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FLORA NORMAL

EFRIDA WARGANEGARA

Introduction
 Many of m.o. this form what is
termed the ‘indigenous’ or
‘normal flora’ of the body, a
collection of spesies routinely in the
normal, healthy individual
 Some of this species are positively
benefecial to the host
 M.O. that benefit from this
association without harming the

host are referred to as
‘commensals’

o. Introduction  Term ‘flora’ is used because the majority of the m. are bacteria.  Antibiotic therapi can eliminated normal flora. but is not possible to eliminate the normal flora of the skin or intestine antibiotica can drastically reduce their number to a minimum  The host may then be overun by introduce patogens or by overgrowth .

of m.o. normally present in small
number

Commensalism
 The normal flora (commensals) is
aquired rapidly during and shortly after
birth and changes continously
throughout life.
 It has been estimated that human have
approximately 1013 cells in the body and
something like 1014 bacteria associated
with them, the majority in the large
bowel.
 Virus, fungi and protozoa can also be
found in healthy individuals, although

these form only a minor component of
the total population or resident organism

that take up residence on its skins and in the digestive tract. in food. are derived from the mother or others who come into contact with the infant.o.  Some of these m. and in the environment soon also become established as residents on the newborn .o.  Various m. but at delivery m. on other human.o. come into contact with the infantbaby is exposed to a variety of m.o. Commensalism  Before birth the fetus is essentially in a steril environment.

 Constituent organism present at any given time reflect the age. nutrition and environment of the individual concerned .

but others establish themselves and produce microcolonies colonized the host microflora established (resident)  Not all area of the body are occupied by commensal spesies  There are appreciable numbers of m. and skin .o. Tract. Commensalism  Most m. are transient paserby that are destroyed by conditions in the host. lower intestinal tract. in the : Upper Resp.o.

 The blood. urine and endothelial tissues are normally steril . urinary tract and stomach contain few m.o. spinal fluid. Esophagus.

diatery alteration. at any body site are : 1. The availability of appropriate receptor sites for attachment 3. The availabiliy or unavailability oxygen 2. The pH of the host site . with only minor changes resulting disease. Commensalism  Microflora remain with the host for life.o. or hormonal changes  The factors that influence the kind and number of m.

The influence exerted by other m.o. The availability of nutrient 5. The immunological respone of the host to the presence of the m. at the site. .4.o. 6.

B12. k) certain vitamine deficiencies in human diet can be remedied by bacterial vitamin synthesis in the intestinal tract . riboflavin. . vit. for example : 1) some m. in intestinal capable sinthesizing vitamin (pathothenic acid. Advantages of Flora Normal  Many of the flora normal may be important in maintaining the health of the host.o.

2) some flora normal produce metabolic product that are effective in preventing invasion by parasites (flora normal in intestinal tract produce fatty acid that inhibit ingested bacteria that attempt to colonize the host .

together with lack of available . b) consuming available nutrients. which. and c) producing compound toxic to other bacteria 4) Gut bacteria release a number of factors with antibacterial activity (bacteriocin. Advantages of Flora Normal 3) Normal flora excludes patogen by : a) covering binding sites that might otherwise be used for attachment. colicin) and metabolic waste product.

oxygen. prevent the establishment of other species 5) Vaginal lactobacilli maintain an acid environment that supresses growth of other organism .

.skin is broken.  This may happen under a variety of circumstance : .when intestine perforated or . Disadvantages of Flora normal  Disadvantages of Flora normal lie primarily in the potential for spread into previously sterile parts of the body.

. coli from the perianal skin ascend the urethra .during extraction of teeth. .E.

potential pathogens take the opportunity to increase .the composition of the flora normal changes (after antibiotics).when the immune system becomes ineffective (AIDS)  Under these conditions.when the local environment changes (increases in stomach or vaginal pH) or . .Disadvantages of Flora normal  Overgrowth by potentially pathogenic members of the normal flora (Candida albicans. Clostridium difficille) can occur when : .

their population size or invade tissues. so becoming harmful to the host .

as direct result of the activities of the human host (consuming food) . and .Physiological variation within the host ( hormonal changes). The Dynamic Nature of the Flora Normal  Composition of normal flora is dynamic – can change change occur in response to : .

Obese more members Clostridium and Bacillus sp. of obese and lean/thin is differ : .lean/thin more members Bacteroides sp. The intestinal m. and . .o.

Contoh Flora Normal Flora Normal in Human Site Normal Flora Nose Staphylococcus Corynebacterium Mouth Streptococcus Leptotrichia Fusobacterium Veillonella Actinomyces Throat Streptococcus Haemophillus Moraxella Neisseria Corynebacterium Mycoplasma Skin Staphylococcus Propionibacterium Large - Bacteroides Streptococcus Intestine Escherichia Candida .

Proteus Clostridium Klebsiella Pseudomonas Lactobacillus Enterococcus Urethra Streptococcus Escherichia Mycobacterium Bacteroides Vagina Lactobacillus .

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PATHOGENESIS OF INFECTION EFRIDA WARGANEGARA .

3. PATHOGENESIS PATHOGENESIS .PATHOGENESIS OF INFECTION 1. PATHOGENESIS OF BACTERIAL INFECTION 2.

OF VIRAL INFECTION OF FUNGAL INFECTION .

causes ) or . ) causing disease capable of  Some microoragnism : - pathogenic . PATHOGENESIS OF BACTERIAL INFECTION  A Pathogenic microoragnism  .1.

.mayority harmless .causes disease  under certains conditions: * introduced into a normally steril body site * infection of an immunocompromized host .

PATHOGENESIS OF BACTERIAL INFECTION Bacterial Pathogenesis includes : .the mechanism that lead to the development of signs and symptoms of disease Many infections caused by bacteria that are commonly considered to the pathogens are inapparent or asymptomatic .initiation of the infectious process.1. and .

 Disease occurs if the bacteria or immunologic reactions to their presence cause sufficient harm to the person .

1. to host cells 3. and . adhesion of the m. propagation of the organism -> invasion of the host cells and tissues 4. entry into the host. with evasion of host primary defences 2. PATHOGENESIS OF BACTERIAL INFECTION  The infectious prosses generaly : 1.o. damage to host cells by bacterial toxins or an inflamatory response of the host.

evasion of host secondary defences  exit and transmission to another person .5.

o. or penetrating -> body surface of the normal healthy host 2. Every Infection is a Race Infection is a race : between the capasity of the m. M.o has spesific mechanism  attaching. to multiply. is introduced into normal healthy host  biting arthropod . spread. and cause disease and the ability of the host to control and finally terminate the infection  Four type of infection : 1. M.o.

is unable infect a normal.3. M.O.O. healthy host  unless there is impairment of surface or systemic defences . is introduce into an otherwise normal. healthy host  skin wound or animal bite 4. M.

tissues)  Receptor molecules  benefit for infectious agents thus critical determinant of cell susceptibility at the body surface and all tissue .always face of these natural mechanism  Succesfull m. have spesific molecules  bind to receptor molecules host (body surface. transversing these body surface  M. possess efficient mechanism for attaching.o.o. Entry in the Host  All these body surface have : cleansing and defence mechanism  m.o.

 After binding can multiply at the surface or
enter the cell and infect it.

Entry in the Host
 If m.o. to be transmitted to a fresh host  must also exit
from the body.

 They are either shed in :
- a large numbers in secretion, excretion, or
- available in blood  for uptake by blood-
sucking artheropods, needles and so on

 Body surface as sites of m.o. infection and
sheding : 1. Skin of a site of entry
2. Respiratory tract of a site of
entry 3. Intestinal tract of a site
of entry

4. Urogenital tract of a site of
entry 5.Oropharynx of a site of
entry

Skin as a site of entry  Skin (fatty acid. saliva and feces) . biting arthropoda (mosquitoes. sebaceous glands. contaminating mouth. fleas and sandflies. teat canal. aberasions or burns. penetrating the skin during feeding. wounds. substances in sebaceous/other gland. a small break in the skin. and material producted by the normal flora of the skin) inactive microorganism  Skin bacteria can introduce by : hair follicle. ticks.1.

. microorganism have efficient attachment mechanism to infect normal conjunctiva. it is keep clean by flushing action of tears. Conjunctiva.

Respiratory tract as a site of entry  In the upper or lower tract : inhaled microorganism like other particle entrapped in mucus back of the throat by cilliary action and swallowed (forming the mucocilliary sheets). encouter alveolar macrophage (function is to remove .2. Inhibiting ciliary activity  invading microorgansm  establish themselves in the respiratory tract  Inhaled microorganism the alveoli.

.foreingn particle and keep these air space clean) most are destroyed by macrophage but one or two pathogens have learnt either to avoid phagocytosis or to avois destruction after phagocytosis.

perhaps acting as a mechanical barrier to infection * contain molecules that binding to microbial adhesins.3. acids. thus blocking attachment to host cells . Intestinal tract as a site of entry  Infection in the intestinal tract  affected by the presence of mucus. enzymes and bile  Mucus : * protect epithelial cell.

o.( V.cho. Salm) can propel themselves through the mucus layers and are thus likely to reach epithelial cells to make spesific attachment . * containing secretory IgA antibodies which protect the immune individual against infection  Motile m.

urethra much shorter (5 cm) but also suffers from anus.go. urethra is 20 cm long. and b) female. Urogenital tract as a site of entry  The UGT is a continuum m. nearly always invade from the exterior. via the urethra. spread easily from one part to another.4. Chlamydia) have specialized attachment mechanism * Urinary infection (cystitis) in : a) male. * Urine in the bladder is sterile.o. which is a constant source of intestinal bacteria  The invading bacteri : begin by colonizing the mucosa around the urethra and probably have special attachment mechanism to cells in this area  and . unless used catheter or flushing activity is impaired. succesfull invaders (N. rare.

invasion by mechanical deformation of the urethra and surrounding region that occurs during sexual intercourse .

4. and certain lactobacilli colonize the vagina. the vaginal epithelium contain glycogen. and repeated introduction of a contaminated pathogen-bearing foreign object (the penis) make the vagina particularly vulnerable to infection (STD) * During reproductive life. Urogenital tract as a site of entry  The vagina : no particular cleansing mechanism.0 inhibits colonization by all. except the . metabolizing glycogen to produce lactic acid pH : 5.

o. lactobacilli and certain Streptococci and diphtherois  If other m.are to colonize and invade must either have spesific mechanism (for attaching).o. oestrogen imbalance) these are the m. Responsible for STD . or take advantages of impaired defences (tampon.

or due to changed resident flora after broad spectrum antibiotics  When salivary flow is decreased for 3-4 hours (as between meals) or dehydrated patient.5. leucocyte present on mucosal surface and in saliva). normal flora. there is .  Additional defences : IgA and antimicrobial substances (lysozyme.  Factor that reduce mucosal resistance : Vitamine C defeciency. cheek and lips. aided by masticatory and other movement of the tongue. Oropharynx as a site of entry A natural cleansing mechanism is : flushing action of saliva.

a four-fold increase in the number of bacteria in saliva .

Virulence and Pathogenicity  Virulenceand Pathogenicity are often interchangeably  Virulencecan quantified by how many m. are required to cause disease in fifty percent of those exposed to the pathogen ( ID50 and LD50)  Virulencefactor are those characteristics of a bacterium that enhance its .o.

that is.patgogenicity. the ability to cause disease .

m. Entry into the Host the first step. by one of several ports (resp. must overcome a diversity of host defences before it can establish itself  These include : phagocytosis. urogenital tract. and various hydrolytic and proteolytic enzyme found in tne saliva.o. stomach. and small intestine . and skin)  Once entry is achieved. GI tract. the acidic environments of the stomach and urogenital tract. Tract. Virulence Factor 1.

 Bacteria that have an outer polisacharida capsule have a better chance of surviving these primary host defences .

Virulence Factor 2. or washed from organs with significant fluid flow (urinary and GI tract)  Adherence also allows each attached bacterial cell to form a microcolony . or hydrophobic adhesion (particularly hydrophobic cell walls interaction)  Adherence enhance virulence by preventing the bacteria from being carried away by mucus.pyogenes). Adherence to Host Cells Some bacteria use pilus/fimbrial adhesion (N. S.go. or afimbrial/cell sutface adhesion molecule.

spreading from the initial site of infection  Invasiveness is facilitated by several bacterial enzyme. which can be either pyogenic or granulomatous. Virulence Factor 3. the most of which are collagenase and hyaluronidase degrade component of the extracellular matrix. depending on . providing the bacteria with easier acces to host cell surface  Invasion is followed by inflamation. Invasion of Host Cells & Tissues is central to the infectious process (for many disease- causing bacteria)  Invasive bacteria are those that can enter host cells or penetrate mucosal surface.

m. granulomatous – fibroblast. (pus -neutrophyl. and macrophage) .o. lymphocyt.

of which there are two general type : the exotoxin and (protein. Virulence Factor 4. Exotoxin : * Some of the most poisonous substance (tetanus) * Exotoxin protein generaly have 2 polypeptide component (for binding and for toxic effect) * most are rapidly inactivated by moderate heating (60o C) * treatment with dilute formaldehyd : destroyed the toxic activity of most exotoxin but does not affect their . bacteria) A. bacteria) the endotoxin (lipopolysacharida. not secreted. and Gram neg. but are integral component of the cell walls of Gram neg. secreted by both Gram pos. Bacterial toxin some bacteria cause disease by producing toxins.

are usefull in preparing vaccines) .antigenicity (called toxoid.

Virulence Factor  Some of the Exotoxin are : a. Toxic Shock Syndrome Toxin-1 (TSST-1) – Staph. Alpha toxin – lecithinase – C. erythrogenic toxin – streptococcal . perfringens d. Pyrogenic exotoxin A. Diphtheria toxin – Coryn. Tetanospasmin – Clost.aureus e. tetani c. diphtheriae b.

cholerae. Vib. Yers. Staphylococcal. perfringens. enterocolitica.f. parahemolyticus . Clost. Enterotoxin : Vib.

lipopolysacharides/LPS  They are released into the host’s circulation following bacterial cell lysis  LPS consist of polysacharide O (somatic antigen. Endotoxin These are heat stable. do not contain LPS. core polysacharide) and lipid A (responsibility for the toxixity)  Gram pos. their cell wall peptidoglycan can elicit shock syndrome but not . and severa million . lipopolysacharides (LPS) component of the outer membrane of Gram Negatif Bacteria – but not Gram positive. Virulence Factor B.bacteria  Molecular weight : 3000-5000 – lipooligosacharides/LOS.

severe. because so different and also less potent generally not considered to be endotoxin .

early leucopenia. secondary leucocytosis occurs later. and thrombosis collectively referred to as Septic Shock 5.. Disseminated intravascular coagulation (DIC). shock. The main physiologic effects of LPS endotoxins are : 1. lowerd cardiac out put. hypoglycemia because LPS enhances glycolysis in many cell types 4. hypotension. 3.peripheral vascular dilatation. peripheral vasoconstrictie. stagnation in the microcirculation. as does bacteriemia with Gram neg org. after 60-90 minutes for the body to release IL-1 2. fever. increaed vascular permeability. is a frequent complication of Gram neg bacteria and can also occur in the other infection . and impaired organ perfusion and its consequences. Hypotension . decrease venous return.

6. . LPS causes platellet to adhere to vascular endothelium and occlusion of small blood vessel – causing ischemic or hemorrhagic necrosis in various organ.

Virulence Factor 5.. Perfr. Enzymes : many species of bacteria produce enzyme that are not intrinsically toxic but do play important role in the infectious process. and promotes spread of infection in tissue Clost.collagenase (proteolytic) – degrades collagen.lecithinace – damages cell membranes by splitting lecithin Clost. the mayor protein of fibrous connective tissue . a). b) causes deposition of fibrin on the surface of Staph. perfringens . . lesions. which helps them persist in tissues.coagulase – contribute to the a) formation of fibrin walls around Staph. Tissue-degrading Enzymes : . which may help .

protect them from phago-cytosis or from destruction within phagocytic cells. .

Streptokinase (fibrinolysin) – a substance that activates a proteolytic enzyme of plasma able to dissolve coagulated plasma and probably aids in in the rapid spread of Strept.hyaluronidase – enzyme that hydrolyze hyaluronic acid – constituent of the ground substance of connective tissue aid in their spread through tissues. Through tissues . Tissue-degrading Enzymes : . . Virulence Factor a).

(in treatment myocardial infarction to dissolve fibrin clots) .Cytolysins – are hemolysin (dissolve RBC) or leucocidins (kill tissue cell or leucocyte) .

IgA 1 Proteases – is the secretory antibody on mucosal surface. it has 2 primary forms (IgA 1 and IgA 2) Some bacteria that causes disease. produce enzyme Ig A 1 proteases – that split IgA 1 and to inactive the primary antibody found on mucosal surface and thereby eliminate protection of the host by the antibody . Virulence Factor b).

N. . IgA 1 is an important virulence factor of the N. H. and S..meningitidis.inf.go.pneu.

Antiphagocytic Factor – many bacterial pathogens are rapidly killed once they are ingested by poly-morphonuclear cells or macrophages .some pathogen evade phagocytosis or leucocyte microbicidal mechanism by adsorbing normal host components to their surface  protein A Stap. have : polysacharide .Other pathogens have surface factors that impade phagocytosis. Virulence Factor 6. aureus .

protein M  Strep.capsules Strep. pneu. pili  N.meningitis. N. pyogenes.go .

Phase variation is the genetically reversible ability of certain bacteria to turn off and turn on the expression of genes coding for surface antigens b. Antigenic variation involves the modification . Antigenic Switching  A succesfull pathogen must evade the host’s immune system that recognized bacterial surface antigens one important evasive strategy for the pathogen is to change its surface antigens  This is accomplished by several mechanism : a.

of the gene for an expressed surface antigen can assume many different antigenic structure .

Number of m.o.o. shed 2. Stability in the environment 3. The number of m. Exit and Transmission  Transmissiondepends in the first place on three factors : 1. required to infect a fresh host .

Types of Transmission  Transmission is at its most effective when it takes place directly from human to human  Thecommonest. or veneral route . world-wide infectiopns are spread by the respiratory. fecal- oral.

either directly from verteberates or from biting arthropods .A separated set of infection acquired from animal.

Transmission from the skin and skin glands tract 6. Transmission from the oropharynx tract 5. Transmission from the urogenital tract 4. Transmission from the respiratory tract 2. Transmission from the intestinal tract 3. Transmission from blood . Types of Transmission  Type of transmission are : 1.

Vertical and Horizontal Transmission 8. Transmission from animal .7.

and is helped by sneezing and coughing  In sneezing up to 20000 droplets are produced and during a common cold many of them will contain virus particles . Type of transmission 1. Transmission from the respiratory tract  Effective shedding from the nasal cavity depends on an increase in nasal secretion.

throat. a smaller number of m. and lung . Duringcoughing. Are expelled from the mouth.o. larynx.

rather than water and flies . Transmission from the intestinal tract  During most of human. Type of transmission 2. there has been a large scale recycling of fecal material back into the mouth and this continues in developing country  Intestinal infection are still spread in developed countries but via food and fingers.

that appear in feces have generally multiplied in the lumen or wall of the intestinal tarct. but there are a few that are shed into bile . Them.o.

o. induce dischage  Other are transmitted effectively from mucosal sore/ulcers – T. shows displasia and contain infected cells . drink and living space. Type of transmission 3. most are not spread via urine  M. although apparently normal. Shed from the UGT are generally transmitted as a result of mucosal contact with susceptible individuals (sexual activity and cause STD)  If there is a discharge – some of the most succesfull STD transmitted m. Transmission from the urogenital tract  Urine can contaminate food. but UTI are common.O.pall or HS  The Human Papilloma Virus are transmitted from genital warts or from foci of infection in the cervix where the epithelium.

 It may be expected thar semen is involved in the transmission of infection (human cytomegalo virus. hepatitis B. During passage down an infected birth canal m. leading to conjuctivitis. can be wiped onto the conjuctiva of the infant or inhaled. penumonia. HIV)  The female genital tract can also be a source of infection for the newborn child. bacterial meningitis and so on.o. .

Type of transmission 4. but certain virus infect salivary glands and are transmitted in this way.o.  In young children fingers and the other objects are regularly contaminated by saliva and each of these infection is aquired via this route . Transmission from the Oropharynx  Saliva is often the vehicle of transmission m.reach saliva during upper and lower respiratory tract infection.

O. From the skin are generally transmitted by direct contact rather than folowing release into the environment (Staphylococci and HPV) . Transmission from the Skin and the Skin glands  M. Type of transmission 5.

 Dermatophyte are shed from skin and also from hair and nails .

Spread by blood-sucking athropod can be said to have been shed into the blood. Type of transmission 6.  Infectious agents present in blood (hepatitis virus. . Transmission from Blood  Blood is often the vehicle of transmission m.o.HIV) are transmissible also by needles.

either in transfused blood or when contaminated needles are used.  The blood is also the source of infection in transplacental t ransmission and yhis generally involves initial infection of the placenta .

ovum. an individual infecting unrelated individuals by contact. HORIZONTALLY transmitted. placenta. in contrast. blood etc  VERTICAL  Other infection. Vertical and Horizontal Transmission  When transmission is direct from parents to offspring via sperm. Type of transmission 7. milk. respiratory or fecal-oral spread  Vertical transmitted infection. subdivided as in type : a) prenatal (route placenta -> Lues). .

d) germline (viral DNA sequences in human genom -> many retrovirus) . c) postnatal (milk or direct contact -> hepatitis B. Chlam. conjuctivitis).b) perinatal (infected birth canal -> Go.CMV).

indirect (via intervertebrate vector) . ticks and mites)  a mayor source of infection bloodsuckers  Other invertebrate vector (shellfish : moluscs and crustacea) food poisoning and GE  Zoonosis (infection transmitted to humans from infected animal).direct (by contact or eating) or . Type of transmission 8. Transmission from Animals  Animal-tansmission infections can be divided into two categories : 1) involving arthropod and other intervertebrate vectors. wether this is : . and 2) transmitted directly from vertebrates (zoonoses)  Arthropod (Mosquitoes.

 A very large number of pathogens are transmitted in this way by a veriety of different routes : contact. contamination of food or water.o. inhalation. bites and scratches. are spread by : contact. scratch. vectors and contamination with fecal material . bites. or ingestion as food  Dogs and cats are the commonest domestic pets both are reservoir of infection for their owner m.

Terima Kasih .