1. Microorganisms are classified based on their relationship with humans as commensals, pathogens, parasites, and opportunistic pathogens.
2. Pathogens have the ability to cause disease, known as pathogenicity, while virulence refers to the degree of pathogenicity.
3. Microbes can be transmitted via various routes including ingestion, inhalation, direct contact, sexual contact, bloodborne transmission, vectors, and vertical transmission.
4. For an infection to occur, a pathogen must first adhere to and invade host tissues, then survive the host's immune response through various mechanisms.
Serological test for virus identificationPlock Ghosh
This presentation consist of detailed study of serological method of virus identification. Basically ELISA is vastly used for virus detection. Western blot method is used for HIV identification.
Serological test for virus identificationPlock Ghosh
This presentation consist of detailed study of serological method of virus identification. Basically ELISA is vastly used for virus detection. Western blot method is used for HIV identification.
A introduction on Viral vaccine for medical students.Although most attenuated vaccines are viral, some are bacterial in nature. Examples include the viral diseases yellow fever, measles, rubella, and mumps, and the bacterial disease typhoid.
Mechanism of pathogenicity-Exotoxin and endotoxinaiswarya thomas
Brief description on mechanisms of pathogenicity, actions of toxins produced by various bacteria and notable endotoxins and exotoxins. Mechanism of action of some of the commonest endotoxins and exotoxins are explained.
Introduction
Disease
Important Properties
Transmission & Epidemiology
Risk factor of reactivation
Pathogenesis
Clinical Findings
Laboratory Diagnosis
Approaches to the diagnosis of latent infections
Treatment
Prevention
A introduction on Viral vaccine for medical students.Although most attenuated vaccines are viral, some are bacterial in nature. Examples include the viral diseases yellow fever, measles, rubella, and mumps, and the bacterial disease typhoid.
Mechanism of pathogenicity-Exotoxin and endotoxinaiswarya thomas
Brief description on mechanisms of pathogenicity, actions of toxins produced by various bacteria and notable endotoxins and exotoxins. Mechanism of action of some of the commonest endotoxins and exotoxins are explained.
Introduction
Disease
Important Properties
Transmission & Epidemiology
Risk factor of reactivation
Pathogenesis
Clinical Findings
Laboratory Diagnosis
Approaches to the diagnosis of latent infections
Treatment
Prevention
review on virulence factors of bacteria done by Mohammed Bushera
knowledge about bacterial virulence factors is a key for medicene or vaccine production, that why I want to share this ppt to the public
Microorganisms cause virtually all pathoses of the pulp and periapical tissues.
Once bacterial invasion of pulp tissues has taken place, both non-specific inflammation and specific immunologic response of the host have a profound effect on the progress of the disease.
Endodontic infection develops in root canals devoid of host defenses,
pulp necrosis (as a sequel to caries, trauma, periodontal disease,or iatrogenic operative procedures)
or pulp removal for treatment.
Biofilm-induced oral diseases.
ROUTES OF ROOT CANAL INFECTION
Caries
• Trauma-induced fractures
• Cracks
• Restorative procedures
• Scaling and root planing
• Attrition
• Abrasion
• Gaps in the cementoenamel junction
at the cervical root surface
• Dentinal tubules
• Direct pulp exposure
• Periodontal disease
• Anachoresis
Mechanisms of Microbial Pathogenicity and Virulence Factors
Pathogenicity : The ability of a microorganism to cause disease.
Virulence: Degree of pathogenicity of a microorganism.
Some microorganisms routinely cause disease in a given host and are called primary pathogens.
Other microorganisms cause disease only when host defenses are impaired and are called opportunistic pathogens by changing the balance of the host–bacteria relationship.
Bacterial strategies that contribute to pathogenicity include the ability to coaggregate and form biofilms.
In the pathogenesis of primary apical periodontitis
Bacteria in caries lesions form authentic biofilms adhered to dentin.
Diffusion of bacterial products through dentinal tubules induces pulpal inflammation
After pulp exposure, the exposed pulp tissue is in direct contact with bacteria and their products
and responds with severe inflammation. Some tissue invasion by bacteria may also occur.
Bacteria in the battlefront have to survive the attack from the host defenses and at the same time acquire nutrients to keep themselves alive.
In this bacteria–pulp clash, the latter invariably is “defeated” and becomes necrotic, so bacteria move forward and “occupy the territory”—that is, they colonize the necrotic tissue.
These events advance through tissue compartments, coalesce, and move toward the apical part of the canal until virtually the entire root canal is necrotic and infected.
At this stage, involved bacteria can be regarded as the early root canal colonizers or pioneer species (play an important role in the initiation of the apical periodontitis disease process, modify the environment, making it conducive to the establishment of other bacterial groups)
Navigating Challenges: Mental Health, Legislation, and the Prison System in B...Guillermo Rivera
This conference will delve into the intricate intersections between mental health, legal frameworks, and the prison system in Bolivia. It aims to provide a comprehensive overview of the current challenges faced by mental health professionals working within the legislative and correctional landscapes. Topics of discussion will include the prevalence and impact of mental health issues among the incarcerated population, the effectiveness of existing mental health policies and legislation, and potential reforms to enhance the mental health support system within prisons.
R3 Stem Cells and Kidney Repair A New Horizon in Nephrology.pptxR3 Stem Cell
R3 Stem Cells and Kidney Repair: A New Horizon in Nephrology" explores groundbreaking advancements in the use of R3 stem cells for kidney disease treatment. This insightful piece delves into the potential of these cells to regenerate damaged kidney tissue, offering new hope for patients and reshaping the future of nephrology.
Defecation
Normal defecation begins with movement in the left colon, moving stool toward the anus. When stool reaches the rectum, the distention causes relaxation of the internal sphincter and an awareness of the need to defecate. At the time of defecation, the external sphincter relaxes, and abdominal muscles contract, increasing intrarectal pressure and forcing the stool out
The Valsalva maneuver exerts pressure to expel faeces through a voluntary contraction of the abdominal muscles while maintaining forced expiration against a closed airway. Patients with cardiovascular disease, glaucoma, increased intracranial pressure, or a new surgical wound are at greater risk for cardiac dysrhythmias and elevated blood pressure with the Valsalva maneuver and need to avoid straining to pass the stool.
Normal defecation is painless, resulting in passage of soft, formed stool
CONSTIPATION
Constipation is a symptom, not a disease. Improper diet, reduced fluid intake, lack of exercise, and certain medications can cause constipation. For example, patients receiving opiates for pain after surgery often require a stool softener or laxative to prevent constipation. The signs of constipation include infrequent bowel movements (less than every 3 days), difficulty passing stools, excessive straining, inability to defecate at will, and hard feaces
IMPACTION
Fecal impaction results from unrelieved constipation. It is a collection of hardened feces wedged in the rectum that a person cannot expel. In cases of severe impaction the mass extends up into the sigmoid colon.
DIARRHEA
Diarrhea is an increase in the number of stools and the passage of liquid, unformed feces. It is associated with disorders affecting digestion, absorption, and secretion in the GI tract. Intestinal contents pass through the small and large intestine too quickly to allow for the usual absorption of fluid and nutrients. Irritation within the colon results in increased mucus secretion. As a result, feces become watery, and the patient is unable to control the urge to defecate. Normally an anal bag is safe and effective in long-term treatment of patients with fecal incontinence at home, in hospice, or in the hospital. Fecal incontinence is expensive and a potentially dangerous condition in terms of contamination and risk of skin ulceration
HEMORRHOIDS
Hemorrhoids are dilated, engorged veins in the lining of the rectum. They are either external or internal.
FLATULENCE
As gas accumulates in the lumen of the intestines, the bowel wall stretches and distends (flatulence). It is a common cause of abdominal fullness, pain, and cramping. Normally intestinal gas escapes through the mouth (belching) or the anus (passing of flatus)
FECAL INCONTINENCE
Fecal incontinence is the inability to control passage of feces and gas from the anus. Incontinence harms a patient’s body image
PREPARATION AND GIVING OF LAXATIVESACCORDING TO POTTER AND PERRY,
An enema is the instillation of a solution into the rectum and sig
One of the most developed cities of India, the city of Chennai is the capital of Tamilnadu and many people from different parts of India come here to earn their bread and butter. Being a metropolitan, the city is filled with towering building and beaches but the sad part as with almost every Indian city
Telehealth Psychology Building Trust with Clients.pptxThe Harvest Clinic
Telehealth psychology is a digital approach that offers psychological services and mental health care to clients remotely, using technologies like video conferencing, phone calls, text messaging, and mobile apps for communication.
Medical Technology Tackles New Health Care Demand - Research Report - March 2...pchutichetpong
M Capital Group (“MCG”) predicts that with, against, despite, and even without the global pandemic, the medical technology (MedTech) industry shows signs of continuous healthy growth, driven by smaller, faster, and cheaper devices, growing demand for home-based applications, technological innovation, strategic acquisitions, investments, and SPAC listings. MCG predicts that this should reflects itself in annual growth of over 6%, well beyond 2028.
According to Chris Mouchabhani, Managing Partner at M Capital Group, “Despite all economic scenarios that one may consider, beyond overall economic shocks, medical technology should remain one of the most promising and robust sectors over the short to medium term and well beyond 2028.”
There is a movement towards home-based care for the elderly, next generation scanning and MRI devices, wearable technology, artificial intelligence incorporation, and online connectivity. Experts also see a focus on predictive, preventive, personalized, participatory, and precision medicine, with rising levels of integration of home care and technological innovation.
The average cost of treatment has been rising across the board, creating additional financial burdens to governments, healthcare providers and insurance companies. According to MCG, cost-per-inpatient-stay in the United States alone rose on average annually by over 13% between 2014 to 2021, leading MedTech to focus research efforts on optimized medical equipment at lower price points, whilst emphasizing portability and ease of use. Namely, 46% of the 1,008 medical technology companies in the 2021 MedTech Innovator (“MTI”) database are focusing on prevention, wellness, detection, or diagnosis, signaling a clear push for preventive care to also tackle costs.
In addition, there has also been a lasting impact on consumer and medical demand for home care, supported by the pandemic. Lockdowns, closure of care facilities, and healthcare systems subjected to capacity pressure, accelerated demand away from traditional inpatient care. Now, outpatient care solutions are driving industry production, with nearly 70% of recent diagnostics start-up companies producing products in areas such as ambulatory clinics, at-home care, and self-administered diagnostics.
ICH Guidelines for Pharmacovigilance.pdfNEHA GUPTA
The "ICH Guidelines for Pharmacovigilance" PDF provides a comprehensive overview of the International Council for Harmonisation of Technical Requirements for Pharmaceuticals for Human Use (ICH) guidelines related to pharmacovigilance. These guidelines aim to ensure that drugs are safe and effective for patients by monitoring and assessing adverse effects, ensuring proper reporting systems, and improving risk management practices. The document is essential for professionals in the pharmaceutical industry, regulatory authorities, and healthcare providers, offering detailed procedures and standards for pharmacovigilance activities to enhance drug safety and protect public health.
1. PRESENTED BY- DR. SARITA KUMARI SAHU
PG 1ST YEAR
Dept. of MICROBIOLOGY
SCB MCH,CUTTACK
2. Depending upon relationship of microbes with humans
microorganisms are of following types:-
Commensals:
Harmless microorganisms living on the host and
causing no ill effect/injury to the host.
Pathogens:
Microorganisms capable of causing disease.
Parasites:
Microbes that live on living host, derieve nutrition,
cause harm to host.
3. Saprophyte:
Free living microbes that live on dead or
decaying organic matter.
Opportunistic pathogens:
Cause disease in immunocompromised people
(HIV, Solid organ transplant patient,
Chemotherapy)
4. Pathogenicity :
It is the organism’s ability to produce disease in a
host.
Virulence :
It refers to the measure of degree of pathogenicity of
the microorganism.
Different strains of same species may exhibit varying
degree of virulence.
Virulence of a strain may undergo spontaneous or
induced variation which can be;
Exaltation- Enhancement of virulence.
Attenuation- Reduction of virulence.
8. Infective dose of the organism is minimum inoculum
size that is capable of initiating an infection.
Low infective dose :
Shigella ( Just 10 bacilli)
Large infective dose:
Vibrio cholera (106 -108 bacilli)
Infective dose varies depending upon the factors
such as
Virulence of the organism
Host’s age and immune status
Ability to resist gastric acid
10. Human body surfaces are colonized with a wide
variety of microorganisms which may lead to either
infection or colonization where as;
Colonization:
Pathogen enters, multiplies at the site of
attachment, but does not invade, neither cause
disease nor elicit specific immune response.
Infection:
Growth, multiplication and invasion of a
microorganism in the body with or without the
production of disease.
11.
12. Initial event of pathogenicity.
Exception- organism are directly introduced by trauma or
other means into deeper tissues.
Organisms which are not a part of normal human microbiota,
requires to outcompete the normal microbiota for a place on
body surface.
13. Non specific
Hydrophobic and
electrostatic attractions
Atomic and molecular
vibrations.
Brownian movement
Specific
Capsule
Fimbriae
Flagella
Lipoteichoic acid
Outer membrane
protein
Bacterial biofilms.
14. Commonly bacterial surface and the host cell surface
have a net negative charge so repulsive forces exist
between the two.
This repulsive forces can be overcome by
hydrophobic forces.
More hydrophobic the bacterial surface, greater will
be the adherence.
15. Loose, relatively unstructured network of polymers that
covers the surface of an organism.
▪ Protects the bacterium from phagocytosis.
▪ Prevents complement mediated bacterial cell lysis.
▪ Prevents dessication.
▪ Protects the bacterium from action of lysozyme and
bacteriophages.
eg- Pneumococcus, Meningococcus, H.influenzae,
Klebsiella, Pseudomonas, Bacillus etc.
18. FIMBRIALADHESION MECHANISM EXAMPLES
•FIMBRIAE/PILI
A) Mannose sensitive
Fimbriae
B) Mannose-resistant
Fimbriae
These are the main
mechanism by which
bacteria adhere to host cell.
These are the fibers that
extends from bacterial
surface, mediate attachment
of bacteria to specific
receptor on host cell.
E . Coli ,
Neisseria gonorrhoea,
Vibro cholerae
NON-FIMBIAL ADHESION ORGANISMS INVOLVED
Haemaglutinin ( filamentous,mannose
resistant,fibrillar)
Biofilm
Curli (surface protein)
Fibronectin
Exopolysaccharide
Bordetella pertusis, Helicobacter pylori,
Salmonella typhimureum
CONS, Staphylococci, E.coli,Viridans group
of streptococci
E. coli, Salmonella, Shigella
Streptococcus pyogenes
Streptococcus mutans
19. Gram negative and many gram positive bacteria has
numerous thin, rigid,rod-like structures called fimbriae or
pili.
Mediate attachment of some bacteria to cell surface.
Fimbriae are classified into:
1. Mannose sensitive fimbriae
2. Mannose resistant fimbriae
20. Type I- (mannose sensitive):
hemagglutination of untreated RBCs.
Eg Escherichia ,klebsiella ,serratia ,salmonella spp.
Type II - No adhesiveness.
Type III- (mannose resistant):
adhesive to RBCs treated with tannic acid/heated to 70o C.
Eg. klebsiella, serratia
Type IV- (mannose resistant):
adhesive to untreated RBCs.
Eg. proteus spp.
Type VI-
no adhesiveness
Eg. Non fimbriated strains of K.ozaenae.
21. Non fimbrial adhesions include protein or polysaccharide
structures that are surface exposed on bacterial cell or
secreted.
Protein based adhesins include
▪ filamentous hemagglutinin of B.pertussis
▪ A mannose resistant hemagglutinin of salmonella
enterica serotype typhimurium
▪ A fibrillar hemagglutinin from H.pylori.
Exopolysaccharides present on surface of gram positive
bacteria involved in adhesion.eg S.mutans
22. Teichoic acid and surface proteins of Coagulase
negative staphylococcus aureus, mediate adherence
to prosthetic device and cathetors.
Flagella acts as adhesins in V.cholera and C.jejuni.
Bacterial motility helps in chemotaxis of V.cholera,
C.jejuni and H.pylori as well as in penetration through the
mucous layer during colonization
23. Outer membrane proteins-
Gram negative cell wall contains certain proteins called
OMP.
These are target sites for phages, antibiotics and
bacteriocins.
▪ Eg:- EPEC-OMP(EAF) helps in adherence of EPEC
to the mucosa of SI.
▪ Non pilated gonococci can still bind to the urethra
and other mucosal surfaces by OMPII/PII
24. Biofilm is an aggregate of interactive bacteria
attached to a solid surface or to each other and
encased in an exopolysaccharide matrix.
They form a slimy coat on solid surfaces, implants
and prosthetic devices.
It may be single species (Monomicrobic aggregation)
or more than one (Polymicrobic aggregation).
The bacteria in the exopolysaccharide matrix may be
protected from the host’s immune mechanisms.
25. Matrix functions as a diffusion barrier for some
antimicrobials.
They have complex antibiotic resistant profile indicating
failure of antibiotics to penetrate the polysaccharide matrix.
Eg -: Pseudomonas aeruginosa
Staphylococcus aureus
Candida albicans
After biofilm is formed quorum sensing molecules produced
by the bacteria in the biofilm accumulate resulting in a
modification of the metabolic activity of bacteria.
26.
27. Quorum sensing is the regulation of gene expression in
response to fluctuations in cell-population density.
Gram-positive Bacteria:
Gram-positive bacteria use autoinducing peptide (AIP)
(autoinducer).
When Gram-positive bacteria detect high concentration of
AIP in their environment, AIP binds to a receptor to activate
a kinase that phosphorylates a transcription factor, which
regulates expression of virulence genes.
Gram-negative Bacteria:
Gram-negative bacteria produce N-acyl homoserine lactones
(AHL) as their signaling molecule.
AHL binds directly to the transcription factor (LuxR) to
regulate expression of virulence genes
28.
29.
30. Cell to cell signalling is made possible by activation of two
genes.
I gene codes for synthase responsible for synthesis of
autoinducer.
Autoinducer is often N-acyl homoserine lactone .
The autoinducer can diffuse freely through the cell membrane.
The R-gene codes for a transcriptional regulator protein that
combines with the autoinducer to become an activator for
transcription of various virulence genes.
32. Ability of microorganism to enter host tissue.
Once surface attachment is secured microbial invasion
into subsurface tissues and organs is accomplished by
disruption of the skin and mucosal surfaces by several
mechanisms such as;
Disruption of skin and mucosal surface by-
Trauma
Inhalation of toxic gases / particulate matter / smoking
Implantation of medical device
33. Childbirth
Overuse of antibiotics
Diseases like Malignancy, Diabetes mellitus , previous
repeated infection
By direct action of an organism’s virulence factors-
Some microorganisms produce factors that force
mucosal surface phagocytes to ingest them and then
release them unharmed into the tissue below the
surface.
34. In staphylococci and streptococci produce an array
of enzymes(Hyaluronidase, Nuclease, Collagenase)
that hydrolyse the host proteins and nucleic acids
destroying host cells and tissues.
Destruction allows the pathogens to burrow through
minor openings in the outer surface of the skin and
into deeper tissues.
Once a pathogen has penetrated the body, it uses a
variety of strategies to survive attack by host’s
inflammatory and immune responses.
35. Invasion of the tissue is enhanced by following
factors:
(1) Invasin
(2) Enzymes
(3) Antiphagocytic factor
(4) Intra-cellular survival
36. INVASIN: Bacterial surface protein that affect physical
proportion of tissue matrices , intracellular spaces,
thereby promoting the spread of pathogens.
ENZYMES: Many pathogens secrete enzymes that
enable them to:
1. Dissolve structural chemicals in the body.
2. Maintain an infection.
3. Invade further.
4. Avoid body defenses.
5. Inactivate antibiotic
37. 1. Hyaluronidase:
“Spreading Factor”.
Digests hyaluronic acid
cement substance between cells.
2 .Collagenase:
Breaks down collagen.
3. Neuraminidase:
Produced by intestinal pathogens.
(Vibrio cholerae and Shigella dysentriae).
Degrades neuraminic (sialic) acid; an
intercellular cement of the epithelial cells of
the intestinal mucosa
38. 4. Coagulase:
Coagulates blood proteins.
Providing a “hiding place” for bacteria
within a clot.
5. Kinases:
Such as staphylokinase and streptokinase.
Kinase enzymes convert inactive plasminogen
to plasmin which digests fibrin and prevents
clotting of the blood.
39. 6. Ig A Proteases:
Split IgA at specific bonds.
Inactivates Ab activity.
40. 7. Lecithinase:
Produced by Clostridium perferingens.
Destroys lecithin (phosphatidylcholine) in cell membranes.
8. Phospholipases (alpha toxin).
Produced by Clostridium perferingens.
Hydrolyzes phospholipids in cell membranes by removal
of polar head groups.
9. Hemolysins
Produced by staphylococci (alpha toxin), streptococci
(streptolysins) and various Clostridia.
May be phospholipases or lecithinases that destroy red
blood cells and other cells (phagocytes) by lysis.
41. Cell wall proteins :
The cell wall proteins such as protein A and protein M
of S.aureus and S.pyogenes are antiphagocytic.
eg protein A of S.aureus binds to IgG and prevents the
activation of complement.
Cytotoxins :
Some bacteria produce cytotoxins that interfere with
chemotaxis or killing of phagocytes.
Eg S.aureus produces hemolysin and leukocidin that
lyse and damage RBCs and WBCs.
42. Surface antigens :
Surface antigens of bacteria like Vi antigen of S.typhi
and K antigen of E.coli make the bacteria resistant to
phagocytosis and lytic activity of complement.
Inhibition of the phagocytic “oxidative burst”:
No formation of reactive o2 radicals in
phagocytes.
eg- Legionella,salmonella
43. Some bacteria grow inside PMNL, macrophages or in
monocytes.
They survive by several mechanisms:-
Avoid entry into phagosome.
Prevent phago-lysososme fusion
(Mycobacterium tuberculosis).
Acquire resistance to lysosomal activity.
Examples: Mycobacterium tuberculosis, Brucella, Listeria
44.
45. For a pathogen to survive action of phagocytes and the
complement , inflammation must be avoided or controlled.
Avoidance of complement activation by-
1.By masking its activating molecules.
2.Produce enzymes disrupt crictical biochemical
components of complement pathway.
Rapid invasion and multiplication resulting in damage
to the host before the immune response can be fully
activated.
46. Invasion and destruction of cells involved in the
immune response.
Avoiding detection by the immune system.
Masking the organisms antigens with a capsule or
biofilm so that an immune response is not activated.
Altering the expression and presentation of antigens
so that the immune system is constantly fighting a
primary encounter.
Production enzymes to directly destroy or inactivate
antibodies .
47. Mycobacterium tuberculosis, L.monocytogenes,brucella sp &
Legionella sp live and grow in the hostile environment within
PMN cells,macrophages or monocytes.
They do so by
▪ avoiding entry into some phagolysosome and live within
the cytosol of phagocyte.
▪ Prevent phagosome lysosome fusion and live within
phagosome.
▪ May be resistant to lysosomal enzymes and survive
within the phagolysosome.
48.
49. Antigenic type of bacteria can be a marker of virulence.
V.cholera O Ag type 1 and O Ag type139 produce cholera
toxin.
Some group A streptococci M protein types are associated
with a high incidence of post streptococcal
glomerulonephritis.
N.meningitides capsular polysaccharide types A &C are
associated with epidemic meningitis.
Some bacteria make frequent shifts in the antigenic form of
their surface structures invitro and presumably
invivo.eg.Borrelia spp
Gonococcus has 3 surface exposed Ags that switch forms
which allows it to evade the host immune system ,survive and
cause disease.
50. Essential for the interaction of bacteria with the eukaryotic
cells of the host.
It helps in transport of proteins that make pili or flagella and
secretion of enzymes or toxins into the extracellular
environment.
Both gram positive and negative bacteria have general
secretion (Sec) pathway as major mechanism for protein
secretion.
52. Type III (sec independent)
Yersinia species -ysc-yop system,toxins that block phagocytosis
Ps.aeruginosa -cytotoxin
Shigella spp -controls host signalling,invasion&death
Salmonella enterica -effectors from SP1 &SP2,which promote
attachment & invasion.
Type IV (Sec dependant and independent)
▪ Protein substrates-Bordetella pertussis-PT
H.pylori-cytotoxin
▪ DNA substrates-N.gonorrhoea-DNA export system
H.pylori-DNA uptake and release system
55. • They are lipid A portion of lipopolysaccharide .
• Present as an integral part of the cell wall of gram
negative bacteria.
56. They are heat labile proteins
Secreted by certain species of both gram positive and
gram negative bacteria.
57. 1. Released from the cell before
or after lysis
2. Protein
3. Heat labile
4. Antigenic and immunogenic
5.Toxoids can be produced
6. Specific in effect on host
7. Produced by gram-positive and
gram-negative organism
8. No fever
1. Integral part of cell wall
2. Endotoxin is LPS; Lipid A is toxic
component
3. Heat stable
4. Antigenic immunogenicity
5.Toxoids cannot be produced
6. Many effects on host
7. Produced by gram-negative
organisms only
8. Fever present
58. Iron is essential nutrient for growth and metabolism and cofactor of
numerous metabolic and enzymatic process.
Iron availability affects the virulence of many pathogens.
Eg. P.aeruginosa.
E.coli, klebsiella and some staphylococci produce extracellular iron
chelators called siderophores for scavenging iron.
C.jejuni & N.meningitides obtain iron by siderophores produced by other
species.
H.influenzae type B, H.parainfluenzae, N.meningitides ,S.aureus &
S.epidermidis have specific receptors for transferrin and lactoferrin on
their surface which bind these protein and remove bound iron.
Bacteroid species remove iron by proteolytic cleavage of the chelator.
L.monocytogenes reduce Fe3+ to Fe2+ which reduces the affinity for the
chelator.
59.
60. Large groups of genes that are associated with pathogenicity and
are located on the bacterial chromosome (PAIs).
One or more virulence genes present.
Occupy large chromosomal regions (10-200 Kbp).
Present in genome of pathogenic member of a species but absent
in nonpathogenic member of same species.
Often found with parts of genome associated with mobile genetic
elements.
Genetic instability present.
61. Different G+C content (lower) from host chromosome.
Associated with tRNA genes, which act as sites for recombination into
the DNA.
Carry functional genes (e.g- integrases), to enable insertion into host
DNA.
Properties of PAIs suggest that they originate from gene transfer from
foreign species(lysogenic bacteriophage and plasmid).