bacteraial infections

1. 1
Bacterial infections

2. 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

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

4. Scarlet Fever (Scarlatina)
 Systemic infection produced commonly by group A, β –
hemolytic streptococci.
 Organisms elaborate an erythrogenic toxin
 Attacks blood vessels, produces characteristic skin rash
4

5. Clinical features
• The microorganism enters the body usually through pharynx
• Incubation period: 3-5 days
• Pharyngitis
• Tonsillitis
• Headache, chills, fever (102 -104 ), vomiting.
5

6. • 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

7. Sand paper skin
7

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. “White Strawberry Tongue”
9

10. “Raspberry Tongue”
10

11. o 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
11

12. Complications
 Peritonsillar abscess
 Rhinitis
 Sinusitis
 Otitis media
 Mastoditis
 Meningitis
 Pneumonia
 Rheumatic fever
 TREATMENT
Penicillin, dicloxacillin
12

13. Tetanus (Lock-Jaw)
 Acute infection of the nervous system
 Causative organism: exotoxin of anaerobic gram +ve bacilli
“Clostridium tetani”.
 Its is characterized by intense activity of motor neurons & results
in the severe muscle spasm.
13

14. Clinical features
 Incubation period: there is wide range of incubation period but the
clinical manifestations starts with in 14 days of onset
Pain, stiffness in jaws & neck muscles
Muscle rigidity producing trismus & dysphagia
14

15. Facial muscle rigidity also occur producing a typical “Risus
Sardonicus”.
Some times the muscles of entire body are affected leading to
the condition called as “Opisthotonus”
“Cephalic Tetanus” is a condition which occurs in association
with 7th cranial nerve palsy
15

16. Opisthotonus
16

17. Treatment
 Surgical wound care
 Active & passive immunization.
 Antibiotics
17

18. Diphtheria
 Acute contagious disease
 Causative organism: Corynebacterium diphtheriae
 Produces lethal exotoxin causing tissue necrosis.
 Humans sole reservoir
 Mode of spread: 1. Direct contact
2. Droplets
18

19. Clinical features
 Incubation period: 1-10 days
 Listlessness, malaise, headache, fever & vomiting
 Sore throat
 Mild redness & edema of pharynx
 Cervical lymphadenopathy – involvement of tonsils
 Edema of neck, submandibular region & anterior part of the
neck giving “bull neck” appearance
19

20.  Involvement of nasal cavity – prolonged mucoid or hemorrhagic
discharge
20

21. Oral manifestations
 Oropharyngeal exudate – begins on 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

22. Diphtheritic membrane
22

23. 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

24. Treatment
 Anti diphtheritic toxins combined with antibiotics.
 Erythromycin, procaine penicillin or i.v. penicillin
 Prevention : By immunization of “diphtheria toxoid”
 DPT vaccination
24

25. Tuberculosis (Koch's disease)
 It is an chronic granulomatous inflammation.
 Causative organism: Mycobacterium tuberculosis (acid fast
bacilli)..
 Incidence: more common in poor countries of Africa, Latin
America &Asia.
25

26. • Mode of transmission: inhalation, ingestion, inoculation &
transplacental routes.
• 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..
• Pathogenesis: in open case of TB, bacilli is shed in respiratory
secretion.
26

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

28. 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

29.  Reactivation of organisms in previously infected person –
Secondary TB
 Diffuse dissemination through vascular system producing
multiple small foci of infection – Miliary TB
29

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

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

32. Scrofula
32

33. 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 & subsequently
proliferate & ulcerate the overlying mucosa.
33

34.  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

35. Tubeculous ulcer
35

36. Tuberculous gingivitis
36

37. TB of alveolus
37

38.  Tuberculous osteomyelitis – reported in jaws.
 Appears as ill defined radiolucency
38

39. Histopathology
 Microscopically the lesions of TB exhibits the granuloma /
caseating granuloma. (tubercle)
 Circumscribed collections of epitheloid
cells, lymphocytes, multinucleated giant cells & macrophages
with central caseous necrosis.
 Langhan’s giant cells
39

40. Granuloma; Langhan’s Giant cells
40

41. Caseation necrosis
41

42. Diagnosis.
 Staining of the smear prepared from sputum by Ziehl-Neelsen
stain
 Chest radiograph
 Bacterial culture in Lowenstein-Jensen media
 Tuberculin test
42

43. TUBERCULIN TEST
Mantoux Test:
Ten tuberculin units of purified derivative in 0.1 ml normal
saline intradermally in flexor aspect of the forearm.
Test is positive if 2-4 days later there is at least induration
with surrounding erythema.
43

44. Treatment
 By antitubercular drugs in different regimens
RIFAMPICIN
ISONIAZID
ETHAMBUTOL
PYRAZINAMIDE
STERPTOMYCIN
Regimens:
6 months, 9 months, 12 months.
Initial phase ( 2 months): PYRAZINAMIDE + ETHAMBUTOL +
RIFAMPICIN+ ISONIAZID
Continuation phase (4 months): RIFAMPICIN+ ISONIAZID
44

45. Prevention
 Through BCG (Bacille Calmette Guerin)
Strain of bovine TB
Intradermal vaccination (0.1 ml)
Protection for up to 7 years
45

46. Leprosy(Hansen's Disease)
 Chronic granulomatous infection.
 Causative organism: Mycobacterium leprae (AFB)
 Slightly contagious disease.
 Mostly documented in Brazil, India, Indonesia, Myanmar
& Nigeria
46

47. 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 rare
47

48. Tuberculoid Leprosy
48

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

50. Lepromatous Leprosy
50

51.  Decreased sensation of light touch, pain & temperature.
 Begins in extremities & spreads to most of body.
51

52. 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

53. Leonine facies
53

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

55. Lepromas
55

56. 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

57. Tuberculoid leprosy
57

58. Lepromatous – no granulomas
58

59. Acid fast stain
59

60. Treatment
 Paucibacillary – 6 months regimen of rifampicin & dapsone
 Multibacillary – 24 months of rifampicin, dapsone &
clofazimine
60

61. 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 or debilitated
from infections
61

62. 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
62

63. 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

64. Large masses of tissue may slough out, 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 in
advance of other adjoining tissues.
Odor arises from the gangrenous tissue which is extremely
foul.
Occasionally the tongue & palate are involved.
64

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

66. Cancrum Oris
66

67. 67

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

69. 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

70. Classification
 Classified anatomically according to the location of the lesion
1) Cervico-facial Actinomycosis
2)Abdominal Actinomycosis
3)Pulmonary Actinomycosis
70

71. Clinical features
 May either be an acute, rapidly progressing infection, or
slow, 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

72. 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.
72

73. 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, meninges
or the brain itself.
73

74. 74

75. 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 lesional 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)
 The colonies are surrounded by a fibrous tissue wall at the
outer margin.
75

76. 76

77. Treatment
 The treatment of the disease is difficult & has not been
uniformly successful.
 Penicillin & Tetracycline have been used more frequently.
77

78. 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

79. 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

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

81. 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
81

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

83. 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 &
nipples, etc.
(at these sites the spirochetes undergo rapid replication and
enter into the lymphatics or blood stream)
83

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

85. 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

86. Chancre
86

87. 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

88.  Skin lesions may also 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

89. Secondary Syphilis
89

90. 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

91.  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

92. Mucous patches – “snail track ulcers”
92

93. 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
93

94. 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

95. Nodular gumma
95

96. 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

97. Gumma perforating palate
97

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

99. Syphilitic Glossitis
99

100. 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

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

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

103. 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

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
104

105. 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

106. 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

107.  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

108. 108

109. DEMONSTATION OF TREPONEMES
DARK GROUND MICROSCOPY: Treponema pallidum
appears as a slender, spiral organism showing
rotational as well flexion and extension movements
109

110. SILVER IMPREGNATION METHOD
 Treponemes in tissues can be demonstrated by silver
impregnation method
110

111. Silver staining for Spirochaetes
111

112. Laboratory Tests
 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
 ELISA.
 Histopathology.
112

113. 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

114. 114