1. Diagnosis and Management of
Odontogenic Infections

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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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. 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%.

30. 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.

31. 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.

32. 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.

33. Cazuri clinice

36. 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.

37. 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.

38. 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.

40. 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.

42. 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.

43. 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)

44. 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.

45. 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.

46. 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.

47. 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.

48. Classification
• Acute (în stadie de
infiltrație seroasă și
purulente)
• Chronic nespecific
and
specific
(tuberculoz, actino
micoz, HIV).
• Superficial
and
deep localization

49. 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.

50. 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.

51. 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.

52. 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.

53. 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

54. 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

55. Complications of OI
• suppurative jugular thrombophlebitis and
carotid artery erosion,
• septic cavernous sinus thrombosis,
• osteomyelitis of the jaw,
• mediastinitis,
• brain abscess

57. 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

58. •
•
•
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

59. 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)