INFECTIONS

Dr Salma Mohamed BDS, MSc Oral Surg.,

MSc Oral Path, LDS RCS
DEFINITION OF INFECTION
Invasion by & multiplication of pathogenic
microorganisms in a bodily part or tissue, which
my produce subsequent tissue injury & progress
to overt disease through a variety of cellular or
toxin mechanisms. Cellular injury may be due to
competitive metabolism, toxins, intracellular
replication or antigen-antibody response
Airborne infection : is the one that contracted by
inhalation of microorganisms or spores suspended in air
or dust particles

Droplet infection : due to inhalation of respiratory

pathogens suspended on
liquid particles exhaled by some one already
infected(droplet nuclei)
RELATED TERMS
• Colonisation:- is the usual presence of non-pathogenic
& even potentially pathogenic microbes on the skin, in the
nose,mouth,bowel mucosa as a part of normal human flora
in the amount not harmful to the body. This is not an
infection e.g. presence of Lactobacillus acidophilus in the
colon.
• Contamination:- is the presence of germs which do not
multiply e.g. in a contaminated (not infected) wound.
Infected or septic wound contain multiplying microbes
.Contamination also refer to presence of pathogenic
microbes on medical equipments, in the water, food etc.
TYPES OF INFECTIONS
• Systemic infection :- like influenza affect the whole
body & cause systemic symptoms like malaise ,muscle
pains, fever, nausea etc
• Localised infection :- cellulitis , is limited to one or
few body parts & presents with localised symptoms like
redness, swelling, or localised ear, nasal discharge.
• Acute infection :- like common cold appear suddenly &
lasts days to one month.
• Chronic infection:- like TB or AIDS may last from
several weeks to several yrs.
• Recurrent infection:- is the one that frequently affect
the person like fungal infection in those with lowered
immunity.
• Asymptomatic infection:- causes no symptoms e.g.
EBV that cause infectious mononucleosis often trigger no
 CAUSES OF INFECTIONS

•Bacteria e.g.
staphylococcus,
salmonella
•Viruses:- influenza,
HIV
•Fungi :-candida
albicans, aspergillus
• Airborne infections industrial cooling or hot water system, air condition& room air
humidifier can be a source for Legionella

• Soil during walking barefoot (Clostridium tetani) , eating with soil contaminated
hands

• Hospital acquired infection

Infection acquired in hospital can be dangerous since the causing microbes are
often resistant to regular antibiotics & patients infected are already seriously ill
UTI from catheter
surgical site wound infection
staphylococcus skin, lung, &heart valve can be infected.
fungal oral thrush in patients with low immune system or cancer pt.
receiving chemotherapy
legionella may be found in tap water in newly opened hospitals or poorly
maintained hospitals
BACTERIAL INFECTION
Dental abscess
• Its an infection of the mouth , face, jaw or throat
• Begins as tooth infection or cavity

• May occur in patients with poor oral hygiene

• In patients with underlying autoimmune disorder e.g. Sjögren
syndrome
• Patients with weakened immune system e.g. diabetes mellitus post
radiation/chemotherapy
• May also triggered by minor trauma to the oral cavity

• Bacteria from dental caries may extend into the gums, cheeks ,
throat beneath the tongue or into the jaw or facial bones
• May be very painful
Cause
Direct growth of bacteria from an existing tooth cavity
into soft tissues & bones of the face & neck

Symptoms
Pain, swelling, redness of the neck & face
Nausea, vomiting, fever with advanced infection

Signs
Cavity ,gum inflammation, oral swelling, tenderness with
touch. Sometimes difficulty fully opening the mouth or
swallowing.
Tenderness on palpation of the infected area.
DIAGNOSIS
• Organisms most commonly isolated in acute
dentoalveolar abscess are facultative or strict
anaerobes.
• The most frequently isolated microorganisms are
anaerobic gram negative rods.
• However other organisms have also been isolated
including
haemolytic streptococci
anaerobic gram negative bacilli
anaerobic streptococci
S. anginosus group
Actinobacillus actinomycetem comitans
Actinomyces species
• Aspiration of dental abscess is necessary to obtain samples
containing the likely causation organisms
SAFETY CONSIDERATION
Specimen collection
• Avoid accidental injury when pus aspirated
• It should be before starting antimicrobial therapy where
possible.
• Specimen should be transported & processed as soon as
possible

Microscopy
• Swabs prepare a thin smear on a clean microscope slide
for gram staining after performing culture.
• Pus using a sterile pipette place one drop of neat
specimen or centrifuged deposit as applicable into a clean
microscopic slide.
ULCERATIVE GINGIVITIS

ANUG
• Acute infection of the gingiva without involvement of the
tissue of the periodontium
• May occur at any age.
• The prevalence in the normal population is less than 0.1%
although in stressed population the frequency increases up
to 7%
• May occur in very young children suffering from
malnutrition
• If progress deep into the periodontal tissue it is necrotising
ulcerative periodontitis (NUP).
• May refer to ANUG as Vincent angina.

Eatiology
Caused by bacterial infection that include
CAUSE
• Caused by over abundance of normal bacteria coupled
with
• poor oral Hygiene,
• poor nutrition & / or vitamin deficiency
• Stress
• Smoking
• Possible immune suppression
• Medical conditions
• Blood dyscreases
• Diabetes mellitus
• gingivitis
SIGNS & SYMPTOMS
• Interdental papillae are highly inflamed, eodematous &
haemorrhagic.
• Necrosis &/or ulceration of the interdental papillae or
gingival margin.
• Gray pseudomembranous formation.
• Painful ,bright red marginal gingiva that bleed upon
manipulation.
• Halitosis .
• Occasionally lymphadenopathy, malaise & fever may occur.
• If the infection extend through the mucosa to the skin of
the face then it is termed noma (cancrum orris) .
DIAGNOSIS

Made by clinical
examination
ulceration
cyanosis
erythema
blunting of the
TREATMENT
• Irrigation & debridement of necrotic area
• Topical or local aneasthetic may be required before
debridement of the tissue
• Oral hygiene instructions (OHI)
• Mouth washes (chlorhexidine, warm saltwater, or diluted
hydrogen peroxide)
• Antibiotic medications such as metronidazole or penicillin
specially in the presence of fever or lymphadenopathy.
• Pain medication
• Proper management of the underlying systemic disorder is
appropriate
• Supportive therapy e.g. rest, appropriate fluid intake, soft
nutritious diet
• Follow-up to reinforce the home care instructions & to
rule out the recurrence.
MYCOBACTERIUM TUBERCLOSIS

• Chronic infectious disease caused by Mycobacterium

tuberculosis.
• It is estimated that about 2 billion people infected world
wide.
• Classic human disease
 PATHOGENESIS
• Inhaled aerosols Engulfed by
alveolar macrophages Bacilli replicate
Macrophages die
• Infected macrophages migrate local lymph nodes
• Develop Ghon’s focus Primary complex
• Cell mediated immune response
stops cycle of destruction and spread
• Viable but non replicating bacilli present in macrophages

EVIDENCE OF INFECTION WITH M TUBERCULOSIS

Chest x-ray / positive skin test
 CLINICAL PRESENTATION
Pulmonary tuberculosis

Primary complex
Asymptomatic
HEALS

Acute pulmonary disease REACTIVATION

Systemic spread Post-primary
tuberculosis
Asymptomatic /symptomatic

LATER DISEASE MILIARY TUBERCULOSIS

Renal / CNS etc Pulmonary
meningitis
• Head & neck involvement may occur.
• Cervical lymph nodes followed by larynx &
middle ear.
• Much less common sites include nasal cavity,
nasopharynx, oral cavity ,parotid gland,
eosophagus, & spine
• Oral lesions appear as chronic painless ulceration
• When present primary oral TB involves the
gingiva, mucobuccal fold,& areas of
inflammation adjacent to teeth or in extraction
sites.
• Secondary lesions are present on the tongue,
palate,& lip.
 DIAGNOSIS
Pulmonary tuberculosis

1 1 Primary complex
Asymptomatic
HEALS
2
3

Acute pulmonary disease REACTIVATION

Systemic spread Post-primary
tuberculosis
Aymptomatic /symptomatic

LATER DISEASE MILIARY TUBERCULOSIS

3
Renal / CNS etc Pulmonary 3
meningitis
DIAGNOSIS
Evidence of infection
Chest x-ray - hilar lymphadenopathy
calcification of primary focus/LN
Delayed hypersensitivity response to purified protein
derivative (PPD) MANTOUX /HEAF TEST
Evidence of active disease
Sputum for AFB (Acid Fast Bacillus) positive
Evidence of active disease
Indirect evidence of infection (Mantoux)
Direct evidence of infection PCR / culture
Histo-pathological evidence
HISTOPATHOLOGY
• Cell mediated hypersensitivity reaction is responsible for
the histopathologic reaction.
• Granulomas formation which are circumscribed collections
of epithelioid histiocytes, lymphocytes& multinucleated
giant cells with central caseous necrosis.
• These granulomas are called tubercle.
• Special stains such as Ziehl-Neelsen or acid- fast stains are
required to demonstrate mycobacteria
• Due to scarcity of the organisms a negative result does not
completely rule out the possibility of TB.
TREATMENT
• Anti-tuberculous drugs
• INAH (Isonicotinic Acid Hydrazide)
• Rifampicin
• Ethambutol
• Pyrazinamide

• DOT (Directly Observed Therapy)

• Multi-drug resistant tuberculosis
 PREVENTION
• Incidence declined after availability of anti-tuberculous
drugs
• Improved social conditions - housing /nutrition
• Case detection & treatment
• Contact tracing
• Evidence of infection / disease
• Treatment of infected / diseased contacts

ROLE OF IMMUNIZATION
BCG (bacillus Calmette Guerin)
ACTINOMYCOSIS
• An infection caused by filamentous branching, gram-
positive anaerobic bacteria (Actinomyces israelii)
• Actinomycetes are normal saprophytic.
• Sites of colonisation include the tonsillar crypts, dental
plaque & calculus, carious dentin, gingival sulci &
periodontal pockets.
CLINICAL FEATURES
• May be either acute rapidly progressing infection or a
chronic slowly spreading lesion that associated with
fibrosis.
• 55%cervicofacial region, 25%in the abdominal & pelvic
region,15% in the pulmonary system
• The suppurative reaction discharge large yellowish flecks
that represent colonies of bacteria called sulfur granules.
• The organism enters tissue through an area of prior trauma
soft tissue injury
periodontal pocket
nonvital tooth
extraction socket
infected tonsil
HISTOPATHOLOGY
• Peripheral band of fibrosis encasing a zone of
chronically inflamed granulation tissue
surrounding large collections of
polymorphonuclear leukocytes & may be
colonies of the organisms.
• The colonies consist of club-shaped filaments
forming a radiating rosette pattern.
• With H&E stain the central core stains
basophilic & the peripheral portion is
eosinophilic
TREATMENT
• In chronic cases prolonged high doses of antibiotics in
association with abscess drainage.
• Although penicillin is the standard of care but others
recommend amoxicillin or tetracycline.
• Localised acute actinomycotic infection such as periapical,
pericoronal actinomycosis, tongue abscess & focal
subacute sialadenitis with intraductal involvement respond
well to surgical removal of infected tissue.
MORE TO COME
 SYPHILIS

• Definition
• A sexually transmitted disease (STD), which in its
late stages can cause mental disorders ,
blindness, & death
DANGER OF SYPHILIS
CAUSES, INCIDENCE,& RISK
FACTORS
• Syphilis caused by a corkscrew-shaped bacterium called
Treponema pallidum
• Originally a disease prevalent in the 15th century, syphilis
is making a come back
• This is largely been attributed to changes in
sexual habits
drug abuse , particularly trading sex for crack
unsafe sexual practice among teenagers
and declining support for public health services
• The infection is acquired by direct contact with the sores
of infected individuals
• The bacterium is usually transmitted through the mucous
membrane of the genital area ,the mouth, or the anus, it
can pass through a broken skin anywhere on the body
• The open sores of syphilis are believed to make it easier
for AIDS virus to enter the body
• The syphilis bacterium is very fragile, however, & the
infection is rarely if ever , spread by contact with objects
such as toilet seats or towels
• Because the early symptoms of syphilis can be very mild,
many people do not seek treatment when they first
become infected
• However, untreated infected people can infect others
during the first two stages of the disease, which can last
up to 2 yrs
• The disease charecterised in three stages
primary
secondary
tertiary
 PRIMARY
• Incubation period is three weeks from initial infection
• A painless ulceration called a chancre (shang-ker) occurs
at the site of infection
• In men the lesion is usually on the penis or anus
• In women on the vulva or within the vagina or cervix
( these lesions may be missed)
• Chancres are highly infective but self limiting & heal
within 4-6 weeks
PRIMARY SYPHILIS CHANCRE
 SECONDARY
• The secondary stage represent s systemic disease
• Follows 2 months after initial lesions appear
• Symptoms include
fever
widespread rash
wart like lesions on the genitals
snail track ulcers on the buccal mucosa
generalised lymphadenopathy
• This stage is also self limiting &followed by a latent period
between 2-20 yrs
SECONDARY SYPHILIS
SNAIL TRACK ULCER
 HISTOPATHOLOGY
• Histopathologic picture of the oral lesions are not specific
• During the first two stages the pattern is similar
the surface epithelium is ulcerated in primary lesions
may be ulcerated or hyperplastic in secondary stage
there may be an increase in the number of vascular channels in the
lamina propria & intense chronic inflammatory reaction which is
composed of lymphocytes & plasma cells
in secondary syphilis the epithelium demonstrate hyperplasia with
spongiosis & exocytosis
the presence of the corkscrew like spirocheatal organisms in the
surface epithelium can be demonstrated by immunoperoxidase
reaction ,Steiner stain or Warthium-Starry , direct fluorescent antibody
testing
oral tertiary syphilis exhibit surface ulceration pseudoepitheliomatous
hyperplasia
the underlying inflammatory infiltrate demonstrate foci of
granulomatous inflammation with well circumscribed collection of
histiocytes & multinucleated giant cells
FOLLICULAR PUSTULE SECONDARY SYPHILIS NODULAR COLLECTION
 DIAGNOSTIC PROCEDURES
• Dark ground examination
• Serological tests for syphilis
standard tests for syphilis (STS)
specific tests for syphilis
• Treponema pallidum immobilisation test (TPI)
• Fluorescent Treponema antibody test (FTI)
• Treponema pallidum haemagglutination test (TPHA)
• Biopsy
 TERTIARY SYPHILIS
• Chronic granulomatous lesion in the skin , mucosa& bones
• Vascular lesions (aortic aneurysm)
• CNS lesions leading to general paralysis & syphilitic
madness, tabes dorsalis
• Neurosyphilis progresses rapidly in HIV patients
TERTIARY SYPHILIS
 PREVENTION
• Safe sex behavior
• Wearing condoms
• Early diagnosis & treatment with antibiotics
 COMPLICATIONS
• Syphilitic madness
• Generalised paralysis
• Tabes dorsalis leading to
altered pain & positional sense
which in turn leads to joint destruction (Charcot joints)
• Congenital defects
• Death
CONGENITAL SYPHILIS
VIRAL INFECTIONS
HAND FOOT AND MOUTH
DISEASE
What is Hand, Foot & Mouth Disease ( HFDM)
• Hand, foot,& mouth disease ( HFMD) is a common illness of
infant & children caused by a virus. It most often occurs in
children under 10 yrs old. It is characterized by fever ,
sores/ulcers in the mouth , & a rash with blisters. The
blisters may appear in the , palm of the hands & soles of
the feet. The rashes may also appear on buttock & on the
legs & arms. The ulcers in the mouth usually appear on the
tongue, the sides of the cheeks, gums or near the throat.
 WHAT CAUSES HFMD?
• The most common causes of Hand, Foot & Mouth
disease are coxsackie virus A16 , enterovirus
71 (EV71) & other enteroviruses. The
enterovirus group includes poliovirus,
coxsackievirus ,echoviruses & other
enteroviruses.
 WHEN & WHERE DOES HFMD
OCCUR?
• Individual cases & outbreaks of HFMD occur
worldwide, more frequently in summer & early
autumn ( in temperate countries) .
 IS HFMD SERIOUS?
• HFMD caused by coxsackie virus A16 is a mild
disease & nearly all patients recover within 7 to
10 days. Complications are uncommon. HFMD
caused by Enterovirus E71 may be associated
with neurological complications such as aseptic
meningitis & encephalitis.
 IS HFMD CONTAGIOUS?
• Yes, HFMD is moderately contagious. A person is
most contagious during the first week of the
illness . The virus can be transmitted from
person to person via direct contact with nose &
throat discharges , saliva, fluid from blisters, or
stool of infected persons. The virus may continue
to be excreted in the stool of infected
individuals up to 1 month. HFMD is not
transmitted to or from pets or other animals.
 HOW SOON THE PERSON BECOME ILL

• AFTER
The usual periodGETTING INFECTED?
from infection to onset of
symptoms ( incubation period) is 3 to 7 days.
Fever is often the first symptom of HFMD
followed by blister/ rash.
 WHAT ARE THE CLINICAL
SIGNS & SYMPTOMS?
• HFMD begins with
A mild fever
Poor appetite ( feeling sick)
Frequently sore throat

One or 2 days after the fever begins ,painful

sores develop in the mouth
They begin as small red spots that blisters&
become ulcers
They are usually located in the tongue,
gums,& inside of the cheeks
The skin rash develop over 1 to 2 days flat or
raised red spots ,some with blisters on the
 HOW HAND, FOOT & MOUTH
DISEASE DIAGNOSED
• Based on a complete history & physical
examination of the child
• It is generally suspected on the appearance of
blister-like rash on hands, feet& mouth in
children with a mild febrile illness
• Usually the doctor can distinguish between HFMD
& other causes of mouth sores based on the age
of the patient, the pattern of the symptoms
reported by the patient or parents & appearance
of the rash & sores on examination
• A throat &/ or blister swab collected preferably
within 2 days of onset of HFMD may be sent to a
laboratory to determine which enterovirus
caused the illness
 HISTOPATHOLOGY
• The areas of the affected epithelium exhibit
intracellular & intercellular eodema which leads
to extensive spongiosis & the formation of an
intraepithelial vesicles
• The vesicles enlarge & ruptures through the
epithelial basal cell layer forming a subepithelial
vesicle
• Epithelial necrosis & ulceration soon follow
• Inclusion bodies & multinucleated epithelial cells
are absent
HISTOPATHOLOGY IMAGES
 HOW IS HFMD TREATED
• In most instances the infection is self limiting
without significant complications
• Therapy is directed towards symptomatic relief
• Antipyretic & topical aneasthetic are often
beneficial
• Dehydration is of concern because the mouth
sores may make it difficult & painful for children
to eat & drink
• Taking enough liquids is very important as well as
monitoring the body temperature
 WHO IS AT RISK FOR HFMD
• Mainly children under 10 yrs old, but may also
occur in adults
• Everyone is at risk of infection , but not everyone who
is infected become ill
• Infants, children & adolescents are more likely
to be susceptible to infection & illness from
these viruses because they are less likely than
adults to have antibodies & be immune from
previous exposures
• Infection results in immunity to the specific virus
but a second episode may occur following
infection with a different virus belonging to the
enterovirus group
 HERPANGINA
• Acute onset of sore throat, dysphagia & fever
• Occasionally cough, rhinorrhea, anorexia,
vomiting, diarrhea, myalgia & headache
• However most cases are mild or subclinical
• Oral lesions usually 2 to 6 develop on the
posterior areas of the mouth (soft palate or
tonsillar pillars)
• The affected areas begin as red macules which
form fragile vesicles that rapidly ulcerate
• The ulcer will be about 2 to 4 mm in diameter
• The systemic symptoms resolve within a few
days, the ulceration usually take 7 to 10 days to
heal