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  1. 1. Diagnosis and Management of Odontogenic Infections
  2. 2. Infection is the invasion of a host organism's bodily tissues by disease-causing organisms, their multiplication, and the reaction of host tissues to these organisms and the toxins they produce. Infections are caused by microorganisms such as viruses, prions, bacteria, and viroids, and organisms like macroparasites and fungi.
  3. 3. Infection in maxillo-facial area in children Infections of the oral cavity are often odontogenic in origin, and include dental caries, pulpitis, periapical abscesses, and gingivitis. They can progress to periodontal and deep fascial space infections if not properly treated.
  4. 4. Infection and the host • In establishing the presence of an infection, there is interaction among three factors • host • environment • organism In a state of homeostasis, balance exists among three factors. • Three major components of the host defense system: 1. Local skin and mucous membrane - epiyhelial lining - secretion and drainage - microbial interference 2. Humoral - immunoglobulin - complement 3. Cellular - limphocytes - phagocytes
  5. 5. Nature of the oral microbiota • Gram-pozitiv cocci : (Streptococci, peptostreptococci, stafilococci, 50%) • Gram-negativ cocci (Neisseria, Veillonela spp. 5% - 10%) • Gram-pozitiv rods an Filaments (Diphtheroizi, Lactobacili, Actinomyces spp) • Gram-negativ rods and Filaments (Pseudomonas, Coliforn bacteria) • Spirochetes • Funji and Yeasts • Viruses • Protozoa Quantitative estimations of the number of microorganisms in saliva and plaque range as high as 1011/ml.
  6. 6. Microbial flora in children • The microbiota of the mouth at new-born is predominantly aerobic: lactobacilli, streptococci, staphylococci, enterococci, veillonela e, neisseriae and coliforms. • At the end of first year of life: streptococci, staphylococci, veillonelae and neisseriae are found cosistently in all mouth. (actinomycetes, nocrdiate, lactobacili and fusobacteria – one half of mouths, and bacteroides, leptotrichia, corynbacteria and coliforns – in less half of mouths. • In early childhood facultative species are dominant (because of lack of sites were anaerobiosis can be achieved) and than various obligate anaerobous are added. • Bacteria increase throughout childhood. Some bacteria (Prevotella species – Bacteroids - and spirochetes are not common until adolescence
  7. 7. MICROBIOLOGY OF ODONTOGENIC INFECTIONS • Usually caused by endogenous bacteria • Aerobic bacteria alone rarely causative agents • Streptococcus species are usually the etiologic organisms if aerobic bacteria present. • Half odontogenic infections: anaerobes. • Most odontogenic infections due to mixed flora • Mixed infections may have 5-10 organisms present • Odontogenic infections are mixt, polymicrobial and nonspecific
  8. 8. MICROBIOLOGY OF ODONTOGENIC INFECTIONS • Bacterial composition 1. 5%-aerobic bacteria 2. 60%-anaerobic bacteria 3. 35% mixed aerobic and anaerobic bacteria • Commonly cultured organisms: alpha-hemolytic Streptococcus, Peptostreptococcus, Peptococcus, E ubacterium, Bacteroides (Prevotella) melaninogenicus, and Fusobacterium.
  9. 9. Social biological factors Disability Genotype and Maturation BIOLOGICAL Parenting/ parenting styles Factors affecting development Culture Approval/ interactions SOCIAL Education Housing Disease and illness NATURE/NURTURE DEBATE Social Class
  10. 10. Social biological factors • First group – social – birth weight, childhood material circumstances, parental divorce, smoking behaviour, educational attainment, • Second group – social hygienic – personal and public hygiene measures. When an individual disregards his personal hygiene, it will not only affect his comfort but will also cause harm to his physical and psychological aspects. (poor oral hygiene, neglect the profilaxy, sport, prevention treatment). • Third group – poor medical prophylaxis activities (group of children that are not cover with oral prevention and people have to refer to hospital in urgent situation.
  11. 11. Constitutional factors are those associated with race, sex, inherent immunity, inherent disease traits, anatomic anomalies. • a high ratio of cancellous to cortical bone and a thick layer of soft tissue covering. • higher elasticity, poor pneumatization (by sinuses), thick surrounding adipose tissue, and stabilization of the mandible and maxilla by the unerupted teeth. • mixed dentition, unerupted teeth, on going growth, growth areas on bone. • immature dental root with an open apex (immature tooth). • large Hawers canals in the jaw bone. • a higher presence of organic substance than unorgaanic
  12. 12. Constitutional environment • • • • • • • • diabetes obesity intravenous drug abuse weakened immune system due to underlying illness or medication Immature immune system in children frequent infection (more than 3 per year) artificial feeding Predominance of parasympatic nerve system over simpatic.
  13. 13. Sighns of infection • Rubor - or redness is seen when the infection is close the tissue surface in individuals with light complexions and is the result of vasodilation. • Tumor – or swelling, results from the accumulation of fluid exudate or puss. • Calor – or heat is the result of the inflow of relatively warm blood from the deeper tissues, increased velocity of blood flow and increased rate of metabolism. • Dolor – or pain, results from pressure on sensory nerve endings from distention of tissues caused by edema or the spreading of infection. The action of activated factors (kinins, histamine, metabolites on nerve ending also is responsible for pain. • Functia laesa or loss of function, is reflected in difficulty in chewing and swallowing and respiratory embarrassment
  14. 14. Ethiological factors • Odontogenic: • • • • • • • • dental and periodontal lession (dental pulp gangrene, apical periodontities, dental fracture, eruption disorders in permanent and primary teeth); injuries of jaw and dental tissues; Jaw osteomyelitis Salivary gland infection; Jaw tumors; Nasopharyngeal infection; Skin infection (pyodermitis, furuncle); Complication of local anesethezia; Foreign body; Complication of dental exarticulation.
  15. 15. Classification of odontogenic infection • Teeth and adjacent tissuer: a) pulpitis (acute, cronic, exacerbation), b) apical periodontitis (acute, cronic, exacerbation), c) pericoronarit (acute, cronic), e) alveolite. • Maxillary bone: a) dento-alveolar infection (acute serous and purulent), b) ostitis (acute, cronic rarefiată și hiperplastic, primary cronic, exacerbată), c) osteomielytis (acute, destructive cronic, cronic distructiv-productiv, hiperplastic – Garre) . • Soft tissure of head and neck area: a)limphadenitis (acute serouse, acute purulent, cronic (speciphyc, nonspeciphyc), exacerbate. b) celiulitis. c) abcesses. d) flegmon. d) adenoflegmon.
  16. 16. Treatment options • Medical support • • Antibiotic therapy Penicillin V: 25-50 mg/kg/d PO divided q6-8h Penicillin G: Mild-to-moderate infection: 100,000-250,000 U/kg/d IV divided q4-6h Severe infection: 250,000-400,000 U/kg/d IV divided q4-6h; not to exceed 24 million Azithromycin (Zithromax) U/d>6 months: Day 1: 10 mg/kg/dose PO/IV once; not to exceed 500 mg Days 2-5: 5 mg/kg/dose PO/IV daily; not to exceed 250 mg Amoxicillin and clavulanate (Augmentin) 80-90 mg/kg/d PO divided q12h (dose based on amoxicillin component) • • Removal of source • • Incision and drainage • • Re-evaluation
  17. 17. Pathways of Odontogenic Infection • Dental pulp – neural, vascular, conecive tissue; • Bacteria – inflamation and edema cause venous congestion or avascular necrosis; • Lack of collateral blood supply contribute to the death of the pulp; • Absence of an adequate blood supply – reduce host defense response to the infection; • Further progression leads to medullary space infection and osteomyelitis • More commonly, get fistulous tracts through alveolar bone • Fistulous tract may penetrate oral mucosa or facial skin
  18. 18. Infection in children • Systemic effects from infection are more pronounced in children. The younger the child, the less well controlled is temperature regulation and rapid temperature elevations may occur with infection. • Dehydration associated with fever and failure to take adequate oral fluids during infection is of greater significance in children than in adults. Oral fluids should be offered frequently to the febrile child. Hospitalization and rehydration should be considered early in the course of an odontogenic infection in the child
  19. 19. Infection in children • Normal values for the white blood cell count and differential in children, as well as pulse, blood pressure and other vital signs and laboratory measurements, differ from those in adults. • The bones of the jaws in children are less dense, with wider marrow spaces, than those in adults. This is thought to be responsible for more rapid spreading of infection. If infection are not treated vigorously and promptly, they may lead to osteomyelitis, proliferative periostites and involvement of the condyle with subsequent growth deformity.
  20. 20. Infection in children • In children infection caused by dentoalveolar abscesses may involve the buds of permanent teeth, resulting in hypoplasia or destruction of teeth. • Abscesses with fistula formation present on skin surface rather than in the vestibule more often in children than in adults because of the relative height of muscle attachments to the developing alveolar process. • Cutaneous fistulae in children are frequently of odontogenic origin. • Failure to recognize dental problems and to treat them properly by pulpal and canal therapy or tooth extraction has resulted in repeated courses of antibiotic therapy and unnecessary surgical procedures to excise fistulous tracts
  21. 21. Infection in children • Infection in children involving the upper face (orbits, paranasal sinuses, maxillary teeth, and cheeks) occur most often in younger children with unknown cause. Those of the lower face (mandibular teeth and submental, sublingual and submandibular structures) occur more often in the older children (mean age 5.6 years) • Because children become rapidly dehydrated and infection may spread readily early hospitalization may be essential to shorten the course of the illness and reduce morbidity
  22. 22. Serious dental infection • - originates in the dental pulp and is usually secondary to dental caries. Dental caries erode the protective layers of the tooth (ie, enamel, dentin) and allow bacteria to invade the pulp, producing a pulpitis. Pulpitis can progress to necrosis, with bacterial invasion of the alveolar bone, causing an abscess.
  23. 23. Serious dental infection • Symptoms of a dental abscess typically include localized redness on the gum (1 or 2 teeth), pain and swelling (may progress over a few hours to days) extending toward the buccal side of the gum (sometimes lingual), tenderness with touch. With an advanced infection, child can experience nausea, vomiting, fever, and chills.
  24. 24. Treatment options • 1. Surgical or dental therapy a. treatment of the offending teeth: - endodontic elimination of the infected pulp, deep periodontal scaling, extraction. • The method of treatment of the offending teeth is determined by: extend of the infection, the patients general status, the degree of trismus prezent, biomechanical necessity of retaining the teeth.
  25. 25. Dentoalveolar abscess The gums surrounding the affected tooth is swell and turn red or slightly white or pale, since they are filled with pus. The gums have diffused borders and are extremely painful when touched. The infiltration is not limited, and extent to 3-4 teeth. But the swell is located only in one side of the gum (vestubular or lingual site). The vestibular sulcus is elivated by pus. The cause tooth can be mobile. Tooth abscess lead to local severe facial swelling. Formula leucocitară: VSH-3040mm, Leucocitoză 20,0-25,0.10 9/l.
  26. 26. Localization of the dentoalvelar abscess is related ro the anatomic pozition of the dental root from which is originated, espacially in relationship to muscle attachments, particularly the buccinator and mtlohyoid muscles. Bulging submucosal vestibular abscesses or fistula in the labial sulcus. A grneralized cellulitis of the upper lip or mid face Examination reveals deep caries, periodontal inflamation, or impacted or fractured teeth. Treatment: incision and drainage; antibiotic therapy
  27. 27. Complications  Dentocutaneous fistulae arise from chronic dental infections. The fistulous pathway develops as the chronic inflammation erodes through the alveolar bone, perforates the periosteum, and spreads into the surrounding soft tissues. The diagnosis is often missed because a chronic asymptomatic dental infection is usually present and the skin lesion is mistakenly thought to arise locally.  Acute suppurative osteomyelitis was common before the era of antibiotic therapy. Osteomyelitis is an inflammation of the medullary cavity and adjacent cortex of bone. The mandible is more commonly involved than the maxilla because the maxilla has a better blood supply. Maxillary sinusitis may occur from direct extension of an odontogenic infection.  Facial-space swelling secondary to spread of the infection most often involves the following areas: Submandibular swelling is caused by dental abscesses from the second or third molars whose roots lie below the attachment of the mylohyoid bone, Sublingual swelling is caused by any lower tooth whose apex is above the mylohyoid muscle attachment (ie, incisors, canines, premolars, mesial roots of the first molar). Buccal swelling originates from infected maxillary or mandibular molars. Less frequently involved facial-space swellings include submental, masticator, canine, lateral pharyngeal, and retropharyngeal
  28. 28. Periostita cronică Două forme: simplă și osificantă. Cauza: focare cronice odontogene, periostita acută, osteomielita cronică. Tabloul clinic: tumefiere limitată, dură, indoloră sau ușor doloră la palpare. Periostita cronică simplă regresează, cea osificantă trece în hiperostoză. Tratamentul: înlăturarea factorilor cauză (înlăturarea dinților cu focare periapicale, tratament rezolutiv cu acțiunea undelor de lazer, ionoforeză cu soluții de KI 5%.
  29. 29. Definition of acute odontogenic osteomyelitis Osteomyelitis is an necrotic purulent inflammation of the medullary cavity and adjacent cortex of bone. Inflammation of all layers of bone : Starting by medullar cavity (bone marrow ) Cancellous bone with high tendency to spread Then it spreads to Cortical bone Then extends to the periosteum The mandible is more commonly involved than the maxilla because the maxilla has a better blood supply.
  30. 30. Classification Etiology classification: odontogic (80%), hematogic (9%) și traumatic (11%). Before 3 years – most common hematogenic osteomyelitis, 3-12 ani – most common odontogenic osteomyelitis. Three detaching theories: embolic BobrovLexer; sensibilization – Derijanov; neuroreflection disturbance Semencenco.
  31. 31. Clinical picture of acute odontogenic osteomyelitis General clinical picture are estubleshed first in children: vomiting, naursa, anorexie, stări de neliniște, insomnie). Suppurative ostemyelitis begins with deep and intense pain in the jaw, high intermittent fever, and a obvious cause, most often a deeply carious or discolored tooth. A swelling are placed on the mucosa of the alveolar bone, bilateral and diffuse, vestibular sulcus are elivated, teeth movemnets on the affected side. During the course of several days facial swelling devoloped and in 10 to 14 days, teeth begins to loosen, pus exudes around the gingival sulcus, and multipal mucosal or cutaneus sinus tracks. A firm cellulitis is present in the soft tissues accompanied by trismus and cervical lymphadenopathy. A leukocytosis ranging from 20-30 cells mm3, neutrofiloză 7080%, lympfopenia 10%, no eozinophyl, low monocytis.
  32. 32. Cazuri clinice
  33. 33. Acute jaw infant infection Ostemyelitis of the jaw in infants is an uncommon disease but merits special mention because of the riscs of the involvement of the eye, extention to the dural sinusis and the potential for facial deformities and loss of teeth resulting from delayed inappropriate treatment. Infantile osteomyelitis occurs most often a few weeks after birth and ussualy affects the maxilla. Infantile osteomyelitis is believed to occur by the hematogenous route or from perinatal trauma of the oral mucosa from the obstretrician’s finger or the mucosa suction bulbused to clear the airway immediately after birth. The infection arise from neonatal trauma to oral tissues, hematogenous spread from skin, middle ear, mastoid, or tonsils. Infection invovlving the maxillary sinus and contaminated human or artificial nipples also have been implicated as sourses of infant infection.
  34. 34. Clinical appearance • Facial cellulitis centered about the orbit. Irritability and malaise, cellulitis, hyperpyrexia, anorexia, and dehydration. Convultions and vomiting may occur. • Pus is often present in the nostril on the affecte side. Inner and outer canthal swelling, palpebral edema, closure of the eye, conjunctivitis, and proptosis may result. A purulent dischurge may associated with the nose or with an inner canthal sinus. A concomitent subperiosteal abscess caused by acute ethmoiditis may be present. Intraorally the maxilla in the affected side is swollen both buccally and palatally, espacially in the molar regeon. Fluctuance often is present and fistulas may exist in the alveolar mucosa. During the early acute phase little radiographic change is noted. Leukocytosis is present with a shift to the left. S. Aureus usualy is the offending organism, although mny other organisms, particularly streptococci, can occasionally be found.
  35. 35. Treatment • Treatment should be prompt and agrressive to prevent permanent optic damage, neurological complcations, and loss of tooth buds and bone. Treatment consists of intravenous antibiotics and drainage of all abcecces. Intravenous penicillin and a penicillinase-resistant penicillin, ampicillin/sulbactam (Unasyn), or clindamicyn should be given, and drainage of all flictuant areas should be established. Specimens shoul be obtained repeadetly for sensitivity testing with appropriate adjusment of the antibiotic regimen. Supportive treatment consist of antypiretics, fluid, and proper diet. Antibiotics should be continued orally for 2 to 4 weeks after all sighns of infection have subsided. A conservative approach to sequestrectomy is advisable because of the dainger of damage to tooth buds. Occationally roots tooth buds are extruded and siquestra form. When teeth in the area eventually erupt they may be dicolored. Scarring beneath the eyelid also have been noteed, causing an ectoprion. Corrective lid surgery sometimes is required for corection.
  36. 36. Destructive Chronic Osteomyelitis After 10 days to 20 weeks of acute odontogenic osteomyelitis, radiographs may show scattered areas of bone destruction suggestive of a moth-eaten appearance and periosteal reaction characterized by the laying down of new bone commonly is seen. Considaration should be given to sequestrectomy, saucerization or the placement of closedwound irrigation and suction.
  37. 37. Garre chronic osteomyelitis This condition also known as chronic nonsuppurative sclerosing osteomyelitis and proliferative osteomyelitis of Garre is notable bacause of the similarity of some of its characteristics to those to other neoperiostoses. It is characterised by a localized, hard, nontender swelling of the mandible. Lymphadenopathy, hyperpyrexia, and leukocytosis are not present. It is associated commonly with a carious teeth, usually the lower first molar and a history of a past toothache. It is also may be associated with a recent dental extraction or an infected flap of tissue over an erupting tooth. Radiographs are showing a focal area of well-calcified bone proliferation that is smooth and that often has a laminated or onion-peel appearance.
  38. 38. Garre chronic osteomyelitis • Garre osteomylitis is thought to be a • response to a low-grade stimulus, such a dental infection, that influences the potentionally active periosteum of young individuals. Its appearance resembls that of infantile cortical hyperostosis (Caffey disease), osteosarcoma and Ewing sarcoma and must be distinguished from them. Treatment consists of extraction or endodontic treatment of the involved tooth, with continued clinical and radiographic follow-up of the patient to ensure that the new bone formation does not progress. Ordinarly remodeling occurs over time, but biopsy should be performed to rule out neoplasm. expansion of the inferior border of the mandible (onion-skin appearance)
  39. 39. Complications • Loss of primary or permanent teeth. • Sequestration of segments of the jaws. • Growth defects, such a mandibular hypoplasia, asymmetry, and ankylosis. • Disfiguring facial scar and cutaneus fistulas. • Lesion suggestive of malignacy, which requireopen biopsy.
  40. 40. Lymphadenopathy Lymph nodes, in conjunction with the spleen, tonsils, adenoids, and Peyer patches, are highly organized centers of immune cells that filter antigen from the extracellular fluid. Directly interior to the fibrous capsule is the subcapsular sinus. This allows lymph, an ultrafiltrate of blood, to traverse from the afferent lymph vessels, through the sinuses, and out the efferent vessels. The sinuses are studded with macrophages, which remove 99% of all delivered antigens. The lymph node, with its high concentration of lymphocytes and antigenpresenting cells, is an ideal organ for receiving antigens that gain access through the skin or gastrointestinal tract. Nodes have considerable capacity for growth and change. Lymph node size depends on the person's age, the location of the lymph node in the body, and antecedent immunological events. In neonates, lymph nodes are barely perceptible, but a progressive increase in total lymph node mass is observed until later childhood. Lymph node atrophy begins during adolescence and continues through later life.
  41. 41. Lymphadenopathy • Recognize that most children have palpable lymph nodes in the anterior cervical, inguinal, and axillary regions that, if evaluated by adult standards, would qualify as lymphadenopathy. Lymphoid mass steadily increases after birth until age 8-12 years, and undergoes progreIn young children, anterior cervical lymph nodes as large as 2 cm, axillary nodes as large as 1 cm, and inguinal nodes as large as 1.5 cm in diameter are normal, and further evaluation is usually not indicated. In a series of 457 children, malignancy was usually associated with nodes larger than 3 cm in diameter.8 However, the presence of even shotty (<0.5 cm) supraclavicular or epitrochlear adenopathy may be associated with malignancy and warrants further evaluation. Newborns usually have small adenopathy (<0.5 cm), and larger nodes not associated with a focus of inflammation are an indication for further evaluation.
  42. 42. Lymphadenopathy • Generalized lymphadenopathy is defined as enlargement of more than 2 noncontiguous lymph node groups. A thorough history and physical examination are critical in establishing a diagnosis. Causes of generalized lymphadenopathy include infections, autoimmune diseases, malignancies, histiocytoses, storage diseases, benign hyperplasia, and drug reactions. • Cervical lymphadenopathy: Cervical lymphadenopathy is a common problem in children.1 Cervical nodes drain the tongue, external ear, parotid gland, and deeper structures of the neck, including the larynx, thyroid, and trachea. Inflammation or direct infection of these areas causes subsequent engorgement and hyperplasia of their respective node groups. Adenopathy is most common in cervical nodes in children and is usually related to infectious etiologies. Lymphadenopathy posterior to the sternocleidomastoid is typically a more ominous finding, with a higher risk of serious underlying disease.
  43. 43. Classification • Acute (în stadie de infiltrație seroasă și purulente) • Chronic nespecific and specific (tuberculoz, actino micoz, HIV). • Superficial and deep localization
  44. 44. Causes • Cervical adenopathy is a common feature of many viral infections. Infectious mononucleosis often manifests with posterior and anterior cervical adenopathy. Firm tender nodes that are not warm or erythematous characterize this lymph node enlargement. Other viral causes of cervical lymphadenopathy include adenovirus, herpesvirus, coxsackievirus, and CMV. In herpes gingivostomatitis, impressive submandibular and submental adenopathy reflects the amount of oral involvement. • Bacterial infections cause cervical adenopathy by causing the draining nodes to respond to local infection or by the infection localizing within the node itself as a lymphadenitis. Bacterial infection often results in enlarged lymph nodes that are warm, erythematous, and tender. Localized cervical lymphadenitis typically begins as enlarged, tender, and then fluctuant nodes. The appropriate management of a suppurative lymph node includes both antibiotics and incision and drainage. Antibiotic therapy should always include coverage for Staphylococcus aureus and Streptococcus pyogenes. • In patients with cervical adenopathy, determine whether the patient has had recent or ongoing sore throat or ear pain. Examine the oropharynx, paying special attention to the posterior pharynx and the dentition. The classic manifestation of group A streptococcal pharyngitis is sore throat, fever, and anterior cervical lymphadenopathy. Other streptococcal infections causing cervical adenopathy include otitis media, impetigo, and cellulitis. • Atypical mycobacteria cause subacute cervical lymphadenitis, with nodes that are large and indurated but not tender. The only definitive cure is removal of the infected node.12 • Mycobacterium tuberculosis may manifest with a suppurative lymph node identical to that of atypical mycobacterium. Intradermal skin testing may be equivocal. A biopsy may be necessary to establish the diagnosis.
  45. 45. Cat scratch disease • • • • • • • • • • Cat scratch disease is usually a self-limited infection by a curved pleomorphic gramnegative, bacteria Bartonella henselae. The bacteria form filaments up to 10 micrometer or longer. It is easily seen in tissue sections of the skin, lymph nodes, and conjunctiva, when stained by a silver impregnation technique. Cats are the principal reservoir of Bartonella henselae, the etiologic agent in most cases of CSD. Infection begins when the organism is inoculated into the skin by the claws of cats and rarely by other animals, or by thorns or splinters. Sometimes the conjunctiva is contaminated by close contact with a cat, possibly by licking around the eye. Infections are more common in children (80%) than in adults, and there may be clustering when a stray cat or kitten joins a family. Most patients have a papule at the site of inoculation, but it may be small and overlooked. The papule, which begins 3 to 14 days after inoculation may persist for 8 weeks, is followed by tenderness and enlargement of the regional lymph nodes. The nodes remain enlarged for 3 to 4 months and may drain through the skin. About onehalf of the patients have other symptoms, including fever and malaise and (rarely) splenomegaly, Parinaud’s oculoglandular syndrome, rash encephalitis (which typically has a sudden onset and sudden resolution), and erythema nodosum. Rare complications of B. henselae infection is bacillary angiomatosis.
  46. 46. Cat scratch disease • At the site of inoculation the bacteria multiply in the wall of the small vessels and about collagen fibers from which they move through draining lymphatics to regional lymphnodes, where they produce a pyogranulomatous lymphadenitis. • In early lesions clusters of bacteria expand and obliterate the walls of small vessels. • The lesions in the skin and lymphnodes progress from abscesses to suppurating granulomas and finally to necrosis. • Bacteria are abundant in early lesions and rare in late ones. • Without biopsy and the visualization of the characteristic bacteria, the diagnosis is supported when three criteria are met : i) contact with a cat, a cat scratch, or a primary lesion of the skin or conjunctiva : ii)a positive skin test for cat scratch antigen : ii)and negative results from laboratory studies for other causes of lymphadenopathy. • Although serologic testing is the reference method for diagnosis, successful use of immunohistochemical (IHC) stain of regional lymph nodes for the diagnosis of CSD has been reported.
  47. 47. Folliculitis • Staphylococcal folliculitis affects hair follicles on the face, scalp, neck, trunk or limbs but not the hands, soles and mucous membranes where there are no hair follicles. Folliculitis usually appears as a group of red bumps, which may develop into pus-filled blisters. Itch or pain are main symptoms; follicles may open and drain pus. Low grade fever may be present. Folliculitis barbae is a folliculitis of the beard in men. A stye or hordeolum is folliculitis affecting one or more hair follicles on the edge of the upper or lower eyelid.
  48. 48. Boil – Skin Abscess • • A furuncle develops from an infected hair follicle, when the adjacent skin tissue is involved. It most commonly appears on the neck, arms or legs as a red nodule up to 1 cm in size, and usually after some time opens and drains pus. Furuncles may be itchy and painful, local swelling and erythema. The overlying skin – thin and tender. The lesion are filled with creamy yellow pus. Facial infection may enter the venous sunuses, rezulting in sinus thrombosis and brain abscess. When several furuncles coalesce, it forms a carbuncle. Carbuncles most often appear on the nape of the neck in persons with lowered immunity, friction of clothes or bad hygiene
  49. 49. Furunculus • Clinical findings • Severe orbital / periorbital/ infraorbital swelling • Ptosis, proptosis,chemosis , occulomotor palsy • Headache in frontal &retro-orbital areas • Photophobia, eye pain,dysesthesia, generali zedsepsis
  50. 50. Complications of OI • suppurative jugular thrombophlebitis and carotid artery erosion, • septic cavernous sinus thrombosis, • osteomyelitis of the jaw, • mediastinitis, • brain abscess
  51. 51. IMAGING STUDIES 1.Contrasted CT focal hypodensity>enhances after ivcontrast>ring-enhanced lesion Frequently located inwatershed areas,regular thin-walledcapsule with peripheralenhancement Brain tumor: irregular border & diffuseenhancement
  52. 52. • • • Impetigo Impetigo is a crust-forming staph infection of the skin, mainly occurring in pre-school children.. It is highly contagious and easily spreads to other parts of the skin. Fever is not common, but the local lymph nodes may be affected. Infection usually heals on its own in 2-3 weeks (3). It most often occurs in summer and autumn. Impetigo contagiosa starts like red bumps which rupture, ooze fluid or pus, and form honey colored crusts. It mostly appears around the child’s nose and mouth (Picture 4). Bullous impetigo mostly appears in infants in the form of vesicles of various size on the trunk or limbs. Ecthyma is a severe form of impetigo with thick crusts. It affects deeper layers of the skin, it is painful, it may develop into an ulcer and leave scars. Complications of impetigo are rare and include scars, permanent hypo- or hyper-pigmented skin patches and cellulitis
  53. 53. Profilaxia, asistența medicală și reabilitarea copiilor cu procese inflamatorii Factorii nefaforabili: Prima grupă - social-biologici (dezvoltarea fizică, afecțiunile acute și cronice suportate, acțiunea factorilor nefavorabili în perioada de nou născut și sugari ca alimentarea artificială, alrgiile la copi). Grupa 2 – social igienică (nerespectarea igienii cavității orale, nivel scăzut de cultură al părinților, ignorarea sportului, neglijarea tratamentului la medic) Grupa 3 - activitățile de tratament și profilaxie la nivel scăzut (grupuri de copii care nu sunt acoperite d asanarea cavității orale, adresarea la medic numai în cazuri urgente)