INFECTION AND IMMUNITY Flashcards by Christha Cabusas

entrance and multiplication of a microorganism in or on a host

INFECTION

How well did you know this?

Not at all

Perfectly

an infection w/ functional and structural harm to the host that is usually accompanied by signs and symptoms

INFECTIOUS DISEASE

How well did you know this?

Not at all

Perfectly

presence and multiplication of new microorganisms that may cause an infectious disease or eliminated by host defense

COLONIZATION

How well did you know this?

Not at all

Perfectly

a microbe capable of causing a disease

PATHOGEN

How well did you know this?

Not at all

Perfectly

study of the structural and functional manifestations of a disease

PATHOLOGY

How well did you know this?

Not at all

Perfectly

a physician specializing in pathology

PATHOLOGIST

How well did you know this?

Not at all

Perfectly

the ability to cause a disease by overcoming host’s defenses

PATHOGENICITY

How well did you know this?

Not at all

Perfectly

steps or mechanisms involved in the development of a disease; disease process

PATHOGENESIS

How well did you know this?

Not at all

Perfectly

- 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

How well did you know this?

Not at all

Perfectly

number of organisms needed to kill half of the hosts/population

50% of lethal dose (LD50)

How well did you know this?

Not at all

Perfectly

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)

How well did you know this?

Not at all

Perfectly

study of the cause/s of disease

Etiology

How well did you know this?

Not at all

Perfectly

environment or place of origin of the infecting agent

Reservoir

How well did you know this?

Not at all

Perfectly

• 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

How well did you know this?

Not at all

Perfectly

	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

How well did you know this?

Not at all

Perfectly

Causative agent is present or incubating at the time of admission into the health care facility
Ascariasis

COMMUNITY-ACQUIRED INFECTION

How well did you know this?

Not at all

Perfectly

Results from organisms that are part of the patient’s normal flora

ENDOGENOUS INFECTION

How well did you know this?

Not at all

Perfectly

microorganisms (bacteria, parasites, viruses, fungi, PRIONS) capable of causing an infectious disease

PATHOGENS

How well did you know this?

Not at all

Perfectly

has the ability to infect a host w/ a healthy immune system as well as those in immunosuppressed state. Bacillus anthracis

TRUE PATHOGEN

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

Microorganisms normally residing in a particular body site; they do not usually cause an infection; also known as usual or indigenous flora

NORMAL FLORA

How well did you know this?

Not at all

Perfectly

2 TYPES OF NORMAL FLORA

Resident microbial flora

* Transient flora

How well did you know this?

Not at all

Perfectly

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 1. Entry 2. Attachment 3. Multiplication 4. Invasion or Spread 5. Evasion of host defenses 6. 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

1. Incubation stage 2. Prodromal stage 3. Clinical stage 4. Stage of Decline 5. Convalescent stage

* Time interval between the initial infection and the first appearance of any signs and symptoms. * No signs or symptoms (s/s)

1. 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

1. Innate/Natural Immunity (Non-Specific) | First Line of Defense

* Skin * Mucous membranes * Normal microbiota

Second Line of Defense

* Phagocytosis | * Inflammation

2. 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. 1. Phagocytosis 2. 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

1. 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?

1. Attachment 2. Invasion 3. Survival against inflammation 4. Survival against immune system 5. Microbial toxins

Microbial activities contributing to colonization of Host Surfaces

1. Survival against environmental conditions 2. Attachment and adherence to host cell surfaces 3. Motility 4. Production of substances that compete w/ host for acquisition of essential nutrients 5. Ability to co-exist w/ other colonizing microorganisms

Factors contributing to disruption of skin and mucosal surface

1. Trauma 2. Inhalation 3. Implantation of medical devices 4. Other diseases 5. Childbirth 6. Overuse of antibiotics

Microbial strategies for surviving inflammation

1. Avoid killing by phagocytes | 2. Avoid effects of the complement system

MAJOR MECHANISMS BY WHICH PATHOGENS CAUSE DISEASE

1. 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

INFECTION AND IMMUNITY Flashcards

(156 cards)