4: Bacterial

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.

Bacterial Infections

Scarlet Fever

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 organism expresses an erythrogenic toxin that acts on the blood vessels to produce the typical skin rash.

Clinical features

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).

Once the rash resolves, a 3–8 months phase of desquamation begins, which is characterized by peeling away of the skin in large flakes.

Oral manifestations

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.


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.

General clinical and oral manifestations

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.

Diphtheria involving the skin causes excoriation of the skin of the nasal and perinasal regions.

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.

Tularemia (Rabbit Fever, Deer-fly Fever, Francis’ Disease, Tick-Borne Disease, Ohara’s Disease)

Tularemia is caused by gram-negative pleomorphic bacterium, Francisella tularensis (named after the extensive work on tularemia done by Dr Edward Francis).

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.

Clinical manifestations

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.

Based on the type of the tularemia, specific clinical manifestations are seen (Table 1).

Table 1

Clinical manifestations and types of tularemia

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


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.

It has also been referred to as St. Anthony’s fire after the name of the Egyptian monk who is believed to have had the powers to cure this disease.


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.

Clinical features

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.

There are two types of impetigo: non-bullous (impetigo contagiosa) and bullous.

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.


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.

Alfred Whitmore, a pathologist and his assistant CS Krishnaswami in 1911, first described melioidosis as a ‘glanders-like’ disease among morphia addicts in Rangoon, Myanmar (formerly Burma).

Stanton and Fletcher in 1932 renamed this disease as meliodosis, which is a derivative from the Greek words ‘melis’ (distemper of asses) and ‘eidos’ (resemblance).

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.

Clinical features

Melioidosis can present in an acute or chronic form.

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 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.

Clinical features

Tetanus is usually seen in young adults who are prone to traumatic injuries. Four types of tetanus are recognized based on the clinical presentation: localized, generalized, cephalic and neonatal.

The localized form of tetanus is characterized by a limited area of muscular spasm that is confined to the area of the entry of the bacilli.

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.

Generalized tetanus is the most common form of the disease and carries the highest mortality. Incubation periods for the generalized form range from a few hours to greater than 1 month.

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.

Prevention and management

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.

Finally the source wound should be thoroughly debrided, with removal of all foreign bodies and devitalized tissue. Metronidazole, 500 mg IV every 6 hours, is recommended as the first-line antibiotic.

As a part of the supportive measures, sympathetic over-activity can be managed with a labetalol infusion at 0.2–51 mg/min. Diazepam may be used to sedate the patient.

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.

Clinical features

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.

Actinomycosis often involves lymphatic nodes but by the direct extension of a primary lesion. Occasionally, the masticatory muscles and tongue may be involved resulting in trismus and dysphagia.

Noma (Cancrum Oris, Gangrenous or Necrotizing Stomatitis)

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.

Clinical features

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.

Many authors believe that noma, occurs secondary to the extension of necrotizing ulcerative gingivitis.

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.

Botryomycosis (Bacterial Pseudomycosis)

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.

Clinical types and features

Winslow (1959) categorized botryomycosis into two types based on their site of involvement: integumental and visceral.

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).

The typical botryomycotic lesions are indurated fibrotic masses that may form draining sinuses and fistulas.

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.

Rhinoscleroma (Respiratory Scleroma)

Rhinoscleroma is an endemic, chronic, slowly progressive granulomatous disease caused by Klebsiella rhinoscleromatis (a gram-negative rod-shaped bacteria, 2.5 μm in length).

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.

Rhinoscleroma is contracted by direct inhalation of droplets or contaminated material.

Clinical stages

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.

Rhinoscleroma occurs in three overlapping stages: catarrhal-atrophic (sometimes called ozaena), granulomatous (proliferative or nodular) and sclerotic (cicatricial or fibrotic).

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.

In the sclerotic stage, clinical examination shows granulomatous lesions surrounded by dense fibrotic tissue.

Cat-Scratch Disease

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.

Cat-scratch disease is considered as a self-limiting granulomatous condition characterized by suppurative regional lymphadenitis.

Clinical features

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’.

Several skin reactions have been reported, including erythema nodosum, erythema marginatum and erythema multiforme.

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:

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.

Viral Infections

Infectious Mononucleosis (Monoglandular Fever, Kissing Disease)

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.

Clinical features

The characteristic clinical features of IM include, malaise, fatigue and anorexia. These symptoms are immediately followed by high fever (about 104°F) which lasts for almost 2 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.

Other clinical features include the presence of tonsillar enlargement, hepatosplenomegaly, jaundice, rhinitis and pharyngitis.

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.

Acute Lymphonodular Pharyngitis

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.

Jan 12, 2015 | Posted by in Oral and Maxillofacial Radiology | Comments Off on 4: Bacterial
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