INFECTION AND IMMUNITY Flashcards
entrance and multiplication of a microorganism in or on a host
INFECTION
an infection w/ functional and structural harm to the host that is usually accompanied by signs and symptoms
INFECTIOUS DISEASE
presence and multiplication of new microorganisms that may cause an infectious disease or eliminated by host defense
COLONIZATION
a microbe capable of causing a disease
PATHOGEN
study of the structural and functional manifestations of a disease
PATHOLOGY
a physician specializing in pathology
PATHOLOGIST
the ability to cause a disease by overcoming host’s defenses
PATHOGENICITY
- steps or mechanisms involved in the development of a disease; disease process
PATHOGENESIS
- degree of pathogenicity •Quantitative measure of pathogenicity • Measured by the number of organisms required to cause disease •50% of lethal dose (LD50) •50% of infectious dose (ID50)
Virulence
number of organisms needed to kill half of the hosts/population
50% of lethal dose (LD50)
number of organisms needed to cause infection in half the hosts/population.
EX. -ID of Shigella is less than 100
- ID of Salmonella is about 100,000
50% of infectious dose (ID50)
study of the cause/s of disease
Etiology
environment or place of origin of the infecting agent
Reservoir
• Acquired in the HOSPITAL or other health care settings
• Causative agent is not present and not incubating in the patient on entry or admission into the health care facility
Examples: UTIs, Surgical wound infections; LRT infections, bacteremia
NOSOCOMIAL INFECTION
Staphylococcus aureus Escherichia coli Enterococcus faecalis Pseudomonas aeruginosa Most of these nosocomial pathogens are resistant to multiple antibiotics!
Bacteria most often associated w/ Nosocomial Infections
- Causative agent is present or incubating at the time of admission into the health care facility
- Ascariasis
COMMUNITY-ACQUIRED INFECTION
Results from organisms that are part of the patient’s normal flora
ENDOGENOUS INFECTION
microorganisms (bacteria, parasites, viruses, fungi, PRIONS) capable of causing an infectious disease
PATHOGENS
has the ability to infect a host w/ a healthy immune system as well as those in immunosuppressed state. Bacillus anthracis
TRUE PATHOGEN
attacks a debilitated host but presents no danger to a healthy individual. Candida albicans
-Infections of the immunocompromised hosts that do not cause a disease in individuals w/ a
normal immune system
-In immunosuppressive conditions, the host’s immune system is unable to effectively battle those microorganisms considered to be normal flora for the general population
OPPORTUNISTIC PATHOGEN
Opportunistic infections are increasing due to:
- Widespread use of broad-spectrum antibiotics that can alter normal flora
- Increased use of immunosuppressive drugs (in organ transplantation)
- Chemotherapeutic agents (cancer)
- Increased and prolonged use of urethral catheters
Individuals at risk for Opportunistic Pathogens include:
- Dialysis patients, Individuals on heart pumps
- Diabetics, burn victims
- Those w/ chronic medical problems; those undergoing invasive medical procedures
- Those w/ foreign body implants (heart valves, prosthetic devices, IV catheters)
- Alcoholics and IV drug users
Microorganisms normally residing in a particular body site; they do not usually cause an infection; also known as usual or indigenous flora
NORMAL FLORA
2 TYPES OF NORMAL FLORA
- Resident microbial flora
* Transient flora
colonize an anatomical area for months or years
• Resident microbial flora
– temporarily present at an anatomical site
• Transient flora
Distribution of normal flora
- Skin, Mouth and oral cavity, nasopharynx
- Stomach and upper small intestine, colon
- Urethra
There are anatomical sites considered to be STERILE (no normal flora):
- BLOOD,
- CEREBROSPINAL FLUID and
- URINARY BLADDER
Normal flora can become pathogenic if they are moved to another site. Examples
- E. coli of the colon (normal flora of the colon) is an important cause of UTI
- Viridans streptococcus of the mouth (normal flora of oral cavity) is a significant cause of bacterial endocarditis when established in the heart
The slightly acidic pH (5.5-6.0) results from the presence of acids produced by its normal flora:
SKIN
Common NF of skin:
- Staphylococcus spp.
- Propionibacterium acnes
- Micrococcus
- Candida
- Clostridium
- Diphtheroids
Less Common NF of skin:
- Streptococcus
- Enterococcus
- Acinetobacter
- Bacteroides
- Moraxella
- Gram negative rods
MOUTH & ORAL CAVITY
- Viridans streptococcus
- Staphylococcus epidermidis
- Neisseria (non-pathogenic spp.)
- Moraxella catarrhalis
- Lactobacilli
- Diphtheroids
Anaerobic NF include:
- Actinomyces
- Veilonella
- Bacteroides
-May serve as a site of asymptomatic carriage of several microorganisms
NASOPHARYNX
Common NF NASOPHARYNX
- Staphylococcus aureus
- Staphylococcus epidermidis
- Diphtheroids
- Haemophilus parainfluenzae
- Streptococcus
Less Common NF NASOPHARYNX
- Streptococcus pneumoniae
- Moraxella catarrhalis
- Haemophilus influenzae
- Neisseria meningitidis
- Other Moraxella spp.
Asymptomatic carriers maintain a reservoir for the organism but do NOT have an infectious disease BUT serve as an infectious source for others
- Staphylococcus aureus
* Neisseria meningitidis
-Are usually sterile containing less than 1000 organisms/ml
-Organisms entering the stomach are usually killed by HCl and gastric enzymes
-When organisms are passed in the small intestine, they may be destroyed by bile and pancreatic enzymes
-When the gastric pH increases to over 5.0, colonization from bacteria of oral, nasopharyngeal, or colon may occur
• Lactobacilli
• Bifidobacteria
STOMACH & UPPER SMALL INTESTINE
-Heavily colonized and serves as a reservoir for infection for numerous body sites, including the urinary tract and peritoneal cavity
COLON
Normal flora of Colon
- Bacteroides
- Lactobacillus
- Clostridium
- Eubacterium
- Coliforms such as Escherichia coli
- Aerobic and anaerobic streptococci
- Yeast
Normal flora of the distal urethra in both males and females may contain
- Diphtheroids
- Streptococci (alpha and non-hemolytic)
- Peptococcus
- Staphylococcus epidermidis
- Bacteroides
NF of the GUT
- Lactobacillus spp.
- Bacteroides spp.
- Clostridium spp.
- Peptostreptococcus
- S. aureus
- S. epidermidis
-Environment or the place of origin of an infecting agent is referred to
ROUTES OF INFECTION
Reservoirs:
- Humans, Animals
* Water, food, air, soil
when the host directly contacts the microbial reservoir or
DIRECT
when the host encounters the microorganism by an intervening agent
INDIRECT
The intervening agent can be a:
- Vector
* Vehicle/Fomite
living entity
Vector
non-living entity
Vehicle/Fomite
DIRECT TRANSMISSION
- Congenital contact
- Sexual contact
- Hand-to-hand contact
- Droplet infection
- May occur across the placenta or during passage at the birth canal
- Rubella virus and Treponema pallidum may be acquired during pregnancy
- Streptocccus agalactiae and Neisseria gonorrhoeae are examples of bacteria that may be transmitted to the infant during delivery
CONGENITAL/ VERTICAL
TRANSMISSION
- Serves as a route for many respiratory viruses and bacterial pathogens including:
- Streptococcus pyogenes
- Neisseria meningitidis
- Infectious secretions may come from coughing, sneezing, kissing and nasal drainage
- Respiratory secretions can become dried on clothing, bedding, or floors and converted to dust, which may serve as a route of indirect transmission
DROPLET INFECTION
Route of infection for many sexually transmitted infections (STIs)
Examples: Gonorrhea, SyphilisChlamydia, HIV InfectionHerpes, Hepatitis B infection
SEXUAL CONTACT
-Mode of direct contact seen w/ the
• spread of common cold due to rhinovirus
• transmission of GI infections (poor hand-washing, fecally contaminated hands)
HAND-TO-HAND CONTACT
- Fomites
- Ingestion of contaminated food and water
- Airborne routes
- Animal or arthropod vectors
INDIRECT TRANSMISSION
- Inanimate objects such as eating utensils, medical instruments, clothing, money, doorknobs, etc.
- Frequent routes of nosocomial infections
FOMITES
-Result of improper or poor sanitary measures
-Associated microorganisms include:
• Salmonella
• Shigella
• Escherichia coli
• Hepatitis A virus
CONTAMINATED FOOD & WATER
-Infections may be incidentally transmitted to humans through infected animals or insect (arthropod vectors) Examples:
• Rabies, Pasteurellosis, Tularemia
• Malaria, Lyme disease, Dengue fever
VECTORS
-Inhalation of infectious particles (aerosols) suspended in air. Examples:
• Tuberculosis
• Coccidioidomycosis
AIRBORNE
• High-grade, spiking fever
- Chills
- Vasodilation w/ flushing
- Increased pulse rate
Acute infection
- Intermittent, low-grade fever
- Weight loss
- Fatigue
Chronic or subacute infection
- Pain (dolor)
- Heat (calor)
- Redness (rubor)
- Swelling (tumor)
Local signs of infection
- Elevated white blood cell count
- Differential wbc count – determine the type of infection
- Increased ESR – fibrinogen enters the blood in high amounts in an inflammatory process —red cells stick together increased ESR
- Presence of C-reactive protein (infection-resisting protein)
- Presence of type-specific antibodies
Laboratory Diagnosis
– increased percentage of neutrophils
• Bacterial infections
increased percentage of lymphocytes
• Viral infections
pulmonary infiltrates, gas and swelling in tissues, accumulation of fluid in body cavities
Radiographic signs (X-ray)
number of people in a population who develop a disease during a particular period of time; an indicator of the spread of a disease; refers only to new cases
INCIDENCE
the number of people in a population who develop a disease at a specified time, regardless of when it first appeared; old and new cases of a disease
PREVALENCE
-Disease that spreads from one host to another either directly or indirectly
Ex: chickenpox, measles, genital herpes, typhoid fever and tuberculosis
COMMUNICABLE DISEASE
-Disease that easily spreads from one person to another.
Ex: measles, chickenpox
CONTAGIOUS DISEASE
SPECIFIC GROUP of signs or symptoms may always accompany a particular disease
SYNDROME
-If disease is not spread from one host to another
-Caused by microorganisms that normally inhabit the body and only occasionally produce disease.
Ex. E. coli infection
-Caused by microorganisms that reside outside the body and produce a disease only when introduced into the body.
E.g. tetanus
NON-COMMUNICABLE DISEASE
– when many immune people are present in a community that they would act as barriers to the spread of infectious agents; people who are immune will not become carriers, thereby reducing disease occurrence
HERD IMMUNITY
blood poisoning
Septicemia –
presence of bacteria in the blood
Bacteremia
presence of toxins in the blood (tetanus)
Toxemia
presence of viruses in the blood
Viremia
A definite sequence of events occurs during infection and disease
Reservoir of infection—Transmission—Invasion—Pathogenesis
source of pathogens for an infectious disease to occur
Reservoir of Infection
pathogen is transferred from the reservoir to a susceptible host
Transmission
the pathogen enters the host and multiplies
Invasion
– pathogen injures the host
- Entry
- Attachment
- Multiplication
- Invasion or Spread
- Evasion of host defenses
- Damage to host tissue/s
. Pathogenesis
Certain bacteria have specialized structures or contain substances that allow them to adhere:
- Pili
- Adherence proteins
- Biofilms
- Various protein adhesins
STAGES OF INFECTIOUS DISEASE
- Incubation stage
- Prodromal stage
- Clinical stage
- Stage of Decline
- Convalescent stage
- Time interval between the initial infection and the first appearance of any signs and symptoms.
- No signs or symptoms (s/s)
- Incubation stage
- First signs and symptoms appear
- Early, mild symptoms of disease such as general aches and malaise
- Pathogen may be highly communicable
Prodromal stage
- Peak of characteristic signs and symptoms
* Person exhibits overt signs and symptoms
Clinical stage
- Condition of host deteriorates possibly to death OR
- Signs and symptoms begin to subside as host condition improves
- Patient is vulnerable to secondary infections
Stage of Decline
- Full recovery of surviving host OR
* Chronic infection develops or death
Convalescent stage
- Innate/Natural Immunity (Non-Specific)
First Line of Defense
- Skin
- Mucous membranes
- Normal microbiota
Second Line of Defense
- Phagocytosis
* Inflammation
- Adaptive/Acquired Immunity (Specific)
- Humoral Immunity (B cells)
* Cellular Immunity (T cells)
Active Immunity
(Antigen)
Passive Immunity
(Antibody)
- Defenses that are present at birth
- Involves the 1st and 2nd lines of defense against invading microorganisms
- Occurs regardless of the type of invading organism (no specific recognition); acts against all microbes in the same way
- Does not have a memory (cannot recall previous contact w/ a foreign molecule)
Innate/Natural/Nonspecific Immunity
- Defense once microorganisms breached innate immunity
- Involves the 3rd line of defense against invading microorganisms
- Customized protection against invading microorganisms
- Has a memory (can recall previous contact w/ a foreign molecule)
Adaptive/Acquired/Specific Immunity
- The stratified and cornified epithelium serve as mechanical barriers
- Fatty acids secreted by sebaceous glands have antibacterial and antifungal properties
- Low pH (pH 3-5) due to fatty acids also has antimicrobial effect
- Desquamation of the skin surfaces – keratinized squamous epithelium
- Those capable of penetrating a normal, healthy skin are few like: leptospires, Francisella tularensis, treponemes, and some fungi
Intact Skin
- Mucous membrane of the RT is lined with cilia and covered w/ mucus w/c trap bacteria
- The RT has also lysozymes that lyse bacterial cell walls
- The GIT has hydrolytic enzymes in saliva and stomach acids that can break down bacteria
- The stomach’s low pH and presence of gastric enzymes limit the number of microbes.
Mucous Membranes
- They compete w/ pathogens for nutrients and space. This competition limit the growth of pathogens, thereby, lessening the chance for colonization – COLONIZATION RESISTANCE
- Some NF produce BACTERIOCINS that inhibit the growth of closely related bacteria
- They may SERVE A NUTRITIONAL FUNCTION. Intestinal bacteria produce several B vitamins and Vit K. Poorly nourished people who are treated w/ oral antibiotics can have vitamin deficiencies as a result of the reduction in normal flora.
Normal Microbiota
Once surface barriers have been bypassed, the host responds to microbial presence in various ways to prevent the microorganism’s multiplication and invasion to vital tissues that could result in severe damage.
- Phagocytosis
- Inflammatory response
2ND LINE OF DEFENSE
- Cells that ingest bacteria and other foreign particles by endocytosis and engulf them through their phagosome
- PMNs/ neutrophils and macrophages
- Phagocytosis is the primary mechanism in the host defense against extracellular bacteria, viruses and fungi
ACTION OF PHAGOCYTES
- Reinforcement mechanism against microbial survival and proliferation; activated by trauma / tissue injury
- Hallmark is the accumulation of large numbers of phagocytes
- Manifested by swelling, redness, heat and pain at the site of infection
- Has cellular and biochemical components:
INFLAMMATORY RESPONSE
caused by increased flow of fluid and cells to the infection site
• Swelling/Edema
continued accumulation of phagocytes
• Pus formation
results from vasodilation at the infection site
• Redness
– results from increased temperature of affected tissue
• Heat
due to tissue damage and pressure from increased flow of fluid and cells
• Pain
-involves the host’s immune system/ immune response
3RD LINE OF DEFENSE
Immunity is induced; that is, it adapts to a microbial invader
ADAPTIVE
Acts only to a specific type of invader (antigen) Customized defense against invading microorganisms
SPECIFIC
Immunity is developed only after exposure to a suitable antigen; or after transfer of antibodies
ACQUIRED
“nonself” or foreign substances made up proteins, nucleoproteins, polysaccharides and some glycolipids to which antibodies respond
Antigens
“self” substances or immunoglobulins that are made up of glycoproteins present in serum and tissue fluids; produced by B cells
Antibodies
- Group of cells, molecules, and organs that act together to defend the host against foreign invaders
- Customized defense against invading microorganisms
- Has a “MEMORY” so that if a microorganism is encountered a 2nd or 3rd time, an immune-mediated defensive response is immediately available
IMMUNE SYSTEM
- ANTIBODIES OR IMMUNOGLOBULINS
- Central molecule of the immune response
- Specific proteins produced by B cells in response to antigens
- Circulate in serum and are present in secretions
- 2 active areas: Ag binding site and phagocyte binding site
COMPONENTS OF THE IMMUNE SYSTEM
5 classes of immunoglobulins
IgG, IgA, IgM, IgE, IgD
TWO ARMS OF THE IMMUNE SYSTEM
- HUMORAL IMMUNITY
- CELL-MEDIATED IMMUNITY
- Mediated by by B cells
- Centered on the production of antibodies
- Becomes activated upon encounter w/ an antigen
HUMORAL IMMUNITY
- Helping phagocytic action
- Neutralizing microbial toxins
- Promoting bacterial clumping (agglutination)
- Inhibiting bacterial motility
- Combining w/ microorganisms to activate the complement system and inflammatory response
Antibodies protect the host by
- Mediated by T cells
- T cells recognize and destroy human host cells infected w/ microorganisms that are able to survive Ab action
- T cells are activated by interaction w/ other cells that process microbial Ags and present them on their surface (eg macrophages and B cells)
CELL-MEDIATED IMMUNITY
CELLULAR COMPONENTS OF THE IMMUNE RESPONSE
- B cells.
2. T cells
TYPES OF ACQUIRED IMMUNITY
PASSIVELY ACQUIRED IMMUNITY
ACTIVELY ACQUIRED IMMUNITY
• Temporary resistance to infectious agents by administration of preformed ANTIBODIES
• The host DOES NOT PRODUCE ANTIBODIES since preformed Abs are already given
Examples: gamma globulin and antitoxin to Clostridium botulinum toxin;
fetus acquiring mother’s Abs through blood during gestation;
newborns acquiring Abs from mother’s breastmilk
PASSIVELY ACQUIRED IMMUNITY
• Resistance to infectious agents by contact/administration of an ANTIGEN
• The host PRODUCES ANTIBODY in reaction to antigens
Examples: infectious process/ active infection immunization (injection of live attenuated microorganisms or its components)
ACTIVELY ACQUIRED IMMUNITY
Factors that provide a microorganism w/ the capacity to:
Damage host cells, tissues and organs
Avoid host defenses
VIRULENCE FACTORS
What are these virulence factors?
- Attachment
- Invasion
- Survival against inflammation
- Survival against immune system
- Microbial toxins
Microbial activities contributing to colonization of Host Surfaces
- Survival against environmental conditions
- Attachment and adherence to host cell surfaces
- Motility
- Production of substances that compete w/ host for acquisition of essential nutrients
- Ability to co-exist w/ other colonizing microorganisms
Factors contributing to disruption of skin and mucosal surface
- Trauma
- Inhalation
- Implantation of medical devices
- Other diseases
- Childbirth
- Overuse of antibiotics
Microbial strategies for surviving inflammation
- Avoid killing by phagocytes
2. Avoid effects of the complement system
MAJOR MECHANISMS BY WHICH PATHOGENS CAUSE DISEASE
- Exoenzymes
2. Toxins
– enzymes released by pathogens enabling them to:
• Evade host defense mechanisms
• Cause damage to body tissues
Exoenzymes
poisonous biochemically active substances released by microbes.
Toxins
released by Gram (-) bacteria
• Capable of inducing fever;
• Have devastating effects on the host’s metabolism e.g. endotoxic shock
Endotoxins
released by Gram (+) and Gram (-) bacteria
• Not associated w/ the production of fever
• Effects tend to be more limited and specific than endotoxins
Exotoxins
– destroy tissues. Examples:
• Proteases by flesh eating strains of Streptococcus pyogenes
• Proteases and lipases by Clostridium species cause gas gangrene
Necrotizing enzymes
forms clots; identifying feature of Staphylococcus aureus;
• binds to prothrombin producing staphylothrombin causing conversion of fibrinogen to fibrin
• Enables Staphylococcus aureus to clot plasma forming a sticky coat of fibrin around themselves for protection
Coagulase
lyse or dissolve clots, thereby enabling them to escape clots
• Streptokinase – by Streptococci
• Staphylokinase – by Staphylococci
Kinases /Fibrinolysins
“spreading factor”; enables pathogens to spread through connective tissues by breaking down hyaluronic acid, the polysaccharide “cement” that holds tissue cells together
• Secreted by several pathogenic species of Staphylococci, Streptococci and Clostridia
Hyaluronidase
breaks down collagen; Clostridium perfringens spreads deeply within the body secreting both collagenase and hyaluronidase
Collagenase
cause damage to erythrocytes and also a source of Fe to pathogens
Hemolysins
breaks down lecithin hence destroying rapidly extensive areas of tissue, esp. muscle tissues (C. perfringens); destructive to cell membranes of rbcs and other tissues
Lecithinase
from the outer membrane of Gram negative bacteria (LPS); very toxic
• Lipid A/endotoxin
chills, fever, rapid breathing, reduced mental alertness, confusion; as shock worsens several organs begin to fail, blood clots may form within blood vessels
• Endotoxic shock/Septic shock
- Lipid A/endotoxin
- Endotoxic shock/Septic shock
- 30-35% mortality rate
ENDOTOXINS
Neurotoxins
Enterotoxins
Exfoliative /Epidermolytic toxins
EXOTOXINS
– affect CNS; most potent among exotoxins
Neurotoxins
affects control of nerve transmission leading to spastic rigid type of paralysis (muscle contraction)
• Tetanospasmin (C. tetani)
blocks nerve impulses leading to generalized, flaccid type paralysis (muscles are relaxed)
• Botulinal toxin (C. botulinum)
affect GIT, causing diarrhea and vomiting. Examples are: • Bacillus cereus • Certain serotypes of Escherichia coli • Clostridium difficile • Clostridium perfringens • Salmonella spp. • Shigella spp. • Some strains of S.aureus
Enterotoxins
causes epidermal layers to slough away leading to a disease called Scalded Skin Syndrome
Exfoliative /Epidermolytic toxins
TSST-1) caused by S. aureus and less
commonly S. pyogenes primarily affect
integrity of capillary walls
Toxic Shock Syndrome toxin
destroy wbcs; produced by Staph, Strep and Clostridia
• Leukocidins
causes scarlet fever by some strains of S. pyogenes
• Erythrogenic toxin
by C. diphtheriae; inhibits CHON synthesis; kills mucosal cells and phagocytes and adversely affects the heart and nervous system
• Diphtheria toxin
- Shiga toxin (Shigella spp.)
- P. aeruginosa toxin (Pseudomonas aeruginosa)
- Shiga-like toxins (certain serotypes of E. coli)
Other toxins which inhibit CHON synthesis are