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PATHOGENESIS is the steps or mechanisms involved in the development of the disease PATHOGENICITY is the ability to cause disease PATHOGEN a microorganism capable of causing disease PATHOLOGY is the study of the structural and functional manifestations of the disease
Infection Versus Infectious Disease
• Infectious Disease
-is a disease caused by a microbe and the microbes that cause infectious disease are collectively referred to as pathogens.
-according to many microbiologists, infection means colonization by a pathogen.
WHY INFECTIONS DOES NOT ALWAYS OCCCUR
• The microbe may land at an anatomical site where it is unable to multiply • Many pathogens must attach to specific receptor site before they are able to multiply and cause damage • Antibacterial factors that destroy or inhibit the growth of microbes maybe present at the site where the pathogen lands • The indigenous microflora at the site may inhibit growth of the foreign microbe by occupying space and using up the available nutrients • The indigenous microflora at the site may produce antibacterial factors (bacteriocins) that destroy the newly arrived pathogen. • The individuals nutritional and overall health status often influences the outcome of the pathogen/host encounter • The person maybe immune to that particular pathogen as a result of prior infection or vaccination • Phagocytic white blood cells may engulf and destroy before it has an opportunity to multiply, invade and cause disease
FOUR PERIODS IN THE COURSE OF AN INFECTIOUS DISEASE
INCUBATION PERIOD- is the time that elapses between
the arrival of the pathogen and the onset of symptoms.
FACTORS INFLUENCING THE INCUBATION PERIOD:
• • • Overall health and nutritional status of the host Virulence of the pathogen Numbers of the pathogens that enters the body
PRODROMAL PERIOD- time during which the patient starts to feel
something wrong but does not yet experience the actual symptoms of the disease
PERIOD OF ILLNESS- time when the person experience the typical
symptoms of the disease. Communicable diseases are most easily transmitted during this stage.
CONVALESCENT PERIOD- time when the person recovers.
Person may recover from the illness but there may be permanent damage of tissues of the affected area
The course of an infectious disease
Exposure to pathogen
Period of Illness Convalescence
Localized Versus Systemic Infections
• LOCALIZED INFECTIONS
-an infection that remains localized at one site or it may spread.
• SYSTEMIC/GENERALIZED INFECTIONS
-an infection that has spread throughout the body.
Acute, Subacute, and Chronic Diseases
• ACUTE DISEASE
-has rapid onset usually by a relatively rapid recovery
• CHRONIC DISEASE
-has an insidious (slow) onset and lasts a long time
• SUBACUTE DISEASE
- diseases that come on more suddenly than chronic diseases but less suddenly than acute diseases
Symptoms of a Disease Versus Signs of a Disease
• SYMPTOM OF A DISEASE
- some evidence of a disease that is experienced or perceived by the patient.
Asymptomatic disease (clinical disease)
-a disease in which the patient is experiencing symptoms
Symptomatic disease (subclinical disease)
-a disease that the patient is unaware of because she/he is not experiencing any symptoms.
SIGN OF A DISEASE
- some type of objective evidence of a disease
- a disease that may go from being symptomatic to asymptomatic, and then some time later, go back to being symptomatic.
Stages of syphilis
Syphilis infection (3 weeks)
Primary: Chancre (2-6 months)
Secondary: Rash, lesions, fever, hair loss (2-6 months)
Latent Stage: No symptoms (5-10 years)
Tertiary: Destruction of brain, heart, spinal cord, and/or other organs
Primary Versus Secondary Infections
• • • One infectious disease may commonly follow another: PRIMARY INFECTION- the first disease SECONDARY INFECTION- the second disease
STEPS IN THE PATHOGENESIS OF INFECTIOUS DISEASES
• ENTRY of the pathogen into the body. - Portals of entry include penetration of skin or mucous membranes by the pathogen, inoculation of the pathogen into bodily tissues by an arthropod, inhalation, ingestion, introduction of the pathogen into the genitourinary tract or introduction of the pathogen directly into the blood. ATTACHMENT of the pathogen to some tissues within the body. MULTIPLICATION of the pathogen. INVASION/SPREAD OF THE PATHOGEN EVASION OF HOST DEFENSES
• • •
• VIRULENT STRAINS - are capable of causing disease. AVIRULENT STRAINS -not capable of causing disease.
ATTACHMENT • RECEPTORS - receptors and integrin are molecule on the surface of the host cell that a particular pathogen is able to recognize and attach to which are often glycoprotein molecules Adhesins and ligand are used to describe the molecule on the surface of the pathogen that is able to recognize and bind to a particular receptor • BACTERIAL FIMBRIAE (PILI) - long thin hair like, flexible projections composed primarily of an array of proteins called pilin which enable the bacteria to attach to surfaces and cause infection in that part of the body
OBLIGATE INTRACELLULAR PATHOGENS
Rickettsia, Chlamydia as well as Ehrlichia must live within the host cells in order to survive and multiply.
FACULTATIVE INTRACELLULAR PATHOGENS
These are pathogens that are able to survive intracellularly and extracellularly. These microorganisms are able to survive within phagocytes. Once bacteria are ingested by white blood cells like macrophages, the phagosome fuses with the lysosome. Lysosomes contain hydrolytic enzymes, hydrogen peroxide, superoxide anions which will cause the destruction of bacteria. But some organisms like the Mycobacterium tuberculosis contain wax on their cell wall which prevent the digestion of the organism from the enzymes of the macrophages. Rickettsia produce phospholipases that destroy the phagosome membrane thus preventing the fusion of the lysosome and phagosome sparing the bacteria from digestion of hydrolytic enzymes.
The presence of capsules that surround the bacteria protects the bacteria from phagocytes because phagocytes lack receptors for polysaccharide material of which the capsule is made. Because they are not phagocytosed, they are able to multiply and cause disease. Encapsulated bacteria include Klebsiella, Haemophilus and Neisseria meningitides as well as S. pneumoniae.
Bacterial flagella are considered virulence factor because they enable the bacteria to invade aqueous areas of the body that nonflagellated bacteria are unable to reach. Flagella also enable bacteria to evade phagocytosis because of its movement which enable it to move at a faster pace thus making it difficult for the phagocytes to catch a motile organism.
• NECROTIZING ENZYMES - bacteria produce
proteases and lipases which cause destruction of tissues like necrotizing fasciitis by Strep pyogenes and gas gangrene or myonecrosis with Clostridium species
-Staph aureus produce coagulase which enable it to clot plasma and thereby form a sticky coat of fibrin around themselves for protection from phagocytes, antibodies and other host defenses
-or fibrinolysins. This substance will dissolve the fibrin clot that the host will attempt to form in order to wall and prevent the organism to invade deeper into body tissues in order for the organism to escape from the clots. Streptococcus produce streptokinase which is able to dissolve blood clots. Streptokinases are also able to dissolve blood clots in cases of thrombotic stroke or myocardial infarction.
- called spreading factor because it enables the pathogen to spread through connective tissue by breaking down hyaluronic acid, which is a polysaccharide cement that holds tissues together. It is secreted by staph, strep and clostridium species
-breaks down collagen which is the supportive protein found in tendons, cartilage and bones, enabling the pathogen to invade tissues. Clostridium perfringens are able to invade tissues by secreting collagenase and hyaluronidase
-enzymes that cause the destruction of red blood cells producing lysis as well as providing iron to the pathogen. Alpha hemolytic strep causes a green color around the colony whereas beta hemolytic strep produces a clear zone around the colony
-enzyme produced by Clostridium perfringens which breaks down phospholipids collectively referred to as lecithin. This enzyme is destructive to cell membrane of rbc and other tissues
-toxins that are integral part of the cell walls of Gram negative bacteria that can cause adverse physiologic reactions like septicemia which produces chills, fever, prostration and the presence of bacteria and their toxins in the bloodstream. The cell wall contain lipopolysaccharide called Lipid A or endotoxin, causing fever and shock. There is reduced mental alertness,, confusion, rapid breathing, chills, fever and there is low perfusion of organs due to shock leading to organ failure. Blood clots may form within blood vessels. There is 30-35% mortality rate associated with Gram negative sepsis
- poisonous proteins produced by pathogens often named for the target organs they affect
- most potent exotoxin produced by Clostridium tetani and Clostridium botulinum. Tetanospasmin affects control of nerve transmission where there is blockade of the inhibitory impulses producing continuous contraction producing spasm. This is called a spastic paralysis. Botulinal toxin on the other hand blocks nerve impulses producing flaccid paralysis in which the patient’s muscles are relaxed
2. ENTEROTOXINS -cause diarrhea and sometimes vomiting (toxin A). Toxin B produced by Clostridium difficile damages the lining of the colon, leading to pseudomembranous colitis
3. TOXIC SHOCK SYNDROME TOXIN l
-produced by strains of Staph aureus and Strep pyogenes which primarily affects the integrity of capillary walls
4. EXFOLIATIVE TOXIN EPIDERMOLYTIC TOXIN
-cause sloughing of the epidermal layers of the skin leading to SCALDED SKIN SYNDROME
-toxin that destroys leukocytes produced by staph and strep
6. DIPHTHERIA TOXIN
-toxin produced by Corynebacterium diphtheria, which inhibits protein synthesis killing mucosal epithelial cells and PMN’s as well as adversely affecting the heart and nervous system. The toxin is coded for by a bacteriophage gene
MECHANISMS BY WHICH PATHOGENS ESCAPE IMMUNE RESPONSES
• ANTIGENIC VARIATION -pathogens able to periodically change their surface antigens. Ex are influenza viruses, HIV, Neisseria gonorrhea, trypanosomes CAMOUFLAGE AND MOLECULAR MIMICRY -adult shistosomes are able to conceal their foreign nature by coating themselves with host proteins. In molecular mimicry, the pathogen’s surface closely resemble host antigens and are therefore not recognized as foreign DESTRUCTION OF ANTIBODIES - H. influenza. Neisseria gonorrhea and streptococci produce an enzyme IgA protease that destroys IgA antibody
Reporters: Ana Micca dela Rosa Niña Scarlet Nahilat Angelique Silvestre Prisvic Llamera Clark Llamera Roscel Melody Lavarias
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