2. Introduction
• Definition: invasion of a living tissue by
harmful organisms.
• Routes:
–Exogenous:inhalation, injestion, contact.
–Endogenous: as bacteria normally present
in the body, the infection occurs with low
immunity.
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3. Bacterial infection
• Pathogenesis of tissue injury with bact inf:
– Adhesion To cells causing death.
– Production of toxins.
– Hypersensitivity reaction.
• Effects :
– Cell injury: necrosis & degeneration.
– Inflammation.
– Immunity or hypersensitivity.
– Blood invasion.
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4. Bacteraemia
• Definition: transient invasion of blood with bateria
without significant toxemia.
• Pathogenesis:
– After tooth extraction.
– Dlood spread from septic focus.
– During incubation period (typhoid).
• Effects:
– Rapidly eliminated by immune mechanism (in most)
– Localize in tissues causing lesions (uncommon &
preceded by predisposing factor).
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5. Toxemia
• Definition: circulating bacterial toxins (endo or
exotoxins) in blood causing harmful effect.
• Types:
• Pathological & clinical manifestations:
– Signs & symptoms: fever, rigors, headache, pallor,
weakness.
– Degeneration , necrosis, acute adrenal insufficiency , ARDS
(due to DAD), septic shock & DIC, amyloidosis (chronic),
According to onset According to type of toxin Saparaemia
•Acute toxemia: as acute
abscess, pneumonia & with
septicemia & pyemia.
•Chronic: chronic lung
abscess & TB.
•Endotoxic: as E coli, typhoid.
•Exotoxic: cholera &
diphtheria.
•Special type occurs in
gangrene due to action of
saprophytes on dead tissues.
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6. Septicaemia
• Definition: large number of virulent bacteria circulate &
multiply in blood+ sever toxemia.
• Aetiology:
– Causative organism: cocci, bacilli
– Predesposing factor: low immunity
– Source of infection: septicaemia complicate severe infections or
ordinary infection in low resistant patients.
• Pathological features: (of strept. Haemolyticus)
– Effects of acute toxemia (except amyloidosis & exotoxin effect).
– Vascular & hematological disorder: hemolysis, petechial hrge
– Serous memb.: serofibrinous or suppurative.
– Heart (3 layers), toxic injury of liver & kidney & acute splenic
swelling. 6
7. Pyaemia
• Defintion: development of multible small abscesses within 1 or
> organs caused by circulation of septic emboli derived from
septic thrombi. Fatal.
• mechanism (pathogenesis): start in veins or heart septic
thrombi septic emboli impacted multiple pyemic
abscesses in periphery of the organ
• Types: Pulmonary (lung), systemic, portal (liver abscesses).
• pathological features:
– Distribution.
– Gross:
• multiple, small, most superficially located in the organ, hyperemic walls,
some pus in the centre.
• Surrounding tissue:degeneration (parynchemal organ).
– M/P:PMN, pus cells, debris, macrophages, congested capillaries.
– Manifestations of toxemia.
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10. Tuberculosis (TB)
• Definition: ch. Infectious granulomatous ds.
• Aetiology:
– Causative organism:
• Caused by Mycobacterium tuberculosis (tubercle bacilli) which
are gram +ve acid fast bacilli, best stained with Ziehl-Neelsen
stain.
• 2 types can cause ds in man: human tubercle bacilli & bovine
tubercle bacilli.
• Have outer lipid capsule covering a body composed of
polysaccharides & proteins (tuberculoprotein).
• Pathogenesis: hypersensitivity reaction to tuberculoprotein
(which is highly antigenic), but no toxin production. The
common toxemia with TB due to 2ry bacterial infection. 10
11. Aetiology of TB (cont.):
–Predesposing factor: low natural resistance
due to low standards of nutrition & housing
(low socioeconomic).
–Mode of infection:
• Human TB bacilli:Inhalation, swallowing or skin
contact to contaminated dust from infected
sputum.
• Bovine TB bacilli: Swallowing of infected milk.
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12. Tissue reaction in TB
• Proliferative (the tubercle): basic lesion of TB
– Mode of formation: nutrophils, macrophages that become
epithelioid cells that fuse (Langhan’s giant cells), sensitize T
lymphocytes (aquired imm. In 10-14d) that produce lymphokines
causing macrophage stimulation & promote caseation.
– Gross: tubrcles are microscopic, when fuse give grossly small
yellow grey, soft, cheesy (caseation) nodules.
– M/P: each tubercle: caseation necrosis in the centre surrounded
by epithelioid cells, Langhan’s giant cells & lymphocytes (form a
peripheral zone).
– Michanism of caseation: cytotoxic lymphokines & ischemic
necrosis (no angiogenesis + endarteritis).
– Fate of tubercle:
• localization [(fibrosis+/- dystrophic calcifications) of small or large
(encapsulation, dormant bacilli, reactivation)] or spread acc. To immunity.12
14. Tissue reaction in TB (cont.)
• Exudative:
– In serous membranes.
– In lungs: proliferative or exudative or both.
– Typical exudative reaction in sensitized persons.
– Charecterized by:
• Fluid exudate containing fibrinogen.
• Many lymphocytes & nutrophils (few EC & GC).
• Marked caseation with rapid liqufaction by nutrophils
enzymes.
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15. Spread of TB
• Mechanism: the non motile bacilli carried by
macrophages, tissue fluid, lymph, blood.
• Routes:
– Direct.
– Lymphatic.
– Blood: depends on bacterial number.
• No effects: small number.
• Isolated organ TB: settle in one or few organs.
• Miliary TB: in immunocompromised persons large number in
the blood, so many organs show huge number of small (1-
2mm), adjacent TB lesions.it is rapidly fata.
– intracanalicular: coughed sputum spread it to larynx, tonsils &
tongue. 15
16. Factors influencing the course of
TB
• Dose & virulence of organism.
• Immunity & hypersensitivity:
– Innate immunity is of great importance.
– Degree of acquired immunity & delayed
hypersensitivity mediated by T lymphocytes.
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17. Types of TB
1ry
• Infection for the 1st
time.
• Mainly affect children.
• Spread of infection is common.
• Less marked tissue destruction
• Slow tissue reaction.
• Coarse of infection affected by
innate immunity.
2ry (reinfection or reactivation)
• Infection of sensitized individual.
(previously infected with TB).
• Mainly affects adults.
• Less common (aquired immunity).
• > tissue destruction (hypersensit).
• Accelerated tissue reaction.
• Course is determined by innate,
acquired imm. & hypersensitivity.
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18. Complications of TB
• Spread.
• Hemorrhage.
• Organ destruction & sever fibrosis.
• Amyloidosis (chronic cases).
• Recurrence (reactivation).
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19. syphilis
• Infective disease caused by Treponema pallidum
spirochaetes.
• Aetiology & mode of infection:
– Acquried :
• venereal(most common): by sexual contact.
• Non venereal: touching lesion or blood transfusion.
– Congenital: transplacental transmission.
• Syphilitic tissue reaction (M/P):
– Progressive endarteritis obliterans.
– Chronic proleferative inflammatory reaction (rich in plasma cells & poor in fluid
exudate).
– Granulation tissue & fibrosis.
– Necrosis (mainly gamma of 3ry stage) 19
20. Viral infections
• viruses: smallest organisms, obligate IC agent, with
core & capsid, classified to DNA & RNA viruses.
• Mode of infection: according to type of virus
(inhalation, ingestion, injection, sexual, inoculation,
bites of vectors.
• Clinical forms: asymptomatic, acute, chronic (=/- acute
phase)carrier, oncogenic.
• Michanism of virus-induced cell injury:
– Interference with cellular synthesis of DNA or RNA.
– Cell membrane injury (HIV).
– Cell lysis (influenza).
– Hypersensitivity host reaction (hepatitis). 20
21. • Tissue reaction to viruses:
– Cell changes:
• Viruses infect the cell & form IC inclusion
bodies (cytoplasmic or nuclear).
• Some May infect specific cells or many cell
types.
• Variable tissue reaction:
–No (latent viral infections).
– cell degeneration & necrosis.
–Cell proliferation (papilloma virus).
– Inflammation: lymphocytes & macrophages.
• E.g: hepatitis (A,B,C,D,E), EBV, HIV,HPV, CMV. 21
