Sunday, March 31, 2013

Prevalence of concurrent deep vein thrombosis in patients with lower limb cellulitis: a prospective cohort study.

Prevalence of concurrent deep vein thrombosis in patients with lower limb cellulitis: a prospective cohort study.

Mar 2013

Source

Department of Infectious Diseases, Christchurch Hospital, Christchurch, 8002, New Zealand. Michael.Maze@cdhb.health.nz.

Abstract

BACKGROUND:

Lower limb cellulitis and deep vein thrombosis share clinical features and investigation of patients withcellulitis for concurrent DVT is common. The prevalence of DVT in this group is uncertain. This study aimed to determine the prevalence of deep vein thrombosis (DVT) in patients with lower limb cellulitis and to investigate the utility of applying the Wells algorithm to this patient group.

METHODS: Patients admitted with lower limb cellulitis prospectively underwent a likelihood assessment for DVT using the Wells criteria followed by investigation with D-dimer and ultrasonography of ipsilateral femoral veins as appropriate. Diagnoses of contralateral DVT or pulmonary embolism during admission were recorded.

RESULTS:

200 patients assessed for DVT. 20% of subjects were high risk by Wells criteria. D-dimer was elevated in 74% and 79% underwent insonation of the affected leg. Ipsilateral DVT was found in 1 patient (0.5%) and non-ipsilateral VTE in a further 2 (1%).

CONCLUSIONS:

Deep vein thrombosis rarely occurs concurrently with lower limb cellulitis. The Wells score substantially overestimates the likelihood of DVT due to an overlap of clinical signs. Investigation for DVT in patients with cellulitis is likely to yield few diagnoses and is not warranted in the absence of a hypercoaguable state.

TRIAL REGISTRATION:

ACTRN: 12610000792022 (https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=320662).


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Sunday, March 03, 2013

Genetic susceptibility to non-necrotizing erysipelas/cellulitis.

Genetic susceptibility to non-necrotizing erysipelas/cellulitis.

2013

Source

Department of Medical Genetics, University of Helsinki, and Folkhälsan Institute of Genetics, University of Helsinki, Helsinki, Finland.

Abstract


BACKGROUND:

Bacterial non-necrotizing erysipelas and cellulitis are often recurring, diffusely spreading infections of the skin and subcutaneous tissues caused most commonly by streptococci. Host genetic factors influence infection susceptibility but no extensive studies on the genetic determinants of human erysipelas exist.

METHODS:

We performed genome-wide linkage with the 10,000 variant Human Mapping Array (HMA10K) array on 52 Finnish families with multiple erysipelas cases followed by microsatellite fine mapping of suggestive linkage peaks. A scan with the HMA250K array was subsequently performed with a subset of cases and controls.

RESULTS:

Significant linkage was found at 9q34 (nonparametric multipoint linkage score (NPL(all)) 3.84, p = 0.026), which is syntenic to a quantitative trait locus for susceptibility to group A streptococci infections on chromosome 2 in mouse. Sequencing of candidate genes in the 9q34 region did not conclusively associate any to erysipelas/cellulitis susceptibility. Suggestive linkage (NPL(all)>3.0) was found at three loci: 3q22-24, 21q22, and 22q13. A subsequent denser genome scan with the HMA250K array supported the 3q22 locus, in which several SNPs in the promoter of AGTR1 (Angiotensin II receptor type I) suggestively associated with erysipelas/cellulitis susceptibility.

CONCLUSIONS:

Specific host genetic factors may cause erysipelas/cellulitis susceptibility in humans.

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Wednesday, February 20, 2013

Serratia marcescens: an unusual pathogen associated with snakebite cellulitis.


Serratia marcescens: an unusual pathogen associated with snakebite cellulitis.


Feb 2013 

Source

Sri Devaraj Urs Academy of Higher Education and Research, Tamaka, Kolar, India. mjchand@gmail.com.

Abstract

This study reports a case of Serratia marcescens cellulitis following a snakebite in a 50-year-old woman. The bite was on the dorsum of the right hand with symptoms of envenomation. She developed swelling and cellulitis with tissue necrosis. Wound debridement was performed.  Pus and tissue biopsy cultures yielded Serratia marcescens sensitive to fluoroquinolones, aminoglycosides, third-generation cephalosporins and carbapenems. The patient responded to anti-snake venom (ASV) therapy, ciprofloxacin, local wound management and recovered uneventfully.
Full Text Article

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Saturday, February 16, 2013

Innate immune cocktail partially protects broilers against cellulitis and septicemia.

Innate immune cocktail partially protects broilers against cellulitis and septicemia.

2012

Source

Vaccine and Infectious Disease Organization (VIDO), International Vaccine Centre (Intervac), University of Saskatchewan, 120 Veterinary Road, Saskatoon, SK, Canada, S7N 5E3.

Abstract

Antimicrobial/host defense peptides (A/HDP) are natural compounds that are found in leucocyte cells and on the skin and bodily fluids of birds, reptiles, and mammals. Not only do they possess antibacterial, antiviral, and antiparasitic characteristics but they also stimulate the host immune system to combat infectious diseases and may play a role in the promotion of wound repair. Gamma-amino butyric acid (GABA) is an amino acid-based inhibitory neurotransmitter in the brain that has also been shown to promote wound healing on skin. The objective of this study was to establish a therapeutic cocktail that protects birds against Escherichia coli-related disease and lesions in broilers. We injected a cocktail of six A/HDPs with or without GABA into 3-wk-old broilers by a subcutaneous or intramuscular route followed 24 hr later by challenge with a field isolate of serogroup O2 E. coli. Birds were examined for 5-6 days post-E. coli challenge and clinical, pathologic, and bacteriologic assessments were conducted. Birds that were subcutaneously injected with an A/HDP plus GABA cocktail had significantly higher survival rates and lower levels of bacteremia (P < 0.05), but a similar percentage of the surviving birds had large cellulitis lesions compared to the surviving phosphate-buffered saline-injected control birds. When this cocktail was administered intramuscularly, there was a trend towards protection against E. coli-related death, although the results were not statistically significant and there was no reduction in bacteremia. A significant number of birds had a reduced bacterial load on cellulitis lesions but no reduction in lesion size, which suggests that when the cocktail was administered intramuscularly it failed to protect against cellulitis. These results suggest that the route of administration of the cocktail influences disease outcome. Gene expression analysis was performed to investigate whether the cocktail induced immunomodulatory functions in avian cells that complemented their antimicrobial and anti-endotoxic effects. A/HDP plus GABA mediated temporal induction of pro-inflammatory cytokines but no induction of any of the chemokines under investigation. This cocktail shows potential to protect against E. coli-related death, which is a major economic burden to the poultry industry.

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Wednesday, January 30, 2013

Primary cutaneous Nocardia brasiliensis cellulitis in immunocompetent child


Primary cutaneous Nocardia brasiliensis cellulitis in immunocompetent child


2012

[Article in Hebrew]

Source

Pediatric Infectious Disease Unit, Meyer Children's Hospital, Rambam Health Care Campus, Haifa, Israel. y_shahor@rambam.health.gov.il

Abstract


Primary cutaneous nocardiosis is an infrequent infection among children, generally affecting immunocompromised hosts. It is caused by Gram positive bacteria, partially alcohol and acid resistant which are saprophytes of the soil, water and organic matter. In most cases the causal agent enters through inhalation, and hematogenous dissemination may occur mainly among the immune compromised patients. Direct cutaneous inoculation is less frequent, especially among children. We report an 8-year old female who lives in an urban house with a small garden, who presented with an ulcer on her right shin accompanied by surrounding cellulitis, pain, swelling and fever. The patient's medical history was unremarkable, with no exposure to animals or travelling, except for rafting on the Jordan River the previous week. Culture from the ulcer grew Nocardia brasiliensis, and she recovered after 8 weeks of therapy with trimethoprim-sulphamethoxazole.

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Necrotizing cellulitis of the abdominal wall, caused by Pediococcus sp., due to rupture of a retroperitoneal stromal cell tumor.


Necrotizing cellulitis of the abdominal wall, caused by Pediococcus sp., due to rupture of a retroperitoneal stromal cell tumor.


Jan 2013

Source

3rd Department of Surgery, Aristotle University of Thessaloniki, AHEPA University Hospital, Thessaloniki, Greece. Electronic address: nickos.michalopoulos@gmail.com.

Abstract


INTRODUCTION:

Soft tissue necrotizing infections are a significant cause of morbidity and mortality. The aim of this study is to present a patient with necrotizing infection of abdominal wall resulting from the rupture of a retroperitoneal stromal tumor.

PRESENTATION OF CASE:

We present a 60-year-old Caucasian male patient with necrotizing infection of abdominal wall secondary to the rupture of a retroperitoneal stromal tumor. The patient was initially treated with debridement and fasciotomy of the anterior abdominal wall. Laparotomy revealed purulent peritonitis caused by infiltration and rupture of the splenic flexure by the tumor. Despite prompt intervention the patient died 19 days later. The isolated microorganism causing the infection was the rarely identified as cause of infections in humans Pediococcus sp., a gram-positive, catalase-negative coccus.

DISCUSSION:

Necrotizing infections of abdominal wall are usually secondary either to perineal or to intra-abdominal infections. Gastrointestinal stromal cell tumors could be rarely complicated with perforation and abscess formation. In our case, the infiltrated by the extra-gastrointestinal stromal cell tumor ruptured colon was the source of the infection. The pediococci are rarely isolated as the cause of severe septicemia.

CONCLUSION:

Ruptured retroperitoneal stromal cell tumors are extremely rare cause of necrotizing fasciitis, and before this case, Pediococcus sp. has never been isolated as the responsible agent.

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Monday, January 21, 2013

Disseminated Cryptococcosis presenting as cellulitis in a renal transplant recipient.


Disseminated Cryptococcosis presenting as cellulitis in a renal transplant recipient.


Jan 2013

Source

Apollo BGS Hospitals, Mysore, Karnataka, India. drchayadr17@yahoo.com.

Abstract


Cellulitis is an unusual presentation of  renal transplant  in renal allograft recipients. In such patients, disseminated cryptococcal infection can result in significant morbidity and mortality. Patients are often treated with antibiotics before a definitive diagnosis is made, delaying appropriate therapy. We describe the case of a 43-year-old post renal transplant recipient presenting with fever and swelling in the right thigh. On physical examination, the patient was found to have features suggestive of cellulitis with minimal slurring of speech. Material obtained from incision and drainage of the wound showed yeast cells resembling Cryptococcus spp. Blood culture and cerebrospinal fluid culture were also found to have growth of Cryptococcus neoformans. He received treatment with amphotericin B 6 mg/kg daily intravenously for two weeks, then continued with fluconazole 400 mg daily for three months. The patient showed a remarkable improvement. There was no recurrence of cryptococcosis after four months of follow-up. The diagnosis of disseminated cryptococcosis should be considered in differential diagnosis of cellulitis among non HIV immunocompromised hosts. A high clinical suspicion and early initiation of therapy is needed to recognize and treat patients effectively.

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Saturday, December 29, 2012

Cellulitis lesions in broiler chickens are induced by Escherichia coli Vacuolating Factor (ECVF).


Cellulitis lesions in broiler chickens are induced by Escherichia coli Vacuolating Factor (ECVF).


Nov 2012

Source

Departamento de Genética, Evolução e Bioagentes, Instituto de Biologia, Universidade Estadual de Campinas (UNICAMP), Rua Monteiro Lobato, 255, Campinas, SP, CEP 13083-862, Brazil.

Abstract

Keywords

  • APEC; 
  • Avian cellulitis; 
  • Escherichia coli Vacuolating Factor (ECVF); 
  • Purification; 
  • Cytokines; 
  • Inflammatory response; 
  • Dermatopathology

Escherichia coli Vacuolating Factor (ECVF) is a heat-labile, vacuolating cytotoxin produced by avian pathogenic E. coli (APEC) isolated from avian cellulitis lesions. In this report, we intend to demonstrate that purified ECVF induces the inflammatory process of cellulitis. Our group is the first to demonstrate the effect of ECVF in a histological analysis by in situ inoculation of broiler chickens with purified ECVF. The animals were inoculated with the APEC AC53 and with purified ECVF subcutaneously on their ventral surface (in the sternum region). The histological analysis showed different grades of an acute inflammatory response in the epidermis, dermis and panniculus. An increase in mRNA expression of the proinflammatory cytokine TNF-α was also demonstrated in the inflamed tissue. When ECVF was systemically administered, increased levels of TNF-α and IL-10 were observed in the serum. These results suggest that ECVF plays a key role in the inflammatory process associated with cellulitis that is mainly mediated by TNF-α. In addition, this inflammation can be down regulated by the anti-inflammatory. 
cytokine IL-10.

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Tuesday, December 25, 2012

Genome Sequence of the Human-Pathogenetic Bacterium Vibrio vulnificus B2.



Genome Sequence of the Human-Pathogenetic Bacterium Vibrio vulnificus B2.


Dec 2012


Abstract

Vibrio vulnificus, which can lead to rapidly expanding cellulitis or septicemia, is present in the marine environment. Here, we present the draft genome sequence of strain B2, which was isolated from a septicemia patient in 2010.

Genome Announcement

Vibrio vulnificus is a human-opportunistic, Gram-negative pathogen, which is always present in marine environments and has been isolated from sediments, water, and many kinds of seafood, such as shrimp, fish, and oysters. This bacterium is highly lethal (>50%) and has been reported to be the leading cause of seafood-borne death in the United States (3). It has also been widely isolated from Chinese seafood markets (14). Infection with this bacterium can lead to rapidly expanding cellulitis or septicemia in predisposed individuals .......

Full Text Article

Journal of Bacteriology

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Wednesday, December 19, 2012

A case of community-acquired Acinetobacter junii-johnsonii cellulitis


A case of community-acquired Acinetobacter junii-johnsonii cellulitis.


Jun 2012

Source

Division of Infectious Diseases, University of Colorado, Denver, USA.

Abstract


Key words: Acinetobacter, cellulitis, community-acquired infections, bacteremia, blister, therapy.

Acinetobacter skin and soft tissue infection outside of the traumatic wound setting are rare occurrences. The majority of cases occur in the presence of significant comorbilities and by Acinetobacter baumanii. Herein a case is reported of community-onset, health-care-associated, non-traumatic cellulitis caused by Acinetobacter, species junii-johnsonii with bacteremia. This is the first reported case of Acinetobacter junii-johnsonii skin and soft tissue infection. Hemorrhagic bullae might be one of the clinical features of Acinetobacter cellulitis.
Case report 
In August 2010, a 48 year old man with a history of metastatic, stage IV, prostate cancer was admitted to the University of Colorado Hospital after being transferred from an outside hospital. The case was complicated by bladder obstruction, T8 fracture, spinal cord involvement and had been treated with androgen-deprivation therapy and local radiation therapy. The patient had been admitted one month prior to this presentation with a pulmonary embolus, methicillin-sensitive Staphylococcus aureus (MSSA) bacteremia of unclear origin and also with a multidrug resistant (MDR) Serratia marcescens urinary tract infection. The patient recovered from that episode and was discharged to his home on intravenous (IV) ertapenem, 1gram every 24 hours. Several weeks later, the patient was readmitted to an outside hospital after developing a rapid progression of symptoms characterized by the following: marked fatigue, light headedness, fever, chills and right lower extremity swelling, erythema, tenderness and warmness. On admission the patient was found to be in septic shock, requiring intensive care unit care. He received aggressive fluid resuscitation therapy and pressor support; and he was placed empirically on IV vancomycin, piperacillin-tazobactam and levofloxacin. His hemodynamic parameters improved over the next two days, and he was transferred to our hospital with the documentation of a non fermenting gram negative rod (GNR) in blood culture (1 of 2 bottles). Computerized tomography (CT) scan of his leg showed a marked subcutaneous edema. The positive culture was from a peripheral site. The physical examination was remarkable for marked right lower extremity swelling, with erythema involving the distal 2/3 of the leg, and local tenderness, warmness and the presence of a purpuric rash and hemorrhagic bullae. The PICC line was present and was without local signs of inflammation. The laboratory tests were significant for leukopenia, anemia and thrombocytopenia. The gram negative rod was a nonmotile, catalase-positive, oxidase-negative bacteria; finally identified using the Vitek 2 system (an automated system for bacterial identification using a phenotypic approach) as Acinetobacter junii-johnsonii, sensitive to quinolones and B-lactams, and intermediate to aztreonam. His antibiotic therapy was narrowed to Levofloxacin only, and the patient was discharged 4 days later. He was seen again in the clinic 4 weeks later; complete resolution of his local right leg inflammatory changes were noted.

Full text with diagnostic images:


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Tuesday, December 11, 2012

Campylobacter fetus infection presenting with bacteremia and cellulitis in a 72-year-old man with an implanted pacemaker: a case report.


Campylobacter fetus infection presenting with bacteremia and cellulitis in a 72-year-old man with an implanted pacemaker: a case report.


Nov 2012

Abstract


INTRODUCTION: Campylobacter is an important causative agent of intestinal infections in humans. Bacteremia is detected in less than 1% of patients, mainly in immunocompromised patients and in extreme age groups. Cellulitis is a relatively common manifestation of Campylobacter infection, but concomitant bacteremia is a rare event. Infections of the pacemaker area are caused primarily by staphylococci, followed by fungi, streptococci and Gram-negative rods. To the best of our knowledge, this is the first case report of pacemaker pocket infection and bacteremia caused by Campylobacter fetus.

CASE PRESENTATION:

A 72-year-old Croatian Caucasian man with myelodysplasia, impaired fasting glucose levels and a recently implanted permanent pacemaker was admitted to hospital after six days of fever, development of red swelling of the pacemaker pocket area and worsening of his general condition. No antibiotic therapy was introduced in the outpatient setting. He denied any recent gastrointestinal disturbances. With the exception of an elevated leukocyte count, erythrocyte sedimentation rate, and C reactive protein and blood glucose levels, other laboratory findings were normal. Treatment with vancomycin plus netilmicin was introduced, and a surgical incision with drainage of the pacemaker pocket was performed. The entire pacemaker system was removed and a new one re-implanted after 14 days of antibiotic therapy. Transesophageal echocardiography showed no pathological findings. Three subsequent blood cultures obtained on admission as well as swab culture of the incised pacemaker area revealed Campylobacter fetus; stool and pacemaker lead cultures were negative. According to the microbiological results, antibiotic therapy was changed to ciprofloxacin plus netilmicin  A clinical examination and the results of a laboratory analysis performed after two weeks of therapy were within normal limits.

CONCLUSION:

Myelodysplasia, impaired fasting glucose levels and older age could be contributing factors for the development of bacteremic Campylobacter fetus cellulitis. Emergent surgical and antibiotic treatment are mandatory and provide the optimal outcome for such types of pacemaker pocket infection.

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Sunday, December 09, 2012

Risk factors for abscess formation in patients with superficial cellulitis (erysipelas) of the leg.


Risk factors for abscess formation in patients with superficial cellulitis (erysipelas) of the leg.


Dec 2012

Source

Department of Dermatology, Inserm U905, Institute for Research and Innovation in Biomedicine (IRIB), Rouen University Hospital, University of Normandy, Rouen, France Nutrition unit and EA4311, Institute for Research and Innovation in Biomedicine (IRIB), Rouen University Hospital, University of Normandy, Rouen, France.

Abstract


Background:  Superficial cellulitis of the leg (erysipelas) is a frequent skin infection. Abscess formation is the most frequent local complication. Determinants of abscess formation in patients with leg cellulitis have not been clearly established yet. 

The aim of this study was to assess risk factors for abscess formation in patients with leg cellulitis.

Patients and methods:  The clinical, biological and bacteriological records of all patients referred to the Dermatology Department of a University Hospital for superficial cellulitis of the leg during a 3-year period were retrospectively reviewed. Using univariate and multivariate analysis, main patients' characteristics at baseline were compared between the group of patients who developed abscess and the group who did not. 

Results:  One-hundred-and-sixty-four patients (93 females, 71 males) of mean age 65±18 years were included. Abscess occurred in 13 cases (8%). The following general factors were positively associated with abscess formation: male gender, smoking, alcohol abuse, delayed introduction of antibiotic treatment. Based on multivariate analysis, only chronic alcohol abuse (OR=4.3, 95%CI:1.08-20.57) and delayed antibiotic treatment initiation (OR=1.4, 95%CI:1.02-2.04) remained independently associated with abscess formation. 

Conclusion:  Alcohol abuse and delayed initiation of antibiotic treatment are risk factors for abscess formation in patients with cellulitis of the leg. Patients with these predictors must be monitored carefully for abscess formation.

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Friday, November 30, 2012

The risk of cellulitis in cirrhotic patients: a nationwide population-based study in taiwan.


The risk of cellulitis in cirrhotic patients: a nationwide population-based study in taiwan.


Oct 2012

Source

Department of Family Medicine, Buddhist Dalin Tzu Chi General Hospital, Chiayi, Taiwan. ; Tzu Chi University School of Medicine, Chiayi, Taiwan.

Abstract


BACKGROUND/AIMS:

Cellulitis is a common infectious disease. However, the risk of cellulitis in cirrhotic patients is not well established, and whether liver cirrhosis is a risk factor for cellulitis remains unknown. This study evaluated the relationship between cellulitis and liver cirrhosis.

METHODS:

The National Health Insurance Database, which was derived from the Taiwan National Health Insurance program, was used to identify patients. The study group consisted of 39,966 patients with liver cirrhosis, and the comparison group consisted of 39,701 randomly selected age- and sex-matched patients.

RESULTS:

During the 3-year follow-up period, 2,674 (6.7%) patients with liver cirrhosis developed cellulitis, and 1,587 (4.0%) patients without liver cirrhosis developed cellulitis. Following a Cox's regression analysis adjusted for age, sex, and underlying medical disorders, the cirrhotic patients demonstrated a greater risk for the occurrence of cellulitis than the non-cirrhotic patients during the 3-year period (hazard ratio [HR], 1.66; 95% confidence interval [CI], 1.55 to 1.77; Additionally, cirrhotic patients with complications also had a greater risk for the occurrence of cellulitis than those patients without complications (HR, 1.23; 95% CI, 1.14 to 1.33; ).

CONCLUSIONS:

We conclude that cirrhotic patients have a greater risk of cellulitis than non-cirrhotic patients.

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