Microorganism Virulence and Pathogenicity

• If a microorganism can cause disease, it is a pathogen
• Only a minority of microorganisms are pathogenic
• Some organisms are highly virulent and cause disease in healthy individuals, even with a small amount of the organism
• Others cause disease only in compromised individuals with weak defenses; these are opportunistic organisms
• Opportunists take the opportunity offered by reduced host defenses to cause disease
• Opportunists are members of the body's normal flora

Virulence

• Virulence is a quantitative measure of pathogenicity related to:
  • Toxigenic potential
  • Invasiveness
• Virulence is measured by the number of organisms needed to cause disease
• LD50 (50% lethal dose) specifies the number of organisms needed to kill half the hosts (laboratory animals)
• ID50 (50% infectious dose) specifies the number needed to cause infection in half the hosts
• Virulence is designated as: LD50 or ID50
• If 300 bacteria injected into 10 animals results in 50% being infected, the rest will not be infected

Communicable Infections

• Communicable infections spread from host to host
• Many, but can be spread via host to host contact, they are called ‘communicable diseases
• Tuberculosis is communicable via airborne droplets
• Staphylococcal food poisoning is not, as the exotoxin contaminates food
• A highly communicable disease is called a 'contagious disease', like chickenpox
• Endemic prevalence of a disease is constant within a community
• Endemic infection is constantly present at a low level in a specific population, like malaria in some African countries
• Epidemic infections occur much more frequently than usual, like influenza in the winter
• Pandemic infections have a worldwide distribution, like the AIDS, Swine influenza, and Covid-19 before few years
• Degree of incidence and prevalence dictate term :
  • Endemic
  • Epidemic
  • Pandemic

Natural History of Infectious Disease

• An acute infection progresses through 4 stages

Stages of Infection progression

• Causative agent example Chickenpox
• Incubation Period: Time between pathogen acquisition to conference of symptoms
  • Varies from hours to weeks
• Prodromal Period (1-2 days before rash)
  • Includes mild fever, fatigue, headache, loss of appetite, malaise
• Period of Invasion (5-7 days)
  • Fever, malaise and loss of appetite is evident as a pathogen with exponential growth and peak in patient sample
• Convalescent Period (5 days
  • Illness subsides and person is better
  • Symptoms of the diseases are evident in a defined period after the onset period
  • Icthing decreases and person feel better

Acute Infections Elicited by Organisms

• Infections that are inapparent or subclinical cause no overt symptoms
• Body may completely eliminate pathogen after initial infection
• Individuals may become
  • Chronic Carriers
  • Remain in Latent state
• Primary herpes infections establish latent states in trigeminal ganglia
• Chronic carriers may shed the virus, spreading disease
• Latent infections may reactivate with recurrence of symptoms

Trigeminal Ganglion

• Herpes labialis or facial herpes is a recurrence of facial herpes infection
• It happens due to reactivation of the latent virus in the trigeminal ganglion
• The initial presentation is on the mucocutaneous junction of the upper lip
• Initial presentation includes burning pain followed by small blister or sore on lips or mouth but disappear then reappear

Pathogenesis of disease

• The following ways and means occurs and affect bacterial cause
• Transmission is a important key step that allow pathogen to cause the disease
• Most infections are acquired via transmission from external sources, i.e. they are exogenous in origin
• Others are caused by members of the normal flora, behaving as opportunist pathogens i.e. they are endogenous in origin
• Transmission methods:
  • Inhalation - the airborne route
  • Ingestion - faecal contamination of food
  • Inoculation - by sexual contact, contaminated needles, skin contact, blood transfusions, or biting insects

Portals of Entry of Pathogens

• 4 important portals (or gates) of entry for pathogens
• Skin:
  • Tetanus, hepatitis B, C
• Respiratory tract (R.T):
  • Pneumonia, T.B
• Gastrointestinal tract (G.I):
  • Cholera, Poliomyelitis
• Genitourinary:
  • Syphilis, AIDS
• Adherence is the first step toward organisms of a disease

Adherence to Host Surface

• Surface structures help with colonization
• Bacteria and fungi use specialized structures to adhere to host surfaces
• If adherence does not succeed, the body cannot cause the infection
• Mutant non-pathogenic adhere mechanism examples
• The adherence has a link to pili type structure and ut epilthium

Biofilm Formation

• Once organisms adhere via mechanisms and intelligent communities for disease
• Biofilms are defined as bacteria attached to a solid surface in an organic matrix
• Up to 65% of human infections associate with microbial biofilms for dental disease and formation

Biofilm and Quorum sensing

• Once organism produce biofilms that are resistance to outer chemicals and can maintain high population
• The biofilms has specific factors, those factors has the role to produce high amount of gene activation for resistance to chemicals.
• Infections associated with biofilms are difficult to eradicate than those with plank tonic bacteria

Biofilm Resistance and components

• Protection is offered by the extracellular polysaccharide matrix from host immune resistance
• Poor penetration will not allow antimicrobials to penetrate the deeper layers of the biofilm
• Degradation of antimicrobials will not allow to penetrate
• pH gradients, that is not suitable for the optimal activity of the drug
• Gene expression will cause the organism to have a resistant organism to antibiotics
• 4 ways biofilms can resistance is show in figure
  • Polysaccharide matrix and bacteria
  • Substraum and antibiotics

Recalcitrant Human infection examples

• Pseudomonas aeruginosa infections of the respiratory tract
• Chronic periodontal infections from dental plaque

Invasiveness of Bacteria

• Invasiveness relates to the ability of bacteria to secrete bacterial enzyme
• Examples:
  • Collagenase and hyaluronidase degrade intercellular substances to allow bacterial spread through tissues (e.g., skin infections caused by Streptococcus pyogenes)
  • Coagulase, produced by Staphylococcus aureus, accelerates the formation of a fibrin clot, helping protect the organisms from phagocytosis by walling off the infected area
  • Immunoglobulin A (IgA) protease degrades protective IgA on mucosal surfaces which allows Haemphilus influenzae and other organisms to infect and colonize

Resistance Components

• Leukocidins destroy neutrophils and macrophages. The periodontopathic organism actinomycetemcomitans has this enzyme
• Mutants exhibit anti-phagocytosis to show enzymatic power
• The polysaccharide capsule in the pneumonia pathogens show anti capsular
• Neisseria Meningitdes can prevent phagocytosis against
  • (S. Pneumoniae) strepiscocsans type b
  • (Nesit tooniningitpic) Capsular
  • Haemophilu influenae (type b) vaccine
• Opsonization is required to prevent pneumococcal activity and produce antibody

Cell Wall Proteins

• The M of gram positive bacteria wall, that has antigen and complexes to form phagocytes
• M protein of group A streptococcus pyogenes
• Protein of A of staphylococci

Mechanism Function for Bacterial Infections

• Receptors recognize the infections, as body ingest the viral presence
• Then body will form phagocytosis, that is followed a lysosome
• Once viral load are formed, body excrete material and residual body
• Viruses evade and replicate within the system
• Histiocytes tissue helps macrophages with infection resistance

Toxigenicity of infections

• Toxin Production comes under several classes:
• Endoxins has a relation lipid and gram -ve bacteria
• Exoxins has relation to ++ gram bacteria
• Toxins causes, shock and other dissemiatedxtravascular conditions
• Endoxins releases active cells to help repair but can be a fever agent

Lipopolysaccharide (LPS) Diagram

• In inner leaflet, there is
  • Core Poly saccharides
  • Sugs
  • O antigens
• In Outer leaflet, Manase unit with protein

Tables Comparing Features across categories

• Property
• Source
• Origin
• Chemistry
• Toxicity
• Clinical effects
• Antigenicity
• Vaccine
• Heat Stablity
• Typical diseases

Exotoxins and Endotoxins

• Exotoxins and endotoxins differ by these and possess different structures and origins, with exotoxins being more potent
• Exotoxins are bacterial products, highly toxic & can befatal. Used as vaccines. Bacterial cause
• CTetanus: Broa @Botulinum: ozonskills lab animals with in

Cytotoxic and Neurotoxins

• Neurotoxins are cytotoxic
• Tetanus toxins and diphtheria all relate to neuro toxins
• Neuro toxin causes receptor for signal of neuron.
• Those types of toxins can affect part binds and produce death side effect
• Neurotoxins are toxins that are specifically poisonous or destructive to nerve tissue
• The component binds to the receptor in the membrane, causing toxic

Dipthteria Toxin

• Diphtheria toxin produced by Corynebacterium
• It has 2 part that cause, paralysis
• One part causes inhibition of cell death
• The other component helps the molecule and transport in membrane

Enterotoxins toxins

• These toxins act on the surface or mucosa of Gut
• That cause disturbance with g.d function and electrolyte disfunction
• the heat labile, as the bacterial bind with that type of toxins
• E coli related to heat toxin
• It has to part
  • bbind to gangiolside in membrane
  • heat labile is activate at 65C IN 30 minute

Virsus Replication Functions

• Permissive infection
• Virus that are not replicate with host and Viral replicate which are caused and lysis to infection

Non-Permissive Infection

• The viruses will lead to death
• ineffective immune responses: (no antibody
  • There are four categories
• cell-mediated host that causes death and not cell death virus death. The permissive virus.

Latent Viral Infections

• Latent viral infections persist in the cell and has a host
• Ganglion transfer is known from this activity
• Detection are made
• CMI is needed to recover the viral cell types

Long Term Functions

• 2- vhas long term period from infection or transmission- varciell

Carries

• They contain large load for prolonged period
• It has high infection load to patient
• They need treatment for dental and care unit

Main Carrier Difference

• Carrier and late and they may have
• Continuous infection and infection may not be detected

Oncogenic Infection

• Have connection to cancer and
• That it has infection infecti is a Burkholderia species
• Lymph node cell 4- slow

Slow Long Infections

• infection will last month or year
• And lead ti severe infection
• Incubation perod s long There infection period

Clinical and diagnostic features

• A cell that May be infected
• May be virus and not virus
• Cell fusion with viral protein

Laboratory Infection and Components

• There cells that are Infection
• Haemo
• The body and haemo
• Red infection call membrane And host cell

Viral replications and Cytopathtic Effect

• Cell Fusion Infected cell in virus, that causes the CD4 cell to die
• Poly carriers
  • A process
  • Long trans
  • This has protein spikel that attack immune

Persisters and Non- Peristal

• Non perster cell infection has that not lead ccell death
• It that The ineffective that can infect that and cell death
• They will create or not, create a a perster cycle and attack body or cells There type viral load and has a different that it causes Hepatitis , papilloma virus and long death