This seminar consisits of description of various bacterial diseases along with their oral manifestations,diagnosis and treatment.an addition of suitable case reports for better understanding and associated disorders

1. ORAL MANIFESTATIONS OF BACTERIAL DISEASES
Karishma
III MDS

2. CONTENTS
• INTRODUCTION
• BACTERIAL INFECTIONS
• IMPETIGO
• ERYSIPELAS
• STREPTOCOCCAL TONSILITIS
• SCARLET FEVER
• SYPHILIS
• TUBERCULOSIS
• LEPROSY
• CAT SCRATCH DISEASE
• DIPTHERIA
• ACTINOMYCOSIS
• NOMA
• CONCLUSION
• REFERENCES

3. Introduction
3
• Oral cavity presents as ideal environment for growth and maintenance of microorganism.
• Certain microorganisms produce the disease, some of these lesions are specific to the oral
cavity and some are not.
• Pathogenic microorganisms evoke anatomic and functional damage to the host by
– Directly by production of toxins.
– Indirectly by sensitizing the host to microbial products that subsequently causes
immunologic reactions of the host (AKPATA ES 1974)

4. Sources of infection
a)Endogenous sources-Eg: Staphylococcus aureus in nostrils, staphylococcus
epidermidis in skin.
b)Exogenous sources- Eg: cornyebacterium diptheriae
Types of carriers
a) Convalescent
b)Intermittent
c)Chronic
d)contact
Primary pathogens cause disease as a result of their
presence or activity within the normal, healthy host, and
their intrinsic virulence.
Opportunistic pathogens can cause an infectious disease in
a host with depressed resistance.

5. • Following factors determine the ability of an
organism to produce disease.
– Appropriate portal of entry
– Innoculum must be sufficient for the organism to survive in
the host environment.
– Organism must be capable of obtaining or creating the
proper environment for their survival within the host.
– Organism must be capable of multiplying within the host’s
tissues either by increasing locally or spreading throughout
the body.
Bowteb,hamillton survival of oral acteria (rev oral biomed 1998)

6. Cardinal signs of acute infection
- Fever, Anorexia ,Pain, Dysfunctions and Convulsions in children.
- Shock, Haemorrhage, Intravascular coagulation and Organ failure in adults in
severe cases.
-Less common features are erythematous rash, arthritis, pericarditis,
encephalitis, peripheral neuropathy, hemolytic anemia and toxin mediated
nephritis.
Chronic infection - loss of weight, muscle wasting, stunted growth, anaemia,
tissue destruction are seen.
EFFECTS OF INFECTIONS

7. CAUSES OF BACTERIAL RESISTANCE
A) Within the host:
-Inducing cellular and metabolic changes at target areas.
-Decreasing cellular uptake of a drug
-Reducing the attraction for a drug at receptor centres
B) Within bacterial population
-Natural resistance to certain drugs
-Resistant mutants may arise spontaneously and proliferate
-Transfer of resistance thro plasmids

8. • Impetigo refers to a very localized bacterial infection of the skin..
• It causes red sores that can break open, ooze fluid, and develop a yellow-brown crust.
• These sores can occur anywhere on the body but most often appear around the mouth
and nose.
• Either by st.pyogenous /st.aureus
• Pervious cuts or insects bites.
• Causative Agent:
– Two Types:
• Bullous caused by staphylococci
• Non-bullous (epidemic) caused by streptococci
IMPETIGO

9. ETIOLOGY AND PREVELENCE
• Insect bites,
• children with below 4 years (84%) and in those aged 5–14 years
(54%).
• the incidence of insect bite only varied between 3 and 5% for males
and between 5 and 9 %for females. (Alex J Elliot 2006)
Non-Bullous:
 Thick, adherent-yellowish-
brown crusted lesions
(coalesce to form large
lesion).
 Cornflakes glued to surface
 Found in face and
extremities.
Bullous:
 Flaccid large bullae (anywhere),
rupture in 2-3 days to form discrete
round lesion
 Clear - turbid
 Intraoral lesions of this disease is
rare, unless there is secondary
infection from the skin lesion

10.  NON-BULLOUS:
Minimal type:
• Water soaks to remove crust- Mupirocin ointment (Bactroban)/retapamulin
for few small lesions in absence of lymphadenopathy.
• Apply to lesions tid for 5 d; clean lesions prior to application.
• If no healing, systemic antibiotics.
• Cephalexin
– 25-50 mg/kg/divided dose qid
• Erythromycin
– 30-50 mg/kg/divided qid for 7 d
TREATMENT
BULLOUS:
• Topical - insufficient
• Systemmic A/B – 1 week
• Cephlexin,doxy,amox-clav

11. ERYSIPELAS
 It is a superficial skin infection most commonly associated with
beta-heomolytic streptococi.
 It is rapidly spreads through the lymphatic channels.
 Can be confused with facial cellulitis from dental infection.
Clinical Features:
 Seen in young and elderly patient those who are diabetic.
 Facial erysipelas – winters and spring
 Lower extremities - summer
 Butterfly-shaped lesions that may resemble lupus erythematous.
 Affected skin surface resembles orange peel(peau d’orange)

12. Diagnostic cultures are usually not beneficial
Treatment: Penicillin, Erythromysin, cephalosporins, fluoroquinilones.
• On initiation of therapy, the area of skin involvement often enlarges,
probably secondary to the release of toxins from the dying
streptococci. A rapid resolution is noted within 48 hours.

13. SCARLET FEVER (SCARLATINA)
• Highly contagious systemic infection
• Predominantly seen in children
• Group A,β -hemolytic streptococci.
• Begins as tonsillitis with pharyngitis – erythrogenic toxins
• Incubation period : 1-7 days

14. Clinical features
• Common in children
• Entry – pharynx
• Pharyngitis and tonsillitis
• Head ache, fever, chills
• Enlargement and tenderness
of regional lymph nodes
• 2/3 rd day : diffuse bright
scarlet skin rash appear

15. • Begins first on the upper trunk,
spreading to involve extremities
• Spares palms and soles
• Small papules of normal color
appear through the rash ”sandpaper
feel to the skin “
“Sun burn with goose pimples”
• Skin folds – “pastia lines”
• Face: erythematous cheek and
circum oral pallor
• Subside- 6-7 days

16. 16
BEGINS WITH
¤ Pharyngitis
¤ Tonsillitis
¤ Headache
¤ Chills & fever
¤ Vomiting
¤ Cervical
lymphadenopathy
2-3 DAYS
¤ Scarlatiniform
exanthem –diffuse ,bright
red skin rash
blanches on pressure
¤ Petechiae –
sand paper, goose pimple
¤ Pasta lines
END OF THE WEEK:
Desquamation starting
from the face and
continuing down the
trunk and limbs

17. Oral manifestation
Stomatitis scarlatina
Palate
 congested ,petechiae
 Fiery red
Fiery red, congested palatal
mucosa,hyperemic, edematous
tonsils covered with gray – white
exudate
Flushed cheeks
Circumoral pallor

18. White strawberry
tongue
Loss of coating
RED STRAWBERRY
TONGUE/
RASPBERRY TONGUE
Severe cases:
Ulceration of buccal mucosa and palate
because of secondary infection

19. Complications:
Due to bacterial dissemination / hyper sensitivity reaction,
Peritonsillar abscess ,Rhinitis and sinusitis , Mastoiditis ,Meningitis
Diagnosis
 Routine blood culture
 Rapid antigen detection test
 Throat culture
Treatment
 Penicillins/amoxicillin
 Cephalosporins, macrolides
 ibuprofen

20. TONSILLITIS & PHARYNGITIS
CLINICAL FEATURES
• Mild to intense
• Sore throat, fever, dysphagia,
cervical lymphadenopathy Redness of
Orophry &tonsils
Palatal petechiae
CAUSE: Group A,Beta hemolytic streptococci,
enteroviruses, influenza, Epstein-barr virus.
• Spread – infectious nasal or oral secretions

21. CLINICAL FEATURES
• Systemic symptoms –headache, malaise, anorexia, abdominal pain, vomiting(in younger children)
• Asso. With viral infection --- rhinitis, laryngitis, bronchitis
DIAGNOSIS
 Clinical Features
 Throat culture, Rapid antigen detection
• Conjunctivitis, cough, hoarseness,
discrete ulcerative lesions - viral cause
TREATMENT
• Penicillin G
• Cephalosporins(e.g :Cephalexin,Cefadroxil)
• Macrolides(e.g :Clarithromycin,azithromycin)

22. • Acute life threatening infectious
• Corynebacterium diptheriae (termed Klebs Loffler bacillus)
• Produces lethal exotoxin that causes tissue necrosis – peripheral
spread
• Local Inflammation and grayish adherent pseudo membrane
• Children
• Humans are sole reservoir
• Acquired through : contact with an infected person or carrier
DIPHTHERIA

23. Toxemia
Bacteria multiplies
liberate toxin
Initial edema and hyperemia
Epithelial necrosis and a/c
inflammation
Pathogenesis
• Air born mode of transmission
• Localize in the mucous membrane of respiratory tract
• Invade open skin lesions
Systemically
• Myocarditis
• Neuritis
• Focal necrosis in
various organs
Locally
• Coagulation of fibrin
&purulent exudates
• Pseudo membrane
• Local inflammation
• Vascular congestion

24. 24
Nasal
Diphtheria
Tonsillar/
Pharyngeal
Diphtheria
Cutaneous
Diphtheria
Laryngeal
Diphtheria
• Characterized by nasal discharge
Serous
Sero-
sanguinous
Mucopurulent

25. Clinical features
• Incubation period :1-5 days
• Initial systemic symptoms :-
– Low grade fever
– Anorexia
– Sore throat
– Vomiting
• Predominantly affects mucosal surface

26. Pseudo membrane
Oro pharyngeal exudates begin on one/both
tonsils
Patchy,yellow-white , thin film
Thickens to form an adherent grey covering
Superficial epithelium ( integral part )
Attempt to remove result in bleeding
Dead cells
Leukocytes
Erythrocytes
Bacterium

27. Severity of infection correlate with spread of
the membrane
Larynx or trachea :
 Hoarseness in voice
 Respiratory stridor& dyspnoea
 Severe respiratory obstruction and death
Cutaneous manifestation
 Deep punched out ulcer with leathery
discharge

28. Oral manifestations
-Grayish green thick fibrinous gelatinous
appearing exudates with overlying necrotic
ulcerated areas of mucosa
-Asymmetric
-Extends to involve tonsils ,soft palate, tongue
-Advancing border is reddened
-Bleeding occurs on scrapping
 Severity – spread of diphtheritic membrane
 Cervical lymphadenopathy – Bull neck
 Toxin related paralysis
 Soft palate paralysis – nasal regurgitatn during swallowing

29. Complications
• Myocarditis
• Polyneuritis
• Interstitial nephritis
• Airway obstruction
• a/c circulatory failure
• Pneumonia
• Otitis media
Diagnosis
Clinical features
Culture of organism
PCR
Prevention
Prophylactic active
immunization with toxoid
Treatment
Antibiotics
Antitoxins

30. • Vaccinations for diphtheria are part of the routine NHS childhood vaccination
schedule.
• In total, children should receive five doses of the diphtheria vaccination.
• It's usually combined with other vaccines.
• DPT vaccine
• Currently, the inoculation has been combined into the Tdap vaccine that includes
tetanus, diphtheria, and pertussis.

31. •Acid fast bacilli
• Mycobacterium
tuberculosis
All ages
Males >
females
•Droplet
Infection
•Direct contact
Months to years
TUBERCULOSIS
 Chronic infection caused by Mycobacterium tuberculosis.
 Non-tuberculous mycobacterial disease can occur from a variety of
organisms(many cases arise from the consumption of milk infected with
Mycobacterium bovis)

32. Primary
 Prev.unexposed
 Always involves lungs
 Airborne
 From active disease
patient
 Only local
fibrocalcific nodule
 Dormant for years
Secondary
 Reactivation
 Compromised host
defense
 Diffuse dissemination
 Multiple small foci
 Miliary TB
 Only 5-10% of patients with TB progress from infection to
active disease

33.  Primary TB is asymptomatic, occasionally fever and pleural effusion may occur.
 Secondary TB lesions are located at the apex of lung but may spread to many
different sites by expectorated infected material or through the lymphatic or
vascular channels.
 Typically, patients have a low-grade fever, malaise, anorexia, weight loss, and night
sweats. With pulmonary progression, a productive cough develops, often
with hemoptysis or chest pain.
 Wasting syndrome
CLINICAL FEATURES

34.  Extrapulmonary TB exhibits with extrapulmonary lesions. Any
organ system may be involved, including the lymphatic system,
skin, skeletal system, CNS, kidneys, and gastrointestinal tract.
 Involvement of the skin may develop with ulcerated papulary
nodules and has been called lupus vulgaris.
 The most common extrapulmonary sites in the head and neck are
the cervical lymph nodes followed by the larynx and middle ear

35. SCROFULA
• Nontuberculous mycobacterial infections from contaminated milk
• Infection of submaxillary /cervical lymph node
• Progress –abscess /granulomatous lesion
• Obvious clinically
• Tender
• Inflammation of overlying skin
• Actual abscess perforate and discharge pus
POTT’S DISEASE
• Tuberculous spondylitis
• Involvement of spine (osteomyelitis+arthritis)

36.  Oral lesions of TB are uncommon.
 The most common presentations for oral involvement are Chronic tongue
ulcerations are seen most frequently and followed closely in prevalence by
mandibular swellings associated with intrabony involvement.
 Other affected sites in order of decreasing frequency include the gingiva, lips,
buccal mucosa, soft palate, and hard palate.
Primary oral TB without
pulmonary involvement is
rare and is more common
in children and adolescents.
ORAL MANIFESTATIONS

37. Foci of caseous necrosis
Surrounded epithelioid
cells
Lymphocytes
Occasional giant cells
Histological features
DIFFERENTIAL
DIAGNOSIS
• Squamous cell
carcinoma
• Sarcoidosis
• Syphilis
• Aphthous ulcer
• Deep mycotic infections
• Traumatic ulcer
• Wegner’s
granulomatosis
• Tularemia
• Foreign body reaction

38. Diagnosis
• Acid fast bacilli in sputum smear – gold
standard
 Ziehl-Neilson staining
 Kinyoun’s cold staining
 Flourscence microscopy of auramine-
rhodone stain
• X ray
• Tuberculin test
• PCR

39. • Multiple drug therapy
 Isoniazid+rifampin+Pyrazinamide+ethambutol : 8 week
 Isoniazid+rifampin: 18 weeks
Prevention
BCG (Bacille Calmette-Guerin)
Treatment
A different protocol termed chemoprophylaxis is used for patients who have a positive skin
test but no signs or symptoms of active disease. Although this situation does not mandate
therapy, several investigators have demonstrated the value of therapy, especially in young
individuals.

40. DOTS (directly observed treatment, short-course)
five main components:
 Government commitment
 Case detection by sputum smear microscopy.
 Standardized treatment regimen directly of six to eight months observed by a
healthcare worker or community health worker for at least the first 2 months.
 A regular, uninterrupted drug supply.
 A standardized recording and reporting system that allows assessment of
treatment results.

41.  Evaluation of the patient
• Constant risk of contacting the disease while treating
• Evaluated by the physician
 Delay elective dental treatment : culture is positive
• Use rubber dam
• Minimum use of ultrasonic scaler and high speed hand
piece
• Operating air should be vented outside
Dental considerations

42. Surendran Thavagnanam, Louise M McLoughlin, Chris Hill, and Paul T Jackson
Atypical Mycobacterial Infections in Children: The Case for Early Diagnosis
Our 3-year old patient presented with a firm inflamed swelling in the right submandibular area. Initial medical
management with intravenous antibiotics was ineffective. Fine needle aspiration of the lesion revealed acid-fast bacilli on
Ziehl-Nielsen staining. Subsequent biopsy demonstrated a granulomatous reaction in keeping with a Mycobacterial
infection.
Specific questioning revealed no family history of tuberculosis, abscesses or infections; there were no family pets, no
exposure to birds and no unpasteurised milk consumption. An initial chest x-ray was normal and Mantoux testing was
negative. Conventional anti-tuberculous therapy (Isoniazid, Rifampicin, and Pyrazinamide) was commenced. Definitive
Culture at 6 weeks isolated Mycobacterium avium intracellulare. The prescription was altered to include Clarithromycin.
This boy remained on antimicrobial therapy for 9 months. When the therapy was discontinued the lesion appeared to be
quiescent. However, following a minor episode of local trauma 6 months later, the lesion became swollen, inflamed and
started to discharge. The original antibiotic therapy regimen was restarted. Subsequent referral was made to a supra-
regional Paediatric Infectious Diseases unit because of failed medical management. Full surgical excision by a paediatric
plastic surgeon was recommended as offering the best chance of complete recovery.

43. Seven month old Saudi boy presented with fever, multiple neck and axillary swellings with two weeks of
fatigability. Two weeks prior to presentation, he had intermittent fever associated with sweating and loss of
appetite but no weight loss. There was no history of raw milk ingestion, recent travel, animal contact or blood
transfusion. He was a product of an uncomplicated spontaneous vaginal delivery, and all of his vaccinations
were up to date.
There were multiple neck swellings with enlarged, matted, nontender submandibular and anterior cervical
lymph nodes with no overlying skin change. In addition, the patient had a similar enlarged axillary lymph node
that measured seven centimeters in diameter.
Chest X–ray showed bilateral hilar lymphadenopathy. Histopathological report of lymph node biopsy showed
acute granulomatous infiltrations with AFB. Culture after six weeks was positive for mycobacterium
tuberculosis. An antibiotic sensitivity test was done and the patient was treated with isoniazid, rifampicin,
pyrazinamide and ethambutol.
Atypical mycobacterial infection in pediatric age group: Case report and
literature review. Albar Rawia F1, Selati Saife A2, Alghamdi Abdullah A2, Salahi Ahmed S2, Ahmed Mohammed Alfaidi2*
AFB: Acid Fast Bacilli

44. Two months later, the patient was readmitted with a febrile seizure. Lumbar
puncture was done and the cerebrospinal fluid culture was negative. A second
excisional biopsy was taken and revealed granulomas with AFB. The patient was
discharged on the same medications as before. Three weeks later, histopathology
report demonstrated granulomatous infiltration formed from sheets of histiocytes
filled with AFB, which was consistent with MAC infection.
The patient was kept on rifampicin and ethambutol as the earlier regimen, with
the addition of clarithromycin and streptomycin. One month later, the patient
was readmitted with a relapse and the culture of lymph node biopsy grew MTB
and MAC. The patient was transferred for further workup and treatment of
combined MTB and MAC infection. Two months later, the patient was diagnosed
with IL-12 deficiency.
AFB: Acid Fast Bacilli; CD: Cluster of Differentiation; MAI: Mycobacterium avium
intracellulare; WBC: White Bloodcells; IL: Interleukin; Ig: Immunoglobulin

45. Phagocytosis by macrophages occurs, triggering a complex immune response that leads to the activation of
other macrophages and the release of cytokines such as, IFN-G, IL-12 and tumor necrosis factor-alpha. With
intact immunity, this response results in intracellular elimination of the organism. However, patients with
compromised immunity are unable to achieve this, resulting in further multiplication of the organism and
subsequent dissemination.
In conclusion, in an infant or a child who is presenting with chronic multiple unilateral lymphadenitis with
weak reaction to tuberculin skin test and unresponsiveness to anti-mycobacterium antibiotics, the clinician
should suspect NTM. Patients with IL12 deficiency have a significant susceptibility to NTM.
AFB: Acid Fast Bacilli;MAI: Mycobacterium avium intracellulare; NTM: Non tuberculous mycobacterial infection.

46. LEPROSY (HANSEN’S DISEASE)
• Chronic Infectious Disease
• Cause : Mycobacterium leprae
• TYPES:
• Tuberculoid leprosy
• Lepromatous leprosy
• Paucibacillary leprosy
• Multibacillary leprosy
Pathogenesis:

47. CLINICAL FEATURES
GENERAL FEATURES
TUBERCULOID LEPROSY
1. Hypo pigmented patches
2. Total loss of cutaneous sensation
3.light touch to be affected first
4.Thickening of nerves
1. Small,well circumscribed
hypopigmented lesions.
2. Dermal & peripheral nerve
trunk involvement
3. Loss of sensation
4. Loss of sweating
LEPROMATOUS LEPROSY
1.Numerous ill defined hypopigmented macules
which become thick – distorted face
2. Dermal & peripheral nerve trunk involvement
3. Loss of sensation begins in extremities and
spreads to most of the body.
4. Loss of sweating

48. MULTIBACILLARY LEPROSY
Numerous ill-def
macules
Numerous
papules

49. Oral lesions
 Hard palate > soft palatate> labial max gingiva > tongue > lips > buccal max gingiva > labial
mand gingiva> buccal mucosa.
 Effected tissue – yellowish – red, sessile, firm, enlarging papules  ulceration & necrosis 
healing by secondary intention.
-Unique pattern of facial destruction
Facies leprosa
Atropry of atrophy of ant endonasal
ant nasal spine max alv ridge inflammatory changes
bone erosion
loss of teeth

50. IN CHILDREN (LEPROSY)
-Enamel hypoplasia
-Short tapering roots
- pulp infections
Internal resorption
(red discoloration)
- Facial paralysis  uni/bilateral
- Any branch of Trigeminal nerve
Pulpal necrosis

51. HISTOPATHOLOGIC FEATURES
Biopsy specimens of tuberculoid leprosy typically reveal granulomatous
inflammation with well-formed clusters of epithelioid histiocytes,
lymphocytes, and multinucleated giant cell.
A paucity of organisms exists; when present, they can be demonstrated
only when stained with acid-fast stains, such as the Fite method.
Lepromatous leprosy demonstrates no well-formed granulomas; the typical
finding is sheets of lymphocytes intermixed with vacuolated histiocytes
known as lepra cells .
Unlike tuberculoid leprosy, an abundance of organisms can be
demonstrated with acid-fast stains in the lepromatous variant .

52. TREATMENT & PROGNOSIS
-Paucibacillary leprosy : Rifampicin - Dapsone
Multibacilary Leprosy : Rifampicin +dapsone+clofazimine
-Reconstruction
-Physiotherapy
-Education of patient
DIAGNOSIS
• Clinical presentation
• Presence of Organism on smear or in tissue

53. • Caused by Bartonella henselae
• Rare in India
• Predominantly in children and young adult
• Arise after a traumatic break in the skin due to the scratch
or bite of house hold cat
CAT -SCRATCH DISEASE

54. Clinical features
• Papule, pustule or vesicle ,that develops at the site of
injury
• Regional lymphadenitis
- 1 or 2 weeks later
- Lymph nodes are painful and several
centimeter in diameter
- Overlying skin – inflamed
- last for 1-6 months
• Low grade fever, headache , chills ,nausea , malaise ,or
even abdominal pain
• Non pruritic macular or maculopapular rash, parotid
swelling ,conjunctivitis and grand mal seizures

55. • Oculoglandular syndrome of parinaud
• Localized grannuloma of eye & preauricular lymphadenopathy
• Soft and fluctuant – necrosis and suppuration
• Pus –sterile
• Occasionally –perforate skin and drain

56. Diagnosis
• Positive intradermal shin test
• Indirect flurescent antibody assay
• ELISA for detecting antibodies to Bartonella.henselae
Treatment
 Local heat with analgesics
 Self limiting
 Drainage of the abscess
 Antibiotics

57. Rapidly spreading mutilating gangrenous stomatitis that occurs due to
Fusobacterium necrophorun ,F,nucleatum and prevotella intermedia
usually in debilitated or nutritionally deficient person
• Children
• Predisposing factors
 Malnutrition
 Debilitating infections
 Blood dyscrasiasis
• Specific infection (vincent’s )
a/c necrotizing gingivostomatitis –secondary infection
Noma (cancrum oris )

58. Clinical features
• Begins as a small ulcer of the gingival mucosa
• Rapidly spreads and involves the surrounding
tissues by gangrenous necrosis
• overlying skin –inflamed& edematous –necrotic
• Skin sloughs out –jaws exposed
• Gangrene : blackening of the skin, necrosis of fat
• Extremely foul odor
• High temperature & secondary infections
• Toxemia & Pneumonia

59. General treatment aspect
.
 Conservative debridment of gross necrotic areas
 Adequate nutrition
 Hydration
 Electrolyte imbalances
 AB :- Penicillin and metronidazole
Noma Neo Natorum:- A gangrenous process affecting the nose, lips, mouth, anal
region, and occasionally the scrotum and eyelids, affects neonates
 Piperacillin, gentamicin, clindamycin
 Complication : pneumonia, diarrhea, septicemia ,Trismus.

60. Department of Health Guidance recommend a Start Smart then Focus approach for
all antibiotic prescriptions [W Lloyd]
 Start smart
 Do not start antibiotics in the absence of clinical evidence of bacterial infection
 If there is evidence/suspicion of bacterial infection, use local guidelines to initiate
prompt effective antibiotic treatment
 Document on drug chart and in medical notes: clinical indication, duration or
review date, route and dose
 Obtain cultures first
Then focus is:
 Review the clinical diagnosis and the continuing need for antibiotics by 48 hours
and make a clear plan of action

61. SYPHILLIS
Cause: Treponema pallidum
Primary mode of transmission
 Sexual
 Mother --- fetus
•Blood transfusion
• Pt highly infectious – first 2 stages
• Pregnant women  latent stage
• Maternal transmission  1st ,2 stages
Causes miscarriage, still birth,infant with congenital
malformations

62. Characterized by chancresite of inoculation
most common sites  85% external genitalia, 10% anus, 4% oral
Papular lesion - central ulceration
PRIMARY SYPHILIS
less than 2% -other locations
- most common oral cavity

lips, tongue, palate, gingiva,
tonsils
oral lesion - painless, clean –based ulceration
 Regional lymphedenopathy –uni /bilateral

63. •4-10 wks after infection
• SKIN: macules or papules, painless
Non pruritic, maculo - papular rash over entire body – notably on palms and soles
•ORAL LESIONS: Mucous patches, multiple,painless gray white plaques
overlying ulcerated surface. Tongue, gingiva, buccal mucosa
• Explosive, widespread form : LUES MAILGNA MUCOUS PATCHES
•Resembles viral papillomas called condyloma lata.
SECONDARY SYPHILIS/disseminated

64. TERTIARY SYPHILIS/ latent syphilis
• Do not appear for years
• CVS & CNS
• Non-infectious
• Scattered foci affect skin,mucosa,softtissue,bones,internal organs.
• GUMMA: result of hypersensitivity. Focal, granulomatous inflammatory Process with central
necrosis i/o gumma : tongue ,palate
• Palate: perforation by sloughing
• Herxheimer reaction.
Interstitial glossitis
Luetic glossitis

65. In 1958 ,Sir Jonathen Hutchinson described changes found in congenital syphillis
- Pathognomonic diagnostic features :
Hutchinson’s triad
1. Hutchinson’s teeth
2. Ocular interstitial keratitis
3. Eight nerve deafness
CONGENITAL SYPHILIS
Mulberry molar / Fournier’s molars
Moon’s molar

66.  Transplacental transmission
 If treatment begun in infected pregnant women before 4th
month of pregnancy – approximately 95% offspring free of
disease
66
• 1- 2 years of
life
Early
signs
• 1st to 2nd
decade of life
Late
signs

67. 67
• Hepatospleenomegaly, jaundice, biliary stasis,
lymphadenopathy, thrombocytopenia
• Osteochondritis and periostitis of lower limbs -
refuses to move involved extremity – Pseudo
Paralysis Of Parrot
EARLY SIGNS

68. Frontal Bossing
Saddle nose
Short maxilla
Relative prognathism
of mandible
Higoumenakis sign
CLUTTON’S JOINT
SABER SHIN
(ibia)

69. TREATMENT
• Customized therapeutic approach
• Penicillin (Benzathine Penicillin) – Primary,secondary
• Penicillin – IM – weekly for 3 weeks
• Allergic to penicillin - Doxycyclin
DIAGNOSIS
 Dark field microscopy
 Serological tests - Venereal Disease Research Laboratory (VDRL) and the rapid plasma
reagin (RPR).
 Fluorescent treponemal antibody absorption (FTA-ABS),
T. pallidum hemagglutination assay (TPHA),
T. pallidum particle agglutination assay (TPPA), and
Microhemagglutination assay for antibody to T. pallidum (MHA-TP)

70. A CASE OF CONGENITAL SYPHILIS PRESENTING WITH UNUSUAL SKIN ERUPTIONS
Alexander K. C. Leung, Kin Fon Leong, Joseph M. Lam, Case Reports in Pediatrics, vol. 2018
A 2-week-old male infant presented with asymptomatic, erythematous, desquamative lesions on the hands and feet
which were noted at birth. He was born to a 30-year-old mother who had poor prenatal care for social and economic
reasons. The mother did not have a venereal disease research laboratory (VDRL) test or rapid plasma reagin (RPR) test
during the pregnancy. Parents were sexually active and had multiple sexual partners. They were non consanguineous,
asymptomatic, and apparently healthy. The infant was born at 38 weeks gestation following a normal spontaneous
vaginal delivery.Birth weight was 2.8 kg, length 45.8 cm, and head circumference 33 cm. The infant was formula fed.
He had a poor appetite and was not thriving.

71. The infant was pale and mildly irritable. He had nasal congestion and snuffles. Multiple
linear scaly fissures were noted at the angles of his mouth. The fingernails and toenails
were thick and long. The abdomen was slightly distended. The liver was 2 cm below the
costal margin, and the spleen tip was palpable. There was no lymphadenopathy. The
ophthalmologic examination was normal. The rest of the examination was
unremarkable. In particular, there was no mucous membrane involvement or hair
abnormality.
A complete blood cell count showed normal values, Serologic tests for toxoplasmosis,
rubella, cytomegalovirus, Epstein–Barr virus, and herpes simplex virus were all negative.
The infant had a positive VDRL titer of 1 : 256 and a positive Treponema
pallidum hemagglutination (TPHA) test. Concurrently, the mother had a positive VDRL
titer of 1 : 16 and a positive TPHA test. No microorganism was identified in culture
specimens of blood, urine, or CSF. Radiographs of long bones were normal. Hearing test
was normal.
The patient was treated with intravenous aqueous crystalline penicillin
50,000 u/kg/dose every 8 hours for a total of 10 days. His skin eruption, except the thick
nails, resolved after 14 days of treatment

72. ACTINOMYCOSIS
– Filamentous, branching,G+ive bact.
– Normal site in healthy pt : tonsillar crypts, dental plaque &calculus, carious dentin, gingival sulci,
periodontal pocket
– Actinomyces israelii >A.viscous>A.naeslundii>A.odontontolyticus>A.meyeri>A.bovis
CLINICAL PATTERN:-
 Acute , rapidly progressing
 Chronic, slow progressing
 Cervicofacial region – 55%
 Abdominal & pelvic – 25%
 Pulmonary – 15%
 Superficial skin – 5%
TYPES:
1. Cervicofacial
2. Abdominal
3. Pulmonary

73.  The suppurative reaction of the infection may discharge large
yellowish flecks that represent colonies of the bacteria
called sulfur granules
 Infection :- enters through trauma, periodontal pocket, nonvital
tooth, extraction socket, infected tonsils
 Abscess - “wooden indurated”area of fibrosis - central,softer
area
 Extent upto surface – sinus tract
 Mandible , maxilla , tounge – common sites
 Salivary glands- submandibular , parotid

74. Infection of the soft tissues
Involve mandible and maxilla [actinomycotic osteomylitis]
Cranium, meninges ,brain
• Lesions of the bone localize near the apex of the tooth root can
simulate a peri apical granuloma
 Abdominal actinomycosis is an extremely serious form of the
disease and carries a high mortality rate. In addition to general ized
signs and symptoms involvement of other organs such as the liver
and spleen.
 Pulmonary actinomycosis produces similar findings of fever and
chills accompanied by a productive cough and pleural pain.

75. DIAGNOSIS :-
– Clinical findings
– Demonstration of organism in tissue section or
smear
TREATMENT :-
– Abscess drainage
– Excision of sinus tract
– Penicillin
Acute systemic febrile reaction – Jarisch – Herxheimer Reaction
– exacerbation of lesions, 15-20% of all patients – during
treatment – not an indication for discontinuation of drug

76. 76
• Disease of the nervous system characterized by intense activity of motor neurons
and resulting in severe muscle spasms
•Clostridium tetani-
anaerobic, gram positive
•Acts at the synapse of
the interneurons of the
inhibitory pathways and
motor neurons to
produce blockade of
spinal inhibition
• All ages
•10- 60 %
mortality rate
• Contaminated
wounds
•Contamination of
umbilical stump in
neonates
(developing
countries)
• Non
communicable
• 4-21 days (10 avg)
TETANUS

77. SIGNS AND SYMPTOMS
• Pain and stiffness in the muscles of jaws and neck
producing the common early sign – trismus or Lock jaw
and dysphagia due to massetric spasm
• Rigidity of facial muscles produces a so called sardonic
smile – Risus sardonicus

78. • When the paralysis extends to the abdominal, lumbar, hip and thigh muscles the
patient – Opisthotonus
• Laryngeal and respiratory muscle spasm can lead to airway obstruction and
asphyxia.
• Does not affect sensory nerves and cortical function – patient is always conscious,
in extreme pain and in fearful anticipation of the next seizure

79. Manifests 3-
12 days after
birth
∙ Difficulty in
feeding
∙ Associated
hunger
∙ Crying
Paralysis with
diminished
movement
with or with
opisthotonus
NEONATAL TETANUS

80. Neonatal tetanus in St. Mary’s Hospital Lacor: A case report
Ronald Okidi ,Vanusa Da Consolação Sambo ,Jacob Eyul
A 5‐day‐old male neonate was delivered by spontaneous vertex delivery and weighed 3.0 kg. He presented with a
3‐day history of high‐grade fever, refusal to breastfeed, excessive crying, and difficulty in breathing. He had
episodic provoked spasms. His mother, an 18‐year‐old, and was treated for malaria at 24 weeks of gestation.
However, she did not receive the routine TTCV vaccines during all her visits.
The baby was sick, on supplemental oxygen via nasal prongs,
the umbilical cord stump had a mild purulent discharge. The
abdomen was of normal fullness, with a tense abdominal muscle.
There was no bacterial growth on blood culture.
The neonate was admitted to the intensive care unit, and initiated on intravenous phenobarbital 10 mg/kg daily,
intravenous diazepam 2.5 mg 6‐hourly, intravenous metronidazole 15 mg/kg loading dose followed 7.5 mg/kg
bodyweight 12‐hourly and oxygen therapy. The umbilical stump was cleaned using hydrogen peroxide daily and
dressed. However, he had no administration of TTCV and tetanus immunoglobulin due to nonavailability and
eventually expired on day 7 of life.

81. TREATMENT
•Surgical wound care
Contaminated
wounds
•Penicillin G 1,00,000 U/Kg /day- 4-6 hours IV for
10-14 days
•Metronidazole 500mg every 8 hours IV
•Erythromycin and tetracyclin
Antimicrobial
drugs
•Diazepam – 0.1-0.2 /Kg 3-6 hours IV initially then
taper over 2-6 weeks
•Midazolam, Chlorpramazine, Baclofen,
Dantrolene , Magnesium sulphate
Muscle
relaxants

82. • Give soon to neutralize toxin before it binds to
muscle groups
• Single dose, IM 500 U- as high as 3000-6000U
Human tetanus
immunoglobulin
• It has 4-90 U/ ml of Tetanus immunoglobulin
Human
intravenous
immunoglobulin
• Equine and bovine tetanus antitoxin – 50,000 –
1, 00, 000 U - half IM half IVAlternative
• DPT vaccine
• Tetanus toxoid
Prevention
Current recommendations for treatment of tetanus during humanitarian emergencies WHO
Technical Note January 2010

83. GRANULOMA INGUINALE
• Chronic, infectious granulomatous disease
• Campylobacter granulomatis
(Donovania granulomatis)
• Mildly contagious
venereal disease
The lesions of the oral cavity are usually secondary to active
genital lesions. Lesions may occur in any oral location such as the lips,
buccal mucosa, or palate, or they may diffusely involve the mucosal surfaces

84. The varied clinical appearance of the lesions is the basis for their classification into one of
three types:
 Ulcerative,
 Exuberant,
 Cicatricial.
They are manifested as papules or nodules, which ulcerate to form clean, granular lesions
with rolled margins and which show a tendency for peripheral enlarge ment.
Satellite lesions often arise through lymphatic extension

85. Ulcerative
Painful ulcerated
Bleeding
Exuberant
Proliferative
granular masses
with intact
epithelial
covering
Inflamed
edematous
mucous
membrane
Cicatricial
Cicatrization
Fibrous scar
formation may
become
extensive
May limit mouth
opening

86. TREATMENT
 Tetracycline, chloramphenicol, streptomycin garamycin, and cotrimoxazole
are effective in the treatment of this disease.
 Complete healing usually occurs within two to three weeks
 Tetracycline – 500mg/day (tid) for 3 weeks

87. CONCLUSION
 There are wide variety of organisms present, each with a distinctive
property.
 This determines the ways in which they will react with their hosts
therefore contribute to the characteristics of the disease they cause.
 The normal flora play a very important role in protection against these
established pathogenic microbes.
 Identification of the microorganisms found during the different phases
of the disease process is technically challenging.
 Technologic advances in molecular microbiology have improved the
ability to detect specific bacteria and their products, which may serve
as markers of ongoing disease or predictors of future disease.

88. REFERENCES:
1. Neville Damm,Oral & Max facial pathology; 4th edition; 2016.
2. Rajendran R, Shafer's textbook of oral pathology; 7th edition; 2012.
3. R. Ananthanarayan . C. K. J.Paniker, Text book of Microbiology; 10th
edition; 2018.
4. Marsh P, Martin M, Oral microbiology; 6th edition; 2018.
5. Essentials of orl pathology – Purkait 3rd edition

89. THANK YOU