x x

INFECTIOUS DISEASE

BACTERIOLOGY IMMUNOLOGY MYCOLOGY PARASITOLOGY VIROLOGY

VIDEO LECTURE

 
INFECTIOUS DISEASE

CHAPTER TWO

Upper Respiratory Tract Infections and Other Infections of the Head and Neck 

Charles Bryan MD

Let us know what you think
FEEDBACK

SEARCH

 

TEST YOUR KNOWLEDGE
Headache
Kidney Transplant
Inclusion bodies

Text links in orange go to a dictionary definition

Text links in blue go to basic science chapters in this book

Figure 1
Anatomic predispositions to upper respiratory tract infections (orange = normal colonizing flora)

 

Upper respiratory tract infection (URI) causes at least of one-half of all symptomatic illness in the community, exacting huge tolls that can be measured as morbidity, absenteeism from school and work, direct health care costs, and overuse of antibiotics leading to the emergence of drug-resistant bacteria. This disease burden is largely explained by anatomy. The nose, mouth, and pharynx are exposed to circulating viruses and are normally colonized by large numbers of bacteria including potential pathogens such as S. aureus, S. pneumoniae, H. influenzae, and group A streptococci (figure 1). Mucosal injury caused by viral infection, allergy, or other factors compromises the mucociliary barriers designed to maintain sterility of the middle ears, paranasal sinuses, and lungs. Most URIs are self-limited but progression to life-threatening acute illness occurs and progression to chronic disease is common.

 

rhino.jpg (189986 bytes)  Figure 2 Human rhino virus © Dr J-Y Sgro, University of Wisconsin. Used with permission

rsv.jpg (51649 bytes)  Figure 3
Transmission electron micrograph of respiratory syncytial virus. Long
filamentous form.
CDC/Dr. Erskine Palmer

Figure 4
Orthomyxovirus structure
Lower image: CDC PHIL

para-4a.gif (107465 bytes) Figure 5  Paramyxovirus © Dr Linda Stannard, University of Cape Town, South Africa (used with permission) 

 

 

 

Figure 6
Pathogenesis of symptoms attributable to the common cold

The Common Cold

The common cold is as an acute, self-limited catarrhal (Latin catarrhus, to flow down) syndrome limited to the mucosal membranes of the upper respiratory tract. Recently, "viral rhinosinusitis" has been suggested as the technically correct term, since CT scanning shows abnormalities of the paranasal sinuses in most cases. However, "cold" is preferred for clinical use since "rhinosinusitis" suggests to patients the need for antibiotics. The common cold accounts for up to three-quarters of all illnesses in young infants and up to one-half of illnesses in adults. Elimination of the common cold would also eliminate in the United States each year an estimated 27 million office visits, 23 million days of work absenteeism, 26 million days of school absenteeism, and nearly $2 billion worth of over-the-counter remedies.

Rhinoviruses (figure 2), of which there are more than 100 serotypes, cause an estimated 30% to 50% of colds. Coronaviruses account for perhaps 10% of cases. Respiratory syncytial virus (RSV) (figure 3) is an important cause of cold symptoms in young children and among the elderly. Influenza virus (an orthomyxovirus, figure 4) and parainfluenza virus (a paramyxovirus, figure 5) can cause colds, but more often cause lower respiratory tract infection or systemic symptoms. Adenoviruses, of which there are at least 47 antigenic types, cause 5% to 10% of colds. Although echoviruses and coxsackieviruses have been associated with colds, they more commonly cause an undifferentiated flu-like illness or distinctive syndromes such as aseptic meningitis or pharyngitis. Rhinoviruses and parainfluenza viruses cause outbreaks of cold symptoms during the fall and late spring; RSV, adenoviruses, and coronaviruses cause outbreaks during the winter and early spring. Viruses that remain to be discovered probably cause a substantial fraction of colds.

Rhinoviruses are transmitted most efficiently by direct contact. Hand contact with the eyes and nose is very common in everyday life. Rhinoviruses remain viable on skin and also on objects (fomites) for at least 2 hours. Rhinoviruses can be recovered from hands in 40% to 90% of persons with colds and from up to 15% of objects near persons with colds. However, brief exposure such as a handshake or even being around an infected person for 36 hours causes transmission in less than 10% of subjects and in one study transmission was only 38% between spouses. Rhinoviruses can also be transmitted by aerosolization, for example, by being in a crowded room where people are sneezing. Kissing does not seem to be a common mode of transmission, probably because only about 10% of persons with colds have demonstrable virus in their saliva. Studies carried out in Antarctica dispel the popular idea that cold weather increases susceptibility to rhinovirus infection.

The nasal epithelium of persons with colds is remarkably intact even when studied with the electron microscope. Symptoms are best explained by physiologic responses:

  • release of chemical mediators of inflammation;

  • sensitization and irritation of airway receptors, with stimulation of the parasympathetic nervous system.

After an incubation period of 24 to 72 hours, most patients develop a sore or scratchy throat which is followed by nasal obstruction, rhinorrhea, and sneezing (figure 6). A green or yellow nasal discharge should not be construed as evidence of secondary bacterial infection (neutrophils cause yellow-green discoloration because of their natural myeloperoxidase activity). By the second and third day of the illness, rhinitis with nasal congestion replaces sore throat as the major complaint. By the fourth and fifth day, nasal symptoms have usually decreased but in about 30% of cases are replaced by cough or "chest cold".

 

 

Acute Bacterial Sinusitis

Few common problems in primary care are as confusing as sinusitis. Acute bacterial sinusitis is vastly over diagnosed, but chronic sinusitis can be frustrating and disabling. The paranasal sinuses are accessible to direct examination only by sophisticated instruments. Adequate specimens for cultures can be obtained only by invasive procedures. Low-grade sinusitis is an intrinsic feature of the common cold. Clinicians must distinguish between self-limited viral rhinosinusitis and acute bacterial sinusitis, which usually calls for antibiotic therapy.

Sinusitis is usually caused by obstruction of the ostia, as from edema, damage to ciliated epithelial cells, and/or increased volume or viscosity of the mucous secretions. The pathogenesis of acute sinusitis can be discussed in three complementary ways: anatomy, physiology, and microbiology.

Anatomically, the outflow tract of the maxillary sinus sits in an awkward position high on the medial wall of the sinus cavity and is connected to the nasal cavity by a narrow tubular passage known as the infundibulum. Gravitational drainage of the maxillary sinus is therefore tenuous and easily disrupted. A small area between the middle and inferior nasal turbinates where drainage from the maxillary, ethmoid, and frontal sinuses converges is known as the ostiomeatal complex. Anatomic or physiologic compromise of the ostiomeatal complex predisposes not only to maxillary sinusitis but also to infection of multiple sinuses (pansinusitis). Causes of mechanical obstruction of sinus drainage include deviated nasal septum, polyps, foreign bodies, tumors, concha bullosa (enlarged middle turbinates from pneumatization, present in 10% of the population), ethmoid bullae, choanal atresia, and―most commonly―mucosal swelling. Mucosal swelling is usually due to viral infection or allergic inflammation, but can also be caused by systemic disorders (such as cystic fibrosis and the dyskinetic cilia syndromes) or injury brought about by trauma, swimming or diving, or overuse of topical medication (rhinitis medicamentosa) or cocaine.

Physiologically, the sinuses are kept sterile mainly by a mucociliary blanket that changes two to three times per hour, a rate sufficient to prevent mucus from accumulating in the sinuses. Sinusitis results when mucociliary drainage of the paranasal sinuses fails because of mucosal edema, dysfunction of the ciliated epithelial cells, or both. Viral rhinitis and allergic rhinitis disrupt the epithelium as do cigarette smoking and intranasal cocaine use. Swimming predisposes to sinusitis for reasons that are somewhat unclear, although chlorine is known to irritate the mucosa. Other factors that may help to preserve the normal sterility of the paranasal sinuses include cellular and humoral immunity and nitric oxide.

Microbiologically, acute sinusitis typically starts with viral infection that paves the path for pathogenic bacteria. The major pathogens are Streptococcus pneumoniae and non-typeable strains of Haemophilus influenzae. Other bacteria associated with community-acquired sinusitis include group A streptococci, S. aureus, Moraxella catarrhalis, and viridans streptococci. Whether Chlamydia pneumoniae commonly causes sinusitis is currently being studied. Patients who have had nasogastric tubes in place are vulnerable to sinusitis caused by aerobic gram-negative rods such as Pseudomonas aeruginosa and Klebsiella pneumoniae. Anaerobic bacteria are associated with acute sinusitis mainly in the setting of dental disease. Anaerobic bacteria possibly play a role in chronic sinusitis (discussed separately, below).

Sinusitis usually begins with symptoms of the common cold such as runny nose, nasal obstruction, sore throat, cough, and the sensation of “pressure” or “tightness” in the face. The symptoms differ somewhat between children and adults. Children with sinusitis can have either of two presentations. The more common presentation consists of persistent cold symptoms that is, symptoms lasting more than 10 days. Children with persistent sinusitis seldom complain of headache or facial pain. Parents of young children often report malodorous breath. The less common presentation consists of severe cold symptoms―that is, cold symptoms that are accompanied by high fever (> 39° C) and purulent nasal discharge. Some of these children experience headaches usually located behind or around the eye, occasionally with periorbital edema. Adults with sinusitis, compared with children, tend to have more prominent facial pain, sometimes with local tenderness, swelling, and erythema. Pain patterns and other findings vary according to which sinuses are involved:

  • Maxillary sinusitis (the most common location): Pain is over the cheekbones or above the maxillary 2nd molar teeth.

  • Ethmoid sinusitis (common): Pain is between the orbits and the nasal bridge.

  •  Frontal sinusitis (uncommon): Pain is over the frontal bones.

  • Sphenoid sinusitis (least common, but dangerous): Pain can be frontal, temporal, orbital, or occipital; facial pain due to Vth nerve involvement is characteristic; pain is occasionally perceived over the vertex of the skull.

Low-grade fever is often present. Physical examination may reveal tenderness on percussion of the maxillary or frontal sinuses, and pinching the bridge of the nose may bring out tenderness if the ethmoid sinuses are involved. However, the sensitivity and specificity of these findings are unknown, and the clinical findings are often subtle.

Acute bacterial sinusitis is often self-limited, but the frequency with which this condition resolves spontaneously is unknown. Direct sinus puncture for accurate diagnosis has not been carried out in placebo-controlled clinical trials. Serious complications occur often enough to justify close follow-up, especially in the clinically more severe cases. The most common complication is progression to chronic sinusitis (see below). Cavernous sinus thrombosis can result from ethmoid, frontal, or sphenoid sinusitis. Ethmoid sinusitis can also cause orbital cellulitis. Frontal sinusitis can also cause osteomyelitis of the frontal bone with swelling and edema of the forehead (Pott’s puffy tumor) and subdural empyema. Sphenoid sinusitis can be a medical emergency.

 

 

Chronic Sinusitis

When acute sinusitis fails to resolve and becomes chronic, cultures may reveal a variety of opportunistic pathogens including anaerobic bacteria. Some authorities feel that the problem is no longer mainly “infectious” but rather reflects permanent mucosal injury. It has been estimated that chronic sinusitis causes morbidity, measured as absenteeism from school, work, or social activities, of the same magnitude as heart disease and arthritis.

The prevailing view holds chronic sinusitis to be a disorder of abnormal anatomy and physiology of the paranasal sinuses with one or more causes:

  • previous acute sinusitis

  • nasal polyposis (as in the triad of asthma, allergies, and aspirin sensitivity)

  • previous sinus surgery

  • cystic fibrosis

These processes lead to anatomic changes including obstruction of the infundibula and ostia, mucosal edema and scarring, bone hypertrophy, polypoid degeneration, and/or mucosal fibrosis, rendering the mucociliary clearance mechanism defunct.

Numerous microorganisms can be isolated from patients with chronic sinusitis, but correlation between culture results and the disease process is often poor. Mixtures of aerobic and anaerobic bacteria are common. The general conclusion at this time is that in most patients, no single microorganism can be assigned a pathogenic role. In some patients, however, Pseudomonas aeruginosa or Staphylococcus aureus seems to be clearly pathogenic, and there are data suggesting roles for Haemophilus influenzae and Moraxella catarrhalis (in children). Patients with chronic sinusitis often have exacerbations analogous to the acute exacerbations of chronic obstructive lung disease. In these instances, especially in children, Streptococcus pneumoniae and Haemophilus influenzae may be important. Numerous bacteria including gram-negative rods have been isolated with patients with post-operative sinusitis. Some investigators believe that many patients with chronic sinusitis have allergic fungal sinusitis (discussed further below), the disease manifestations being caused by an immune response to extramucosal fungi.

The typical history consists of nasal drainage, obstruction, and postnasal drip lasting for at least several months, often against a background of chronic “sinus trouble.” Patients often complain of headache or “sinus pain,” nocturnal cough, and bad breath. Loss of smell may also be present. Fever is unusual. A history of inhalant allergy is 4.5 times more common in patients with chronic sinusitis than in persons without chronic sinusitis.

Although physical examination can reveal findings such as nasal septal deviation or mucosal changes, imaging studies are necessary to make a correct diagnosis. The coronal CT scan represents the current gold standard, but axial CT scans are often useful especially in children. Sinus endoscopy an also provide invaluable information.

Chronic sinusitis may have a relapsing or remitting course, but, untreated, patients seldom become entirely free of symptoms related to the paranasal sinuses. Complications include remodeling of the facial bones, osteomyelitis, and―occasionally―invasive disease of the CNS caused by bacteria or fungi.

 

  This chest radiograph shows probable aspergillosis with an aspergilloma, or fungus ball in the upper lobe of the right lung. Lung diseases that damage a lung can cause cavities that can leave a person more susceptible to developing an aspergilloma, or fungus ball. The fungus can then begin secreting toxic and allergic products, which may make the person feel ill.  CDC/M. Renz


This patient presented with a case of a periorbital fungal infection known as mucormycosis, or phycomycosis.
Mucormycosis is a dangerous fungal infection usually occurring in the immunocompromised patient, affecting the regions of the eye, nose, and through its growth and destruction of the periorbital tissues, it will eventually invade the brain cavity. CDC



Pseudallescheria boydii is pathogenic in humans, especially those who are immunocompromised, causing infections in almost all body regions, and which are classified under the broad heading of “Pseudallescheriasis”. CDC

 

Fungal Sinusitis

Fungal sinusitis is relatively uncommon, but should be considered in patients with chronic sinusitis because of its potentially serious complications. Aspergillus species are the most common causes of fungal sinusitis, and fungi of the order Mucorales are the most dangerous (rhinocerebral mucormycosis). Various widely distributed pigmented fungi that are collectively known as dematiaceous molds can cause a variety of syndromes that include life-threatening disease; examples of these organisms include Alternaria, Bipolaris, Cladosporium, Curvularia, and Exserohilum. Numerous other fungi sometimes cause sinusitis.

      Five syndromes are currently recognized.

  • Simple colonization of the paranasal sinuses by fungi may be relatively common, although the incidence is unknown.

  • Sinus mycetoma (fungus ball) presents most often as a mass in the maxillary sinus. Underlying disease is usually not present although some patients have nasal polyps and chronic bacterial sinusitis. Patients usually seek medical attention for nasal obstruction, facial pain, symptoms of chronic sinusitis, or fetid breath (cacosmia). Seizures have been reported as a presenting manifestation.

  • Allergic fungal sinusitis usually presents as intractable sinusitis with nasal polyposis in patients with atopy. Some patients also have allergic bronchopulmonary aspergillosis. Children with allergic sinusitis may develop hypertelorism or proptosis when the frontal or ethmoid sinuses are involved. As mentioned above, some investigators believe that allergic fungal sinusitis is present in a majority of patients who carry the diagnosis of "chronic rhinosinusitis".

  • Acute (fulminant) invasive fungal sinusitis is essentially synonymous with rhinocerebral mucormycosis, which usually occurs in patients with diabetes mellitus or severe immunosuppression from other causes. The sinuses have been called "way stations to the brain" in this medical emergency, which classically presents as a painless black eschar on the palate or a nasal turbinate followed by epistaxis, headache, changes in mental status, and focal neurologic symptoms and signs (such as diplopia). Other fungi including Aspergillus species, Fusarium species, and Pseudallescheria boydii can cause an identical syndrome, typically in patients who are severely immunosuppressed from disease (including AIDS) or chemotherapy for cancer or organ transplantation.

  • Chronic invasive fungal sinusitis can occur not only in immunocompromised patients but also in patients who are immunologically normal. Most of these latter patients have chronic sinusitis and nasal polyposis. Causative organisms include the dematiaceous molds noted above; the condition is known as phaeohyphomycosis. Dense masses of fungal elements resembling mycetoma are found, but there is also invasion into the mucosa and then into bone. Patients present with headache and localizing symptoms such as decreased vision and loss of eye movement (orbital apex syndrome) or behavioral changes (mycetoma of the frontal lobe).

 


Erysipelas is a dermatologic condition, which involves the inoculation of the skin and subcutaneous tissue with streptococcal bacteria causing edema and bright red erythema of the affected areas. It is sometimes referred to as cellulitis. CDC
 

Otitis Externa

Otitis externa, a spectrum of conditions caused by infection, allergy, or primary skin disease, affects up to 10% of all people during their lifetimes. Necrotizing (malignant) otitis externa is a medical emergency seen usually in patients with diabetes mellitus or a compromised immune system or in patients who have had prior irradiation of the head.

Otitis externa begins with breakdown in the cerumen barrier. Cerumen, although commonly considered a nuisance, protects against infection by (1) creating an acidic environment hostile to bacterial and fungal growth; (2) promoting a dry environment through its hydrophobic properties; and (3) trapping debris by its sticky nature. Excessive cleaning or scratching of the ear canal promotes breakdown of the cerumen barrier. Swimming notoriously predisposes to otitis externa, the main effect being promotion of a more alkaline pH, which in turn promotes bacterial growth. However, increased moisture of any origin leads to maceration of the skin and breakdown. Mechanical trauma from devices such as ear plugs (used for hearing conservation in many industries), headphones, hearing aids, and diving caps also predisposes to otitis externa.

Pseudomonas aeruginosa and S. aureus are common causes of otitis externa. Group A streptococci and various gram-negative rods sometimes cause this condition, and anaerobic bacteria are involved in up to 25% of cases. About 10% of cases are caused by various fungi, with Aspergillus species being the most common followed by Candida species.

·        Acute localized otitis externa presents as a single or several pustules or furuncles located in the ear canal, usually due to S. aureus. Initial symptoms include itching, pain, swelling, redness, and sometime decreased hearing. A small furuncle that would be inconspicuous on most parts of the skin becomes intensely painful in the confines of the narrow ear canal.

·        Acute diffuse otitis externa (swimmer’s ear) typically presents with pain (otalgia), itching, discharge, and hearing loss. The pain can become intolerable. There is often a history of recent exposure to water. Mobile redwood hot tub systems were associated with a severe hemorrhagic form of the disease. Pseudomonas aeruginosa is the most common pathogen. Other patients give a history of ear instrumentation, excessive cleaning, previous infection, otitis media, tinnitus, or vertigo. Examination reveals the ear canal to be diffusely red and edematous.

·        Erysipelas involving the concha and canal is caused by group A streptococci, the pathogenesis being similar to that of erysipelas elsewhere. Patients present with a diffusely red and painful ear. Examination may reveal hemorrhagic bullae on the walls of the canal and on the tympanic membrane, and there may be tender regional lymphadenopathy.

·        Chronic otitis externa presents with mild discomfort and flaking of the skin of long duration, often with a history Otitis media can be graded in severity from mild (minor pain and pruritus, minimal edema of the ear canal) to severe (severe pain and pruritus, complete occlusion of the ear canal, auricular and periauricular erythema, and, frequently, fever and lymphadenopathy).

  •  Malignant otitis externa is a medical emergency usually encountered in patients with diabetes mellitus. A history of chronic otitis media with drainage is often obtained. Pseudomonas aeruginosa is the usual causative organism. Complications include osteomyelitis of the temporal bone (a defining feature of the disease) and extension to the base of the skull, with cranial nerve palsies, meningitis, and other serious consequences.

 Diagnosis of otitis externa is nearly always made by the history and physical examination. Pressure on the tragus or pulling the auricle superiorly causes pain; the latter maneuver is a valuable diagnostic aid. Examination of the ear canal shows erythema and edema and, in severe cases, partial or complete occlusion of the canal. To exclude otitis media, one should demonstrate with pneumatic insufflation that the tympanic membrane is mobile. However, the tympanic membrane is often partially or totally obscured by edema in the ear canal.

Although otitis externa is usually considered a self-limited condition, serious complications can occur. Perforation of the tympanic membrane can be caused by extension of the disease process or by misguided attempts by patients or health care providers to relieve the condition through mechanical manipulation. Other complications include stenosis of the ear canal, auricular cellulitis, or chondritis.

 

 

Acute Otitis Media

The importance of otitis media in primary care cannot be overemphasized, especially in pediatrics practice, where it accounts for about 25% of all office visits, 50% of office visits for illness, and 40% of antibiotic prescriptions. By age 5, between 75% and 95% of children have had at least one episode of otitis media. This disease is responsible for some 25 million office visits each year, with annual health care costs estimated to be between 3 and 5 billion dollars. Although 80% of patients with otitis media are less than 15 years of age, more than one-fourth of all oral antibiotic prescriptions in the United States are written for this condition. Heavy prescribing of β-lactam antibiotics for otitis media is thought to be responsible in large measure for the decreasing drug susceptibility of S. pneumoniae strains.     

Acute otitis media is often preceded by viral URI that causes edema and obstruction of the eustachian tube, causing an ex vacuo serous transudate into the middle ear and paving the way for pathogenic bacteria. Children are predisposed because their eustachian tubes are shorter, wider, and straighter compared with those of adults. Appreciation of otitis media requires knowledge of the relationship of the eustachian tube to the nasopharynx, the middle ear, and the mastoid air cells. The eustachian tube normally serves to regulate pressure in the middle ear, to protect against nasopharyngeal sound pressure and secretions, and to afford a pathway for the drainage of secretions produced within the middle ear into the nasopharynx. The latter function requires an intact mucociliary system. Factors predisposing to eustachian tube dysfunction and otitis media include allergy, cleft palate, ciliary dysmotility, immunodeficiency, exposure to tobacco smoke, exposure to frequent upper respiratory tract infections (notoriously, in day care centers), early age of first infection, and race. Native Americans are markedly predisposed to otitis media for reasons that are unclear. Adults can be predisposed to otitis media on account of diabetes mellitus, cancer, immune deficiencies, and injection drug use. The adenoids have long been implicated in the pathogenesis of otitis media, for better or worse, since

  • inflammation of the adenoids causes inflammatory obstruction of the adjacent eustachian tube orifices;

  • colonization of the adenoids by pathogenic bacteria promotes invasion of the middle ear by these same bacteria;

  • yet the adenoids provide local immunity in the form of secretory IgA secretion.

The microbiology in otitis media is similar in adults and children when tympanocentesis is carried out. In about 40% of cases, culture of middle ear fluid fails to show a bacterial pathogen. This might reflect a viral etiology or sterile inflammation. Respiratory syncytial virus has been found relatively commonly, with a special tendency to cause the disease in children. Influenza viruses and parainfluenza viruses also predispose to otitis media. Streptococcus pneumoniae causes about 30% to 40% of cases, and the prevalence of strains with reduced susceptibility to penicillin is increasing. H. influenzae causes between 20% and 30% of cases, and M. catarrhalis between 10% and 15% of cases, especially in children. Group A streptococci cause less than 5% of cases but can cause up to 10% during the winter months.

Acute otitis media in children usually presents with rapid onset of otalgia, fever, and/or irritability. Otalgia in young infants is manifest by pulling on the ear. Young children can also have anorexia, loose stools, and vomiting. Otalgia tends to be the major symptom in adults. A minority of patients experience spontaneous perforation of the tympanic membrane.

The tympanic membrane is abnormal, often bulging, with loss of the usual landmarks. Erythema of the tympanic membrane alone is not diagnostic; it can be caused, for example, by crying. Purulent fluid is sometimes seen behind the tympanic membrane. The key procedures are pneumatic otoscopy and, when indicated, tympanocentesis. Pneumatic otoscopy, which is done by gently squeezing and then releasing a rubber bulb attached to the otoscope, provides information about the mobility of the tympanic membrane. Tympanocentesis provides fluid for culture, which is becoming more important due to the emergence of drug-resistant bacteria. Cultures of the nasopharynx correlate poorly with cultures of fluid obtained by tympanocentesis, and are therefore of limited usefulness.

Acute otitis media must be distinguished from otitis media with effusion (serous otitis media). The latter consists of an asymptomatic or hyposymptomatic middle ear effusion, which can be acute (less than 3 weeks), subacute (3 weeks to 3 months), or chronic. Although hearing loss is frequently present in both acute otitis media and otitis media with effusion, patients with otitis media and effusion lack systemic signs and symptoms such as otalgia and fever.

The natural history of untreated otitis media continues to prompt debate whether most cases should be treated with antibiotics. A meta-analysis of the literature based on data obtained from 5400 children in 33 studies indicates that 81% percent of children have spontaneous resolution. However, it is difficult to predict on clinical grounds whether an individual patients disease will resolve spontaneously, and the current consensus opinion in the United States is that all patients should be treated.

 

 

Chronic suppurative otitis media and mastoiditis

Chronic suppurative otitis media is a complication of acute otitis media, usually occurring when there is a defect in the tympanic membrane, such as a "central" perforation or a tympanostomy tube. It is accompanied by purulent discharge (otorrhea). Mastoiditis is invariably present. The associated bacteria seem to vary depending on whether an infected cholesteatoma is present. Cholesteatoma is often associated with anaerobic bacteria and “skin flora” microorganisms, and the otorrhea often has a foul odor. When cholesteatoma is not present, gram-negative rods including Pseudomonas aeruginosa and E. coli are often found.

In the pre-antibiotic era, mastoiditis was often a dramatic and severe illness with retroauricular inflammation and serious intracranial complications. Today, mastoiditis is more typically an indolent, low-grade, often painless infection of the temporal bone that tends to be clinically silent ("masked mastoiditis") unless a complication such as brain abscess develops. Patients at high risk of complications include newborn infants, persons with diabetes mellitus, the elderly, and the immunocompromised.

Spontaneous resolution is rare, if it occurs at all. Local complications of chronic suppurative otitis media and mastoiditis include bone destruction, subperiosteal abscess, facial paralysis, labyrinthitis, and petrositis. Intracranial complications include brain abscess, subdural abscess, epidural abscess, septic thrombosis of the lateral sinus, meningitis, and hydrocephalus. Patients with chronic suppurative otitis media and/or mastoiditis should be referred to an otolaryngologist, as effective treatment usually requires surgical intervention.

 

Figure
Staphylococcal parotitis, face of elderly woman.
CDC

Acute suppurative parotitis 

Acute suppurative parotitis, an uncommon condition, usually results from decreased salivary flow, allowing retrograde ascent of bacteria from Stenson’s duct. It can also result from ductal obstruction from mucus or fibrinous plugs, tumors, or foreign bodies). The clinical signs and symptoms include an acutely swollen, indurated check with fever and pain. Pus can be expressed from Stenson’s duct. More than 80% of cases are caused by Staphylococcus aureus. Most patients are elderly, debilitated, and dehydrated. Mortality is high.

 

 

Acute pharyngitis

Acute pharyngitis (sore throat) is one of the most common problems encountered in clinical practice. Viruses cause most cases as part of the common cold. However, about 15% of cases, and up to 50% of cases in children during some periods, are caused by group A β-hemolytic streptococci (S. pyogenes). Although usually self-limited, streptococcal pharyngitis demands respect as a cause of acute rheumatic fever and―less commonly―major suppurative complications, acute glomerulonephritis, and even the streptococcal toxic-shock syndrome. The clinician’s task is to determine in a cost-effective manner which patients need treatment and which do not.

Acute pharyngitis has many known etiologies, and pathogens remain to be discovered for an estimated 30% of cases. Viral infections cause sore throat, it is thought, by generating bradykinin and lysyl bradykinin, which stimulate nerve endings. Group A streptococci and certain other pathogens including some of the respiratory viruses cause pain by invading the mucosa.

Group A streptococci are carried in the human nasopharynx and transmitted from person to person usually by direct contact with saliva or nasal secretions. Acquisition is greatest in school-aged children, suggesting the gradual development of immunity over time. Children also serve as a reservoir for spread among family members. Asymptomatic pharyngeal carriage of group A streptococci is relatively common, and the factors that cause some persons to develop acute pharyngitis and other complications are poorly understood. Group C and group G streptococci cause a pharyngitis syndrome clinically indistinguishable from that caused by group A streptococci, sometimes recognized as outbreaks related to a common food source. Group C streptococci (S. dysgalactiae subspecies equisimilis) appear to be a frequent cause of pharyngitis in college-aged students.

Pharyngitis due to group A streptococci occurs most frequently in children between 5 and 15 years of age, usually during the winter and early spring. In its severe form the disease starts abruptly with fever, sore throat, and odynophagia. Chills, headache, and abdominal pain are sometimes present. Examination reveals diffuse erythema of the pharynx and tonsils accompanied by a patchy, purulent tonsillar and pharyngeal exudate, hypertrophy of the lymphoid nodules in the posterior pharyngeal mucosa, and tender cervical lymphadenopathy. Occasional strains of S. pyogenes elaborate the erythrogenic toxin of scarlet fever, resulting in a striking rash and "red strawberry tongue" with enlargement of the papillae. Rhinorrhea and cough are usually not present, but may occur. However, these dramatic manifestations are absent in many, perhaps most cases of streptococcal pharyngitis. Because the features of group A streptococcal pharyngitis blend imperceptibly with those of other causes of sore throat, numerous students of the disease have concluded that the diagnosis must be secured by laboratory methods prior to definitive treatment (see below). Other syndromes include the following:

  • The common cold is often accompanied by sore throat, which is frequently the first symptom but is usually not the main complaint when patients seek medical care. Rhinorrhea, postnasal drainage, and cough are usually more prominent symptoms than sore throat. Fever is seldom prominent and severe sore throat with odynophagia are uncommon.
     

  • Influenza sometimes presents with sore throat as the chief complaint, but is usually accompanied by other symptoms suggesting influenza such as myalgia, headache, and cough. In pharyngitis due to the common cold or to influenza, purulent pharyngeal or tonsillar exudates and tender cervical lymphadenopathy are not present. Tracheal tenderness may be present in influenza, indicating diffuse viral infection of the respiratory mucosa.
     

  • Adenoviral pharyngitis, on the other hand, often presents with sore throat as the chief complaint. Fever, chills, headache, malaise, and myalgias can be prominent. About one-third to one-half of patients with adenoviral pharyngitis also have follicular conjunctivitis; this syndrome is known as pharyngoconjunctival fever. Patients with adenoviral pharyngitis often have pharyngeal exudate, so the disease can mimic streptococcal pharyngitis. Epidemics of pharyngoconjunctival fever occur during the summer months in civilian populations and during the winter months in military recruits.
     

  •  Infectious mononucleosis due to the Epstein-Barr virus causes exudative tonsillitis or pharyngitis in about one-half of cases. Tonsillar and pharyngeal exudates can be prominent. If examined with Wright’s stain, the exudates of mononucleosis consist mainly of mononuclear cells in contrast to the exudates of streptococcal pharyngitis, which consist mainly of polymorphonuclear neutrophils. Tender cervical lymphadenopathy is often prominent in the posterior triangles of the neck (spinal accessory chain of nodes), contrasting with the prominent anterior nodal enlargements (jugulodigastric chain) typical of bacterial pharyngitis. Patients with mononucleosis usually have headache, fatigue, and other features of the disease such as palpable splenomegaly (about one-half of cases). Peripheral blood smear typically shows lymphocytosis with atypical lymphocytes. Cytomegalovirus mononucleosis can also cause sore throat, but pharyngeal exudate is rare.
     

  • Primary infection with HIV, known as the acute retroviral syndrome, sometimes presents with fever and pharyngitis. Pharyngeal erythema can be marked but exudates do not seem to occur. This illness usually occurs within 3 to 6 weeks of the initial infection, during a phase of initial viral multiplication and prior to the appearance of HIV antibodies. Fever, lethargy, arthralgia, and myalgia are usually prominent and many patients have a nonpruritic maculopapular rash. Lymphadenopathy, which can be in the anterior and/or posterior triangles, appears about one week after the onset of pharyngitis.
     

  • Herpes simplex virus infection can cause pharyngitis, which can sometimes resemble viral or streptococcal pharyngitis. Vesicles and shallow ulcers on the palate suggest the herpetic etiology. These can be extensive and confluent, causing severe oral pain (see “Mouth Ulcers,” below). Herpangina is an uncommon syndrome caused by coxsackieviruses and is seen mainly in children. It is characterized by small (1 to 2 mm) vesicles on the soft palate, uvula, and anterior tonsillar pillars, which rupture to form small white ulcers. Fever, sore throat, and dysphagia can be severe and occasional patients experience anorexia and abdominal pain suggesting acute appendicitis.
     

  • Chlamydia pneumoniae can cause pharyngitis with or without infection of the lower respiratory tract. No distinctive features have been described. There is some epidemiologic evidence that Mycoplasma pneumoniae causes pharyngitis, usually mild and again without distinctive features.
     

  • Diphtheria should be mentioned, as it still causes occasional cases of pharyngitis in the United States in patients who have not been vaccinated. Classical diphtheria (Corynebacterium diphtheriae) has a slow onset followed by marked systemic toxicity. Sore throat is usually not severe despite the finding of a gray "pseudomembrane" adherent to the tonsillar and pharyngeal mucosa. Arcanobacterium hemolyticum (formerly known as Corynebacterium hemolyticum) has been increasingly recognized as a cause of exudative pharyngitis in adolescents and young adults, associated with a diffuse and sometimes pruritic maculopapular rash on the trunk and extremities. Rarely, this disease can mimic diphtheria. Corynebacterium ulcerans is a rare cause of pharyngitis associated with the ingestion of raw milk.

  • Anaerobic pharyngitis (Vincent’s angina) presents with a purulent exudate and often a foul odor to the breath. This uncommon infection is caused by a mixture of anaerobic bacteria and spirochetes, with group A streptococci and S. aureus sometimes playing a role. This infection sometimes progresses to peritonsillar abscess (quinsy) or to septic thrombophlebitis of the internal jugular vein (Lemierre syndrome).
     

  • Yersinia enterocolitica can cause exudative pharyngitis with a fulminant course associated with high mortality. Fever, tender cervical lymphadenopathy, and abdominal pain with or without diarrhea are prominent features. This illness can occur in outbreak form due to ingestion of contaminated food or beverages.
     

  • Tularemia can present as pharyngitis in the typhoidal form of the disease due to inhalation of the organisms, which can occur while skinning an infected rabbit.

  •  Kawasaki syndrome, a systemic vasculitis affecting mainly infants and young children, can present with fever and sore throat. Diffuse oropharyngeal erythema without exudate is found during the acute febrile phase of the illness. Other features include bilateral, nonpurulent conjunctivitis, erythema with fissuring, cracking, and bleeding of the lips, strawberry tongue, edema of the hands and feet with erythema of the palms and soles, and an erythematous rash.

Miscellaneous causes of sore throat include juvenile rheumatoid arthritis, systemic lupus erythematosus, bullous pemphigoid, Behçet’s disease, paraquat ingestion, and drug reactions.

 

 

Acute Laryngitis 

Acute laryngitis is extremely common, usually occurring as part of upper respiratory tract infection. Treatment is symptomatic, but prolonged hoarseness mandates the search for other etiologies. Acute laryngitis is most often caused by respiratory viruses, but vocal abuse or gastroesophageal reflux must also be considered. Parainfluenza viruses are the usual cause in patients between ages 5 and 15. Hoarseness complicates up to 29% of rhinovirus infections, 35% of influenza virus and adenovirus infections, and 63% of coronavirus infections according to various studies. Hoarseness can also complicate acute streptococcal pharyngitis. H. influenzae and Moraxella catarrhalis are often isolated, but their pathogenic roles are unclear. Rarely, fungi such as Candida species, Cryptococcus neoformans and Coccidioides immitis can cause laryngitis. Uncommonly, laryngitis can also be caused by tuberculosis and blastomycosis.

Acute laryngitis presents as hoarseness. Speech and/or swallowing may be painful. The voice is hoarse, harsh, broken, or nearly absent. There are often concomitant symptoms of common cold including sore throat. Diagnosis of acute laryngitis is made on clinical grounds, typically by the history. Direct or indirect laryngoscopy shows erythema and edema of the vocal folds, sometimes with submucosal bruising or micro-hemorrhages (if the patient continues major voice use or has a bad cough). Viral cultures and special studies are seldom indicated.

 

 

Odontogenic Infections

Odontogenic infections, the most common infections of the oral cavity, begin in and around the teeth and can spread to cause life-threatening local or systemic complications.

The normal oral cavity contains dense masses of bacteria, of which more than 80% or more are anaerobic. Viridans streptococci (such as S. mitis, S. sanguis, S. salivarius, and S. mutans) preferentially colonize one or another anatomic site. Streptococcus mutans is the major cause of dental caries (cavities). As is well known, poor oral hygiene facilitates development of dental plaque, composed mainly of anaerobic bacteria. Diet high in simple sugars and carbohydrates predisposes to plaque. Periodontal disease, on the other hand, is unrelated to diet but is associated with poor oral hygiene, increasing age, and with various congenital immunodeficiency diseases and juvenile diabetes mellitus. Gingivitis and periodontitis are caused mainly by anaerobic bacteria. Once established, suppuration arising in and around the teeth can spread along fascial planes, invade bone, or enter the bloodstream. Deeper infections requiring surgical drainage, such as periapical abscesses and deep fascial space infections, are usually associated with numerous anaerobic bacterial species.

      Odontogenic infections present as one of several syndromes:

  • Periapical abscess and acute alveolar abscess represent infection of the tooth pulp. In the early stages, the tooth is sensitive to touch and also to both hot and cold. In the later stages, the tooth is extremely painful to heat, the pain being relieved by cold.
     

  • Gingivitis is often first manifest by friability and bleeding of the gums. A more severe form, known as acute necrotizing gingivitis (Vincent’s angina or trench mouth), presents with sudden onset of severe pain and necrosis of the gingiva, typically with a grayish pseudomembrane, halitosis, and systemic symptoms including fever, malaise, and generalized lymphadenopathy.
     

  • Periodontitis, broadly defined as infections of the periodontium (the supporting structures of the teeth, which include alveolar bone, cementum, and the periodontal ligament as well as the gingiva) begins gradually, usually in early adulthood, and is associated with plaque below the gingival margin. Patients sometimes complain of itchy sensations of the gums in between the teeth, bad taste in the mouth, vague jaw pains, and sensitivity to both hot and cold. Pus can sometimes be expressed by pressure on the gingival margin. Periodontal abscess can present as a red, fluctuant swelling of the gingival margin. Pus can readily be expressed after probing.
     

  • Pericoronitis consists of acute localized pain over a partially erupted or impacted wisdom tooth. The gums are red and swollen, and a small amount of pus can usually be expressed by pressing on the gum flap overlying the partially erupted tooth. Trismus caused by irritation of the masseter or medial pterygoid muscle is often marked.

Diagnosis of dentoalveolar infections, gingivitis, and periodontal infections is based upon symptoms, examination, and, when indicated, dental x-rays. Dental x-rays are especially valuable for visualizing periapical abscess and acute alveolar abscess.

 

 

Mouth Ulcers

Careful examination of the oral cavity often provides evidence of important systemic and local disease. More commonly, primary care clinicians evaluate patients with self-limited diseases such as stomatitis due to the herpes simplex viruses and aphthous stomatitis (canker sores). Here we will briefly review these latter conditions and their differential diagnosis.

Herpes simplex viruses 1 and 2 cause fever blisters and, less commonly, lesions elsewhere in the mouth including the palate. The cause of aphthous stomatitis is unknown. Current opinion favors an immunopathogenesis involving T-cell immunity, possibly a delayed-type hypersensitivity reaction to an antigen residing within the epithelium. Some cases of aphthous stomatitis have been attributed to drugs. Stress, smoking, hormonal factors, and food allergy have also been invoked, but the evidence is unconvincing.

Herpes simplex stomatitis begins with small, 1 to 2 mm vesicles that rupture, leading to ulceration. Confluent lesions can give rise to large areas of ulceration. Lesions typically occur on keratinized or attached oral mucosal surfaces such as the lips, the gingiva, the lateral surfaces of the tongue, or the palate. Aphthous stomatitis begins with ulcers of various sizes, usually from several mm to 1 cm or more in diameter. Lesions typically occur on non-keratinized, unattached mucosal surfaces. Both types of lesions are painful.

 

Return to the Infectious Disease Section of Microbiology and Immunology On-line

This page copyright 2011, The Board of Trustees of the University of South Carolina
This page last changed on Thursday, February 24, 2011
Page maintained by
Richard Hunt