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BACTERIAL INFECTIONS. Dr Shruti Nayak Dept. of Oral Pathology. Bacteria. They are prokaryotic microorganisms which can be spheroidal (coccus), rod / cylindrical (bacillus) and spirillar (spirochetes) They are the causative agents of many human diseases. Bacterial species.
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BACTERIAL INFECTIONS Dr Shruti Nayak Dept. of Oral Pathology
Bacteria • They are prokaryotic microorganisms which can be spheroidal (coccus), rod / cylindrical (bacillus) and spirillar (spirochetes) • They are the causative agents of many human diseases
Some of the important specific bacterial infections • TUBERCULOSIS • SYPHILIS • ACTINOMYCOSIS • SCARLET FEVER • NOMA • LEPROSY • DYPHTHERIA • CAT – SCRATCH DISEASE • PYOGENIC GRANULOMA
Tuberculosis is a chronic systemic infectious disease of worldwide prevalence. • It is a granulomatous infection and is caused by Mycobacterium tuberculosisor rarely by Mycobacterium bovis • Incidence of tuberculosis has declined greatly • In patients with AIDS, M. aviumintercellulareis a common cause of opportunistic infections
Pathogenesis • Caused by mycobacterium tuberculosis which is aerobic, slender, non-motile, non-spore forming, rod shaped, acid fast organism • Mode of spread: droplet infection • Since TB spread through droplet infection, optimal conditions for transmission include: • Overcrowding • Poor personal hygiene • Poor public hygiene
Contributing factors • Social issues: poverty, overcrowding • Political issues:war time, resettlement, immigration • Health issues: malnutrition, drug abuse, HIV infection, immunosuppression, • Economic issues: drug cost, health care housing, case identification and management • Microbial: drug resistance
Patients with the active disease expel the bacilli into the air by: • Coughing/Sneezing/Shouting • Any other way that expels bacilli into the air • Once inhaled by a tuberculin free person, the bacilli multiply in 4-6 weeks and spreads throughout the body. The bacilli implant in areas of high partial pressure of oxygen: • Lung • Renal cortex
This is known as the Primary Tuberculosis. The lesion will heal and a scar will appear in the infected loci. • The bacteria at this time goes into a dormant state • When a person's immune system is depressed, a secondary reactivation occurs and is called Secondary Tuberculosis. • Diffuse disseminated infection through vascular channels may occur and has been termed “Miliary Tuberculosis”.
Airborne (droplet) infections Tissue hypersensitivity to the bacilli Transient inflammatory reaction in lung (PMNL’s & macrophages) Macrophages phagocytose the organism Bacilli start to multiply within the macrophage Formation of epitheloid cells Epitheloid cells fuse together and form Langhan's giant cells
Caseation necrosis begins in the center of the infected tissue Lymphocytes and fibroblasts accumulate in the periphery Leads to formation of an avascular granuloma (Tubercle) Most of the lesions heal by fibrosis and calcification Micro-organisms may remain dormant for a long time Reinfection as a result of reactivation whenever the patient's body resistance is suppressed Called Secondary Tuberculosis
Clinical Features • Commonly occurs in adult males • Primary TB is usually asymptomatic • Secondary TB shows features such as • General • Fever, Weight loss, Anorexia, Night sweats, Weakness, “Consumption” • Organ specific • Lungs: Pneumonia (cough, sputum +/- blood) • Lymph nodes : Swollen lymph nodes (scrofula) • Genitourinary: Sterile pyuria • Bone: tuberculous osteomyelitis, fracture • Brain: Headache, Meningitis • skin: Lupus vulgaris
Oral Manifestations • TB of Oral cavity is rare. • Tuberculous lesions of the oral cavity are mostly secondary to the pulmonary infections • Primary oral tuberculosis may occur in some cases
Intact oral mucosa does not permit tuberculous bacilli to enter into the tissue. • Pre-existing oral lesions may facilitate the entry of these organisms into various oral structures (oral ulcers, periodontitis, dental abscess, cyst, granuloma & leukoplakia ) • Organisms can also reach through hematogenous route to sub mucosa, subsequently proliferate & ulcerate the mucosa.
Dentist may get infected by contact with infected persons • The important tuberculous lesions of the oral cavity are • Tuberculous ulcers • Tuberculous gingivitis • Tuberculous osteomyelitis • Tuberculosis of the salivary glands • May also produce nodules, vesicles, fissures, plaques, granulomas or verrucal-papillary lesions
Tubercular ulcers • Single or multiple ulcers which are irregular , superficial or deep, painful & tend to increase slowly in size. • Have a granulating floor with minimum induration and surrounding mucosa is inflamed and edematous • May occur in any intraoral site, however tongue is the most common site. (Palate, buccal mucosa, gingiva, lips, alveolar ridge and vestibules may also be affected).
Tubercular granuloma • Seen as soft, non-tender swelling • May occur in any intraoral site, palate is the most common site. • May develop in the periapical region of a grossly decayed tooth due to the entry of organism through the pulp canal- Tubercular periapical granuloma / tuberculoma • Tubercular Gingivitis Small granulating ulcers or erosive lesions with concomitant gingival hyperplasia
Tuberculous osteomyelitis • Develop due to entry of organisms through decayed tooth or due to hematogenous spread. • Pain, swelling, sinus/fistula formation, trismus, paresthesia. • Tuberculosis of salivary gland • Generalized glandular swelling or abscess formation along with pain, facial palsy & fistula formation
Scrofula • Enlarged oropharyngeal lymphoid tissue with involvement of cervical lymph nodes. Caseous necrosis &numerous draining fistula through overlying skin • Lupus vulgaris – Tuberculous involvement of skin
Microscopic presentation is in the form of granulomas, which are circumscribed lesions. • granulomas have a central area of caseous necrosis surrounded by multinucleated giant cells and epithelioid cells. • Rimming -Epitheloid cells are macrophages. • The nuclei of multinucleated giant cells are seen at the periphery, having a horse shoe shaped arrangement and these cells are called Langhans’ giant cells.
This is surrounded by a zone of lymphocytic infiltration and fibrosis. • Tubercular organisms may be demonstrated in the tissue sections by Ziehl – Neelsen or other acid fast stains.
Investigations • Staining of the smear prepared from sputum by Ziehl-Neelsen stain • Chest radiograph • Bacterial culture in Lowenstein-Jensen media (materials used for culture may be sputum, laryngeal swab, gastric lavage, urine, cerebrospinal fluid and pus, etc.) • Animal inoculation • Histopathology • Tuberculin test / Mantoux test • Enzyme-linked immunosorbent assay (ELiSA) test • PCR (polymerase chain reaction)
Treatment • By antitubercular drugs in different regimens
Historical Perspective • It was first described in the 1500’s • Also called as LUES • Was known as “The Great Imitator” because so many of the signs and symptoms are indistinguishable from those of other diseases
Syphilis is a sexually transmitted disease (STD)caused by a microscopic bacterium called the Treponemapallidum, which enters the blood stream and infects the entire body. • Syphilis has an incubation period of 1-13 weeks before any signs or symptoms. • The disease is generally classified into two: • Acquired syphilis • Congenital syphilis
4 Stages of Syphilis Acquired syphilis • Primary Stage • Secondary Stage • Latent Stage • Tertiary Stage
Acquired Syphilis • Is acquired from an infected person • It can be either through • Sexual contact with an infected partner • Careless handling of the infected patients by the health professionals • Drug abusers • Manifests in four stages: • Primary syphilis • Secondary syphilis • Latent syphilis • Tertiary (late) syphilis
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)
Characteristic primary lesion of syphilis is called “Chancre” • It is a solitary, painless, indurated, nontender, nonhemorrhagic, ulcerated or eroded lesion. • Chancre starts as a dull red macule or papule, which later on becomes eroded or ulcerated and produces Regional lymphadenopathy • Resolves within 3 - 8 weeks
Primary Syphilis: Oral manifestations • Chancre occurs on the lips, tongue, palate, gingiva, uvula and tonsils • May be painful due to secondary infection and are highly contagious in nature • Chancres are ulcerated, indurated lesions covered by a grayish white membrane • Often mistaken for an early carcinoma
Tongue lesions- seen on the lateral surface of the anterior two-third area or on the dorsal surface and often there is enlargement of the folate papilla. • Tonsils show edema, redness and surface erosions or ulcerations. • Lymph nodes are enlarged bilaterally, these are painless and rubbery in consistency. • Heals by scarring within 3-6 weeks time
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
Skin lesions may also occur in the form of nodular, flat-papillary (condylomalata) or pustular lesions. • Circinate (coin-like) lesions on the face are characteristic of secondary syphilis. • Areas of hyperpigmentations may be seen on the palms and soles.
Constitutional symptoms with secondary syphilis include-headache, anorexia, fever, joint and muscle pain, laryngitis and pharyngitis, etc. • Generalized lymphadenopathy is common and the nodes are painless, discrete and not fixed to the surrounding tissues. • With or without treatment secondary lesions usually heal within 2-4 weeks time • At times in immunocompromised patients , it become wide spread & is referred to as ‘ Leus Maligna’
Secondary Syphilis: Oral manifestations • The secondary lesions are mucocutaneous in nature and they usually occur 6 to 8 weeks after the primary infection. • The oral lesions in this stage are called “mucous patches”, and these are commonly seen over the tongue, gingiva, tonsils, larynx, pharynx and cheek, etc. • These patches are characterized by multiple, flat, irregular or circular, slightly raised, painless, round erosions.