Etiopathogenesis and Causative Factors

Most infections of the head and neck are initiated by streptococci and perpetuated by anaerobes. This pattern probably applies to nonodontogenic as well as odontogenic abscess-forming head and neck infections. The streptococci are able to elaborate hyaluronidases that lyse the ground substance of connective tissue, allowing the bacteria to spread through soft tissue planes. Then, these bacteria are able to synthesize nutrients upon which the anaerobic members of the infecting flora depend. Further, the streptococci are able to consume local oxygen supplies, and by their acidic by-products, reduce the pH of the infected site. In this manner, the invading streptococci are able to create a favorable environment for the later growth of obligate anaerobic bacteria. Thus, in the first 3 days of symptoms, a predominantly aerobic or facultative flora is cultivated from head and neck infections. Thereafter, a mixed flora of aerobic or facultative organisms plus anaerobes can be isolated. Once an infection matures and the local oxygen supplies have been consumed, such as within an abscess cavity, a purely anaerobic flora is often identified.

Many of the anaerobic bacteria, however, are able to synthesize penicillinases. This capability allows the anaerobic members of the infecting flora to “return the favor” to the invading species by neutralizing many β-lactam antibiotics, such as penicillin, providing protection for otherwise penicillin-sensitive organisms. This phenomenon has been demonstrated in a recent case series of severe odontogenic infections requiring hospitalization, in which penicillin therapy failed in 21% of patients receiving it and in 60% of the cases in which one or more penicillin-resistant organisms was isolated.

The usual pathogens of head and neck infections are listed in Table 116-1 . The similarities among the pathogens associated with the various types of head and neck infection lend further credence to the concept that the primary pathogenic agents of head and neck infections are streptococci plus anaerobes. One may add to that list certain respiratory pathogens, such as Haemophilus influenzae, and S taphylococcus aureus for skin-related or nosocomial infection, such as poststernotomy osteomyelitis of the sternum. Necrotizing fasciitis occurs in four types, according to the microbial etiology. In the head and neck, the polymicrobial and the streptococcal types occur most frequently.

Some head and neck infections are caused by pathogens other than bacteria. Of course, there are viral infections such as herpes simplex stomatitis and herpangina. Fungal infections, such as mucormycosis and noma, may also occur in the immunosuppressed or malnourished patient. Mycobacterial infections are divided into tuberculous and nontuberculous types. Table 116-2 lists the comparative diagnostic features of tuberculous and nontuberculous infections of the head and neck. This information may assist the clinician in choosing diagnostic maneuvers for identifying mycobacterial infections.

A new association between syphilis and HIV among men who have sex with men (MSM) may present as orofacial infection. There has been a dramatic increase in syphilis among MSM in the United States in recent years. This spread of syphilis has been facilitated by the misconception that unprotected oral sex is safe, since HIV is not carried in saliva at infective levels. On the other hand, the syphilitic chancre and the mucus patches of secondary syphilis are highly infective with Treponema pallidum. The ulcerated lesions of primary and secondary syphilis serve as very effective portals of entry for HIV. In this manner, syphilis may serve as a potentiating cofactor in the spread of HIV infection. An oral chancre is illustrated in Figure 116-1 .

A primary chancre of syphilis on the ventral surface of the tongue.

(From Flynn TR, Hunter GJ, Johnson MM. Case records of the Massachusetts General Hospital. Case 6-2010. A 37-year-old man with a lesion on the tongue. N Engl J Med. Feb 25;362:740-748, 2010.)

Pathologic Anatomy

The usual pathogens of head and neck infections are the oral streptococci and anaerobes. Both of these groups are excellent abscess-formers, and when these organisms are introduced deeply into the tissues, such as in a dental periapical infection, the infection tends to pass through the stages of infection. These are inoculation, the spread of bacteria into soft tissue spaces; edema, the initial inflammatory response to bacteria and their by-products; cellulitis, a highly inflamed spreading induration; abscess, characterized by central fluctuance and suppuration; and finally resolution, when spontaneous or surgical drainage is achieved. Further, the infection tends to spread through recognized anatomic compartments, such as bone, fascial spaces, the paranasal sinuses, or vascular structures, especially the valveless head and neck veins. The anatomic presentation of various head and neck infections is presented later, in the chapter on the surgical therapy of head and neck infections.

Other types of head and neck infections, however, also follow characteristic anatomic patterns. For example, viruses and treponemes tend to cause spreading surface mucosal infections, such as herpes and syphilis. The superficial form of necrotizing fasciitis follows the platysma muscle from the inferior border of the mandible down the neck and onto the chest wall. This phenomenon is illustrated in Figure 116-2 , which depicts the end result of necrotizing fasciitis, osteomyelitis, and split-thickness skin grafting in a patient with uncontrolled HIV infection, multiple periapical abscesses, and osteomyelitis of the mandible.

Clinical result of odontogenic abscess, mandibular osteomyelitis, necrotizing fasciitis, and skin grafting in a 37-year-old male with previously uncontrolled HIV infection.

Fungal infections tend to follow microvascular patterns. Their propensity to invade and occlude capillaries and other small vascular channels causes the necrosis seen in mucormycosis and other related infections. On the other hand, bacterial infections may occasionally follow the larger vascular pathways. Odontogenic cavernous sinus thrombosis, as illustrated in Figure 116-3 , follows recognized venous pathways from the face into the cranium. Small emissary veins that perforate the inner table of the cranium may allow bacteria from chronic sinusitis to pass into the brain, causing brain abscess, as illustrated in Figure 116-4 . Sometimes these small emissary veins also allow infection to pass through paper-thin layers of bone from the sinuses into the orbit, as illustrated in Figure 116-5 , in which a maxillary and ethmoid sinusitis passed through the lamina papyracea into the orbit, causing orbital subperiosteal abscess.

Cavernous sinus thrombosis due to an upper right first molar.

(From Flynn TR, Topazian RG: Infections of the oral cavity. In Waite D, editor: Textbook of practical oral and maxillofacial surgery. Philadelphia, 1987, Lea & Febiger.)

CT of frontal lobe brain abscess caused by nearby frontal sinusitis.

Subperiosteal orbital abscess. A, Clinical view. B, CT demonstrating left maxillary and ethmoid sinusitis, soft tissue thickening along the left medial orbital wall, and lateral displacement of the globe.

(From Simos C, Flynn TR, Piecuch JF, Topazian RG: Infections of the oral cavity. In Feigin RD, Cherry JD, Demmler-Harrison GL, et al, editors: Textbook of pediatric infectious diseases, ed 6. Philadelphia, 2009, Lippincott.)

Necrotizing fasciitis may also have a deep anatomic pattern. Cases historically described as descending necrotizing mediastinitis may represent the same process as necrotizing fasciitis, only on a deeper anatomic plane. Rapidly developing cases of mediastinitis, characterized by necrotic tissue found deep in the neck at surgical exploration, may simply be cases of necrotizing fasciitis that have followed the deep fascial planes of the neck into the danger space and from there into the mediastinum.

Pathologic Anatomy

The usual pathogens of head and neck infections are the oral streptococci and anaerobes. Both of these groups are excellent abscess-formers, and when these organisms are introduced deeply into the tissues, such as in a dental periapical infection, the infection tends to pass through the stages of infection. These are inoculation, the spread of bacteria into soft tissue spaces; edema, the initial inflammatory response to bacteria and their by-products; cellulitis, a highly inflamed spreading induration; abscess, characterized by central fluctuance and suppuration; and finally resolution, when spontaneous or surgical drainage is achieved. Further, the infection tends to spread through recognized anatomic compartments, such as bone, fascial spaces, the paranasal sinuses, or vascular structures, especially the valveless head and neck veins. The anatomic presentation of various head and neck infections is presented later, in the chapter on the surgical therapy of head and neck infections.

Other types of head and neck infections, however, also follow characteristic anatomic patterns. For example, viruses and treponemes tend to cause spreading surface mucosal infections, such as herpes and syphilis. The superficial form of necrotizing fasciitis follows the platysma muscle from the inferior border of the mandible down the neck and onto the chest wall. This phenomenon is illustrated in Figure 116-2 , which depicts the end result of necrotizing fasciitis, osteomyelitis, and split-thickness skin grafting in a patient with uncontrolled HIV infection, multiple periapical abscesses, and osteomyelitis of the mandible.

Clinical result of odontogenic abscess, mandibular osteomyelitis, necrotizing fasciitis, and skin grafting in a 37-year-old male with previously uncontrolled HIV infection.

Fungal infections tend to follow microvascular patterns. Their propensity to invade and occlude capillaries and other small vascular channels causes the necrosis seen in mucormycosis and other related infections. On the other hand, bacterial infections may occasionally follow the larger vascular pathways. Odontogenic cavernous sinus thrombosis, as illustrated in Figure 116-3 , follows recognized venous pathways from the face into the cranium. Small emissary veins that perforate the inner table of the cranium may allow bacteria from chronic sinusitis to pass into the brain, causing brain abscess, as illustrated in Figure 116-4 . Sometimes these small emissary veins also allow infection to pass through paper-thin layers of bone from the sinuses into the orbit, as illustrated in Figure 116-5 , in which a maxillary and ethmoid sinusitis passed through the lamina papyracea into the orbit, causing orbital subperiosteal abscess.

Cavernous sinus thrombosis due to an upper right first molar.

(From Flynn TR, Topazian RG: Infections of the oral cavity. In Waite D, editor: Textbook of practical oral and maxillofacial surgery. Philadelphia, 1987, Lea & Febiger.)

CT of frontal lobe brain abscess caused by nearby frontal sinusitis.

Subperiosteal orbital abscess. A, Clinical view. B, CT demonstrating left maxillary and ethmoid sinusitis, soft tissue thickening along the left medial orbital wall, and lateral displacement of the globe.

(From Simos C, Flynn TR, Piecuch JF, Topazian RG: Infections of the oral cavity. In Feigin RD, Cherry JD, Demmler-Harrison GL, et al, editors: Textbook of pediatric infectious diseases, ed 6. Philadelphia, 2009, Lippincott.)

Necrotizing fasciitis may also have a deep anatomic pattern. Cases historically described as descending necrotizing mediastinitis may represent the same process as necrotizing fasciitis, only on a deeper anatomic plane. Rapidly developing cases of mediastinitis, characterized by necrotic tissue found deep in the neck at surgical exploration, may simply be cases of necrotizing fasciitis that have followed the deep fascial planes of the neck into the danger space and from there into the mediastinum.

Diagnostic Studies

The Gram stain is a simple and rapidly available diagnostic test that can quickly identify broad categories of bacteria. This test indicates the ability of the sampled bacteria to bind Gram’s iodide stain. The cell morphology and the growth pattern of the bacteria, such as cocci or rods, and distribution in pairs, chains, or clumps can also be observed.

The most widely used and currently dependable method for diagnosing bacterial infections is culture and sensitivity. Since 94% of odontogenic infections contain anaerobic bacteria, it is important for the clinician to identify both aerobic and anaerobic bacteria by using culture swabs for each type. Certain types of swab culture systems, however, are capable of preserving both aerobic and anaerobic bacteria, at least for reasonably brief periods of time. The surgeon should check the expiration date of culture swabs before using them because of their short shelf life.

A major limitation of conventional culture methods is that approximately 60% of the oral flora, for example, are not yet culturable by available methods. Therefore a large proportion of the species found in a given specimen may not be identified. On the other hand, it is reassuring to note that conventional culture methods do seem to yield clinically useful information. Another limitation of conventional culture methods is the time required for identification of fastidious organisms such as the slow-growing oral pathogens. Often, species identification cannot be made until 7 days or more after sampling. By this time, the patient’s clinical course has usually either improved or deteriorated dramatically. Antibiotic sensitivity testing may require up to another 7 days in the case of slow-growing organisms. More timely availability of culture and sensitivity results would be most useful to clinicians. Practical clinical indications for culture and sensitivity testing are listed in Table 116-3 .