1. Professor of Pathology Faculty of Medicine Ain Shams University
Dr. Riham Abu-Zeid
Professor of Pathology
Faculty of Medicine
Ain Shams University
Inflammation 6

2. Toxemia
Septicemia
Bacterial infection
of blood
Bacteremia
Pyemia

3. Effects and complications: Fever, headache, rigors ,pain
1-Toxemia:
A-Acute Toxemia
presence of bacterial toxins in blood.
typhoid fever, diphtheria, pneumonia ,bacillary dysentery
Effects and complications:
Fever, headache, rigors ,pain
Fatty change of parenchymatous organs.
Toxic myocarditis >> acute heart failure.
necrosis of the liver.
Necrosis of suprarenal cortex > acute adrenal insufficiency and death.
Bilateral tubular necrosis of the kidney > acute renal failure.
Endotoxic (septic) shock.
pain allover the body.
necrosis of the liver.
Necrosis of suprarenal cortex > acute adrenal insufficiency and death.
Bilateral tubular necrosis of the kidney > acute renal failure.
Endotoxic (septic) shock.

4. Endotoxic (septic) shock
Acute Toxemia
Myocarditis
AHF
Bil. TN & ARF
acute adrenal insufficiency
Liver
Necrosis
Endotoxic (septic) shock
Fever
Toxins produced by pathogens cause an immune response; in gram-negative bacteria these are endotoxins, which are bacterial membrane lipopolysaccharides
At high levels of LPS, the syndrome of septic shock supervenes; the same cytokine and secondary mediators, (TNF )now at high levels, result in systemic 1-vasodilation (hypotension), 2-diminished myocardial contractility, widespread 3-endothelial injury and activation, causing systemic leukocyte adhesion and diffuse alveolar capillary damage in the lung 4-activation of the coagulation system, culminating in disseminated intravascular coagulation (DIC).
The hypoperfusion from the combined effects of widespread vasodilation, myocardial pump failure, and DIC causes multiorgan system failure that affects the liver, kidneys, and central nervous system, among others.  Unless the underlying infection (and LPS overload) is rapidly brought under control, the patient usually dies.
TN :tubular necrosis
ARF:Acute renal failure

5. Loss of weight and prolonged low grade fever.
B-Chronic toxaemia as in TB
Effects and complications:
Loss of weight and prolonged low grade fever.
Amyloidosis.
Normocytic anemia due to bone marrow depression.

6. 2-Bacteremia presence of small number of bacteria in the blood which
do not multiply significantly
commonly not detected by direct microscopy.
Blood culture is done for their detection
e.g. infection with Salmonella typhi,
Streptococcus viridians and Escherichia coli.

7. presence of rapidly multiplying
3-Septicemia
presence of rapidly multiplying
highly pathogenic bacteria in the blood.
Causative organisms:
Pyogenic cocci
Bacilli of plague… etc.
N.B
It is a very serious condition with
severe toxemia and shock.
An Atypical Inflammatory Reaction
In a typical inflammatory reaction, the local pro-inflammatory processes are balanced by systemic anti-inflammatory processes and are automatically terminated within a short time. In sepsis, however, cytokine production continues unending and the circulatory spread of the cytokines then causes increased cytokine production at distant sites
Endotoxin is a lipopolysaccharide in the cell wall of Gram-negative bacteria. When it gets into the circulation, endotoxin strongly activates the coagulation and complement systems throughout the body.
Endothelial Damage
a normal inflammatory reaction activates local endothelial cells but it also damages those same cells. Sepsis multiplies this effect by activating and damaging endothelial cells in patches throughout the entire vascular tree.
In sepsis there are many places in the body where the barrier between the bloodstream and the surrounding tissues has become leaky and crowded with immune cells
The damaged endothelial surface inhibits anticoagulant properties as well as increases antifibrinolysis, which can lead to intravascular clotting, the formation of blood clots in small blood vessels, and multiple organ failure 
Organ Damage
Sepsis can evolve to multiple organ dysfunction syndrome (MODS), An organ with significant damage to its vascular endothelium ends up poorly perfused and ischemic. Such an organ will function poorly (organ dysfunction) or it will fail altogether.
Progression to Shock
Severe sepsis occurs when organ dysfunction progresses to organ failure. If arteries fail to constrict,dt excessive production of chemicals that dilate blood vessels such as nitric oxide, a deficiency of chemicals that constrict blood vessels such as vasopressin, and activation of ATP-sensitive potassium channels.septic shock occurs.

8. Pathological features(postmortum);
3-Septicemia
Pathological features(postmortum);
Petechial hemorrhages.
Massive adrenal hges & DIC
Acute bacterial endocarditis
Acute splenic swelling.
Petechial haemorrhages allover the body.(leaky blood vessels)
Acute bacterial endocarditis
if streptococci invade cusps of valves

9. 3-Septicemia Acute splenic swelling. Normal spleen Gross enlarged,
soft with semifluid cut surface
that can be washed by tap water.
Microscopically
lymphoid follicles are atrophied,
sinusoids are congested &
contain acute & chronic
inflammatory
cells.
spleen is moderately enlarged,
very soft with semifluid cut surface
that can be washed by tap water.
Normal spleen

10. Characters of pyemic abscess; are multiple small abscesses
bacteria
Trombus
4-Pyemia
Dissemination of small septic emboli in the blood resulting in pyemic abscesses at the sites where they are lodged
Characters of pyemic abscess;
are multiple small abscesses
nearly of the same size
surrounded by zone of congestion. .
Inflamed (stasis +endoth inj )…>>thrombi +infection ..arteries give branches of arterioles >arrest of thrombi necrosis dt cut of supply necrosis with superdeed bacteria begin abscess as usual

12. Systemic Pyemia Portal To liver Into arterial side To lung
eg.GIT
To liver
Into venous side
Into arterial side
eg.left side of heart
lung
Live\ may be involved in both portal and systemic (arterial) pyemia
NB internal hemorroides drain into porta>>portal pyemia
External hemooroides drain to systemic veins go to lung
To lung
To brain, liver, kidney, spleen

13. when septic emboli are carried by systemic circulation
Types of pyemia
Systemic pyemia
Portal pyemia
when septic emboli are carried by systemic circulation
when septic emboli are carried by portal circulation
Acute hematogenous osteomyelitis.
Puerpural sepsis
Suppurative otitis media
Suppurative lung disease e.g. abscess (emboli arising from lung veins).
Acute bacterial endocarditis
Acute suppurative appendicitis.
Infected internal piles
Suppuration of gall bladder and large intestine.

14. venous side (a, b & c) >>pyemic abscesses in LUNG.
Types of pyemia (cont )
Systemic pyemia
Portal pyemia
Emboli arising from
venous side (a, b & c) >>pyemic abscesses
in LUNG.
-Emboli in general arterial circulation(d& e) producing pyemic abscesses in brain, liver, kidney, spleen, skin, intestine… etc.,
Emboli arrested in LIVER,
producing multiple abscesses

15. Toxins in blood Bacteremia Toxemia Septicemia
Not detected in blood –needs blood culture
Toxins in blood
Rapidly multiplying highly pathogenic bacteria
Moving
Infected thrombus
Bacteremia
Toxemia
Pyemia
Septicemia

16. Exudate Transudate Inflammatory cause
alteration in normal vascular permeability.
Transudate
Diminished colloid osmotic pressure in the plasma.
Increased hydrostatic pressure across the vessel wall
No or minmal increase in vascular permeability.
alteration in normal vascular permeability in the area of injury.