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Bacterial infections
Bacterial infections
Bacterial infections
Bacterial infections
Bacterial infections
Bacterial infections
Bacterial infections
Bacterial infections
Bacterial infections
Bacterial infections
Bacterial infections
Bacterial infections
Bacterial infections
Bacterial infections
Bacterial infections
Bacterial infections
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Bacterial infections

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bacteraial infections

bacteraial infections

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  • 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

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