Chapter 9 Bacterial , Viral & Mycotic

infections

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• I ) Bacterial infections of oral cavity :

• 1- Acute necrotizing gingivitis.• 2-Acute streptococcal gingivitis • 3-Scarlet fever • 4-Diphtheria• 5-Syphilis.

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1) Acute necrotizing ulcerative gingivitis : ( Trench mouth , fusospirochetal infection & Vincent,s infection )

Definition : Acute necrotic marginal gingiva & interdental papilla.Etiology : Fusobacterium nucleatum, Treponema vincentii. Predisposing factors are

emotional stress, smoking, poor oral hygiene, local trauma, and mainly HIV infection

- Fusospirochetal infection with certain local & systemic factors acting to lower the resistance of the gingival tissue

A) Local factors B) Systemic diseases 1- Poor oral hygiene 1) Vitamin B , C deficiency 2- Plaque & calculus 2) Debilitating disease 3- Food impaction 3) Leukopenia

Causative microorganism : - fusiform bacilli G +ve - Spirochetes ( Borrelia vencenti )

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Severe necrotizing gingivitis in a 32-year-old HIV- seropositive homosexual

Necrotizing gingivitis and stomatitis in a 30-year-old man with AIDS. Note the extensive soft-tissue necrosis beyond the gingiva.

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Clinical features : 1- Acute gingivitis ( Margial gingiva & interdental papilla)2- Erosion of the interdental papillae & covered by grey necrotic

pseudomembrane3- Spontaneous bleeding4- Foul foetid odour due to necrosis & bad oral hygiene5- Severe pain 6- Increased salivation7- Metallic taste8- General symptoms: fever , headach , malaise & regional lymphadenopathy.Histopathology : ( non – specific) 1-Necrosis of surface epithelium with a structureless mass of

( pseudomembrane) - Fibrin - Tissue debris - PNL - M.O.2- C.T. : Vasodilatation & edema & PNL infiltration

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Acute inflammation with ulceration

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2) acute streptococcal gingivitis : Causative microorganism : B haemolytic streptococcus, it is due gingival infection

from streptococcal tonsillitisClinically : 1) Gingival margin : fiery red & bleeding 2) Regional lymphadenitis 3) Leucocytosis Histopathology : acute inflammation

3) Scarlet fever : Acute pharyngitis with skin rashCausative microorganism : B haemolytic streptococcus ( Lancifield group A ) Mode of infection : droplet infection Clinical features : 1- incubation period 2-4 days 2-Severe pharyngitis & tonsillitis 3- Fever , headach , chills 4- Regional lymphadenitis 5- Skin rash : diffuse , papular• Erythema except skin over orbicularis oris muscle , this zone is called circum oral

pallor

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Streptococcus pyogenes

Strawberry tongue The exudative pharyngitis typical of scarlet fever

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Scarlet fever is a disease caused by an infection with group A beta-hemolytic streptococcal bacteria that occurs in a small percentage of people with strep throat. The illness typically begins with a fever and sore throat. It may be accompanied by chills, vomiting, abdominal pain and malaise. The streptococcal bacteria produces a toxin that causes a rash that appears one to two days after the onset of illness. The rash initially appears on the neck and chest, then spreads over the body. While the rash is still red, the patient may develop Pastia's lines, bright red coloration of the creases under the arm and in the groin.

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Oral manifestations of Scarlet fever : The pharynx is the primary site of involvement & the toxins are produced through the following local pharyngitis.

1- congested palate 2- fiery red throat 3- swollen , yellow exudate tonsils

Tongue : 1- early : white coating through which inflammed edematous

fungiform papillae project. 2- late : the tongue coating desquamate leaving red , raw

surface ( since the fungiform papillae still appear prominent on the erythematous base ( strawberry tongue)

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4) Diptheria • It is an acute infection , which involves the pharynx & characterized by

formation of pseudomembrane.• Caused by Corynebacterium diphtheria ( G+ve bacillus that elaborate

potent toxins).Mode of infection : - Direct contact - Droplet infectionClinical features : fever , headach , malaise , vomiting . Sore throat , redness ,

edema of the pharynx , cervical lymphadenopathy.Oral manifestations : - Adherent grey pseudomembrane covering the uvula , tonsils , soft

palate , hard palate & dorsum of the tongue , leaving a bleeding surface if stippled away .

- the soft palate has a temporary paralysis due to neurotoxic involvementHistopathology ( non-specific) : 1- Pseudomembrane , which is composed of fibrin , tissue debris &

microorganisms with PNL. 2- C.T. vasodilatation , PNL , lymphocytes , plasma cells & histiocytes.

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5- Oral Tuberculosis : • It is a chronic granulomatous disease. It is an infectious disease. The oral primary

form is a rare type.Caused by Mycobacterium tubercle bacilliMode of infection : - Sputum - Blood.Clinical feature : any age , any sex , site : oral cavity : lip & tongue• - Pulmonary T.B. is first present then the oral cavity is affected. Characters : 1- ulcer with special characters : undermined edges , irregular outlines , painful &

covered by yellowish fibrous layer.2- nodule in the palate or gingiva3- osteomyelitis in the mandible or maxilla , vertebra & long bones : firm swelling then

softens with discharge through sinuses , enlarged lymph nodes X ray : irregular radiolucent areas with worm eaten appearance ( radioopaque) ,

subperiosteal new bone formation.Histopathology : • 1- Central caseous necrosis 2- Epitheliod cells ( histiocytes)• 3- Langhan,s giant cells 4- lymphocytes 5- Fibrosis ( fibroblasts , collagen , & B.V.)

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Tuberculosis ulcer on lower alveolar attached mucosa with minimal induration and hemorrhagic periphery.

Original ulcer on the alveolar mucosa (arrowheads) and a "satellite" ulcer on the buccal mucosa (arrows).

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granulomatous inflammation with Langhans’ giant cells and focal caseous necrosis (hematoxylin and eosin stain, . B. Acid-fast bacillus (arrows) engulfed in a histiocyte (Ziehl-Neelsen stain,

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6- Syphilis• It is a chronic specific granulomatous infectious disease.• Caused by Treponema pallidum , which is a motile spirochete , & demonstrated

microscopically by dark field examination.• Classification : • A- Acquired ( extrauterine ) : • I- primary stage ( chancre): 1- I.P 3-5 weeks 2- Site : a) genital 90% & b- extragenital ( lips , tongue , gingiva) 3- At the site of entry of M.O the chancre develop as papules ( red , indurated &

solitary ) then ulcerates ( serous exudate – indurated base) 4- Lymphadenopathy ( regional painless unilateral ) 5- Regress spontaneously in 2 weeks to 2 months. This stage is infectious.• II- Secondary stage ( infectious) 1- 6-8 weeks after the onset of the 1ry lesion ( chancre) 2- Skin rash : macules or papules , generalized , symmetrical , painless

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3- Lymphadenopathy ( generalized) 4- Oral manifestations : -Mucous patches : grayish white plaques , multiple , painless , ovoid , irregular ,

surrounded by red zone. - Ulcers : oval , coalesce ( snail track)• III- Tertiary stage ( non-infectious) : • After 2-3 years • Due to : - delayed type of hypersensitvity or • - Thickening of the wall of B.V. : narrow lumen ( endarteritis obliterans) , • decrease nutrition • -Lymph nodes are not involved.• Types : 1) Gumma (localized) • 2) Diffuse syphilitic lesions ; bone ( osteomyelitis) & tongue ( diffuse

syphilitic glossitis ) • Gumma : A- palate : nodule ulcerates , perforation the occur.• B- Tongue lingual lobulata : - fibrosis , nodule • & ulcer : large , circular , irregular , soft edge , depressed base & gummy center

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• 2- diffuse syphilitic lesion : • i-bone ( diffuse syphilitic osteomyelitis) • ii-Tongue ( diffuse syphilitic glossitis)• Diffuse syphilitic glossitis : Because “ Treponema pallidum” has predilection for

active motile tissues , large number of them concentrate in the tongue during 2nd stage producing diffuse vasculitis leading to endartiritis obliterans with relative ischaemia , which results in :

• 1- Atrophy of tongue papillae ( bald tongue).• 2- Atrophy of the lingual muscles resulting in ( surface wrinkles) • 3- Atrophy of the lingual papillae depriving the tongue from it is natural protection

then chronic irritation lead to leukoplakia ( premalignant) then malignant transformation ( SCC).

• Microscopically : 1- Granulation tissue : fibroblasts , collagen fibers , B.V. , lymphocytes , plasma

cells & histiocytes giant cells. 2- Coagulative necrosis in the center gummy material, due to endarteritis

obliterans.

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B) Congenital syphilis : • It is acquired by the fetus from his mother during I.U. life from his infected mother

through the placenta.• Clinical features : Infant , both sex . 1- Rhagades : linear scars radiating from the corners of the mouth representing

healed fissures. 2- Gummata : palate , nasal bridge causing saddle nose. 3- White mucous patches. 4-Hutchison,s triad : a- Interstitial keratitis b- 8th nerve involvement lead to deafness c- Hutchinson,s tooth. Dental abnormalities : - Hutchinson,s tooth in centrals - Mulberry molar usually first molar - Moon,s molar usually first molar

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Solitary chancre on the ventral surface of the tongue.

Two chancres on the tongue.

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Primary chancre. The lower lip is a typical site for extragenital chancres but they are rarely seen.

Tertiary syphilis; gummas of the palate. Necrosis in thecentre of the palate has caused perforation of the bone and two typical round punched-out holes.

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• II- Mycotic or fungal infections : 1) Candidiasis ( Moniliasis – Candidosis - Thrush) : • It is a fungal infection caused with candida albicans , which commonly inhibitant of

oral cavity , GIT & vagina. • It is an opportunistic M.O.• Normal flora introduction of antibiotics lead to imbalance of oral flora with

increase number of fungi.• It is classified into two groups : Mucocutaneous ( oral esophagus , vagina ) &

systemic ( eye , kidney , skin)• 1) Acute pseudomembrane candidiasis ( thrush) : • It is a common form of candidiasis• Any age ( low body resistance ) • Site : buccal mucosa , tongue , palate , floor of mouth .• Character : soft , white , slightly elevated plaque, milk curds ; can be wiped away

leaving mucosa red.• Histopathology : fungal hyphae , necrotic debris , fibrin , desquamated epithelium.• Acute atrophic candidiasis : As a sequlae of pseudomembrane .

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• II- Chronic • 1- chronic hyperplastic candidiasis : leukoplakic candidiasis , firm , persistant

plaque. There is definite relationship between presence of M.O & focal atypia.• It is considered that has a premalignant potentiality. • 2- chronic mucocutaneous candidiasis : • A- chronic familial M.C.C. inherited : young before 5 years• B- chronic localized M.C.C. severe form at early age , affect also widespread affect

skin ( horny masses). C- chronic diffuse M.C.C. : at late age about 55 years , crusty sheets. D- chronic craniopathy syndrome inherited : 1- oral cavity candidal inked. 2- hypoadrenalism ,or hypoparathyroidism , or hypothyroidism , or diabetes

mellitus 3- Chronic atrophic candidiasis : denture sore throat , it is diffuse inflammation

of the denture bearing area accompanied with angular stomatitis. It occurs in female more than male.

Differential diagnosis : leukoplakia , lichen planus.

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Pseudomembranous candidiasis on the palate.

Nodular candidiasis

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Chronic mucocutaneous candidiasis: multiple lesions on the tongue.

Chronic biting of the buccal mucosa.

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Thrush. The lesions consist of soft, creamy patches or flecks lying superficially on an erythematous mucosa. This soft palate distribution is particularly frequent in those using steroid inhalers.

Thrush. At high power the components of a plaque may beclearly seen. The surface layers of the epithelium are separated by inflammatory oedema and are colonised by fungal hyphae and infiltrated by neutrophils

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Direct smear from thrush. The tangled mass of Gram positive hyphae of Candida albicans is diagnostic. A few yeast cells may be present as well, but it is the large number of hyphae which is diagnostic.

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• 2- Actinomycosis : it is a chronic suppurative granulomatous disease caused by false fungus called actinomyces.

• Etiology : it is now believed to be caused by bacterium called actinomyces israeli which is a normal inhabitant of oral mucosa as this microorganism is anerobic one. “It is found in carious cavities of teeth , deep peridontal pockets & GIT.

• Types of actinomycosis : • 1- Cervicofacial actinomycosis : • - It represent two thirds of all cases of actinomycosis ( most common type) • - It causes typical swelling below the mandible called ( lumpy jaw).• - This type is believed to be triggered by trauma * usually tooth extraction or fracture precedes the clinical manifestations. * tooth extraction offer an excellent mechanism for the organism to be introduced

into traumatized tissue deep in the bottom of the socket ( anaerobic environment )

* infection can spread along alveolar bone to subcutaneous tissue , which appears under the skin as red blue painless nodule.

* many nodules may appear on the indurated swelling forming a sinus tract oozing yellow pus containing the characteristic sulphur granules containing colonies of the organism . * Regional lymph node is involved.

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• Histopathology : • 1- multiple foci of suppuration separated from each other by dense scar tissue or

fibrous septa.• 2- colonies of the organism appear in the center of large number of neutrophils.• 3- on the periphery of these foci , macrophages appear .• 4- the colony if the microorganism is consisted of : • a) oval mass of filaments arranged radially from the center of the colony ,

deeply basophilic• b) club shaped end appears as swelling at the end of each filament ( bright

eosinophilic ) • 2- Actinomycotic osteomyelitis: - this type is less common than cervicofacial type. - infection extend into the bone itself causing osteomyelitis - it is more common in the mandible. - when it affects the maxilla , it may perforates into the maxillary sinus. - the course is benign & chronic unless secondary infection occurs. - in most cases , fibrosis is extensive walling off the infection to a certain limit.

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• 3- Actinomycosis of the tongue : - it affects the anterior third of the tongue in one side of midline near tip of the

tongue. - the swelling is painful , lasts after many weeks. - early , the lesion is small rounded , slightly tender & well defined with hyperemia

of the overlying mucosa. - later on the nodule increases in size , & becomes softer , with bluish coloration of

the mucosa. - this nodule may rupture discharging pus containing sulphur granules. - if untreated , this lesion becomes multilocular with abscesses formation with

perforation through the skin into the submental region.

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Actinomycosis. This single, complete loculus was from an early case of actinomycosis that followed dental extraction. The colony of actinomyces with its paler staining periphery (a 'sulphur' granule) is in the centre; around it is a dense collection of inflammatory cells, surrounded in turn by proliferating fibrous tissue. It will be apparent that an antibiotic cannot readily penetrate such a fibrous mass and must begiven in large doses to be effective.

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III- Virus• General properties of virus : • 1- size : ultramicroscopic• 2- obligatory intracellular• 3- Shape : spherical or filamentous• 4- Structure : Nucleic acid core & protein envelop.• 5- Type : DNA & RNA virus groups.• I-Reproduction of virus ( life cycle) : • A-Attachment phase B- Penetration phase• C- Eclipse phase D- Maturation • II-Reaction against virus : • A- local cellular reaction • B- Local inflammatory reaction ( acute inflammatory reaction around the attacked

cells) vasodilation & exudate contain lymphocytes & macrophages.• C- General body reaction ( general immunity).

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• Local cellular reaction : 1- necrosis poliomyelitis 2- Ballooning herpes simplex 3- Proliferation ( Burkitt,s lymphoma – verruca vulgaris) 4- No reaction latent virus infection e.g. the epithelium of the lip & face may

harbour the herpes simplex virus without showing any lesion . HIV virus may enter & remain latent in circulating lymphocytes for years

• General body reactions : 1- Humoral immunity : plasma cells & B lymphocytes produce neutralizing

antibodies . Bind to viral capsid or protein envelop so prevent virus attachment 2- Cellular immunity : T lymphocytes destroy virus infected cells. 3- Inerferon : produced by virus infected cells & T lymphocytes ( prevent virus

multiplication )

• Classification of major virus group & disease. I - DNA viruses II- RNA viruses

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I) DNA viruses : A) Herpes virus group : 1- Herpes simplex virus Herpes simplex 2- Varicella zoster virus : chicken pox , herpes zoster 3- Epstein Barr virus (EBV) : Burkitt,s lymphoma , infectious

mononucleosis . 4- Cytomegal virus : cytomegalic inclusion disease.

B) Pox virus group : small pox , Molluscum contahiosum

C) Papova virus : Verruca vulgaris.

II) RNA viruses : 1- Orthomyxo virus infulenza 2- Paramyxo virus : Measles – Mumps 3- Retrovirus : Human immunodeficiency virus HIV.

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I) DNA virus 1- Herpes Simplex • It is a viral infection , which is caused by Herpes simplex virus Types : • 1- Primary herpetic gingivostomatitis• 2- Recurrent herpetic infection ( labialis)

1- Primary herpetic gingivostomatitis : Clinically : - Age : children & young adult , fever , headach , cervical lymphadenitis• Acute gingivitis , vesiculr eruption lip , tongue , buccal mucosa palate , pharynx ,

tonsils . • Ulcer covered by a grey membrane & surrounded by a red halo.• Healing occurs spontaneously within 7-14 days without scar.Histopathology : 1- vesicle : - intraepithelium , - ballooning degeneration , - intranuclear inclusion bodies ( Lipschutz inclusion bodies), - C.T. infiltration by PNL.

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2- Ulcer : A- epithelium : ( surface exudate – degenerated epithelium – fibrin , PNL ) B- C.T. infiltration by PNL , lymphocytes , plasma cells , vasodilatation & edema.• Healing by proliferation of adjacent epithelium at the periphery.

2- Recurrent herpetic infection : • Activation of the latent virus due to : fatigue , pregnancy , trauma , exposure to

sunlight , gastrointestinal tract disturbance.Clinical features : adult age , equal sex , lip site. 1- Burning sensation , pruritis & pain., vesicle , which ulcerated & surrounded by

red halo small & localized .Lesions will coalesce into large lesion & crust formation.Histopathology : - inclusion bodies |( Lipschutz inclusion bodies) - Ballooning degeneration - Intraepithelial vesicle

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Herpetic stomatitis. Pale vesicles and ulcers are visible on thepalate and gingivae, especially anteriorly, and the gingivae areerythematous and swollen.

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A smear from a herpetic vesicle. The distended degenerating nuclei of the epithelial cells cluster together to give the typical mulberry appearance.

Herpetic ulcer. The vesicle has ruptured to form an ulcer(right) and the epithelium at the margin contains enlarged, darkly staining virus-infected cells liberating free virus into the saliva.

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Herpetic vesicle. The vesicle is formed by accumulation of fluid within the prickle cell layer. The virus-infected cells, identifiable by their enlarged nuclei, can be seen in the floor of the vesicle and a few are floating freely in the vesicle fluid.

Herpes labialis. A. Typical vesicles. B. Crusted ulcers affecting the vermilion borders of the lips.

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2- Varicella zoster A) Varicella ( chicken pox) • Varicella zoster virus ( DNA virus) belongs to herpes virus group.• Clinically : children ( non-immune) , fever , headache , nasopharyngitis. In skin

produce maculopapulary or vesicular eruption then rupture. Ulcer , crust , desquamate which heal without scar.

• Orally vesicle ulcerated & surrounded by red margin.B) Herpes zoster : caused by varicella zoster virus , the skin supplied by the nerve of

the affected ganglia. - varicella zoster virus infect the child & produce chicken pox - The virus pass via the blood to be latent in the sensory root ganglia - Activation of the virus in adult that affect the skin or mucous membrane\ - Unilateral vesicles soon rupture , healing occur after while - Hyperaesthesia of the surrounding area Oral manifestation: vesicles : unilateral , painful , along the course of mandibular &

maxillary nerve branches ,ulcer surrounded by red margin. Histopathology : Ballooning degeneration , intraepith V. , intrnuclear Ic. bodies

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Herpes zoster. A severe attack in an older person shows confluent ulceration on the hard and soft palate on one side.

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3- Burkitt,s lymphoma ( african jaw lymphoma )• It is malignant neoplasm , caused by Epstein-Barr virus ( DNA , herpes like virus) ,

3-8 years , male more than female , over 50% of cases affect the jaws.• Characters : Rapidly growing swelling ; in the maxilla appears on both buccal &

palatal surface & extends to maxillary sinus- ethmoid sinus or orbit. Looseness of teeth.

• Radiograph : loss of lamina dura , small radiolucent area coalesce large radiolucent area , erosion of the cortical bone.

• Histopathology : • - primitive lymphoid cells , abundant mitotic activity• - nucleus = large , round & vesiclar• - Nucleoli = prominent & up to 5 in number• - cytoplasm = scanty & haematoxyphilic • Histiocytes ( macrophages) : large cells , clear vacuolated cytoplasm , scattered

between the lymphoid cells giving “starrysky appearance “( characteristic feature)

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Burkitt's lymphoma. Small darkly staining neoplasticlymphocytes form sheets in which the macrophages containing cellular debris form round, pale holes (starry sky appearance).

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• 4- Infectious mononucleosis ( glandular fever ) : • - It is caused by Epstein – Barr (EB) virus , herpes like virus . • -The mechanism of transmission is unknown but it may be due initimate oral

exchange of saliva. • -Oral excretion of EB virus may continue for 18 months following onset of the

disease. Clinical features : -young adult age , very sore throat , headach , chills , cough , nausea , vomiting ,

lymphadenopathy . -The cervical lymph nodes are enlarged followed by the nodes of the axilla &

groin. Oral manifestations : -White or grey membrane in various areas , palatal petechae , oral ulcers. Lab. Findings : ( paul - bunnle test ) : - Atypical lymphocytes in the circulating blood. - Antibodies to EB virus - Increased heterophil antibody titre.

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5- Acquired immune deficiency syndrome ( AIDS) • - Retro virus caused by human immune deficiency virus ( HIV) , incubation period 6

months – 6 years.• Immunopathology aspects : destruction of T helper lymphocytes specific

apportunistic infections & malignancies ( kaposi,s sarcoma.• Transmission of HIV virus : Sexual contact , parentral transfer of blood or blood

products , shared needles & synringes , transplacental & perinatal transfer from mother to child ( in utero or mother,s milk)

• Clinical features : asymptomatic carriers , persistent lymphadenopathy , AIDS related complex , fully expressed AIDS.

• Fully expressed AIDS : symptomatic with opportunistic infection .High fever , enlargement lymph node , splenomegaly , sudden loss of weight.

• Recurrent infection : pneumonia , oral infection , malignancies.• Malignancies associated with aids : • 1- Kaposi,s sarcoma • 2- Oral SCC• 3- Burkitt,s lymphoma • 4- Leukaemia

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• Oral manifestations of AIDS : • Oral infection : - dental caries - candidiasis -herpes simplex - stomatitis - periodontal disease - hairy leukoplakia • Malignancies: - Kaposi,s sarcoma - oral SCC - Burkitt,s lymphoma

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