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 **

F. Jacobsen, C. Fisahn, M. Sorkin, . Thiele,T. Hirsch, I. Stricker, T. , A. Roemer, B. Fugmann, and L. Steinstraesser^,*T. Klaassen,

^{Author information ► Article notes ►} 

2011 May

ABSTRACT

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:

PubMed - Antimicrobial Agents and Chemotherapy

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

Sept 2010

Giordano CN, Kalb RE, Brass C, Lin L, Helm TN.

Source

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

Abstract

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.

Dermatology Online Journal

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

2012

Singh SN, Tahazzul M, Singh A, Chandra S.

Source

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

Abstract

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 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 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.

BMJ

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**

Glatz M, Degen D, French LE, Aberer W, Müllegger RR.

Source

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

Abstract

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.

Karger

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Infections in Medicine

For further information:

Lymphedema Erysipelas

Classification and External Resources

ICD-10	A46.0 -  Excludes: postpartum or puerperal erysipelas ( O86.8 )
ICD-9	035 -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)
DiseasesDB	4428
MedlinePlus	000618
eMedicine	derm/129
MeSH	D004886

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

Jan 2013

McCusker RH, Kelley KW.

Source

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.

Abstract

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:

Journal of Experimental Biology

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

Babu S, Nutman TB.

Source

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

Abstract

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).

Springerlink