Microbiota- grp of microorganism that exist in specific environment

UNIT 1 : Microbiota of the human body and introduction to

pathogenicity and infection

Significance of microbiome (Normal microflora)

ADVANTAGE
1. Contribute to the maturation of immune system
2. Defense against pathogen→ bacterial interference→ normal microflora interferes with colonization of pathogen on our
body
- competition for nutrient
- Competition for receptors
- Inhibition of pathogen due to toxic metabolite production- acid/ certain chemical toxic to pathogen
- Antimicrobial compound (bacteriocins) ( ex- colicins )
3. Aid in digestion process
- Absorption of nutrient
- Vitamin synthesis ( E.coli is known to synthesize vit K in gut )
4. Pathogen producing toxin→ metabolized by normal microflora
5. Endotoxin produced by microflora may help in defense mechanisms by triggering alternative complement pathways.
DISADVANTAGE
1. Normal microflora can sometimes act as opportunistic pathogen
- Location changes
( skin microflora→ by chance introduced into blood stream → infection )
- Immune system weak
2. Can be possible source of carcinogen
- Cyclamate ( cyclohexylamine sulfate)--> can be converted to bladder carcinogen → by bacteria
3. Abnormal multiplication can cause disease ( enteritis & endotoxic shock )
4. Cause confusion in diagnosis
- are ubiquitous
- Resemblance to some pathogen
5. Penicillinase producing organism - ca aggravate infection- by interfering with therapy/ medication

TYPES

RESIDENT MICROFLORA TRANSIENT MICROFLORA

Presence Permanent flora Temporary flora

(Reside long-term unless disturbed) (Remain on the body for a short period)

Colonization & Can’t be removed. Removed

removal If disturbed, reestablish themselves again Usually do not reestablish

Transmission of Usually non pathogenic + not associated with Pathogenic + usually associated with transmission
infection transmission of infection ( sometimes of infection
opportunistic pathogen )+ bacterial interference

Immune response Tolerated by the host immune system May trigger immune response if recognized as
foreign

Ex- Staphylococcus epidermidis, Ex- E.coli

propionibacterium acnes
#NOTE-
Gnoblastic- germ free organism/ animal

Microbiota of skin
1. skin
- Physical & immunologic barrier
- Large no. of microbes colonize here (most of which are harmless or even beneficial to the host)
- Because of its constant exposure to and contact with the environment, the skin is particularly apt to contain transient
microorganisms. ( can’t be removed )
- there is a constant and well-defined resident flora, modified in different anatomic areas
- Extent of skin microflora depend on individuals personal hygiene, clothing, work, environment
2. Factors discouraging microbial colonization on skin-
- Dryness
- inhibit growth
- Some region lie toes, armpit have high no. of microflora as compared to dry area- 10^6 Cfu/m^2
- Low PH (3-5) - acid production
- Antimicrobial compound
- Lysosome- produced by sweat gland
- secretion of sebum/complex lipids - by sebaceous gland - which can be degraded by certain bacteria(
propionibacterium acnes ) to produce long chain fatty acid- toxic to other bacteria
- salts
3. Pathogen- infection- transmission
- Injury
- Needle
- Mosquito bite
4. mechanism for this selectivity-
- Despite being constantly exposed to large no. of microbes- skin can distinguish between harmless and harmful
pathogenic microbe
- Keratinocytes
(continuously sample the microbiota colonizing the skin surface through pattern recognition receptors (eg, Toll-like
receptors, mannose receptors)
- activation of keratinocyte PRR (pattern recognition receptor)→by PAMP (pathogen-associated molecular
patterns)-->PAMP initiates the innate immune response→ resulting in the secretion of antimicrobial peptides, cytokines,
and chemokines.
5. Microflora
- Staphylococcus epidermidis
- Staphylococcus aureus
- Propionibacterium acnes ( aerobic and anaerobic diphtheroid bacilli )
- streptococcus viridans ( α-hemolytic )
- Enterococcus species
- Acinetobacter
- candida

Microbiota of throat/ respiratory tract

1. [preventive mechanism
- Ciliated cells
- Mucous ( mucociliary escalator )
- lysozyme
2. Nose - nasal hairs ( trap )
3. Nasopharynx & upper resp. Tract (URT )
- Mucous ( trap )
- Natural habitat of pathogens ( acts like reservoir )
- Favorable conditions
- Humidity
- Low PH
- separate/ protected environment
4. No microbe in lower resp. Tract (LRT)
5. Transient microflora
- There may be E.coli or pseudomona or other gut microbe in nasopharynx due to food contamination.
6. Normal microflora
- strepto, Corynebacteria ( prominent )
- Staph epidermidis, Staph aureus
- Neisseria ( non- gonococcal ), moraxella
7. Change in flora
- Nasopharynx -sterile at birth
- Within 12 hrs- alpha hemolytic streptococci-found in URT
- Pharynx & trachea- flora similar to mouth
- Bronchi & alveoli - normally sterile
- Within 2-3 das- acquires normal & pathogenic flora ( carried by mother & attendants )
#note-
● Vaginally delivered infant's harbor bacterial communities - similar in composition to the vaginal communities of
the mothers;
● C-section babies lack bacteria from the vaginal community- harbor bacterial communities similar to the skin
communities of the mother

Microbiota of gastrointestinal tract (including mouth )

1. GI tract include
- Upper GI tract= mouth + pharynx+ esophagus+ stomach+ duodenum
- Lower GI tract
- small intestine= duodenum, jejunum, ileum
- large intestine= cecum, colon, rectum, anal canal

2. facts
- sterile at birth, but colonization begins soon after with introduction of organisms through food and environmental
exposure
- Microbial populations vary across gastrointestinal sections, influenced by factors like pH and oxygen availability.
- Antibiotic use or medical conditions altering stomach pH can significantly impact microbial flora.
- Imbalance in gut microbiota associated with inflammatory bowel diseases and possibly intestinal malignancies.

3. Mouth
- Favorable condition- humid, exposed envt, nutrients availability ( saliva )- lipid, AA, water, etc
- Microflora-
- streptococcus salivarius ( uniformly present in large no on dorsal surface of tongue )
- strepto, staph, lactobacillus, nisseria, candida
- Change in flora
- Teeth aane se pahele- aerobic condition- aerobic/ facultative aerobes
- Teeth aane ke baad- anaerobic condition ( in between the teeth)- obligate anaerobes
- At puberty-
- Treponema
- bacteroides, melaninogenicus ( colonize b/w teeth & gum )- anaerobic cond.
- Trichomonas tenax (protozoa)- in gingival margins & teeth cavity

Role of the Normal Mouth Microbiota in Dental Plaque and Caries .

- commonly known as tooth decay
- is the breakdown of teeth starting from the surface and progressing inward due to demineralization.
- Dental plaque- a complex biofilm- primarily composed of bacteria originating from the mouth's normal flora- adheres to
tooth surfaces- making a thin organic film covering tooth surfaces.
- Plaque formation involves dynamic interactions between bacteria and the pellicle, as well as among different
bacterial species within the biofilm
- Streptococcus mutans
- Can convert sucrose to glucan/ extracellular glucan polymers that bind the plaque biofilm together- help in
adherence of bacteria to the surface.
- They ferment fructose or other carb to lactic acid→ low PH→ demineralization of enamel (enamel decay)
- Dietary sugars, particularly sucrose, provide substrates for bacterial glycolysis and acid production, leading to
tooth demineralization
- Effective management= physical plaque removal, controlling sucrose intake, maintaining good nutrition, and
oral hygiene practices.
 - Lactobacillus actinomyces - secondary invaders
4. Intestinal tract
- Factors discouraging microbial growth
- Low PH- acid in stomach/ gastric juice/ bile- acts as barrier
( some tolerant lactobacillus or candida sp)
(Stomach's acidic environment limits microbial growth, except for Helicobacter pylori)
- 2 possibility
1) Acid tolerant bacteria - cross the barrier, number increase
2) Low acid production- weak barrier

5. Small intestine-
- Duodenum-10^3-10^6 bact/g
- Jejunum- 10^5-10^8 bact/g
- Ileum- 10^5-10^8 bact/g
6. Large intestine- colon- 10^11 bact/g
7. Microbes are removed-
- Peristalsis
- Mucous
- Desquamation
8. Microbe-
- E.coli, kleb, candida albicans
- Lactobacilli
- Bifidobacterium
- Trichomonas hominis, iodamoeba, entamoeba

Microbiota of urogenital tract

1. Preventive mechanisms
- Flushing action of urine
- Lysozyme in cervical mucosa
2. Urethra
- Male urethra- longer ; female urethra - shorter. Hence females have more chances of urinary tract infection
- Microbe-
- Lactobacilli, staphylococcus epidermidis, streptococcus faecalis,
- Neisseria , corynebacterium
- Enterobacteria, Mycobacterium,
3. Changes in microflora of female GU ( genitourinary tract )
- As per change in physiology
- At birth- sterile
- Within 24 hr- micrococci, diphtheroids, enterococci
- Within 2-3 days - maternal estrin induce glycogen deposition– in vaginal epithelium ( source of nutrients )
This promote lactobacilli growth ( known as doderlein's bacillus )--acid production–adult microflora
(persist as long as the pH remains acidic)
- When maternal estrin removed–no glycogen deposition–bacilli removed–alkaline envt–microflora changed
- pH becomes neutral until puberty, a mixed flora of cocci and bacilli is present.
- Puberty- hormonal changes- estrin production- bacilli reappear- acidic PH- prevent pathogen due to acidic condition
- Menopause- lactobacilli decrease, and a mixed flora returns.
- During pregnancy- staph. Epidermidis, nacilli predominates
 Definitions

1. Microbiota: Microbial flora harbored by normal, healthy individuals

2. Pathogen : microorganisms capable of causing disease.
3. Non pathogen: microorganism that does not cause disease; may be part of the normal microbiota
4. Pathogenicity: ability of an infectious agent to cause disease
5. Infection
- Multiplication of an infectious agent within the body
- Multiplication of the bacteria that are part of the normal microbiota ( GI, skin,etc )- no harm- not considered a infection
- multiplication of pathogenic bacteria ( salmonella sp )- harm- even if asymptomatic - is an infection
6. Disease- possible outcome of pathogen infection–. Development of infection.
7. Invasion
- process whereby bacteria, animal parasites, fungi, and viruses - enter host cells/ tissues & spread in the body.
8. Adherence / adhesion / attachment:
- process by which bacteria stick to the surfaces of host cells.
- After bacteria enters the body, adherence is a major step in the infection process

9. Virulence and its determinants

- quantitative ability of an agent to cause disease
- These agents cause disease when introduced into the host in small numbers.
- involves adherence, persistence, invasion, and toxigenicity
10. Endotoxins and exotoxins
-
11. Toxigenicity
- ability of a microorganism to produce a toxin that contributes to the development of disease
12. Superantigens
- Protein toxins - that activate the immune system by- binding to MHC molecules and T-cell receptors and stimulate large numbers of T
cells to produce massive quantities of cytokines
13. Carriers and their types
- person / animal with asymptomatic infection that can be transmitted to another person / animal.
14. Opportunistic infections
- agent capable of causing disease only when the host’s resistance is impaired (ie, when the patient is “immunocompromised”).
15. Nosocomial infections
- Infection that is contact in certain areas like- hospitals.
- Ex- MRSA- methicillin resistant strep. Aureus ( resistant to antibiotic methicillin )

Association of microbe with specific disease

Koch’s postulates
1. The microorganism should be found in all cases of the disease in question, and its distribution in the body should be in accordance with the
lesions observed.
2. The microorganism should be grown in pure culture in vitro (or outside the body of the host) for several generations.
3. When such a pure culture is inoculated into susceptible animal species, the typical disease must result.
4. The microorganism must again be isolated from the lesions of such experimentally produced disease.

Severity of disease depend on:

D=nV/R DOSE

D- severity of disease Infective dose:

N- dose - no of microbe to which potential host is exposed - Minimal dose necessary to establish/ cause infection
V- virulence - V∝1/n ( n kam toh V jyada )
( the quantitative ability of agents to cause disease. Example-
Involves- adherence, invasion, toxigenicity ) Infective dose of M.tuberculosis- 10 bacilli ( low hai because iski virulence jyada hai→
R- resistance ( include all those factor responsible for thode mein bhi kaam ho jayega ) ( thick cell wall + acid fast bacteria )
resistance ) Whwreas V.cholerae = 1 million ( virulence kam hai )

D ∝ 1/R Lethal dose: (LD)

- amount of the microorganism required to cause death in a specified proportion of
the population or experimental animals within a given period.
- LD is typically expressed as LD50 or LD90
- LD50- dose that kills 50% of infected host
# resistance kam kab hogi?
- Immune system not working properly→ Immunodeficiency, old age
- Less acid production in stomach- more infection
- Vibrio cholerae acid tolerant nhi hai . so jyada microbe chahiye to cross this barrier.

Virulence mechanism
2 possible mechanism-
Many factors determine bacterial virulence or the ability to cause infection and disease.
1. Defensive strategy ( vo strategy jo bacterial cell ko immune system se bachata hai )
a. Capsule→ bacteria produce outer layer of polysaccharides or proteins
- a protective barrier around the cell.
- Also help in adhesion
- enhance bacterial survival by preventing phagocytosis, as they inhibit recognition and engulfment by host immune cells.
- Ex- anthrax, yersinia pestis

b. Biofilm formation
- bacteria adhering to surfaces and producing an extracellular matrix, resulting in the formation of complex microbial
communities.
- provide protection against host immune responses and antimicrobial agents, facilitating bacterial persistence and colonization
of host tissues.

c. Antigenic variation
- refers to the ability of bacteria to alter surface antigens, such as proteins or polysaccharides, to evade host immune
recognition.
- Ex- influenza, african sleeping sickness ( treponema bruce )
d. Adhesins (Adherence factor)
- When bacteria enter the body of the host, they must adhere to cells of a tissue surface. If they did not adhere, they would be
swept away by mucus and other fluids
- Bacteria also have specific surface molecules that interact with host cells- pili, fimbriae
- Ex- spikes, hooks, suction disc ( in giardia )
e. Miscellaneous protein
- M protein in streptococcus
- Waxy coat in tuberculosis

2. Offensive strategy ( vo strategy jo host cell damage krta hai )

a. Toxin
involves the synthesis and release of toxic molecules by bacteria, which can disrupt host cell function or induce tissue damage.
- Endotoxin- toxin released after cell lysis
- Exotoxin- toxins secreted by microbial cell- released outside
Structure
- 2 parts : A & B
- A- activity unit-act on host
- B - binding- cell receptor binding
- A & B ke kitne bhi unt ho sakte hai - A2B, AB2, etc
Toxoid - toxin minus toxicity ( immunogenicity retained )- used in vaccines
( exotoxins, which are modified so that they are no longer toxic)

- Toxin classification
- Based on activity
(i) enterotoxin
- Travelers diarrhea- E.coli
- Cholera
- Clostridial food poisoning
(ii) neurotoxin
- Interfere with transmission of nerve impulse
- Botulism
- Tetanus
- Outcome→ paralysis (2 types- flacid & spastic )
(iii) cytotoxin
- Toxic shock syndrome
- E.coli 0157 ( deadly strain )
 b. Tissue invasion
- Tissue invasion–the ability of bacteria to penetrate and enter host tissues–facilitated by adherence to host cells and subsequent
cellular uptake.
- By invading host tissues, bacteria can establish infection at specific sites, evade immune surveillance, and initiate pathogenic
processes leading to disease.

c. Enzymatic degradation
Many species of bacteria produce enzymes that are not toxic but do play important roles in the infectious process
- Tissue degrading
- Allow spread of infection ( spreading factors )
(i) hyaluronidase- act on hyaluronic acid ( part of connective tissue )
(ii) collagenase - act on collagenase ( framework of connective tissue )
(iii) haemolysin- act on RBC
(iv) leukocidins- act on WBC
(v) kinases - breakdown/ remove clots→ allowing trapped bacteria to cause infection
Ex- staphylokinase, DNAse ( DNAse dna ko cleave karega- viscosity kam pus ki
Helicobacter pylori- produce urease
Ex- streptokinase- Streptokinase has been used in treatment of acute myocardial infarction to dissolve fibrin clots.

Transmission of infection
1. It is the passing of infection- causing communicable disease from the infected host individual to the healthy person.
2. Transmission-
- Bacteria exhibit adaptability to diverse environments ensuring their survival and enhancing transmission.
- Some bacteria employ strategies such as causing asymptomatic or mild infections within hosts, rather than fatal outcomes, to increase
the likelihood of transmission.
- Example-
Clostridium in the environment, transmitted through ingestion or wounds, aided by spore formation for survival.
- Clinical Manifestations and Transmission
- Vibrio cholerae induces diarrhea, contaminating water sources or seafood, facilitating transmission through ingestion.
- Mycobacterium tuberculosis spreads primarily through respiratory droplets expelled during coughing, emphasizing
person-to-person transmission.
- Many bacteria responsible for nosocomial infections are transmitted via hands, underlining the importance of hand hygiene in
infection control.
3. infection-
- Bacteria initiate disease by attaching to host cells
- multiply
- spread directly through tissues or via the lymphatic system into the bloodstream (bacteremia)
- Example-
Vibrio cholerae ingested→attracted to gut epithelium→ adheres to the mucosal surface→Production of cholera toxin disrupts
electrolyte balance→inducing watery diarrhea

Pathophysiological effect of LPS (endotoxin )

LPS of gram -ve bact - are bact cell wall component- often liberated when bacterial cell lyse.
- Heat stable
- Mol wt b/w 3000-5000D
- There are 3 main components-
1) Lipid A- recognized by immune system- responsible for cytokine stimulation
2) Oligosaccharide core
3) Outermost O ag polysaccharide

Endotoxin- Mainly these are LPS→in blood→ detected by Macrophage, monocytes, etc→ reaction/ effects ( listed below )
1. Can bind to TLR→ innate immunity active ( PRR-PAMP )
2. Antigen directly activating complement pathway ( alternative pathway )--> membrane + tissue damage→ MAC formation→ lysis + inflammation
3. Activate immune system
4. Detection by macrophage or monocyte→ secretion of IL & TNF→ inflammation
5. Activate factor 12→
- Activate plasminogen- make plasmin- plasmin breakdown fibrin→ fibrin split product→ decrease in platelet & fibrinogen level
- Activate coagulation cascade→ fibrinogen converted to fibrin→fibrin production→ fibrin clots formed
 6. Symptoms like Fever + leukopenia + hypotension + Shock
- Hypoglycemia ( endotoxin leads to high sugar consumption by cell- low sugar in blood - hypoglycemia )
- All these Result in impaired perfusion of organs ( proper o2 & nutrients nhi pahuchta organ tak )--> Result in DIC ( disseminated
intravascular coagulation )--> organ failure→ death
7. Cause- platelets adherence to endothelial→ occlusion of small blood vessel→ causing Ischemic or haemolytic necrosis→ blood is not able to
reach organ properly→ organ failure→ death
8. Bacteremia- presence of bacteria in blood
Result→
- Leukopenia + fever + hypoglycemia
- Maybe widespread atreolar & venulor constriction→ vascular dilation + increased vascular permeability + decrease in venous return→
lower cardiac output→ peripheral vascconstriction

To detect LPS/ endotoxin→ limulus test ( endotoxin coagulate in limulus gel

Endotoxin - in case of gram -ve

In gram +ve- peptidoglycan and other protein→ can show similar signs

Endotoxin in general are not that toxic but when in large quantity→ highly toxic

Properties Endotoxin Exotoxin

secretion Component of outer membrane of gram -ve organism Excreted out of living cell
( retained inside the cell- released when cell lyse )

Specific receptors not found on cells ( PRR-PAMP Usually bind to specific receptors on cells
interaction) ( innate immunity in action wohoo!! )

organism Only in gram -ve Both gram +ve & -ve

component Mainly these are LPS Mainly these are proteins

( lipid A with KDO ) - 2-keto-3-deoxy- octonicacid

Heat stable Heat stable Unstable ( destroyed by heating over 60 degree )

immunogenicity Weakly immunogenic Highly antigenic and immunogenic ( adaptive immunity in

action )

toxoid Can't make toxoid out of it Toxoid can be made

toxicity Moderately toxic Highly toxic

receptor Effects - due to - binding to TLR, IL, complement Usually have specific receptor on cell

fever Pyrogenic ( fever ) Usually do not produce fever in the host

Encoded by Coded by chromosomal gene Plasmid gene

Jarisch-Herxheimer Reaction
- two dermatologists who independently described it: Adolf Jarisch and Karl Herxheimer
- reaction that can occur shortly after initiating antibiotic treatment for certain infections
- reaction typically manifests within hours of antibiotic administration and is characterized by fever, chills, headache, myalgias, exacerbation of
skin lesions, and sometimes hypotension.
- result from the release of endotoxins or other microbial components following rapid killing ( cell lysis ) of bacteria by antibiotics, triggering an
exaggerated immune response.
 UNIT 2 : Human diseases caused by bacterial pathogens

Bacillus anthracis
1. Properties
- Aerobic
- Spore forming ( centrally located spores- endospore )
- Non motile
- Rods ( with square end )
- Blood agar- medusa head colony ( round ) + non hemolytic
2. Pathogenesis
- Anthrax
- Affect both humans & animals ( usually herbivore- goat, sheep, horse, etc )- mainly gazing animal
- Entrance- mouth / soil spore
In humans-
( when comes in contact with infected person/animal or contaminated animal product )
a. Cutaneous anthrax
b. Pulmonary anthrax
c. Intestinal anthrax
3. Virulence factor
- Majorly capsules- polysaccharide
- Toxin
- Component of toxin= edema factor + lethal factor + protective factor
4. Vaccine available
5. Transmission -
- Spore→ mouth→vegetative form→ edema→ lymphatic & blood stream → germinate & multiply in blood → death
6. Virulence of anthracis
a. Capsule
- Mostly polysaccharide but for bacillus anthracis → poly D-glutamic acid ( anti phagocytic )
- Capsule encoded by plasmid pX02
- Spores phagocytize ho jate hai but cell nhi.
( so spores phagocytize hue lungs mein→ lymph node mein aaye→ germinate→ cell formed→ can not be
phagocytized easily )
b. toxin
- A2B type toxin ( tripartite )
(i) protective - allows binding of toxin to surface
(ii) edema factor- cAMP production increase krta hai- increase in fluid secretion from cell
(iii) lethal factor- to kill host cell - hemorrhage or necrosis mechanism
# genes for these toxins encoded by plasmid pX011

Cutaneous anthrax
1. Anthrax of skin
2. Entry- skin ( face, neck, hand, arms, back, etc
3. Mechanism
- Formation of bumps called papules- pruritic papule ( fluid filled vesicle- itching ) - within 1-7 days after entry of spores
( papule resembles like insect bite )
- Papule changes into vesicle ( fluid secretion starts )
( sometimes small vesicles fuse → necrotic ulcer/ black ulcer )--> black eschar
- Eschar dries and separates from the skin ( sukh ke jhad jate hai )
( but scar remains )- many weeks - to heal this scar
# in 20% patients- it may lead to→ systemic infection or meningitis and death
4. Can also cause
- Lymphangitis and lymphadenopathy } swelling of lymph nodes/ increase in size
5. Least dangerous
Pulmonary anthrax
1. Fatal- deadliest form of anthrax
2. mechanism
- Dust from infected wool ( during wool sorting→ dust → spores→ spores phagocytized in lungs by macrophage→
transported to lymphatic drainage & lymph node ( mediastinal node )- chest area→
- germinate in lymph node→ toxin production
- RESULT-
- Hemorrhagic media stinitis
- Sepsis
- Hemorrhagic meningitis (brain)
- Hemorrhagic pneumonia

3. Early manifestation
- Hemorrhagic necrosis
- Edema of media stinal
- Sub sternum pain ( sternum bone ke niche )
- On x ray→ media stinal widening visible
Lungs enclosed within pleura →hemorrhagic pleural effusion ( inner and outer pleura ke beech fluid )--> X ray
RESULT- coughing + sepsis
- bact enter into blood stream now
- Can reach GI tract
4.

Intestinal anthrax
1. Symptoms- enteritis + bloody diarrhea + abdominal pain+ vomiting

Streptococcus pyogenes
1. Properties -
- Gram +ve
- Non motile
- Non spore forming
- Produce extracellular molecules
- aerobic/ facultative anaerobe
- 37 degree optimum

- Hemolytic bacteria
Can be identified by hemolysis on blood agar
(i) alpha hemolytic type- streptococcus viridans
(ii) beta- S. agalactiae- STREPTOCOCCUS PYOGENES
(iii) gamma- S. pneumoniae ( no hemolysis )
# hemolysis promoted in a 10% CO2 environment.

- Lancefield group A ( rhamnose N acetyl glucosamine cell wall )

- Cause hydrolysis of PYR ( L-pyrrolidonyl 2-naphthylamide )- PYR positive
- Susceptible to - antibiotic Bacitracin
- Hyaluronic acid capsule

- Different strains-
- Virulence strain- matte colonies
- Non-virulent strain- glossy colony
2. Classification
- Based on colony morphology, hemolytic reaction, serological basis, biochemical feature.
- Based on capsule polysaccharide S.pneumoniae- classified into 90 antigenic type
LANCEFIELD CLASSIFICATION
- Based on cell wall carbohydrate composition
- 20 groups- [A-H] & [K-U]
- GroupA- rhamnose N acetyl glucosamine
- Group B- rhamnose glucosamine polysaccharide
- Group D- glycerol teichoic acid
3. Antigenic structure
a. Have M protein
- Play role in virulence
- Inhibit phagocytosis
- Appearance- hair like projection of cell wall
- Rod like coiled structure that separate functional domain
- Heat and acid stable
- Many immuno- antigenic determinant sites→ bohot sare M protein ban sakte hai→ reoccured infection

- Play role in rheumatic fever

( M protein + other cell wall protein→ ab production→ interfere cardiac cycle→ rheumatic fever )

b. Enzyme
(i) streptokinase
- Convert plasminogen to plasmin→ it will digest fibrin and other protein
- Used to treat blood clots
- Anti streptokinase ab → in diagnostics→ to detect this infection
(ii) streptodornase
- DNAse ( pus ki viscosity kam )
- Combination of streptokinase & streptodornase used sometimes
(iii) hyaluronidase
- Also known as pedic factor
- Spreading factor
- Hyaluronic acid in tissue ( helps in joining/ adherence of cells ) degraded by this enzyme
(iv)NADase
- Works as leukosidase- kills leukocyte
(v) hemolysin
- 2 types of hemolysins produced

Streptolysin O Streptolysin S

Oxygen labile Soluble in serum + stable in presence of O2

Leukotoxic activity Not antigenic

Anti streptolysin O Ab used for standard Can’t be used for diagnosis→ antigenic nhi hai→ ab
serological process for retro specific diagnosis nhi banegi
Range - 160-200→ abnormally high–. Suggest
recent infection

c. Toxin
- Pyrogenic toxin ( pyrogenic- fever )
- Erythrogenic toxin
- Acts as superantigen
- 3 types- A, B & C
- Produced by group A streptococci when they have lysogenic bacteriophage→ associated with disease
- Streptococcal toxic shock syndrome
- Scarlet fever
- May cause skin infection
- Generally have M protein type I &II
4.