Infections of the Skin, Eyes and Wounds

I. Bacterial infection of intact skin usually involves invasion via the hair follicle or sebaceous gland. The most significant pathogens to cause infection in this manner are Staphylococcus aureus, several species of Streptococcus including Streptococcus pyogenes and Propionibacterium acnes. Members of the genus Staphylococcus and Streptococcus are pyogenic. This means that they elicit strong inflammatory responses resulting in the production of large amounts of pus. A pus filled infection is referred to as an abscess.

A. Staphylococcus aureus is a gram positive coccus that can cause a primary infection of the glands and hair follicles of the skin. When only the hair follicle is involved it is referred to as a folliculitis or pimple (pimples can also be caused by other bacteria). This type of infection usually remains superficial. If the infection progresses into the subcutaneous layer it is referred to as a furuncle (commonly referred to as a boil). If several furuncles merge a large region of inflamed tissue results which is referred to as a carbuncle.

1. Scalded skin syndrome is a condition that occurs secondary to infection by S. aureus. Certain strains of S. aureus have the capacity to produce and release proteins known as exfoliative toxins or exfoliatins. These toxins are produced and released into the blood stream so that skin far from the site of infection may show the effects of this toxin. Exfoliatins appear to cause the epidermis to delaminate from the dermis. This condition initially presents as a reddened area followed by disseminated fluid filled vesicles. At the site of the vesicles, the epidermis peels away leaving areas that appear as if they were scalded. High fever and bacteremia often accompany this condition.

2. S. aureus is implicated in another skin disorder known as impetigo. Some debate exists as to whether S. aureus or species of Streptococcus are responsible for this condition. Raised, erythematous (reddened) lesions that are covered with a yellow-gray crust characterize this condition. Impetigo is usually highly infectious for children. Transmission occurs by direct contact or via fomites.

B. Members of the genus Streptococcus are gram positive cocci that are responsible for several types of skin disorders. As previously mentioned members of the genus Streptococcus are felt to play a role in the development of impetigo.

1. Scarlet fever is a skin condition caused by the release of an exotoxin by strains of Streptococcus pyogenes. These exotoxins are referred to as erythrogenic toxins cause the skin to become reddened. Usually the site of infection is the pharynx not the skin itself.

2. A less common but considerably more dangerous condition is streptococcal cellulitis or erysipelas. These conditions usually result from the infection of a minor cut or abrasion with a beta hemolytic strain of Streptococcus. Cellulitis usually occurs in the subcutaneous layer resulting in the tissues becoming bright red. The margins of this type of infection are poorly defined. Erysipelas is more superficial occurring in the dermis. These lesions are also bright red but the margins are well defined. In either case, the lesion continues to spread as the bacteria spreads through the tissue. This spread is facilitated by the production of exoenzymes (hyaluronidase, collagenase, etc.) by the pathogen. Dissemination throughout the body can occur via the lymphatics or blood stream. This is extremely serious and can result in death. 

C. Acne is an infection of the sebaceous gland by bacteria; most commonly the etiologic agent is a gram positive rod known as Priopionbacterium acnes. Increased production of androgens (androgens are testosterone and testosterone-like hormones) in the pubescent adolescent leads to increased secretion from the sebaceous gland. This in turn leads to overgrowth of Priopionbacterium acnes and inflammation of the sebaceous gland. Rupture of the gland can lead to spread of the infection into the dermis or subcutaneous layer resulting in considerable scarring.

II. Two viruses, Varicella-Zoster virus and measles virus, cause infections that result in the development of skin lesions. In both cases these viruses are transmitted most efficiently via the respiratory tract not by skin to skin contact.

A. Measles virus or rubeola is an extremely contagious pathogen. Infection results in a diffuse rash. In 0.1% of the cases a noticeable encephalitis occurs and in 10-15% of those showing signs of encephalitis death occurs. Thus roughly 1 in 10,000 persons infected with this virus died. This may have not been a statistic of much significance if the disease was not so contagious. Before the introduction of the vaccine, virtually every child suffered this infection. Secondary infections of the open skin lesions caused by the virus also increased the morbidity for which this pathogen was responsible.

1. Transmission of measles virus is by inhalation of aerosolized respiratory droplets or droplet nuclei. Infected persons shed the virus several days before the rash is apparent. The initial infection results in a runny nose, malaise and fever. Small, ulcerated lesions on the oral mucosa are also apparent and are referred to as Koplik spots. Within several days a generalized rash appears on the skin.

2. The vaccine is a modified-live vaccine. It is part of the MMR received early in childhood. The vaccine appears to have reduced the number of infections in this country to less than 500 per year from a high of 800,000 cases per year.

3. Measles virus is responsible for a condition referred to as subacute or slow sclerosing panencephalitis. This disease is due to the slow growth of the virus in the neurons of the brain. Years after the initial bout with measles, the patient begins a slow, degenerative disease which results in their death. The virus appears to cause many lesions throughout the brain.

B. Varicella-Zoster Virus (VZV) is the causative agent of chicken pox (varicella). The virus can establish a latent infection in the sensory neurons of the trunk. Reactivation of the virus leads to a disease known as shingles (Zoster).

1. In the initial infection (varicella) the virus infects the upper respiratory tract. Replication at that site leads to the development of a viremia. The virus is spread by the blood to various organs within the body. Virus in the skin results in the formation of a rash that develops into vesicles that rupture and eventually scab over. When this initial infection occurs in a child (2-13 years of age) little or no complication usually occurs. Infection of adults can lead to a more serious conditions due to the infection of cells lining the arterioles (endothelial cells) and the subsequent reduction in circulation to tissues serviced by the affected blood vessels. Though rare, spleen and liver damage can be fatal.

a. The virus is most efficiently transmitted through the aerosol route and occurs very easily. Children are infectious during the early stages of the infection when clinical signs are indistinct from those of a common cold. It is during this phase that the virus is most easily spread. Usually by the time the vesicles are apparent and the child is quarantined they are not nearly as infectious. Often transmission is encouraged to ensure that the child has the disease before maturity.

2. Years after the initial infection, immunity begins to wane allowing virus that has latently infected the dorsal root ganglia to cause a vesicular rash. Usually a person only suffers one round of viral reactivation. During this phase virus can be transmitted when the vesicles rupture. This route of transmission is not very efficient.

3. Until recently no vaccine was available. Parents would often intentionally expose children to the virus ("pox parties") to assure that the child had the virus before they reached maturity. Now a modified-live vaccine is available that appears to reliably prevent the infection.

III. Lysozyme and the constant washing action of tears usually protect the eye. Occasionally infection of the eye occurs. Early intervention is imperative as scarring caused by the inflammatory process can cloud the cornea leading to reduced visual acuity or even blindness.

A. Infection of the eye of the new born was once fairly common. This infection was acquired as the child passed through the birth canal. This condition is referred to as ophthalmia neonatorum. Two common pathogens, Neisseria gonorrhoeae and Chlamydia trachomatis, can cause this condition. These pathogens are common sexually transmitted diseases that often cause an inapparent infection of the women. The infection of the neonate’s cornea results in an inflammatory response. The changes elicited by the inflammatory mediators (prostaglandins, interleukins, etc.) result in the overproduction of keratin (keratitis) within the cornea. Keratin is not transparent and so the cornea becomes clouded. If allowed to progress, this will lead to a loss of sight. In this country and most of the developed world the incidence of this disease have been reduced by the routine treatment of the neonate with an antimicrobial ointment at birth.

B. In children and adults infection of the conjunctiva by certain strains of Chlamydia trachomatis due to hand to eye contact, fomite transmission or insect transmission can result in trachoma. This infection results in a scarred and deformed conjunctiva that abrades the surface of the cornea when the infected person blinks. This abrasion and secondary infections that are established in the abraded tissue result in progressive deterioration of the cornea. This in turn leads to blindness. Worldwide this is the leading cause of blindness.

C. Pinkeye is a condition that results when the conjunctiva is infected with a bacterial or viral pathogen. Whether the pathogen is viral or bacterial it is easily transmitted via contact with an infected person. The most common bacterial pathogens include Staphylococcus aureus, Streptococcus pneumoniae, Neisseria gonorrhoeae, several members of the genus Pseudomonas, and Haemophilus influenzae. Treatment of bacterial pinkeye usually involves administration of ophthalmic drops that contain one or more antimicrobial drugs. As this is highly contagious, those suffering from this condition should be isolated.

IV. Infection of wounds usually involves growth of the bacteria in the loosely connected subcutaneous layer or in the disrupted dermal layer. When tissues are badly damaged the disruption of the circulatory bed along with increased cellular activity by the white blood cells (WBC’s) at the site of damage can lead to the tissue become anaerobic. A fibrous capsule that limits amount of oxygen diffusing into the tissue often surrounds deep wounds. Increased WBC activity at the encapsulated site leads to anaerobic conditions developing. It is under these conditions that the spores of the obligate anaerobe Clostridium perfringens and Clostridium tetani. These organisms are found in the soil and as part of the normal flora of the colon of cows and horses.

A. Endospores of Clostridium perfringens are introduced into wounded tissue. When anaerobic conditions develop the spores germinate and begin to grow. The production of exotoxins result in the death of surrounding tissues. Production of exoenzymes allows the bacteria to spread into these necrotic tissues. The metabolic activities of the bacteria lead to the production of gas that cause the tissues to bloat. This condition usually is initiated in an extremity (arm or leg) and will progress until the necrosis reaches the vital organs of the abdominal cavity at which point death occurs.

1. If antimicrobial drugs are given early, this condition can be averted. Once the necrosis has progressed, the lack of profusion into the effected tissues will limit the effectiveness of these drugs.

2. Debridement or, in more serious cases, amputation is often necessary to stop the progression of this condition.

B. Infection of deep wounds by endospores of Clostridium tetani leads to the germination of the spores in these tissues in a manner similar to that seen with C. perfringens. But C. tetani does not lead to progressive tissue necrosis, instead in remains as a local infection and releases an exotoxin known as tetanospasmin. This toxin reduces the function of inhibitory neurons resulting in firing of the motor neurons and constant contraction of the muscle groups that these motor neurons control. 

1. Usually the muscles of the neck, jaw and back are initially affected. The toxin leads to a spastic paralysis of these muscle groups. This condition is referred to as tetanus. Eventually the diaphragm is affected. This leads to death. Early in the progression of this condition undue pain and muscle twitching near the site of the wound indicate production of the tetanospasmin.

2. The vaccine is a toxoid that leads to production of antibodies that bind to the toxin. This allows the body to clear the toxin with no ill effects. Once tetanus begins to develop (in a person who is unvaccinated or has not been received proper boosters) antibodies are given (gamma globulins) that will bind to the toxin.

Here are some links!!

Dermatopathology Table of Contents http://edcenter.med.cornell.edu/CUMC_PathNotes/Dermpath/Dermpath_TOC.html

Here is an in-depth page of explaining the structure, function and pathology that affects the skin.

Medical Microbiology textbook  http://gsbs.utmb.edu/microbook/ch098.htm

Varicella-Zoster Information    http://www.tulane.edu/~dmsander/WWW/335/Herpesviruses.html#VZV