 Infection vs Disease ( so we thought that infection and disease are the same however,

infection is the process specifically, the start; where the pathogen enters the host. The
disease is the end product of it.)
o progression from a pathogen entering a host (infection) to its multiplication within
the host and the resulting damage causing disease. The infection stage can be
asymptomatic or symptomatic, meaning the host may not experience any
symptoms initially.

 Key Concepts/Tips:

1. Infection←The invasion and multiplication of a pathogen in a host.

2. Disease←A condition of impaired health caused by infection or other factors.
3. Asymptomatic↔Showing no symptoms of disease despite the presence of
infection.
4. Symptomatic↔Showing symptoms of disease.
5. Not all infections lead to disease; the host's immune system can often successfully
combat infections before they cause illness


 Infectious disease←It applies when an interaction with a microbe causes damage to the
host and the associated damage or altered physiology results in clinical signs or
symptoms of the host resulting from infection.

 SIGNS
 AND SYMPTOMS??
o Signs←are objective changes such as rash or fever that a physician can
o observe.
o Symptoms←are subjective changes in the body functions such as pain or loss
o of appetite that are experienced by the patient.

 TYPES OF HOST

1. Obligate Host←A host that is absolutely required for a parasite's survival and
reproduction.
 Viruses are obligate parasites that require the metabolic capabilities of a
host to replicate their DNA or RNA and to produce “infectious” viral
particles that can restore and maintain their life cycle.
 CLINICAL ISSUES •

3. Plasmodium vivax←Most widespread human malaria; 2.5 billion people

worldwide at risk of infection
4. Strongyloidiasis←>100 million persons with chronic infection worldwide;
severe infection may occur in immunosuppressed individuals
5. Filarial parasites←8 species infect > 150 million people in tropical and
subtropical regions
 6. Hookworm (Ancylostoma duodenale)←~ 25% of world’s population
infected
7. Schistosomiasis←200 million people infected, 120 million symptomatic,
20 million have severe disease
8. Echinococcus granulosus←Usual cause of human hydatidosis

2. Primary Host/Definitive host←The host in which a parasite reaches sexual

maturity and reproduces.
 For trypanosomes, the cause of sleeping sickness, humans are the primary
host, while the tsetse fly is the secondary host.
3. Secondary Host/ intermediate host←A host that harbors a parasite for a period,
but is not essential for the parasite's life cycle.
4. Transport Host←A host that carries a parasite without being infected itself,
acting as a vector to transmit the parasite to another host.
 Filariasis←is a disease caused by parasitic worms that are spread by
mosquitoes


 CHAIN OF INFECTION

1. Portal of Entry←The infectious agent enters a susceptible host through this

2. Susceptible Host←this is necessary for the infectious agent to establish itself and
potentially cause disease.
 Infection does {{3265111580680409::not occur automatically}} when the
pathogen enters the body of a person whose immune system is functioning
normally. When a virulent pathogen enters an immune-compromised
person, however, infection generally follows.
 Whether exposure to a pathogen results in infection depends on several
factors related to the person exposed (the host), the pathogen (the agent),
and the environment. Host factors that influence the outcome of an
exposure include the presence or absence of natural barriers, the functional
state of the immune system, and the presence or absence of an invasive
device.
3. Infectious Agent←include not only bacteria but also viruses, fungi, and parasites.
 The virulence of these pathogens depends on their
{{8516806624400115::number, their potency, their ability to enter and
survive in the body, and the susceptibility of the host.}}
 For example, the {{14502585270433044::smallpox virus}} is particularly
virulent, infecting almost all people exposed. In contrast, the
{{1828704595079056::tuberculosis bacillus}} infects only a small
number of people, usually people with weakened immune function, or
those who are undernourished and living in crowded conditions.
 Viruses are {{3844112832464943::intracellular}} parasites; Some
viruses, such as HIV and hepatitis B and C, have the ability to enter and
survive in the body for {{7870868257348254::years}} before symptoms
of disease occur.
  Other viruses, such as{{956140165852899:: influenza and COVID-19}},
quickly announce their presence through characteristic symptoms.
 Intracellular parasites←that is, they can only reproduce inside a living
cell.
4. Reservoir (potential)←is any person, animal, arthropod, plant, soil or substance
(or combination of these) in which an infectious agent normally lives and
multiplies. The infectious agent depends on the reservoir for survival, where it can
reproduce itself in such manner that it can be transmitted to a susceptible host.
5. Portal of Exit←is the means by which a pathogen exits from a reservoir.
 For a human reservoir, the portal of exit can include→blood, respiratory
secretions, and anything exiting from the gastrointestinal or urinary tracts.
 Large droplets←settle faster than they evaporate and contaminate
surrounding surfaces.
 Smaller droplets← evaporate faster than they settle, forming droplet
nuclei that can stay airborne for hours (becoming aerosolized) and
may be transported over long distances
6. Mode of Transmission←The infectious agent is transmitted to another potential
host (e.g., airborne droplets, direct contact, vectors).
 Direct vs Indirect Contact
 DIRECT CONTACT
 SARS-CoV-2, the virus that causes COVID-19, spreads
primarily through airborne transmission. People release
virus-carrying respiratory droplets of varying sizes when
they breathe, talk, cough, or sneeze. Larger droplets fall
quickly, but smaller droplets and aerosol particles can
remain suspended in the air for hours, allowing for
transmission over distances greater than six feet, especially
in poorly ventilated indoor spaces. Studies show the virus
can be detected in air and on surfaces in rooms occupied by
infected individuals, even those with mild symptoms. Good
ventilation is crucial in reducing airborne transmission.
 INDIRECT CONTACT
 transmission happens when a pathogen is transferred from a
reservoir to a host via an intermediary. This can be:

2. Vehicle-borne←An inanimate object (e.g., contaminated

food, utensils, surfaces) carries the pathogen.
3. Vector-borne←A living organism (e.g., mosquito, rodent)
carries the pathogen and transmits it through bites, feces, or
other means.


 FACTORS INFLUENCING THE OCCURENCE OF INFECTION
o PORTAL OF ENTRY
o PORTAL OF EXIT
o VIRULENCE OF ORGANISM←extent /degree of pathogenicity
o INFECTIVE DOSE←refers to the minimum number of organisms required to
cause an infection in a host. It can vary based on factors such as the type of
pathogen, host defenses, and immune status
o DEFENSIVE POWERS OF THE HOST
 Gut bacteria protect against intestinal infections in three main ways
 They take up space and resources, preventing harmful bacteria
from settling in.
 They boost the body's natural defenses by increasing mucus
production, antibodies (IgA), and antimicrobial substances
(AMPs).
 They trigger immune responses that strengthen the gut lining and
attract immune cells to fight infection.
 Antibodies←are useful tools for detecting and measuring germs like
viruses, bacteria, fungi, or parasites. They can be obtained from patients
who have recovered from infections or created in animals.
 There are two types of antibodies
 Polyclonal antibodies←These come from various sources
and can recognize many parts (epitopes) of a single germ.

2. Monoclonal antibodies←These are made to target a

specific part of a germ. They are produced by fusing
immune cells from an immunized mouse with cancer cells,
creating a hybridoma that produces one type of antibody.

o PRESENCE OF VECTORS/ CARRIER

o RESERVOIR
o HYGIENE
o MALNUTRITION
o SMOKING AND ALCOHOLISM
 Smoking
 Damaged Respiratory System: Smoking directly damages the
delicate lining of the respiratory system, including the lungs,
airways, and cilia (tiny hair-like structures that sweep out foreign
particles). This damage makes it easier for germs to enter the body
and harder for the body to clear them
 Weakened Immune System: Smoking impairs the immune
system's ability to fight off infections. It reduces the production of
antibodies and weakens white blood cells, making the body more
vulnerable to pathogens
 Increased Inflammation: Smoking causes chronic inflammation
in the lungs and airways, making them more susceptible to
infection

2. Alcoholism
 Impaired Immune Function: Alcoholism weakens the immune
system by suppressing the production and activity of immune cells,
 including white blood cells. This makes it harder for the body to
fight off infections
 Gut Microbiome Disruption: Alcohol consumption can disrupt
the balance of beneficial bacteria in the gut, which plays a crucial
role in immune function. This can lead to increased susceptibility
to infections
 Increased Inflammation: Alcohol can exacerbate inflammation
throughout the body, making it easier for infections to take hold
and spread

o PREGNANCY
o EDUCATIONAL BACKGROUND
o CULTURE

 Portal of Entry
o Mouth (Oral)
o Anus
o Ears
o Nose
o Eyes
o Intact
o skin
o Open
o wound
o Percutaneous
o bites
o Vaginal
o opening
o Urinary
o orifice (urethral meatus)

 Portal of Exit
o Mouth (Oral)
o Anus
o Ears
o Nose
o Eyes
o Intact
o skin
o Open
o wound
o Percutaneous
o bites
o Vaginal
o opening
o Urinary
 o orifice (urethral meatus)

 types of infection
o Primary infection
o Secondary infection
o Reinfection←are recurrences caused by a different pathogen than the original
infection and typically occur weeks to months after the first infection
o Cross infection←the transmission of infectious microorganisms, like bacteria or
viruses, from one person to another, either through direct contact, indirect contact
with contaminated surfaces, or airborne transmission, essentially spreading an
infection from one individual to another
o Nosocomial infection←an infection that occurs in a hospital or healthcare
facility, and was not present at the time of admission
o Opportunistic infection←an infection that occurs more frequently or more
severely in people with weakened immune systems
o Colonization←when germs are present but don't cause illness
 For example, someone might test positive for a virus like COVID-19 but
not have any symptoms.
o Latent infection←A means a microbe is present in the body without causing any
noticeable symptoms, often in a dormant state. Key difference is that a latent
infection can potentially reactivate and become symptomatic later on, while
colonization typically doesn't lead to disease.
o
o Sub-clinical infection←is an infection that occurs without any noticeable
symptoms or signs. It's also known as an inapparent or preinfectional. These
infections cause few or no symptoms. Symptoms are mild enough to go
undetected
o Iatrogenic infection←an infection that occurs as a result of a medical procedure
or treatment, or from a medication prescribed by a doctor.



 TYPES OF INFECTION ACCORDING TO TIME OF OCCURENCE
o PRIMARY INFECTION← the first and original infection that makes a
person ill.
o SECONDARY INFECTION← the second infection that follows as a
complication of the original infection.
o INTERCURRENT INFECTION← two different primary infections occurs
simultaneously.
o MIXED INFECTION← two or more infections occurring with a primary
and a secondary infection.
 TYPES OF INFECTION ACCORDING TO THE EXTENT OF DISTRIBUTION
OF EFFECTS IN THE BODY
o LOCAL/ LOCALIZED INFECTION← occurs when a pathogen remains in
a particular site.
 o SYSTEMIC/ GENERALIZED INFECTION← the pathogen or its products
is spread in the body through the circulation.
o FOCAL INFECTION←original site of pathogen remains in an area from
which it spreads to other parts and set-up another focus/ center of action.
 TYPES OF INFECTION ACCORDING TO SEVERITY
o CHRONIC INFECTION← infection that has a slow evolution of the disease
and usually cures at a longer period.
o ACUTE← infection with a swift and rapid or severe course of development
that usually recovers fast.
o LATENT INFECTION← infection held in check by the by the defensive
forces of the body.
o SUBCLINICAL/ INAPPARENT INFECTION← type of infection where the
signs and symptoms are so mild that it remains undetected or undiagnosed.
o TERMINAL INFECTION←a complicating infection leading to death
 TYPES OF INFECTION ACCORDING TO THE DISTRIBUTION
o SPORADIC←an infectious disease that occurs only occasionally, irregularly,
and in scattered isolated cases, with no clear pattern of transmission or geographic
concentration
o ENDEMIC
o EPIDEMIC←unexpected increase in the number of disease cases in a specific
geographical area. Can refer to a disease or other specific health-related behavior
(e.g., smoking) with rates that are clearly above the expected occurrence in a
community or region.
o PANDEMIC←The World Health Organization (WHO)(link is external and
opens in a new window) declares a ‒‒‒‒‒ when a disease’s growth is exponential.
This means the growth rate skyrockets, and each day cases grow more than the
day prior. In being declared a ‒‒‒‒-. It means a virus covers a wide area, affecting
several countries and populations.
 COURSE OF INFECTIOUS DISEASE/ STAGES OF DEVELOPMENT OF
INFECTION
o INCUBATION PERIOD← interval between the time the pathogen is
received and the appearance of the disease S/S.
o PRODROMAL PERIOD← a short interval described by such ill-defined
symptoms as headache
o INVASION PERIOD← dse. reaching its full development and maximum
intensity either rapid (acute) or insidious (chronic).
o FASTIGIUM / ACME← dse. at its height
o DEFERVESCENCE← period of decline either in crisis (fast) or lysis
(gradual/ slow)
o CONVALESCENCE← period of recovery
 Pattern in the presentation of pathology of infection
o Toxin mediated disease←infections caused by bacteria that release toxins that
damage tissues or organs. ex. Diphtheria, Tetanus.
o Acute pyogenic infection←infections caused by pus-forming bacteria that result
in inflammation, pus, and abscesses. ex. Staphylococcal pharyngitis,
Staphylococcal abscess.
 o Sub-acute infection←Persisting more than 4 weeks, but less than 12 weeks with
total resolution of symptoms. Ex. Sub–acute bacterial endocarditis, Atypical
pneumonia
o Chronic granulomatus infection←a rare genetic disorder that makes it difficult for
the body to fight off bacterial and fungal infections. This is due to a defect in the
white blood cells, called phagocytes, that are responsible for killing germs. Ex.
Tuberculosis, Brucellosis
 source of infection
o Exogeneous Source←when the pathogen comes from outside the body, like from
another person, contaminated environment, or food
o Endogenous Source←means the infection originates from the body's own
microbiota, usually due to an imbalance in the normal flora, like bacteria
overgrowing in a specific area due to disrupted defenses
o
 RESERVOIR
o Homologous←It is applied when another member of the same species is victim.
o Heterologous←When the infections is derived from a reservoir other than man as
for animal, bird infected with salmonella.
 ANIMAL RESERVOIR – ZOONOTIC INFECTIONS
 Bacterial zoonoses
 Viral zoonoses
 Rabies←A fatal disease that affects the nervous system. It's
usually spread by an infected animal biting a person or
another animal.

2. Ebola←A zoonotic disease that is rare and that can cause

recurring outbreaks, especially in parts of Africa. You get it
from contact with body fluids of infected animals or
people. Symptoms include fever, headache, rash, vomiting
and bleeding.
3. COVID-19←A novel coronavirus that has the potential to
cause global pandemics.
4. Avian Influenza←“bird flu,” is a viral infection that
spreads in birds, cows and other animals. It can sometimes
spread to people. In humans, H5 subtypes of influenza A
are the most common cause. It can cause mild to severe
respiratory symptoms and pink eye
5. Hantaviruses←viruses cause diseases like hantavirus
pulmonary syndrome (HPS) and hemorrhagic fever with
renal syndrome (HFRS). People get hantavirus from
contact with rodents like rats and mice, especially when
exposed to their urine, droppings, and saliva. It can also
spread through a bite or scratch by a rodent, but this is rare

 Fungal zoonoses
 1. Ringworm←A fungal infection that can be treated with
antifungal creams or lotions.
2. Blastomycosis←A rare fungal infection that's usually
acquired by inhaling the spores of a fungus.

 Parasitic zoonoses
 Trichinosis←a foodborne disease caused by eating raw or
undercooked meat from an infected animal. It's caused by
the roundworm Trichinella spiralis.
 Giardiasis←an intestinal infection marked by stomach
cramps, bloating, nausea and bouts of watery diarrhea
 Malaria←a life-threatening disease spread to humans by
some types of mosquitoes. It is mostly found in tropical
countries. It is preventable and curable.
 Insect vectors←Mosquitoes, Flies, Mites and Ticks
 Mechanical vector
 Domestic flies carry enteric bacteria on their leg
 Biological vector↑Biological vector ( e.g- rat fleas, female anophales
mosqitoes that transmit Plague, Malaria respectively)
 ( e.g- rat fleas, female anophales mosqitoes that transmit
Plague, Malaria respectively)
 CARRIER CAN BE CLASSIFIED IN FOLLOWING WAYS
o active carrier←is an infected individual who can transmit a disease to others,
even if they don't show symptoms.
o passive carrier←is someone who is contaminated with a pathogen but isn't
infected themselves and can only transmit the disease by accidentally carrying it
on their body or clothes

3. Based on type
 Incubatory carrier←those who can transmit the agent during the ‒‒‒‒
period before clinical illness begins
 Ex. Measles, Polio, Pertussis and Influenza
 Convalescent carrier←those who have recovered from their illness but
remain capable of transmitting to others.
 Ex. Typhoid fever
 Healthy carrier
4. Based on duration
 Temporary carriers←can refer to people or animals that have a disease
but don't show symptoms, or to people or vehicles that transport goods for
a short time. Ex. Incubatory, Convalscent and healthy carriers
 Chronic carriers – Tyhoid fever, Dysentry, Cerebrospinal meningitis
and Gonorrhoea, syphilis

 TYPES OF VIRULENCE FACTORS

o Adherence factors.
o Invasion factors.
 o Capsule.
o Toxins.
o Iron acquisition.
 ADHERENCE OR COLONIZATION FACTORS
o Pathogens and potentially pathogenic commensals adhere to the mucous
membrane surfaces with considerable selectivity
 Fimbriae.
 Slime layer.
 Glyco-calyx.
 Membrane protein.
 Cell bound protein.
 Bacterial biofilms.
 INVASION
o Cell invasion←refers to describe the entry of bacteria into host cells, ability to
avoid humoral host defense mechanisms and potentially provides a niche rich in
nutrients and devoid of comperition from another host.
o Invasion of the tissue is enhanced by following factors
 (1) Invasin;
 (2) Enzymes;
 (3) Antiphagocyic factor;
 (4) Intra-cellular survival.

3. INVASIN←It is the bacterial surface protein that affect physical proportion of

tissue matrices , intracellular spaces, thereby promoting the spread of pathogens.
4.
5. Hyaluronidase
 Organism: Staphylococci, Group A, B, G streptococci, Clostridium
perfringens
 Mechanism of Action: Hydrolyzes hyaluronic acid, facilitating bacterial
spread through subcutaneous tissue.
6.
7.
8. Collagenase
 Organism: Clostridium perfringens
 Mechanism of Action: Hydrolyzes collagen, facilitating bacterial spread
through subcutaneous tissue.
9.
10.
11. Coagulase
 Organism: Staphylococcus aureus
 Mechanism of Action: Converts fibrinogen to fibrin clots, protecting
bacteria from phagocytosis.
12.
13.
14. Streptokinase
 Organism: Group A, C, G streptococci
  Mechanism of Action: Binds to plasminogen, activating plasmin
production to dissolve blood clots.
15.
16.
17.
18. Staphylokinase
 Organism: Staphylococcus aureus
 Mechanism of Action: Prevents fibrin clot formation.
19.
20.
21.
22. Lecithinase
 Organism: Clostridium perfringens
 Mechanism of Action: Hydrolyzes lecithin, destroying the integrity of the
cytoplasmic membrane of many cells.
23.
24.
25. Phospholipase
 Organism: Staphylococcus aureus
 Mechanism of Action: Lyses red blood cells
26.
27. I. IgG IgA1 protease
 Organism: Staphylococcus aureus
 Mechanism: Cleaves IgA at specific pro-ser or pro-thr bonds in the hinge
region, creating Fab and Fc fragments (disrupts antibody function).
28.
29.
30. II. Leukocidins
 Organisms: Streptococcus pneumoniae, Neisseria sp., Haemophilus
influenzae
 Mechanism: Pore-forming exotoxins causing lysosome degranulation
within leukocytes (damages white blood cells).
31.
32.
33. III. Porins
 Organisms: Staphylococci, Streptococci, Pneumococci
 Mechanism: Inhibit phagocytosis by activating the adenylate cyclase
system (interferes with immune cell engulfment).
34.
35.
36. IV. Protein A
 Organism: Staphylococcus aureus
 Mechanism: Binds to IgA by its Fc end, preventing complement
interaction with bound IgG (blocks complement-mediated killing).
37.
38.
 39. V. DNase
 Organisms: Staphylococci, Group A streptococci, Clostridium
perfringens
 Mechanism: Lowers the viscosity of exudates, increasing pathogen
mobility (breaks down DNA in pus, improving spread).
40.
41.
42. VI. Hemolysins
 Organisms: Staphylococci, Streptococci, E. coli
 Mechanism: Lyse erythrocytes, making iron available for microbial
growth (releases nutrients for bacterial growth).
43.
44.
45. VII. Pyrogenic exotoxin B
 Organism: Group A streptococci
 Mechanism: Degrades protein (general tissue damage).
46.
47.
48. VIII. Elastin, alkaline protease
 Organism: Pseudomonas aeruginosa
 Mechanism: Cleaves laminin associated with the basement membrane
(disrupts tissue structure).


 INTRACELLULAR SURVIVAL
o A few mechanisms that are suggested or the intra – cellular survival of bacteria
include
 inhibition of phago – lysosome fusion,
 resisance to action of lysosomal enzymes,
 adaption to cytoplasmic replication.

 TOXINS – derived from Greek (Toxicon) – Bow poison
o Components or products of microorganisms which, when extracted and
introduced into host animals, reproduces disease symptoms normally associated
with infection
 Types of Toxin
 Endotoxin
 Exotoxin
 Exotoxins
o Chemical Nature→are proteins secreted by certain Gram-positive and Gram-
negative bacteria. They are generally heat-labile, meaning they are easily
destroyed by heat.
o Mode of Action & Symptoms→have specific mechanisms of action and cause
specific symptoms. They can be cytotoxins (damaging cells), enterotoxins
(affecting the intestines), or neurotoxins (affecting the nervous system). The
effects are targeted to specific cells or tissues.
 o Toxicity: Exotoxins are highly toxic and can often be fatal.
o Immunogenicity: Exotoxins are highly immunogenic, meaning they stimulate the
body to produce antibodies (antitoxins) that neutralize them. This is the basis for
toxoid vaccines.
o Toxoid Potential: Exotoxins can be converted into toxoids by treatment with
formaldehyde. Toxoids retain their immunogenicity but lose their toxicity,
making them safe for use in vaccines.
o Fever Potential: Exotoxins generally do not cause fever.

 Endotoxins
o Chemical Nature: Endotoxins are lipopolysaccharide-lipoprotein complexes
found in the outer membrane of Gram-negative bacteria. They are released upon
the lysis (breakdown) of bacterial cells and are extremely heat-stable.
o Mode of Action & Symptoms: Endotoxins have a general mode of action and
cause systemic symptoms such as fever, diarrhea, and vomiting. Their effects are
not targeted to specific cells or tissues.
o Toxicity: Endotoxins are weakly toxic and rarely fatal.
o Immunogenicity: Endotoxins are relatively poor immunogens; the immune
response they elicit is not sufficient to neutralize them effectively.
o Toxoid Potential: Endotoxins cannot be converted into toxoids.
o Fever Potential: Endotoxins are pyrogenic, meaning they often cause fever in the
host.

 Parts of Endotoxin
o oligosaccharide ‘O’ side chain
o lipid A
o Core polysaccharide

 Biologic activities of lipid A component of endotoxin:
o Activates macrophages
 IL-1: Fever
 TNF: Fever & Hypotension
 Nitric oxide: Hypotension
o Activates complements
 C3a: Hypotension edema
 C5a: Neutrophil chemotaxis
o Activates tissue factors
 Coagulation cascade - DIC

 Exotoxin
o Types of Exotoxin, toxins
 Neurotoxin (Type 3, ABtoxin)
 Cytotoxin (Type 2 or Type 1) (releases cytokines)
 Enterotoxin (Type 1, superantigen)
o Found in→Gram positive and gram negative species -
 o Soluble protein toxins released from viable bacteria during
{{7747188950045705::exponential growth }}phase
o Are excellent antigens that elicit specific antibodies called→antitoxins
o Enter eukaryotic cells primarily through→receptor mediated endocytosis
 TOXIC SHOCK SYNDROME TOXIN
o Formerly called Pyrogenic exotoxin.
o Massive
o immune activation and pyrogenicity - Superantigens.

 SUMMARY OF TOXINS
 Cytotoxin
o Anthrax: Edematous Papule, Enteritis, Bloody Diarrhea
o Diptheria toxin: Pseudomembrane, Papule
o Staphylococcal α-toxin: Disrupts smooth muscles of blood vessels, cytotoxic to
RBCs, platelets, monocytes, etc.
 Neurotoxin
o Botulinum: Flaccid Paralysis
o Tetanospasmin: Spastic Paralysis
 Enterotoxin
o Cholera toxin: Watery Diarrhea
o Shiga toxin: Dysentery, HUS
 Superantigens
o Toxic Shock Syndrome Toxin: Fever, Hypotension, Erythematous rash, MOF,
Hypovolemic Shock
o Scarlet Fever Toxin: Erythematous Rash, 'Strawberry tongue'
o Scalded skin syndrome toxin: Perioral erythema, Cutaneous blisters

 Endotoxins

1. Source→Gram-negative bacteria only. Located in the outer membrane.

2. Type→Lipopolysaccharide (LPS).
3. Composed of three parts
 Three parts of LPS
 Lipid A: Immunogenic (activates the immune system, causing
problems).
 Core polysaccharide: Not a major focus.
 O antigen: Antigenic (triggers antibody production).
4. Effects: LPS (specifically Lipid A) activates
 Macrophages: Leading to the release of cytokines→(IL-1, IL-6, TNF-α,
nitric oxide).
 These cytokines cause
 Fever: By stimulating the hypothalamus to increase body
temperature.
 Hypotension: Due to increased capillary permeability and
vasodilation, leading to decreased blood pressure. Severe
 hypotension can cause multi-system organ failure and
septic shock.
 Complement system: Leads to the release of C3a and C5a.
 These cause
 Inflammation: C5a increases neutrophil chemotaxis.
 Edema: C3a increases histamine release, causing
vasodilation and increased capillary permeability.
 Hypotension: As above.
 Tissue factor (Factor III): Activates the coagulation cascade, leading to
widespread clotting (DIC - disseminated intravascular coagulation) and
potentially bleeding due to depletion of clotting factors.
5. Exotoxins
 Source: Gram-positive and gram-negative bacteria. Made inside the cell
and then excreted.
 Types: Categorized by mechanism of action:
 Type 1 (Superantigens): Bind to MHC II molecules on antigen-
presenting cells and T cell receptors, enhancing the interaction and
causing a massive cytokine release (cytokine storm), leading to
inflammation, fever, and hypotension (similar to endotoxins but
often more potent). Examples: Toxic Shock Syndrome Toxin 1
(TSST-1), enterotoxins (Staphylococcus aureus), erythrogenic
toxin (Streptococcus pyogenes).
 Type 2 (Membrane-damaging): Directly damage host cell
membranes by forming pores or breaking down the phospholipid
bilayer. Examples: Streptolysin, leukocidin (Staphylococcus
aureus), alpha toxin (Clostridium perfringens).
 Type 3: Exert their effects after entering the host cell, often via an
A-B toxin mechanism (A subunit is active, B subunit binds to the
cell). They can inhibit protein synthesis, alter cell signaling, or
modify enzyme activity. Examples: Diphtheria toxin, cholera
toxin, anthrax toxin, pertussis toxin, tetanus toxin, botulinum toxin.
Some bacteria use injectosomes to directly inject the toxin into the
host cell.
6. Examples of Exotoxins by Type
 Type 1: Staphylococcus aureus (TSST-1, enterotoxins), Streptococcus
pyogenes (erythrogenic toxin).
 Type 2: Staphylococcus aureus (streptolysin, leukocidin), Clostridium
perfringens (alpha toxin).
 Type 3: Corynebacterium diphtheriae (diphtheria toxin), Pseudomonas
aeruginosa (exotoxin A), Shigella (Shiga toxin), E. coli (Shiga-like toxin),
Vibrio cholerae (cholera toxin), Bacillus anthracis (anthrax toxin),
Bordetella pertussis (pertussis toxin), Clostridium tetani (tetanospasmin),
Clostridium botulinum (botulinum toxin).

 Key Differences Between Endotoxins and Exotoxins

o Source: Endotoxins are only found in gram-negative bacteria, while exotoxins
can be produced by both gram-positive and gram-negative bacteria.
 Location: Endotoxins are part of the outer membrane of gram-negative
bacteria. Exotoxins, on the other hand, are made inside the bacterial cell
and then released outside.
 Chemical Nature: Endotoxins are complex molecules called
lipopolysaccharides (LPS). Exotoxins are proteins.
 Toxicity: Exotoxins are generally much more toxic than endotoxins. You
might only need a small amount of an exotoxin to cause significant harm,
whereas endotoxins often require a higher concentration to have a serious
effect.
 Heat Stability: Endotoxins are heat-stable, meaning they can withstand
high temperatures. Exotoxins are usually heat-labile, meaning they are
destroyed by heat.
 Immunogenicity: Exotoxins are more immunogenic than endotoxins,
meaning they are better at triggering an immune response (like antibody
production).
 Mechanism: Endotoxins work by activating immune cells (like
macrophages), the complement system, and the coagulation cascade.
Exotoxins have a variety of mechanisms, including acting as
superantigens, directly damaging cell membranes, or interfering with
cellular processes after entering the cell.