Bacterial infections and its oral manifestations

Bacteria are prokaryotic microorganisms that do not contain chlorophyll. They are unicellular and do not show true branching, except in higher bacteria like actinomycetales.

  • Bacteria of medical importance measure 0.2-1.5 μm in diameter and about 3-5 μm in length.
  • 1 micron (m) or micrometer (μm) = a millionth part of a meter or a thousandth of a millimeter.
  • 1 millimicron (mm) or nanometer (nm) = one thousandth of a micron or one millionth of a millimeter.
  • 1 Angstrom unit (Å) = one tenth of a nanometer.

Depending on shape, bacteria can be classified as:

  1. Cocci: Cocci (from kokkos meaning berry) are spherical, or nearly spherical.
  2. Bacilli: Bacilli (from baculus meaning rod) are relatively straight, rod shaped (cylindrical) cells.
    • In some of the bacilli, the length of the cells may be equal to width and known as coccobacilli.
  3. Vibrios: Vibrios are curved or comma-shaped rods and derive the name from their characteristic vibratory motility.
  4. Spirilla: Spirilla are rigid spiral or helical forms.
  5. Spirochetes: Spirochetes (from speira meaning coil and chaite meaning hair) are flexuous spiral forms.

The morphological study of bacteria requires the use of microscopes. The types of microscope are:

  • Light or optical microscope
  • Phase contrast microscope
  • Dark field/ Dark ground microscope
  • Electron microscope
  • Christian Gram, a Danish Physician in 1884 developed a staining technique to distinguish two types of bacteria.
  • Based on gram staining there are two types of bacteria:
  1. Gram positive bacteria.
  2. Gram negative bacteria.
  • Bacteria are first stained with crystal violet or gentian violet.
  • All bacterial cells will stain blue or purple colour with crystal violet solution. Then the bacterial cells are treated with iodine solution (Lugol’s iodine) solution and washed with alcohol (dc-staining solution).
  • Those bacteria which retain the blue or purple colour of crystal violet are called Gram positive bacteria.
  • Those bacteria which loose the colour of crystal violet after washing with dc-staining solution is called Gram Negative bacteria.
  • Gram negative bacteria are later stained with safranin or fuchsin for observation under microscope. Gram negative bacteria after safranin or fuchsin staining colour red or pink colour.
  • Gram staining differentiates bacteria by the chemical and physical properties of their cell walls by detecting the properties of peptidoglycan.
  • Gram staining method is useful in differentiating majority of bacterial species into two broad categories. 

  Charactristic

Gram positive

Gram negative

  Gram Reaction

Retain crystal violet dye and stain blue or purple

Accept safranin and stain pink or red

  Cell Wall Thickness

Thick (20-80 nm)

Thin (8-10 nm)

  Chemical Composition of Cell Wall

Peptidoglycan, Teichoic acid Lipotechoic acid

Lipopolysaccharide, Lipoproteins and Peptidoglycans

  Peptidoglycan Layer

Thick (Multilayered)

Thin (Single layered)

  Teichoic Acid in Cell Wall

Present

Absent

  Lipopolysaccharide Layer (Outer Layer)

Absent

Present

  Lipid Content

Absent or lower content of lipids than Gram Negative bacteria

Contains higher content of lipids than Gram positive bacteria (due to presence of outer membrane)

  Porin Proteins

Absent

Present

  Flagellar Structure

2 rings in basal body

4 rings in basal body

  Periplasmic Space

Absent

Present

  Mesosome

More prominent

Less prominent

  Ratio of RNA:DNA

8:1

Almost 1

  Toxins Produced

Primarily Exotoxins

Endotoxins and Exotoxins (Primarily Endotoxins)

  Resistance to Physical Disruption

High

Low

  Cell Wall Disruption by Lysozyme

High.

After digestion of peptidoglycan layer, Gram +ve bacteria become Protoplast

Low.

After digestion of peptidoglycan layer, Gram -ve bacteria become Spheroplast.

  Susceptibility to Penicillin and     Sulphonamide

High

Low

  Susceptibility to Streptomycin,     Chloramphenicol and Tetracycline

Low

High

  Inhibition by Basic Dyes

High

Low

  Susceptibility to ionic detergents

High

Low

  Resistance to Sodium Azide

High

Low

  Resistance to Drying

High

Low

  Isoelectric Range pH

2.5-4.0

4.5-5.5

  Nutritional Requirements

Relatively Complex

Relatively Simple

  Rendering

They can rendered Gram -ve by increasing acidity

They can rendered Gram +ve by increasing alkalinity

  Morphology

Usually cocci or spore forming rods (exception : Lactobacillus and Corynebacterium)

Usually non-spore forming rods (Exception : Neisseria)

  Examples

Staphylococcus

Streptococcus

Bacillus

Clostridium

Nocardia

Propionibacterium

Enterococcus

Corynebacterium

Listeria

Lactobacillus

Gardnerella

Escherichia

Salmonella

Klebsiella

Proteus

Helicobacter

Hemophilus

Vibrio

Shigella

Neisseria

Enterobacter

Pseudomonas

  • There are two types of organisms and tiny single-celled bacteria called aerobic and anaerobic bacteria.
  • Aerobics are able to use oxygen, whereas anaerobic bacteria can sustain itself without the presence of oxygen.
  • Aerobic bacteria can detoxify oxygen, whereas anaerobic bacteria cannot sufficiently break down food molecules as muchas aerobic bacteria.
  • Aerobic bacteria gets energy from food when compared to anaerobic, that can survive in places where there is less oxygen, such as human guts.
  • Some anaerobic bacteria also causes diseases in those areas of the human body where there is less oxygen supplied. Aerobic bacteria cannot grow without an ample supply of oxygen involved in a chemical reaction, whereas the anaerobic term does not imply this.
  • Culture media contains nutrients and physical growth parameters necessary for microbial growth.
  • All microorganisms cannot grow in a single culture medium and in fact many can’t grow in any known culture medium.
  • Organisms that cannot grow in artificial culture medium are known as obligate parasites.
  • Mycobacterium leprae, rickettsias, Chlamydias, and Treponema pallidum are obligate parasites.

On Consistency:

  1. Solid medium
    • Solid medium contains agar at a concentration of 1.5-2.0% or some other mostly inert solidifying agent. Solid medium has physical structure and allows bacteria to grow in physically informative or useful ways (e.g. as colonies or in streaks).
    • Solid medium is useful for isolating bacteriaor for determining the colony characteristics of the isolate.
  2. Semisolid media
  3. They are prepared with agar at concentrations of 0.5% or less. They have soft custard like consistency and are useful for the cultivation of micro-aerophilic bacteria or for determination of bacterial motility.

  4. Liquid (Broth) medium

These media contains specific amounts of nutrients but don’t have trace of gelling agents such as gelatin or agar. Broth medium serves various purposes such as propagation of large number of organisms, fermentation studies, and various other tests. e.g. sugar fermentation tests, MR-VR broth.

On Chemical Composition:

  1. Routine Laboratory Media
  2. Synthetic Media: These are chemically defined media prepared from pure chemical substances. It is used in research work.

Routine Laboratory Media classified into six types:

  1. Basal media.
  2. Enriched media.
  3. Selective media.
  4. Indicator media.
  5. Transport media.
  6. Storage media.

Basal media

Basal media are those that may be used for growth (culture) of bacteria that do not need enrichment of the media. Eg.

  • Nutrient broth, nutrient agar and peptone water.
  • Staphylococcus and Enterobacteriaceae grow in these media.

Enriched media

These media are prepared to meet the nutritional requirements of fastidious organisms. (e.g. Streptococcus pneumoniae, Neisseria gonorrhoea, Neisseria meningitis, Hemophilus influenzae) These organisms are more exacting in nutritional needs and extra supplements like blood, serum or egg has to be added to a basal medium. e.g. Blood agar, Chocolate agar, Bordet-Gengou agar, Loffler’s serum slope, Dorsett’s egg medium

Selective media

These media favour the growth of a particular bacterium by inhibiting the

growth of undesired bacteria and allowing growth of desirable bacteria. Eg: MacConkey agar, Lowenstein-Jensen media, tellurite media (Tellurite inhibits the growth of most of the throat organisms except diphtheria bacilli).

Antibiotic may be added to a medium for inhibition.

Indicator media

An indicator is included in the medium. A particular organism causes change in the indicator, e.g. blood, neutral red, tellurite. Examples: Blood agar and MacConkey agar are indicator media.

Transport media

These media are used when specimen cannot be cultured soon after collection. Eg: Cary-Blair medium, Amies medium, Stuart medium.

Storage media:

Media used for storing the bacteria for a long period of time. Examples: Egg saline medium, chalk cooked meat broth.

  • Scarlet Fever.
  • Diphtheria.
  • Tuberculosis.
  • Leprosy.
  • Actinomycosis.
  • Botryomycosis.
  • Tularemia.
  • Melioidosis.
  • Tetanus.
  • Syphilis.
  • Gonorrhea.
  • Granuloma Inguinale.
  • Rhinoscleroma.
  • Noma.
  • Cat-scratch Disease.
  • First described by Robert Koch in 1882.
  • It is a chronic infectious disease caused by a Mycobacterium tuberculosis
  • This complex consists of tuberculosis, which is the main causative agent of TB, as well as of M. bovis, M. africanum, and M. microti.
  • Mycobacterium tuberculosis is a gram positive, acid-fast, aerobic bacillus.

The factors favouring the spread of tuberculosis, both its pulmonary and extra-pulmonary forms, are:

  • HIV epidemic.
  • Higher life expectancy.
  • Poverty expansion.

Other predisposing factors include:

  • Prolonged immunosuppressive therapy.
  • Diabetes.
  • Alcoholism.
  • Drug addiction.
  • Lymphomas and other malignant tumors.
  • Fever.
  • Chills.
  • Night sweats.
  • Weight loss
  • Fatigue.
  • Hemoptysis may be observed in people with cavities in the lungs, but it is seldom the first sign of TB.
  • Oral lesions secondary to pulmonary changes can precede systemic symptoms.
  • Systemic symptoms rarely appear in the primary oral tuberculosis

Oral TB classification based on five different oral changes:

  • Ulcers.
  • Tuberculomas (granules that collapse forming ulcerations).
  • Tuberculous fissures.
  • Tubercle papillomas (overgrowths of the tuberculous fissure margins).
  • Cold abscesses.
  • Oral TB lesions may be either primary or secondary.
  • Tongue is most frequent site of oral lesions but cheeks, lips and palate also involved.
  • Tuberculous apical dental granulomata: looseness of teeth.
  1. Oral lesions on lip:
  • Begin as small “tubercles” or “pimples” that breakdown and form painful ulcers.
  • Additional small tubercles characteristically develop about the periphery of the ulcer and process is repeated.
  • Corners of the mouth is commonly involved.
  1. Oral lesions on cheek:

Tubercular ulcers of cheek have irregular, undermined borders.

  1. Oral lesions on tongue:
  • Develops along the lateral margins of the tongue which rest against rough, sharp, or broken teeth or at the site of other irritants.
  • Deep tubercular ulcers of the tongue are typical in appearance with a thick mucous material at the base.
  • Tongue lesions are characterized by severe unremitting and progressive pain that profoundly interferes with proper nutrition and rest.
  • Tubercular ulcers of the tongue may involve the tip, lateral margins, dorsum, the midline, and base of the tongue.
  • They are irregular, pale, and indolent with inverted margins and granulations on the floor with sloughing tissue.
  • Tuberculosis involvement of cervical lymphnode is called scrofula.
  • Tuberculous lymphadenitis (scrofula) was known as the “king’s evil” in Europe.
  • Diagnosis is usually by fine-needle aspiration, excisional biopsy.

Tuberculosis involvement of spine, usually in childhood is k/a pott’s disease.

  Variable

Primary oral TB

Secondary oral TB

  Occurrence

Very rare, found predominantly in children

More often found than the primary, especially

in the middle-aged and elderly

  General and local risk factors

Immunodeficiency (e.g. in diabetes, neoplasms, alcoholism, states after graft procedures, HIV

infection, prolonged steroid therapy), tobacco smoking, oral mucosa traumas, hyperkeratotic

disorders, poor oral hygiene, periodontitis

  Clinical manifestations

Ulcer – superficial and covered with granular

tissue or larger and deeper

Ulcer – with undermined, irregular edges, covered

with Trelat granules (they are numerous yellowish submucosal points)

  Soreness of the lesion

No

Yes

  Local lymph nodes

Enlarged, painful

Enlarged or not, usually not painful

  Duration

Tubercular ulcerations last for a long time showing no tendency to heal, and increase slowly in size

  Management

Anti-tubercular therapy (antibiotics), topically administered anti-inflammatory and protective agents, elimination of chronic traumatic factors

  • Tuberculous osteomyelitis is quite rare and constitutes <2 % of skeletal tuberculosis.
  • Bone involvement of the maxilla and mandible can produce tuberculous osteomyelitis by occult spread of the microorganism.
  • Most commonly involves young children.
  • Mandible is rarely involved due to the less amount of cancellous bone.
  • The chief routes of spread are from infected sputum, surrounding soft tissue and haematogenous route, wound following extraction of a tooth.
  • The angle and the ramus of mandible are commonly involved.
  • Destruction and erosion of the cortex occurs which is replaced by soft granulation tissue.
  • Caseation occurs resulting in softening, liquefaction and formation of a subperiosteal abscess which can either burst intraorally or extraorally.
  • Radiographically, TB lesions appears as a blurry radiolucency with erosion of cortex.
  • High-resolution CT may reveal occult abscesses, pathological cavities, and the extent of disease 
  • Based on carefully collected medical history.
  • In every oral ulcer lasting for more than 3 weeks, an incisional biopsy is required.
  • Histopathological assessment may reveal the presence of granulomatous inflammatory infiltration with Langhans giant cells and lymphocytes.
  • Foci of caseous necrosis of the tissue.
  • Microbiological culture of sputum and of the material taken from the surface of the oral lesion.
  • Ziehl-Nielsen staining of sputum swab for acid-fast bacilli can be positive.
  • Posterior-anterior (PA) and lateral view chest radiograph is mandatory.
  • Disseminated infiltrations, nodules, fibrotic scars, cavities in the lungs, hilar or mediastinal lymphadenopathy, pleural effusion are the findings suggestive of TB.
  • Mantoux tuberculin skin test, but its positive result does not always mean active TB.
  • TB blood tests or interferon-gamma release assays or IGRAs: Measure the ability of the Mycobacterium tuberculosis antigens to react with immune system. Two IGRAs that are approved by the U.S. Food and Drug Administration are:
  1. QuantiFERON®-TB Gold In-Tube test (QFT-GIT): Uses an ELISA format to detect whole blood production of interferon γ with great sensitivity (89%).
  2. T-SPOT.TB test: Measures T cells primed to Mycobacterium tuberculosis (MTB) antigens.
  • Nucleic acid amplification testing (NAAT): Is a molecular technique used to directly detect the genetic material of the infecting organism or virus. NAAT may speed the diagnosis in smear-negative cases and may be helpful to differentiate non-tuberculous mycobacteria. NAAT may utilize polymerase chain reaction (PCR) technique or transcription-mediated amplification (TMA) or other forms of nucleic acid amplification methods to detect mycobacterial nucleic acid. The two most common commercially available tests are amplified Mycobacterium tuberculosis direct test (AMTD, Gen-Probe) and amplicor (Roche Diagnostics). The AMTD test appears to perform better than other currently available commercial tests.
  • Bacille Calmette-Guerin (BCG) vaccination.
  • The treatment if initiated early results in complete resolution of the lesion. According to RNTCP the treatment advocated is of 6 months comprising of an intensive therapy of 2 months with Isoniazid, Rifampicin and Pyrazinamide and a maintenance therapy of 4 months with Rifampicin and Isoniazid.

Syphilis, actinomycosis, histoplasmosis, planoepithelial cancer, traumatic lesions, recurrent aphthous stomatitis (RAS), leukemia, pemphigoid, erosive form of lichen planus.

  • Also known as Scarlatina.
  • Scarlet fever is a bacterial infection caused by Streptococcus pyogenes, which is classified as Group A streptococcus (GAS; also known as Group A beta-haemolytic streptococcus).
  • The “A” refers to the presence of a surface antigen. 
  • Spread by coughing, sneezing or breathing out of bacteria during the subclinical and acute phases of the illness.
  • The incubation period is between two and four days.
  • Incidence of infection is highest in children aged four to eight years.
  • The strep bacteria make a toxin (poison) that causes a bright red, bumpy rash. The rash spreads over most of the body and is what gives scarlet fever its name.
  • Sore throat and fever (usually above 38.5C).
  • Bright red (“scarlet”) rash developing within a day or so.
  • Rash is due to the production of an erythrogenic toxin by the bacteria, which passes into the bloodstream via the infected throat.
  • The rash starts as small spots on the neck, upper chest, and spreads to the rest of the body. It blanches when pressed and has a “sandpaper” feel.
  • Rash that is prominent in the areas of skin folds is called ‘pastia lines’.
  • Rash subsides after 6 or 7 days followed by the desquamation of palms and soles.
  • The color of the rash varies from scarlet to dusky-red.
  1. Stomatitis scarlatinaThe mucosa of palate may appear congested and have petechiae scattered on soft palate.
  • Palate and throat is fiery red.
  • Tonsils and faucial pillars are swollen and covered by grayish exudates.
  1. Strawberry tongue: In early course of disease, tongue exhibits a white coating and the fungiform papillae are edematous and hyperemic, projecting above the surface as small red knobs.
  2. Rasp berry tongue: The coating of the tongue is soon lost; beginning at the tip and lateral margins, and this organ becomes deep red, glistening and smooth except for the swollen, hyperemic papillae. This phase is known as ‘rasp berry tongue’.
  • Made from samples obtained from biopsies, smears, wound aspirates, pharyngeal secretions, blood, or CSF.
  • Diagnoses are confirmed via culture and identification from blood agar or from serology with antigen detection.
  • PYR (Pyrrolidonyl Aminopeptidase) Test and susceptibility to bacitracin, antistreptolysin O and antihyaluronidaste titers, or anti-D Nase B will all prove positive for Strep. pyogenes.
  • Direct carbohydrate antigen.
  • Nucleic acid probe detection.
  • Phenoxymethyl penicillin or erythromycin for those allergic to penicillin.
  • The duration and frequency of the antibiotic regimen is a matter for debate. Most studies regard oral penicillin V given six-hourly for 10 days 
  • It is an acute, life-threatening, infectious, and communicable disease of the skin and mucous membrane.
  • Disease caused by Corynebacterium diphtheriae.
  • It is characterized by local inflammation and the formation of a grayish adherent pseudomembrane, which bleeds on removal.
  • Transmitted via respiratory droplets.
  • Diphtheriae in the respiratory tract are classified as:
  1. Diphtheria cases if the pseudomembrane is present
  2. Diphtheria carriers if the pseudomembrane is absent.
  • The clinical features are caused by a toxin produced by C. diphtheriae after it colonizes the upper respiratory tract.

Clinical features:

  • Fever
  • Malaise
  • Sore throat.
  • Cervical lymphadenopathy.
  • Soft tissue swelling of the neck.
  • Stridor .
  • Difficulty breathing.
  • Within a few days, a grayish white pseudomembrane develops over the tonsils, posterior pharyngealwall, and/or larynx.

Systemic absorption of the toxin can result in:

  • Myocarditis.
  • Acute Tubular Necrosis.
  • Polyneuropathy.
  • Diphtheritic membrane: It is a false membrane which is grayish-green, thick, and fibrinous, and is composed of dead cells, leukocytes and bacteria overlying necrotic, ulcerated areas of the mucosa tends to be adherent and leaves a bleeding surface if stripped away.
  • This membrane involves the tonsil, soft palate and tongue, lips, gingiva, buccal mucosa and site of erupting teeth.
  • Husky voice.
  • Submandibular and anterior cervical nodes are enlarged with soft tissue edema giving bull neck appearance.
  • Soft palate may become temporarily paralyzed, during the third to fifth weeks of the disease.
  • Pai agar.
  • Cystine-tellurite agar.
  • Chocolate agar.
  • Rogosa’s medium.

Special stains:

  • Albert’s stain.
  • Ponder’s stain.
  • Neisser’s stains to demonstrate metachromatic granules.
  • Based on clinical signs and symptoms.
  • Isolation of organisms beneath the membrane or a portion of the membrane itself can be submitted for culture.
  • Once the culture reveals  C. diphtheriae, one or both of the following tests are used to identify whether the strain is toxigenic:
  1. Elek’s test.
  2. Polymerase chain reaction.

What is treatment of diphtheria?

  • The CDC recommends either
  1. Metronidazole
  2. Erythromycin (orally or injection) for 14 days(40mg/kg per day with a maximum of 2 g/d)

Or

  1. Procaine penicillin G given intramuscularly for 14 days(300,000 U/d for patient weighing.>10kg and 600,000 U/d for those weighing for those weighing > 10kg).
  • Patients with allergies to penicillin G or erythromycin can use rifampin or clindamycin.
  • Disease may be prevented by prophylactic active immunization with diphtheria toxoid.
  • Also known as Lock-jaw.
  • Tetanus is a neurotoxin-mediated disease characterized by a progressive spastic paralysis of multiple muscle groups.
  • Clostridium tetaniis an anaerobic gram-positive bacillus.
  • Its natural habitat is soil and it is distributed worldwide.
  • It occurs when a wound is contaminated with  tetanispores; the anaerobic environment of the wound allows the spores to germinate and produce a toxin, tetanospasmin, which is transported to the central nervous system.
  • Tetanospasmin then binds irreversibly to neurons and prevents release of inhibitory neurotransmitters, thereby allowing unopposed motor and autonomic activity.

Mode of transmission:

Through a contaminated puncture wound,

Risk factors:

  • Dental procedures.
  • Surgery.
  • Intramuscular injections.
  • Intravenous drug use.
  • Burns.
  • Incubation period ranges from 3 days to 4 weeks.
  • Muscle rigidity and spasms are typical clinical hallmarks of generalized tetanus g.trismus (lockjaw) and opisthotonus (spasm of the muscles causing backward arching of the head, neck, and spine).
  • Ablett classification is mostly used, which ranges from mild to moderate trismus with no spasms to prolonged spasms with severe autonomic disturbance :
GradeClinical features
  IMild: mild to moderate trismus; general spasticity; no respiratory embarrassment [respiratory distress]; no spasms; little or no dysphagia
  IIModerate: moderate trismus; well-marked rigidity; mild to moderate but short spasms; moderate respiratory embarrassment with an increased respiratory rate greater than 30 [breaths/min]; mild dysphagia
  IIISevere: severe trismus; generalized spasticity; reflex prolonged spasms; increased respiratory rate greater than 40 [breaths/min]; apneic spells; severe dysphagia; tachycardia greater than 120 [beats/min]
  IVVery severe: grade III and violent autonomic disturbances involving the cardiovascular system; severe hypertension and tachycardia alternating with relative hypotension and bradycardia, either of which may be persistent

Generalized tetanus is characterized by:

  • Lock-jaw or trismus due to spasm of masseter,
  • Dysphagia,
  • asphyxia.
  • risus sardonicus.
  • opisthotonus.

Local tetanus manifests as spasm of muscles near the wound and is uncommon.

A facial expression characterized by raised eyebrows and grinning distortion of the face resulting from spasm of facial muscles especially in tetanus.

  • It is a state of extreme hyperextension of the head, neck and spine that presents as severe, prolonged spasm characterized by a strongly arched and rigid back, hyperextended neck and arms, with the heels bent back.
  • Opisthotonus occur in tetanus, rabies, cerebral malaria, neurosyphilis, meningitis, encephalitis, cerebral palsy, partial seizures, strychnine poisoning and adverse effects of medications.

Characterized by trismus and facial palsy is rare one, and may occur after head injury or ear infection.

  • Penicillin 10–12 million units IV for 10 days.
  • Metronidazole 1 gm every 12 hours.
  • Clindamycin or erythromycin is an alternative for penicillin allergic patients.
  • Antitoxin is injected to neutralize circulating toxin and unbound toxin.

Human tetanus immunoglobulin (TIG) 3000–6000 units IM individual doses. A 500 unit dose is as effective as higher doses.

  • Prophylaxis. Wound debridement and booster doses of TT.
  • Unimmunized individuals: Anti-tetanus serum 1500 units or TIG 250 units should be given.
  • An active immunization schedule requires three doses triple vaccine in the first year of life with subsequent doses or booster doses of TT at school entry and at 5–10 year interval should be given.
  • Also known as Lues
  • Syphilis is a sexually transmitted infectious disease caused by Treponema pallidum (gram-positivea, motile, microaerophilic spirochete).
  • Characterized by episodes of active disease interrupted by the period of latency. 

Transmission occurs via oral-genital, oral-anal, or other sexual contact, transfusion with contaminated blood, direct contact with contaminated material, and intra-uterine transmission.

Syphilis can be classified as:

  • Congenital
  • Acquired.

The acquired form can be classified as primary, secondary, latent and tertiary.

  • Lesion is called chancre.
  • Develops at site of inoculation approximately 3–90 days after contact with the infection.
  • Occurring in ano-genital and oral regions.
  • In oral cavity it involves lips, tongue, palate, gingiva, and tonsils.
  • Intraoral chancre is an ulcerated lesion covered by a grayish-white membrane, may be painful due to secondary infection.
  • Regional lymphadenopathy.
  • Spontaneous healing occurs within three to six weeks without scar.
  • IgG antibodies to T. pallidum become positive.
  • Microscopically appear as a superficial ulcer showing intense inflammatory infiltrate, numerous plasma cells
  • Microorganisms in the tissue and may be demonstrated by silver stain.
  • Lesions contain highly contagious spirochetes.
  • Occur from four to eight weeks after chancre emergence.
  • Characterized by diffuse eruptions of the skin and mucous membranes.
  • On the skin, lesions appear as multiple painless macules or papules.
  • Oral lesions known as ‘mucous patches’ are usually multiple, painless, grayish-white plaques overlying an ulcerated surface that found frequently on the tongue, gingiva, or buccal mucosa as ovoid or irregular in shape surrounded by an erythematous zone.
  • Lesions undergo spontaneous remission within a few weeks, but exacerbations may continue to occur for months or several years.
  • Lues maligna characterized by fever, headache, and muscle pain followed by necrotic ulcerations involving the face and the scalp.
  • Commonly found in AIDS patients.
  • After second-stage as lesions got healed and symptoms disappears patient enter the latent stage which may last for 1–30 years till the next stage, tertiary syphilis, develops.
  • Patients demonstrate reactive serological test for syphilis.
  • Also known as late syphilis.
  • Does not usually appear for several years and involves CVS, CNS and certain organs.
  • It is non-infectious.
  • Classic lesions known as gumma.
  • Due to hypersensitivity reaction between the host and treponemes or their breakdown products.
  • Found in the skin and mucous membranes, liver, testes, and bone.
  • It consists of a focal, granulomatous inflammatory process with central necrosis.
  • Size of lesions from a millimeter or less to several centimeters in diameter.
  • Intraoral gumma involves tongue and palate.
  • Lesion appears as a firm nodular mass in the tissue, which may subsequently ulcerate, to form a deep painless ulcer.
  • Palatal lesions cause perforation by sloughing of the necrotic mass of tissue.
  • In syphilitic glossitis, surface of the tongue gets broken up by fissures due to atrophy and fibrosis of tongue musculature; and hyperkeratosis frequently follows.
  • Glossitis is found almost exclusively in males.
  • Syphilitic glossitis sometimes may  undergo carcinomatous transformation

Lesions of congenital syphilis include:

  • Frontal bossae.
  • Short maxilla.
  • High palatal arch.
  • Saddle nose.
  • Mulberry molars.
  • Higoumenakis sign or irregular thickening of the sternoclavicular portion of the clavicle.
  • Relative protuberance of mandible.
  • Rhagades.
  • Saber shin.

Systemic manifestations of late congenital syphilis are recognized by Hutchinson’s triad:

  • Interstitial keratitis of the cornea.
  • Eighth nerve deafness.
  • Dental abnormalities.

Dental abnormalities are probably caused by spirochetal infection of the enamel organ, causing screwdriver-shaped incisor (Hutchinson’s incisors) and Mulberry molars.

  • Diagnosis is commonly made by serologic testing.
  • The most commonly used screening tests are the Rapid Plasma Reagin (RPR) and the Venereal Disease Research Laboratory (VDRL).
  • The most specific serologic tests for syphilis are the fluorescent treponemal antibody absorption test and the micro-hemagglutination test.
  • These detect antibodies that are produced against treponemal antigens.
  • Dark-field microscopic examination to detect spirochetes.

Treatment of primary, secondary and early latent syphilis

DrugDose, administrationTreatment duration
Benzathine penicillin2.4 million units, IMSingle dose
Procaine penicillin600 000 units once daily, IM10–14 days
ALTERNATIVES
Doxycycline200 mg once daily, PO14 days
Tetracycline500 mg 4× daily, PO14 days
Erythromycin500 mg 4× daily, PO14 days
Azithromycin 2 g, POSingle dose
Ceftriaxone500 mg once daily, IM10 days

Also known as Hansen’s disease, is a chronic infectious disease caused by Mycobacterium leprae, discovered by G. H. Armauer Hansen of Norway in 1873.

  • It multiplies very slowly and the incubation period is about five years.
  • It may take as long as 20 years for the symptoms to develop.
  • Spreads through droplets from the nose or mouth of a patient to the skin and respiratory tract of another person.
  • Transmission requires close and frequent prolonged contact with untreated, infected person.
  • Indirect transmission is very unlikely.

Clinical, histopathological, and immunological criteria identify five forms of leprosy:

  • Tuberculoid polar leprosy (TT).
  • Borderline tuberculoid (BT).
  • Midborderline (BB).
  • Borderline lepromatous (BL).
  • Lepromatous polar leprosy (LL).

For therapeutic purposes it divided in to:

  • Paucibacillary (TT, BT)
  • Multibacillary (midborderline (BB), BL, LL).

Characteristics

 

Tuberculoid

 

Borderline tuberculoid

 

 

Midborderline

Borderline

lepromatous

 

Lepromatous leprosy
Number of lesions Single or upto 3A Few (up to 10)Several (10–30)

Numerous,

asymmetrical

(>30)

Innumerable,

symmetrical

Size Variable, usually largeVariable,some are largeVariable,

Small, some

can be large

Small
Surface changesHypopigmented

Dry, scaly, look bright,

and infiltrated

Dull or slightly shinyshinyshiny
Sensations AbsentMarkedly diminishedModerately diminished

Slightly

diminished

Minimally diminished
Hair growthNilMarkedly diminishedModerately diminished

Slightly

diminished

Not affected initially
Skin smearNegativeNegative or 1+1–3+3–5+Plenty, including globi (6+)
Lepromin test Strongly positiveWeakly positiveNegativeNegativeNegative
  • Presence of lepromas(small tumor like masses) on the tongue, lips, or hard palate.
  • Lepromas show a tendency to break down and ulcerate.
  • Gingival hyperplasia.
  • Loosening of the teeth.
  • Paralysis of facial and maxillary division of trigeminal nerve.
  • Dental manifestations known as odontodysplasia leprosa.
  • Premaxilla is affected in childhood
  • Circumferential hypoplasia,
  • Shortening of roots (maxillary anteriors).
  • Long standing lepromatous lesions show granulomatous invasion of pulp and pinkish discoloration of crowns.
  • Based on clinical and bacteriological examination.
  • Nasal smears and scrapings stained with modified Ziehl- Nielsen method for lepra bacilli  count more than 1011 gm of tissue.
  • Morphological index measures the number of AFB in skin scrapping that stain uniformly bright correlated with viability.
  • Bacteriologic index, a logarithmic scaled measure of density of leprae in the dermis.

Other tests are:

  • Monoclonal antibodies.
  • ELISA.
  • PSR.
  • Sweat function test.

The BI is an index of the bacillary load in the patient. This is expressed on a semi-logarithmic scale as given below.

BI Interpretation

  • 1+ 1 to 10 bacilli per 100 high power (oil immersion) fields.
  • 2+ 1 to 10 bacilli per 10 high power fields.
  • 3+ 1 to 10 bacilli per high power field.
  • 4+ 10 to 100 bacilli per high power field.
  • 5+ 100 to 1000 bacilli per high power field.
  • 6+ >1000 bacilli per high power field.

Reference may be made to the term ‘globi’ in some reports. These are clumps of bacilli and are generally found in LL. The clumps are derived from micro-colonies in macrophages.

  • The MI is an index of viability of the bacilli.
  • Solid bacilli are deemed to be viable while fragmented or granular bacilli are considered to be non-viable.
  • The MI is equal to the percentage of viable bacilli. The MI in untreated multi-bacillary leprosy usually ranges between 25 and 75 and should decline to 0 after 4 to 6 months of effective modern chemotherapy.
  • The treatment for leprosy is called multidrug therapy (MDT).
  • MDT treatment is provided in blister packs, each containing four weeks’ treatment. Specific blister packs are available for multibacillary (MB) and paucibacillary (PB) leprosy as well for adults and children.
  1. Standard adult treatment regimen for MB leprosy:
  • Rifampicin: 600 mg once a month
  • Clofazimine: 300 mg once a month, and 50 mg daily
  • Dapsone: 100 mg daily
  • Duration: 12 months (12 blister packs)
  1. Standard adult treatment regimen for PB leprosy:
  • Rifampicin: 600 mg once a month
  • Dapsone: 100 mg daily
  • Duration: six months (six blister packs)
  1. Standard child (ages 10 – 14) treatment regimen for MB leprosy:
  • Rifampicin: 450 mg once a month
  • Clofazimine: 150 mg once a month, and 50 mg every other day
  • Dapsone: 50 mg daily
  • Duration: 12 months (12 blister packs)
  • Appropriate dose for children under 10 years of age can be decided on the basis of body weight. [Rifampicin: 10 mg per kilogram body weight, clofazimine: 1 mg per kilogram per body weight daily and 6 mg per kilogram monthly, dapsone: 2 mg per kilogram body weight daily.

Sarcoidosis, leishmaniasis, lupus vulgaris, lymphoma, syphilis, yaws.

  • Caused by Neisseria gonorrhoeae a gram-negative, nonmotile, nonspore forming organism that grows in pairs (diplococci).
  • N. gonorrhoeae thrives in a warm, moist environment.
  • gonorrhoeae is a fragile bacterium that cannot tolerate a dry environment, so it is rarely transmitted by contact with contaminated fomites (inanimate objects).
  • Transmission occurs almost exclusively by sexual activity:
  1. Genital-to-genital contact
  2. Oral-to-genital contact
  3. Rectal-to-genital contact.

Uncommonly, an infected mother may transmit the disease to her child during childbirth.

Risk factors for gonorrhea include sexual contact with an infected person or someone from an endemic area; previous gonorrhea, STIs or human immunodeficiency virus (HIV); being a sexually active youth; having multiple partners; and being a sex worker, street youth and/or man who has sex with men (MSM).

  • Gonorrhea is often asymptomatic in females and symptomatic in males.
  • When symptomatic, the clinical presentation in females includes:
  1. Vaginal discharge.
  2. Dysuria.
  3. Dyspareunia.
  4. Abnormal uterine bleeding.
  5. Lower abdominal and/or rectal pain.

In males:

  1. Urethral discharge and/or itch,
  2. Dysuria
  3. Testicular or rectal pain.
  4. The urethra and cervix are the most frequently affected anatomical sites, followed by anal and pharyngeal areas.
  • Fever.
  • Regional lymphadenopathy.
  • Acute painful ulceration of lips with limiting motion.
  • Gingiva may become erythematous, with or without necrosis.
  • Tongue become red, dry, ulcerated, glazed and swollen with painful erosions.
  • Buccal mucosa and palate are also involved.
  • Gonococcal pharyngitis and tonsillitis appear as vesicles or ulcers with a
  • Gray or white pseudomembrane.
  • Gonococcal parotitis.

Diagnosis based on:

  • History and physical examination.
  • Nucleic acid amplification testing (NAAT)
  • For males, a urethral swab is sufficient for NAAT
  • For females receive a vaginal or endometrial swab.
  Type of InfectionRegimenDuration of Therapy
Uncomplicated  gonococcal infections of  the   cervix, urethra, and rectum

Recommended: ceftriaxone 250 mg IM + azithromycin 1 g po Alternative: cefixime 400 mg po+ azithromycin 1 g po

Cephalosporin allergy: gemifloxacin320 mg po + azithromycin 2 g po

Azithromycin allergy: ceftriaxone 250 mg IM + doxycycline 100 mg po bid

Recommended: Ceftriaxone and azithromycin are both single doses Alternative: Cefixime and azithromycin are both single doses

Cephalosporin allergy: Gemifloxacin and azithromycin are both single doses.

Azithromycin allergy: Ceftriaxone is a single dose. Continue doxycycline for 7 days

Uncomplicated gonococcal infections of the pharynxRecommended: ceftriaxone 250 mg IM + azithromycin 1 g poRecommended: Ceftriaxone and azithromycin are both single doses
Gonococcal arthritis

Recommended: ceftriaxone 1 g IM or IV q24h + azithromycin 1 g po

Alternative: cefotaxime 1 g IV q8h + azithromycin 1 g po

Recommended: Continue ceftriaxone for ≥7 days. Azithromycin is a single dose

Alternative: Continue cefotaxime for ≥7 days. Azithromycin is a single dose

Gonococcal  meningitis endocarditisRecommended: ceftriaxone 1-2 g IV and q12-24h + azithromycin 1 g poRecommended: For meningitis, continue ceftriaxone for 10-14 days. For endocarditis, continue ceftriaxone for 4 wk. Azithromycin is a single dose
  • Actinomycosis is a chronic suppurative granulomatous infection caused by the Actinomyces genus.
  • These are non-spore-forming, anaerobic, or microaerophilic gram-positive bacilli.
  • Some human-associated Actinomyces species including israelii, Actinomyces gerencseriae, and Actinomyces graevenitzii, may be involved in classical actinomycosis.
  • Actinomyces meyeri, Actinomyces neuii, and Actinomyces turicensis are emerging, to cause such infections at many body sites.
  • israelii and A. gerencseriae are responsible for about 70% of orocervicofacial infections.
  • Infection characterised by contiguous spread, suppurative and granulomatous inflammation, and formation of multiple abscesses and sinus tracts that may discharge ‘sulfur granules’.
  • Actinomycetes are prominent among the normal flora of the oral cavity but less prominent in the lower gastrointestinal tract and female genital tract.
  • As these microorganisms are not virulent, they require a break in the integrity of the mucous membranes and the presence of devitalized tissue to invade deeper body structures and cause human illness.
  • Infection typically spreads contiguously, frequently ignoring tissue planes and invading surrounding tissues or organs. Ultimately, the infection produces draining sinus tracts.
  • Hematogenous dissemination to distant organs may occur in any stage of the infection, whereas lymphatic dissemination is unusual.

According to the body site, actinomycosis can classify as:

  • Orocervicofacial.
  • Thoracic.
  • Abdominopelvic.
  • Most common form of the disease.
  • Characterized by a painless lumpy jaw.
  • Chronic soft tissue swelling, abscesses, woody fibrosis, and sinus discharge of sulfur granules.
  • Swellings are firm, and often lead to misdiagnosis of malignancy
  • Infection can spread directly to adjacent muscles and bones.
  • Mandible most commonly affected, less commonly, the maxilla which results in actinomycotic osteomyelitis

Differential diagnosis: abscess by other typical bacteria, cyst, neoplasm, tuberculosis, or nocardiosis.

Follows aspiration of endogenous organisms of the oropharynx into the lungs in persons with poor oral hygiene or from extension of cervicofacial infections.

Clinical manifestations:

  • Productive cough.
  • Low-grade fever.
  • Blood tinged sputum
  • Chest X-rays range from small nodular lesion to cavitating lesions with pleural, chest wall, transdiaphragmatic, or spine involvement
  • CT findings include patchy, nodular, or cavitating pulmonary lesions, as well as pleural or mediastinal lesions
  • Ultrasound or CT guided biopsy used for the diagnosis of patients with peripheral lung lesions.
  • Pelvic actinomycosis mostly occurs in women who use IUDs.
  • Actinomycosis may involve the abdominal wall, segments of the colon, uterus, ovaries, bladder, liver, gallbladder, and pancreas.
  • The portions of the gastrointestinal tract commonly involved are sigmoid colon, rectum, cecum, appendix, distal ileum, and ascending colon. 

Symptoms and signs:

  • Abdominal pain with or without palpable mass.
  • Body weight loss.
  • Fever.
  • Vaginal discharge.
  • Constipation or diarrhea.
  • In laboratory analyses the dominating sign are leukocytosis, positive inflammation markers, and anemia.
  • Radiology findings in a barium study include mural invasion with structure formation, mass effect with tapered narrowing of the lumen, and thickened mucosal folds but these findings are not specific for abdominopelvic actinomycosis.
  • CT findings may show concentric bowel wall-thickening, enhancing homogeneously, and forming fistula.

Laboratory Studies

  • CBC count: Anemia and mild leukocytosis are common.
  • Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels are often elevated.
  • Chemistry results usually are normal, with the exception of a frequently elevated alkaline phosphatase level in hepatic actinomycosis.
  • Organism cultures.
  • Nucleic acid probes and polymerase chain reaction (PCR)
  • Examination of sulfur granules: Granules should be crushed between 2 slides, stained with 1% methylene-blue solution, and examined microscopically for features characteristic of actinomycetes.
  • Imaging Studies: Chest X-ray & CT Scan. A chest radiograph may reveal a poorly defined mass or pneumonitis or cavitary lesion, with or without pleural involvement.
  • CT scanning (irrespective of the anatomic area of involvement) usually reveals an infiltrative mass with focal areas of decreased attenuation that enhance with contrast.
  • FNAC
  • Histopathological examination
  • High-dose penicillin [Adult: Penicillin G – 12-24 million U/d IV by continuous infusion or in divided doses q4h for 1-2 wk, then switch to PO (penicillin VK) for 6-12 mo] administered over a prolonged period (6 months to 1 year)
  • Alternative to Penicillins, if the patient is hypersensitive to penicillin or the causative organisms are resistant to Penicillin are Ceftriaxone (Adult: 2 g IV/IM q12-24h; not to exceed 4 g/d), Imipenem/Cilastin (Adult: 500 mg1000mg IV q8h; not to exceed 4 g/d), Clindamycin (Adult: 600 mg IV q8h, or 150 – 300 mg PO q8h), Amoxycillin/Clavulanic acid (Adult: 500 mg PO q8h, or 875 mg PO q12h), Doxycycline (Adult: 100 mg PO/IV q12h), Tetracycline, Lincomycin, Macrolides (erythromycin, Carbomycin, Spiramycin, Oleandomycin) – all these are effective.
  • Surgical treatment: Surgery is indicated for biopsy specimen, to drain abscesses, to extirpate (wide excision) a fibrotic sinus tract (not responsive to conservative treatment) or a recalcitrant fistula tract, to decompress or remove a intra-cranial or intra-spinal space occupying lesion, to remove severely damaged segment of lung or liver, relieving obstruction.
  • Also known as Cancrum oris, gangrenous stomatitis
  • Noma, or cancrum oris, is a multi-stage, opportunistic, rapidly progressive, and painless necrotizing stomatitis. 
  • Infection is multifactorial in nature and not clearly understood.
  • Predisposing factors: Presence of pre-existing malnutrition, poor oral hygiene, and an inciting illness, in combination. This triad allows for a polymicrobial infection to take hold.
  • Triggers for the illness include:
  1. Systemic febrile illness (e.g., from measles, varicella, or malaria).
  2. Neurotrophic viral infection (e.g., herpes).
  3. Periodontal disease,
  4. Other trauma leading to mucosal ulceration.

Micro-organisms: Treponema vincentii, other spirochetes or fusiform bacteria, Staphyloccus aureus, a-hemolytic Streptococcus, and Pseudomonas.

Noma occurs almost exclusively in children.

Systemic manifestations:

  • Fever.
  • Tachycardia.
  • Lymphadenopathy.
  • High respiratory rate.
  • Anorexia.
  • General edema.
  • Ascites.
  • First recognized sign of noma is edema of cheek, or gingiva or both.
  • A greyish black area appears on the external surface of the cheek opposite to the intraoral lesion within the next few days, which later on becomes a well-defined black necrotic zone.
  • This necrotic zone acquires a cone shape and rapidly sloughs away.
  • Sequestration of the exposed bone and teeth,
  • Halitosis.
  • Pseudomembranes.
  • Excessive salivation.
  • Spontaneous gingival bleeding.
  • Loss of tips of interdental gingival papilla.
  • Sometimes the necrosis is very severe that both maxilla and mandible are completely destroyed extending up till the nose, upper lip, pre-maxilla and the infraorbital margin.
  • Blood examination reveals a low hemoglobin concentration and white blood cell count, elevated erythrocyte sedimentation rate and hypoalbuminaemia.
  • HIV patients with noma may have a very low CD4 count.

Leprosy, leishmaniasis, post kala-azar dermal leishmaniasis, oral cancer, clostridial or streptococcal gangrene and Stewart’s granuloma

  • Untreated, acute noma in children is 80%–90% lethal.
  • Antibiotic treatment and nutritional support.
  • Plastic orofacial reconstruction is often necessary for both functionality and cosmesis (is the preservation, restoration, or bestowing of bodily beauty).
  • Also known as Bacterial actinophytosis, actinobacillosis, bacterial pseudomycosis ,pyoderma vegetans.
  • First reported by Bollinger in lung of horse in 1870.
  • Rare chronic bacterial granulomatous disease that usually involves skin and rarely viscera.
  • Common causative bacteria are Staphylococcus aureus and occasionally Pseudomonas spp., Escherichia coli, Proteus spp., and Streptococcus spp.

Risk factors: Impaired immunity or underlying systemic conditions such as diabetes mellitus, cystic fibrosis or HIV infection.

  • Affect the patient 9 months to 80 years of age.
  • Males are more affected than females.
  • Present in cutaneous or visceral forms.

Cutaneous form

  • It is a chronic persistent condition that presents with chronic, suppurative, and granulomatous skin lesions.
  • It may be preceded by trauma.
  • Presence of nodules, abscesses, and sinuses with purulent discharge.

Visceral form:

  • It is usually with pulmonary involvement.
  • Associated with cystic fibrosis and reaches skin forming sinuses and irregular masses.
  • Intra-orally tongue is common site of involvement.
  • Present as a firm, nodular infiltration of the body and base of the tongue.

Pathologically, botryomycosis is characterized by the presence of eosinophilic granules, with eosinophils surrounding central foci of necrosis, known as the Splendor-Hoeppeli effect.

Biopsy specimens should be routinely examined with a battery of stains (PAS, GMS, Brown-Brenn and Ziehl-Neelsen).

There are three ways to establish the diagnosis:

  • Identify granules in pus from draining sinus.
  • Culture the bacterium from ulcers or exudates with clinical findings of bortryomycosis.
  • Recognize granules in fine needle aspirates, biopsies or autopsy specimen.
  • Prolonged (2 weeks to 2 months) antibiotic administration.
  • Duration of therapy depends solely upon clinical response.
  • Selection of antibiotic based upon the culture results and associated sensitivity studies.
  • Penicillin G, erythromycin, trimethoprim-sulfamethoxazole and minocycline can be used successfully.
  • Also known as Francis’ disease, deer-fly fever, rabbit fever, water-rat trappers’ disease, wild hare disease. 
  • It is a particularly adaptive zoonotic disease caused by a small, non-motile, aerobic and fastidious gram-negative pleomorphic coccobacillus bacterium,  tularensis.
  • Infection spread by: arthropod bites, handling infected animal tissues or fluids, direct contact with or ingestion of contaminated water, food, or soil, and inhalation of infective aerosols.
  1. Ulceroglandular
    • Most common form.
    • Occurs following a tick or deer fly bite or after handling of an infected animal.
    • A skin ulcer appears at the site where the bacteria entered the body.
    • The ulcer is accompanied by swelling of regional lymph glands, usually in the armpit or groin.
  2. Glandular:
    • Similar to ulceroglandular tularemia but without an ulcer.
    • Acquired through the bite of an infected tick or deer fly or from handling sick or dead animals.
  3. Oculoglandular:
    • Occurs when the bacteria enter through the eye.
    • Symptoms: irritation and inflammation of the eye and swelling of lymph glands in front of the ear.
  4. Oropharyngeal
    • Results from eating or drinking contaminated food or water.
    • Symptoms: sore throat, mouth ulcers, tonsillitis, and swelling of lymph glands in the neck.
  5. Pneumonic
    • Serious form of tularemia.
    • Symptoms: cough, chest pain, and difficulty breathing.
    • Results from breathing dusts or aerosols containing the organism.
    • Also occur when other forms of tularemia (e.g. ulceroglandular) are left untreated and the bacteria spread through the bloodstream to the lungs.
  6. Typhoidal
    • This form is characterized by any combination of the general symptoms (without the localizing symptoms of other syndromes)

Occur most frequently in adults.

Symptoms

  • Headache.
  • Nausea.
  • Vomiting.
  • Chills.
  • Fever.
  • Lymphadenopathy.

Oral manifestations:

  • The oral lesions manifested as necrotic ulcers of the oral cavity or pharynx, accompanied by severe pain.
  • Generalized stomatitis
  • Single nodular, masses develops into abscesses.
  • Lymphadenitis may arise in the submaxillary and cervical lymphadenopathy.
  • Tularemia confirmed by the demonstration of an antibody response to  tularensis, that occurs about 2 weeks after the onset of the disease.
  • The detection of serum antibodies is achieved by agglutination or an ELISA.
  • PCR-based assays: nested PCR assay allowed the detection of 1 CFU of F. tularensis.

Since F. tularensis is easy to aerosolize, highly infective, and the number of organisms needed to infect is very less, it is considered to be a biological weapon.

The aminoglycosides streptomycin and gentamicin are bactericidal against F. tularensis 

  • First described by the dermatologist Ferdinando Von Hebra in 1870.
  • It is a chronic granulomatous disease caused by Gram negative bacillus called Klebsiella rhinoscleromatis or Frisch bacillus.
  • Altered immune response with impaired cellular immunity plays an important role.
  • Spreads from person-to person by air-borne transmission.
  • Females are more frequently affected.
  • Affect the age between 10–30 years of age.
  • Nasal cavity is the most common predilection site.
  • Other sites of involvement are: nasopharynx, oropharynx, larynx, trachea and bronchi.
  • Rhinoscleroma is mostly endemic in tropical countries.
  • Disease evolves through three stages:
  1. Catarrhal stage: It is characterized by foul smelling purulent nasal discharge and crusting resembling atrophic rhinitis.
  2. Granulomatous stage: In this painless and non-ulcerative granulomatous, nodules form in the nasal mucosa. There is also sub-dermal infiltration of external nose and upper lip giving a ‘woody’ feel.
  3. Cicatricial stage: This causes stenosis of nares, distortion of upper lip, adhesions in the nose, nasopharynx and oropharynx.
  • Oral lesions appearing as proliferative granulomas.
  • Impairment of the sensation of taste, anesthesia of the soft palate and enlargement of the uvula and upper lip.
  • Diagnosis requires a high index of suspicion (“awareness and concern for potentially serious underlying and unseen injuries or illness”) and clinicopathological correlation.
  • Warthin-Starry is the most helpful type of stain as it stains the organisms black, leading to easier detection.
  • Specific diagnosis is made with bacterial isolation by culture on blood or MacConkey agar.
  • Histopathologicaly characterized by a chronic granulation tissue with abundant plasma cells and Mikulicz cells, Russell bodies (plasma cells with retained globules of immunoglobulins).
  • MRI in the hypertrophic stage shows a soft tissue mass with mild to marked high signal intensity in both T1- and T2-weighted images.
  • Drug treatment may be combined with surgery in cases with granulomatous lesions or scarring stenosis.
  • Streptomycin has severe side effects.
  • Tetracycline requires a prolonged course of treatment and has adverse effects.
  • Rifampicin provides good results but requires effective monitoring of toxicity.
  • Trimethoprim-sulphamethoxazole may be effective.
  • Quinolones, ciprofloxacin and fluoroquinolone readily penetrate the tissues and are clinically effective.

Tuberculosis, leprosy, leishmaniasis, blastomycosis, cryptococcosis, and syphilis.

  • Also known as Cat-scratch fever, benign lymphoreticulosis, benign nonbacterial regional lymphadenitis.
  • First reported by Debre and his coworkers in 1950.
  • Caused by Bartonella henselae, a gram-negative bacillus demonstrable with silver stain.
  • Occur at any age, but predominantly in children and young adults.
  • Primary lesion appears as papule, pustule or vesicle that develops at the site of the injury, within one to three weeks, a regional lymphadenitis without lymphangitis develops.
  • Nodes becomes painful and increases in size.
  • Overlying skin may be inflamed.
  • Lymphadenopathy may persist for 1 to 6 months.
  • Preauricular, submaxillary, or cervical chain of nodes involvement.

Early stage shows:

  • Low-grade fever.
  • Headache.
  • Chills.
  • Nausea.
  • Malaise.
  • Abdominal pain.
  • This consists of a localized granuloma of the eye and preauricular lymphadenopathy.
  • The lymph nodes gradually become soft and fluctuant, owing to necrosis and suppuration.
  • Positive intradermal skin test of antigen.
  • Indirect immunofluorescent antibody assay.
  • IgM antibodies to the organism by ELISA.
  • Self limiting and regresses within a period of weeks or months.
  • Incision and drainage of the involved node may be necessary.
  • Lymph node penetration of antibiotics and effective intracellular and pericellular concentrations may be essential for treatment; azithromycin penetrates lymph node tissue and is concentrated intracellularly.
  • Described by McCarthy in 1949.
  • It is a very rare oral manifestation with unknown pathogenesis. 
  • Lesion has strong association with Inflammatory Bowel Disease (IBD).
  • Crohn’s disease is also associated with pyostomatitis vegetans.
  • Affect any age group but it is commonest in young and middle aged adults.
  • Has predilection for males with male to female ratio of 2:1 to 3:1.
  • Pyostomatitis vegetans is a very rare oral disorder characterized by pustules that affect oral mucosa.
  • Multiple white or yellow pustules on erythematous base may rupture and form folded, fissured appearance resembling a “snail-track”.
  • The labial gingiva, soft and hard palate, buccal and labial mucosa are most commonly affected.
  • Skin lesions (pyodermatitis vegetans) characterized by: vesicular, pustular, exudative and vegetating plaques and usually involved the scalp, face, axillae and genital regions.
  • Cutaneous lesions can appear after or prior to the occurrence of Pyostomatitis vegetans lesions but Pyostomatitis vegetans can be seen without skin lesions.
  • Based on clinical features (snail tracks appearance).
  • Association with inflammatory bowel disease.
  • Peripheral eosinophilia.
  • Characteristic histological features (intraepithelial abscesses with large amount of eosinophils).
  • Direct and indirect immunofluorescence is usually negative or may be weakly positive in direct immunofluorescence and the results are inconclusive.
  • Management is based on treatment of the underlying gastrointestinal disease.
  • Oral lesions without any gastrointestinal problem, can be managed with:
  1. Local therapies such as antiseptic mouthwashes (chlorhexidine).
  2. Topical corticosteroids (triamcinolone acetonide paste or betamethasone mouthwash).
  3. Systemic steroid therapy (azathioprine and sulfamethoxypyridazine).

Once a bacterium has been obtained in pure culture, it has to be identified. Identification schemes are classified into one of the two categories:

  1. Phenotypic characteristics.
  2. Genotypic characteristics.

Identification of bacteria of only pure culture (single strain) was made by phenotypic methods:

  1. Microscopic morphology.
  2. Staining reactions.
  3. Metabolism differences:
    • Macroscopic morphology or cultural characteristics
    • Fermentation and other biochemical reactions.
  4. Serology.
  5. Antibiotic tolerance (resistance) tests, dye tolerance, and other inhibition tests.
  6. Bacteriophage and bacteriocin typing.
  7. Pathogenicity.

An alternative approach to identification involves the application of modern, rapid molecular methods and identification of a bacterial species from a complex population. Methods:

  • Nucleic acid hybridization.
  • PCR-Amplifying specific DNA sequences.
  • Sequencing rRNA genes.
  • Urine dipstick test: is a bedside test that can assist with diagnosing bacterial infection.
  • Wet prep microscopy: for the diagnosis of sexually transmitted infections in women.
  • Bedside Gram stain: Helpful for identifying Gram-negative diplococci in a joint aspirate to confirm gonoccocal arthritis, for rapid diagnosis of meningococcaemia from a skin scraping of a petechial rash.

General bacteriology available from: http://generalbacteriology.weebly.com/culture-media.html

Differences between Gram Positive and Gram Negative bacteria available from: https://laboratoryinfo.com/differences-between-gram-positive-and-gram-negative-bacteria/

Bacteriological culture media / Types of culture media Available from:

Bacterial culture media: classification, types and uses available from: https://microbeonline.com/types-of-bacteriological-culture-medium/

Types of culture media used in microbiology. Available from: http://www.aladdin-e.com/up_files/docs/Types%20of%20culture% 20media% 20used%20in%20microbiology.pdf

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Krawiecka E, Szponar E Tuberculosis of the oral cavity: an uncommon but still a live issue Postępy Dermatologiii Alergologii 2015;4:302-6.

Kamath AT, Raghu Radhakrishnan R, Manish Bhagania M,  Mohan A Tuberculous Osteomyelitis of the Mandible J Maxillofac Oral Surg. 2015;14: 200–202.

Kannaperuman J,Gowri Natarajarathinam G, Rao AV, Palanimuthu S. Primary tuberculous osteomyelitis of the mandible: A rare case report Dent Res J 2013;10: 283–286.

Rodriguez JT, Fernandez RL, Jurado RR, Hayde Nallely Moreno-Sandoval HNM, Francisco Martinez-Perez FM, Barrios JAG Mycobacterium tuberculosis as a cause of mandibular osteomyelitis in a young woman: a case report J Med Case Rep. 2016;10:366.

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