by Al Kline DPM¹

Podiatry Internet Journal  1 (1):3  

Abstract 

 

A case presentation of pseudomonas aeruginosa infection is discussed.  Typical case presentation with review of diagnosis and treatment is discussed.  

 

Pseudomas aeurginosa is a gram-negative rod bacterium that is opportunistic and can infect the foot. The disease process usually begins with the pathogen circumventing normal host defenses as seen in the immunocompromised hosts. It can lead to a wide range of infections including urinary tract infections, pneumonia, endocarditis, osteochondritis and dermatitis and associated cellulitis. [1]  Commonly, as in group A streptococcal pyogenes infections of the foot, they are caused by an underlying secondary infection associated with tinea pedis in the foot. The condition usually presents following blister formation seen in tinea pedis. These blisters burst and allow entry and colonization of infectious organisms such as pseudomonas, streptococcus and staphylococcus bacteria. Any condition that causes a breakdown in skin integrity or injury will lead to changes conducive to secondary infections. Burn wounds are especially susceptible to pseudomonas for this reason alone. On the cellular level, the fimbriae of the pseudomonas pathogen will adhere to epithelial cells and bind to specific galactose , mannose or sialic acid receptors. A mucoid exopolysacchardie is a repeating polymer of mannuronic and glucuronic acid referred to as alginate. The alginate slime forms a matrix of pseudomonas biofilm which will then anchor cells to their environment. [1]  This alginate slime protects the bacteria from host defenses such as lymphocytes, phagocytes and other host defenses. P. aeruginosa can produce the blue-green pigment pyocyanin. [1]  Pseudomonas generally has a sweet, pungent odor. Generally, skin manifestations presents with acute erythema and even a ‘greenish’ drainage. The pathogens are common in soil, water, plants and animals. The infection is most commonly seen in the immunocompromised host. The bacterium is invasive and can colonize rapidly as a local or disseminating systemic disease. The bacterium is also a nosocomial pathogen. According to the CDC, average hospital infections are on the average of 4 per 1000 patient discharges and is the fourth most commonly isolated nosocomial pathogen accounting for about 10.1% of all hospital-acquired infections. [2]  A case presentation of a Pseudomonas aeurginosa infection of the foot is presented.

 

Case Presentation

 

A 48 year old Caucasian male presented to the emergency room after a progressive history of left foot ‘cellulitis’. The patient works as an oil-field worker and began experiencing left foot erythema and blisters.  He began developing “blisters” 3 month prior to his ER visit. About a month later, the blisters did not go away and he was given Bactrim. He states he had a reaction by development of “more blisters to the hand and foot” which progressed to increased erythema and a green-yellowish drainage from the digits and in between the toes. He began to develop local chills and fever and was transferred admitted through the emergency room setting. Cultures, radiographs and labs were performed in the emergency room. The patient was then put on intravenous Vancomycin and Zosyn and admitted to the floor. The patient has an unremarkable medical history. He does abuse alcohol and related to a history of drug abuse when he was in his 20’s. He now denies any drug use and relates his alcohol consumption as drinking “a couple of six-packs a week”. His family history includes diabetes mellitus. His x-ray report reveals no signs of gas in the tissue and no signs of osteomyelitis. His laboratory data was relatively normal with a 6,900 white blood cell count. No left shift was seen. His culture report revealed +3 tiny gram negative rods and +1 gram positive cocci. On day 1, presumptive +4 Pseudomonas aeruginosa was identified. Diptheroids and coagulase negative staphylococcus species were also identified. His aerobic and anaerobic blood cultures were negative.In the photo on left, it is interesting how just his left foot is infected and his right foot is completely spared.

 

Discussion and Treatment

 

This case is interesting because the host does not initially appear to be immunocompromised. However, he has a history of drug use and consumes alcohol quite heavily during the week. His work conditions are also conducive to these type of infections. He works as an oil working on an oil platform in the country. He also wears steel toe type boots and rubber-type boots in the field. Soil contaminates and moisture would play an important role in pathogenesis of this infection. The patient also had exposure to Bactrim early in his treatment which may have played a role in the ability of his immune system to fight the infection in its early stage. Two extracellular proteases and extracellular protein toxins are produced in the initial infective stage. Elastin protease and alkaline protease destroy the cells ground substance and lysis its supporting structure of fibrin and elastin. Exotoxin A has a tissue necrotizing effect and has the same mechanism of action as the diphtheria toxin. Exoenzyme S is also thought to be a tissue destructive exoenzyme that is commonly seen during pseudomonas colonization on burn wounds. [1,2]

 

The picture at left represents local colonization of pseudomonal infection of the foot. Here, the skin is erythematous and has a scalded-skin type appearance. This is likely due to extracellular toxins and proteases causing local ground substance disruption. You can also readily see the alginate slime layer that forms a matrix of the pseudomonas biofilm. This alginate biofilm is representative of pseudomonas colonization and the bacterial attempt at protecting the colony from host defenses. Treatment should include primary coverage for pseudomonal infection. Sensitivity reports revealed bacteriocidal activity using Ciprofloxacin. Ciprofloxacin 750mg to be taken orally twice daily was prescribed . Oral bioavailability of Ciprofloxacin is identical to the bioavailability of the intravenous form. The oral form of 750 mg of Ciprofloxacin has the same serum concerntration of 400mg of IV Ciprofloxacin given over 60 minutes every 12 hours. [3]  He was also placed on Dicloxycillin for empiric coverage of possible streptococcal infection and suprainfection. Griseofulvin 250mg daily was also prescribed as empiric coverage for dermatophytosis. Parenteral treatments are similar to that of streptococcal infections that included daily washes with chlorohexidine gluconate soap, acetic acid dressings (0.25% to 5% topically applied), Domeboro’s soaks (Aluminum Acetate), interspace separation with 2×2 gauze, whirlpool and daily dressing changes. There have also been reports of treating P. aeruginosa by topical acetic acid alone. This is a common method of treatment in burn wounds secondarily infected with P.aeruginosa.

 

Summary

 

This case describes the clinical evaluation and diagnosis of Pseudomonas aeruginosa infection of the foot. The patient underwent aggressive treatment after what appears to have been a chronic type infection. Pseudomonas infections can cause an erythematous and ‘wheeping’ skin similar to that of group A streptococcal infections (GAS). However, there does not appear to be the aggressive necrotizing appearance as seen in GAS infections of the foot. Typically, there is an alginate slime layer that is classic for this type of infection. Any green driainage or ‘fruity’ odor to the foot should be considered pseudomonas and treated aggressively with antibiotics bacteriocidal to the pseudomonas bacterium. This case is in progress and I hope to have a followup report on this patients condition in the near future.

 

 

References

 

1.  Today’s Online Textbook of Bacteriology: Pseudomonas aeruginosa, Online reference, 2004.

 

2.  Qarah, S, Cunha, B.: Pseudomonas Aeruginosa Infections: eMedicine, Online , 2005

 

3.  Cipro: Bayer Corp, Drug insert, Online reference.

¹Dr. Kline is in private practice in Corpus Christi, Texas.  He can be reached by email at al@kline.net.

© Podiatry Internet Journal , 2006