This document discusses various types of bacterial and viral infections. It defines key terms like infection, bacteraemia, toxemia, septicaemia, pyaemia, and chronic bacterial infections. It also summarizes the pathogenesis, effects, and clinical manifestations of these conditions. Tuberculosis and syphilis are discussed in further detail regarding their causative organisms, modes of transmission, tissue reactions, and complications. Viral infections are also briefly introduced.

1. infection
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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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8. 8

9. Chronic bacterial infections
• Non specific
• specific granulomatous (TB,
leprosy, syphilis &
actinomycosis).
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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

13. 13

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