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BACTERIOLOGY > INFECTION AND IMMUNITY > Flashcards

INFECTION AND IMMUNITY Flashcards

1
Q

entrance and multiplication of a microorganism in or on a host

A

INFECTION

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2
Q

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

A

INFECTIOUS DISEASE

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3
Q

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

A

COLONIZATION

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4
Q

a microbe capable of causing a disease

A

PATHOGEN

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5
Q

study of the structural and functional manifestations of a disease

A

PATHOLOGY

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6
Q

a physician specializing in pathology

A

PATHOLOGIST

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7
Q

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

A

PATHOGENICITY

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8
Q
  • steps or mechanisms involved in the development of a disease; disease process
A

PATHOGENESIS

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9
Q 
- 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)
A

Virulence

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10
Q

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

A

50% of lethal dose (LD50)

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11
Q

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

A

50% of infectious dose (ID50)

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12
Q

study of the cause/s of disease

A

Etiology

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13
Q

environment or place of origin of the infecting agent

A

Reservoir

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14
Q

• 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

A

NOSOCOMIAL INFECTION

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15
Q 
	Staphylococcus aureus
	Escherichia coli
	Enterococcus faecalis
	Pseudomonas aeruginosa
	Most of these nosocomial pathogens are resistant to multiple antibiotics!
A

Bacteria most often associated w/ Nosocomial Infections

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16
Q
  • Causative agent is present or incubating at the time of admission into the health care facility
  • Ascariasis
A

COMMUNITY-ACQUIRED INFECTION

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17
Q

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

A

ENDOGENOUS INFECTION

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18
Q

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

A

PATHOGENS

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19
Q

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

A

TRUE PATHOGEN

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20
Q

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

A

OPPORTUNISTIC PATHOGEN

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21
Q

Opportunistic infections are increasing due to:

A
  1. Widespread use of broad-spectrum antibiotics that can alter normal flora
  2. Increased use of immunosuppressive drugs (in organ transplantation)
  3. Chemotherapeutic agents (cancer)
  4. Increased and prolonged use of urethral catheters
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22
Q

Individuals at risk for Opportunistic Pathogens include:

A
  • 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
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23
Q

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

A

NORMAL FLORA

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24
Q

2 TYPES OF NORMAL FLORA

A
  • Resident microbial flora

* Transient flora

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25
Q

colonize an anatomical area for months or years

A

• Resident microbial flora

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26
Q

– temporarily present at an anatomical site

A

• Transient flora

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27
Q

Distribution of normal flora

A
  • Skin, Mouth and oral cavity, nasopharynx
  • Stomach and upper small intestine, colon
  • Urethra
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28
Q

There are anatomical sites considered to be STERILE (no normal flora):

A
  • BLOOD,
  • CEREBROSPINAL FLUID and
  • URINARY BLADDER
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29
Q

Normal flora can become pathogenic if they are moved to another site. Examples

A
  • 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
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30
Q

The slightly acidic pH (5.5-6.0) results from the presence of acids produced by its normal flora:

A

SKIN

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31
Q

Common NF of skin:

A
  • Staphylococcus spp.
  • Propionibacterium acnes
  • Micrococcus
  • Candida
  • Clostridium
  • Diphtheroids
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32
Q

Less Common NF of skin:

A
  • Streptococcus
  • Enterococcus
  • Acinetobacter
  • Bacteroides
  • Moraxella
  • Gram negative rods
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33
Q

MOUTH & ORAL CAVITY

A
  • Viridans streptococcus
  • Staphylococcus epidermidis
  • Neisseria (non-pathogenic spp.)
  • Moraxella catarrhalis
  • Lactobacilli
  • Diphtheroids
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34
Q

Anaerobic NF include:

A
  • Actinomyces
  • Veilonella
  • Bacteroides
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35
Q

-May serve as a site of asymptomatic carriage of several microorganisms

A

NASOPHARYNX

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36
Q

Common NF NASOPHARYNX

A
  • Staphylococcus aureus
  • Staphylococcus epidermidis
  • Diphtheroids
  • Haemophilus parainfluenzae
  • Streptococcus
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37
Q

Less Common NF NASOPHARYNX

A
  • Streptococcus pneumoniae
  • Moraxella catarrhalis
  • Haemophilus influenzae
  • Neisseria meningitidis
  • Other Moraxella spp.
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38
Q

Asymptomatic carriers maintain a reservoir for the organism but do NOT have an infectious disease BUT serve as an infectious source for others

A
  • Staphylococcus aureus

* Neisseria meningitidis

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39
Q

-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

A

STOMACH & UPPER SMALL INTESTINE

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40
Q

-Heavily colonized and serves as a reservoir for infection for numerous body sites, including the urinary tract and peritoneal cavity

A

COLON

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41
Q

Normal flora of Colon

A
  • Bacteroides
  • Lactobacillus
  • Clostridium
  • Eubacterium
  • Coliforms such as Escherichia coli
  • Aerobic and anaerobic streptococci
  • Yeast
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42
Q

Normal flora of the distal urethra in both males and females may contain

A
  • Diphtheroids
  • Streptococci (alpha and non-hemolytic)
  • Peptococcus
  • Staphylococcus epidermidis
  • Bacteroides
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43
Q

NF of the GUT

A
  • Lactobacillus spp.
  • Bacteroides spp.
  • Clostridium spp.
  • Peptostreptococcus
  • S. aureus
  • S. epidermidis
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44
Q

-Environment or the place of origin of an infecting agent is referred to

A

ROUTES OF INFECTION

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45
Q

Reservoirs:

A
  • Humans, Animals

* Water, food, air, soil

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46
Q

when the host directly contacts the microbial reservoir or

A

DIRECT

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47
Q

when the host encounters the microorganism by an intervening agent

A

INDIRECT

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48
Q

The intervening agent can be a:

A
  • Vector

* Vehicle/Fomite

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49
Q

living entity

A

Vector

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50
Q

non-living entity

A

Vehicle/Fomite

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51
Q

DIRECT TRANSMISSION

A
  • Congenital contact
  • Sexual contact
  • Hand-to-hand contact
  • Droplet infection
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52
Q
  • 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
A

CONGENITAL/ VERTICAL

TRANSMISSION

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53
Q
  • 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
A

DROPLET INFECTION

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54
Q

Route of infection for many sexually transmitted infections (STIs)
Examples: Gonorrhea, SyphilisChlamydia, HIV InfectionHerpes, Hepatitis B infection

A

SEXUAL CONTACT

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55
Q

-Mode of direct contact seen w/ the
• spread of common cold due to rhinovirus
• transmission of GI infections (poor hand-washing, fecally contaminated hands)

A

HAND-TO-HAND CONTACT

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56
Q
  • Fomites
  • Ingestion of contaminated food and water
  • Airborne routes
  • Animal or arthropod vectors
A

INDIRECT TRANSMISSION

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57
Q
  • Inanimate objects such as eating utensils, medical instruments, clothing, money, doorknobs, etc.
  • Frequent routes of nosocomial infections
A

FOMITES

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58
Q

-Result of improper or poor sanitary measures
-Associated microorganisms include:
• Salmonella
• Shigella
• Escherichia coli
• Hepatitis A virus

A

CONTAMINATED FOOD & WATER

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59
Q

-Infections may be incidentally transmitted to humans through infected animals or insect (arthropod vectors) Examples:
• Rabies, Pasteurellosis, Tularemia
• Malaria, Lyme disease, Dengue fever

A

VECTORS

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60
Q

-Inhalation of infectious particles (aerosols) suspended in air. Examples:
• Tuberculosis
• Coccidioidomycosis

A

AIRBORNE

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61
Q

• High-grade, spiking fever

  • Chills
  • Vasodilation w/ flushing
  • Increased pulse rate
A

Acute infection

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62
Q
  • Intermittent, low-grade fever
  • Weight loss
  • Fatigue
A

Chronic or subacute infection

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63
Q
  • Pain (dolor)
  • Heat (calor)
  • Redness (rubor)
  • Swelling (tumor)
A

Local signs of infection

64
Q
  • 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
A

Laboratory Diagnosis

65
Q

– increased percentage of neutrophils

A

• Bacterial infections

66
Q

increased percentage of lymphocytes

A

• Viral infections

67
Q

pulmonary infiltrates, gas and swelling in tissues, accumulation of fluid in body cavities

A

Radiographic signs (X-ray)

68
Q

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

A

INCIDENCE

69
Q

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

A

PREVALENCE

70
Q

-Disease that spreads from one host to another either directly or indirectly
Ex: chickenpox, measles, genital herpes, typhoid fever and tuberculosis

A

COMMUNICABLE DISEASE

71
Q

-Disease that easily spreads from one person to another.

Ex: measles, chickenpox

A

CONTAGIOUS DISEASE

72
Q

SPECIFIC GROUP of signs or symptoms may always accompany a particular disease

A

SYNDROME

73
Q

-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

A

NON-COMMUNICABLE DISEASE

74
Q

– 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

A

HERD IMMUNITY

75
Q

blood poisoning

A

Septicemia –

76
Q

presence of bacteria in the blood

A

Bacteremia

77
Q

presence of toxins in the blood (tetanus)

A

Toxemia

78
Q

presence of viruses in the blood

A

Viremia

79
Q

A definite sequence of events occurs during infection and disease

A

Reservoir of infection—Transmission—Invasion—Pathogenesis

80
Q

source of pathogens for an infectious disease to occur

A

Reservoir of Infection

81
Q

pathogen is transferred from the reservoir to a susceptible host

A

Transmission

82
Q

the pathogen enters the host and multiplies

A

Invasion

83
Q

– 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
A

. Pathogenesis

84
Q

Certain bacteria have specialized structures or contain substances that allow them to adhere:

A
  • Pili
  • Adherence proteins
  • Biofilms
  • Various protein adhesins
85
Q

STAGES OF INFECTIOUS DISEASE

A
  1. Incubation stage
  2. Prodromal stage
  3. Clinical stage
  4. Stage of Decline
  5. Convalescent stage
86
Q
  • Time interval between the initial infection and the first appearance of any signs and symptoms.
  • No signs or symptoms (s/s)
A
  1. Incubation stage
87
Q
  • First signs and symptoms appear
  • Early, mild symptoms of disease such as general aches and malaise
  • Pathogen may be highly communicable
A

Prodromal stage

88
Q
  • Peak of characteristic signs and symptoms

* Person exhibits overt signs and symptoms

A

Clinical stage

89
Q
  • Condition of host deteriorates possibly to death OR
  • Signs and symptoms begin to subside as host condition improves
  • Patient is vulnerable to secondary infections
A

Stage of Decline

90
Q
  • Full recovery of surviving host OR

* Chronic infection develops or death

A

Convalescent stage

91
Q
  1. Innate/Natural Immunity (Non-Specific)

First Line of Defense

A
  • Skin
  • Mucous membranes
  • Normal microbiota
92
Q

Second Line of Defense

A
  • Phagocytosis

* Inflammation

93
Q
  1. Adaptive/Acquired Immunity (Specific)
A
  • Humoral Immunity (B cells)

* Cellular Immunity (T cells)

94
Q

Active Immunity

A

(Antigen)

95
Q

Passive Immunity

A

(Antibody)

96
Q
  • 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)
A

Innate/Natural/Nonspecific Immunity

97
Q
  • 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)
A

Adaptive/Acquired/Specific Immunity

98
Q
  • 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
A

Intact Skin

99
Q
  • 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.
A

Mucous Membranes

100
Q
  • 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.
A

Normal Microbiota

101
Q

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
A

2ND LINE OF DEFENSE

102
Q
  • 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
A

ACTION OF PHAGOCYTES

103
Q
  • 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:
A

INFLAMMATORY RESPONSE

104
Q

caused by increased flow of fluid and cells to the infection site

A

• Swelling/Edema

105
Q

continued accumulation of phagocytes

A

• Pus formation

106
Q

results from vasodilation at the infection site

A

• Redness

107
Q

– results from increased temperature of affected tissue

A

• Heat

108
Q

due to tissue damage and pressure from increased flow of fluid and cells

A

• Pain

109
Q

-involves the host’s immune system/ immune response

A

3RD LINE OF DEFENSE

110
Q

Immunity is induced; that is, it adapts to a microbial invader

A

ADAPTIVE

111
Q

Acts only to a specific type of invader (antigen) Customized defense against invading microorganisms

A

SPECIFIC

112
Q

Immunity is developed only after exposure to a suitable antigen; or after transfer of antibodies

A

ACQUIRED

113
Q

“nonself” or foreign substances made up proteins, nucleoproteins, polysaccharides and some glycolipids to which antibodies respond

A

Antigens

114
Q

“self” substances or immunoglobulins that are made up of glycoproteins present in serum and tissue fluids; produced by B cells

A

Antibodies

115
Q
  • 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
A

IMMUNE SYSTEM

116
Q
  • 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
A

COMPONENTS OF THE IMMUNE SYSTEM

117
Q

5 classes of immunoglobulins

A

IgG, IgA, IgM, IgE, IgD

118
Q

TWO ARMS OF THE IMMUNE SYSTEM

A
  • HUMORAL IMMUNITY

- CELL-MEDIATED IMMUNITY

119
Q
  • Mediated by by B cells
  • Centered on the production of antibodies
  • Becomes activated upon encounter w/ an antigen
A

HUMORAL IMMUNITY

120
Q
  • Helping phagocytic action
  • Neutralizing microbial toxins
  • Promoting bacterial clumping (agglutination)
  • Inhibiting bacterial motility
  • Combining w/ microorganisms to activate the complement system and inflammatory response
A

Antibodies protect the host by

121
Q
  • 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)
A

CELL-MEDIATED IMMUNITY

122
Q

CELLULAR COMPONENTS OF THE IMMUNE RESPONSE

A
  1. B cells.

2. T cells

123
Q

TYPES OF ACQUIRED IMMUNITY

A

PASSIVELY ACQUIRED IMMUNITY

ACTIVELY ACQUIRED IMMUNITY

124
Q

• 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

A

PASSIVELY ACQUIRED IMMUNITY

125
Q

• 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)

A

ACTIVELY ACQUIRED IMMUNITY

126
Q

Factors that provide a microorganism w/ the capacity to:
Damage host cells, tissues and organs
Avoid host defenses

A

VIRULENCE FACTORS

127
Q

What are these virulence factors?

A
  1. Attachment
  2. Invasion
  3. Survival against inflammation
  4. Survival against immune system
  5. Microbial toxins
128
Q

Microbial activities contributing to colonization of Host Surfaces

A
  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
129
Q

Factors contributing to disruption of skin and mucosal surface

A
  1. Trauma
  2. Inhalation
  3. Implantation of medical devices
  4. Other diseases
  5. Childbirth
  6. Overuse of antibiotics
130
Q

Microbial strategies for surviving inflammation

A
  1. Avoid killing by phagocytes

2. Avoid effects of the complement system

131
Q

MAJOR MECHANISMS BY WHICH PATHOGENS CAUSE DISEASE

A
  1. Exoenzymes

2. Toxins

132
Q

– enzymes released by pathogens enabling them to:
• Evade host defense mechanisms
• Cause damage to body tissues

A

Exoenzymes

133
Q

poisonous biochemically active substances released by microbes.

A

Toxins

134
Q

released by Gram (-) bacteria
• Capable of inducing fever;
• Have devastating effects on the host’s metabolism e.g. endotoxic shock

A

Endotoxins

135
Q

released by Gram (+) and Gram (-) bacteria
• Not associated w/ the production of fever
• Effects tend to be more limited and specific than endotoxins

A

Exotoxins

136
Q

– destroy tissues. Examples:
• Proteases by flesh eating strains of Streptococcus pyogenes
• Proteases and lipases by Clostridium species cause gas gangrene

A

Necrotizing enzymes

137
Q

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

A

Coagulase

138
Q

lyse or dissolve clots, thereby enabling them to escape clots
• Streptokinase – by Streptococci
• Staphylokinase – by Staphylococci

A

Kinases /Fibrinolysins

139
Q

“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

A

Hyaluronidase

140
Q

breaks down collagen; Clostridium perfringens spreads deeply within the body secreting both collagenase and hyaluronidase

A

Collagenase

141
Q

cause damage to erythrocytes and also a source of Fe to pathogens

A

Hemolysins

142
Q

breaks down lecithin hence destroying rapidly extensive areas of tissue, esp. muscle tissues (C. perfringens); destructive to cell membranes of rbcs and other tissues

A

Lecithinase

143
Q

from the outer membrane of Gram negative bacteria (LPS); very toxic

A

• Lipid A/endotoxin

144
Q

chills, fever, rapid breathing, reduced mental alertness, confusion; as shock worsens several organs begin to fail, blood clots may form within blood vessels

A

• Endotoxic shock/Septic shock

145
Q
  • Lipid A/endotoxin
  • Endotoxic shock/Septic shock
  • 30-35% mortality rate
A

ENDOTOXINS

146
Q

Neurotoxins
Enterotoxins
Exfoliative /Epidermolytic toxins

A

EXOTOXINS

147
Q

– affect CNS; most potent among exotoxins

A

Neurotoxins

148
Q

affects control of nerve transmission leading to spastic rigid type of paralysis (muscle contraction)

A

• Tetanospasmin (C. tetani)

149
Q

blocks nerve impulses leading to generalized, flaccid type paralysis (muscles are relaxed)

A

• Botulinal toxin (C. botulinum)

150
Q 
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
A

Enterotoxins

151
Q

causes epidermal layers to slough away leading to a disease called Scalded Skin Syndrome

A

Exfoliative /Epidermolytic toxins

152
Q

TSST-1) caused by S. aureus and less
commonly S. pyogenes primarily affect
integrity of capillary walls

A

Toxic Shock Syndrome toxin

153
Q

destroy wbcs; produced by Staph, Strep and Clostridia

A

• Leukocidins

154
Q

causes scarlet fever by some strains of S. pyogenes

A

• Erythrogenic toxin

155
Q

by C. diphtheriae; inhibits CHON synthesis; kills mucosal cells and phagocytes and adversely affects the heart and nervous system

A

• Diphtheria toxin

156
Q
  • Shiga toxin (Shigella spp.)
  • P. aeruginosa toxin (Pseudomonas aeruginosa)
  • Shiga-like toxins (certain serotypes of E. coli)
A

Other toxins which inhibit CHON synthesis are

BACTERIOLOGY (6 decks)

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