Tuesday, February 26, 2013

Gram-negative Bacteria Infections

Gram-negative Bacteria Infections

General Information about gram-negative bacteria.

Gram-negative bacteria cause infections including pneumonia, bloodstream infections, wound or surgical site infections, and meningitis in healthcare settings. Gram-negative bacteria are resistant to multiple drugs and are increasingly resistant to most available antibiotics. These bacteria have built-in abilities to find new ways to be resistant and can pass along genetic materials that allow other bacteria to become drug-resistant as well. CDC’s aggressive recommendations, if implemented, can prevent the spread of gram-negatives.
Gram-negative infections include those caused by KlebsiellaAcinetobacter, Pseudomonas aeruginosa, and E. coli., as well as many other less common bacteria.

CDC guidelines to address gram-negative bacteria

  • CDC Multi-Drug Resistant Organism Guidelines address reducing infections caused by all drug-resistant bacteria, including gram negatives.
  • CDC Guidance for Control of Infections with Carbapenem-resistant or Carbapenemase-producing Enterobacteriaceae in Acute Care Facilities contains specific recommendations for prevention and control of a specific emerging drug-resistant gram-negative.    

    Outbreak investigations

    Outbreak investigations have led to a better understanding of how to control these bacteria in healthcare. In the past 3 years, the Division of Healthcare Quality Promotion has assisted in at least 10 investigations of outbreaks of gram negative infections.
      • CDC has collaborated with state health departments in Maryland and Arizona to successfully control outbreaks of Multidrug-resistant-Acinetobacter infections occurring among intensive care unit patients.
      • CDC has worked with the Puerto Rico health department to control an outbreak of highly resistant Klebsiella at a neonatal intensive-care unit in Puerto Rico.
      • CDC assisted the Ohio health department’s investigation of infections caused by Acinetobacter. These outbreaks have occurred in various healthcare facilities in the state of Ohio and have been controlled by aggressive infection control interventions.
      • CDC worked with the state health department of Texas on separate outbreaks of B. cepacia and Pseudomonas
      • Additionally, CDC worked with the state health department in Georgia on an unrelated outbreak of B. cepacia.
      • CDC worked with the Department of Defense to investigate and control Acinetobacter infections occurring in soldiers injured in the Middle East. This collaboration led to important improvements in infection control in military medical facilities.
    • In addition to these outbreaks, CDC’s reference laboratory has confirmed carbapenemase resistance in bacteria for 32 other U.S. states.

    Laboratory tests for detecting resistance

    • CDC is collaborating with laboratory standards-setting institutions to identify and recommend laboratory tests for the accurate detection of carbapenemase-mediated resistance.  
    • CDC is working with states to identify isolates with unusual resistance and to determine new mechanisms of resistance among multidrug-resistant gram-negatives, including the recent identification of a new mechanism of resistance in patients returning from Asia.

    Monitoring gram-negative healthcare-associated infections

    • CDC’s National Healthcare Safety Network (NHSN) captures information on antibiotic resistance patterns in gram-negative bacteria in healthcare settings. 
    • The percentage of gram-negatives that are resistant to drugs is increasing. 
    • In 2008, based on NHSN data, 13% of E. coli and Klebsiella, 17% of P. aeruginosa and 74% of A. baumannii in intensive-care units were multidrug-resistant.

Pseudomonas bacteria

*Thought it might be good to have a brief apge on Psuedomonas, as it is an infection that so many lymphedema patients (including myself) see to "catch."*
Pseudomonas bacteria are any bacteria of the Pseudomonas genus of gamma proteobacteria. This type of bacteria is often infectious and has many characteristics in common with other pathogenic bacteria. They occur very commonly in water and some types of plant seeds, and for this reason, were observed very early on in the history of microbiology. The name Pseudomonas literally means “false unit.”
Pseudomonas bacteria are rod-shaped like many other bacterial strains, and are Gram-negative. This means that when stained with a certain violet-red dye according to the Gram staining protocol, they do not retain the dye’s color after being washed. This fact gives important clues about the structure of the cell wall of Pseudomonas bacteria. It shows that it is resistant to certain types of antibiotics, which fact is proving to be increasingly relevant.
One type of Pseudomonas bacteria is the Pseudomonas aeruginosa, which is responsible for an increasing number of infections in hospital patients, particularly those suffering from cancer or severe burns. This opportunistic pathogen has very minimal nutritional requirements, evidenced by the fact that it has been found growing in distilled water. Its preferred temperature for growth is 98.6 degrees Fahrenheit (37 degrees C), making it especially suited for infecting the tissues of the human body. It is important to note, though, that this bacterium is often found harmlessly on the skin and in the bodies of healthy persons.
Some kinds of Pseudomonas bacteria are also pathogenic to plant life. Many of these, interestingly enough, show a tendency to only infect certain plants in certain ways, and to use specific tactics in doing so. Even when not strictly a plant pathogen, Pseudomonas bacteria can affect agriculture in other ways, often causing problems in the cultivation of mushrooms.
Because of the infectious nature of these bacteria, they can actually be used to combat other agricultural pathogens. Since the 1980s, certain types of Pseudomonas bacteria, such as Pseudomonas fluorescens, have been applied directly to soils and seeds in order to prevent the growth of crop pathogens. This practice of deterring one type of pathogen with another is generally referred to as biocontrol. Another member of the Pseudomonas genus which has biocontrol properties is Pseudomonas chlororaphis, which itself produces an antibiotic which is active against certain fungi that attack plants. There is still much study to be done in the area of biocontrol, and Pseudomonas bacteria may yet prove to have additional helpful qualities.

From Wisegeek

Wednesday, February 13, 2013

Role of Bacterial Lipopolysaccharide in Enhancing Host Immune Response to Candida albicans.

Role of Bacterial Lipopolysaccharide in Enhancing Host Immune Response to Candida albicans.



Tissue Engineering and Reparative Dentistry, School of Dentistry, College of Biomedical and Life Sciences, Cardiff University, Heath Park, Cardiff CF14 4XY, UK.


Human infections involving yeast of the genus Candida often occur in the presence of bacteria, and, as such, it is important to understand how these bacteria influence innate host immunity towards Candida. Dectin-1 is a cell receptor of macrophages for Candida albicans recognition. The aim of this study was to examine dectin-1 expression by monocytes after stimulation with bacterial lipopolysaccharide (LPS), followed by heat-killed C. albicans (HKC). Freshly isolated human peripheral blood monocytes (PBMCs) and human monocytes cell line (THP-1) cells expressed low levels of dectin-1. Stimulation with LPS and GM-CSF/IL-4 was found to increase dectin-1 expression in both CD14(+) human PBMC and THP-1 cells. Enhanced dectin-1 expression resulted in increased phagocytosis of Candida. When THP-1 cells were challenged only with HKC, detectable levels of IL-23 were not evident. However, challenge by LPS followed by varying concentrations of HKC resulted in increased IL-23 expression by THP-1 cells in HKC dose-dependent manner. Increased expression of IL-17 by PBMC also occurred after stimulation with Candida and LPS. In conclusion, bacterial LPS induces an enhanced immune response to Candida by immune cells, and this occurs through increasing dectin-1 expression.

Thursday, February 7, 2013

Symptom burden and infection occurrence among individuals with extremity lymphedema.

Symptom burden and infection occurrence among individuals with extremity lymphedema.



School of Nursing, Vanderbilt University, Nashville, TN 37240, USA. sheila.ridner@vanderbilt.edu


Currently, there is a lack of data related to differences in symptoms and infection across different types and anatomical sites of lymphedema. The objective of this study was to examine differences in symptoms and infection status among individuals with lymphedema of the upper or lower extremities. The National Lymphedema Network initiated an online survey of self-report lymphedema data from March 2006 through January 2010. Descriptive statistics, Mann-Whitney tests, and Chi-square tests were used to analyze data. 723 individuals with upper extremity lymphedema and 1114 individuals with lower extremity ymphedema completed the survey. Individuals with extremity lymphedema experienced high symptom burden and infectious complications. Compared with individuals with upper extremity lymphedema, individuals with lower extremity lymphedema experienced more frequent and more severe symptoms (p<.001), infection episodes (p<.001), and infection-related hospitalizations (p<.001). No statistically significant differences of symptom burden and infection status were identified between individuals with lower extremity primary and secondary lymphedema. Individuals with extremity lymphedema experience substantial symptom burden and infectious complications; however, those with lower extremity lymphedema have more severe symptoms and more infections than those with upper extremity lymphedema.

Wednesday, January 30, 2013

Efficacy of Topically Delivered Moxifloxacin against Wound Infection by Pseudomonas aeruginosa and Methicillin-Resistant Staphylococcus aureus

Efficacy of Topically Delivered Moxifloxacin against Wound Infection by Pseudomonas aeruginosa and Methicillin-Resistant Staphylococcus aureus

**Recently, many full text articles have become available through that fantastic site Pub Med - National Institutes of Health.  Although this was written two years ago, I found it quite interesting and informative and wanted to share it with you. Several years ago, I had a systemic infection of both pseudomona and staph aureaus.  Thanksfully, the staph was not the resistant type.  Even then I was on IV antibiotics for three solid months. Pat **

2011 May


Wound infection is a common risk for patients with chronic nonhealing wounds, causing high morbidity and mortality. Currently, systemic antibiotic treatment is the therapy of choice, despite often leading to several side effects and the risk of an insufficient tissue penetration due to impaired blood supply. If systemically delivered, moxifloxacin penetrates well into inflammatory blister fluid, muscle, and subcutaneous adipose tissues and might therefore be a possible option for the topical treatment of skin and infected skin wounds. In this study, topical application of moxifloxacin was investigated in comparison to mupirocin, linezolid, and gentamicin using a porcine wound infection and a rat burn infection model. Both animal models were performed either by an inoculation with methicillin-resistant Staphylococcus aureus (MRSA) or Pseudomonas aeruginosa. Wound fluid, tissue, and blood samples were taken, and bacterial counts as well as the moxifloxacin concentration were determined for a 14-day follow-up. A histological comparison of the rat burn wound tissues was performed. Both strains were susceptible to moxifloxacin and gentamicin, whereas mupirocin and linezolid were effective only against MRSA. All antibiotics showed efficient reduction of bacterial counts, and except with MRSA, infected burn wounds reached bacterial counts below 105 CFU/g tissue. Additionally, moxifloxacin was observed to promote wound healing as determined by histologic analysis, while no induction of bacterial resistance was observed during the treatment period. The use of topical antibiotics for the treatment of infected wounds confers many benefits. Moxifloxacin is therefore an ideal candidate, due to its broad antibacterial spectrum, its high efficiency, and its potential to promote wound healing.

Read the full text article:

Monday, January 21, 2013

Nodular lymphangitis: Report of a case with presentation of a diagnostic paradigm.

Nodular lymphangitis: Report of a case with presentation of a diagnostic paradigm.

Sept 2010


University at Buffalo School of Medicine and Biomedical Sciences, USA.


A 54-year-old man with asthma, mitral valve prolapse, and a back injury developed erythematous nodules that progressed along the lymphatic drainage of his right arm. Skin biopsy revealed granulomatous inflammation with microabscess formation. Culture confirmed Mycobacterium marinum infection. 

The patient was treated with clarithromycin, ethambutol, rifampin, and topical silver sulfadiazine. Oral doxycycline hyclate was later added because of slow healing. Mycobacterium marinum is one of a group of infectious agents that can cause nodular lymphangitis. Sporotrichoid lesions most commonly develop after cutaneous inoculation with Sporothrix schenckii, Leishmania species, Nocardia species, and Mycobacterium marinum.

A thorough clinical history and physical examination can narrow the differential diagnosis by eliciting information about the etiologic setting, incubation time, clinical appearance of the lesions, and presence or absence of systemic involvement for each of the causative organisms. Skin biopsy and microbiological tissue cultures are essential for diagnostic confirmation. The differential diagnosis and a suggested diagnostic paradigm will be reviewed.

Monday, January 14, 2013

Varicella infection in a neonate with subsequent staphylococcal scalded skin syndrome and fatal shock.

Varicella infection in a neonate with subsequent staphylococcal scalded skin syndrome and fatal shock.



Department of Paediatrics, Chhatrapati Shahuji Maharaj Medical University (formerly King George's Medical College), Lucknow, Uttar Pradesh, India.


A male term neonate, at day 23 of life, presented with vesicular lesions over the trunk, which spread to allover the body on the next day. Five days later, he started developing blistering of the skin over the trunk and extremities, which subsequently ruptured, leaving erythematous, tender raw areas with peeling of the skin. The mother had vesicular eruptions, which started on the second day of delivery and progressed over the next 3&emsp14;days. Subsequently, similar eruptions were noticed in two of the siblings before affecting the neonate. On the basis of the exposure history and clinical picture, a diagnosis was made of varicella infection with staphylococcal scalded skin syndrome (SSSS). The blood culture and the wound surface culture grew Staphylococcus aureus. Treatment included intravenous fluid, antibiotics, acyclovir and wound care. However, after 72&emsp14;h of hospitalisation, the neonate first developed shock, refractory to fluid boluses, vasopressors and catecholamine along with other supports; and he then succumbed. In all neonates, staphylococcal infection with varicella can be fatal due to SSSS, the toxic shock syndrome or septicaemia.

Monday, January 7, 2013

Erysipelas of the Thigh and the Gluteal Region: Retrospective Multicenter Analysis of a Very Rare Entity in 39 Patients.

Erysipelas of the Thigh and the Gluteal Region: Retrospective Multicenter Analysis of a Very Rare Entity in 39 Patients.

**Editor's note: Not all infection we lymphers get can correctively be labled as cellulitis.  Often it is another form of infection referred to as erysipelas. This brief article is important specifically due to the closing line where it speaks of the disruption of the lymphatic vessels.  We know of course this can lead to secondary lymphedema**


Department of Dermatology, University Hospital Zurich, Zurich, Switzerland.


Background: Erysipelas of the thigh and the gluteal region are rarely described and not well characterized. Therefore we aim to describe the prevalence, clinical characteristics, and risk factors of these erysipelas types. 

Methods: The files of 1,423 patients with erysipelas were analyzed. Data from patients with erysipelas of the thigh or the gluteal region were compared between the two groups and with a control group with erysipelas of the lower leg. 

Results: The thigh was exclusively affected in 2.1%, and the gluteal region in 0.6% of erysipelas patients. Gluteal erysipelas had conspicuous irregular borders and sometimes appeared bilaterally. Major risk factors for erysipelas of both sites were previous surgical interventions. Gluteal erysipelas was common in patients with the metabolic syndrome and required a more intense antibiotic therapy. 

Conclusion: Erysipelas of the thigh and the gluteal region are rare and significantly associated with prior surgical disruption of lymphatic vessels.

Diagnostic Image:

Access Medicine

Infections in Medicine

For further information:

Classification and External Resources
ICD-10A46.0 - 
Excludes:postpartum or puerperal erysipelas O86.8 )
ICD-9035 -Erysipelas (gangrenous) (infantile) (newborn) (phlegmonous) (suppurative) 035 
  • 035 is a specific code that can be used to specify a diagnosis
  • 035 contains 9 index entries

035 excludes:

  • postpartum or puerperal erysipelas (670)

Immune-neural connections: how the immune system's response to infectious agents influences behavior.

Immune-neural connections: how the immune system's response to infectious agents influences behavior.

Jan 2013


Integrative Immunology and Behavior Program, Department of Animal Sciences, College of ACES and Department of Pathology, College of Medicine, University of Illinois at Urbana-Champaign, 250 Edward R. Madigan Lab, 1201 W. Gregory Drive, Urbana, IL 61801-3873, USA.


Humans and animals use the classical five senses of sight, sound, touch, smell and taste to monitor their environment. The very survival of feral animals depends on these sensory perception systems, which is a central theme in scholarly research on comparative aspects of anatomy and physiology. But how do all of us sense and respond to an infection? We cannot see, hear, feel, smell or taste bacterial and viral pathogens, but humans and animals alike are fully aware of symptoms of sickness that are caused by these microbes. Pain, fatigue, altered sleep pattern, anorexia and fever are common symptoms in both sick animals and humans. 

Many of these physiological changes represent adaptive responses that are considered to promote animal survival, and this constellation of events results in sickness behavior. Infectious agents display a variety of pathogen-associated molecular patterns (PAMPs) that are recognized by pattern recognition receptors (PRRs). These PRR are expressed on both the surface [e.g. Toll-like receptor (TLR)-4] and in the cytoplasm [e.g. nucleotide-binding oligomerization domain (Nod)-like receptors] of cells of the innate immune system, primarily macrophages and dendritic cells. These cells initiate and propagate an inflammatory response by stimulating the synthesis and release of a variety of cytokines. 

Once an infection has occurred in the periphery, both cytokines and bacterial toxins deliver this information to the brain using both humoral and neuronal routes of communication. For example, binding of PRR can lead to activation of the afferent vagus nerve, which communicates neuronal signals via the lower brain stem (nucleus tractus solitarius) to higher brain centers such as the hypothalamus and amygdala. 

Blood-borne cytokines initiate a cytokine response from vascularendothelial cells that form the blood-brain barrier (BBB). Cytokines can also reach the brain directly by leakage through the BBB via circumventricular organs or by being synthesized within the brain, thus forming a mirror image of the cytokine milieu in the periphery. Although all cells within the brain are capable of initiating cytokine secretion, microglia have an early response to incoming neuronal and humoral stimuli. Inhibition of proinflammatory cytokines that are induced following bacterial infection blocks the appearance of sickness behaviors. 

Collectively, these data are consistent with the notion that the immune system communicates with the brain to regulate behavior in a way that is consistent with animal survival.
Full Text:

Tuesday, January 1, 2013

Immunopathogenesis of lymphatic filarial disease.

Immunopathogenesis of lymphatic filarial disease.

Nov 2012

**Editor's Note:As individuals with a immunocompromised limb, we are susceptible to both bacterial and fungal infections, and problems from both that can be connected with a parasitic infection as is the case with lymphatic filariasis. Pat**

Nov 2012


NIAID/TRC (now NIRT) ICER, Chennai, India, sbabu@mail.nih.gov.


Although two thirds of the 120 million people infected with lymph-dwelling filarial parasites have subclinical infections, ∼40 million have lymphedema and/or other pathologic manifestations including hydroceles (and other forms of urogenital disease), episodic adenolymphangitis, tropical pulmonary eosinophilia, lymphedema, and (in its most severe form) elephantiasis. Adult filarial worms reside in the lymphatics and lymph nodes and induce changes that result in dilatation of lymphatics and thickening of the lymphatic vessel walls. Progressive lymphatic damage and pathology results from the summation of the effect of tissue alterations induced by both living and nonliving adult parasites, the host inflammatory response to the parasites and their secreted antigens, the host inflammatory response to the endosymbiont Wolbachia, and those seen as a consequence of secondary bacterial or fungal infections. Inflammatory damage induced by filarial parasites appears to be multifactorial, with endogenous parasite products, Wolbachia, and host immunity all playing important roles. This review will initially examine the prototypical immune responses engendered by the parasite and delineate the regulatory mechanisms elicited to prevent immune-mediated pathology. This will be followed by a discussion of the proposed mechanisms underlying pathogenesis, with the central theme being that pathogenesis is a two-step process-the first initiated by the parasite and host innate immune system and the second propagated mainly by the host's adaptive immune system and by other factors (including secondary infections).