Bacterial Infections

1. 1
Bacterial infections
Dr. Arun Panwar
18/06/2020

2. Contents:
Introduction
Bacterial Infections:
• Scarlet Fever
• Syphilis
• Gonorrhea
• T.P
• Actinomycosis
• Necrotizing ulcerative gingivitis (NUG)
• Noma
• leprosy
• Tetanus
Conclusion
References

3. BACTERIA
2
Bacteria constitute a large domain or kingdom of
prokaryotic microorganisms. Typically a few
micrometres in length, bacteria have a wide range of
shapes, ranging from spheres to rods and spirals

4. Classification
BACTERIA
Gram Negative
- Spirochaetes
Gram Positive
- Staphylococcus
- Streptococcus
- Clostridium
- Actinomyces
- Corynebacterium
3

5.  Highly contagious systemic infection
 Predominantly in children
 β – hemolytic streptococci (Streptococcus pyogens)
 Organisms produce an erythrogenic toxin
 Attacks blood vessels, produces characteristic skin rash
Scarlet Fever (Scarlatina)
4

6. Clinical features
• The microorganism enters the body usually through pharynx
• Incubation period: 3-5 days
• Pharyngitis
• Tonsillitis
• Headache, chills, fever, vomiting.
• Sand paper skin
5

7. • Enlargement & tenderness of cervical lymph nodes
• Characteristic diffuse, bright scarlet skin rash which appears on
the 3rd day– “sun burn” with “goose pimples”
• When the rash is prominent in areas of skin folds – “Pastia
lines”
• Rash clears in 1 week followed by period of desquamation for
3 – 8 weeks.
6

8. Oral manifestations
 Scattered petechiae on soft palate.
 First 2 days – white coating on dorsal surface of tongue
through which only fungiform papillae seen (white strawberry
tongue)
 By 4th or 5th day – white coating desquamates, reveals
erythematous dorsal surface with hyperplastic fungiform
papillae – (red strawberry tongue or raspberry tongue)
8

9. 11
Stomatitis Scarlatina- small punctate red macules appear on hard &
soft palate & uvula
o Congested mucosa of palate
o Fiery red colour throat
o Tonsils-swollen & grayish exudate
 Complications:
 Peritonsillar abscess
 Rhinitis
 Sinusitis
 Otitis media

10. Treatment

11. Tetanus (Lock-Jaw)
 Acute infection of the nervous system
 Causative organism: exotoxin of anaerobic gram +ve bacilli
“Clostridium tetani”.
 Characterized by intense activity of motor neurons & results
in the severe muscle spasm.
13
 Incubation period: 6-10 days
 Can enter body through trauma
 Pathogenesis- Tetanospasmin

12. Clinical features
 Characterised by involvement of multiple muscles
 Lock Jaw- Trismus due to spasm of masseter, rigid abdomen and
stiff proximal limb muscles.
 Prolonged contraction of facial muscles results in grimace or
sneer called as Risus scardonicus.
 Contraction of back muscles produces an arched back called
opisthotomus.
 Spasms occur spontaneously/ slight stimulation
14

13. Other features- Dsyphagia, restricted chest movement, layrngeal
spasm leading to asphyxia.
Local Tetanus:
• Manifest as spasm of muscles near the wound
•Cephalic Tetanus- trismus and facial palsy
•Occur after head inury or ear infection
15

14. Treatment
Aim:
• To remove spores at the sites of the wound
• Prevent toxin production
• Neutralize unbound toxins
• Prevent muscular spams
• Antibiotics should be given to erradicate source of toxins:
• Penicillin 10-12 million units IV x 10 days
• Metronidazole 1g / 12hrs
17

15. Antitoxin:
• Injected to neutralize circulating toxin and unbound toxin within
wound.
• Human tetanus immunoglobin (TIG)
Prophylaxis
• Wound debridement and booster dose of TT
• ATS (Anti tetanus sera) 1500 units or TIG 250 units
• Active Immunization: 3 doses of triple vaccine in 1st year of life
• Booster dose – 5 to 10 year interval

16. Diphtheria
 Acute Infectious and communicable disease
 Skin and mucous membrane
 Causative organism: Corynebacterium diphtheriae
 Produces lethal exotoxin causing tissue necrosis.
 Humans only reservoir
 Characterised by local inflammation and grayish
pseudomembrane
 Mode of spread: 1. Direct skin contact
2. Respiratory droplets
18

17. Clinical features
19
 Incubation period: 2-5 days
 Types of diphtheria: Tonsillar, Pharyngeal, Laryngeal
Clinically:
 Malaise, headache, fever , Sore throat
 Mild redness & edema of pharynx
 Tender enlargement of lymph nodes
 Edema of neck, submandibular region & anterior part of the
neck giving “bull neck” appearance

18. Oral manifestations
 Oropharyngeal exudate – begins from one or both tonsils as
patchy, yellow white, thin film.(diphtheritic membrane)
 Thickens to form adherent grayish green covering.
 May develop patches of green or black necrosis.
 Involve entire soft palate, uvula, larynx or trachea.
21

19. Laboratory Diagnosis
 Direct Microscopy: smear stained with albert stain
show “Chinese Letter” or “Cuneiform Arrangement”.
 The bacilli look green and
 Metacromatic granules appear bluish black
23

20. Treatment
 Antidiphtheritic toxins (ADS) combined with
antibiotics – Once disease has developed
 Erythromycin, procaine penicillin or i.v. penicillin
 Prevention : By immunization of “diphtheria toxoid”
 DPT vaccination (Diptheria toxoid, tetanus toxoid
and pertusis.
 Given 3 doses from age of 3 years , interval of 4-6
weeks
 Booster dose after 1 year.
24

21. Tuberculosis (Koch's disease)
(acid fast
 It is an chronic granulomatous inflammation.
 Causative organism: Mycobacterium tuberculosis
bacilli)..
 Incidence: more common in poor countries of Africa, Latin
America &Asia.
• Mode of transmission: Small air borne droplets generated by
coughing, sneezing, talking of a person with tuberculosis.
Pulmonary TB is the chief form of the disease although it may
also occur in any part of the body including major organs such
as kidney, liver, bone etc..
25

22. Types of tuberculosis
 Primary TB
 Secondary TB
 Pulmonary TB
 Miliary TB
27

23. Pathogenesis of Primary tuberculosis
Droplet spread & inhalation
Goes in to the lung alveoli
Engulfed by alveolar macrophages
Multiply within macrophages
Either host cells overcome bacteria, or vice versa
28

24. Clinical features
• Episodic fever, chills, fatigability, malaise.
• Gradual loss of weight
• Persistent cough with or with out hemoptysis.
• Night sweating, dyspnea.
30

25. Extra – pulmonary TB
• May involve lymph nodes, skin, skeletal system, CNS, kidneys
& GIT
Scrofula: Involvement of cervical lymph nodes
• Swelling, tenderness of lymph nodes.
• Involvement of TMJ
• Involved nodes may develop:
• Cold Abscess
• Lupus vulgaris –
• involvement of the skin
31

26. Oral manifestation
 Do occur but are relatively uncommon (0.1%)
 Lesions of oral mucosa are seldom primary, but they are
secondary to pulmonary diseases.
 Organisms are carried in the sputum & enter the mucosal tissues
only if there is a break or a breach in the mucosal surface.
 Organisms may be carried to the oral tissues by the
hematogenous route, deposited in the submucosa & may
proliferate & ulcerate the overlying mucosa.
33

27.  Lesions may occur at any site in oral mucosa, but the tongue is the
most common site followed by palate, lips, buccal mucosa,
gingiva & frenum.
 Usually the TB lesion is irregular, superficial or deep, painful ulcer
which tends to increase in size.
 Less frequent –nodular, granular or firm leukoplakic areas
 TB gingivitis – manifests as diffuse, hyperemic, nodular or
papillary proliferation of gingival tissues.
34

28. Tubeculous ulcer
35

29. Diagnosis.
 Staining of the smear prepared from sputum by Ziehl-Neelsen
stain
 Chest radiograph
 OPG
 Fine needle aspiration of Lymph nodes
 Bacterial culture in Lowenstein-Jensen media
 Mantoux Test (Tuberculin test)
42

30. TUBERCULIN TEST
Mantoux Test:
•Hypersensitivity reaction to tubercular antigen
• Ten units of purified derivative in 0.1 ml normal saline
is injected intradermally in flexor aspect of the forearm.
• Test is positive if 2-4 days later there is inflammatory
reaction with surrounding erythema (not less than
5mm).
• Inference: Size of the inflammatory reaction
43

31. Treatment
• First line of drugs: Rifampicin, Isoniazid, Ethambutol,
Pyrazinamide, Sterptomycin
• Second line of drugs: Cycloserine, ethionamide, Amikacin,
Levofloxacin, Moxifloxacin
Regimen:
Initial phase ( 2 months): PYRAZINAMIDE + ETHAMBUTOL +
RIFAMPICIN+ ISONIAZID
Continuation phase (4 months): RIFAMPICIN+ ISONIAZID
44

33. Directly Observed Therapy (DOT)
• Means that a Trained healthcare worker or other designated
individual (excluding a family member) provides the prescribed
TB drugs and watches the patient swallow every dose.
BCG Vaccine
•Prepared from the strain of attenuated live bovine tuberculosis
bacillus, Mycobacterium Bovis.
•80 % effective in preventing TB for 15 years

34. Leprosy(Hansen's Disease)
 Chronic granulomatous infection.
 Causative organism: Mycobacterium leprae (AFB)
 Slightly contagious disease.
 Mostly documented in Brazil, Indonesia, Myanmar &
Nigeria
 Modes of transmission: Direct contact, Materno fetal
transmission
 Types: Paucibacilliary and Multibacillary
46

35. Clinical features
Tuberculoid lesions: (paucibacillary)
 Small number of well circumscribed, hypopigmented skin lesions
 Nerve involvement results in anesthesia of affected skin
 Accompanied by loss of sweating.
 Oral lesions are rare
47

36.  Lepromatous lesions: (multibacillary)
 Begins slowly with numerous, ill defined, hypopigmented
macules or papules.
 With time, lesions become thickened
 Hair on eyebrows & eyelashes often lost.
 Nerve involvement – leads to loss of sweating
49

37. Oral manifestations
 Facial involvement common
 Skin enlargement leads to distorted facial features (leonine facies)
 Nasal involvement – nose bleeds, stuffiness, loss of smell
 Collapse of bridge of nose – pathognomonic
52

38.  Small tumor like masses-“LEPROMAS” develop on the
tongue, lips & hard palate – break down & ulcerate.
 Gingival hyperplasia with loosening of the teeth.
54

39. Histopathologic features
 Paucibacillary type – granulomatous inflammation with well formed
clusters of epitheloid histiocytes, lymphocytes & giant cells.
 Paucity of organisms – can be demonstrated only with acid fast
staining.
 Multibacillary type – no well formed granulomas.
 Sheets of lymphocytes mixed with vacuolated histiocytes called as
“Lepra cells”
56

40. Treatment
 Paucibacillary – 6 months regimen of rifampicin & dapsone
 Multibacillary – 12 months of rifampicin, dapsone &
clofazimine
60

41. Acute Nectrotizing Ulcerative Gingivitis
Also called as:
• Vincent infection
• Trench mouth
• Fetid stomatitis
Etiology:
• Borrelia vincentii, Prevotella intermedia
• Poor oral hygiene
• AIDS
• Stress

42. Stages of ANUG
According to Pindborg et al

43. Clinical feature:
• Characterised by development of painful, hyperemic gingiva
and sharply punched out erosions of interdental papilla.
• Gingiva bleeds freely when touched
• Covered by grey, necrotic pseudomembrane
• Metallic foul taste
• Malaise, low grade fever, headache, excessive salivation,
regional lymphadenopathy

44. Treatment
First visit

45. Antibiotic regimen:

46. Patient instructions:

47. Second Visit:

48. Third visit:

50. Noma (Cancrum Oris, Gangrenous
Stomatitis)
It is a rapidly spreading gangrene of the oral & facial tissues.
Seen commonly in debilitated or nutritionally deficient
children.
Occurs chiefly in persons who are undernourished
61
Considered a 2o complication of systemic disease rather then a
primary disease.
Appears to originate as a specific infection by the Vincent’s
organism.
Fusobacterium, Prevotella intermedia, Borrelia
vincentii, Porphyromonas gingivalis

51. Clinical features
Begins as a small ulcer of the gingival mucosa.(NUG)
Rapidly spreads and involve the surrounding tissues of the
jaws, lips & cheeks by gangrenous necrosis.(NUS)
The over lying skin becomes inflamed, edematous & finally
necrotic.
Line of demarcation develops between healthy & dead tissue.
63

52. • Large masses of tissue may sloghout,
leaving the jaw exposed
• Commencement of the gangrene is denoted
by the appearance of blacking of the skin.
• Subcutaneous fat pad & buccal fat pad
undergo necrosis.
• Odor arises from the gangrenous
tissue which is extremely foul.
• Occasionally the tongue & palate are
involved.

53. Lesion not restricted by tissue planes.
Patients have high temperature during the course of the
disease.
They usually suffer from 2o infections and may die from
toxemia or pneumonia
65

54. Treatment
 Systemic Antibiotics (penicillin & metronidazole)
 Wound care
 Correction of nutrition, hydration & electrolyte imbalance
68

55. Actinomycosis
 Chronic granulomatous, suppurative & fibrosing disease.
 Caused by anaerobic, gram+ve, non
acid fast, branched, filamentous
bacteria.
 Actinomyces israelii most common causative agent,
 A. viscosus second
 It is characterized chiefly by the formation of abscesses
which tends to drain by the formation of sinus tracts.
69

56. Classification
 Classified anatomically according to the location of the lesion
1) Cervico-facial Actinomycosis
55%
1) Abdominal Actinomycosis
25%
1) Pulmonary Actinomycosis
15%
70

57. Clinical features
 May either be an acute, rapidly progressing infection or
slow progressing, chronic lesion.
 Organism enters the tissue though the oral mucous
membrane.
 May either remain localized in the mucous membrane itself
or might spread to involve the salivary glands, bones or skin
 Swelling & induration of the tissues
 Develop into one or more abscesses which later rupture to
liberate pus which contain “sulphur granules”.
71

58. o Skin over these abscesses is purplish red in color.
o These abscess areas after rupturing do heal but due to
chronicity of the disease , by the time one abscess heal the
other abscess is ready to rupture & perforate the skin
surface.
o Thus the patient over a period of time shows scars and
disfigurement of skin.
o The induration of soft tissues my get extended to
the underlying bones (maxilla & mandible)
o Mandible is more commonly involved than maxilla, if at
all maxilla is involved it may also involve cranium.
72

59. Histopathology
 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 periphery.
 The individual colony appear round or lobulated, made up
of a meshwork of filaments in a rosette pattern.
 Filaments stain with hematoxylin, but shows eosinophilia
of the peripheral club shaped end of the filaments (ray
fungus)
75

60. Treatment
 Chronic fibrosing cases – Antibiotics along with
drainage and excision of sinus tracts.
 Mild Cases:
 Oral Penicillin V 3-4 g/day or 4million units i.m daily
 If allergic to penicillin – Tetracycline 500mg/6hrs
 In case of Cervicofacial actinomycosis- 5- 6 weeks
 Deep seated – 12 months
 Severe Cases:
 Penicillin 20 million unit IV for 2-6 weeks followed
by Oral dose for for 6- 12 months
77

61. Syphilis (Lues)
 Syphilis is a sexually transmitted chronic infection caused by
Treponema pallidum
 Characterized by an incubation period of about 2 to 6 weeks.
 Infection goes through a classic evolution characterized by 3 stages
- Primary syphilis
- Secondary syphilis
- Tertiary syphilis
78

62. Etiology
 The usual mode of transmission is through
- sexual intercourse
- secretions by intimate contacts
- transplacental transmissions
Pathogenesis:
 T. pallidum gains entry through the intact mucosa or through
microscopic abrasions in the skin.
 From here it enter the blood and lymphatics to eventually produce
systemic infections.
79

63. Classification
80
 The disease is generally classified into two:
 Acquired syphilis
 Congenital syphilis
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

64.  Manifests in three stages:
1. Primary syphilis
2. Secondary syphilis
3. Tertiary (late) syphilis
82

65. Primary Syphilis
 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.
(at these sites the spirochetes undergo rapid replication and
enter into the lymphatics or blood stream)
83

66. non -
 Characteristic primary lesion of syphilis is called “Chancre”
 It is a solitary, painless, indurated, nontender,
hemorrhagic, 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 3 - 8 weeks
84

67. 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
85

68. 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
87

69.  Skin lesions occur in the form of nodular, flat- papillary
(condyloma lata) or pustular lesions.
 Circinate (coin-like) lesions on the face & skin are
characteristic of secondary syphilis.
 Areas of hyperpigmentations may be seen on the palms and
soles.
88

70. 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”;
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.
90

71.  Covered by a thin yellowish-grey (glistening) slough; surrounded
by a painful erythematous halo
 Multiple mucous patches in the oral cavity coalesce together and
from “snail track” like ulcers.
 Highly contagious.
91

72. 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 proceed to tertiary stage
93

73. 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",
 Localized, chronic granulomatous lesion having either nodular or
ulcerated surface.
 Often appears as a "punched-out" ulcer, having vertical walls and a
dull red granulomatous base with an irregular outline.
94

74. Tertiary Syphilis :Oral manifestations
 Gumma are commonly seen on the hard and soft palate, lips and
tongue
 This stage is not contagious.
 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.
96

75.  Tongue may be diffusely involved with gummata
 Appear large, lobulated & irregularly shaped. (interstitial glossitis)
 Diffuse atrophy & loss of papillae – syphilitic glossitis
98

76. Congenital Syphilis
 Congenital syphilis is a rare entity that occurs in children born of an
infected mother.
 The condition occurs due to transplacental infection with
Treponema pallidum during fetal development
 Congenital infection is associated with several adverse
outcomes, including:
 Perinatal death
 Premature delivery
 Low birth weight
 Congenital anomalies
100

77.  Clinical manifestations after birth are divided
arbitrarily into:
- Early Congenital syphilis (<=2 years of age)
- Late Congenital syphilis ( >2 years of age)
101

78. Clinical Manifestations of Early Congenital
syphilis
 Maculopapular rash
 Hepatosplenomegaly
 Jaundice due to the hepatitis
 Anemia
 Lymphadenopathy
 Mucous patches
102

79. Clinical Manifestations of Late Congenital
syphilis
 Frontal bossing
 Short maxilla
 High -arched palate
 Saddle nose
 Mulberry molars
 Hutchinson's incisors
 Higoumenaki's sign
 Enlargement of clavicle adjacent to the sternum
 Relative prognathism of mandible
 Interstitial keratitis
103

80. 104
 Rhagades
 Premature perioral fissuring
 Saber shin
 Anterior bowing of tibia as a result of periostitis
 Eighth nerve deafness
 Scaphoid scapulae
 Concavity of vertebral border of the scapulae
 Clutton's joint
 Painless synovitis and enlargement of joints, usually the knee

81. 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
105

82. 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
 Resulting tooth resembles a straight - edge screwdriver.
 The incisal edge often exhibits a central hypoplastic notch.
106

83.  Mulberry molars - taper toward the occlusal surface with a
constricted grinding surface.
 The occlusal anatomy is abnormal
 Numerous disorganized globular projections that resemble the
surface of a mulberry
107

84. Demonstation Of Treponemes
DARK GROUND MICROSCOPY: Treponema pallidum
appears as a slender, spiral organism showing
rotational as well as flexion and extension movements
109

85. Laboratory Tests
 Detection
microscopy
 Bacterial culture in artificial media.
 Serological tests
 Wasserman reaction, Khan test, Venereal disease research laboratory
(VDRL) test
 ELISA
 Western blot
112
of bacteria in smear by dark ground illumination

86. Treatment
 Penicillin will cure a person that has had syphilis for less than a
year.
 Blood tests should check to make sure the infection has been
eliminated.
 Tertiary syphilis is incurable as it has damaged body organs.
113

87. References
1. Harrison’s Infectious diseases, 3rd Edition
2. Shafer’s textbook of oral pathology
3. Burket’s Oral Medicine
4. .

88. Thank You