweet's syndrome is unknown, though it is presumed to be a type of hypersensitivity reaction which leads to stimulation of a cascade of cytokines that precipitate neutrophil activation and infiltration.[2,4,5, 6] A T-cell mediated immune response has been postulated.[7] HLA analyses have given variable results. Mizoguchi[8] described an increase in the frequency of HLA Bw54 in Japanese patients with Sweet's syndrome. However, recently in a series of 41 European, caucasian patients, no significant HLA associations were found.[9]

Differential Diagnosis

Bowel bypass-related dermatosis
Cellulitis/erysipelas
Disseminated erythema nodosum
Erythema elevatum diutinum
Erythema multiforme
Leukocytoclastic vasculitis
Pyoderma gangrenosum

Associated Diseases

Von den Dreisch[2] summarized seven series and catagorized Sweet's syndrome cases into four groups: classic/idiopathic(71%), parainflammatory(16%), paraneoplastic(11%), and pregnancy-related(2%). However, more recently, in a large series of patients from Mayo Clinic, 54% had either a a malignancy or some type of hematologic disease.[3] The classic/idiopathic form has a significant female predominance whereas the malignant form does not.[2] In addition, paraneoplastic Sweet's syndrome is more likely to show slightly atypical lesions with more pustular/bullous forms as well as a greater localization to the upper body and face.[3] Paraneoplastic cases are most commonly associated with hematologic malignancies, though a wide variety of solid tumors are also found.[2] In one study, 160f patients who had no evidence of malignancy at presentation developed a malignancy within a year.[6] Hence, Sweet's syndrome may develop very early in the course of a malignancy, possibly at a curable stage. The Mayo Clinic series found 190f cases to have an associated immunologic disease which included relapsing polychondritis, rheumatoid arthritis, d ermatomyositis, non-specific connective tissue disease, and inflammatory bowel disease.[3] A variety of infections have been associated with the syndrome, and these include upper respiratory infections, urinary tract infections, viral pneumonia, Yersinia infection, typhus, salmonellosis, toxoplasmosis, tuberculosis and other mycobacterial infections, histoplasmosis, cytomegalovirus infections, tonsillitis, hepatitis, vulvovaginitis, and Helicobacter pylori infection.[2,3,11] In addition,drug-related cases have been recognized.[12] Granulocyte-Colony Stimulating Factor(G-CSF) has been reported to precipitate Sweet's syndrome as well as other neutrophilic dermatoses.[13,14,15] Chemotherapy with all trans-retinoic acid also stimulated Sweet's syndrome, which occurred concommitantly with the neutrophilic differentiation induced by the drug.[16] Trimethoprim-sulfamethoxazole, hydralazine, oral contraceptives, minocycline, Lithium, and furosemide have all been reported as offending drugs.[2,12,17] About 20f cases have been associated with pregnancy.[2,18] Onset was in the first or second trimester and most cases resolved spontaneously. No fetal mortality or morbidity occurred.

Laboratory/Special Examinations

he erythrocyte sedimentation rate is said to be elevated in most patients with Sweet's disease. The white blood cell cournt is said to be greater than 8000 in 80%, and greater than 10000 in 600f affected individuals.[2] Neutrophilia is less commonly found in association with drug-related causes.[12] Anemia and elevated alkaline phosphatase are present about half the time. The presence of anemia and low platelet count have been associated with an underlying malignancy.[10] Patients with Sweet's syndrome should undergo an age-appropriate work-up for malignancy. Earlier reports suggested an association of Sweet's disease with ANCA positivity, however further evaluation has cast doubt on this association.[2]

Management

Systemic Corticosteroids
Systemic corticosteroids have been the treatment of choice in most large series of patients reported.[2,3,19] Generally prednisone or prednisolone is used with an initial dose of 0.5-1.5 mg per kg per day. Reduction is begun within two to four weeks.[2] A good response can be anticipated with resolution of malaise within hours and mucosal lesions and fever within two days.[2] Skin lesions should resolve within one to four weeks.[2,3] However, recurrance is common (25%). Chronic relapsing disease is seen in about 15%.[2]
Topical Corticosteroids
Topical and intralesional corticosteroids have frequently been used as adjunctive treatment along with systemic modalities. They are occasionally used as solo therapy and can be effective in mild cases.[3,4]
Non-steroidal Anti-inflammatory Drugs
Indomethacin appears promising as an alternative to corticosteroids. It was first reported as useful in 1977.[20] Most recently,17/18 patients responded with clearing to indomethacin.(6) No recurrances were noted in a mean follow-up of 20 months. The dosage used was as follows: 150 mg per day for one week, 100 mg per day for two weeks. Indomethacin was then stopped. Fever and arthralgia were attenuated within 48 hours. The eruption clea red within 7-14 days. Naproxen was used successfully in one patient with CML.[21]
Potassium Iodide
Some authors state that potassium iodide may be as effective as corticosteroids and that relapses may be less frequent.[2] However, the reports of KI use tend to be older and smaller numbers of patients were treated than in reports utilizing corticosteroids. Nevertheless, several studies have shown effective clearing with the use of KI.[19,22,23,24] In these studies, 900 mg per day was initiated. Symptoms improved within 48 hours and cutaneous lesions cleared within one week in most cases. In some cases the drug was withdrawn after only 2 weeks and no recurrance was seen.[22] Two patients developed a severe vasculitis that was attributed to KI.
Cyclosporine
Several cases have been reported to respond to cyclosporine.[26,27,28] Initial doses have varied widely, from 2-10 mg per kg per day. Response was rapid (within one week). Tapering was difficult in some cases.
Doxycycline
Joshi [29] reported two cases of successful treatment with doxycycline. Treatment was initiated with 100 mg BID. The lesions resolved within 3-4 weeks. Doxycycline was stopped after 6-8 weeks. No recurrances were noted in either patient, but follow up time was not stated.
Dapsone
A few cases have responded to the use of dapsone in doses of 100-200 mg per day.[3,30] It has also been used in combination with prednisone.[3,19] However, it has also been reported as a failure.[24]
Colchicine
Colchicine has been effective in a few case reports.[31,32] The initial dose used was 0.5 mg TID. Usually the drug could be stopped in seven days. Alternatively, the dosage could be tapered over three weeks. However, others found it to be ineffective.[3]
Clofazamine
Clofazamine has been used in only a few cases, but appeared effective in doses of 200 mg per day.[2,33] Improvement began within one week, but it is unclear how long treatment was continued.
Pentoxifylline
Pentoxifylline was given as a trial at 400 mg TID in two patients with Sweet's syndrome, but neither responded.[34]

Dermatology OnLine