1. BACTERIAL INFECTIONS
Dr Shruti Nayak
Dept. of Oral Pathology

2. Bacteria
They are prokaryotic microorganisms which can be spheroidal (coccus), rod / cylindrical (bacillus) and spirillar (spirochetes)
They are the causative agents of many human diseases

3. Bacterial species

4. Some of the important specific bacterial infections
TUBERCULOSIS
SYPHILIS
ACTINOMYCOSIS
SCARLET FEVER
NOMA
LEPROSY
DYPHTHERIA
CAT – SCRATCH DISEASE
PYOGENIC GRANULOMA

5. TUBERCULOSIS

6. Tuberculosis is a chronic systemic infectious disease of worldwide prevalence.
It is a granulomatous infection and is caused by Mycobacterium tuberculosis or rarely by Mycobacterium bovis
Incidence of tuberculosis has declined greatly
In patients with AIDS, M. avium intercellulare is a common cause of opportunistic infections

7. Mycobacterial tuberculosis- species

8. Pathogenesis
Caused by mycobacterium tuberculosis which is aerobic, slender, non-motile, non-spore forming, rod shaped, acid fast organism
Mode of spread: droplet infection
Since TB spread through droplet infection, optimal conditions for transmission include:
Overcrowding
Poor personal hygiene
Poor public hygiene

9. Droplet infection

10. Contributing factors Social issues: poverty, overcrowding
Political issues: war time, resettlement, immigration
Health issues: malnutrition, drug abuse, HIV infection, immunosuppression,
Economic issues: drug cost, health care housing, case identification and management
Microbial: drug resistance

11. Patients with the active disease expel the bacilli into the air by:
Coughing/Sneezing/Shouting
Any other way that expels bacilli into the air
Once inhaled by a tuberculin free person, the bacilli multiply in 4-6 weeks and spreads throughout the body. The bacilli implant in areas of high partial pressure of oxygen:
Lung
Renal cortex

12. This is known as the Primary Tuberculosis
This is known as the Primary Tuberculosis. The lesion will heal and a scar will appear in the infected loci.
The bacteria at this time goes into a dormant state
When a person's immune system is depressed, a secondary reactivation occurs and is called Secondary Tuberculosis.
Diffuse disseminated infection through vascular channels may occur and has been termed “Miliary Tuberculosis”.

13. Airborne (droplet) infections
Tissue hypersensitivity to the bacilli
Transient inflammatory reaction in lung (PMNL’s & macrophages)
Macrophages phagocytose the organism
Bacilli start to multiply within the macrophage
Formation of epitheloid cells
Epitheloid cells fuse together and form Langhan's giant cells

14. Caseation necrosis begins in the center of the infected tissue
Lymphocytes and fibroblasts accumulate in the periphery
Leads to formation of an avascular granuloma (Tubercle)
Most of the lesions heal by fibrosis and calcification
Micro-organisms may remain dormant for a long time
Reinfection as a result of reactivation
whenever the patient's body resistance is suppressed
Called Secondary Tuberculosis

15. Clinical Features Commonly occurs in adult males
Primary TB is usually asymptomatic
Secondary TB shows features such as
General
Fever, Weight loss, Anorexia, Night sweats, Weakness, “Consumption”
Organ specific
Lungs: Pneumonia (cough, sputum +/- blood)
Lymph nodes : Swollen lymph nodes (scrofula)
Genitourinary: Sterile pyuria
Bone: tuberculous osteomyelitis, fracture
Brain: Headache, Meningitis
skin: Lupus vulgaris

16. Oral Manifestations TB of Oral cavity is rare.
Tuberculous lesions of the oral cavity are mostly secondary to the pulmonary infections
Primary oral tuberculosis may occur in some cases

17. Intact oral mucosa does not permit tuberculous bacilli to enter into the tissue.
Pre-existing oral lesions may facilitate the entry of these organisms into various oral structures (oral ulcers, periodontitis, dental abscess, cyst, granuloma & leukoplakia )
Organisms can also reach through hematogenous route to sub mucosa, subsequently proliferate & ulcerate the mucosa.

18. Dentist may get infected by contact with infected persons
The important tuberculous lesions of the oral cavity are
Tuberculous ulcers
Tuberculous gingivitis
Tuberculous osteomyelitis
Tuberculosis of the salivary glands
May also produce nodules, vesicles, fissures, plaques, granulomas or verrucal-papillary lesions

19. Tubercular ulcers
Single or multiple ulcers which are irregular , superficial or deep, painful & tend to increase slowly in size.
Have a granulating floor with minimum induration and surrounding mucosa is inflamed and edematous
May occur in any intraoral site, however tongue is the most common site.
(Palate, buccal mucosa, gingiva, lips, alveolar ridge and vestibules may also be affected).

20. Tubercular Gingivitis
Tubercular granuloma
Seen as soft, non-tender swelling
May occur in any intraoral site, palate is the most common site.
May develop in the periapical region of a grossly decayed tooth due to the entry of organism through the pulp canal- Tubercular periapical granuloma / tuberculoma
Tubercular Gingivitis
Small granulating ulcers or erosive lesions with concomitant gingival hyperplasia

21. Tubercular Gingivitis

22. Tuberculous osteomyelitis
Develop due to entry of organisms through decayed tooth or due to hematogenous spread.
Pain, swelling, sinus/fistula formation, trismus, paresthesia.
Tuberculosis of salivary gland
Generalized glandular swelling or abscess formation along with pain, facial palsy & fistula formation

23. Scrofula
Enlarged oropharyngeal lymphoid tissue
with involvement of cervical lymph nodes.
Caseous necrosis &numerous draining
fistula through overlying skin
Lupus vulgaris – Tuberculous involvement of skin

24. Scrofula / lupus vulgaris

25. Histopathology

26. Microscopic presentation is in the form of granulomas, which are circumscribed lesions.
granulomas have a central area of caseous necrosis surrounded by multinucleated giant cells and epithelioid cells.
Rimming -Epitheloid cells are macrophages.
The nuclei of multinucleated giant cells are seen at the periphery, having a horse shoe shaped arrangement and these cells are called Langhans’ giant cells.

27. This is surrounded by a zone of lymphocytic infiltration and fibrosis.
Tubercular organisms may be demonstrated in the tissue sections by Ziehl – Neelsen or other acid fast stains.

30. Investigations
Staining of the smear prepared from sputum by Ziehl-Neelsen stain
Chest radiograph
Bacterial culture in Lowenstein-Jensen media
(materials used for culture may be sputum, laryngeal swab, gastric lavage, urine, cerebrospinal fluid and pus, etc.)
Animal inoculation
Histopathology
Tuberculin test / Mantoux test
Enzyme-linked immunosorbent assay (ELiSA) test
PCR (polymerase chain reaction)

31. Treatment
By antitubercular drugs in different regimens

32. Syphilis

33. Historical Perspective
It was first described in the 1500’s
Also called as LUES
Was known as “The Great Imitator” because so many of the signs and symptoms are indistinguishable from those of other diseases

34. The disease is generally classified into two: Acquired syphilis
Syphilis is a sexually transmitted disease (STD) caused by a microscopic bacterium called the Treponema pallidum, which enters the blood stream and infects the entire body.
Syphilis has an incubation period of 1-13 weeks before any signs or symptoms.
The disease is generally classified into two:
Acquired syphilis
Congenital syphilis

36. 4 Stages of Syphilis Acquired syphilis Primary Stage Secondary Stage
Latent Stage
Tertiary Stage

37. Acquired Syphilis Is acquired from an infected person
It can be either through
Sexual contact with an infected partner
Careless handling of the infected patients by the health professionals
Drug abusers
Manifests in four stages:
Primary syphilis
Secondary syphilis
Latent syphilis
Tertiary (late) syphilis

38. Primary Syphilis Clinical symptoms appear at the site of inoculation
Develops at the site of inoculation approximately 3 weeks after infection
Clinical symptoms appear at the site of inoculation
male and female genitalia
extra genital site like-fingers, oral region, perianal region & nipples, etc.
(at these sites the spirochetes undergo rapid replication and enter into the lymphatics or blood stream)

39. Characteristic primary lesion of syphilis is called “Chancre”
It is a solitary, painless, indurated, nontender, nonhemorrhagic, ulcerated or eroded lesion.
Chancre starts as a dull red macule or papule, which later on becomes eroded or ulcerated and produces Regional lymphadenopathy
Resolves within weeks

40. Chancre

42. Primary Syphilis: Oral manifestations
Chancre occurs on the lips, tongue, palate, gingiva, uvula and tonsils
May be painful due to secondary infection and are highly contagious in nature
Chancres are ulcerated, indurated lesions covered by a grayish white membrane
Often mistaken for an early carcinoma

43. Tongue lesions- seen on the lateral surface of the anterior two-third area or on the dorsal surface and often there is enlargement of the folate papilla.
Tonsils show edema, redness and surface erosions or ulcerations.
Lymph nodes are enlarged bilaterally, these are painless and rubbery in consistency.
Heals by scarring within 3-6 weeks time

44. Secondary Syphilis Also called Metastatic Stage
Appears in about 6-8 weeks after the appearance of the primary chancre
Occurs due to the generalized hematogenous dissemination of the infection in the body
Characterized by skin lesions, mucosal lesions, few constitutional symptoms and generalized lymphadenopathy

45. Skin lesions may also occur in the form of nodular, flat-papillary (condyloma lata) or pustular lesions.
Circinate (coin-like) lesions on the face are characteristic of secondary syphilis.
Areas of hyperpigmentations may be seen on the palms and soles.

46. Constitutional symptoms with secondary syphilis include-headache, anorexia, fever, joint and muscle pain, laryngitis and pharyngitis, etc.
Generalized lymphadenopathy is common and the nodes are painless, discrete and not fixed to the surrounding tissues.
With or without treatment secondary lesions usually heal within 2-4 weeks time
At times in immunocompromised patients , it become wide spread & is referred to as ‘ Leus Maligna’

47. Secondary Syphilis - condymalata

49. Leus Maligna’

50. Secondary Syphilis: Oral manifestations
The secondary lesions are mucocutaneous in nature and they usually occur 6 to 8 weeks after the primary infection.
The oral lesions in this stage are called “mucous patches”, and these are commonly seen over the tongue, gingiva, tonsils, larynx, pharynx and cheek, etc.
These patches are characterized by multiple, flat, irregular or circular, slightly raised, painless, round erosions.

51. Mucous patches are covered by a thin yellowish-grey (glistening) slough and are surrounded by a painful erythematous halo
Multiple mucous patches in the oral cavity coalesce together and from “snail track” like ulcers. This stage is also contagious.
Diffuse maculo- papular eruptions of the palate and other parts of the oral mucosa often occurs.
Tongue is often fissured .
Oral condyloma lata often presents round, pale or white, velvety lesions.

52. Secondary Syphilis: Snail track ulcers

53. Latent Syphilis Called the Hidden Stage
Begins when the Secondary symptoms disappear
The bacteria begins to infest the bone marrow, lymph glands, vital organs, and the central nervous system
It may last up to a month or a lifetime
1/3 of the cases left untreated will proceed to tertiary stage

54. Latent Syphilis

55. trophic degeneration of knee joint
Latent Syphilis
trophic degeneration of knee joint

56. Tertiary (Late) Syphilis
Occurs about 5-10 years after the primary infections and it affects nearly every organs of the body
It mainly affects skin, mucous membrane, CNS & CVS
Typical lesions of tertiary syphilis is called " Gumma", which is a localized, chronic granulomatous lesion having either nodular or ulcerated surface.
Granulomatous ulcerative lesion often appears as a “punched-out” ulcer, having vertical walls and a dull red granulomatous base with an irregular outline.

57. Skin lesions heal very slowly and often they leave "tissue paper" like scars.
Tertiary syphilis occurring in pregnancy often results in congenital syphilis of the newborn
The most serious complication of tertiary syphilis is the destruction of the walls of large blood vessels, resulting in aneurysm and cardiac insufficiency.
Involvement of central nervous system (neurosyphilis) results in generalized paresis, dementia and strokes.

59. Tertiary Syphilis :Oral manifestations
Gumma are commonly seen on the hard and soft palate, lips and tongue
This stage is not contagious.
These lesions begin as firm, small, pale, nodular masses in the midline of the palate.
They frequently ulcerate by central necrosis and have a punched-out edge with a wash-leather floor.
The ulcers are either single or multiple and are mostly painless.

60. In tertiary syphilis, progressive necrosis and sloughing often leads to perforation of the palate.
In the tongue, often there is presence of a superficial glossitis called “Syphilitic/Leutic/interstitial/Atrophic glossitis”.
Loss of filliform and fungiform papilla results in a bald tongue.
However an ulcerative gummatous lesion of the tongue may closely resemble squamous cell carcinoma.

62. Congenital Syphilis
Congenital syphilis is a rare entity that occurs in children born to an infected mother.
The condition occurs due to transplacental infection with T. Pallidum during fetal development.
Congenital infection is associated with several adverse outcomes, including:
Prenatal death
Premature delivery
Low birth weight
Congenital anomalies

63. Two-thirds of live-born neonates with Congenital syphilis are asymptomatic at birth.
Overt infection can manifest in the fetus, the newborn, or later in childhood.
The infant may have many or even no signs until 6-8 weeks of life (delayed form).
Clinical manifestations after birth are divided arbitrarily into:
- Early CS (<=2 years of age)
- Late CS ( >2 years of age)

64. Clinical Manifestations of Early Congenital syphilis
Condyloma Lata
Maculopapular rash
Hepatosplenomegaly
Jaundice due to the hepatitis
Anemia
Osteochondritis
Pseudoparalysis
Lymphadenopathy
Mucous patches

66. Clinical Manifestations of Late Congenital syphilis
Frontal bossing
Saddle nose
Short maxilla
High -arched palate
Relative prognathism of mandible
Hutchinson's tooth
Mulberry molars
Hutchinson's incisors

67. Interstitial keratitis
Eighth nerve deafness
Rhagades
Premature perioral fissuring
Higoumenaki's sign
Enlargement of clavicle adjacent to the sternum
Saber shin
Anterior bowing of tibia as a result of periostitis
Scaphoid scapulae
Concavity of vertebral border of the scapulae
Clutton's joint
Painless synovitis and enlargement of joints, usually the knee

68. Saddle Nose

69. Higoumenaki's sign

70. Saber Shins

71. Clutton’s Joints

72. https://classconnection. s3. amazonaws

73. Hutchinson's triad Described by Sir Jonathan Hutchinson in 1858.
Defined the following three pathognomonic diagnostic features
Hutchinson's teeth
Ocular interstitial keratitis
Eighth nerve deafness
Few patients exhibit all three features

74. Hutchinson's teeth
The infection alters the formation of both the anterior teeth (Hutchinson's incisors) and the posterior dentition (Mulberry molars, Fournier's molars, Moon's molars).
Hutchinson's incisors exhibit their greatest mesiodistal width in the middle third of the crown.
The incisal third tapers to the incisal edge, and the resulting tooth resembles a straightedge screwdriver.
The middle lobe is affected. The incisal edge often exhibits a central hypoplastic notch.

75. Mulberry molars taper toward the occlusal surface with a constricted grinding surface.
The occlusal anatomy is abnormal, with numerous disorganized globular projections that resemble the surface of a mulberry

78. Interstitial keratitis
Not present at birth, but usually develops between the ages of 5 and 25 years
May lead to permanent blindness

80. Histopathology
Histopathologic picture of the oral lesions - not specific.
During the first two stages, the pattern is similar
The surface epithelium is ulcerated in 10 lesions & may be ulcerated/hyperplastic in the 20 stage.
The underlying lamina propria may demonstrate an increase in the number of vascular channels, and an intense chronic inflammatory reaction.
The infiltrate is composed predominantly of lymphocytes and plasma cells and often demonstrates a perivascular pattern.

81. Histopathology
Oral tertiary lesions typically exhibit surface ulceration, with peripheral pseudo epitheliomatous hyperplasia.
The underlying inflammatory infiltrate usually demonstrates foci of granulomatous inflammation with well-circumscribed collections of histiocytes and multi-nucleated giant cells.
Even with special stains, the organisms are hard to demonstrate in the third stage

82. Histopathology

83. Histopathology

84. Diagnosis
Detection of bacteria in smear by dark ground illumination microscopy
Bacterial culture in artificial media.
Serological tests
Wasserman reaction, Khan test, Venereal disease research laboratory (VDRL) test, Rapid Plasma Reagin (RPR) test, T pallidum hemagglutination assay (TPHA) & Fluorescent treponemal antibody absorption(FTA-ABS)
ELISA.
Histopathology.

85. Treatment Penicillin- In high doses
Erythromycin or tetracycline – In case of patients allergic to penicillin
Blood tests - to make sure the infection has been eliminated.
Tertiary syphilis is incurable

87. ACTINOMYCOSIS
Actinomycosis is a chronic granulomatous, suppurative and fibrosing infection.
Although the term actinomycosis seems to imply a fungal infection, it is an infection of filamentous, branching, gram-positive anaerobic, non acid fast bacteria
Actinomyces-israelii
A viscosus
A naeslundii
A odontolyticus
A, meyeri
A. bovis

89. The microorganisms are normal inhabitants of the oral cavity
Sites of colonization in healthy patients include the tonsillar crypts, dental plaque and calculus, carious dentin, gingival sulci, and periodontal pockets.
Takes entry into the tissues during trauma or tooth extraction to produce infection
Occurs in three forms:
Cervicofacial (commonest form)
Abdominal
Pulmonary actinomycosis

90. Pathogenesis
The organisms enter tissue through an area of prior trauma or soft tissue injury, periodontal pocket, extraction socket, or infected tonsil.
The infection does not spread along the typical facial plain and usually disregards the normal lymphatic and vascular routes.
Direct extension soft tissue is seen producing indurated swellings which become fluctuant and later organisms drain through multiple sinuses.
Lymph nodes become involved only if they are in the path of the process.
Lymphadenopathy associated due to secondary infections

91. Clinical Features Cervicofacial
Age: disease occurs mostly in the fourth and fifth decade of life.
Sex: More prevalent among males.
Site: The soft tissues of the submandibular, submental, and cheek areas are common areas of involvement, with the area overlying the angle being the most frequently affected site.

92. The organism enters tissue through an area of prior trauma or soft tissue injury, periodontal pocket, extraction socket, or infected tonsil
The infection does not spread along the typical facial plain and usually do not take normal lymphatic and vascular routes
Direct extension through soft tissue is seen and lymph nodes become involved only if they are in the path of the process.
Lymphadenopathy associated with this disease may be due to secondary infections caused by some other organisms.

93. Starts as a swelling over upper part of the neck or below the ear, or over mandible with minimal pain.
The overlying skin appears purplish red & indurated.
Later on the swelling becomes fluctuant and some areas of the skin breaks down to produce multiple pus discharging sinuses.
Similar sinuses may be seen intraorally.
The pus contains clinically visible, small yellowish flecks known as “Sulfur Granules” and each of them represents a colony of organisms.

96. The pus discharging sinuses heal up, but later on, some new sinuses appear in the region and the process continues for years and causes great deal of scarring and disfigurement of the skin.
Involvement of the jaw bones by this disease often results in chronic osteomyelitis
Lesions localize at the apices of teeth and may simulate periapical granulomas or cyst

97. Sulfur Granules

98. Abdominal Extremely severe form High mortality rate
Exhibit as a mass fixed to the underlying skin or as abscess involving any organ
Accompanied by symptoms such as fever, chills, nausia, vomiting etc
THORACIC FORM
Fever & chills with productive cough and pleural pain

100. Histopathology
Actinomycosis is essentially a granulomatous inflammation showing central abscess formation, which shows typical bacterial colonies.
Colonies appear to be floating in a sea of PMNL’s with giant cells & macrophages around the lesional periphery.
The individual colony appear round or lobulated, made up of a meshwork of filaments that stains with hematoxylin, but shows eosinophilia of the peripheral club shaped end of the filaments

101. The periphery of each colony shows club-shaped filaments that form a radiating rosette pattern and produce a "ray fungus" like appearance.
The colonies are surrounded by a fibrous tissue wall at the outer margin.

102. RAY FUNGUS

103. Diagnosis Culturing of organisms Histopathological diagnosis
Immunofluorescent techniques

104. Treatment
High doses of any of the drugs like-penicillin, cephalosporin, clindamycin and lincomycin, etc.

106. SCARLET FEVER
Scarlet fever is a rare specific bacterial disease caused by Group A, β-hemolytic streptococcus
It commonly occurs in children during winter months.
The disease begins as streptococcal tonsillitis with pharyngitis in which the organisms elaborate an erythrogenic toxin
The toxin attacks the blood vessels and cause the characteristic skin rash

107. Clinical Features Incubation period ranges from 1-7 days
Significant clinical findings: Fever, Enanthem & Exanthem
Also seen are headache, vomiting, tonsillitis, pharyngitis and cervical lymphadenopathy, etc.
Fever develops abruptly around second day
Temperature peaks around 1030 & returns to normal within 3 days

108. A diffuse, bright red skin rash appears on the second or third day of the disease, that starts on the chest and gradually spreads to the other body surfaces.
The skin rash is particularly more noticeable in areas of pressure & skin folds.
Characteristic skin rash is referred to as “ Sunburn with goose pimples”.
Skin of the trunk & extremities have a Sand paper texture.

109. Sunburn with goose pimples
Pastia lines

110. Transverse red streaks known as “Pastia’s lines” are seen in zones of stress.
Skin rashes last for about one week following which the affected area undergoes desquamation, starting with the face
Period of desquamation may last from 3-8 weeks

112. Oral Manifestations
Chief oral manifestations of scarlet fever are referred to as “Stomatitis Scarlentina”
The oral mucosa involves the tonsils, pharynx, soft palate & tongue.
The tonsils, pharynx, & soft palate becomes erythematous & edematous.
Tonsillar crypts may be filled with a yellowish exudate.
The palate appears congested and inflamed, and the hard palate exhibits punctiform redness.

113. The tongue may be covered with a white coating, through which the enlarged and reddened fungiform papillae project like small red knobs, and this phenomenon is called “Strawberry tongue”.
Later on, the white coating on the tongue is lost, leaving a deep red, glistening & smooth surface except for the swollen hyperimic papillae and is called “Raspberry tongue”.

115. Raspberry Tongue

117. Treatment Administration of penicillin or erythromycin.
With appropriate treatment prognosis is excellent.
No available methods for prevention

119. NOMA
Also called as “Cancrum oris; Gangrenous stomatitis & Necrotizing stomatitis”
Derived from the Greek word “Nomein” meaning "to devour."
Rapidly progressing, gangrene of the oral & facial tissues that occurs in debilitated or nutritionally deficient persons.
An opportunistic infection caused by components of the normal oral flora that becomes pathogenic during periods of compromised immune status.

120. Main causative organisms are Fusobacterium necrophorum or F
Main causative organisms are Fusobacterium necrophorum or F. nucleatum & Prevotella intermedia.
They interact with one or more other bacterial organisms, of which the most commonly implicated are Borrelia vincenti, S. aureus, & Non hemolytic Streptococcus species.
May be considered as a secondary complication of a systemic disease rather than a primary disease.

121. Predisposing factors include:
Poverty
Malnutrition or dehydration
Poor oral hygiene
Poor sanitation
proximity to livestock
Recent debilitating illness
Immunodeficiency disorder

122. Clinical Features
In many instances. the infection begins as necrotizing ulcerative gingivitis (NUG).
May be considered as an extension of necrotizing ulcerative gingivitis
Often begins on the gingiva as NUG, which may extends to involve the adjacent soft tissue by ganngrenous necrosis and forms areas called necrotizing ulcerative mucositis.

123. Typically arises in children aged 1 to 10 years
A line of demarcation develops between the healthy tissue & dead tissue
Jaw is exposed as large masses of tissue sloughs out
Commencement of gangrene is denoted by blackening of the skin.
Fetid odor, significant pain, fever, malaise & regional lymphadenopathy are typical.

124. A related disorder, “Noma Neonatorum”, arises in the first month of life in low-birth weight infants
who also demonstrate malnutrition and frequently a debilitating illness
These patients almost always have infection with Pseudomonas aeruginosa. often combined with E. coli, Kiebsiella species, or
Staphylococcus species

125. necrotizing ulcerative mucositis/gangreneous-stomatitis

126. Complications Severe facial disfigurement Death, as a result of
Toxemia
Pneumonia
Diarrhea

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