Transcript Infectious-Diseases

Infectious Diseases
INFECTION
• Definition:
• Invasion of the body by pathogens and the
development of pathological changes.
Mode of Infection
Exogenous infection:
• From the environment, a patient or a carrier.
• The routes of exogenous infection are:
• (a) Skin and mucous membrane! contact,
• (b) Inhalation,
• (c) Ingestion.
• Endogenous infection:
• By pathogenic bacteria normally present in the body as
streptococcus viridans in the mouth, pneumococci in the
nasopharynx and E. coli in the intestine.
• Infection occurs when the defensive mechanisms of the
body are overcome.
Host Barriers to Infection
• The outcome of infection is determined by the ability of the
microbe to infect, colonize, and damage host tissues and
the ability of host defense mechanisms to eradicate the
infection.
• Host barriers to infection prevent microbes from entering the
body and consist of :
• Innate immune defense mechanisms .
• Adaptive immune responses
Effects of Infection:
• Inflammation.
• Toxaemia.
• Blood invasion by bacteria (bacteraemia,
septicaemia and pyaemia).
• Immunity and hypersensitivity.
TOXAEMIA
• Definition: Circulation of bacterial toxins in the
blood causing pathological and clinical
manifestations. Bacterial toxins are of two types:
• Exotoxins: Produced by gram positive bacteria as
diphtheria bacilli and some types of streptococci.
• Endotoxins: Released from the bodies of dead
gram negative bacteria as typhoid bacilli.
• Types:
• Acute toxaemia: Occurs in acute infections as
diphtheria.
• Chronic toxaemia: Occurs in chronic infections as
tuberculosis.
TOXAEMIA
• Manifestations of Toxaemia:
• Constitutional signs and symptoms:
Fever, rigor, headache, weakness and increased rate of
tissue metabolism.
• Degeneration:
Mainly in the heart, kidney and liver in the form of
cell swelling and fatty change.
Severe toxaemia causes acute heart failure.
Chronic toxaemia may cause amyloidosis.
• Necrosis and haemorrhage of the adrenal cortex: May
be fatal due to acute adrenal cortical insufficiency.
• Anaemia: Due to bone marrow depression by the
toxins.
BACTERAEMIA
• Definition:
• Transient presence of small number of bacteria
in the blood stream without toxic manifestations.
• Pathogenesis: Bacteria enter the blood stream
from a septic focus in the body e.g. tonsillitis,
sinusitis, cholecystitis, salpingitis ... etc.
• A common example of bacteraemia is that
occurring after tooth extraction.
SEPTICAEMIA
• Definition:
• The circulation and multiplication of large number
of virulent bacteria and their toxins in the blood
stream. The condition is highly fatal.
• Causative organisms:
• The commonest is streptococcus haemolyticus.
• Sources: Important sources are infected, septic
wounds, puerperal sepsis and acute osteomyelitis.
SEPTICAEMIA
Pathology of Streptococcus Haemolyticus Septicaemia:
(1) Red cell haemolysis by haemolysin causing anaemia
and red staining of the intima of the vessels by the
liberated haemoglobin
(2) Petechial haemorrhage in the skin, mucous and serous
membranes due to capillary destruction by the
streptococcal toxins
(3) Cloudy swelling, fatty change and focal necrosis in the
heart, liver and kidney
(4) Serofibrinous or suppurative inflammation in the serous
sacs
(5) Acute splenic swelling
PYAEMIA
• Definition: Pyaemia is the circulation of septic
emboli in the blood. Pyaemia has a high
mortality rate.
• Pathogenesis: When a septic focus involves a
vein, fragments from the septic thrombus
circulate in the blood stream as septic emboli.
• Next the septic emboli get impacted in the small
vessels of different organs producing multiple
small pyaemic abscesses.
PYAEMIA
• Types:
1) Systemic pyaemia: The septic emboli circulate in the
systemic venous blood. They are derived from acute
osteomyelitis, puerperal sepsis, suppurative otitis media,
cellulitis and acute bacterial endocarditis. They get
arrested in the lung forming multiple pyaemic abscesses.
Smaller emboli from the lung reach the kidney, liver,
brain ... etc.
2) Portal pyaemia: The septic emboli circulate in the portal
venous blood. They are derived from acute suppurative
appendicitis, infected piles, acute cholecystitis,
diverticulitis and septic lesions in the colon. The emboli
get arrested in the liver forming multiple pyaemic
abscesses
Bacterial, Fungal &
Parasitic Infection
Tuberculosis
Syphilis
Leprosy
Actinomycosis
Mycetoma
Schistosomiasis
TUBERCULOSIS
Definition:
Chronic infective granuloma caused by tubercle bacilli
Causative organism:
• Two types of bacilli infect man: Human and Bovine
• Its growth is strict aerobic and inhibited by acidic ph
• It has no known exotoxins, endotoxins or histolytic
enzymes
• It consists of complex lipid, carbohydrate around
tuberculoprotein
• The bacteria is non-motile and are carried by
macrophages to spread by various methods
TUBERCULOSIS
Methods of infection:
• Inhalation: is the commonest method
• The human bacilli are inhaled in coughed droplets or
dust contaminated with sputum from a case with opened
TB
• The inhaled bacilli infect the tonsils or the lung
• Most infections are acquired by sustained exposure
rather than casual contact
• Ingestion: of raw milk contaminated with bovine or human
bacilli. They infect the tonsils or intestine
• Skin inoculation: by handling infected material. This
method is not common
PATHOGENESIS
• The pathogenesis of tuberculosis in the
previously unexposed immunocompetent
individual is centred on the development of cellmediated immunity associated with tissue
hypersensitivity to tubercular antigens
• The pathologic features of tuberculosis, such as
caseating granulomas and cavitation, are the
result of the destructive tissue hypersensitivity
PATHOGENESIS
• The sequence of events from inhalation of bacteria to
formation of the primary focus is as follow:
• The earliest phase of primary tuberculosis (<3 weeks) in
the nonsensitized individual is characterized by
unchecked bacillary proliferation within the pulmonary
alveolar macrophages and airspaces, with resulting
bacteremia and seeding of multiple sites
• • The development of cell-mediated immunity occurs (> 3
weeks after exposure. Processed mycobacterial
antigens are presented to T lymphocytes, resulting in
macrophage activation, monocytes recruitment &
granuloma formation
PATHOGENESIS
TISSUE REACTION IN
TUBERCULOSIS
I - Proliferative tissue reaction
Composed mainly of inflammatory cells
II – Exudative tissue reaction
Having excess inflammatory fluid exudate
TUBERCLE
Definition:
• Is the unit of proliferative
tissue reaction
• Composed of a compact
collection of
 Epithelioid cells
 Langhan’s giant cells
 Lymphocytes
Microscopic Picture of Tubercles
1-Epithelioid cells:
With abundant pale red
cytoplasm, indistinct cell borders
and round or oval vesicular nuclei
2- Langhan’s giant cells
3- Lymphocytes
4- Central caseation
TB bacilli inside epithelioid cells
Tuberculosis
Clinical patterns
• Primary type: occurring in individuals following the
initial infection, this type is called childhood type, as
it is frequent in children leading to formation of
primary complex
• Post primary (secondary type): tend to be more
chronic and slowly progressive. It is associated with
significant (although inadequate) resistance
Primary Tuberculosis
Primary complex
Sites:
• Tonsil
• Lung
• Intestine
• Skin
Primary Pulmonary Complex
• Ghon’s Focus
Under the pleura,
small in size (1cm)
with late caseation
• Tuberculous lymphangitis
• Tuberculous lymphadenitis
Fate of Primary Complex
I- Healing
- Fibrosis & calcification
- Very small foci
- Bacilli may persist for life
II- Spread: low immunity
1- Direct: focus enlarges and gives new lesions with
extensive caseation
2- Haematogenous
 Small No of bacilli
 Moderate number of bacilli
 Large number of bacilli
Miliary TB
3- Bronchial spread
III- Encapsulation and reactivation
Secondary Tuberculosis
• This type of tuberculosis arises in a previously sensitized
individual, whether the TB bacilli are derived from
endogenous or exogenous sources
• Most cases of secondary TB represent reactivation of
asymptomatic primary disease
• The reactivation is the result of shift in the balance
between host and organism due to such factors as
reduced immunity, poor nutritional status, alcoholism or
advanced age
Secondary Pulmonary Tuberculosis
Apical lesion
• Are almost always near the apex of
the lung at sites of high oxygen
tension (where the bacilli had
localized at the time of original
bacillemia)
•
The minimal lesion at the apex
consists of 1-3 cm focal area of
caseous consolidation, usually within
1 -2cm from pleural surface
TB cavities with caseation
Secondary Pulmonary Tuberculosis
Course of Apical lesion
a) Healing, scarring and calcification giving fibrocalcific 'arrested‘
tuberculosis
b) Progressive local spread:
Fibrocaseous foci may undergo softening and erode through airways
and emptying of this soft material into the bronchus (open case)
leaving a cavity lined by caseous material and surrounded by fibrous
tissue (Chronic fibrocaseous T.B)
Retrograde spread of caseous material through the distal airways
produce small caseating (acinar lesions) mainly at the base of the
lung. These lesions subsequently fuse into larger lesion
Chronic firocaseous TB
Secondary Pulmonary Tuberculosis
Course of Apical lesion
c) Tuberculous pneumonia: In the highly susceptible,
highly sensitized individual, the tuberculous infection
may spread rapidly throughout large areas of lung
parenchyma and produce a diffuse bronchopneumonia,
or lobar exudative consolidation
d) Further local contiguous dissemination:
– To the pleural space (tuberculous empyema) or,
– Spread along contiguous passages
(tracheobronchial) to the larynx - then to intesine
Isolated Organ Tuberculosis
• Reactivation of bacilli that
had widely distributed at the
time of bacteraemia, but
undergoes proliferation in
only one area, meninges,
kidney, adrenal, cervical
lymph nodes, bone with
subsequent local extension
((eg.. TB nephritis —>
cystitis and salpingitis or
epididymitis)
Pott’s disease
Miliary Tuberculosis
• With very low body resistance lesions may
spread into lymphatics and blood vessels—->
then wide dissemination
• The distribution of miliary lesions depends on
the pathways of dissemination
• Favored targets for miliary seeding are the bone
marrow, liver, spleen, and retina
Miliary tuberculosis
Miliary tuberculosis
Schistomiasis
Schistomiasis ( Bilharziases)
Definition
Chronic granuloma caused by schistosomal
infection
Three species are present:
1.Schistosoma Haematobium
2.Schistosoma Mansoni
3.Schistosoma Japonicum
Life Cycle of Schistomiasis
Schistosomal Lesions
• Cercaria:
Cause acute dermatitis
• Adult worms:
o Living worms: ingest blood and excrete
brown bilharzial pigment
o Dead worms: cause severe allergic
inflammation with necrosis and
eosinophilic infiltrate
Schistosomal Lesions
• Ova:
Produce granulomatous reaction formed of:
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Macrophages
Lymphocytes
Plasma cells
Eosinophils
Few giant cells
Fresh or calcified bilharzial ova
Intestinal Bilharziasis
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Pathological features
Mild Infection: Petechial haemorrhage,
Bilharzial granulomas in submucosa
• Severe prolonged infection:
In addition to bilharzial granulomas the
following lesions develop
1. Sandy patches
2. Bilharzial ulcer
3. Bilharzial polyps
Bilharzial polyp
Multiple bilharzial polyps
Bilharziasis of the Liver
• Common disease, secondary to closed
intestinal bilharziasis
• Emboli of the ova and dead worms reach the
liver by portal blood
• Types:
1. Fine B portal fibrosis
2. Coarse B portal fibrosis
3. Mixed type
• Complications
Portal hypertension
Effects:
1. Splenomegaly
2. Opening of porto-systemic
anastomosis
Oesophageal varices
Piles
Caput medusa
3. Ascites
Complication of
Portal
hypertension
Oesophageal varices
Splenomegaly
Ascites
Caput Medusae
Urinary Bladder Bilharziasis
• Pathological Features:
1- Sandy patches
2- Bilharzial polyps
3- Bilharzial ulcers
4- Epithelial changes
a- Hyperplasia
b- Brunn’s nests
c- Cystitis cystica d- Cystitis glandularis
e- Squamous metaplasia
Actinomycosis
ACTINOMYCOSIS
• Chronic infective suppurative granuloma
caused by an anaerobic Gram-positive
bacterium “actinomyces Israel”.
• The infection may be endogenous as the
organism is a normal saprophyte of the mouth,
tonsils, carious teeth and intestinal tract
• Previously thought to be a fungal infection, but
these organisms are actually gram-positive,
filamentous bacteria
ACTINOMYCOSIS
• Actinomycosis is a chronic disease
characterized by the production of suppurative
abscesses or granulomas that eventually
develop draining sinuses.
• These lesions discharge pus containing the
organisms.
• The organisms are found in firm, yellowish
granules called sulfur granule
ACTINOMYCOSIS
• The disease is divided into three major clinical
types:
1.Cervicofacial
2.Thoracic
3.Abdominal
• But primary infections may involve almost any
organ.
Cervicofascial Actinomycosis
Mycetoma Pedis
Mycetoma Pedis ( Nocardiosis)
Chronic infective
suppurative
granuloma, affects mainly
the foot, caused by free living
saprophytes called Nocardia
Pathological features
Gross:
Multiple sinuses discharging
pus containing the fungal
colonies
Madura foot
( Mycetoma)
Syphilis
Syphilis
• Definition: Infective granuloma caused by a
spirochete called Tropenema pallidum
Mode of Mode of Infection:
1. Direct contact of the body with a source of
infection, commonly during sexual
intercourse. The spirochaetes can penetrate
the intact skin or mucous membrane.
2. Congenital infection of the foetus from the
mother through the placenta
Syphilis
Lesions in Syphilis
 Primary Stage: Chancre
 Secondary stage:
 Tertiary
stage:
 Skin rash
 Gumma
 Mucous patches
 Condyloma latum
 Generalized lymphadenopathy
 Diffuse syphilitic
reaction
Tissue Reaction in Syphilis
Chronic inflammatory reaction formed of
Perivascular infiltrate of:
• Plasma cells
• Lymphocytes
• Few small giant cells
• Blood vessels show endarteritis obliterans
• II. Secondary Stage:
(2) Mucous Patches: Occur in
the mouth, pharynx, vagina, cervix
and anal canal. They are round or
oval slightly raised above the
surface, covered by whitish or
greyish membrane and surrounded
by a red border Some of these
lesions may ulcerate. The resulting
small ulcers may coalesce together
and form a snail tract ulcer.
(3) Generalized lymphadenitis:
Specially the epitrochlear and
posterior cervical. Microscopically
their changes are the same as the
node draining the primary stage.
Splenic enlargement
Mucous patches
Alopecia
III. Tertiary Stage:
• Secondary lesions also heal spontaneously and the disease pass
into a latent phase that may extend for years (2-10 years) until
tertiary lesions develop which are of two types:
(l)Gumma: Localized area of syphilitic granulation tissue which
undergoes slow caseation necrosis. Gumma affects any organ, but
the common sites are the liver, meninges, bone, tongue, testis, heart
and lung.
• Gross picture: Gumma may be solitary or multiple, variable in size
and rubbery in consistency. The cut surface is greyish yellow with
greyish white fibrosis in the periphery.
• Fate:
• (a) Gumma in solid organs as the liver is gradually replaced by
fibrous tissue which contracts and distorts the shape of the organ.
• (b) Gumma near the surface as in the subcutaneous tissue or
tongue ulcerates. The gummatous ulcer is serpiginous in shape. The
edge is deep and punched out (sharp). The floor is greyish yellow
and caseous. The base is firm
Tertiary syphilis
Gumma of nose & palate
Ulcerative gumma of hand
Gumma of skull
III. Tertiary Stage
(2) Diffuse syphilitic inflammation: This type of lesion is
more common than gumma. It is a diffuse syphilitic reaction
with minimal areas of caseation (microscopic gummata)
which develop very slowly. Replacement fibrosis occurs in
the usual way. The affected organ is firm and its cut surface
is greyish white. The lesion occurs in the larynx, aorta,
testis, bone and meninges.
Tertiary Syphilis of Cardiovascular System
I. Syphilis of The Heart:(1) Gumma
in the septum
(2) Diffuse syphilitic myocarditis and
pericarditis.
II- Syphilitic Arteritis: (End arteritis
obliterans)
III- Syphilitic Aortitis: affects the ascending
syphilitic aortitis
(Coronary ostea stenosis)
thoracic aorta because of its rich lymphatics
(1)Aortic Incompetence
(2)Aortic Aneurysm
(3)Stenosis of Coronary Orifices
syphilitic aneurysm
Congenital Syphilis
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The untreated syphilitic mother is very liable to transmit the
disease to her foetus after the fourth month of pregnancy,
when the Langhan’s layer of the placenta disappears.
Abortion may result, or else a severely affected infant may
die soon after birth. More frequently the child survives and
he may develop syphilitic lesions early or late in life.
Pathological Lesions:
Placenta: Pale, enlarged, heavy and firm. Spirochaetes are
present in large numbers.
Early Manifestations of Congenital Syphilis: Appear
soon after birth or within two years. They are similar to
secondary syphilitic lesions
Late Manifestations of Congenital Syphilis: The patient
develops
syphilitic lesions within 2-30 years
congenital syphilis
Hutchinson teeth
Hepar lobatum
perforated palate
Leprosy
LEPROSY
(HANSEN’S DISEASE)
• Leprosy is an ancient disease characterized by a long
incubation period and a unique predilection for skin and nerves
in the cooler parts of the body.
• It is a slowly progressive mycobacterial infection caused by
Mycobacterium leprae which is an obligate intracellular acid
fast bacteria.
Mode of infection:
• Human-to-human transmission is the usual cause of
transimission, but requiring “prolonged and intimate contact.”
• The organisms enter through or mucous membranes of nose
and respiratory tract.
• The incubation period is 5-10 years
LEPROSY
(HANSEN’S DISEASE)
• Types
• There is wide spectrum of the disease depend on the
competent of host immune response to the organisms.
1- Tuberculoid leprosy (TL):
Patients with (TL) have partial T-lymphocyte immunity.
2- Lepromatous leprosy (LL).
Patients with LL have little or no T-lymphocyte immunity to
M. leprae.
3- Brderline: between the two polar types of the disease with
variable degrees of host immunity & resistence
LEPROSY
(HANSEN’S DISEASE)
• Tuberculoid leprosy (TL):
• The classic early skin lesion is an anesthetic asymetrical plaque with
erythematous borders.
• Nerve involvement is dominant. The nerves are enclosed in granulomatous
reaction with damage of nerves (mainly sensory nerves with trophic changes)
LEPROSY
(HANSEN’S DISEASE)
Lepromatous leprosy (LL).
• Symmetric skin nodules, plaques, and dermal thickening.
• “leonine facies” (coarsening of the facial features due to
massive infiltration of
• the dermis by M. leprae).
• Nasal lesions: nodules causing ulceration & nasal obstruction.
• Peripheral nerve involvement The nerves become enlarged,
and the anesthesia
• results in severe ulcerations and loss of tissue ( Trophic
lesions).
• Hypergammaglobulinemia and secondary amyloidosis.
Lepromatous leprosy (LL).
leonine facies
Lepromatous leprosy (LL).
Skin nodules
LEPROSY
(HANSEN’S DISEASE)
Peripheral nerve involvement dominates the clinical features of both types of
leprosy. The nerves become enlarged, and the anesthesia results in severe
ulcerations and loss of tissue
•
(Trophic Lesions).
CANDIDIASIS (MONILIASIS)
• Definition:
• Infection by the fungus monilia albicans.
• Mode of Infection: The fungus is found in the mouth,
intestine and vagina of healthy persons.
• Candidiasis is seen in newborns, debilitated patients,
children receiving oral corticosteroids for asthma, and
after a course of broad-spectrum antibiotics that
destroy competing normal bacterial flora.
• The other major risk group includes HIV-positive
patients
CANDIDIASIS (MONILIASIS)
• Pathology:
• Mucous membranes: The mucosa is hyperaemic
and shows small white patches which could be rubbed off.
• The patches consists of the fungus filaments and necrotic
surface epithelial cells.
• The lesion in the oral cavity is called thrush.
• Skin: Cutaneous candidiasis can present in many different forms, including
infection of the nail proper (onychomycosis), nail folds (paronychia), hair
follicles (folliculitis), moist, intertriginous skin such as armpits or webs of the
fingers and toes (intertrigo), and penile skin (balanitis).
• Candida Vaginitis is an extremely common form of vaginal infection in women,
especially those who are diabetic or pregnant or on oral contraceptive pills.
• It is usually associated with intense itching and a thick, curd-like discharge.
• "Diaper rash" is a cutaneous candidial infection seen in the perineum of infants,
in the region of contact of wet diapers.
CANDIDIASIS (MONILIASIS)
• Pathology:
• Visceral Candidiasis: is common in AIDS patients and in those with
hematolymphoid malignancies
• Lung lesions in the form of tiny yellow nodules. The lesion is a necrotic
focus with inflammatory cellular infiltrate around.
• Candida Esophagitis. These patients present with dysphagia (painful
swallowing) and retrosternal pain; endoscopy demonstrates white plaques
and pseudomembranes resembling oral thrush on the esophageal mucosa.
• Invasive (disseminated) Candidiasis, implies bloodbome dissemination of
organisms to various tissues or organs.
• Common patterns include (1) renal abscesses, (2) myocardial abscesses and
endocarditis, (3) brain involvement (most commonly meningitis, but
parenchymal microabscesses occur), (4) endophthalmitis , (5) hepatic
abscesses, and (6) Candida pneumonia
Hydatid Disease
The disease is caused by development of the larval stage
of Echinococcus granulosus in man
Pathologial Features:
In any organ ( e.g liver or lung) the
embryo becomes
distended by clear fluid forming
Hydatid cyst:
• The wall of the cyst is formed is
formed of inner germinal layer and
outer cuticular layer
• From the germinal layer, new cysts
may originate
• The cysts are surrounded by
macrophages, eosinophils, giant
cells and fibrosis
Hydatid cyst of brain