Bacterial, Viral and Fungal Infections
Many of the systemic diseases are caused by a wide range of bacteria, viruses and fungal organisms. Some of these microbial diseases can exhibit oral manifestations. However, some of the microbial diseases such as dental caries and periodontal diseases are localized to the oral cavity. Systemic microbial diseases with oral manifestations are discussed in this chapter.
Scarlet fever is also known by the names scarlatina, scarlatinella and scarlatiniform rash. It is caused by an infection with a pyogenic exotoxinproducing group A β-hemolytic streptococci. The upper respiratory tract is the usual portal of entry. Most cases occur between 1 and 10 years of age and may occasionally be seen in adults.
The incubation period of the bacteria ranges from 1 day up to a week. Patients will present with fever and skin rashes within the first 2 days of the infection. The fever and rash usually resolve in about 7 days. Other associated clinical features include headache, tonsillitis, pharyngitis and lymphadenopathy.
The scarlet fever rash appears bright red and mimics a sunburn appearance. Normal pin head-sized areas of the skin may project through the rash giving rise to a sandpaper like surface texture, which is popularly referred to as ‘sandpaper rash’ or ‘sunburn with goose bumps or goose pimples’.
The skin rashes are commonly seen over the trunk, extremities, neck, groin and specifically along Pastia’s lines (darkening of the normal skin fold/creases, such as the axillary crease, anticubital crease).
Patients may present with circumoral pallor. The soft palate, pharynx, tonsillar region and the tongue are commonly affected. The oral cavity appears extensively erythematous and edematous (stomatitis scarlatina). Occasionally a yellowish-white exudate may be seen in the tonsillar crypts.
During the first 2 days of the infection the dorsal surface of the tongue exhibits a white coat through which the fungiform papillae are visible. Such an appearance is referred to as ‘white strawberry tongue’. After about 4 days the white coat on the tongue desquamates to reveal an erythematous dorsal surface with hyperplastic fungiform papillae, which is referred to as ‘red strawberry tongue’.
The complications of untreated scarlet fever may occur either due to streptococcal toxin (myocarditis), or bacterial invasion (septic arthritis, meningitis, osteomyelitis) or by an allergic reaction (rheumatic fever, glomerulonephritis).
The diagnosis can be made based on the characteristic clinical presentations, culture of the secretions from the pharynx or tonsillar regions and detection of antigens specific for group A β-hemolytic streptococci.
A single episode of scarlet fever will usually confer permanent antitoxin immunity. However, recurrences are not unusual. This is due to the fact that toxin produced by other strains is not neutralized and the bacterial immunity is temporary.
Penicillin is the drug of choice. Erythromycin may be used in patients who are allergic to penicillin. Acetaminophen or ibuprofen may be used to alleviate pain and manage fever. Analgesic mouthrinses (benzydamine hydrochloride) may be used for stomatitis.
Diphtheria is an acute infectious disease caused by toxin-producing Corynebacterium diphtheriae or Klebs-Löffler bacillus (after Klebs who discovered the bacillus and Loffler who isolated the bacillus in pure culture).
The bacteria reside in the upper respiratory tract of the infected individual and cause local infection of the upper respiratory tract and occasionally the skin and the heart, kidneys, and peripheral nerves.
It spreads through droplet infection and direct contact. The incubation period lasts for a few days, following which the bacterium expresses an exotoxin that causes tissue necrosis that subsequently spreads peripherally.
Tonsillitis is usually the first clinical finding. Patients present with fever, malaise, headache, sore throat, foul taste/breath and cervical lymphadenopathy. The exotoxin causes necrosis of the soft tissues producing a thick, grayish white membrane. As the infection progresses patients may complain of difficulty in speech, swallowing and breathing.
The grayish pseudo membrane (diphtheritic membrane–covers necrotic ulcerated areas of the mucosa and contains dead cells, leukocytes and bacteria) initially forms on the tonsils and subsequently spreads to involve the larynx, pharynx, uvula, soft palate and occasionally the gingiva. Removal of this mildly adherent membrane leaves a raw bleeding surface. Some patients may exhibit transient paralysis of the soft palate.
Extensive involvement of the respiratory tract may lead to respiratory obstruction. The other serious complications include effects of the toxin on the cardiovascular system, nervous system and renal system to cause myocarditis, polyneuritis and acute interstitial nephritis.
It is transmitted to men from animals (chiefly rabbits and also by muskrats and squirrels) by contact with diseased or dead animals, by the bites of deer flies, fleas, and ticks; by contact with contaminated animals or their products; by ingestion of contaminated food or water or by inhalation of aerosolized bacteria. Young and middle-aged individuals who are actively involved in outdoor activities are more susceptible to the disease.
The incubation period of tularemia usually varies from 3 to 4 days. The initial symptoms include fever, chills, myalgias and malaise. Disseminated form of the disease can cause tularemic meningitis, pericarditis, peritonitis, endocarditis and osteomyelitis. Occasionally a severe form of tularemia, typhoidal tularemia may be seen.
|Type of tularemia||Mode of transmission||Clinical features|
|Ulceroglandular tularemia||Bite of infected insects and animals (ticks, rabbits)||Ulcers at the site of inoculation (fingers, hands, feet) Inflammation of the regional glands. Tender nodes|
|Glandular tularemia||Similar features as that of the ulceroglandular variety except that there is no evidence of ulcer|
|Pneumonic tularemia||Inhaling of airborne bacteria from soil or inhalation of the bacteria by healthcare workers||Pneumonia is the characteristic feature. Other symptoms include dry cough, dyspnea, and pleuritic chest pain|
|Oropharyngeal tularemia||Eating undercooked meat of an infected animal or drinking contaminated water||Vomiting, diarrhea and other digestive problems|
|Oculo-glandular form||Occurs following exposure of the conjunctiva to infected blood||The affected eye is tender and erythematous. Occasionally purulent exudate may be seen along with inflamed regional glands|
In the initial stages solitary nodular masses may be appreciated which may eventually form abscesses or ulcerate. Generalized stomatitis along with extremely painful necrotic ulcers may be seen affecting any part of the oropharynx. Regional lymphadenopathy is usually a prominent feature.
Erysipelas is an acute inflammation of the skin, with marked involvement of cutaneous lymphatic vessels. It is usually caused by β-hemolytic Streptococcus pyogenes of group A. Erysipelas has to a lesser extent been caused by group B, C, or G streptococci, and occasionally by Staphylococcus aureus.
The typical lesion of erysipelas is evident as an erythematous, well defined area that may be warm to touch. Occasionally a butterfly rash mimicking lupus erythematosus may be seen when the bridge of the nose is involved. Fever of sudden onset is a typical feature. Erysipelas is usually seen in young or old patients and in systemically compromised patients.
The typical rash of erysipelas can affect skin on any part of the body. However previous sites of trauma are the most commonly affected. The common sites affected include the legs, cheeks, eyelids and bridge of the nose.
Impetigo is a highly contagious superficial skin infection caused by β-hemolytic streptococci and Staphylococcus aureus. Impetigo is considered as the most common bacterial dermal infection in children. It is more common in children receiving dialysis.
Impetigo usually affects children in the age group of 2–6 years. It spreads via direct skin contact. The incidence of impetigo is greatest in the summer months, and the infection most often occurs in areas with poor hygiene and in crowded living conditions.
The host response to the infection results in the non-bullous type of impetigo. On the other hand, the bullous form is not dependent on the host response but results from the direct action of the staphylococcal toxin.
The skin of the face and the hands and legs are commonly affected sites. The infection begins as a solitary red macule or papule that almost immediately turns into a vesicle. The vesicle ruptures to form an erosion, and the contents dry to form characteristic honey-colored crusts that may be pruritic. These lesions may spread to surrounding areas by autoinoculation.
Meliodosis is a potentially fatal bacterial infection caused by exposure to soil or water contaminated with the bacterial species Burkholderia pseudomallei. The causative organism, Burkholderia pseudomallei, was thought to be a member of the Pseudomonas genus and was previously known as Pseudomonas pseudomallei.
Melioidosis is regarded as endemic to southeast Asia and northern Australia. In the Indian subcontinent a survey conducted by Kang et al (1996) revealed a seroprevalence of 7% in a rural rice-growing area near Vellore.
Diabetes, thalassemia, excessive consumption of alcohol, renal disease, and frequent history of occupational or recreational exposure to mud or pooled surface water are common risk factors resulting in melioidosis.
The average incubation period of acute melioidosis is about 9 days. However patients can exhibit a period of latency. Such patients do not present any clinical symptoms. Literature review reveals that the longest duration between presumed exposure and clinical presentation was 62 years. Such prolonged periods of incubation were recognized in American soldiers involved in the Vietnam War, and was referred to as the ‘Vietnamese time-bomb’.
The typical clinical presentations of acute melioidosis usually include pain and fever. Other clinical findings are cough or pleuritic chest pain suggestive of pneumonia, bone or joint pain suggestive of osteomyelitis or septic arthritis, or cellulitis, thyroid, lymph node and scrotal abscess and ocular infection. Parotid abscess has been reported specifically in Thai children.
The chronic form of melioidosis is seen in about 10% of the patients. A chronic form is characterized by the presence of symptoms for longer than 2 months. Patients may present with chronic pneumonia, ulcers on the skin surface and chronic dermal infections. Since the chronic form closely resembles tuberculosis, some authors term chronic melioidosis as ‘Vietnamese tuberculosis’.
The bacterium can be cultured from the tissue fluid from the abscesses and the patient’s blood and sputum. The drugs of choice include antibiotics such as trimethoprim-sulfamethoxazole and ceftazidime orally. However serious infections are best managed with intravenous tetracycline, chloramphenicol, and trimethoprim-sulfamethoxazole.
The word tetanus comes from the Greek tetanos, which is derived from the term teinein, meaning to stretch. Tetanus, commonly called lockjaw, is an acute neurologic disease that results from wound contamination with Clostridium tetani, an anaerobic, gram-positive, motile, spore-forming rod characterized by generalized muscle rigidity and spasm, sometimes associated with autonomic dysfunction.
It is believed that although most wounds may be contaminated with the spores of Clostridium tetani, the germination and toxin production occurs only in wounds with low oxidation reduction potential, such as those with devitalized tissue, foreign bodies, or active infection. The bacteria produce two exotoxins: tetanolysin (role still unclear) and tetanospasmin. Tetanospasmin is the neurotoxin responsible for the clinical manifestations of the disease. The toxin spreads hematogenously to the peripheral nerves and travels in a retrograde fashion along the nerve fibers to reach the central nervous system where it blocks the release of gamma-aminobutyric acid (GABA) from presynaptic inhibitory neurons. This loss of inhibitory impulses results in the cardinal clinical manifestations of reflex irritability and autonomic hyperactivity.
The cephalic subtype of tetanus is characterized by cranial nerve palsies that often precede trismus. Patients present with cranial nerve palsy (usually facial nerve is affected). Approximately two thirds of cases progress to generalized tetanus. The incidence of cephalic tetanus ranges from 0.9 to 3.0%. The cephalic form results from injuries sustained to the head and neck region, tooth extraction or chronic tympanitis. Some patients may present with incomplete Bell’s palsy.
Trismus or lockjaw is the initial presentation in 75% of cases. Facial muscle spasm may cause the classic sneering grin of risus sardonicus. Motor findings progress to involve the neck, trunk and extremities, eventually leading to abdominal rigidity and opisthotonus. The muscle spasms may be sustained or paroxysmal. In severe cases the spasm of intercostal, diaphragmatic and pharyngeal muscles leads to breathing difficulties which may eventually lead to death.
Neonatal tetanus is a fatal yet preventable disease that accounts for 14% of annual neonatal deaths worldwide. The neonatal form of tetanus has a high mortality rate. It results from unhygienic delivery practices, application of harmful substances on the umbilical cord, and lack of maternal TT immunization. Risk for contamination and subsequent occurrence of neonatal tetanus remains high for several days after delivery until the baby’s cord wound heals. The incubation period varies from 3 to 10 days. Neonate’s failure to suckle is often the first sign of infection in the neonate, and typically occurs between the 3rd and 10th day of life. In spite of efforts by the infant, spasms of the masseter muscle impede feeding. The newborn becomes irritable and cries constantly. Exhaustion may subsequently bring about cessation of audible crying. Sometimes the lips are pursed as if to whistle. Variable degree of muscle spasm develops leading to asphyxia.
Fascial space infections causing trismus, dystonic reactions induced by such drugs as phenothiazines and metoclorpropramide, hypocalcemia, meningitis, encephalitis, rabies and strychnine poisoning can be considered in the differential diagnosis for tetanus.
A simple bed side test may be used effectively to diagnose tetanus. The spatula test is said to have a sensitivity of 94% and specificity of 100%. The posterior pharyngeal wall is touched with a spatula. The test is considered positive if there is a reflex spasm of masseter and negative if there is a normal gag reflex.
The first step should include rapid-sequence intubation with midazolam and succinylcholine. Passive immunization with human tetanus immune globulin (5,000 IU) will help to neutralize free tetanospasmin. It should be given after airway control and before wound debridement.
The WHO recommends that an individual should receive 3 doses of DTP in infancy, followed by a TT-containing booster at school-entry age (4–7 years), in adolescence (12–15 years), and in early adulthood.
Actinomycosis is subacute to chronic, suppurative granulomatous disease that tends to produce draining sinus tracts. It is caused by anaeroboic gram-positive, non-acid fast bacilli. The common isolates in humans include Actinomyces naeslundii, A. israelii, A. meyeri, A. viscosus and rarely A. odontolyticus. Kalfas et al (2001) identified a new species, Actinomyces radicidentis that was isolated from apical periodontitis.
Von Langenbeck noted the first case of human actinomycosis in 1845. Bollinger and Harz in 1877, named the genus Actinomyces when they described the etiologic agent of bovine actinomycosis (‘lumpy jaw’) and called it Actinomyces bovis.
Actinomycosis is mostly found in young adults. Women are less frequently affected than men. Based on the site of involvement, actinomycosis can be grouped into the cervicofacial (55%), pulmonary (15%), abdominal and pelvic (25%) and cutaneous and genitourinary actinomycosis (5%). Cutaneous actinomycosis is extremely rare and these are said to arise from wounds contaminated with saliva or as a consequence of hematogenous dissemination following a dental procedure. However primary cutaneous actinomycosis have also been reported. The genitourinary form has been reported in patients using intrauterine contraceptive devices.
The presenting symptoms of pulmonary actinomycosis are fever, cough, thoracic pain and dyspnea. The sputum is mucopurulent or even sanguineous. With the appearance of fistulae, the disease spreads to the mediastinum, the pericardium, and finally to the skin of the chest.
Actinomycosis is believed to be acquired by endogenous implantation into deep tissues where anaerobic conditions prevail. Actinomyces israelii is an anaerobic normal inhabitant of the mouth, especially in the teeth and tonsils.
In the cervicofacial region, puncture wounds, dental extractions, or compound fractures are some of the routes of infection. The cervicofacial variant is characterized by the appearance of solid sub- or supramandibular nodules or swellings and the overlying skin becoming purple to violet.
Clinical presentation of cervicofacial actinomycosis is characterized by the presence of suppurative or ‘wooden’ indurated mass with discharging sinuses. Pus from the discharging sinuses contains tiny yellow sulfur granules. Common initial symptoms of infection including pain, fever, erythema, edema, and suppuration may be absent.
Periapical actinomycosis is believed to be a non-resolving periapical lesion associated with actinomycotic infection and has been suggested as a contributing factor in the perpetuation of periapical radiolucencies after root canal treatment. A diagnosis is usually made by identifying the typical actinomycotic colonies in a surgical specimen. Occasionally, the periapical actinomycotic lesion may appear radiopaque mimicking condensing osteitis.
Sinus tracts may reveal the presence of yellowish granules (1–6 mm in diameter) referred to as ‘sulfur granules’. On histological examination, the sulfur granules consist of a central tangled mass of gram-positive mycelia surrounded at the periphery by gram-negative, club-shaped rods.
The word noma is derived from the Greek word ‘nomein’ that means ‘to devour’. It is rapidly progressive opportunistic infection which is caused primarily by Fusobacterium necrophorum, Fusobacterium nucleatum and Prevotella intermedia. Other reported organisms isolated from the Noma lesions include α-hemolytic Streptococci, Actinomyces spp., Peptostreptococcus micros, Veillonellaparvula, Staphylo-coccus aureus, Corynebacterium pyogenes, Bacteroides fragilis, Bacillus cereus and Pseudomonas species.
The predisposing and/or risk factors for noma include poverty, malnutrition, immunosuppression (including HIV infection), poor oral hygiene, unsanitary environment, leukemia, and infectious diseases caused by measles and herpesviridae.
Noma is considered to represent the ‘face of poverty’ because many of the risk factors that are associated with poverty. The World Health Organization (1998) has reported an estimated worldwide incidence of 140,000 cases per year.
Noma is usually seen in children between the age of 3 and 12 years mainly in the developing countries especially sub-Saharan Africa. Children at risk for noma have been seen to have low plasma concentrations of zinc, retinol, ascorbate, and essential amino acids with increased plasma and saliva levels of free cortisol.
In the initial stages ulcerative areas from the gingiva extend to involve the adjacent soft tissues. Subsequently the necrotic areas spread both into deeper tissue planes and superficially. The overlying skin turns deep blue to black and eventually sloughs away. Extensive necrosis can lead to exposure of bone and osteomyelitis. Patient may present with pain, fever, malaise, foul odor and regional lymphadenopathy. The differential diagnosis for noma must include mucocutaneous leishmaniasis, lupus erythematosus, leprosy, agranulocytic ulcerations, injuries associated with physical trauma (including burns), syphilis, oral cancer and yaws.
‘Noma neonatorum’ is characterized by gangrenous process of the nose, oral cavity, eyelids, and perineum usually seen in premature infants at births or within the first month of life. The causative organism for noma neonatorum is usually Pseudomonas.
Extensive necrosis can cause premature loss of deciduous teeth, damage to the permanent tooth buds, sequestration of the jaws, trismus, and bony or fibrous ankylosis of the temporomandibular joint. Occasionally, infection from the oral cavity can extend to other parts of the body causing systemic complications such as toxemia, dehydration and bronchopneumonia. Untimely intervention can lead to death.
Botryomycosis arises from chronic infections produced by low-virulence organisms in an altered host environment. Staphylococci have been the most common organisms implicated, but various other bacteria have also been identified in lesions of human botryomycosis.
The disease, later referred to as botryomycosis, was first described involving the lung of a horse by Bollinger in 1870. Sebastiano Rivolta in 1884 coined the term botryomycosis (‘botryos’ from Greek for bunch of grapes) after he found globular granules in a tumor from the cut spermatic cord of a horse.
The integumental botryomycosis affects the exposed body surfaces such as the hands, feet or the head. It occurs in the site of a contaminated wound, foreign body or trauma and manifests as a localized granulomatous infection. Occasionally it causes osteomyelitis.
The visceral form is relatively rare. It is usually seen in immunocompromised individuals. It affects the lung, liver, kidney, spleen, brain, prostate, bowel and the lymphatic tissues (tonsil, lymph node).
Literature review reveals a few reports of botryomycosis affecting the orofacial region. Small and Kobernick (1967) reported a patient with botryomycosis of the tongue. Rawal and Rawal reported a patient with gingival botryomycosis and Alavandar (1979) reported botryomycosis affecting the mandible.
Within the areas of the purulent inflammation, Bollinger’s granules are seen. These are relatively small, but frequently microscopically visible, pale yellow or yellow-white granules consisting of irregular aggregates or colonizations of gram-positive cocci, usually staphylococci.
Bollinger’s granules are surrounded by an amorphous, eosinophilic, refringent matrix called the Splendore-Hoeppli phenomenon (this phenomenon is also seen around colonies of certain bacteria, fungi, helminthes, actinomyces, mycetoma, nasofacial and subcutaneous phycomycosis and around silk sutures).
In 1882, von Frisch identified K. rhinoscleromatis as the etiologic agent. In 1870 Ferdinando Von Hebra, a dermatologist described the disease for the first time. It was later named respiratory scleroma. The word ‘skleroma’ in Greek meaning hard tumefaction, was adopted in 1932 at the International Clinical Otorhinolaryngology Conference (in Madrid), emphasizing involvement of upper and lower airways.
Humans are the only identified host of K. rhinoscleromatis. It usually affects individuals in the 2nd to 4th decades of life. It affects people living in crowded conditions with poor hygienic and nutritional conditions (including iron deficiency anemia). Rhinoscleroma affects women more commonly than men (13:1).
The nose is the most common site of infection, although the nasopharynx, paranasal sinuses, and pharynx may also be involved. Other affected organs include the paranasal sinuses, eustachian tubes, middle ear, orbital tissues and the brain.
In the catarrhal stage, patient may complain of foul smelling purulent nasal discharge and nasal obstruction. On clinical examination atrophy and crusting of the nasal mucosa or hyperemia and exudates in the respiratory tract mucosa are evident.
In the granulomatous stage, epistaxis, nasal deformity and destruction of the nasal cartilage (Hebra nose), hoarseness of voice, anosmia and anesthesia of the soft palate are common signs and symptoms. Clinical examination may reveal a bluish red and rubbery granulomatous lesion. These lesions over a period of time turn into a pale hard granulomatous mass.
The diagnosis of rhinoscleroma is made by the bacterial isolation by culture on blood or MacConkey agar. Histopathological specimens can be stained with periodic acid-Schiff, Giemsa and Warthin-Starry stain. The presence of Mikulicz cells (clear cytoplasm vacuolated histiocytes containing the bacillus) and degenerated plasmocytes in Russel bodies are diagnostic of rhinoscleroma.
Nasal or pharyngeal obstruction is best managed surgically along with antibiotic therapy. Many authors recommend the use of cephalosporins and clindamycin. Shaer et al (1981) have shown that the topical application of 2% acriflavine solution is an effective and safe treatment option for rhinoscleroma. Tracheostomy may be required if laryngeal scarring causes airway obstruction.
Cat-scratch disease arises from the inoculation of the gram-negative bacillus Bartonella henselae following a cat’s scratch, lick or bite. It is estimated that almost 40% of the domestic cats may have an asymptomatic B. henselae infection accompanied by bacteremia, which can persist for more than a year. It is believed that domestic cats tend to rapidly develop antibodies and therefore appear healthy in spite of the bacteremia.
The first description in the literature of cat-scratch disease is credited to Henri Parinaud in 1889. Dr Robert Debre in 1931 described a case of a boy with a cat-scratch on his hand associated with a suppurative epitrochlear lymph node. He is credited with recognizing the cat as the vector of this illness and coined the term ‘cat-scratch disease’. Regnery and coworkers (1992) identified B. henselae as the causative organism for cat-scratch disease.
The incubation period varies from 7 to 15 days. It usually affects individuals in the second decade of life. Patients may present with mild fever, fatigue and malaise. The initial lesion occurs as a pustule or papule seen at the site of the trauma (cat-scratch or bite). These initial lesions are followed by regional lymphadenopathy that lasts for a couple of months. The lymph nodes can enlarge to a size of about 10 cm.
Other systemic manifestations include parotitis, osteomyelitis, hepatosplenomegaly, neurological conditions (seizures, altered behavior or consciousness, peripheral facial nerve paresis, myeloradiculitis) and hematological conditions (hemolytic anemia, thrombocytopenia and eosinophilia).
When a pet’s saliva contaminated (as the cat constantly licks its fur) fur is groomed, organisms from the fur are transferred to the individual’s hand. Such contaminated fingers, when used to rub the eyes might cause self-inoculation of the organisms to the conjunctiva. Conjunctival involvement will result in preauricular lymphadenopathy. This association of conjunctival involvement and preauricular lymphadenopathy in cat-scratch fever is referred to as ‘Parinaud oculoglandular syndrome’.
B. henselae and B. quinata are implicated in the causation of bacillary angiomatosis and peliosis in immunocompromised hosts such as in AIDS. Orally these lesions mimic Kaposi’s sarcoma and appear as vascular lesions and within bone may cause alveolar bone loss.
Neville and coworkers enumerated certain criteria for the diagnosis of cat-scratch fever. Evidence of at least three of the following four criteria is considered to be positive for cat-scratch disease:
This skin test was first developed by Hanger and Rose in 1946. Aspirated material from a lymph node of a patient with known cat-scratch disease is pasteurized, standardized, and tested for sterility. It is then injected subdermally and skin reaction is noted.
However, serological test (ELISA for IgM antibodies to B. henselae) is the gold standard for the diagnosis of cat-scratch disease. Elevated serum titers are seen 1–3 weeks after the onset of the disease process.
The condition is self-limiting and usually resolves in about 6 months duration. Suppurative nodes may be aspirated to evacuate the pus. The recommended surgical procedure to evacuate the pus is to introduce the needle into the skin 1 to 2 cm away from the swelling and then burrow beneath the surface of the skin to reach the affected node. The technique helps to hasten the healing and prevent formation of a persistent sinus.
Infectious mononucleosis (IM) is a clinical syndrome caused by Epstein-Barr virus-4 (EBV, human herpes virus-4). EBV replicates primarily in beta-lymphocytes but also may replicate in the epithelial cells of the pharynx and parotid duct.
Children and young adults are usually affected. The virus is transmitted via intimate contact. Children may acquire the virus through sharing of saliva contaminated fingers, toys and serving spoons. Direct transfer of contaminated saliva may occur in adults following kissing (hence the name kissing disease) or sharing of straws. The incubation period is 4–8 weeks.
The most striking feature of IM is the presence of lymphadenopathy. Any or all lymphatic chains may be enlarged. Lymphadenopathy is always bilateral and symmetrical in all patients. Bilateral posterior and anterior cervical lymphadenopathy is highly suggestive of EBV infectious mononucleosis.
Hoagland’s criteria (1975) for the diagnosis of IM include: at least 50% lymphocytes and at least 10% atypical lymphocytes in the presence of fever, pharyngitis, and adenopathy, and confirmed by a positive serologic test.
Oral manifestations include hard and soft palate petechiae, necrotizing ulcerative mucositis, necrotizing ulcerative gingivitis and pericoronitis. Occasionally, the parotid gland may be affected along with facial nerve palsy.
Warwick et al (2003) reported a patient with IM, ruptured spleen and Cullen’s sign (periumblical ecchymosis). They also suggest that the presence of abdominal pain is an uncommon symptom in infectious mononucleosis and its occurrence is therefore a danger sign that may forewarn a potentially life threatening complication of ruptured spleen.
The complications of IM include myocarditis and cardiac conduction abnormalities, neurologic abnormalities, meningitis, encephalitis, cranial nerve palsies, retrobulbar neuritis, acute interstitial nephritis, hemolytic anemia, thrombocytopenia and upper airway obstruction.
The Paul-Bunnell test is a serological test that detects heterophile antibodies by agglutination of sheep or horse red blood cells. However, in the 1st week of infection, the false-negative rate is as high as 25%.
Infectious mononucleosis usually resolves in about 6 weeks. IM is best managed with extensive palliative and supportive healthcare. Patient should be adequately hydrated. Fever and malaise may be managed with acetaminophen and NSAIDs. Though steroids have been used frequently, they are best used only in an emergency to relieve the patient of respiratory compromise secondary to pharyngeal edema.
Acute lymphonodular pharyngitis is caused by Coxsackie virus A10. It is characterized by prodromal fever, anorexia, headache and sore throat. Like most viral infections, the condition is self-limiting and generally resolves in about 2 weeks.
Acute lymphonodular pharyngitis is usually seen in children and young adults. Clinically, the hyperplastic lymphoid aggregates are evident as discrete yellow to dark pink colored nodules or white to yellow papules surrounded by an erythematous ring, generally 1–5 in number. These lesions are typically found on the tonsillar pillars, uvula, soft palate and oropharynx.