Bacteria

 They are prokaryotic microorganisms which

can be spheroidal (coccus), rod / cylindrical
(bacillus) and spirillar (spirochetes)

 They are the causative agents of many human

diseases
Some of the important specific bacterial
infections

TUBERCULOSIS
SYPHILIS
ACTINOMYCOSIS
SCARLET FEVER
NOMA
LEPROSY
DYPHTHERIA
CAT – SCRATCH DISEASE
PYOGENIC GRANULOMA
TUBERCULOSIS
 Tuberculosis is a chronic systemic infectious
disease of worldwide prevalence. It is a
granulomatous infection and is caused by
Mycobacterium tuberculosis or rarely by
Mycobacterium bovis

 Incidence of tuberculosis has (had) declined

greatly

 Alarming come back as a result of HIV epidemic

 In patients with AIDS, M. avium intercellulare is a

common cause of opportunistic infections
Pathogenesis
 Caused by mycobacterium tuberculosis which is
aerobic, slender, non-motile, non-spore forming,
rod shaped, acid fast organism

 Mode of spread: droplet infection

 Since TB spread through droplet infection, optimal

conditions for transmission include:
Overcrowding
Poor personal hygiene
Poor public hygiene
Contributing factors
 Social issues: poverty, overcrowding
 Political issues: war, resettlement, immigration
 Health issues: malnutrition, drug abuse, HIV
infection, immunosuppression,
 Economic issues: drug cost, health care housing,
case identification and management
 Microbial: drug resistance
 Patients with the active disease expel the bacilli
into the air by:
 Coughing/Sneezing/Shouting
 Any other way that expels bacilli into the air

 Once inhaled by a tuberculin free person, the

bacilli multiply in 4-6 weeks and spreads
throughout the body. The bacilli implant in
areas of high partial pressure of oxygen:
 Lung
 Renal cortex
 This is known as the Primary Tuberculosis.
The lesion will heal and a scar will appear in
the infected loci.

 The bacteria at this time goes into a dormant

state

 When a person's immune system is depressed,

a secondary reactivation occurs and is called
Secondary Tuberculosis.

 Diffuse disseminated infection through

vascular channels may occur and has been
termed “Miliary Tuberculosis”.
 Airborne (droplet) infections

Tissue hypersensitivity to the bacilli

Transient inflammatory reaction in the lung (PMNL’s & macrophages)

Macrophages phagocytose the organism

Bacilli start to multiply within the macrophage

Formation of epitheloid cells

Epitheloid cells fuse together and form Langhan's giant cells

Caseation necrosis begins in the center of the infected tissue

Lymphocytes and fibroblasts accumulate in the periphery

Leads to formation of an avascular granuloma (Tubercle)

Most of the lesions heal by fibrosis and calcification

Micro-organisms may remain dormant for a long time

Reinfection as a result of reactivation

whenever the patient's body resistance is suppressed

Called Secondary Tuberculosis

 Clinical Features
 Commonly occurs in adult males
 Primary TB is usually asymptomatic
 Secondary TB shows features such as
General
Fever, Weight loss, Anorexia, Night sweats,
Weakness, “Consumption”
Organ specific
Lungs: Pneumonia (cough, sputum +/- blood)
Lymph nodes : Swollen lymph nodes (scrofula)
Genitourinary: Sterile pyuria
Bone: tuberculous osteomyelitis, fracture
Brain: Headache, Meningitis
skin: Lupus vulgaris
Oral Manifestations
 TB of Oral cavity is rare.

 Tuberculous lesions of the oral cavity are

mostly secondary to the pulmonary
infections

 Primary oral tuberculosis may occur in

some cases
 Intact oral mucosa does not permit tuberculous
bacilli to enter into the tissue.

 Pre-existing oral lesions may facilitate the entry of

these organisms into various oral structures
(oral ulcers, periodontitis, dental abscess, cyst, granuloma &
leukoplakia )
 Organisms can also reach through hematogenous
route to sub mucosa, subsequently proliferate &
ulcerate the mucosa.
 Dentist may get infected by contact with infected
persons
 The important tuberculous lesions of the oral
cavity are
 Tuberculous ulcers
 Tuberculous gingivitis
 Tuberculous osteomyelitis
 Tuberculosis of the salivary glands

 May also produce nodules, vesicles, fissures,

plaques, granulomas or verrucal-papillary
lesions
 Tubercular ulcers
 Single or multiple ulcers which are irregular ,
superficial or deep, painful & tend to increase
slowly in size.
 Have a granulating floor with minimum
induration and surrounding mucosa is
inflamed and edematous
 May occur in any intraoral site, however
tongue is the most common site.
(Palate, buccal mucosa, gingiva, lips, alveolar ridge and
vestibules may also be affected).
 Tubercular granuloma
 Seen as soft, non-tender swelling
 May occur in any intraoral site, palate is the
most common site.
 May develop in the periapical region of a grossly
decayed tooth due to the entry of organism
through the pulp canal- Tubercular periapical
granuloma / tuberculoma

 Tubercular Gingivitis
Small granulating ulcers or erosive
lesions with concomitant gingival
hyperplasia
 Tuberculous osteomyelitis
Develop due to entry of organisms through decayed
tooth or due to hematogenous spread.
 Pain, swelling, sinus/fistula formation, trismus,
paresthesia.

 Tuberculosis of salivary gland

 Generalized glandular swelling or abscess formation
along with pain, facial palsy & fistula formation

 Scrofula
Enlarged oropharyngeal lynphoid tissue
with involvement of cervical lymph nodes.
Caseous necrosis &numerous draining fistula
through overlying skin
 Lupus vulgaris – Tuberculous involvement
of skin
 Histopathology
 Microscopic presentation is in the form of
granulomas, which are circumscribed lesions.
 granulomas have a central area of caseous
necrosis surrounded by multinucleated giant
cells and epithelioid cells.Epitheloid cells are
macrophages.
 The nuclei of multinucleated giant cells are
seen at the periphery, having a horse shoe
shaped arrangement and these cells are called
Langhans’ giant cells.
 This is surrounded by a zone of lymphocytic
infiltration and fibrosis.
 Tubercular organisms may be demonstrated in
the tissue sections by Ziehl – Neelsen or other
acid fast stains.
 Investigations

 Staining of the smear prepared from sputum by

Ziehl-Neelsen stain
 Chest radiograph
 Bacterial culture in Lowenstein-Jensen media
(materials used for culture may be sputum, laryngeal swab, gastric

lavage, urine, cerebrospinal fluid and pus, etc.)

 Animal inoculation
 Histopathology
 Tuberculin test / Mantoux test
 Enzyme-linked immunosorbent assay (EL1SA)
test
 PCR (polymerase chain reaction)
 Treatment

 By antitubercular drugs in different regimens

 Historical Perspective
 It was first described in the 1500’s

 Also called as LUES

 Was known as “The Great Imitator”

because so many of the signs and symptoms
are indistinguishable from those of other
diseases
 Syphilis is a sexually transmitted disease (STD)
caused by a microscopic bacterium called the
Treponema pallidum, which enters the blood
stream and infects the entire body.

 Syphilis has an incubation period of 1-13 weeks

before any signs or symptoms.

 The disease is generally classified into two:

 Acquired syphilis
 Congenital syphilis
Acquired Syphilis
 Is acquired from an infected person
 It can be either through
 Sexual contact with an infected partner
 Careless handling of the infected patients by the health
professionals
 Drug abusers
 Manifests in four stages:
1. Primary syphilis
2. Secondary syphilis
3. Latent syphilis
4. Tertiary (late) syphilis
 Primary Syphilis
 Develops at the site of inoculation approximately 3
weeks after infection
 Clinical symptoms appear at the site of
inoculation
 male and female genitalia
 extra genital site like-fingers, oral region, perianal
region & nipples, etc.
(at these sites the spirochetes undergo rapid replication and
enter into the lymphatics or blood stream)
 Characteristic primary lesion of syphilis is called
“Chancre”

 It is a solitary, painless, indurated, nontender,

nonhemorrhagic, ulcerated or eroded lesion.

 Chancre starts as a dull red macule or papule,

which later on becomes eroded or ulcerated and
produces Regional lymphadenopathy

 Resolves within 3 - 8 weeks

Chancre
Primary Syphilis: Oral manifestations
 Chancre occurs on the lips, tongue, palate,
gingiva, uvula and tonsils

 May be painful due to secondary infection and are

highly contagious in nature

 Chancres are ulcerated, indurated lesions covered

by a grayish white membrane

 Often mistaken for an early carcinoma

 Tongue lesions- seen on the lateral surface of the
anterior two-third area or on the dorsal surface
and often there is enlargement of the folate
papilla.
 Tonsils show edema, redness and surface erosions
or ulcerations.
 Lymph nodes are enlarged bilaterally, these are
painless and rubbery in consistency.
 Heals by scarring within 3-6 weeks time
 Secondary Syphilis
 Also called Metastatic Stage

 Appears in about 6-8 weeks after the appearance

of the primary chancre

 Occurs due to the generalized hematogenous

dissemination of the infection in the body

 Characterized by skin lesions, mucosal lesions, few

constitutional symptoms and generalized
lymphadenopathy
 Skin lesions may also occur in the form of
nodular, flat-papillary (condyloma lata) or
pustular lesions.

 Circinate (coin-like) lesions on the face are

characteristic of secondary syphilis.

 Areas of hyperpigmentations may be seen on the

palms and soles.
 Constitutional symptoms associated with secondary syphilis
include-headache, anorexia, fever, joint and muscle pain,
laryngitis and pharyngitis, etc.

 Generalized lymphadenopathy is common and the nodes

are painless, discrete and not fixed to the surrounding
tissues.
 With or without treatment secondary lesions usually heal
within 2-4 weeks time
 At times in immunocompromised patients , it become wide
spread & is referred to as ‘ Leus Maligna’
Secondary Syphilis
Secondary Syphilis: Oral manifestations
 The secondary lesions are mucocutaneous in
nature and they usually occur 6 to 8 weeks after
the primary infection.

 The oral lesions in this stage are called “mucous

patches”, and these are commonly seen over the
tongue, gingiva, tonsils, larynx, pharynx and
cheek, etc.

 These patches are characterized by multiple, flat,

irregular or circular, slightly raised, painless,
round erosions.
 Mucous patches are covered by a thin yellowish-
grey (glistening) slough and are surrounded by a
painful erythematous halo
 Multiple mucous patches in the oral cavity
coalesce together and from “snail track” like
ulcers. This stage is also contagious.
 Diffuse maculo- papular eruptions of the palate
and other parts of the oral mucosa often occurs.
 Tongue is often fissured .
 Oral condyloma lata often presents round, pale or
white, velvety lesions.
 Latent Syphilis
 Called the Hidden Stage

 Begins when the Secondary symptoms disappear

 The bacteria begins to infest the bone marrow,

lymph glands, vital organs, and the central
nervous system

 It may last up to a month or a lifetime

 1/3 of the cases left untreated will proceed to

tertiary stage
 Tertiary (Late) Syphilis
 Occurs about 5-10 years after the primary infections and it
affects nearly every organs of the body

 It mainly affects skin, mucous membrane, CNS & CVS

 Typical lesions of tertiary syphilis is called " Gumma", which

is a localized, chronic granulomatous lesion having either
nodular or ulcerated surface.

 Granulomatous ulcerative lesion often appears as a

“punched-out” ulcer, having vertical walls and a dull red
granulomatous base with an irregular outline.
 Skin lesions heal very slowly and often they leave
"tissue paper" like scars.

 Tertiary syphilis occurring in pregnancy often results

in congenital syphilis of the newborn

 The most serious complication of tertiary syphilis is

the destruction of the walls of large blood vessels,
resulting in aneurysm and cardiac insufficiency.

 Involvement of central nervous system

(neurosyphilis) results in generalized paresis,
dementia and strokes.
 Tertiary Syphilis :Oral manifestations
 Gumma are commonly seen on the hard and soft
palate, lips and tongue

 This stage is not contagious.

 These lesions begin as firm, small, pale, nodular

masses in the midline of the palate.

 They frequently ulcerate by central necrosis and

have a punched-out edge with a wash-leather floor.

 The ulcers are either single or multiple and are

mostly painless.
 In tertiary syphilis, progressive necrosis and sloughing often
leads to perforation of the palate.

 In the tongue, often there is presence of a superficial glossitis

called “Syphilitic/Leutic/interstitial/Atrophic glossitis”.

 Loss of filliform and fungiform papilla results in a bald

tongue.

 However an ulcerative gummatous lesion of the tongue may

closely resemble squamous cell carcinoma.
Perforation of the palate Leutic glossitis
 Congenital Syphilis
 Congenital syphilis is a rare entity that occurs in
children born of an infected mother.

 The condition occurs due to transplacental

infection with T. Pallidum during fetal
development.

 Congenital infection is associated with several

adverse outcomes, including:
 Prenatal death
 Premature delivery
 Low birth weight
 Congenital anomalies
 Two-thirds of live-born neonates with Congenital syphilis are
asymptomatic at birth.

 Overt infection can manifest in the fetus, the newborn, or later

in childhood.

 The infant may have many or even no signs until 6-8 weeks of
life (delayed form).

 Clinical manifestations after birth are divided arbitrarily into:

- Early CS (<=2 years of age)
- Late CS ( >2 years of age)
 Clinical Manifestations of Early
Congenital syphilis
 Condyloma Lata
 Maculopapular rash
 Hepatosplenomegaly
 Jaundice due to the hepatitis
 Anemia
 Osteochondritis
 Pseudoparalysis
 Lymphadenopathy
 Mucous patches
 Clinical Manifestations of Late Congenital
syphilis
 Frontal bossing
 Saddle nose
 Short maxilla
 High -arched palate
 Relative prognathism of mandible
 Hutchinson's tooth
 Mulberry molars
 Hutchinson's incisors
 Interstitial keratitis
 Eighth nerve deafness
 Rhagades
 Premature perioral fissuring

 Higoumenaki's sign
 Enlargement of clavicle adjacent to the sternum

 Saber shin

 Anterior bowing of tibia as a result of periostitis

 Scaphoid scapulae
 Concavity of vertebral border of the scapulae

 Clutton's joint
 Painless synovitis and enlargement of joints, usually the knee
Saddle Nose
Saber Shins
Clutton’s Joints
 Hutchinson's triad
 Described by Sir Jonathan Hutchinson in
1858.
 Defined the following three pathognomonic
diagnostic features
 Hutchinson's teeth
 Ocular interstitial keratitis
 Eighth nerve deafness
 Few patients exhibit all three features
Hutchinson's teeth
 The infection alters the formation of both the anterior
teeth (Hutchinson's incisors) and the posterior dentition
(Mulberry molars, Fournier's molars, Moon's molars).

 Hutchinson's incisors exhibit their greatest mesiodistal

width in the middle third of the crown. The incisal third
tapers to the incisal edge, and the resulting tooth
resembles a straightedge screwdriver. The middle lobe
is affected. The incisal edge often exhibits a central
hypoplastic notch.

 Mulberry molars taper toward the occlusal surface with

a constricted grinding surface. The occlusal anatomy is
abnormal, with numerous disorganized globular
projections that resemble the surface of a mulberry
Interstitial keratitis
 Not present at birth, but usually develops
between the ages of 5 and 25 years
 May lead to permanent blindness
 Histopathology
 Histopathologic picture of the oral lesions - not
specific.
 During the first two stages, the pattern is similar
 The surface epithelium is ulcerated in 10 lesions &
may be ulcerated or hyperplastic in the 20 stage.
 The underlying lamina propria may demonstrate an
increase in the number of vascular channels, and an
intense chronic inflammatory reaction.
 The infiltrate is composed predominantly of
lymphocytes and plasma cells and often demonstrates
a perivascular pattern.
 Oral tertiary lesions typically exhibit surface
ulceration, with peripheral pseudoepitheliomatous
hyperplasia.
 The underlying inflammatory infiltrate usually
demonstrates foci of granulomatous inflammation
with well-circumscribed collections of histiocytes and
multi-nucleated giant cells.
 Even with special stains, the organisms are hard to
demonstrate in the third stage
 Diagnosis
 Detection of bacteria in smear by dark ground
illumination microscopy
 Bacterial culture in artificial media.
 Serological tests
 Wasserman reaction, Khan test, Venereal disease research
laboratory (VDRL) test, Rapid Plasma Reagin (RPR) test,
T pallidum hemagglutination assay (TPHA) & Fluorescent
treponemal antibody absorption(FTA-ABS)
 ELISA.
 Histopathology.
 Treatment
 Penicillin- In high doses
 Erythromycin or tetracycline – In case of
patients allergic to penicillin
 Blood tests - to make sure the infection has been
eliminated.
 Tertiary syphilis is incurable
 ACTINOMYCOSIS
 Actinomycosis is a chronic granulomatous,
suppurative and fibrosing infection.

 Although the term actinomycosis seems to imply a

fungal infection, it is an infection of filamentous,
branching, gram-positive anaerobic, non acid fast
bacteria
 Actinomyces-israelii
 A viscosus
 A naeslundii
 A odontolyticus
 A, meyeri
 A. bovis
 The microorganisms are normal inhabitants of the
oral cavity

 Sites of colonization in healthy patients include the

tonsillar crypts, dental plaque and calculus, carious
dentin, gingival sulci, and periodontal pockets.

 Takes entry into the tissues during trauma or tooth

extraction to produce infection

 Occurs in three forms:

 Cervicofacial (commonest form)
 Abdominal
 Pulmonary actinomycosis
 Pathogenesis

 The organisms enter tissue through an area of prior

trauma or soft tissue injury, periodontal pocket, extraction
socket, or infected tonsil.
 The infection does not spread along the typical facial plain
and usually disregards the normal lymphatic and vascular
routes.
 Direct extension through soft tissue is seen producing
indurated swellings which become fluctuant and later
organisms drain through multiple sinuses.
 Lymph nodes become involved only if they are in the path
of the process. Lymphadenopathy associated with this
disease may be due to secondary infections caused by some
other organisms.
 Clinical Features
Cervicofacial
 Age: disease occurs mostly in the fourth and fifth
decade of life.

 Sex: More prevalent among males.

 Site: The soft tissues of the submandibular,

submental, and cheek areas are common areas of
involvement, with the area overlying the angle being
the most frequently affected site.
 The organism enters tissue through an area of prior
trauma or soft tissue injury, periodontal pocket,
extraction socket, or infected tonsil

 The infection does not spread along the typical facial

plain and usually disregards the normal lymphatic
and vascular routes

 Direct extension through soft tissue is seen and

lymph nodes become involved only if they are in the
path of the process.

 Lymphadenopathy associated with this disease may

be due to secondary infections caused by some other
organisms.
 Starts as a swelling over the upper part of the neck or
below the ear, or over the mandible with minimal
pain.

 The overlying skin appears purplish red & indurated.

 Later on the swelling becomes fluctuant and some

areas of the skin breaks down to produce multiple pus
discharging sinuses. Similar sinuses may be seen
intraorally.

 The pus contains clinically visible, small yellowish

flecks known as “Sulfur Granules” and each of them
represents a colony of organisms.
 The pus discharging sinuses heal up, but later on,
some new sinuses appear in the region and the
process continues for years and causes great deal of
scarring and disfigurement of the skin.

 Involvement of the jaw bones by this disease often

results in chronic osteomyelitis

 Lesions localize at the apices of teeth and may

simulate periapical granulomas or cyst
Abdominal
 Extremely severe form
 High mortality rate
 Exhibit as a mass fixed to the underlying skin or as
abscess involving any organ
 Accompanied by symptoms such as fever, chills,
nausia, vomiting etc

THORACIC FORM

Fever & chills with productive cough and pleural pain

 Histopathology
 Actinomycosis is essentially a granulomatous
inflammation showing central abscess formation,
which shows typical bacterial colonies.

 Colonies appear to be floating in a sea of PMNL’s

with giant cells & macrophages around the lesional
periphery.

 The individual colony appear round or lobulated,

made up of a meshwork of filaments that stains with
hematoxylin, but shows eosinophilia of the peripheral
club shaped end of the filaments
 The periphery of each colony shows club-shaped
filaments that form a radiating rosette pattern and
produce a "ray fungus" like appearance.

 The colonies are surrounded by a fibrous tissue wall

at the outer margin.
 Diagnosis

 Culturing of organisms
 Histopathological diagnosis
 Immunofluorescent techniques
 Treatment

 High doses of any of the drugs like-penicillin,

cephalosporin, clindamycin and lincomycin,
etc.
 SCARLET FEVER
 Scarlet fever is a rare specific bacterial disease caused
by Group A, β-hemolytic streptococcus

 It commonly occurs in children during winter months.

 The disease begins as streptococcal tonsillitis with

pharyngitis in which the organisms elaborate an
erythrogenic toxin

 The toxin attacks the blood vessels and cause the

characteristic skin rash
 Clinical Features
 Incubation period ranges from 1-7 days

 Significant clinical findings: Fever, Enanthem &

Exanthem

 Also seen are headache, vomiting, tonsillitis,

pharyngitis and cervical lymphadenopathy, etc.

 Fever develops abruptly around second day

 Temperature peaks around 1030 & returns to normal

within 3 days
 A diffuse, bright red skin rash appears on the second
or third day of the disease, that starts on the chest and
gradually spreads to the other body surfaces.

 The skin rash is particularly more noticeable in areas

of pressure & skin folds.

 Characteristic skin rash is referred to as “ Sunburn

with goose pimples”.

 Skin of the trunk & extremities have a Sand paper

texture.
 Transverse red streaks known as “Pastia’s lines” are
seen in zones of stress.

 Skin rashes last for about one week following which

the affected area undergoes desquamation, starting
with the face

 Period of desquamation may last from 3-8 weeks

 Oral Manifestations
 Chief oral manifestations of scarlet fever are referred
to as “Stomatitis Scarlentina”

 The enanthem of oral mucosa involves the tonsils,

pharynx, soft palate & tongue.

 The tonsils, pharynx, & soft palate becomes

erythematous & edematous.

 Tonsillar crypts may be filled with a yellowish

exudate.

 The palate appears congested and inflamed, and the

hard palate exhibits punctiform redness.
 The tongue may be covered with a white coating,
through which the enlarged and reddened fungiform
papillae project like small red knobs, and this
phenomenon is called “Strawberry tongue”.

 Later on, the white coating on the tongue is lost,

leaving a deep red, glistening & smooth surface
except for the swollen hyperimic papillae and is
called “Raspberry tongue”.
Strawberry Tongue
 General Complications
 The disease usually subsides within a week or 10
days

 Complications may occur in few cases due to

bacterial metastasis or hypersensitivity reactions.

 These complications include peritonsillar abscess,

rhinitis, sinusitis, otitis media, mastoiditis, arthritis,
pneumonia, meningitis, rheumatic fever, acute
glomerulonephritis and septicemia, etc.
 Treatment

 Administration of penicillin or erythromycin.

 With appropriate treatment prognosis is excellent.

 No available methods for prevention

 NOMA
 Also called as “Cancrum oris; Gangrenous stomatitis
& Necrotizing stomatitis”

 Derived from the Greek word “Nomein” meaning "to

devour."

 Rapidly progressing, gangrene of the oral & facial

tissues that occurs in debilitated or nutritionally
deficient persons.

 An opportunistic infection caused by components of

the normal oral flora that becomes pathogenic during
periods of compromised immune status.
 Main causative organisms are Fusobacterium
necrophorum or F. nucleatum & Prevotella
intermedia.

 They interact with one or more other bacterial

organisms, of which the most commonly implicated
are Borrelia vincenti, S. aureus, & Non hemolytic
Streptococcus species.

 May be considered as a secondary complication of a

systemic disease rather than a primary disease.
 Predisposing factors include:
 Poverty
 Malnutrition or dehydration
 Poor oral hygiene
 Poor sanitation
 proximity to livestock
 Recent debilitating illness
 Immunodeficiency disorder
 Clinical Features
 In many instances. the infection begins as necrotizing
ulcerative gingivitis (NUG).

 May be considered as an extension of necrotizing

ulcerative gingivitis

 Descriptions of the initial stages of the disease are

sketchy
 Typically arises in children aged 1 to 10 years

 Often begins on the gingiva as NUG, which may

extends to involve the adjacent soft tissue by
ganngrenous necrosis and forms areas called
necrotizing ulcerative mucositis.

 A line of demarcation develops between the healthy

tissue & dead tissue

 Jaw is exposed as large masses of tissue sloughs out

 Commencement of gangrene is denoted by
blackening of the skin.

 Fetid odor, significant pain, fever, malaise & regional

lymphadenopathy are typical.

 A related disorder, “Noma Neonatorum”, arises in

the first month of life in low-birth weight infants who
also demonstrate malnutrition and frequently a
debilitating illness

 These patients almost always have infection with

Pseudomonas aeruginosa. often combined with E.
coli, Kiebsiella species, or Staphylococcus species
 Complications
 Severe facial disfigurement
 Death, as a result of
 Toxemia
 Pneumonia
 Diarrhea
 4 Stages of Syphilis

 Primary Stage

 Secondary Stage

 Latent Stage

 Tertiary Stage
 
Latent Syphilis
Called the Hidden Stage

 Begins when the Secondary symptoms disappear

 The bacteria begins to infest the bone marrow, lymph glands, vital organs, and the central nervous system

 It may last up to a month or a lifetime

 1/3 of the cases left untreated will proceed to tertiary stage

Latent Syphilis
Latent Syphilis

trophic degeneration of knee joint

 Tertiary Syphilis
Disease is not infectious at this stage
Lesions develop on the skin, bones, and vital organs
Patient experiences lack of coordination, paralysis, gradual
blindness, dementia, and vomiting.
Gummas or painful tumors may appear on the skin
Late syphilis can result in mental illness, blindness, other
neurological problems, heart disease, and death.
Tertiary Syphilis

Gumma on the buttock

 Diagnoses
 Syphilis is diagnosed in 3 ways

1) First recognize the signs and symptoms of

each stage.
2) Blood samples need to be obtained to test for
syphilis antibodies that the body produces
after the infection occurs.
3) A microscopic examination may be performed
of an active lesion to confirm diagnosis.
 Laboratory Tests
In the later stages of syphilis, blood or cerebrospinal fluid for
serological tests are necessary for diagnosis.
 Non-specific non-Treponemal tests RPR, VDRL
 May cross-react resulting in low-level false positive tests during
pregnancy, other infections, drug abuse, connective tissue disease and
aging.
 Levels usually relate to disease activity and are used for monitoring
treatment.
 After effective treatment of syphilis these tests usually become
negative but in some people, may retain positive at low levels
 Laboratory Tests
 Venereal Disease
Research Laboratory
test (VDRL) of the
cerebrospinal fluid
(CSF) is used to
screen for syphilis.
CSF is a clear fluid
that circulates in the
space surrounding the
spinal cord.
 Laboratory Tests
 Specific anti-treponemal antibody tests TPHA, EIA
 These detect antibody due to past or present infection with
Treponema pallidum or another treponema species.
 They cannot distinguish between different types of
Treponema infection ex. Yaws Syphilis of the duration of
the infection.
 Most people with reactive treponemal tests will continue to
have reactive tests for the remainder of their lives,
regardless of treatment or disease activity.
 Treatments
 Penicillin will cure a person that has had
syphilis for less than a year.
 Antibiotics are available as well but over the
counter drugs will not cure syphilis.
 Blood tests should check to make sure the
infection has been eliminated..
 Tertiary syphilis is incurable as it has damaged
body organs.
 Prevention

 Abstinence
 Practicing safer sex by using a condom
before beginning all types of sex (vaginal,
anal, and oral)
 Testing in early pregnancies is the best way to
prevent congenital syphilis.
 See a physician if you suspect you have been
exposed.
 There is a cure to the disease and inexpensive
 CAN SYPHILIS CAUSE OTHER
COMPLICATIONS?
 Syphilis bacteria frequently invade the nervous system during
the early stages of infection.
 3% – 7% of persons with untreated syphilis develop neurosyphilis,
a serious disorder of the nervous system
 May develop 20 years after tie of infection of syphilis
 Some people with neurosyphilis never develop any symptoms
 Others may have headache, stiff neck, and fever that result an
inflammation of the lining of the brain
 Seizures may develop
 People whose blood vessels are affected may develop symptoms
of stroke with numbness, weakness, or visual problems.