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Stephanie Mita, Medical Microbiology
G athophysiology:
G Erosions on the soles of the feet caused by a cutaneous infection with the
bacteria @
   
 (now known as   
)
À

 ʹ T    G mhite patches studded with small, shallow pits that sometimes
join together to form crater-like lesions
G athophysiology: G Àenderness and extreme malodor
G Invasion of the nail bed and the underside of the nail plate by the fungus À

 G Affects males more often than females
G Àhickened, yellow, chalky, dull, rough, crumbly nail G isk factors are sweaty feet, hot/humid weather, unventilated footwear,
G Brownish-yellow debris forming beneath the nail, causing it to separate from the nail bed and increased skin surface pH
(onycholysis) G Àreatment:
G Coexistent tinea pedis (Athlete͛s foot) is commonͶtypically caused by À
 G Keep feet as dry as possible and change socks often
G isk factors are increasing age, diabetes, poor venous and lymphatic drainage, and ill-fitting shoes G Lotions containing antibiotics (erythromycin or clindamycin) that bind to the
G Àransmission: large bacterial ribosome subunit to halt bacterial protein synthesis
G Direct contact with infected persons, animals, soil, or fomites G Injections of botulinum toxin in severe cases
G Àreatment: G Virulence factors:
G Oral antifungal medications (relapses occur after stopping therapy) G Obligate aerobic Gram-positive cocci that produce serine proteases that
G Àerbinafine works by inhibiting an enzyme needed for fungal cell membrane synthesis, which causes fungal degrade human keratin in the stratum corneum
cell lysis G roteases that cut peptide bonds in proteins
G Virulence factors: G Break down keratin to obtain carbon and nitrogen sources
G Dermatophyte that colonizes keratinized tissues (hair, nails, and outer skin layer) G Ability to degrade keratin improves with the presence of NaCl
G Asexual sporulation in the nail bed to produce microconidia (spore form of the organism that allows it to G Nonhalophilic but grows well at 10% NaCl
survive in adverse environmental conditions) G Optimal activity at pH 6.3-6.9 (increased skin surface pH)
G Surface covered with thin rods that favor buoyancy (to be transmitted on air currents) G Optimal activity at temperature 28-36϶C (close to skin temperature)
G roteins providing resistance to dessication, heat, starvation, DNA damage, and osmotic stress without loss
Scanning electron micrograph of (A) the cell wall
of viability
of microconidia directly attaching to the epithelial 2-3 mm crater-like shallow pits. 10x dermoscopic
G Carbohydrate-binding adhesins on surface of microconidia that recognize mannose and galactose cell membrane and (b) some disrupted cells after Scanning electron micrograph of  
. magnification reveals structure of pit walls
G Mannose binding allows for initial recognition of epithelial cell interacting with microconidia. Magnification: A, according to random dissolution of stratum
G Galactose binding allows for invasion of the cell x3000; B, x5500. corneum by bacterial colonies.

T 
    

G athophysiology:
G Bacterial infection of the skin, connective tissues, muscles, and bones that can develop into gangrene if left untreated
G Many different bacteria (polymicrobial) usually involved in establishing the infection, but the most common aerobic
organism is 2     (the most common anaerobic organism is  
  

)
G Most common foot infection leading to lower extremity amputation
G Diabetes mellitus
G Damage to the nervous system prevents person from feeling minor injuries like cuts, scrapes, blisters, and
foot strain (as well as trauma)
G Normal sweat secretion and oil production that lubricate the skin are impaired
G Damage to blood vessels slows down wound healing
Àhe human foot makes up the end of the limb, G Àreatment:
G Debridement (removal of all necrotic tissue and foreign bodies down to viable tissue)
allowing for locomotion and weight-bearing. It G Offloading (using wheelchair, crutches, or custom-made orthotic devices to halt weight bearing and alleviate pressure)
contains more than 26 bones, as well as G Infection control via antibiotics
hundreds of muscles, tendons, and ligaments. G Quinolone ʹ inhibits bacterial topoisomerase II enzyme to block bacterial DNA replication and transcription
Àhe skin of the foot is the most important barrier G Metronidazole ʹ absorbed by anaerobic bacteria, which reduce it and cause the production of toxins that
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  to protect from pathogens. mhen this surface is selectively accumulate in anaerobes and form unstable molecules
G Clindamycin ʹ inhibits bacterial protein synthesis
compromised due to environment (moisture, G Virulence factors:
G athophysiology: pH, trauma, improperly-fitting shoes, diabetes) , G 2    capable of producing a wide variety of toxins (extracellular proteins)Ͷexfoliative toxins
G Acute febrile disease and blister-like rashes resulting from 
 

 famiily viruses Coxsackie G Serine proteases that recognize and cleave desmosomal cadherins only on the superficial layers of the skin
it can allow for colonization by a microbe. mhen
virus A16 or Enterovirus 71 G Desmosomal cadherins are responsible for maintaining adhesion between epithelial cell layers and
G uever, poor appetite, runny nose, sore throat 3-5 days after exposure this happens, this can lead to many types of between epithelial cells within the same layer
G Blister-like rash inside the oral cavity followed by painful vesicular lesions on hands and feet infectionsͶeven ulcers that require amputation G Cause blistering skin and epidermal loss (rashes and large, fluid-filled blisters)
1-2 days after initial symptoms of the limb. G Act as superantigens that induce non-specific proliferation of À cells and cause the deregulation of the
G Non-itchy skin rash (flat or raised red spots, sometimes with blisters) immune response
G Most common in children under 10 years old
G Usually mild with benign symptoms, but it can manifest as paralytic poliomyeletis, meningitis,
encepahlitis, myocarditis, or hemorrhagic conjunctivitis
G Àransmission:
G Direct contact with nose and throat discharges, blisters, and feces of infected people
G Most often spread by people with unwashed, virus-contaminated hands
G Specific immunity can occur, but a second episode is possible from a different Coxsackie virus strain
G Àreatment:
G No specific treatments availableͶjust control fever and maintain good oral hydration
G Virulence factors:
G Single-stranded positive-sense NA allows for rapid translation to proteins
G Naked virus that is able to remain virulent even outside of optimal conditions
G High acid stability allows it to survive in the stomach and pass into the intestine
G High mutation rate due to frequent recombination and low-fidelity replication
G Virus can be shed in the stool for several weeks to months

Desmoglein (a type of desmosomal cadherin) distribution in A) healthy skin

and B) skin exposed to exfoliative toxin. In all layers except the stratum
granulosum, Dsg-3 compensates for hydrolysis of Dsg-1. Dsg-3 is absent in
the stratum granulosum, which explains the cell detachment and splitting
of epidermal layers.

eferences
GBl omqvi s t, Soi l e, et a l . ͞Co-ci rcul ati on of coxs ackievi ruses A6 a nd A10 i n ha nd, foot, a nd mouth di s ea s e outbrea k i n ui nl a nd.͟ *   

 
 A8 (2010): A9-5A. 2 June 2011. m eb.
GBukows ki , Mi cha l , et a l . ͞Exfol i a ti ve toxi ns of 2    .͟ À
 2 (Ma y 2010): 11A8-65. 2 June 2011. m eb.
Molecular structure of Coxsackie GEs quena zi , Da ni el e, et a l . ͞Àhe rol e of s urfa ce ca rbohydra tes on the i ntera cti on of mi croconi di a of À
 menta grophytes wi th epi thel i a l cel l s .͟    @
 @
 

 35 (2003): 113-23. 31 Ma y 2011. m eb.
virus A16 by X-ray crystallography. G͞Ha nd, uoot, a nd Mouth Di s ea s e.͟ . 1 Dec 2010. 27 Ma y 2011 <http://www.cdc.gov/nci dod/dvrd/revb/enterovi rus /hfhf.htm>.
GHunt, i cha rd. ͞Enterovi rus es a nd Genera l uea tures of i cornaviruses.͟ @
 

    
. 12 Apri l 2010. 2 June 2011 <http://pa thmi cro.med.s c.edu/vi rol /pi corna.htm>.
GJeffcoa te, m i l l i a m a nd Kei th Ha rding. ͞Di a beti c uoot Ul cers .͟ À  361 (Ma y 2003): 15A5-51. 31 Ma y 2011. m eb.
GLa dha ni , Sha mez, et a l . ͞Cl i ni ca l, Mi crobi al, a nd Bi ochemi cal As pects of the Exfol i a ti ve Àoxi ns Ca using Sta phyl ococcal Scalded-Ski n Syndrome.͟ 

 @
 

 
  12.2 (Apri l 1999): 22A-A2. 31 Ma y 2011. m eb.
GLeng, m enchua n, et a l . ͞roteomi c profi l e of dorma nt À
 
 

! @ "
 9 (2008): 1-11. 31 Ma y 2011. m eb.
GLongs ha w, C.M., et a l . ͞  
, the orga ni s m a s sociated wi th pi tted kera tol ys i s , produces two kera ti n-degra ding enzymes .͟ *   #
 @
 

 93 (2002): 810-16. 31 Ma y 2011. m eb.
GLockwood, La uren., et a l . ͞Dermos copy of i tted Kera tol ys i s.͟   
   2.2 (Ma y-Aug 2010): 1. 2 June 2011. m eb.
athogenesis of enteroviruses, including Coxsackie A viruses. GKrus e, Ingri d a nd Steven Edel ma n. ͞Eva l ua ti on a nd Àrea tment of Di a beti c uoot Ul cers .͟ 

 

 2A.2 (Apri l 2006): 91-3. 31 Ma y 2011. m eb.
GSi ms , Da vi d, et a l . ͞Compl ete genome s equence of   
 type s tra i n (5A1À).͟ 2 
 "
 2
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GSotto, Al l bert. ͞Vi rul ence otenti a l of 2     Stra i ns Is ol ated urom Di a beti c uoot Ul cers .͟ 

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