Bacterial Conjunctivitis
Lenio S. Alvarenga
Barrett Ginsberg
Mark J. Mannis
Bacterial conjunctivitis is a common form of ocular infection. The incidence and prevalence are difficult to determine, since most patients are treated without laboratory investigation. The clinical characteristics and course of bacterial conjunctivitis are related primarily to the disease-producing capabilities of the infecting microbe, including its invasiveness and its ability to elaborate toxins.
NATURAL DEFENSES
The external eye possesses an indigenous microbial flora1,2 that is acquired early in life.3 The balance between host, normal flora, and pathogenic organisms at the ocular surface is maintained by both native and acquired defense mechanisms of the external eye.4,5
The native (nonspecific) defense mechanisms are dependent upon maintenance of a highly efficient multilayer barrier, designed to minimize the probability of microbial colonization and access to the epithelium.6 The outer components of this barrier are the lid, the lashes, and the lipid layer of the tear film. The second barrier, the aqueous layer of the tear film, is continually renovated. Lacrimal gland secretion is added to the tear film, and the mechanical action of the lids provides continuous pumping that sweeps and flushes debris and potential bacterial pathogens from the ocular surface into the drainage system (nasally). Certain tear film proteins (e.g., lactoferrin, lysozime, lipocalins, IgA) have antimicrobial properties. The final barrier consists of the apical epithelial cells, which are bound by tight cell junctions and are covered by a blanket of mucin. Large glycoproteins are present on all nonkeratinized epithelium and aid in lubrication and water retention and also acts as a barrier4 to pathogens.
Acquired (specific) defense mechanisms are provided by both the cellular and humoral components of the immune system. Human conjunctiva and the lacrimal drainage system have an associated lymphoid tissue (conjunctiva-associated lymphoid tissue- CALT) that contains all components necessary for a complete immune response.4 Polymorphonuclear leukocytes and macrophages in tears are involved in the acute response mechanisms.
Further, the normal bacterial flora may help resist infection by production of metabolic products toxic to other bacteria and other factors that adversely affect the survival of more pathogenic species.7
RISK FACTORS
Abnormalities of the lid margins, incomplete lid closure, inadequate blinking, and abnormalities of lid apposition to the globe (such as ectropion, horizontal lid laxity, or entropion) may compromise the integrity of the aforementioned barriers.
Dry eye or obstruction of the lacrimal drainage system (e.g., infants with nonpatent lacrimal ducts) may decrease tear film turnover. Tear film abnormalities, including defects of the water, lipid, or mucin layers, may compromise the ocular surface. This may lead to altered immune function of the tears, poor wetting of the ocular surface, or surface epithelial cell damage. Surface trauma may promote infection by causing a break in the epithelial barrier and by introducing foreign, potentially virulent bacteria to the eye.
The presence of perinatal vaginitis is an important risk factor for ophthalmia neonatorum.8 Additionally, conjunctivitis is one of the most frequently occurring health care–acquired infections in the neonatal intensive care unit. For these patients, low birth weight is a significant predictor of conjunctivitis, and neonates with respiratory support are at higher risk, probably due to transfer of nasopharyngeal bacteria to the eyes.9
Specific ocular defense mechanisms may be impaired by systemic or local immunosuppression, especially with immunosuppressive therapy. Under these conditions, bacteria not normally pathogenic may become opportunists and sources of conjunctival infection. Further, some bacteria have developed the capability of penetrating host defense mechanisms. These include glycocalyx/extracellular matrix adherence (e.g., Pseudomonas10,11), pili-mediated enhanced surface attachment, and production of IgA proteases (Streptococcus pneumoniae, Neisseria species, and Haemophilus influenzae).12,13
NORMAL OCULAR SURFACE FLORA
The indigenous microbial flora of the ocular surface primarily are Gram-positive organisms, composed of Staphylococcus species (primarily coagulase negative) and diphtheroids. S. epidermidis has developed strategies that allow it to overcome tear defenses and become part of the normal ocular flora. Isolates have demonstrated resistance to the action of lysozyme, lactoferrin, and other constitutive tear proteins.14 Other organisms have been isolated from the conjunctival surface, but they are usually transient. These include S. pneumoniae, Haemophilus species, Moraxella, and S. aureus. Occasionally, Gram-negative coliform rods can be isolated from the lids or conjunctiva. Anaerobic skin and mucous membrane flora, including Propionibacterium acnes, Lactobacillus species, Eubacterium species, and Peptostreptococcus species, have been isolated from the outer eye. Systemic disease (e.g., diabetes15) may alter the proportion of conjunctival colonization, and chronic use of antibiotics may exert a selective pressure in the conjunctival flora.16 Under ordinary conditions, it is difficult for a fungus to remain or proliferate in the conjunctival sac,17 and there is little evidence that there is any significant indigenous fungal flora.
EPIDEMIOLOGY
Bacterial conjunctivitis is ubiquitous in humans. Its frequency, cause, distribution, and course are influenced by age, climate, social and hygienic conditions, and coexisting epidemic disease. Epidemiologic distribution is, to some extent, peculiar to bacterial species. Age is an important factor, with children, adults, and the elderly more likely to be infected, respectively, with specific organisms.
In children, the most commonly isolated organisms are S. pneumoniae and Haemophilus species.18,19 In a recent childhood-based study,20 H. influenzae and S. pneumoniae accounted for more than half of the bacterial conjunctivitis in patients less than 7 years of age. Among 7- to 14-year-old patients S. aureus was the most common isolate. In adults and the elderly, Staphylococcus species and S. pneumoniae often predominate. Some organisms result in more seasonal infections, and others are more common in certain climates. Certain bacteria are responsible for an increased incidence of conjunctivitis during seasons when there is a higher incidence of upper respiratory infection.
Unencapsulated, nontypeable S. pneumoniae may cause outbreaks in school-age children and college students.21,22 Analysis of survey data from a recent college outbreak21 indicated that close contact with a student with conjunctivitis, wearing contact lenses, membership on a sports team, and attending parties at or living in a fraternity or sorority house were associated with conjunctivitis. The rate of diagnosis of conjunctivitis declined after the implementation of distribution of alcohol-based hand gel messages about prevention and after spring break.
CLINICAL CONSIDERATIONS
Clinical determination of a bacterial cause for infectious conjunctivitis without the benefit of laboratory studies is a difficult task. Although some characteristics are cited as indicative of bacterial etiology (involvement of the other eye within 24 to 48 hours, a papillary conjunctival reaction, and mucopurulent or catarrhal discharge), there is no data available to support those assertions.23 A recent cohort study designed to identify diagnostic indicators of a bacterial origin of acute infectious conjunctivitis24 detected that early morning glued eye(s) increased the likelihood of a bacterial cause, whereas itch and a history of conjunctivitis decreased it, but those findings are controversial.
Specific organisms may produce a characteristic clinical picture that is helpful in diagnosis and in specifying a course of treatment. Very often, however, the clinical picture is nonspecific, and cultures provide the criteria for defining a specific bacteria.
Although the clinical expression and severity of conjunctivitis is the result of the pathogenicity, virulence, invasiveness, and toxigenicity of an organism, the basic mechanism underlying each clinical expression is similar. The pathogen elicits a hyperemic response, vascular stasis, cellular exudate, and vascular leakage producing edema. The intensity of these common responses varies with the organism and the host. Signs and symptoms include red eye, mucopurulent or purulent discharge, conjunctival thickening and chemosis, and a papillary reaction. Certain virulent organisms may produce marked lid edema, conjunctival hyperemia, and a copious, purulent, exudative response. Infections by other organisms are characterized by a membranous or pseudomembranous conjunctivitis. The membrane or pseudomembrane consists of condensed fibrin, inflammatory cells, and other exudates. A true membrane results from penetration of the fibrinous exudate into the epithelium, producing bleeding when peeled; pseudomembranes do not bleed when peeled. Specific organisms may produce a follicular response, but this is unusual and more characteristic of chlamydial or viral infections. The follicular response represents a lymphoproliferative reaction to bacterial antigen in the inferior conjunctival cul-de-sac. Enlarged tender preauricular lymph nodes typically are absent but may be present with certain bacteria.
CLINICAL CLASSIFICATION
Bacterial conjunctivitis can be characterized according to the mode of onset, the severity of the clinical response, and the time course of the disease. Descriptions of the three clinical types follow.
Acute Bacterial Conjunctivitis
Acute bacterial conjunctivitis occurs commonly, second only to viral conjunctivitis as an infectious cause. It usually begins unilaterally with irritation, tearing, mucopurulent or purulent discharge, and morning mattering of the lids. The second eye often is involved 24 to 48 hours later. Symptoms are accompanied by epibulbar and tarsal conjunctival hyperemia, and there often is punctate epithelial keratitis. There is generally minimal or no lymphadenopathy. The pathogens most commonly associated with acute bacterial conjunctivitis include S. aureus, coagulase-negative Staphylococcus, S. pneumoniae, and H. influenzae. In children, the most common pathogens are similar, with H, influenzae and S. pneumoniae the more frequent.
S. aureus is the most common cause of bacterial conjunctivitis worldwide. This ubiquitous aerobic Gram-positive organism, which colonizes humans within a few days after birth, is not normally part of the ocular flora. It is seen both singly and in pairs, and, less commonly, in clusters in conjunctival smears. It is 1 μm in diameter, and it produces cream-colored or golden colonies and complete hemolysis on blood agar. Conjunctival infection is probably caused by spread from the adjacent facial skin or nares. The tissue-cytologic response is polymorphonuclear. Although the clinical manifestations of infection induced by S. aureus are numerous, the organism can induce a self-limited inflammatory episode with an acute onset associated with a mucopurulent discharge. There is no seasonal incidence of infection.
S. epidermidis, the most common type of coagulase-negative Staphylococcus species in the normal ocular flora,15 may also produce conjunctivitis, despite its appearance as normal flora in many individuals. It is also involved in the pathogenesis of chronic blepharoconjunctivitis.25
S. pneumoniae is an aerobic, encapsulated, Gram-positive diplococcus carried most commonly in the upper respiratory tract of healthy children of preschool or grammar school age. It is more commonly seen in more temperate climates during the colder months of the year. The serotypes causing eye disease are those that are found in the healthy carrier. On Gram-stained smears of conjunctival scrapings, the organism occurs in pairs, is lancet shaped, and elicits a substantial polymorphonuclear response. Some appear encapsulated (polysaccharide). Colonies grow on blood or chocolate agar. S. pneumoniae produces a self-limited (7 to 11 days), mucopurulent conjunctivitis that generally reaches its peak in 2 to 3 days and commonly resolves without damage to the conjunctiva. It is more common in children and may be associated with institutional epidemics. Other streptococcal species (e.g., Streptococcus viridans group) also may act as pathogens. Streptococcus species usually cause a red eye and a sticky mucopurulent discharge. Subconjunctival hemorrhages and chemosis may occur. In some subjects, beta-hemolytic streptococci may produce a severe purulent conjunctivitis that can progress to pseudomembrane or membrane formation. Outbreaks due to atypical unencapsulated S. pneumoniae have been described.21,22. In a recent outbreak at an elementary school22 the symptoms reported most commonly were red eyes (85%), itchy, painful, or burning eyes (69%), crusty eyes in the morning (65%), gray or yellow discharge from eyes (65%), and swelling of the eyelids (46%); the median duration of symptoms was 3 days (range 1 to 14 days). Since the available pneumococcal vaccines work by inducing type-specific antibodies targeting the polysaccharide capsule, infection-control measures are the only available means of controlling outbreaks and preventing sporadic disease caused by unencapsulated pneumococci. Overall, the potential coverage of the 7-valent pneumococcal conjugate vaccine in conjunctivitis is relatively lower than that reported in other pneumococcal infections.19 New vaccines that are now being developed target highly conserved pneumococcal surface proteins and could prove to be useful as control measures.26
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